Science

 

TABLE OF CONTENTS

Omega-3 science and studies on PUFA (poly-unsaturated-fatty-acids) are continuously updated here! Please keep checking in! We suggest that if you are searching for a specific condition please use ‘ctrl F’ to search or use the table of contents.

TABLE OF CONTENTS

 

 

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Here is a list of Important Functions that rely on proper availability of Omega-3 fatty acids IN YOUR diet:

 

Heart Health, Heart Health, Heart Health – YOUR HEART cannot function without making energy. Energy in the form of ATP is produced in healthy mitochondria relying on omega-3 function!  Meta-analyses of prospective cohort studies indicate that fish consumption is inversely associated with the risk of heart failure.

 

Conclusions: This meta-analysis is consistent with a lower risk of heart failure with intake of marine omega-3 fatty acids. 

This comes at no surprise because Without omega-3 your mitochondria are dying!

Omega3 and Vitamin D are now considered a NEUTRACEUTICAL!

A nutraceutical is a term derived from the combination of the words “nutrition” and “pharmaceutical.” It refers to a food or food component that provides health benefits beyond basic nutritional value, often with the potential to prevent or treat various diseases and health conditions. Nutraceuticals can be naturally occurring in foods or created through a manufacturing process and added to foods or consumed as supplements.

Omega3 has direct effects on: Vision and eye health, Immune Function and Inflammation control, Cell division, Mitochondrial energy production, Liver Detoxification, Reproduction, Brain and Nerve health, Wound Healing and Stem Cell function, Bone-Tendon-Muscle Regeneration, Heart and Lung health, Athletic performance, Digestion, Blood pressure and Kidney Health, Sugar metabolism, Hearing, Memory, Mental Clarity and many more. REDUCTION of  INFLAMATION lies at the center of the mechanism of these chronic diseases!

All modern Nutrition agrees: “Including a variety of omega-3-rich fish in your diet provides numerous health benefits, such as improved cardiovascular health, reduced inflammation, and better cognitive function.”

Omega-3 is essential – How can I get omega-3 in my diet?

Only “grazing-animals” and cold water fish can extract omega3-DHA from algae. Plants do not make make DHA or EPA, some seeds contain ALA (which your body can convert to DHA but only at max 5% and only if your enzymes are working properly! So the best source of proper omega3 is from properly harvested and stabilized fish oil however vegan omega3 oils are available as well. Cattle has to be grass fed and ‘grass finished’ not subjected to a feed lot.

Daley 2010: showed that the omega6/3 index in grass-fed beef is below 2:1 whereas grain-fed can go up as high as 10:1 (Table2). 

 

“YOU ARE WHAT YOU EAT”

 

Table of Contents

 

 

Terminology and abbreviations: FO= fish oil.; PUFA=polyunsaturated fatty acids; Omega-3= ω-3 fatty acids; DHA=Docosahexaenoic acid; RCT=randomly controlled trial (placebo controlled study); MUFA=monounsaturated fatty acids; n6= ω-6=omega6; n3=omega3; SFA=saturated fatty acids; HSF=high saturated fatty acids

EPA=Eicosapentaenoicacid; ALA= Alpha-linolenic acid; Linoleicacid(LA); Arachidonicacid(AA).

1. Introduction: THE DILEMMA – Omega3 fatty acids oxidize quickly and turn rancid

Dilemma #1 Certainly, whole foods should provide the best nutrition. However the reality is that we now consume massive amounts of inflammatory omega6 and our food is devoid of many nutrients due to over farming and processing. Even so-called ‘natural foods’ have to be processed by FDA standards.

Dilemma #2 natural sources of omega3 are simply hard to find because access to fresh fish is rare and grass fed beef loses its omega3 content on the “feed lot”.

Dilemma #3 our tests reveal that most supplements are rancid and provide inadequate amounts of EPA and DHA and 97% of the populations even in traditional fishing countries such as Norway and Taiwan are up to 95% omega3 deficient and end up highly inflammatory.

Dilemma #4 the omega6/3 inflammatory index has been officially adopted into medical science for decades but yet today it is not part of routine blood work. This leaves us in the dark of how to assess other tested inflammatory markers ! Schaky 2007: An omega-3 index of >8% is associated with 90% less risk for sudden cardiac death, as compared to an omega-3 index of <4%.

Dilemma #5 many omega3 studies are done with inadequate and rancid supplements which leaves average consumers questioning. However once a study is done with fresh fish and clearly looks at the omega6/3 index there is a near 100% correlation of omega3 deficiency and inflammation, forming a link to modern chronic disease.

 

Humans are unable to convert omega3 directly from Algae. We rely on the consumption of grazing animals (ruminants) or cold water fish. A constant steady supply of fresh omega3 in our diet is essential to US and our house pets health.

1) Grass fed cows are put on a feed lot – you would have to consume (daily) “grass fed – grass finished” beef

2) Only FRESH cold water fish, krill or roe have high amounts of omega3 – once frozen or processed omega3 content is lost and altered. Although when done properly flash freezing at -80C showed little effect on omega3 content the process leads to an increase in LPL (lysophospholipids) and in free fatty acids accompanied by formation of polar (presumably oxidized) material. Farmed fish does not have access to the necessary algae:  Levels of EPA and DHA in farmed fish have more than halved in the last 20 years.

3) Traditional Pressed oils such as flax seed oil turn rancid quickly and supply only Alpha-linolenic acid but many people cannot convert ALA to vital EPA and DHA anymore.

4) At the same time our intake of inflammatory omega6 has exponentially increased – our test show a very high ratio of omega 6/3.

5) Many people also test deficient in saturated stearic acid (despite the fact the body can synthesize it). People have been told not to consume fatty red meats for over 70 years now. This is a strange suggestion that humans grew up on red meat for over 100000 years. With the exception of coconut, plant oils contain mostly palmitic acid. Stearic acid is shown to be vital for heart functions.

6) Supplements that are not tested for stability especially in pill form are highly rancid. You can simply open a gel capsule let it sit for 5 min and smell its rancidity. These oxidized fish oils are potentially harmful. For Zinzino TOTOX values check below. Supplements are mostly rancid and test badly in many 3rd party laboratories. The aldehyde and ketones give them the unpleasant taste similar to rotten fish and cause burping and indigestion. That is why most supplements are sold in gel caps so you cannot tell unless you open up the pills.

A recent 3rd party test revealed how many supplements are below acceptable standards.

For that reason, Zinzino balance oil is stabilized with phenolic acids in a proprietary formula. It is tested and the results show!

 

 

Here is a short summary of what the long term studies shows:

The FACTS:

→ Western diets are NOW  HIGHLY deficient in omega-3 fatty acids, and have excessive amounts of omega-6 fatty acids compared with the diet on which human beings evolved and their genetic patterns we established. The reasons why we are so deficient in modern times are explained below.

 Watkins and Cordain conducted detailed chemical analysis of the meats people ate up to 10,000 years ago and compared those results to the most common meats people consume today. They found that wild game, such as venison or elk meat, as well as grass-fed beef, contain a mixture of omega 6 and 3 fats that are actually healthy for you and could reduce chronic disease risk (closer to 1:1). Our genome cannot adjust quick enough for the modern changes in our diet with a very low omega-3 intake.

Cordain says anthropological nutritionists have studied isolated hunter-gatherer societies – such as the Nanamiut of Alaska, the Aborigines of Australia and Africa and found that modern disease, such as heart disease, high cholesterol, obesity and diabetes, are rare in these populations.

“Over the past several decades, numerous studies have found that indigenous populations have low serum cholesterol and triglyceride levels,” Cordain says.

There is no doubt that humans were hunters and gatherers for over 200,000 years and have only very recently started farming, ca 9,500BC.

Thousands of studies have indicated that a healthy diet should contain a balance of essential fats. Omega-3 fatty acids, which are often found in high levels in cold water fish, have been shown to reduce the risk of cardiovascular disease. In contrast Omega-6 fatty acid is also is an essential fat, but excess consumption can contribute to inflammatory responses associated with chronic diseases.

At least since 2004 the Omega6/3 index for the purpose of clinical studies was established! The relationship between this marker and risk for eg. CHD death, especially sudden cardiac death (SCD), was since evaluated in many published primary and secondary prevention studies. However not much has happened. Neither is there an established need determined for Omega3 nor has the omega6/3 index become part of the ‘standard of medical care’.

Global recommendations for long-chain omega-3 fatty acids underscore the pressing need to establish Dietary Reference Intake (DRI) for DHA and EPA because DRIs are recognized as the “official” standard by which federal agencies issue dietary guidance or policy directives for the health and well-being of individuals in the United States and Canada. Because of the many health benefits of DHA and EPA, it is important and timely that the National Academies establish DRIs for the individual long-chain (20 carbons or greater) omega-3 fatty acids. – Kris 2009 

Dr. Artemis P. Simopoulos is well-known for her research and advocacy related to the health benefits of omega-3 fatty acids. She has published extensively on the subject since 1965 and is often cited for her work (over 130 publications) on the importance of the balance of omega-3 and omega-6 fatty acids in the diet for optimal health. She has argued and was even criticized for her efforts to change the dietary guidelines that the modern Western diet often contains a ratio heavily skewed towards omega-6 fatty acids, which can lead to a range of health problems, and that increasing intake of omega-3s can help to address this imbalance and promote better health. Almost 60 years later she is still advocating the omega6/3 index with an extensive emphasis on changing the paradigm on cholesterol and fat, but nothing much has changed.

 

Let’s Cut to the chase: Why are EPA and DHA so important for our health?

Offering a comprehensive account of all the metabolic functions in the body involving omega-3 would exceed the scope of this website. Nevertheless, we try out best and here’s a brief overview:

  1. Membrane Function and Fluidity: The omega-3 molecule chain, due to its flexible and curved nature, contributes to the fluidity and volume of cell membranes. This is crucial when a concave membrane structure is required for cell division. DHA, essentially, is integrated into one layer of the membrane (the bottom hemi layer), with the other layer saturated with fatty acid to produce curvature.

  2. Anti-inflammatory Eicosanoids: This is a complex area but it essentially boils down to the contrast between inflammatory omega-6 fatty acids and anti-inflammatory omega-3s. Hence the importance of maintaining the ratio of omega-6 to omega-3 (“6/3 omegas”) below 4:1!

  3. Redox Potential: An often overlooked factor is that omega-3 readily oxidizes, hence, serving as a significant acceptor of electrons within the cell membrane.

  4. Trans-Membrane Protein Function: This includes the functioning of cytochrome C in the mitochondria. Approximately 50% of cardiolipin in the heart muscle lipids is accountable for meeting the high energy demands. Nerve and brain cells rely on the function of potassium channels; without DHA these channels can’t open properly. Furthermore, omega-3 aids in creating lipid rafts—functional units that allow protein complexes to communicate and maneuver.

  5. Epoxy Products: Epoxy products from oxidized PUFAs possess a localized vasodilatory effect, making them vital for the health of the brain, heart, and kidneys. However, these epoxy molecules are rapidly eliminated by specific hydrolases, causing them to be short-lived.

  6. Cellular Repair and Stem Cells: No cell can divide and tissues cannot renew from stem cells without adequate omega-3. Membrane curvatures and repair processes rely on asymmetric lipid bilayer structures.

  7. Fat Metabolism and Ketosis: Omega-3 fatty acids can regulate the expression of certain genes involved in fatty acid metabolism. They can act on nuclear receptors such as PPARs (peroxisome proliferator-activated receptors), which play a role in the expression of genes involved in fatty acid transport and oxidation and keep ketosis alive.

 

What is this omega3 index?

Simply: measuring the amount of inflammatory omega6 and dividing it by the available omega3! A ratio of <4:1 is needed. That roughly means you can only have a 4 times the amount of arachidonic acid compared to the combined amount of EPA and DHA. So the lower the index the better for your health prospects but one of the lowest index we have found in our tests was 1.7:1. Note, that some studies reverse this index by dividing omega 3 over 6!

 

Disclaimer: some of the references herein are not peer reviewed publications but were included for informational purpose. Generally (but not always) pubmed.gov references are peer reviewed scientific or clinical articles. All others references generally show the opinion of the authors with references to other articles. The author of this website does not make any medical claims. It is our goal to inform about research and clinical studies. In the best of our efforts all references to copy rights are provided.

Adopted from Omegaquant 2020: Since the 1960s we have been significantly overwhelmed with inflammatory omega-6 oils while simultaneously deprived of vital omega-3

→ omega6 fatty acids are generally considered pro-inflammatory and omega3s are anti-inflammatory

→ There is evidence that the early human paleo diet consisted of an omega 6 to 3 ratio closer to 1:1.

Fat, fatty acid (ω6, ω3, trans, and total) intake (as percent of calories from fat; hypothetical extrapolation). Data were extrapolated from cross-sectional analyses of contemporary hunter-gatherer populations; Source Simopoulos 2016

→ As you can see above human fat consumption vastly changed. The steep incline of inflammatory omega6 and trans-fats in the last century with a steady decline in omega3 are probably a major root cause of modern diseases.

→ Excessive amounts of omega-6 polyunsaturated fatty acids (PUFA) and a very high omega-6/omega-3 ratio, as in today’s Western diets, promote the pathogenesis of many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases, whereas increased levels of omega-3 PUFA (a low omega-6/omega-3 ratio) exert suppressive effects.

→ Our food supply has been systematically devoid of proper omega-3 supply. Ultra processed foods, the lack of grass fed red meat, cold water fish and other food sources have taken their toll on human health. Most foods advertised as omega 3 rich such as nuts and oils also contain too much omega6. They are often rancid and because of an excess consumption of omega6 foods, they will inhibit omega 3 conversion that results in proper DHA. The bulk of ALA from these omega3 rich foods, which isn’t converted to EPA and DHA, still plays important roles in the body, from the structure of cell membranes to use as energy or energy storage. But it the end, you are lacking vital DHA for your brain and eye function. Most people that take supplement and ‘eat well’ still test up to 80% deficient for DHA, DPA and EPA!

Source: Dailymail.uk

Why Most omega3 supplements do not work: recent meta analyses of available studies don’t show improved mortality with omega3 supplementation. These studies show that supplement really deliver a poor and inadequate supply of omega3. The research clearly shows that your omega 6 to 3 ratio is linked to disease and that our over-consumption of omega 6 fats (eg. vegetable oils) and the lack of omega 3 (eg. grass-fed red meat) is the problem. These studies are done with basically oxidized (rancid) omega 3 supplements and further emphasize the need to get your 6 to 3 ratio as low as possible! Oconnell 2017: Ultimately, we suggest that the main failing of ω3-PUFAs in clinical trials might be a failure to reach a therapeutically effective concentration. 

Kader 2013 provides some more information on the rancidity process of oils here. Often tocopherol or ascorbic acid are added but they do not really stop the process of oxidation.

 

Mediterranean diet

There are many aspects of the Mediterranean diet that makes it the winner in most studies but its omega3 content is among the most important anti-inflammatory aspects.

We have studied the power of the Mediterranean diet extensively. One aspect now shows this diet is high in omega3 and low in omega6. This in turn lowers inflammatory markers such as IL-6, TNFalpha and cRP. A traditional Mediterranean dietary pattern, which typically has a high ratio of monounsaturated (MUFA) to saturated (SFA) fats and ω-3 to ω-6 polyunsaturated fatty acid (PUFAs) has shown anti-inflammatory effects when compared with typical North American and Northern European dietary patterns in most observational and interventional studies and may become the diet of choice for diminishing chronic inflammation in clinical practice.

 

What about olive oil?

Yes extra virgin cold pressed olive oil is very healthy, as it contains little omega-6 and mostly omega-9 and plenty of anti-inflammatory polyphenols. However, Omega-9 mono-unsaturated fat is important but not essential. Your body can produce its own if necessary. Omega-3 is essential and cannot be produced from eating olive oil. As Olive oil (olive is a fruit not a seed) contains less absolute omega6 or 3, you still have to be aware that its inflammatory index is is fairly high (11:1 omega6/3).

 

Does Flaxseed oil provide omega3? By the time a processed oil of any kind arrives in your kitchen it is mostly oxidized/rancid. To avoid the rapid onset of rancidity, flax oil is often supplemented with lipid-soluble vitamins A and E (carotenoids and tocopherols) and stored in dark glass jars. However none of these protection methods are fully satisfactory! Throughout history humans obtained freshly pressed omega3 from the farm but moderns manufactures do little in terms of testing the bio-availability of non-oxidized omega3. But perhaps the most important factor is that these oils contain little EPA or DHA and the ALA has to be converted enzymatically in the body. These enzyme function are highly compromised in older bodies and now even in your people. We can see this problem in our test results (over 1M performed) when ALA is positive but EPA and DHA are still very deficient.

Do EPA or DHA supplements work? Again they are not effective enough to make a significant change! Almost one million fatty acid tests have been performed by Zinzino worldwide! However people who take expensive supplements (such as fish oil or DHA)(, still only test marginally better than people who don’t take these supplements.

 

Why even grass-fed beef hardly contains any omega-3 !

This study by Duckett, 1993 shows how modern way or feeding up the beef even after grazing is detrimental!

→ The severe loss of valuable omega3 does not come as a surprise since Omega-6 is found in high levels in many of the oil seed crops that we consume.

Because many sustainable farmers now care about the omega3 content of their meat a new term was coined:

“grass-fed-grass-finished” beef. However a normal store label of “grass-fed” will not reveal how the cattle is treated right before production. You need to talk to your butcher to find out more details.

Freezing fish and beef

Freezing is a common method used to preserve the freshness and quality of meat and fish. Generally, it is believed that freezing does not significantly alter the nutritional value of fish and beef. Most nutrients, including proteins, fats, vitamins, and minerals, remain relatively stable during freezing. However it is known that freezing can have a significant effect on taste, texture, vitamin content and oxidation. So research in this area is still ongoing.

When done properly, flash-freezing at -80C and only thawing once, the content of the meat is relativly stable. However freezing at higher temperatures and repeated thawing produces oxidized and altered fat content. These studies are ongoing and much has to be done in analyzing the content of frozen food. Dawson 2018: Lipid oxidation of salmon results in the formation of volatile products such as aldehydes and ketones which are detected by humans as rancid flavors and odors. The rancid off flavor of frozen salmon is primarily because of increase in three aldehydes, (E, Z)-2,6-nonadienal with a cucumber odor, (Z)-3-hexenal with a green odor, and (Z, Z)-3,6-nonadienal with a fatty odor which are formed from the oxidation of n-3 unsaturated fatty acids.

 

 

2. What are all the different fats anyhow?

 

Which Vegetable oils are safe to use for cooking?

Well the truth is that there are probably none. The average American consumes up to 15 spoons of vegetable oils per day- unknowingly. That is equivalent of eg. >300g of sunflower seeds. This is only possible because of modern industrial processing. These oils are loaded with inflammatory omega-6 (up to 60%) and contain almost no omega-3. For example, canola oil contains a small but significant amount of omega-3, however due to food processing and long shelf times, by the time it arrives in your kitchen the omega-3 is oxidized and the oil contains mostly omega-6 which is much more stable. Any beneficial micronutrients that should be present, such as polyphenols, tocopherols and phytosterols in eg. rapeseed exert potential benefit to hepatoprotection, BUT most of these micronutrients are removed by the traditional refining process. In addition, you will be consuming some trans fats or other byproducts of the cooking heating process! Even if you get some intact non-oxidized ALA in these vegetable oils there is no guarantee that your body is converting it to vital DHA. Studies show that you only convert about 5% and even less or none in older people. We can see this conversion rate in our balance tests. In summary, it is much safer to use saturated fat for cooking, such as lard, bacon and butter. In some cases, coconut oil maybe acceptable, if you are on a vegan diet. As a side note, olive is a fruit not a vegetable and it contains less omega6 and more omega9, however it generally has a lower smoke point. Never heat any oil to smoking as it can produce unhealthy compounds. However a new study by Ravetti 2018 shows that even higher temperatures do not alter the the PUFA content.  But here you can see that olive oil can contain as much inflammatory omega6 as it does omega9 with an inflammatory index above 11:1…

Here you can see that vegetable oils contain mostly omega-6 (LA) and very little omega-3 (light red, ALA); Source: Nobbs 2020

Table of common cooking oils, including avocado oil, showing their approximate alpha-linolenic acid (ALA) and omega-6 fatty acid content. The values are presented per 100 grams (3.5 ounces) of oil.

Oil ALA (mg) Omega-6 (mg) Omega-6/3 Ratio
Canola oil 9179 19962 2.17
Corn oil 1659 53456 32
Olive oil 103 9763 94
Sunflower oil 5 65341 13068
Safflower oil 0 74807 N/A (No ALA)
Soybean oil (unhydrogenated) 6801 50052 7.36
Peanut oil 0 32051 N/A (No ALA)
Grapeseed oil 1 69045 69045
Coconut oil 2 2437 1218
Flaxseed oil 53588 12815 0.24
Avocado oil 958 9847 10.28

Please note that these values are approximate and the absolute amounts of inflammatory omega6 consumed matters as well.

Omega6/3 index of various food sources. PUFA=polyunsaturatedfatty acids; SFA=saturated fatty acids; n3=omega3; Keep in mind that the absolute intake of each fat matters and not just the relative index of the food. Source Khan 2017

What about omega9?

Omega-9 fatty acids are monounsaturated fats found in various plant sources. Keep in mind that all oils turn rancid and their content can change drastically. Some plant-based foods and oils with the highest amounts of omega-9 fatty acids include:

  1. Olive oil: One of the best-known sources of omega-9, olive oil is a staple in the Mediterranean diet and is praised for its heart-healthy properties.
  2. Almonds: These nuts are rich in monounsaturated fats, including omega-9 fatty acids, and also provide a good source of protein, fiber, and vitamin E.
  3. Avocado: Besides being a great source of omega-9 fatty acids, avocados also contain various vitamins, minerals, and fiber.
  4. Macadamia nuts: These nuts have a high content of monounsaturated fats, including omega-9, and are known for their buttery taste and texture.
  5. Hazelnuts: Rich in omega-9 fatty acids, hazelnuts also provide a good source of vitamin E, magnesium, and other essential nutrients.
  6. Pecans: Pecans are another nut variety high in monounsaturated fats, including omega-9 fatty acids, and are also a good source of fiber and antioxidants.
  7. Canola oil: This oil is a good source of omega-9 fatty acids, although it is not as highly praised as olive oil due to its relatively high omega-6 content.
  8. Sunflower oil: High-oleic sunflower oil is a good source of omega-9 fatty acids and is used in various cooking applications.

Including these plant-based sources of omega-9 fatty acids in your diet can help promote a healthy balance of fats and support overall health. But it is not going to affect your omega3 deficiency.

There is no direct evidence that the body makes more omega-9 fatty acids to compensate for omega-3 deficiency. Omega-3 and omega-9 fatty acids have different roles and functions in the body, so an increase in omega-9 cannot fully compensate for a deficiency in omega-3.

Omega-3 fatty acids are essential fats that the body cannot produce on its own and must be obtained through diet. They play crucial roles in maintaining cell membrane fluidity, regulating inflammation, and supporting brain and heart health.

Omega-9 fatty acids, on the other hand, are not considered essential because the body can produce them from other fatty acids. They are found in many plant-based oils and are known for their role in supporting heart health and regulating blood sugar levels.

While omega-9 fatty acids have their own health benefits, they cannot replace the unique functions of omega-3 fatty acids in the body.

Omega-9 fatty acids, like other unsaturated fats, can become rancid when exposed to heat, light, or oxygen. Rancidity is the process by which fats and oils oxidize, break down, and produce off-flavors and odors.

The rate at which omega-9 fatty acids turn rancid depends on several factors:

  1. Degree of unsaturation: Omega-9 fatty acids are monounsaturated fats, which means they have one double bond in their molecular structure. The presence of a double bond makes them more susceptible to oxidation than saturated fats, which have no double bonds. However, they are less prone to oxidation than polyunsaturated fats, like omega-3 and omega-6 fatty acids, which have multiple double bonds.

  2. Antioxidant content: Antioxidants can help protect fats and oils from oxidation and rancidity. Some sources of omega-9 fatty acids, like olive oil, are rich in antioxidants such as vitamin E and polyphenols, which can help slow down the oxidation process.

  3. Storage conditions: Exposure to heat, light, and oxygen can accelerate the oxidation of omega-9 fatty acids. To minimize rancidity, it is essential to store oils and other fat sources in a cool, dark place and use them within their shelf life.

Overall, omega-9 fatty acids can turn rancid, but proper storage and handling can help prevent or slow down this process. It is important to use fresh, high-quality oils and fats and store them appropriately to maintain their nutritional value and avoid consuming rancid fats, which can have negative effects on health.

Again, both olive and avocado are classified as fruits. They are specifically considered as drupes, which are fruits with a single large seed or pit surrounded by a fleshy outer layer. Olives and avocados contain omega-6 fatty acids because these fatty acids are naturally present in many types of plant-based foods, including fruits, nuts, seeds, and vegetable oils.

Just like Omega3, Omega-6 fatty acids are polyunsaturated fatty acids (PUFAs) that play an essential role in various physiological processes, such as cell signaling, inflammation, and brain function. The human body cannot synthesize omega-6 fatty acids either, so they must be obtained from the diet.

It’s important to note that while both olives and avocados contain omega-6 fatty acids, their overall fatty acid composition is different. Olive oil, for example, is predominantly composed of oleic acid, an omega-9 monounsaturated fatty acid, which is known for its potential health benefits, including reducing inflammation and promoting heart health. Avocados also contain a significant amount of monounsaturated fats, mainly oleic acid, along with smaller amounts of omega-6 and omega-3 fatty acids.

While it’s essential to consume omega-6 fatty acids as part of a balanced diet, it’s also important to maintain a proper balance between omega-6 and omega-3 fatty acids. Consuming too much omega-6 relative to omega-3 can contribute to inflammation and increase the risk of chronic diseases. However, olives and avocados are generally considered healthy food choices due to their high content of monounsaturated fats and other beneficial nutrients.

In summary, Omega9 is non-essential but olive and avocado are good sources of omega9 and other anti-oxidants. Olive and avocado do contain a larger amount of inflammatory omega6 however much less than vegetable-seed oils.

 

Saturated fat and why coconut is a superfood?

Coconut pulp, also known as coconut meat, is the white, fleshy part of the coconut. It is rich in nutrients and has a variety of health benefits. Here is a list of some key nutritional components found in coconut pulp:

  1. Fats: Coconut pulp is high in saturated fats, particularly medium-chain triglycerides (MCTs), which are easily metabolized by the body for energy. The primary fatty acids in coconut pulp are lauric acid, caprylic acid, and capric acid.

  2. Fiber: Coconut pulp is an excellent source of dietary fiber, which aids in digestion and supports overall gut health.

  3. Carbohydrates: Although coconut pulp is relatively low in carbohydrates compared to other fruits, it does contain some simple sugars, such as glucose and fructose.

  4. Protein: Coconut pulp contains a small amount of protein, which is essential for muscle growth, tissue repair, and other bodily functions.

  5. Vitamins: Coconut pulp is a good source of several vitamins, including vitamin C, thiamin, riboflavin, niacin, vitamin B6, and folate.

  6. Minerals: Coconut pulp contains various essential minerals, such as potassium, calcium, magnesium, phosphorus, iron, and zinc.

  7. Phytonutrients: Coconut pulp contains various bioactive compounds, including phenolic acids, flavonoids, and other antioxidants, which have been associated with numerous health benefits, such as reducing inflammation and protecting against oxidative stress.

Keep in mind that the nutritional content of coconut pulp can vary depending on factors like the variety, maturity, and processing methods.

As Coconut is not a good source for omega-3 but it contains very little inflammatory omega-6 as well and mostly saturated fat as you can see in the table above. Coconut is relatively low in omega-6 fatty acids. In 100 grams of raw coconut meat, there is approximately 0.2 grams of omega-6 fatty acids, primarily in the form of linoleic acid. Coconut is mainly composed of saturated fats, particularly medium-chain triglycerides (MCTs), which have different health implications compared to omega-6 fatty acids.

Saturated Fat and Butter

There is much confusion around the topic of saturated fats and cholesterol, both of which have been “badmouthed” for many decades now. Humans grew up on either consuming fatty red meat or fish (see above).

Sources of saturated Fat:

  1. Vegetable oils contain mostly unsaturated fats and therefor are highly inflammatory because they contain mostly omega6 (the little omega3 is rancid by the time you consume it) -that is the reason why essentially over 98% of the population is now testing with an omega 6/3 ratio of above 20:1 (up to 100:1)
  2. That really only leaves a few options for a vegan diet: palm oil and coconut. As explained above coconut contains almost no PUFA and providing more saturated fat.  The inflammatory index of coconut is discussed above.
  3. Again, coconut is the only plant source with over 20% (SA) stearic acid (all others are below 7% and contain mostly PA).

The body can synthesize SA but that is just not what is happening. Apparently, we need large amounts of SA in our diet (apart from the correct ratio of Omega 6/3). If the body does not get any SA or cholesterol it has to make it but that comes at a price. Grass eating animals (or plankton nibbling fish for that matter) are at an advantage because they have direct access to the algae and apparently no need large need for SA. So in a sense humans became dependent on that process – we are at the end of the food chain. In the tropics your metabolism is quite different and you are allowed to have a more “vegan” diet with large amounts of cooling fruit sugar. Naturally there is less need for omega-3 in that environment and tropical fish are not containing much of it. Coconut is a tropical “fruit” as it provides much needed saturated fat, fiber, potassium, magnesium, phenolic acids and many other nutrients.

Adipose tissue, or body fat, is composed of adipocytes, which are cells specialized in storing energy as fat. The fat stored in adipocytes, known as triglycerides, is a mix of different types of fatty acids, including saturated fats (SFA), monounsaturated fats (MUFA), and polyunsaturated fats (PUFA), which include both omega-3 and omega-6 fatty acids.

The specific composition of these fatty acids in adipose tissue can vary widely depending on several factors, including dietary intake, metabolic factors, and genetic factors. For example, a diet rich in saturated fats will result in a higher proportion of saturated fats in adipose tissue, while a diet rich in PUFAs will lead to a higher proportion of PUFAs stored.

A number of studies have been conducted on the fatty acid composition of human adipose tissue. The overall consensus is that the majority of fat in adipose tissue is made up of monounsaturated and saturated fatty acids, but there is a significant amount of polyunsaturated fatty acids as well. The exact proportions can vary, but one study found that the fatty acid composition of adipose tissue in the average American adult was approximately 55% monounsaturated, 25% saturated, and 20% polyunsaturated.

Therefore, It is interesting to see how little saturated fat is actually being stored by the body despite the great need for it. However this has physical chemistry reasons. In other words it is much more difficult to store “solid fat” than liquid PUFA.

From a physical chemistry perspective, there are indeed differences between storing saturated fats (which are typically solid at room temperature) and unsaturated fats like polyunsaturated fatty acids (PUFAs, which are liquid at room temperature). Let’s delve into this:

  1. Molecular Structure: The distinction between saturated and unsaturated fats lies in the presence of double bonds in their molecular structure. Saturated fats don’t have double bonds between the individual carbon atoms, leading to a straight structure. In contrast, unsaturated fats have one (monounsaturated) or more (polyunsaturated) double bonds, introducing kinks into their structure.

  2. Physical Properties: These molecular structures influence the physical properties of the fats:

    • Saturated Fats: The straight structure of saturated fats allows them to pack closely together, leading to a more solid state at room temperature.
    • Unsaturated Fats: The kinks introduced by the double bonds in unsaturated fats prevent them from packing closely, making them more fluid or liquid at room temperature.

  3. Storage in Adipose Tissue: Adipose tissue stores fat as triglycerides, which are molecules made up of three fatty acid chains attached to a glycerol backbone. While it might seem intuitive to think that solid fats would be harder to store than liquid fats due to their physical state, the body can efficiently store both types. In the body’s storage conditions, the distinction between solid and liquid is less pronounced. The body can adjust the composition of the stored fats, affecting the fluidity of the lipid droplets in adipocytes (fat cells).

  4. Preference for Storage: While the physical state might play some role, the body’s storage preference isn’t solely dictated by whether a fat is solid or liquid at room temperature. It’s influenced by various metabolic pathways, enzymatic activities, and dietary intake.

  5. Cell Membrane Composition: The fluidity of cell membranes is crucial for proper cell function, and this is influenced by the types of fats incorporated into the membrane. PUFAs, for instance, increase membrane fluidity. So, while the body stores various fats for energy, the types of fats consumed also play roles in other physiological processes.

In summary, while the physical properties of fats—like being solid or liquid at room temperature—arise from their molecular structures, the body’s ability to store and utilize them isn’t solely based on these properties. The metabolic pathways and overall physiological needs of the body play significant roles in determining how different fats are processed and stored. However as mentioned above only about 25% of stored is saturated.

Salem 2016: After having reached equilibrium on a defined diet composed of 10% total fat, of which 15% was 18:2n-6 and 3% was 18:3n-3, the rats retained 12 wt% as total n-6 PUFA and 2.1% as total n-3 PUFA in the body. Among these, 18:2n-6 accounted for 84% while 20:4n-6 was 12% of the total n-6 PUFA. For the total n-3 PUFA, 18:3n-3 was 59%, 20:5n-3 was 2.1%, and 22:6n-3 was 32%. The white adipose tissue contained the most C18 precursors and the muscle had the most of 20:4n-6 and 22:6n-3. Through these data, we have shown that in the rat body, fatty acid profiles differ greatly from tissue to tissue not only in fatty acid species, but also in carbon length and degree of unsaturation. Here we have demonstrated that there is remarkable specificity of fatty acid tissue accretion in the rat tissues.

Again, Saturated fats, like all dietary fats, play roles in various physiological processes. However, the body regulates the storage and usage of fats, including saturated fats, in a complex manner:

  1. Dietary Fats and Storage: When you consume fats in your diet, whether they’re saturated, monounsaturated, or polyunsaturated, they are typically ingested as triglycerides. If these fats aren’t used immediately for energy or other processes, they can be stored in adipose tissue (body fat).

  2. Saturated Fat Usage: Saturated fats have several roles in the body. They are integral components of cell membranes, can be used as a source of energy, and are involved in the synthesis of various essential compounds, like certain hormones. However, the body doesn’t necessarily prefer saturated fats for storage over other types of fats. The fats you store will reflect your diet’s composition, combined with how your metabolism processes those fats.

  3. Health Implications: Excessive intake of saturated fats has been linked to various health issues but for the wrong reasons. This is discussed below in the context of cholesterol and triglycerides.

  4. The Body’s Preference: The body tends to prefer glucose (from carbohydrates) as its primary energy source. When there’s an excess of energy (calories) from any source, be it carbohydrates, proteins, or fats, it will be stored for future use, primarily as fat in adipose tissue. The type of fat stored (saturated vs. unsaturated) is influenced by the kinds of fats consumed, but the overall storage process is mainly a factor of total caloric intake versus expenditure. The link between Omega3 deficiency and glucose metabolism is summarized above under the umbrella of metabolic disease.

  5. Storage Efficiency: Fats, in general, are stored more efficiently than carbohydrates. This means that excess calories from fats are more readily stored as body fat compared to excess calories from carbohydrates. This is not exclusive to saturated fats but applies to all dietary fats.

In summary, the body does store saturated fats, but the extent to which it does so is influenced by various factors, including total caloric intake, the type of fats consumed, metabolic rate, and individual genetics. It’s essential to maintain a balanced intake of different types of fats and be aware of the potential health implications of consuming excessive saturated fats.

What about butter?

In summary, butter is about 80% fat and 20% water; The fat composition is 50-70% saturated fat and mostly omega-9 for the remaining parts. Butter contains very little inflammatory omega-6. It is an interesting source of fatty acids since it also contains short chain FAs not present in other food sources, such as butyric acid. These have been show to be very beneficial for your gut health. Butter only contains trace amounts protein and therefore not very allergenic. In addition, it is a good source of stearic acid which as discussed below is very important for you heart health and not present in plant sources. Butter also contains small amounts of healthy trans fats such as CLA that are shown to have anti-cancer benefits.

What about dairy in general?

Butter is primarily composed of fat, but it does contain trace amounts of proteins. The main proteins in milk are casein and whey proteins. During the butter-making process, most of these proteins are separated out along with the liquid phase (buttermilk). However, not all proteins are entirely removed; minute amounts can remain in the butterfat.

The proteins that can be found in trace amounts in butter include:

  1. Casein Proteins: These are the primary proteins found in milk and account for about 80% of total milk protein. Even though most are removed during butter processing, tiny amounts might remain.

  2. Whey Proteins: These make up about 20% of milk proteins and include beta-lactoglobulin, alpha-lactalbumin, and serum albumin, among others. Again, while most whey proteins are removed in the butter-making process, trace amounts can remain in the butter.

For individuals with severe milk allergies, even these trace amounts of proteins in butter can potentially trigger an allergic reaction. If someone has a known milk allergy, they should consult with a healthcare professional regarding the safety of consuming butter and may consider alternatives like clarified butter (ghee) or non-dairy butter replacements. Clarified butter has had most of its water and milk solids (which contain the proteins) removed, making it potentially safer for some individuals with milk protein allergies, but it’s not guaranteed to be completely protein-free.

Allergies to whey and casein are types of milk allergies. These allergies are triggered by an immune response to specific proteins found in milk. Here’s a closer look at what happens:

  1. Immune Response: When someone is allergic to a substance, their immune system mistakenly identifies that substance as harmful, even though it’s not. In the case of whey and casein allergies, the body perceives proteins from whey and/or casein as threats.

  2. Antibodies Production: In response to this perceived threat, the immune system produces a specific type of antibody called immunoglobulin E (IgE). When the person consumes milk or milk products containing whey or casein, the IgE antibodies recognize these proteins.

  3. Histamine Release: Once these IgE antibodies bind to the offending proteins (whey or casein), certain cells (like mast cells) release chemicals, the most notable of which is histamine. This release of histamine and other chemicals leads to the symptoms of an allergic reaction.

  4. Symptoms: Symptoms can range from mild (like hives or a stuffy nose) to severe (like anaphylaxis, a life-threatening reaction that requires immediate medical attention). Symptoms can affect various parts of the body, including the skin, lungs, gastrointestinal system, and cardiovascular system.

It’s important to differentiate between a milk allergy and lactose intolerance. Lactose intolerance is not an immune response but rather a digestive issue where individuals lack sufficient amounts of the enzyme lactase, which is needed to digest lactose, the sugar found in milk.

Milk’s composition can vary based on factors such as the type of cow, its diet, the time of year, and other factors. However, on average, here’s a rough breakdown:

Milk:

  • Total protein content: About 3.2% to 3.5%
    • Casein: Represents about 80% of the total protein in milk, which is approximately 2.6% to 2.8% of the total volume of milk.
    • Whey Proteins: Make up the remaining 20% of milk proteins, equating to roughly 0.6% to 0.7% of the total volume of milk.

Butter: Butter is primarily fat, with water, milk solids, and only trace amounts of protein.

  • Total protein content: Generally less than 1% of its composition. This percentage can be even lower in highly purified forms of butter like clarified butter (ghee). 

Butyrate:

  1. What is Butyrate?: Butyrate (or butyric acid) is a short-chain fatty acid produced in the colon through the fermentation of dietary fiber by the gut microbiota.

  2. Benefits:

    • Gut Health: Butyrate is the primary energy source for colonocytes, the cells lining the colon. It helps maintain the health and integrity of the intestinal lining.
    • Anti-inflammatory: Butyrate possesses anti-inflammatory properties and can modulate the immune response in the gut. This has made it of interest in the study of conditions like inflammatory bowel disease.
    • Potential Neuroprotective Effects: There’s emerging evidence suggesting that butyrate might have neuroprotective effects, possibly by influencing gene expression and reducing oxidative stress.
    • Other Benefits: Butyrate may also play a role in metabolism, appetite regulation, and even in cancer protection, though research in these areas is ongoing.

A2 Milk:

  1. What is A2 Milk?: Cow’s milk contains various types of beta-casein proteins, with A1 and A2 being the most common. A2 milk contains only the A2 type of beta-casein protein, while regular milk contains both A1 and A2 types.

  2. Origin: The presence of either A1 or A2 beta-casein depends on the genetics of the cow. Historically, cows produced only A2 milk. However, due to breeding changes over thousands of years, many cows, especially in the Western world, started producing milk with both A1 and A2 proteins.

  3. Why the Interest in A2 Milk?: Some people claim that A2 milk is easier to digest than regular milk and that it might be a better option for those who experience discomfort when consuming regular milk. The underlying idea is that the A1 protein releases a peptide called BCM-7 during digestion, which has been linked (in some studies) to gastrointestinal discomfort and other symptoms. A2 milk, lacking the A1 protein, would not release this peptide.

  4. Scientific Evidence: While there’s some evidence suggesting A2 milk might be easier on digestion for some people, the research is not entirely conclusive. Some studies have found benefits, while others haven’t observed significant differences between A2 and regular milk in terms of digestive comfort.

  5. Not a Solution for Milk Allergy or Lactose Intolerance: It’s essential to differentiate between milk protein intolerance and lactose intolerance. A2 milk still contains lactose, so it’s not suitable for those with lactose intolerance. Similarly, those with a milk protein allergy might still react to A2 milk since it contains the same milk proteins, except for the A1 beta-casein.

In summary, butyrate is a beneficial short-chain fatty acid produced in our gut, while A2 milk is a type of cow’s milk that only contains the A2 variant of beta-casein protein. The potential benefits of A2 milk are still being researched, and while some find it a more digestible option, it’s not a universal solution for all milk-related issues.

So when it comes to butter, the distinction between A1 and A2 becomes less significant. This is because butter is primarily composed of fat, with only trace amounts of protein. The main difference between A1 and A2 milk is in the type of beta-casein protein they contain. Since the protein content in butter is minimal, the difference in beta-casein types (A1 vs. A2) in butter is negligible.

However, for those who are extremely sensitive to A1 proteins, even the tiny amount in butter might be of concern, but for the vast majority of people, there would be no noticeable difference between butter made from A1 milk and that made from A2 milk.

 

What about saturated animal fast – is it good or bad?

Saturated fat is safe and specifically stearic acid is very important for heart health. The alleged danger of eating too much red meat is fabricated by the food and drug industry. In addition there is no danger in Cholesterol quite to the contrary. Read below for more in depth science. 

Stearic acid is a long-chain saturated fatty acid found in both animal and plant sources. It is commonly used in the food, cosmetic, and pharmaceutical industries due to its properties as an emulsifier, thickener, and stabilizer. Some of the main dietary sources of stearic acid include beef, poultry, cocoa butter, dairy products, and vegetable oils, such as palm and soybean oil.

Unlike some other saturated fatty acids, stearic acid does not appear to have the same adverse effects on heart health. In fact, research has shown that stearic acid does not raise blood cholesterol levels as much as other long-chain saturated fatty acids, like palmitic acid, and may have a neutral effect on blood cholesterol levels. A high stearic acid intake, within the context of a balanced diet, is not generally considered a significant health concern. 

For more information about Fat and Digestion see below.

 

 

Why Fish oils are the better source for omega-3!

 

Many sources of omega-3 are available but fish oil is currently the best source. IN short the cold water fish did all the work for you. Vegan algae oils do not contain enough EPA and plant sources only contain ALA which has be converted in your body. This process is very inefficient. Another aspect is that we don’t fully understand rare omega3 species yet and their health benefits, only present in fish oil. Cold water fish for the production of Zinzino balance oil is currently sustainably caught in Island, however there is a Vegan Algae version available as well.

Unlike fresh fish, Fish oil supplements are tested for Total Oxidation Value (see totox below) as well as other pollutants. Zinzino and Lysi have stringent test methods that ensure the product is safe after processing.

Fish oil contains several different types of omega-3 fatty acids. The most well-known and biologically active omega-3 fatty acids found in fish oil are:

  1. Eicosapentaenoic acid (EPA): EPA is a long-chain omega-3 fatty acid that has been linked to various health benefits, such as reducing inflammation, promoting heart health, and supporting brain function.

  2. Docosahexaenoic acid (DHA): DHA is another long-chain omega-3 fatty acid with numerous health benefits, including supporting brain health, visual function, and reducing inflammation.

  3. Docosapentaenoic acid (DPA): DPA is a less-studied long-chain omega-3 fatty acid that is an intermediate between EPA and DHA. It is found in lower amounts in fish oil compared to EPA and DHA. DPA has been associated with some cardiovascular health benefits, but more research is needed to establish its full role in human health.

  4. Alpha-linolenic acid (ALA): ALA is a short-chain omega-3 fatty acid that is found in plant sources such as flaxseeds, chia seeds, and walnuts. It is usually present in fish oil in small amounts. The human body can convert ALA into EPA and DHA, but the conversion rate is relatively low and inefficient.

These are the primary omega-3 fatty acids found in fish oil, with EPA and DHA being the most important for human health. The specific concentrations of these fatty acids can vary depending on the type of fish, the part of the fish from which the oil is extracted, and the processing method used. It’s important to choose high-quality fish oil supplements to ensure you’re getting the most beneficial omega-3 fatty acids.

Cold-water fish don’t actually produce the omega-3 fatty acids EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) themselves. These fatty acids are produced by microorganisms such as algae.

In the food chain, small sea creatures like krill eat phytoplankton (which includes microalgae), thus obtaining the omega-3 fatty acids. Fish then eat these smaller creatures and accumulate the omega-3 fatty acids in their tissues. When humans consume these fish, they then obtain the beneficial omega-3 fatty acids.

This is why oily, cold-water fish such as salmon, mackerel, sardines, and trout are such good sources of these fatty acids. They have consumed a diet rich in these substances and stored them in their own tissues.

Microalgae are primary producers, meaning they are able to synthesize their own food through photosynthesis. As part of this process, they create a range of nutrients, including EPA and DHA. These omega-3 fatty acids are then passed up the food chain when the microalgae are consumed by small sea creatures, and then in turn by larger sea creatures.

This is why algal oil can also be a direct plant-based source of DHA and EPA and is now used to create omega-3 supplements especially suitable for vegetarians and vegans. However tests show that vegan sources are not providing enough EPA among other more rare omega3-species.

There are more rare omega-3 fatty acids found in fish oil and other food sources. They are present in smaller amounts and are not as well-studied as EPA, DHA, and ALA. Some of these lesser-known omega-3 fatty acids include:

  1. Eicosatrienoic acid (ETE): This is a 20-carbon omega-3 fatty acid that has three double bonds. It is present in fish oil but is not as well-researched as other omega-3s.

  2. Eicosatetraenoic acid (ETA): ETA is another 20-carbon omega-3 fatty acid with four double bonds. It is present in small amounts in some fish oils and has been linked to anti-inflammatory effects, but more research is needed to establish its full role in human health.

  3. Docosapentaenoic acid n-6 (DPA n-6): This is a 22-carbon omega-3 fatty acid, an isomer of DPA n-3, with five double bonds. It is found in smaller amounts in fish oil, and its physiological effects are not well understood.

  4. Tetracosahexaenoic acid (THA): THA is a 24-carbon omega-3 fatty acid with six double bonds. It is found in trace amounts in fish oil, and its physiological effects are not well studied.

These additional omega-3 fatty acids are present in fish oil but in smaller amounts compared to EPA and DHA. The roles and health benefits of these lesser-known omega-3 fatty acids are not as well-established, and more research is needed to fully understand their impact on human health.

In Summary, stabilized cold water fish is currently the best source for EPA and DHA  and we do have that evidence from our 1M balance tests.Omega-3 Balance Test

Sardines and mackerel contain the highest amount of essential omega3 and are generally considered safe. Some others are:

  1. Salmon: Wild-caught salmon, particularly sockeye, coho, and king salmon, are high in omega-3 fatty acids. They are also an excellent source of protein, vitamins, and minerals.

  2. Herring: Herring is another fish rich in omega-3s, and it is often available fresh, smoked, or pickled. Atlantic and Pacific herring varieties are good sources of these essential fatty acids.

  3. Anchovies: Anchovies are small, oily fish that are rich in omega-3 fatty acids. They can be consumed fresh, canned, or as a paste, and are often used as a flavor enhancer in various dishes.

  4. Trout: Rainbow trout, lake trout, and other trout varieties are also good sources of omega-3 fatty acids. Trout is a versatile fish that can be prepared in several ways, including grilling, baking, and pan-frying.

  5. Tuna: Albacore tuna, in particular, is a good source of omega-3 fatty acids. However, it is essential to consume tuna in moderation due to potential mercury content, especially for pregnant women and young children.

  6. Arctic char: This cold-water fish, similar in taste and texture to salmon, is another excellent source of omega-3 fatty acids.

Including a variety of these omega-3-rich fish in your diet can provide numerous health benefits, such as improved cardiovascular health, reduced inflammation, and better cognitive function. It is generally recommended to consume at least 5 servings of fatty fish per week to obtain even the lowest adequate benefits of omega-3 fatty acids.

Table showing the approximate omega-3 content (DHA and EPA) in different fish species. These values are approximate and can vary depending on factors such as the fish’s diet, size, and environment. The values are presented per 100 grams (3.5 ounces) of cooked fish.

Fish Species DHA (mg) EPA (mg) Total Omega-3 (mg)
Salmon (Atlantic) 1425 774 2199
Mackerel (Atlantic) 982 698 1680
Herring (Atlantic) 944 710 1654
Sardines (Atlantic) 509 473 982
Trout (Rainbow) 859 277 1136
Tuna (Albacore) 751 228 979
Anchovies 694 211 905
Arctic Char 763 134 897
Halibut 534 134 668
Cod (Pacific) 129 193 322
Tilapia 111 40 151

Please note that these values are approximate and can vary based on factors such as the cooking method, fish’s diet, and environmental conditions. You can see that the proportions of relatively higher EPA vs DHA are only apparent in Sardines, Herring, Mackerel and Salmon. Tropical warm water fish do not contain much omega3.

Why Fish and beef again?

The stability of omega-3 fatty acids in different food sources, such as grass-fed beef or wild game, is influenced by various factors, including the composition of the fats, the presence of antioxidants, and the conditions under which the food is stored and processed. Unlike fish, where phlorotannins (antioxidants found in seaweeds and algae) play a role in stabilizing omega-3 fatty acids, the stability of these fatty acids in meat sources like grass-fed beef or wild game depends on other factors:

  1. Natural Antioxidants in Meat: Grass-fed beef and wild game often have higher levels of natural antioxidants compared to grain-fed counterparts. These antioxidants, such as vitamin E and selenium, can help protect omega-3 fatty acids from oxidative damage.

  2. Fatty Acid Composition: The composition of fatty acids in the meat can also impact stability. Saturated fats, which are more stable than unsaturated fats, can help protect the more sensitive omega-3 fatty acids from oxidation.

  3. Diet of the Animals: The diet of the animals plays a crucial role in the fatty acid profile of the meat. Grass-fed animals typically have a higher omega-3 content due to the omega-3 rich grasses they consume. The natural diet may also contribute to higher levels of certain antioxidants in the meat.

  4. Processing and Cooking: The way meat is processed and cooked can significantly affect the stability of omega-3 fatty acids. High-temperature cooking methods, such as grilling or frying, can increase the risk of oxidation.

  5. Storage Conditions: Exposure to light, air, and high temperatures can accelerate the oxidation of omega-3 fatty acids. Proper storage in cool, dark conditions can help preserve their stability.

So, while meat does not contain phlorotannins like fish, the natural antioxidants present, along with factors like diet, processing, and storage, play a key role in maintaining the stability of omega-3 fatty acids in grass-fed beef and wild game. However, it’s important to note that these meats, in general, have lower omega-3 levels compared to fatty fish. Therefore, the risk of significant degradation of omega-3s may be lower, but proper handling and cooking are still important to preserve their nutritional value.

The physical characteristics of beef meat, particularly its mass and density, can also play a role in the stability of omega-3 fatty acids and their protection from oxidation.

  1. Mass and Density: Beef, being a denser and thicker meat compared to fish, may offer some protection to the omega-3 fatty acids from exposure to oxygen and reactive oxygen species (ROS). The dense muscle fibers and fat composition in beef can act as a barrier, slowing down the penetration of oxygen into the deeper parts of the meat. This reduced exposure to oxygen can potentially slow down the rate of oxidative degradation of sensitive fats like omega-3s.

  2. Oxygen Penetration and ROS: Oxygen penetration is a critical factor in the oxidation of fats. In larger and denser cuts of meat, like those from beef, the interior portions are less exposed to air, which might help in preserving the integrity of omega-3 fatty acids. This is in contrast to fish, which typically has a less dense texture, allowing for more rapid oxygen penetration and potentially faster oxidation of fats.

  3. Protective Components: The presence of other components in the meat, such as saturated fats and antioxidants like vitamin E and selenium (which are often higher in grass-fed beef), also contributes to the stability of omega-3 fatty acids. These components can provide a protective effect against oxidation.

  4. Impact of Cooking and Processing: However, it’s important to note that cooking methods and processing can significantly impact the stability of omega-3 fatty acids in beef. High-temperature cooking methods can increase the exposure of these fats to oxygen and heat, accelerating oxidation.

In summary, the physical characteristics of beef, including its mass and density, along with its composition, can provide some level of protection to omega-3 fatty acids against oxidation. However, factors such as the cut of meat, cooking methods, and storage conditions also play crucial roles in determining the stability of these sensitive fatty acids.

3. Introduction to the inflammatory index

Measuring the amount of inflammatory omega6 and dividing it by the available omega3 is the index that is at the top of all other inflammatory markers! A ratio of  less than 4:1 is needed! A ratio of less than 2:1 is desired. The US average is above 22:1.

How do we know that Zinzino Balance Oil works?

Our customers get tested before and after taking the balance oil!

Our anonymous blood tests show how YOUR 6 to 3 ratio is significantly reduced after taking Zinzino products for more than 120 days. In most cases but depending on your age and starting value an index of less than 4:1 can be achieved in one year!

Here are the steps to health:

  1. Get tested!
  2. Take Zinzino balance oil!
  3. Get retested after 120 days!
  4. Add other products of the Zinzino health protocol such as fiber, probiotics, fucoidans and vitamin D.

 

Here is what you need to know:

 

  1. You CANNOT improve your omega 6 to 3 ratio by eliminating omega 6 rich foods as shown in the Journal of American Medicine – “A much greater change in the dietary ratio of n-6 fatty acids to n-3 fatty acids can be practically achieved by increasing intake of n-3s (eg, going from no intake of oily fish to 1 serving/wk) compared with lowering intake of n-6s (which are widely consumed in cooking oils, salad dressings, and prepared foods)”. 
  2. Omega 3 fatty acids (DHA, EPA, DPA) are essential, which means your body cannot make them!
  3. Most modern disease in linked to a high intake of omega 6 and very limited supply of omega 3!
  4. Vegetable oils contain very high amounts of omega6 and are not only inflammatory, they can also produce dangerous trans-fats and MDA!
Omega 6 in access is producing inflammation!Undesired chronic health disorders, which are made worse by excessive omega-6 hormone actions, can be prevented by eating more omega-3 fats,

YOUR Eicosanoid index ratio!

At least since 2004 the Omega6/3 index for the purpose of clinical studies was established! The relationship between this marker and risk for eg. CHD death, especially sudden cardiac death (SCD), was since evaluated in many published primary and secondary prevention studies.

 

What are the differences of EPA and DHA?

DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) are both types of omega-3 fatty acids that are found in cold-water fatty fish such as salmon, tuna, and mackerel. Although they are both omega-3 fatty acids, there are some differences between DHA and EPA:

  1. Structure: DHA is a 22-carbon fatty acid with six double bonds, while EPA is a 20-carbon fatty acid with five double bonds. This structural difference can affect how they are metabolized and used by the body.

  2. Function: DHA is an important structural component of cell membranes, particularly in the brain and retina. It plays a key role in brain development and cognitive function. EPA, on the other hand, is important for reducing inflammation in the body, supporting cardiovascular health, and improving mood and behavior.

  3. Sources: DHA is found in higher concentrations in fatty fish and seafood, while EPA is found in greater amounts in fish oil supplements.

  4. EPA is particularly important for heart health because it reduces inflammation and is involved in energy ATP production in the mitochondria of the heart muscle.

  5. Dosage: The recommended dosage of DHA and EPA can vary depending on the health condition being treated. For example, the American Heart Association recommends at least two servings of fatty fish per week to obtain EPA and DHA, while some studies have used higher doses of fish oil supplements containing both EPA and DHA to achieve therapeutic effects.

  6. Side effects: Rancid fish oil has GI side effects, so it is important to consume good products. People taking blood-thinning medications should use caution when taking high doses of omega-3 fatty acids, as they can increase the risk of bleeding.

Overall, DHA and EPA have different functions and may be beneficial for different health conditions.

Why ALA is not enough!

Yes, there are sources of ALA in eg. flax seeds but in short ALA is only a precursor to EPA and DHA. The human body does use alpha-linolenic acid (ALA) for several purposes, including energy production. However, ALA does not fulfill all the same biological roles as docosahexaenoic acid (DHA) due to differences in their chemical structure and the physiological functions they support. Here are some reasons why ALA cannot simply replace DHA:

  1. Structural Differences: ALA is a shorter-chain omega-3 fatty acid with 18 carbon atoms, while DHA is a long-chain omega-3 fatty acid with 22 carbon atoms and six double bonds. This longer chain and greater number of double bonds give DHA its unique fluidity and flexibility, which are crucial for its functions in cell membranes, especially in the brain and retina.

  2. Cell Membrane Incorporation: DHA is a critical component of phospholipids in cell membranes, contributing to membrane fluidity and flexibility, which is essential for proper cell signaling, neurotransmitter function, and protection against oxidative stress. ALA does not have the same physical properties and cannot be incorporated into cell membranes in the same way as DHA.

  3. Brain and Eye Health: DHA is particularly important for brain and eye health. It accounts for up to 97% of the omega-3 fatty acids found in the brain and up to 93% in the retina. ALA cannot be utilized as efficiently as DHA in these tissues due to its shorter chain length and lack of conversion.

  4. Conversion Efficiency: The body converts ALA to EPA and then to DHA, but this conversion process is limited and inefficient in humans. Only a small percentage of ALA is converted to EPA, and even less to DHA. This means that even with adequate ALA intake, the body may not be able to produce enough DHA to meet its needs, especially in certain life stages like pregnancy and early childhood, which are critical for brain development.

  5. Physiological Roles: DHA plays specific physiological roles that ALA cannot, such as modulating the activity of ion channels in the nervous system, influencing neurotransmission, and affecting gene expression related to brain growth and repair.

  6. Anti-Inflammatory Effects: While both ALA and DHA have anti-inflammatory properties, DHA is a precursor to specialized pro-resolving mediators (SPMs) like resolvins and protectins, which have potent anti-inflammatory and tissue protective effects. ALA does not directly produce these compounds.

  7. Regulatory Functions: DHA is involved in the regulation of various metabolic processes, including those related to insulin sensitivity, lipid metabolism, and inflammation. These regulatory functions are specific to longer-chain fatty acids like DHA.

In summary, while ALA is an essential fatty acid and serves as a precursor to longer-chain omega-3 fatty acids, the body requires DHA for its unique and specific roles that ALA cannot fulfill due to structural and functional differences and enzymatic conversion is very inefficient. Therefore, dietary intake of DHA, either directly through foods or supplements, is important for maintaining optimal health.

 
 

It is important that you have a simultaneous high intake of EPA and DHA. 

The human body can convert some alpha-linolenic acid (ALA present in seeds) into eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are longer chain omega-3 fatty acids. However, the conversion rate of ALA to EPA is relatively low, estimated to be between 0.2-8% depending on several factors such as sex, age, genetics, and dietary factors.

Several studies have investigated the conversion rate of ALA to EPA, and the results have been variable. Studies found that the conversion rate in men can be as low as 0.2%. Generally, the conversion rate tends to be higher in women than in men.

It’s important to note that dietary sources of EPA and DHA, such as fatty fish or algae-based supplements, are typically more effective in increasing EPA and DHA levels in the body than relying on ALA conversion. It’s therefor recommended that adults consume at least 250-500 mg of EPA and DHA per day for general health, and up to 2-4 grams per day for specific medical conditions. If you have concerns about your omega-3 intake, it’s best to speak with a trained scientific Nutritionist.

Burdge GC, Wootton SA. Conversion of alpha-linolenic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic acids in young women. Br J Nutr. 2002;88(4):411-420. doi: 10.1079/BJN2002689

This study investigated the conversion rate of ALA to EPA, docosapentaenoic acid (DPA), and DHA in young women. The results showed that the conversion rate of ALA to EPA was approximately 21%, while the conversion rates to DPA and DHA were lower at 9% and 1%, respectively.

  1. Goyens PL, Spilker ME, Zock PL, Katan MB, Mensink RP. Conversion of alpha-linolenic acid in humans is influenced by the absolute amounts of alpha-linolenic acid and linoleic acid in the diet and not by their ratio. Am J Clin Nutr. 2006;84(1):44-53. doi: 10.1093/ajcn/84.1.44

This study investigated the effect of dietary ALA and linoleic acid (LA) intake on the conversion rate of ALA to EPA and DHA in healthy men and women. The results showed that the conversion rate of ALA to EPA ranged from 0.2% to 8% in different individuals, and was not significantly influenced by the ratio of ALA to LA in the diet.

  1. Plourde M, Cunnane SC. Extremely limited synthesis of long chain polyunsaturates in adults: implications for their dietary essentiality and use as supplements. Appl Physiol Nutr Metab. 2007;32(4):619-634. doi: 10.1139/h07-034

This review article provides an overview of the limited conversion of ALA to EPA and DHA in humans, and suggests that dietary sources of EPA and DHA are more effective in increasing their levels in the body than relying on ALA conversion.

Overall, while the conversion rate of ALA to EPA is relatively low and variable among individuals, consuming dietary sources of EPA and DHA or taking supplements may be more effective in increasing their levels in the body.

back to the top 
 
 
EPA from DHA reverse conversion:

Yes, the body can convert DHA (docosahexaenoic acid) to EPA (eicosapentaenoic acid) to a limited extent. However, this conversion process is relatively inefficient and can be influenced by several factors, including age, sex, genetics, and dietary factors.

Studies suggest that the conversion rate of DHA to EPA in humans is estimated to be around 4-5% on average. This means that if you consume 1000 mg of DHA, you may only convert about 40-50 mg of that to EPA.

While it’s important to consume both DHA and EPA for optimal health benefits, some research suggests that DHA may be more beneficial for certain health outcomes, such as cognitive function and brain health. On the other hand, EPA may be more effective in reducing inflammation and improving cardiovascular health.

Therefore, it’s important to consume a balanced intake of both DHA and EPA, either through dietary sources such as fatty fish or algae-based supplements, or through a combination of both. 

 

 

 

4. Omega-3 clinical studies and Science

Major Benefits:

-THE EFFECT OF OMEGA 3 ON HEART FUNCTION:
The heart is the core organ in the human body. Influencing factors for the
heart health are the flow properties of the blood as well as cell metabolic processes.
An adequate supply of omega-3 fatty acids indicates that these factors can be positively influenced. EPA and DHA contribute to normal heart function. According to EFSA (European Food and Safety Agency): The positive effect occurs with a daily intake of at least 250 mg EPA and DHA.


-THE EFFECT OF OMEGA 3 ON VISION:
The cells in the human eye contain a particularly large proportion of omega-3
fatty acids. Many studies have demonstrated that the supplementation with omega-3 fatty acids has a positive effect on vision. DHA contributes to the maintenance of normal vision. According to EFSA: The positive effect is
with a daily intake of at least 250 mg of DHA.


-THE EFFECT OF OMEGA 3 ON THE BRAIN
The brain is composed of a high percentage of unsaturated fatty acids. Remarkably, the concentration of DHA approaches almost 50% of all lipids in the phospholipid bilayer of neuronal synapses. About 60% of the brain is comprised of fat and 60% of that should be unsaturated. Recent studies show a clear correlation between the intake of omega-3 fatty
fatty acids and improved brain function. DHA contributes to the maintenance of normal brain function. According to EFSA: The positive effect occurs with a daily intake of at least 250 mg of DHA.


-THE EFFECT OF OMEGA 3 DURING PREGNANCY
The intake of DHA by the mother contributes to the normal development of the eyes and brain in the fetus.
brain in the fetus and in the breastfed infant. According to EFSA: The beneficial effect
is achieved with a daily intake of at least 200 mg of DHA, in addition to the recommended daily
recommended daily intake of omega-3 fatty acids for adults (i.e., at least 250 mg of
DHA and EPA).


-THE EFFECT OF OMEGA 3 ON THE INFANT AFTER THE BIRTH
The intake of DHA by the infant (follow-on formula) contributes to the normal
Development of vision in infants up to 12 months of age. According to EFSA: The
positive effect occurs with a daily intake of at least 100 mg of DHA, via
the follow-on formula.

 

-METABOLIC SYNDROME

Omega3 deficiency is interactively involved in metabolic syndrome which involves autoimmunity, diabetes, obesity, hypertension and cardiovascular disease!

 

 

What do the studies say?

Clinical studies are great – if they are done properly with thoughtful placebo controls and non-rancid omega3 (fresh fish eaters are still the best study group). If a study does not show an effect on omega3 supplementation always look for the omega6/3 ratio.

The omega6/3 index is always accurate when measured correctly in the RBC membranes.  There is a 100% correlation of the high 6/3 ratio and disease! In other words if your 6/3 ratio does not go down you cannot assume that the omega3 used was intact and functional.

 

YOUR brain function relies on omega3!

Without Omega3 your brain shrinks. YOUR Brain is 60% fat and requires >36% PUFAs. Literally spoken it is on fire without proper omega3! This study shows how your brain shrinks without DHA – and remember we all test up to 90% deficient before balance oil supplementation. DHA is positively associated with cortical gray matter volumes

Unique Omega-3 Fatty Acid Lipid Could Revolutionize Our Understanding of Brain Development and Aging

Manage brain capacity!

As shown below your brain literally shrinks without proper DHA!

The management of neurodegenerative diseases in their early stages. Most dementia disease is age related. Our bodies are amazing designs that can operate on below 10% nutrition for a long time, however at certain age and most Parkinson’s is diagnosed above 65 years the inflammation in the brain reaches a limit. A diet rich in omega 3 defeats the outcome of dementia!

BRAIN SIZE: A higher omega-3 index was correlated with larger total normal brain volume

 

BRAIN SIZE: A higher omega-3 index was correlated with larger total normal brain volume!

Source

Pottala 2014: A Higher RBC EPA + DHA corresponds with larger total brain and hippocampal volumes; 1.6% greater EPA + DHA (omega-3 index from red blood cells) level was correlated with 2.1 cm3 larger brain volume; 1.6% greater omega-3 index was correlated with greater hippocampal volume (50 mm(3), p = 0.036) (MRI brain volumes were assessed in over 1100 postmenopausal women )

 

McNamara2010: “DHA deficits, impaired astrocyte mediated vascular coupling, neuronal shrinkage, and reductions in gray matter volume in the prefrontal cortex (PFC). Preclinical studies have also observed neuronal shrinkage and indices of astrocyte pathology in the DHA-deficient rat brain. “

 

DHA is enriched in the central nervous system (CNS), comprising of 5% of the brain by mass and 20% of all lipids in neuronal cell membranes. Here you can see how DHA is built into the structure of a membrane protein that transports lipids. This has implications for a proper blood brain barrier.

Chen 2020: For each interquartile increment (2.02%) in omega-3 index, the average volume was 5.03 cm3 (p < 0.01) greater in the white matter and 0.08 cm3 (p = 0.03) greater in the hippocampus. The associations with RBC docosahexaenoic acid and eicosapentaenoic acid levels were similar. Higher LCn3PUFA attenuated the inverse associations between PM2.5 exposure and white matter volumes in the total brain 

McNamara 2008: The age-related reduction in PUFA composition was inversely correlated with SCD expression and activity resulting in elevations in monounsaturated fatty acid composition. Increasing age was associated with a progressive decline in polyunsaturated fatty acid (PUFA) composition, including DHA and arachidonic acid (AA, 20:4n-6), and transient, apparently compensatory, elevations in elongase and desaturase gene expression.

See below EICOSANOIDS!

Here is a list of potential health claims established by the EFSA, European Commissions Regulations:

  • Health claims on Omega-3 (EPA and DHA) in BalanceOil: EPA and DHA contributes to the normal function of the heart
  •  
  • DHA contributes to the maintenance of normal vision
  •  
  • DHA contributes to the maintenance of normal brain function
  •  
  • With high dosages of BalanceOil, the following claim can be used: DHA and EPA (2 g daily) contributes to the maintenance of normal blood triglyceride concentrations
  •  
  • DHA and EPA (3 g daily) contributes to the maintenance of normal blood pressure  (max 5 g EPA+DHA)

 

 

Aging and stem cells

-> All organs rely on proper omega3 supply in their stem cells!

-> The older we get the more deficient and toxic our stem cells become

-> With age it becomes more difficult to incorporate healthy cells into your organs especially the heart and kidneys = the process of renewal slows down and we age

Kang 2014: PUFA-based interventions to create a favorable environment for stem cell proliferation or differentiation may thus be a promising and practical approach to controlling stem cell fate for clinical applications.

Rashid 2016: Role of Polyunsaturated Fatty Acids and Their Metabolites on Stem Cell Proliferation and Differentiation: The nervous system is highly enriched with long-chain polyunsaturated fatty acids (PUFAs). Essential fatty acids, namely, ω-6 (n – 6) and ω-3 (n – 3) PUFA, and their metabolites are critical components of cell structure and function and could therefore influence stem cell fate.

Telomere length

Omega-3 fatty acids have been shown to have potential benefits for telomere length, which is a marker of cellular aging. Here are some key points:

Recent studies have explored the relationship between omega-3 fatty acid supplementation and telomere length, offering insights into how these nutrients might influence cellular aging and overall health.

  1. Meta-Analysis of Clinical Trials: A mini meta-analysis aimed at assessing the effect of omega-3 fatty acids on telomere length reviewed five clinical trials with a total of 337 participants. The findings revealed an overall beneficial effect of omega-3 fatty acids on telomere length, suggesting a positive impact on cellular aging. The mean difference in telomere length was found to be significant (p = 0.02). This suggests that omega-3 fatty acids may have a protective effect on chromosomes, although larger clinical trials are needed to confirm these findings and to clarify the underlying molecular mechanisms​​.

  2. Systematic Review of Clinical Trials: Another systematic review examined the effect of omega-3 PUFA supplementation on telomere length and telomerase enzyme activity. The review, which included six clinical trials, found that omega-3 PUFA supplementation did indeed statistically affect telomere length in three out of three studies (keep in mind that the omega6/3 index is ignored as usual). It affected telomerase activity in two out of four studies, indicating some influence on cellular mechanisms related to aging and cell maintenance. The supplementation increased telomerase enzyme activity in subjects with first-episode schizophrenia and decreased it in type 2 diabetes subjects. The review highlighted the need for further studies due to methodological differences (rancid supplements) and the limited number of studies on this theme​​.

  3. Randomized Controlled Trial: A specific randomized controlled trial focused on omega-3 PUFAs, oxidative stress, and leukocyte telomere length. This trial included 106 healthy sedentary overweight middle-aged and older adults who received different dosages of omega-3 PUFAs or a placebo. The study found that omega-3 supplementation significantly lowered oxidative stress, as measured by F2-isoprostanes. Although direct group differences for telomerase and telomere length were nonsignificant, a decrease in the n-6:n-3 PUFA plasma ratios (indicating higher omega-3 levels) correlated with an increase in telomere length. This finding suggests a link between omega-3 intake, reduced oxidative stress, and potentially slower cell aging​​.

These studies collectively suggest a complex relationship between omega-3 fatty acid supplementation and telomere length. While direct effects on telomere length are not consistently demonstrated across studies, there is evidence suggesting that omega-3s may influence cellular aging processes, particularly through their impact on oxidative stress and inflammatory markers. Further research is needed to fully understand these relationships and their implications for health and longevity.

 

Aging and longevity is on everyone’s “mind”. You could sum up the process of aging with the ‘quality of your stem cells’. All organs have the ability to renew, some quicker such as intestinal and blood cells and some slowly like heart and nerve cells. In other words, as your stem cells age quickly and their niches die out so will your regenerative quality of your own body. Hair is a good example. As the hair loss progresses in the front of the scalp once the hair follicles are gone you simply cannot  grow more hair. This is no different for the heart or kidney or any other organ. Lucky for us the liver and digestive tract has enormous amounts of ‘healthy’ stem cells otherwise we could not absorb nutrition or detox or for that matter absorb necessary omega3. In principle Aging has to do with the accumulation of all lifetime diseases. EG. a cancer diagnosis can be detrimental to you life span. Only an overall healthy body lives longer but especially diseases of dementia and the nervous system are crucial for longevity.

Aging is primarily visible on the skin. See below.

  • Wrinkles
  • Dullness of skin
  • Dry skin
  • Blotchiness and age spots
  • Rough skin texture
  • Visible pores

Aging of the brain function is and sensory organs is not so visible but a prime factor in aging:

Swanson 2012: Omega-3 [(n-3)] fatty acids have been linked to healthy aging throughout life. Recently, fish-derived omega-3 fatty acids EPA and DHA have been associated with fetal development, cardiovascular function, and Alzheimer’s disease. 

Bourre 2004: Alpha-linolenic acid deficiency decreases the perception of pleasure, by slightly altering the efficacy of sensory organs and by affecting certain cerebral structures. Age-related impairment of hearing, vision and smell is due to both decreased efficacy of the parts of the brain concerned and disorders of sensory receptors, particularly of the inner ear or retina.

 PUFA-based interventions to generate a positive environment for stem cell proliferation or differentiation might be a promising and practical approach to controlling stem cell fate for clinical applications.

Langelier 2010: Long chain-polyunsaturated fatty acids modulate membrane phospholipid composition and protein localization in lipid rafts of neural stem cell cultures  Glomerular filtration rate (GFR) and connexin 43 contents in the rafts were increased by DHA supplementation. The restoration of DHA levels in the phospholipids could profoundly affect protein localization and, consequently, their functionalities.

More on Vision Health below.

As you age your fatty acid conversion enzymes that are supposed to make more DHA do not work as well:

McNamara: The Aging Human Orbitofrontal Cortex: Decreasing Polyunsaturated Fatty Acid Composition is responsible; “The age-related reduction in PUFA composition was inversely correlated with SCD expression and activity resulting in elevations in monounsaturated fatty acid composition. These dynamic age-related changes in OFC gray matter fatty acid composition and biosynthetic gene expression may contribute to the progressive decline in OFC gray matter volume found with advancing age. “

Telomere length (TL) is considered a biomarker of aging: shorter telomeres are associated with a decreased life expectancy and increased rates of age-related chronic diseases. Telomere attrition has been shown to be accelerated by oxidative stress and inflammation.

In the same context “EPA was able to prevent cortisol-induced reduction in neurogenesis and increase in apoptosis, when used in pre-treatment, and both pre- and co-treatment only during the proliferation stage” Borsini 2020 provide the first evidence for treatment with both EPA and DHA to prevent cortisol-induced reduction in human hippocampal neurogenesis and apoptosis.

Crous-Bou 2019 shows how a balanced diet that provides plenty of omega3 including grass fed meat has an effect telomere length:

Telomers: Several observational studies have reinforced the suggestive benefits of adherence to the Mediterranean diet (a plant-rich dietary pattern), consumption of seeds (and its derivatives), and dietary intake of carotenoids on TL, which further supports the research benefits of plant-rich dietary patterns and plant foods to promote health and longevity.

Ali 2022: A total of 5 clinical trials were included for the quantitative meta-analysis, comprising a total of 337 participants. The results revealed an overall beneficial effect of omega-3 fatty acids on the telomere length (mean difference = 0.16; 95% CI, 0.02, 0.30; p = 0.02).

The older people, omega-3, and cognitive health (EPOCH) trial design and methodology: A randomised, double-blind, controlled trial investigating the effect of long-chain omega-3 fatty acids on cognitive ageing and wellbeing in cognitively healthy older adults.

Fish oil–derived n−3 PUFA therapy increases muscle mass and function in healthy older adults. Compared with the control group, 6 mo of n−3 PUFA therapy increased thigh muscle volume (3.6%; 95% CI: 0.2%, 7.0%), handgrip strength (2.3 kg; 95% CI: 0.8, 3.7 kg), and 1-RM muscle strength (4.0%; 95% CI: 0.8%, 7.3%) (all P < 0.05) and tended to increase average isokinetic power (5.6%; 95% CI: −0.6%, 11.7%; P = 0.075).

In summary, the health and longevity of your stem cells that are responsible for the renewal of all your organs rely on the proper availability of omega3.

Sarcopenia in aging adults:

Dietary omega-3 fatty acid supplementation increases the rate of muscle protein synthesis in older adults: Omega-3 fatty acid supplementation augmented the hyperaminoacidemia-hyperinsulinemia-induced increase in the rate of muscle protein synthesis

Omega-3 fatty acids stimulate muscle protein synthesis in older adults!

 

Omega3- lowers telomerase activity:

 

– Gironolamo 2014: Omega-3 fatty acids and protein metabolism: enhancement of anabolic interventions for sarcopenia!

 

– Dupont 2019: We conclude that there is growing evidence for a beneficial effect of omega-3 PUFAs supplementation in sarcopenic older persons!

 

Heart Disease

 

First of all – do a search of “heart disease” on this page and you will see how the heart is at the center of this metabolic problem. While Omega-3 fatty acids, including EPA and DHA, have numerous health benefits, their impact on heart health is indeed one of the most significant and well-studied effects. Omega-3 fatty acids, particularly EPA, have been shown to have profound positive effects on cardiovascular health:

  1. Lowering Triglyceride Levels: Omega-3 fatty acids can significantly reduce blood levels of triglycerides, a type of fat linked to an increased risk of heart disease.

  2. Reducing Inflammation: Chronic inflammation is associated with heart disease. Omega-3 fatty acids have anti-inflammatory properties that can help reduce inflammation throughout the body, including in the blood vessels.

  3. Improving Blood Pressure: Studies have shown that omega-3 fatty acids can help lower blood pressure levels, particularly in individuals with hypertension or high blood pressure.

  4. Reducing Blood Clotting: Omega-3 fatty acids can help prevent blood platelets from clumping together, reducing the risk of blood clots that can lead to heart attacks or strokes.

  5. Improving Endothelial Function: The endothelium is the inner lining of blood vessels. Omega-3 fatty acids can help improve the function of the endothelium, promoting better blood flow and cardiovascular health.

  6. Anti-arrhythmic Effects: Omega-3 fatty acids have been shown to have anti-arrhythmic effects, meaning they can help prevent irregular heartbeats, which can lead to sudden cardiac death.

  7. Impact on Cholesterol Levels: While omega-3 fatty acids may not significantly lower total cholesterol levels, they can improve the overall cholesterol profile by increasing levels of high-density lipoprotein (HDL) cholesterol and reducing the ratio of total cholesterol to HDL cholesterol.

Heart Disease is equivalent to cardiovascular health and chronic inflammatory diseases are all linked to the metabolic syndrome. Simply, the quality of your arteries and their endothelial function in regulating blood pressure tells the story.

Both DPA  (docosahexaenoic acid) and EPA (eicosapentaenoic acid) are integrally involved in heart health in different aspects. Overall, EPA may be particularly important for reducing inflammation, lowering triglycerides, improving blood pressure, and reducing the risk of arrhythmias, which are all important aspects of heart health. However, DHA is also important for heart health and has been shown to improve endothelial function (the health of the lining of the blood vessels), reduce blood pressure, and improve lipid metabolism.

So once again, its all about reducing inflammation: EPA has potent anti-inflammatory properties that can help reduce inflammation in the body, including the arteries. Chronic inflammation is a key contributor to the development of heart disease, so reducing inflammation with EPA can help prevent or reduce the risk of heart disease.

  1. Lowering triglycerides: High levels of triglycerides (a type of fat in the blood) are a risk factor for heart disease. EPA has been shown to reduce triglyceride levels in the blood, particularly in people with high triglyceride levels.

  2. Improving blood pressure: High blood pressure is another risk factor for heart disease. EPA has been shown to help lower blood pressure, particularly in people with hypertension.

  3. Reducing the risk of arrhythmias: Arrhythmias are abnormal heart rhythms that can be life-threatening. EPA has been shown to help reduce the risk of arrhythmias, particularly in people with a history of heart disease.

  4. Improving endothelial function: The endothelium is the lining of the blood vessels, and healthy endothelial function is important for maintaining normal blood flow and preventing the development of atherosclerosis. EPA has been shown to improve endothelial function, which can help reduce the risk of heart disease.

Overall, EPA is an important nutrient for heart health, and getting enough EPA through the diet or supplementation can help reduce the risk of heart disease and improve cardiovascular health.

Omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have significant effects on the heart muscle and mitochondria, contributing to cardiovascular health in several ways:

  1. Mitochondrial Function: Mitochondria are the powerhouse of cells, including heart muscle cells (cardiomyocytes), and are crucial for energy production. Omega-3 fatty acids can improve mitochondrial function, enhancing the efficiency of energy production in the heart muscle. This is particularly important for the heart, as it requires a continuous supply of energy to function effectively.

  2. Cardioprotection: Omega-3 fatty acids have been shown to have cardioprotective effects, reducing the risk of heart failure and improving heart function in patients with existing cardiovascular diseases. They can help maintain the structural integrity of cardiomyocytes and support the repair mechanisms of the heart muscle.

  3. Anti-inflammatory Effects: Chronic inflammation can damage heart muscle cells and mitochondria. Omega-3 fatty acids have anti-inflammatory properties that can help reduce inflammation in the heart and blood vessels, protecting the heart muscle and its mitochondria.

  4. Antioxidant Effects: Oxidative stress can damage mitochondrial DNA and impair mitochondrial function. Omega-3 fatty acids have antioxidant properties that can help protect mitochondria from oxidative damage, thereby supporting their function and overall cardiovascular health.

  5. Regulation of Lipid Metabolism: Omega-3 fatty acids can influence lipid metabolism in the heart, promoting the use of fatty acids for energy production in mitochondria. This can help optimize energy utilization in the heart muscle.

  6. Impact on Heart Rhythm: Omega-3 fatty acids can help regulate the electrical activity of the heart, reducing the risk of arrhythmias (irregular heartbeats) that can lead to sudden cardiac death. This effect is partly mediated by their influence on ion channels in cardiomyocytes and mitochondrial membranes.

  7. Prevention of Cardiac Remodeling: After a heart attack or in chronic heart failure, the heart muscle can undergo detrimental remodeling. Omega-3 fatty acids have been shown to attenuate this remodeling process, preserving heart function and reducing the progression of heart failure.

Overall, the beneficial effects of omega-3 fatty acids on the heart muscle and mitochondria contribute to their protective role in cardiovascular health. Ensuring adequate intake of omega-3 fatty acids through diet or supplementation, as advised by healthcare professionals, can be an important part of maintaining a healthy heart.

The body of research on Omega3 and heart disease is endless. Here are just a few examples:

Yokoyama 2007: In patients with a history of coronary artery disease who were given EPA treatment, major coronary events were reduced by 19% (secondary prevention subgroup: 158 [8.7%] in the EPA group vs 197 [10.7%] in the control group; p=0.048). In patients with no history of coronary artery disease, EPA treatment reduced major coronary events by 18%, but this finding was not significant (104 [1.4%] in the EPA group vs 127 [1.7%] in the control group; p=0.132).

Elagizi 2021: It was proposed that insufficient Ω-3 dosing (<1 g/day EPA and docosahexaenoic acid (DHA)), as well as patients aggressively treated with multiple other effective medical therapies, may explain the conflicting results of Ω-3 therapy in controlled trials. We have thus reviewed the current evidence regarding Ω-3 and CV health, put forth potential reasoning for discrepant results in the literature, highlighted critical concepts such as measuring blood levels of Ω-3 with a dedicated Ω-3 index and addressed current recommendations as suggested by health care professional societies and recent significant scientific data.

“There is mounting evidence that higher doses of Ω-3 interventions appear more likely to demonstrate CVD and other clinical benefits.” – what this recent article shows is that dosage and the omega3 index matters! “For CVD events, the estimates for the slope translate to a risk reduction of 5.8% for each additional 1 g/day intake”

What this article like many others fails to explain: without knowing the omega6/3 index – how do you know that your omega3 is not rancid? Herein lies the problem with many studies. Regardless of this problem, the meta analyses shows even small amounts of omega3 increase make a difference!

Another example in this recent large study below shows a very measurable effect on diabetics but once again the article does not have SINGLE mention of the omega6/3 index. How would you know your omega 3 is rancid otherwise?

Huang 2023: Eight eligible studies involving 57,754 participants were ultimately included. Meta-analysis showed that ω-3 fatty acid supplementation reduces cardiovascular disease (CVD) risk in patients with diabetes. However – “a significant reduction in study heterogeneity was found, suggesting that different types of ω-3 FA supplementation are a source of study heterogeneity” 

Mitochondrial health

Both EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) are important for mitochondrial function and cytochrome c, but they may have different effects.

Mitochondria are the energy-producing organelles in cells, and cytochrome c is a protein that is involved in the electron transport chain, which is the process that generates ATP (adenosine triphosphate) in the mitochondria.

Research has shown that both EPA and DHA can improve mitochondrial function and increase cytochrome c levels in cells. However, some studies suggest that EPA may be more effective than DHA at improving mitochondrial function.

For example, a study published in the Journal of the International Society of Sports Nutrition in 2014 found that supplementation with EPA improved mitochondrial function and increased cytochrome c levels in skeletal muscle cells of older adults, while DHA supplementation had no effect.

 

Benedict 1992: Normal levels of the essential fatty acids in the n-3-enriched mitochondrial membrane phospholipids appear to eliminate the mitochondrial dysfunction observed in essential fatty acid-deficient membranes. = In mitochondria isolated from hearts of dogs fed this diet for 60 wk, the phospholipid content of inflammatory arachidonic acid was replaced by the n-3 fatty acids, eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids.

 

Elevated mitochondrial Ca2+ and increased dehydrogenase activation are linked to inefficient mitochondrial function and limited postischaemic recovery of contractile function. 5. Notably, a distinct decrease in the ratio of mitochondrial membrane omega-3 to omega-6 polyunsaturated fatty acids (PUFA) and a decrease in the mitochondrial phospholipid cardiolipin occurs in aged rat hearts. A diet rich in omega-3 PUFA directly increases membrane omega-3:omega-6 PUFA and cardiolipin content and also facilitates improved tolerance of ischaemia and reperfusion.

Mickleborough, T. D., Sinex, J. A., Platt, D., & Chapman, R. F. (2014). The effects of fish oil supplementation on mitochondrial function and muscle damage in older adults. Journal of the International Society of Sports Nutrition, 11(1), 31. doi: 10.1186/1550-2783-11-31

In this study, 21 older adults (aged 60-85 years) were randomized to receive either 2 grams per day of EPA (eicosapentaenoic acid), 2 grams per day of DHA (docosahexaenoic acid), or a placebo for 8 weeks. The researchers measured mitochondrial function and muscle damage markers before and after the intervention.

The results showed that supplementation with EPA, but not DHA, improved mitochondrial function and increased cytochrome c levels in skeletal muscle cells. The authors suggested that the beneficial effects of EPA on mitochondrial function may be due to its anti-inflammatory properties and ability to increase the production of mitochondria.

Another study published in the journal Nutrition and Metabolism in 2016 found that supplementation with a combination of EPA and DHA improved mitochondrial function and increased cytochrome c levels in healthy young adults, but the effect was greater for EPA than for DHA.

Overall, while both EPA and DHA are important for mitochondrial function and cytochrome c, some studies suggest that EPA may be more effective than DHA at improving these aspects of cellular function. However, more research is needed to fully understand the mechanisms and optimal dosages of EPA and DHA for mitochondrial function and cytochrome c.

 
 

Heart Failure

Arguably the most important health benefit you can get from omega-3 supplementation is improving your heart health. This is what the research shows. To be fair, there are meta analyses studies that do not show any improved mortality with omega3 supplementation. However, scientist agree these studies are done with poor and inadequate supply of omega3. Once you look at the omega6/3 index, there is a 100% correlation: the lower your omega6/3 index – the better your heart health.

For persons with an omega-3 index <4%, risk is tenfold, as compared to persons with an omega-3 index >8% EPA and DHA have anti-arrhythmic and anti-atherosclerotic mechanisms of action. In large-scale intervention studies, intake of EPA and DHA has been demonstrated to reduce SCD and non-fatal cardiovascular events.

Evidence is summarized strengthening the concept that a low “EPA+DHA level” presents a risk for sudden cardiac death and that the administration of 840 mg/day of EPA+DHA ethyl esters raises the “EPA+DHA level” to approximately 6% that is associated with a marked protection from sudden cardiac death. 

•In the secondary prevention of cardiovascular disease, a ratio of 4/1 was associated with a 70% decrease in total mortality.

 

Excess inflammatory omega 6 consumption in the USA compared to a balanced diet in Greenland and Inuit Eskimos causes increased heart disease! Source

 

Heart failure: Oconnell 2017: We also examine mechanistic studies suggesting ω3-PUFAs signal through free fatty acid receptor 4 (Ffar4), a G-protein coupled receptor (GPR) for long-chain fatty acids (FA), thereby identifying an entirely novel mechanism of action for ω3-PUFA mediated cardioprotection. 

Source: Oconnell 2017 omega3 prevents heart fibrosis

 

Opedisano 2021: Dietary supplementation with n-3 polyunsaturated fatty acids (PUFAs) seems to produce good results. In fact, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have anti-inflammatory and antioxidant properties and different cardioprotective mechanisms. Therefore, both the European Society of Cardiology (ESC) and the American College of Cardiology/American Heart Association (ACC/AHA) define dietary supplementation with n-3 PUFAs as an effective therapy for reducing the risk of hospitalization and death in HF patients.

“The free fatty acid receptor 4 (Ffar4) receptor, or the G-protein coupled receptor 120 (GPR120) fibroblast receptors inhibit cardiac fibrosis and protect the heart from HF onset. Furthermore, n-3 PUFAs increase the left ventricular ejection fraction (LVEF), reduce global longitudinal deformation, E/e ratio (early ventricular filling and early mitral annulus velocity), soluble interleukin-1 receptor-like 1 (sST2) and high-sensitive C Reactive protein (hsCRP) levels, and increase flow-mediated dilation.”

 

Djousse 2012: 176,441 subjects and 5480 incident cases of heart failure from 7 prospective studies were included in this analysis. Using random effect model, the pooled relative risk for heart failure comparing the highest to lowest category of fish intake was 0.85 (95% CI; 0.73-0.99). This meta-analysis is consistent with a lower risk of heart failure with intake of marine omega-3 fatty acids. 

AFIB

Several studies have explored the relationship between atrial fibrillation (AFib) and omega-3 fatty acid intake or the omega-3 index. Here are a few studies that highlight these connections:

  1. Mozaffarian, D., Psaty, B. M., Rimm, E. B., Lemaitre, R. N., Burke, G. L., Lyles, M. F., … & Siscovick, D. S. (2004). Fish intake and risk of incident atrial fibrillation. Circulation, 110(4), 368-373. This study found that higher fish consumption, which is associated with a higher omega-3 index, was linked to a reduced risk of incident atrial fibrillation in older adults.

  2. Wu, J. H., Lemaitre, R. N., King, I. B., Song, X., Sacks, F. M., Rimm, E. B., … & Mozaffarian, D. (2012). Association of plasma phospholipid long-chain omega-3 fatty acids with incident atrial fibrillation in older adults: the cardiovascular health study. Circulation, 125(9), 1084-1093. This study demonstrated that higher circulating levels of long-chain omega-3 fatty acids were associated with a lower incidence of atrial fibrillation in older adults.

  3. Virtanen, J. K., Mursu, J., Voutilainen, S., & Tuomainen, T. P. (2009). Serum long-chain n-3 polyunsaturated fatty acids and risk of hospital diagnosis of atrial fibrillation in men. Circulation, 120(23), 2315-2321. This study found that higher serum levels of long-chain omega-3 polyunsaturated fatty acids were associated with a reduced risk of atrial fibrillation in middle-aged men.

  4. Are there any side effects taking fish oil? Brouwer, I. A., Heeringa, J., Geleijnse, J. M., Zock, P. L., & Witteman, J. C. (2006). Intake of very long-chain n-3 fatty acids from fish and incidence of atrial fibrillation: The Rotterdam Study. The American journal of clinical nutrition, 83(5), 1086-1091. This study reported that there was no significant association between long-chain omega-3 fatty acid intake from fish and atrial fibrillation incidence in the general population.

Once again if there is no effect in a study or meta anlyses you have to look at the omega6/3 index. Just giving someone rancid DHA pills says nothing. His index needs to be measured properly!

Mozaffarian D 2004 clearly shows how non-fried fish has an impact on AFIB events- alias: fried fish has a much higher omega6/3 index.
 
 

Cardiovascular disease and Blood pressure

Of course Cardiovascular disease, hypertension and atherosclerosis are all integrally linked to heart disease.

In this Nature article proper omega3 supplementation clearly shows how your blood pressure can be lowered. Cardiovascular disease (CVD) is one of the main causes of death worldwide, and thus is the subject of numerous studies to explore potential new treatment strategies. Cardiovascular risk of stroke, coronary artery disease and hypertensive end organ damage is increased by hypertension. High blood pressure can be reduced by certain dietary modifications, such as an increased consumption of long chain ω-3 polyunsaturated fatty acids (ω-3 PUFAs) found in fatty fish or fish oil. The American Heart Association (AHA) recommends that healthy adults consume a serving of fish at least two times a week, and patients with coronary heart disease take a supplement of 1 g of EPA (eicosapentaenoic acid, 20:5) and DHA (docosahexaenoic acid, 22:6) every day!!! source

Anemia

First of all Anemia is not iron deficiency. It is the inability of red blood cells to bind enough hemoglobin and therefor blood iron becomes depleted. Omega-3 fatty acids have been found to have a relationship with iron metabolism, which is essential for preventing and managing anemia. Studies have shown that omega-3 fatty acids can influence iron metabolism and may affect various iron-related disorders​​. Specifically, in the context of sickle cell anemia, a study found that treatment with omega-3 fatty acids reduced the frequency of pain episodes, severe anemia, and the need for transfusions in patients with sickle cell anemia. This suggests that omega-3 fatty acids could have a beneficial role in managing anemia, particularly in conditions like sickle cell disease. However, very little research has been conducted to fully understand the mechanisms behind these effects and their clinical implications! It is also clear from the science of vegan dieters that iron is not the issue, rather its is the ‘quality of the blood cells’ and their membranes that is the decisive factor. 

In summary, Anemia is a condition in which there aren’t enough healthy red blood cells to carry adequate oxygen to the body’s tissues, and it can have several causes. Iron deficiency anemia is a specific type of anemia caused by a lack of iron, which is necessary for the production of hemoglobin in red blood cells. However, anemia can also be caused by other factors, such as vitamin deficiencies, chronic diseases, or genetic disorders.

Furthermore, iron overload, also known as hemochromatosis, can indeed have serious consequences. It can lead to organ damage, especially in the liver, heart, and pancreas, and increase the risk of diabetes, liver disease, and heart problems. It’s important to have a balanced approach to iron intake and to consult healthcare professionals for proper diagnosis and management of anemia or iron overload.

McBurney 2021: Omega-3 index is directly associated with a healthy red blood cell distribution width. In healthy adults of both sexes, the data suggested that an O3I of > 5.6% may help maintain normal RBC structural and functional integrity.

Blood cell membranes of patients with SCD(sickle cell) have abnormal fatty acids composition characterized by high ratio of pro-inflammatory arachidonic acid (AA) to anti-inflammatory DHA and EPA (high omega-6/omega-3 ratio). In addition, experimental and clinical studies provide evidence that treatment with DHA does confer improvement in rheological properties of sickle RBC, inflammation and hemolysis. The clinical studies have shown improvements in VOC rate, markers of inflammation, adhesion, and hemolysis. In toto, the results of studies on the therapeutic effects of omega-3 fatty acids in SCD provide good body of evidence that omega-3 fatty acids could be a safe and effective treatment for SCD.

Iron deficiency negatively impacts organ functions and is associated with an increased risk of maternal and child mortality, impaired cognitive and body development, reduced physical performance and work capacity in adults, and decreased cognitive function in elderly individuals.

In this context also check the discussion on veganism below.

Our hominin ancestors began consuming meat, fish, seafood, and eggs >2 million years ago. Consequently, humans are genetically adapted to procure nutrients from both plant and animal sources. In contrast, veganism is without evolutionary precedent in Homo sapiens species. Strict adherence to a vegan diet causes predictable deficiencies in nutrients including vitamins B12, B2, D, niacin, iron, iodine, zinc, high-quality proteins, omega-3, and calcium. Prolonged strict veganism increases risk for bone fractures, sarcopenia, anemia, and depression. 

Cancer treatment anemia: Diets enriched with omega-3 PUFA may have beneficial anticancer effects in particular when containing only basal amounts of antioxidants such as vitamin E or C. 

 It was found that 2% AAFA (an omega-3 polyunsaturated fatty acid productaa) in the diet of the CPT-11 treated mice: decreased apoptotic figures in the duodenal crypts; markedly suppressed the inflammatory eicosanoid, prostaglandin E(2) in the liver; prevented liver hypertrophy; improved white blood cell counts; significantly increased red blood cell counts; decreased numbers of CPT-11 induced immature red blood cell and micronuclei in red blood cells of the peripheral blood; increased eicosapentaenoic acid and docosahexaenoic acid in liver cell membranes and maintained normal grooming behaviour. Thus 2% AAFA in the diet reduced the side effects of CPT-11 treatment in mice.

Cancer:

Cancer is linked to excess inflammation and nutrient deficiency. The cancer cells take advantage of the defenseless state of your immune system!

There is increasing evidence suggesting that inflammation plays a significant role in cancer development and progression. Chronic inflammation can lead to DNA damage, which in turn may lead to the formation of cancerous cells.

Marine omega-3 fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been shown to have potent anti-inflammatory effects. These fats, found primarily in fish and seafood, can help reduce the production of molecules and substances linked to inflammation, such as inflammatory eicosanoids and cytokines.

Lee2020: We found that 12 meta-analyses showed evidence of an association between ω-3 fatty acid intake and risk of the following types of cancer: liver cancer (n = 4 of 6), breast cancer (n = 3 of 14), prostate cancer (n = 3 of 11), and brain tumor (n = 2 of 2).

In preclinical studies (i.e., lab studies not done in humans), EPA and DHA have been shown to inhibit breast tumor growth, delay progression, and enhance the effects of some chemotherapy drugs.

While there is always more research needed to fully understand the relationship between omega-3 fatty acids and cancer risk, it is clear that maintaining a diet rich in omega-3s as part of a balanced, nutrient-rich diet, is generally recommended for overall health. In this context keep in mind that most supplements have been shown to be rancid and ineffective and that study biases have to be taken into account. Therefore most studies that look at “fresh fish eaters” show a clear effect whereas supplements can be questionable.

It’s also important to note that while a healthy diet with supplementations of omega3 can help reduce the risk of cancer, it is not a guarantee against cancer, and is only one component of a cancer prevention strategy. 

Source: Kimler 2018 Pathways of obesity-related inflammation in cancer

-> There are multiple preclinical and epidemiologic studies suggesting that the marine omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) help resolve inflammation and reduce the risk for breast cancer. This article shows how your own fat cells become less toxic and less inflammatory with omega3.

->Cancer cells have been shown to be deficient of omega-3 and change their entire cell membrane to become a “closed-off system”. The more omega-3 your membranes contain the higher your bodies defense mechanisms are to combat this change. 

-> Cancer cells create their own membrane to shut off communication with the body. This can be seen in the lipid composition and their high content of saturated fatty acids and also in pH and electrical potentials

-> Cancer is highly depended on inflammation; your inflammatory index matters!! YOU have to get below 4:1 index!

-> Cancer stem cells are hard to be killed, they are clever. By creating your own healthy new stem cells with ‘proper omega3 membranes’ to form a new tissue, you can outcompete the cancer stem cells and your immune system can finally take care of the problem.

-> “Survival of the fittest” – dont allow your cancer cells to be the ‘fittest”

How does omega3 prevent cancer?

Research has indeed indicated that cancer cells may have altered lipid metabolism, which can include a deficiency in omega-3 fatty acids. Omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are crucial components of cell membranes and have several biological functions that may inhibit cancer growth.

One of the proposed mechanisms by which omega-3 fatty acids might inhibit the growth of cancer cells is by incorporating into cell membranes and altering their properties. This can affect the fluidity, flexibility, permeability, and the function of several membrane proteins and receptors. Changes in these properties may in turn impact signal transduction pathways, cell behavior, and ultimately, cancer progression.

Another possibility is that omega-3 fatty acids are metabolized into bioactive derivatives (like resolvins, protectins, and maresins) that possess anti-inflammatory, pro-resolution, and tissue regenerative properties. These compounds might contribute to reducing inflammation, a key factor in the development and progression of many types of cancer.

However, it’s important to note that while the association between omega-3 fatty acids and cancer is promising, the relationship is complex and not fully understood. More research, particularly in the form of randomized controlled trials, is needed to fully elucidate these mechanisms and to develop specific dietary recommendations for cancer prevention and treatment.

•A ratio of 2.5/1 reduced rectal cell proliferation in patients with colorectal cancer, whereas a ratio of 4/1 with the same amount of omega-3 PUFA had no effect.

•The lower omega-6/omega-3 ratio in women with breast cancer was associated with decreased risk.

We conclude that DHA alters breast cancer exosome secretion and microRNA contents, which leads to the inhibition of angiogenesis. 

A plant-based diet LOW in linoleic acid (omega6), complemented by an ample intake of flaxseed and supplemental fish oil, with or without metformin and other D6D-antagonist agents, may aid prevention and control of some cancers.

Many diseases including cancer show an inhibition of the enzymes involved in omega3 (ALA) conversion to necessary EPA,DPA and DHA. The reason maybe a that the negative feedback from accumulation of inflammatory DGLA (omega6). Dihomo- γ-Linolenic Acid (20:3n-6)-Metabolism, Derivatives, and Potential Significance in Chronic Inflammation

A decrease in the number of live cells and an increase in the number of apoptotic cells were also observed with increasing DHA concentrations. p53 is one of the most important cancer mutation genes. In vitro concentrations of DHA equal to human plasma levels, are able to modulate, Wt-p53, survivin, and microRNA-16-1 in CRC cells

Olive products contain omega-9 and phenolic compounds. They indirectly contribute to the effect of omega3. Recent European projects such as EPIC (European Prospective Investigation into Cancer and Nutrition) and EPICOR (long-term follow-up of antithrombotic management patterns in acute coronary syndrome patients) have demonstrated the functional and preventive activities of EVOO showing the relation both between cancer and nutrition and between consumption of EVOO, vegetables, and fruit and the incidence of coronary heart disease. 

Colon cancer study: EPA + FuOx (a chemotherapy drug) caused a reduction in CSC/CSLC (chemo resistant cells) population. The growth reduction by this regimen is the result of increased apoptosis as evidenced by PARP cleavage. Our data suggest that EPA by itself or in combination with FuOx could be an effective preventive strategy for recurring colorectal cancer.

 

Inflammation drives cancer, namely arachidonic acid (omega6). Marks 1998: “A permanent overactivation of arachidonic acid metabolism appears to be a driving force of tumor development in both experimental animals and man. Inhibition of the enzymes involved (such as cyclooxygenases by nonsteroidal antiinflammatory drugs) provides, therefore, a powerful and promising measure of cancer chemoprevention. “

Calder 2017: “Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are n-3 fatty acids found in oily fish and fish oil supplements. These fatty acids are capable of partly inhibiting many aspects of inflammation including leucocyte chemotaxis, adhesion molecule expression and leucocyte-endothelial adhesive interactions, production of eicosanoids like prostaglandins and leukotrienes from the n-6 fatty acid arachidonic acid and production of pro-inflammatory cytokines. In addition, EPA gives rise to eicosanoids that often have lower biological potency than those produced from arachidonic acid, and EPA and DHA give rise to anti-inflammatory and inflammation resolving mediators called resolvins, protectins and maresins. Mechanisms underlying the anti-inflammatory actions of EPA and DHA include altered cell membrane phospholipid fatty acid composition, disruption of lipid rafts, inhibition of activation of the pro-inflammatory transcription factor nuclear factor κB so reducing expression of inflammatory genes and activation of the anti-inflammatory transcription factor peroxisome proliferator-activated receptor γ.”

Tevar 2002: EPA rats had significant reductions in tumor volume compared with isocaloric corn oil and control saline animals (25%, p < .01 and 33%, p < .01, respectively). Rats receiving EPA demonstrated decreased VEGF-alpha mRNA levels (0.023 +/- 0 0.001) compared with those receiving corn oil (0.129 +/- 0.047) or saline (0.150 +/- 0.026; p < .05).

Conclusions: These data demonstrate that EPA/DHA marine supplementation inhibits tumor growth, potentially through alterations in the expression of the pro-angiogenic VEGF-alpha. The mechanism(s) of EPA as an inhibitor of tumor-related angiogenic growth factors may be associated with COX-2 enzyme fatty acid metabolism and merits further study.

Cancer and LDH

The Warburg effect , proposed by Otto Warburg, is a phenomenon where cancer cells predominantly produce energy by a high rate of glycolysis followed by lactic acid fermentation in the cytosol, rather than by a comparatively low rate of glycolysis followed by oxidation of pyruvate in mitochondria as in most normal cells. This implies that even in the presence of oxygen, cancer cells tend to convert glucose into lactate.

Lactate dehydrogenase (LDH) plays a crucial role in this process by converting pyruvate, the end product of glycolysis, to lactate when oxygen is low.

Why Cancer Cells Use Warburg Effect:

1. Rapid Energy Production:
The glycolytic pathway provides ATP more quickly than oxidative phosphorylation, although it is less efficient in terms of ATP produced per molecule of glucose.

2. Biosynthetic Requirements:
This metabolic reprogramming also facilitates the diversion of glycolytic intermediates into biosynthetic pathways, aiding in the synthesis of nucleotides, amino acids, and lipids, which are critical for rapidly proliferating cells like cancer cells.

3. Adaptation to Hypoxic Environment:
Tumors often have regions of low oxygen, or hypoxia. By relying on glycolysis, which doesn’t require oxygen, cancer cells can survive and even thrive in hypoxic conditions.

4. Acidification of the Tumor Microenvironment:
The production of lactate leads to an acidic tumor microenvironment, which can induce tissue remodeling, aid in invasion and metastasis, and can inhibit the response of the immune cells.

5. Evasion of Apoptosis:
Mitochondrial oxidative phosphorylation is associated with apoptosis, a form of programmed cell death. By relying less on mitochondrial metabolism, cancer cells may resist apoptosis.

6. Redox Balance:
Utilizing glycolysis helps cancer cells maintain redox balance, managing reactive oxygen species (ROS) levels, and reducing oxidative stress.

Importance of LDH:
Increased LDH activity is seen as a marker for cellular necrosis and is also correlated with the Warburg effect in cancer cells. It is considered a crucial enzyme for the survival, proliferation, and metastasis of cancer cells, making it a potential therapeutic target in cancer treatment. Blocking LDH activity might impair the ability of cancer cells to sustain the high rate of glycolysis they rely on, potentially leading to reduced growth and survivability of the cancer cells.

Omega-3 fatty acids, particularly EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), have been studied for their potential anti-cancer effects, but the exact mechanisms are not fully understood and are likely multifaceted, involving anti-inflammatory, pro-apoptotic, and anti-proliferative pathways. Research has also explored the modulation of metabolic processes by omega-3 fatty acids, including their possible effects on lactate dehydrogenase (LDH) and cancer metabolism.

1. Omega-3 Fatty Acids and Cancer Cell Metabolism

Omega-3 fatty acids might influence cancer metabolism, which may include effects on LDH levels and activity. By modifying the lipid composition of cell membranes, omega-3 fatty acids could potentially affect the functionality of various membrane proteins involved in metabolic regulation.

2. Inflammation Modulation

Omega-3 fatty acids have well-established anti-inflammatory effects, which can contribute to their anti-cancer properties, given the role of chronic inflammation in cancer development and progression.

3. Cell Apoptosis and Proliferation

Several studies suggest that omega-3 fatty acids can induce apoptosis (programmed cell death) in cancer cells and inhibit their proliferation, which can halt the growth of tumors.

4. Omega-3 and Warburg Effect

Regarding the Warburg effect—where cancer cells preferentially utilize glycolysis over oxidative phosphorylation for energy production—it is conceivable that omega-3 fatty acids, by modulating inflammatory responses and cellular metabolism, could influence this metabolic shift in cancer cells.

5. Research Considerations

While the potential anti-cancer effects of omega-3 fatty acids are promising, it is essential to acknowledge the complexity of cancer biology. Individual studies may show differing results based on cancer type, study design, and other factors. Additionally, clinical relevance and application require extensive validation through well-designed clinical trials.

 

Cancer and VTE

Indeed, some research has shown that Omega-3 fatty acids, which have anti-inflammatory and antithrombotic properties, may reduce the risk of cardiovascular diseases including thrombosis. Omega-3 intake to VTE risk reduction in cancer patients shows a definitive relationship.

Isaksen 2019: Conclusion: A high dietary intake of marine n-3 PUFAs was associated with lower risk of recurrent VTE after unprovoked index events, DVT, and in cancer-free patients.

Cancer itself is a risk factor for venous thromboembolism due to various mechanisms, including the activation of the coagulation system, increased blood viscosity due to high cell turnover, and the release of procoagulant substances from cancer cells. Therefore, optimizing nutritional status, including Omega-3 intake, is an important part of overall cancer care.

Patients with cancer have up to a 7-fold excess risk of venous thromboembolism (VTE)

= this again highlights the importance of omega3 as there is a direct correlation of VTE and omega3 deficiency. It is not difficult to imaging that the quality of the arterial and venous membranes plays a role in this mechanism. 

 

Colorectal Cancer: Fiber and Microbiome

Chapkin 2020: Dietary fiber has been shown to reduce colon tumors in animal models, and, in vitro, butyrate influences cellular pathways important to cancer risk. Furthermore, work from our group suggests that the combined effects of butyrate and omega-3 polyunsaturated fatty acids (n-3 PUFA) may enhance the chemopreventive potential of these dietary constituents. We postulate that the relatively low intakes of n-3 PUFA and fiber in Western populations and the failure to address interactions between these dietary components may explain why chemoprotective effects of n-3 PUFA and fermentable fibers have not been detected consistently in prospective cohort studies.

–Zhang, Y., Chen, L., Hu, G. Q., & Zhang, N. (2018). Omega-3 polyunsaturated fatty acids in the prevention of postoperative complications in colorectal cancer: a meta-analysis. Short-term omega-3 PUFA administration was associated with reduced postoperative infectious complications, inflammatory cytokines, and hospital stay after CRC surgery

-An insight into the role of arachidonic acid derived lipid mediators in virus associated pathogenesis and malignancies

 

 

 

Programmed cell death in cancer  

Ferroptosis is a type of programmed cell death. There appears to be strong relationship between lipid peroxidation and cell death. Intrinsic mitochondrial-mediated programmed cell death resulting from the accumulation of lipid reactive oxygen species (ferroptosis), and epigenetic programming related to lipid catabolism and beta-oxidation-associated genes is strongly related to omega3 and butyric acid and the protection level in your gut.

Prostate Disease


The relationship between omega-3 fatty acid deficiency and prostate disease, including prostate cancer, has been a subject of considerable scientific debate and investigation. The role of dietary fats, particularly omega-3 fatty acids, in the development and progression of prostate disease is complex, with studies showing mixed results. Here’s a summary of the evidence:

Omega-3 Fatty Acids and Prostate Health
Anti-inflammatory Effects: Omega-3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are known for their anti-inflammatory properties. Chronic inflammation is thought to play a role in the development and progression of various cancers, including prostate cancer. Omega-3 fatty acids may help reduce this risk by mitigating inflammation.
Cell Growth Regulation: Omega-3 fatty acids have been shown to influence various molecular pathways that control cell growth, apoptosis (programmed cell death), and angiogenesis (the growth of new blood vessels), all of which are crucial in cancer development and progression.
Research Findings
Protective Effects: Some epidemiological studies suggest that high intake of omega-3 fatty acids is associated with a reduced risk of prostate cancer. For example, populations that consume a diet rich in fish (which is high in EPA and DHA) have lower incidences of prostate cancer.
2013 Study on Prostate Cancer Risk: A highly publicized 2013 study published in the “Journal of the National Cancer Institute” found that high concentrations of omega-3 fatty acids in the blood were associated with an increased risk of prostate cancer. However, this study faced criticism regarding its methodology, including the fact that blood levels of omega-3s were only measured once and may not have accurately reflected long-term dietary intake.
Meta-analyses and Reviews: Subsequent meta-analyses and systematic reviews have yielded mixed results. Some have found no significant association between omega-3 fatty acid intake and prostate cancer risk, while others suggest a potential protective effect, especially in terms of reducing mortality or progression of the disease.

In the polyunsaturated fatty acids (PUFAs), we found that the omega-3 PUFAs level was significantly decreased in patient with BPH and PC and that the omega-6 PUFAs level was increased in PC only.

Conclusion: It can be concluded that association of omega-3 fatty acids with tamsulocin and finasteride may produce better clinical results.

The relationship between dihydrotestosterone (DHT) and omega-3 fatty acids involves complex interactions that can influence various physiological processes, including those related to inflammation, hormone synthesis, and cellular function. Here’s a detailed look at how omega-3 fatty acids might interact with DHT and the potential implications:

Omega3 and DHT

Benign prostatic hypertrophy (BPH), also known as benign prostatic hyperplasia, is indeed closely related to the effects of the androgen hormone 5alpha-dihydrotestosterone (DHT) on the prostate gland. Here’s an overview of how DHT is involved in BPH:

Role of DHT in BPH

  1. Hormonal Conversion: DHT is a metabolite of testosterone, converted from testosterone by the enzyme 5-alpha reductase, which is present in the prostate, skin, and other tissues. DHT binds to androgen receptors with a much higher affinity than testosterone, making it a more potent androgen.

  2. Prostate Growth: DHT’s primary role in the prostate is to stimulate growth. During puberty, DHT is responsible for prostate development and growth. Later in life, continued exposure to DHT can lead to further prostate enlargement.

  3. Cellular Proliferation and Inflammation: DHT stimulates the proliferation of prostate cells and can contribute to the inflammatory processes within the prostate gland. Over time, this ongoing stimulation and cellular proliferation result in an enlarged prostate, characteristic of BPH.

Clinical Aspects of DHT and BPH

  • Symptoms of BPH: As the prostate enlarges, it can press against the urethra and bladder, leading to symptoms such as difficulty in urinating, increased urinary frequency, urgency, a weak urine stream, and incomplete bladder emptying.

  • Treatment Targeting DHT: Treatment strategies for BPH often focus on reducing DHT levels in the prostate to manage the condition. Medications such as finasteride and dutasteride are 5-alpha reductase inhibitors that reduce the conversion of testosterone to DHT, thereby helping to reduce prostate size and alleviate symptoms.

  1. Anti-inflammatory Effects: Omega-3 fatty acids, particularly EPA and DHA, are known for their anti-inflammatory properties. Since inflammation can contribute to conditions exacerbated by DHT, such as benign prostatic hyperplasia (BPH) and possibly certain forms of hair loss, omega-3 fatty acids may help mitigate these conditions by reducing the inflammatory response.

Hormonal Regulation

  1. Influence on Enzyme Activity: Omega-3 fatty acids may affect the activity of enzymes involved in hormone metabolism, including 5-alpha reductase, the enzyme responsible for converting testosterone into DHT. There is some evidence suggesting that omega-3 fatty acids can modulate this enzyme’s activity, potentially leading to lower DHT levels, although more research is needed to confirm these effects.

  2. Impact on Androgen Receptor Activity: Omega-3 fatty acids might also affect the activity of androgen receptors, to which DHT binds. Altering receptor sensitivity or activity could modify how effectively DHT exerts its effects on target tissues.

Effects on Prostate Health

  1. Potential Benefits for BPH: Given their anti-inflammatory effects and potential to modulate 5-alpha reductase activity, omega-3 fatty acids may have a beneficial role in managing BPH. By potentially reducing DHT production or activity, omega-3s might help in reducing prostate enlargement and the associated symptoms.

Cardiovascular Health

  1. Cardiovascular Implications: While the primary context here is the relationship between DHT and omega-3s, it’s worth noting that omega-3 fatty acids are beneficial for cardiovascular health. Since hormone balance, including DHT levels, can influence cardiovascular risk factors, omega-3 fatty acids might indirectly benefit heart health by improving lipid profiles and reducing inflammation.

  • Dietary Sources and Supplementation: For individuals interested in the potential benefits of omega-3 fatty acids, including those related to DHT modulation, incorporating rich sources of EPA and DHA, such as fatty fish (salmon, mackerel, sardines), or considering omega-3 supplements might be beneficial.

In conclusion, while the interaction between omega-3 fatty acids and DHT is complex and not fully understood, the potential for omega-3s to modulate inflammation, enzyme activity, and hormonal effects offers promising avenues for research and therapeutic strategies, particularly in conditions influenced by DHT levels.

Epigenetics and omega3

Changes in epigenetics maybe one of the reasons why our younger teen generations test so much worse compared to over 50 year old adults with an inflammatory index 50:1 not unusual. On average we find 2-3x Higher inflammatory index compared to older generations:

Abbas 2021: “A diet supplemented with omega-3-rich FA (as opposed to an omega-6-rich diet containing corn oil), reduced the risk of developing BCa, and also significantly reduced the incidence of BCa in F1 offspring. 

 

It is possible that changes in epigenetics contribute to the differences in inflammatory indices between younger and older generations. Epigenetics refers to modifications in gene expression that are not caused by changes in the DNA sequence itself but are influenced by external factors, such as diet, lifestyle, and environmental exposure.

Inflammation is a complex physiological response that plays a crucial role in the immune system. While acute inflammation is typically beneficial for fighting off infections and promoting tissue repair, chronic inflammation can lead to various health issues, including cardiovascular disease, obesity, and autoimmune disorders.

There are several factors that might be contributing to the observed differences in inflammatory indices between younger and older generations:

  1. Dietary changes: Modern diets, particularly those rich in processed foods, refined sugars, and unhealthy fats, can contribute to chronic inflammation. The consumption of omega-6 fatty acids has increased over time, resulting in a higher omega-6 to omega-3 ratio in the diet, which is linked to increased inflammation. Older generations may have consumed more balanced diets with a lower inflammatory potential.

  2. Lifestyle factors: Increased sedentary behavior, reduced physical activity, and disrupted sleep patterns in younger generations could also contribute to higher inflammatory indices. Regular exercise and adequate sleep are essential for maintaining a healthy immune system and controlling inflammation.

  3. Environmental factors: Exposure to pollution, environmental toxins, and chronic stress can also impact epigenetic regulation and contribute to inflammation. Younger generations may be more exposed to these factors than older generations.

  4. Genetics and epigenetics: Genetic predispositions, combined with epigenetic changes resulting from the factors mentioned above, might contribute to the observed differences in inflammatory indices between younger and older generations.

It is essential to consider these factors collectively when trying to understand the differences in inflammatory indices between age groups. Further research is needed to establish a clear connection between epigenetic changes and the higher inflammatory indices observed in younger generations. Public health interventions targeting diet, lifestyle, and environmental factors may help reduce inflammation and improve overall health in younger populations.

Some studies and predictions suggest that current younger generations might be at a higher risk of developing cancer, dementia, and other chronic diseases due to various factors. Several contributing factors include lifestyle changes, environmental exposures, and increased prevalence of risk factors:

  1. Lifestyle changes: Younger generations are exposed to several lifestyle factors that increase the risk of cancer and dementia, such as unhealthy diets, sedentary behavior, and disrupted sleep patterns. For example, high consumption of processed foods, refined sugars, and unhealthy fats, along with low consumption of fruits and vegetables, can increase the risk of certain types of cancer. Additionally, lack of physical activity and poor sleep hygiene have been linked to increased risks of both cancer and dementia.

  2. Obesity: The prevalence of obesity has increased dramatically in recent decades, especially among younger populations. Obesity is a significant risk factor for many types of cancer, and it has also been associated with an increased risk of dementia.

  3. Environmental factors: Younger generations may be more exposed to pollution, environmental toxins, and chronic stress, which can contribute to the development of cancer and dementia. For example, air pollution has been linked to lung cancer and neurodegenerative diseases like Alzheimer’s.

While these factors suggest that younger generations might be at a higher risk of developing cancer and dementia, it is important to note that improvements in medical care, early detection, and preventive measures can help mitigate these risks. Encouraging and promoting healthy lifestyle choices, such as a balanced diet, regular exercise, and stress reduction, can significantly reduce the risk of developing these chronic diseases. Additionally, further research and public health initiatives are needed to address the specific challenges faced by younger generations.

  1. Kalmijn, S., van Boxtel, M. P., Ocké, M., Verschuren, W. M., Kromhout, D., & Launer, L. J. (2004). Dietary intake of fatty acids and fish in relation to cognitive performance at middle age. Neurology, 62(2), 275-280.

  2. Niculescu, M. D., Lupu, D. S., & Craciunescu, C. N. (2011). Perinatal manipulation of α-linolenic acid intake induces epigenetic changes in maternal and offspring livers. The FASEB Journal, 25(1), 216-227.

  3. Gao, H., Geng, T., Huang, T., & Zhao, Q. (2016). Fish oil supplementation and insulin sensitivity: a systematic review and meta-analysis. Lipids in Health and Disease, 15(1), 1-10.

  4. Calder, P. C. (2018). Omega-3 fatty acids and inflammatory processes: from molecules to man. Biochemical Society Transactions, 46(5), 1105-1115.

  5. Joffre, C., Rey, C., Layé, S., & Nadjar, A. (2020). N-3 polyunsaturated fatty acids and the resolution of neuroinflammation. Frontiers in Pharmacology, 11, 1147.

 

More articles on epigenetics topic:

  1. Omega-3 fatty acids and DNA methylation in prostate cancer: epigenetic and transcriptomic implications. Fernández-Real et al., Clinical Epigenetics 2021. PMID: 34020618 investigated the effects of omega-3 fatty acids on DNA methylation patterns in prostate cancer cells.

  2. Omega-3 fatty acids and epigenetic regulation of adipose tissue inflammation. Acevedo et al., Molecular Nutrition & Food Research 2021. PMID: 33555446 explored the epigenetic mechanisms by which omega-3 fatty acids may reduce inflammation in adipose tissue.

  3. Omega-3 fatty acids and epigenetic regulation in brain health and disease. Chang et al., Trends in Molecular Medicine 2020. PMID: 32046816 discusses the potential for omega-3 fatty acids to modulate epigenetic processes in the brain and influence brain health.

  4. The effect of omega-3 fatty acids on DNA methylation and histone modifications in patients with major depressive disorder. Ahmadpanah et al., Journal of Affective Disorders 2020. PMID: 32679495 This randomized controlled trial, published in the journal Journal of Affective Disorders in 2020, investigated the effects of omega-3 fatty acid supplementation on epigenetic modifications in patients with major depressive disorder.

  5. The role of omega-3 fatty acids in epigenetic regulation of inflammation and aging. Simonovic et al., Nutrients 2019. PMID: 31658730 summarizes the current knowledge on the epigenetic mechanisms by which omega-3 fatty acids may modulate inflammation and aging.

 

Inflammatory markers and Arthritis:

There is no question that both inflammatory arthritis and osteo-arthritis are linked to a high omega6/3 index. As a matter of fact rheumatoid arthritis although presenting with different symptoms initially will develop in to OA.

The term “leaky gut” refers to a proposed medical condition in alternative medicine wherein there is increased permeability of the gut lining. Increased permeability allows substances like bacteria, toxins, and undigested food particles to leak from your intestines into your bloodstream, which may potentially lead to systemic inflammation.

The concept of “leaky joints” then results as this long term systemic inflammation caused by a leaky gut could potentially impact the joints, leading to symptoms such as pain and stiffness. Certain studies also suggest that the gut microbiome could play a role in the development of such autoimmune disorders.

There is evidence suggesting that an imbalance in the omega-6 to omega-3 fatty acid ratio, specifically a high omega-6/3 index, can contribute to the development and progression of inflammatory arthritis, such as rheumatoid arthritis (RA), and osteoarthritis (OA).

Omega-6 and omega-3 fatty acids are both essential polyunsaturated fatty acids that play crucial roles in human health. However, they have opposing effects on inflammation. Omega-6 fatty acids, particularly arachidonic acid (AA), are precursors to pro-inflammatory molecules, while omega-3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have anti-inflammatory properties.

Rheumatoid arthritis is an autoimmune disease characterized by chronic inflammation in the joints. Inflammation plays a critical role in the pathogenesis of RA. A high omega-6/3 ratio can exacerbate inflammation and contribute to the development and progression of the disease. Studies have shown that increasing omega-3 fatty acid intake can help reduce inflammation and alleviate RA symptoms.

Osteoarthritis, on the other hand, is a degenerative joint disease primarily caused by wear and tear on the joints over time. While OA is not typically considered an inflammatory disease, low-grade inflammation has been shown to play a role in the cartilage breakdown and joint damage seen in OA. A high omega-6/3 ratio can contribute to this low-grade inflammation, potentially worsening OA symptoms and progression.

Although rheumatoid arthritis and osteoarthritis are distinct diseases with different underlying mechanisms, it is possible for an individual with RA to eventually develop OA due to the long-term joint damage caused by chronic inflammation. In both cases, maintaining a balanced omega-6/3 ratio may help reduce inflammation and improve joint health.

What the studies say:

•A ratio of 2-3/1 suppressed inflammation in patients with rheumatoid arthritis. This can be measured by markers such as cortisol, IL-6, -12 and TNFalpha.

Madison et al 2021 found: Omega-3reduced overall cortisol (p = 0.03) and IL-6 (p = 0.03) throughout the stressor; the 2.5 g/d group had 19% and 33% lower overall cortisol levels and IL-6 geometric mean levels, respectively, compared to the placebo group. By lowering overall inflammation and cortisol levels during stress and boosting repair mechanisms during recovery, omega-3 may slow accelerated aging and reduce depression risk.

 

 

Osteoarthritis:

Loef 2018: While all polyunsaturated fatty acids reduced markers of oxidative stress, omega-3 polyunsaturated fatty acids additionally decreased prostaglandin production. Human intervention studies with omega-3 polyunsaturated fatty acid supplementation may indicate a beneficial effect on pain and function and might be associated with less structural damage. 

Conclusions: Krill oil was safe to consume and resulted in modest improvements in knee pain, stiffness, and physical function in adults with mild to moderate knee OA.

 

 

Osteoporosis:

The Omega-6/3 index, also known as the fatty acid index, is a measure that represents the balance between omega-6 and omega-3 polyunsaturated fatty acids (PUFAs) in the body. This balance plays a crucial role in maintaining overall health and preventing various chronic diseases, including osteoporosis.

Osteoporosis is a bone disease characterized by reduced bone mass, weakened bone structure, and increased risk of fractures. It is more prevalent in older adults, particularly postmenopausal women. The exact relationship between the Omega-6/3 index and osteoporosis is still being researched, but evidence suggests that the balance of these fatty acids can impact bone health.

Omega-6 and omega-3 PUFAs are essential fatty acids, meaning they must be obtained through the diet. Omega-6 fatty acids are generally pro-inflammatory, while omega-3 fatty acids have anti-inflammatory properties. Inflammation is thought to contribute to the development of osteoporosis, as it can trigger bone resorption (the process of breaking down bone and releasing minerals into the bloodstream).

A balanced Omega-6/3 index is important for maintaining optimal bone health. An imbalance, particularly with a high omega-6 to omega-3 ratio, may contribute to increased inflammation and bone loss, thus increasing the risk of osteoporosis. A healthy ratio is generally considered to be around 4:1 (omega-6 to omega-3) or lower. Some researchers even suggest aiming for a 1:1 ratio for optimal health benefits.

To maintain a healthy Omega-6/3 index, it is important to consume a balanced diet that includes a variety of foods rich in omega-3 fatty acids, such as fatty fish (salmon, mackerel, sardines), flaxseeds, chia seeds, and walnuts. At the same time, try to reduce the intake of omega-6-rich foods, like vegetable oils (soybean, corn, sunflower), and processed foods.

While the Omega-6/3 index is just one factor that can impact bone health, it’s essential to consider other factors as well, such as adequate calcium and vitamin D intake, regular physical activity, and avoiding smoking and excessive alcohol consumption. If you are concerned about your Omega-6/3 index or your risk for osteoporosis, consult with a healthcare professional or registered dietitian for personalized advice.

 

Studies related to the Omega-6/3 index, fatty acid balance, and bone health. 

  1. -Weiss, L. A., Barrett-Connor, E., & von Muhlen, D. (2005). Ratio of n-6 to n-3 fatty acids and bone mineral density in older adults: the Rancho Bernardo Study. American Journal of Clinical Nutrition, 81(4), 934-938. 

  2. -Orchard, T. S., Cauley, J. A., Frank, G. C., Neuhouser, M. L., Robinson, J. G., Snetselaar, L., … & Lu, B. (2010). Fatty acid consumption and risk of fracture in the Women’s Health Initiative. The American Journal of Clinical Nutrition, 92(6), 1452-1460. 

  3. -Farina, E. K., Kiel, D. P., Roubenoff, R., Schaefer, E. J., Cupples, L. A., & Tucker, K. L. (2011). Protective effects of fish intake and interactive effects of long-chain polyunsaturated fatty acid intakes on hip bone mineral density in older adults: the Framingham Osteoporosis Study. The American Journal of Clinical Nutrition, 93(5), 1142-1151. 

  4. -Virtanen, J. K., Mozaffarian, D., Cauley, J. A., Mukamal, K. J., Robbins, J., & Siscovick, D. S. (2010). Fish consumption, bone mineral density, and risk of hip fracture among older adults: the cardiovascular health study. Journal of Bone and Mineral Research, 25(9), 1972-1979. 

  5. –Lavado-García, J., Roncero-Martin, R., Moran, J. M., Pedrera-Canal, M., Aliaga, I., Leal-Hernandez, O., … & Calder, P. C. (2018). Long-chain omega-3 polyunsaturated fatty acid dietary intake is positively associated with bone mineral density in normal and osteopenic Spanish women. PLoS ONE, 13(1), e0190539. 

  6. – 432,924 subjects: Positive effects on bone were found in 3% of subjects with MeatDiet and in 12% with FishDiet. 

These studies investigate the relationship between the Omega-6/3 index, fatty acid consumption, and bone health in various populations. Some of them indicate a positive association between omega-3 fatty acid intake and bone mineral density, while others emphasize the importance of maintaining a balanced ratio of omega-6 to omega-3 fatty acids. 

 

Lung health:

•ratio of 5/1 had a beneficial effect on patients with asthma, whereas a ratio of 10/1 had adverse consequences. Higher omega-6 intake associated with increased odds of increased asthma severity 

Seasonal Allergy

Kitz 2010: Ratios of n-3/n-6 PUFA were significantly lower in asthmatics than in healthy controls. Levels of eNO were significantly higher in Q25 asthmatics than in Q75 asthmatics (p = 0.040). There was a trend of higher bronchial hyperreactivity in Q25 asthmatics (median PD(20) 0.27 vs. 0.14; n.s.), induced by specific bronchial challenge with grass pollen (FEV(1) decrease 16.7 vs. 23.1%; n.s.).

 

ADHD, Mental Health, Dementia, Parkinson’s, Alzheimer’s disease

Mental health problems start early in life:

ADHD: Children are deprived of proper brain development:

Yes, all mental diseases maybe related to one problem! Research is clear on that. Synaptic vesicles do not function, channels and receptors malfunction and your brain is simply “on fire”! This problem slowly gets worse over a lifetime and your brain is slowly degrading. And the problem is getting worse. The number of diagnosed mental diseases will almost double almost every 20 years!

Dysfunctional and 30:1 inflammatory neuronal membranes simply cannot produce a healthy state.

  1. -Omega3 deficiency early in life is now linked to mental disease and dementia later in life. This is simply related to the functional neuronal brain function. Receptors and synapses cannot function properly without omega3.
  2. -Omega 3 and brain health in our Kids: consider that up to 60% of your brain mass is comprised of fat and lipids and over 60% of that fat is supposed to be unsaturated PUFA; On average our kids test at 60 – 85% deficiency in PUFA which results in a functional brain fat composition of less than 7%!! Here is an ADHD study showing there is evidence that n-3 PUFAs supplementation monotherapy improves clinical symptoms and cognitive performances in children and adolescents with ADHD.
  3. -Depression: n-3 PUFAs and their role in depression: These fatty acids are critical for development and function of the central nervous system. Increasing evidence from epidemiological, laboratory, and randomized placebo-controlled trials suggests deficiency of dietary n-3 PUFAs may contribute to development of mood disorders, and supplementation with n-3 PUFAs may provide a new treatment option. 

 

There is evidence suggesting that omega-3 fatty acid deficiency early in life may be linked to an increased risk of developing mental health disorders. Omega-3 fatty acids, particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), are crucial for brain development and function throughout life.

DHA is a major structural component of neuronal cell membranes and plays a vital role in maintaining their integrity and fluidity, while both DHA and EPA have anti-inflammatory and neuroprotective properties. Adequate omega-3 fatty acid intake during critical periods of brain development, such as during pregnancy and early childhood, is essential for optimal cognitive and behavioral outcomes.

Some of the mental health disorders potentially linked to omega-3 deficiency early in life include:

  1. Attention Deficit Hyperactivity Disorder (ADHD): Some studies have found that children with ADHD have lower levels of omega-3 fatty acids, particularly DHA, compared to their peers. Omega-3 supplementation has shown potential benefits in improving ADHD symptoms in some clinical trials, although more research is needed to confirm these findings.

  2. Autism Spectrum Disorder (ASD): While the exact cause of ASD is not fully understood, some research has suggested that omega-3 fatty acid deficiency during early brain development may be a contributing factor. Some studies have reported improvements in ASD symptoms following omega-3 supplementation, but more research is necessary to establish a clear link.

  3. Depression and anxiety: Omega-3 fatty acids have been shown to play a role in regulating mood and reducing inflammation, which can contribute to the development of depression and anxiety. Some studies have suggested that low omega-3 levels during early life may be associated with an increased risk of developing these mental health disorders later in life.

  4. Schizophrenia and other psychotic disorders: There is some evidence suggesting that omega-3 fatty acid deficiency during early brain development may increase the risk of developing schizophrenia and other psychotic disorders. Some studies have reported improvements in symptoms with omega-3 supplementation, but more research is needed to confirm these findings.

  5. Chronic deficiencies of certain minerals such as zinc, iron, magnesium and iodine and insufficient dietary intake of long-chain polyunsaturated fatty acids may have a significant impact on the development and deepening of the symptoms of ADHD in children. A crucial role in the diet of pregnant and lactating women, and child plays also polyunsaturated omega-3 fatty acids, mainly DHA, which are necessary for proper development and function of brain. 
  6. Omega-3 supplement is the latest dietary treatment with positive reports of efficacy, and interest in the additive-free diet of the 1970s is occasionally revived. A provocative report draws attention to the ADHD-associated “Western-style” diet, high in fat and refined sugars, and the ADHD-free “healthy” diet, containing fiber, folate, and omega-3 fatty acids. 

It is important to note that while omega-3 deficiency may be a contributing factor to the development of mental health disorders, it is not the sole cause. Mental health disorders are complex and multifactorial, involving genetic, environmental, and lifestyle factors. However it is evident that Ensuring adequate omega-3 intake during pregnancy and early childhood may be beneficial for promoting optimal brain development and reducing the risk of mental health disorders.

Parkinson’s Disease

There is growing interest in the potential role of omega-3 fatty acids in the prevention and management of Parkinson’s disease (PD), a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra region of the brain. While the exact cause of PD is not yet fully understood, factors such as oxidative stress, inflammation, and mitochondrial dysfunction are believed to contribute to the development and progression of the disease.

Omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are known to have anti-inflammatory and neuroprotective properties, which could be beneficial in the context of Parkinson’s disease. Some potential mechanisms by which omega-3 fatty acids may influence PD include:

  1. Reducing inflammation: Omega-3 fatty acids can modulate the production of inflammatory cytokines and other molecules involved in the inflammatory response, which could help protect dopaminergic neurons from damage associated with inflammation.

  2. Protecting against oxidative stress: EPA and DHA have antioxidant properties and can help counteract the harmful effects of reactive oxygen species (ROS), which contribute to oxidative stress and neuronal damage in PD.

  3. Supporting neuronal membrane integrity: DHA is a major structural component of neuronal cell membranes and plays a crucial role in maintaining their integrity and fluidity. Adequate DHA levels may support neuronal function and protect against neurodegeneration.

  4. Promoting neurogenesis: Some studies have suggested that omega-3 fatty acids could stimulate the growth of new neurons and support the survival of existing ones, which could be beneficial in slowing the progression of PD.

Evidence from preclinical studies and epidemiological research suggests that omega-3 fatty acids may have protective effects against Parkinson’s disease. Current data is not yet conclusive due to the fact of inadequate supplements. Randomized controlled trials investigating the effects of proper omega-3 supplementation in individuals with PD are necessary to establish the potential therapeutic benefits of these fatty acids in the prevention and management of the disease. However fish eaters and PD show a clear benefit.

Several studies have examined the potential relationship between fish consumption and the risk of Parkinson’s disease, with somewhat mixed results.

Many fish are high in omega-3 fatty acids, which have been suggested to have neuroprotective effects and could potentially lower the risk of Parkinson’s disease. Additionally, fish is a significant source of dietary vitamin D, which has also been suggested to have a protective effect against Parkinson’s.

It is important to get your omega-3 from tested small cold water fish to minimize the environmental toxins such as mercury, which could potentially increase the risk of neurodegenerative diseases such as Parkinson’s.

A large Swedish study published in 2014 in the American Journal of Epidemiology found no overall association between fish consumption and Parkinson’s disease risk. However, they found a lower risk among those who ate fatty fish and fish rich in omega-3.

Another study published in Neurology in 2003, suggested that even moderate consumption of dietary vitamin D may be associated with a lower risk of Parkinson’s disease.

Particularly DHA is important in brain development and function as well as vision health.

  1. DHA can ward off Parkinson’s symptoms!
  2. Parkinson’s studies show Indeed, treatment with omega-3 fatty acids, being safe and well tolerated, represents a valuable and biologically plausible tool in the management of neurodegenerative diseases in their early stages. Most dementia disease is age related. Our bodies are amazing designs that can operate on below 10% nutrition for a long time, however at certain age and most Parkinson’s is diagnosed above 65 years the inflammation in the brain reaches a limit. A diet rich in omega 3 defeats the outcome of dementia!

    How does this work? – dysfunctional lipid rafts

    Evidence suggests the greatest benefit may been seen with DHA in non-cognitively impaired older people. Purified lipid rafts from the frontal cortex of postmortem samples from patients with early motor stage PD and incidental PD exhibit significant reductions in DHA (and AA), but not EPA or DPA, compared to controls (Fabelo et al., ).  Dyall SC. Long-chain omega-3 fatty acids and the brain: a review of the independent and shared effects of EPA, DPA and DHA. Front Aging Neurosci. 2015;7:52. doi: 10.3389/fnagi.2015.00052 https://pubmed.ncbi.nlm.nih.gov/25954194/

Alzheimer’s

 

Alzheimer’s disease: Neuroinflammation is strongly implicated in Alzheimer’s disease (AD). Inflammation is not only controlled by inflammatory eicosanoids (system-2 pge, pgp, pgf and many others) but also by local epoxy products from rapidly oxidized PUFAs. However epoxys are then rapidly removed by hydrolases. These hydrolases are predominantly expressed in astrocytes and are elevated in postmortem brain tissue from patients with AD. In other words local epoxy anti-inflammatory effects to reduce inflammation in the brain are not effective in AD patients.

 

The newest study on the relationship between omega-3 fatty acids and Alzheimer’s Disease (AD), as well as dementia and cognitive decline, offers significant insights:

  1. Study Focus and Participants: The study aimed to assess the longitudinal relationships of omega-3 polyunsaturated fatty acid intake and blood biomarkers with the risk of AD, dementia, or cognitive decline. It included data from 1135 participants without dementia, averaging 73 years old, from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort.

  2. Findings on Omega-3 Supplement Use: In the ADNI cohort, long-term users of omega-3 fatty acid supplements showed a 64% reduced risk of developing Alzheimer’s Disease. This was measured over a 6-year follow-up period.

  3. Meta-Analysis of Dietary Intake: The study also incorporated a meta-analysis of 48 longitudinal studies involving 103,651 participants to test the impact of dietary intake of omega-3 and its peripheral markers on all-cause dementia or cognitive decline. The findings suggest that dietary intake of omega-3 fatty acids could lower the risk of dementia or cognitive decline by approximately 20%, particularly with docosahexaenoic acid (DHA) intake.

  4. Dose-Response Analysis: The analysis indicated that each increment of 0.1 g/day of DHA or eicosapentaenoic acid (EPA) intake was associated with an 8% to 9.9% lower risk of cognitive decline. Additionally, elevated levels of plasma EPA and erythrocyte membrane DHA were linked to a lower risk of cognitive decline.

  5. Conclusion: The study concludes that dietary intake or long-term supplementation of omega-3 fatty acids may help reduce the risk of Alzheimer’s Disease or cognitive decline​

Here are more studies on the potential benefits of omega-3 fatty acids in the prevention and treatment of Alzheimer’s disease:

  1. A higher omega-3 index was correlated with larger total normal brain volume ! Pottala JV, Yaffe K, Robinson JG, et al. Higher RBC EPA + DHA corresponds with larger total brain and hippocampal volumes: WHIMS-MRI study. Neurology. 2014;82(5):435-442. doi:10.1212/WNL.0000000000000080 

  2. DHA is also protective against several risk factors for dementia including head trauma, diabetes, and cardiovascular disease. DHA is specifically protective against AD via additional mechanisms: It limits the production and accumulation of the amyloid β peptide toxin Cole GM, Ma QL, Frautschy SA. Omega-3 fatty acids and dementia. Prostaglandins Leukot Essent Fatty Acids. 2009;81(2-3):213-221. doi: 10.1016/j.plefa.2009.05.015 

  3. A total of 131 sample participants developed Alzheimer disease. Participants who consumed fish once per week or more had 60% less risk of Alzheimer disease! Zhang Y, Chen J, Qiu J, Li Y, Wang J, Jiao J. Intake of fish and n-3 fatty acids and risk of dementia and Alzheimer’s disease: a meta-analysis. Ageing Res Rev. 2016;25:1-12. doi: 10.1016/j.arr.2015.11.005 

  4. A subgroup (n = 32) with very mild cognitive dysfunction (MMSE >27 points), a significant (P<.05) reduction in MMSE decline rate was observed in the omega-3 fatty acid-treated group compared with the placebo group; Freund-Levi Y, Eriksdotter-Jönhagen M, Cederholm T, et al. Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease: OmegAD study: a randomized double-blind trial. Arch Neurol. 2006;63(10):1402-1408. doi: 10.1001/archneur.63.10.1402 

These studies suggest that omega-3 fatty acids, particularly EPA and DHA, may have a protective effect against the development of Alzheimer’s disease and improve cognitive function in individuals with mild to moderate Alzheimer’s disease. Omega-3 fatty acids may also improve brain volume and reduce brain inflammation.

Note: There are several reasons why some studies might not show a benefit for a particular intervention, like omega-3 supplementation, and why researchers often conclude that “more research is needed.” Some of the most common issues are:

  1. Lack of Quality Control: Without quality control measures in place, it’s hard to ensure that all participants are receiving the same type and quality of supplement. This is especially true for omega-3 supplements, which can become rancid if not properly stored and handled.

  2. High Dropout Rates: In many studies, a significant proportion of participants discontinue participation before the study is completed. This can bias the results, as the people who drop out might differ in important ways from those who stick with the study.

  3. Subjective Measurements: Diseases like dementia and depression often rely on subjective measures, such as self-reported mood or cognitive function. These measures can be influenced by a host of factors beyond the treatment being studied, making it difficult to isolate the treatment’s effects.

  4. Lack of Biomarkers: Without objective biomarkers to measure disease status, it’s hard to gauge the true impact of a treatment. This can make the results of a study difficult to interpret and can lead to under- or over-estimation of the treatment’s effects.

  5. Short Study Durations: Many studies are only conducted over a short period, such as six months. This might not be enough time to see the full effects of a treatment, particularly for chronic diseases that develop and progress slowly.

  6. Inadequate Control Groups: Without appropriate control groups, it’s hard to account for the placebo effect or other factors that might influence the results. For example, people who drop out of a study might have been more likely to experience negative outcomes, which could skew the results if they’re not properly accounted for.

  7. Lack of Inflammatory Index Testing: Without testing the inflammatory omega-6/3 index, it’s hard to know how much quality, non-oxidized omega-3 participants are actually consuming.

All of these issues can contribute to bias in research studies and can make it challenging to draw firm conclusions from the results. That’s why researchers often call for more studies to further investigate and confirm their findings.

IN SUMMARY, research shows your brain shrinks without proper omega3 and neurons are dysfunctional and inflammatory. Just like heart disease, the brain suffers from a very omega6/3 index of over 20:1 and only less than 1% of people show an index of less than the required 4:1.

 

ALS

Amyotrophic lateral sclerosis  or Lou Gehrig’s disease is a motor neuron disease (MND) that results in the progressive loss of motor neurons that control voluntary muscles. Again this disease is highly depended on inflammation and the destructive process in the brain. Omega3 can reduce this risk significantly.

Fitzgerald 2014: Longitudinal analyses based on 1,002,082 participants (479,114 women and 522,968 men) in 5 prospective cohorts. A total of 995 ALS cases were documented during the follow-up. A greater ω-3 PUFA intake was associated with a reduced risk for ALS. The pooled, multivariable-adjusted RR for the highest to the lowest quintile was 0.66 (95% CI, 0.53-0.81; P < .001 for trend). Consumption of both α-linolenic acid (RR, 0.73; 95% CI, 0.59-0.89; P = .003 for trend) and marine ω-3 PUFAs (RR, 0.84; 95% CI, 0.65-1.08; P = .03 for trend) contributed to this inverse association. Intakes of ω-6 PUFA were not associated with ALS risk.

  1. Mariosa D, Hammar N, Malmstrom T, et al. Dietary intake of fish, omega-3, omega-6 polyunsaturated fatty acids and vitamin D and the prevalence of amyotrophic lateral sclerosis in a Swedish cohort. J Neurol Neurosurg Psychiatry. 2017;88(9):818-826. doi:10.1136/jnnp-2016-315721

  2. Wills AM, Hubbard J, Macklin EA, et al. Hypercaloric enteral nutrition in patients with amyotrophic lateral sclerosis: A randomised, double-blind, placebo-controlled phase 2 trial. Lancet. 2014;383(9934):2065-2072. doi:10.1016/S0140-6736(14)60222-1

  3. Khan F, Patterson A, Lewington A, et al. The Role of Omega-3 Fatty Acids in the Management of Amyotrophic Lateral Sclerosis (ALS): A Systematic Review. Nutrients. 2018;10(6):773. doi:10.3390/nu10060773

  4. Long J, Gao F, Tong L, et al. The Anti-Inflammatory Effects of Omega-3 Fatty Acids in the Brain: Implications for the Treatment of Amyotrophic Lateral Sclerosis. Open Biol. 2019;9(8):190165. doi:10.1098/rsob.190165

These studies suggest that omega-3 fatty acids may have anti-inflammatory effects in the brain and could potentially improve motor function and survival in patients with ALS.

 

 

IQ development

-> Fetus development means building a brain and nervous system from scratch. This cannot be done properly without the availability of omega3

-> Our balance tests show how the baby desperately uses every DHA molecule available and both mother and baby end up deficient.

– > Brain health is essential to your children’s IQ development at any age. There is a direct link of omega3, IQ and dementia at a later age.

 

Omega-3 fatty acids, particularly EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), are essential for brain health and development. They play crucial roles in cognitive function, neuronal communication, and maintaining the integrity of cell membranes. Research suggests that omega-3 fatty acids may have a positive impact on IQ development in children and potentially help reduce the risk of dementia in later life.

  1. IQ Development in Children:

Gómez-Pinilla, F. (2008). Brain foods: the effects of nutrients on brain function. Nature Reviews Neuroscience, 9(7), 568-578. Link: https://www.nature.com/articles/nrn2421

This review article discusses the effects of various nutrients, including omega-3 fatty acids, on brain function. The author highlights that a diet rich in omega-3 fatty acids is crucial for brain development and cognitive function, particularly during prenatal and early childhood periods.

Helland, I. B., Smith, L., Saarem, K., Saugstad, O. D., & Drevon, C. A. (2003). Maternal supplementation with very-long-chain n-3 fatty acids during pregnancy and lactation augments children’s IQ at 4 years of age. Pediatrics, 111(1), e39-e44. Link: https://pediatrics.aappublications.org/content/111/1/e39

This study found that maternal supplementation with omega-3 fatty acids during pregnancy and lactation resulted in higher IQ scores in children at 4 years of age, suggesting that early omega-3 intake may positively impact cognitive development.

  1. Dementia in Later Life:

Yurko-Mauro, K., Alexander, D. D., & Van Elswyk, M. E. (2015). Docosahexaenoic acid and adult memory: a systematic review and meta-analysis. PloS one, 10(3), e0120391. Link: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0120391

This systematic review and meta-analysis concluded that DHA supplementation may improve memory and cognitive function in older adults with mild cognitive impairment, which could potentially help delay the onset of dementia.

Cederholm, T., & Palmblad, J. (2010). Are omega-3 fatty acids options for prevention and treatment of cognitive decline and dementia?. Current Opinion in Clinical Nutrition & Metabolic Care, 13(2), 150-155. Link: https://journals.lww.com/co-clinicalnutrition/Abstract/2010/03000/Are_omega_3_fatty_acids_options_for_prevention_and.8.aspx

This review paper explores the potential role of omega-3 fatty acids in the prevention and treatment of cognitive decline and dementia. The authors suggest that increasing the intake of omega-3 fatty acids, especially DHA, could be beneficial for maintaining cognitive function in older adults.

Overall, research indicates that omega-3 fatty acids, particularly DHA, play a crucial role in cognitive development in children and may help maintain cognitive function and reduce the risk of dementia in older adults. Conclusion. Maternal intake of very-long-chain n-3 PUFAs during pregnancy and lactation is favorable for later mental development of children.

 

Basak 2021: During the last trimester of gestation and for the first 18 months after birth, both docosahexaenoic acid,22:6n-3 (DHA) and arachidonic acid,20:4n-6 (ARA) are preferentially deposited within the cerebral cortex at a rapid rate. 

 

The study estimates that increasing maternal docosahexaenoic acid (DHA) intake by 100 mg/day increases child IQ by 0.13 points. Children whose mothers had eaten fish (whether oily or non-oily) in late pregnancy had a verbal IQ that was 7.55 points higher (95% CI .75 to 14.4) than those whose mothers did not eat fish. This study even suggests that at age7 it maybe too late to make a difference. However we think its never too late because remember most of these studies are done with with inadequate or rancid omeg3 supply and it is really important to analyze the 6:3 ratio.

Mueller 2020: A vegan diet can be potentially critical for young children with risks of inadequate supply in terms of protein quality and energy as well as long-chain fatty acids, iron, zinc, vitamin D, iodine, calcium, and particularly vitamin B12. Deficiencies in these nutrients can lead to severe and sometimes irreversible developmental disorders. If such a diet is chosen for ethical, ecological, or health reasons, a well-planned, diversified diet with additional supplementation of vitamin B12, vitamin D, iodine, and potentially other micronutrients is crucial to ensure a healthy and nutritious intake during childhood.

Gaps in meeting nutrient needs in healthy toddlers: In Hungary, DHA levels in breast milk are spectacularly lower than median DHA levels usually reported in the literature; therefore, more awareness of the importance of DHA intake during pregnancy should be created.

 

Blurry Vision, Dry eyes, Glaucoma and Macular Degeneration

We are visual people and the eye literally sucks out every last DHA molecule available to it, because the retina has priority.

The retina of the eye, specifically the photoreceptor cells in the retina, is exceptionally rich in DHA (docosahexaenoic acid), an omega-3 fatty acid. DHA comprises over 50% of the total fatty acid content in the retina.

The high concentration of DHA in the retina is vital for maintaining the fluidity of photoreceptor membranes, which in turn supports the function of proteins within these membranes. These proteins are essential for photoreceptor cells to absorb light and convert it into electrical signals that the brain interprets as visual information. Thus, a deficiency in DHA can negatively impact vision and may contribute to conditions such as retinal degeneration.

Moreover, DHA also serves as a precursor to neuroprotectin D1, a molecule that has anti-inflammatory effects and protects retinal cells from oxidative stress, further underscoring the importance of DHA in eye health

Nine studies provided data on a total sample of 88 974 people, including 3203 AMD cases. A high dietary intake of omega-3 fatty acids was associated with a 38% reduction in the risk of late AMD. Loss of DHA from the nerve cell membrane leads to dysfunction of the central nervous system in the form of anxiety, irritability, susceptibility to stress, dyslexia, impaired memory and cognitive functions, and extended reaction times. A high intake of dietary omega-3 PUFA or fish was associated with a reduced risk of developing of AMD, which further supports that consumption of omega-3 PUFA-rich foods. DHA plays an important role in ensuring a healthy ageing, by thwarting macular degeneration, Alzheimer’s disease, and other brain disorders. Molecular risk factors [for macular degeneration] are [low] High-Density Lipoprotein Cholesterol (HDL-C), Docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), zeaxanthin and lutein.  Increase macular pigment optical density (MPOD) was significantly associated with higher plasma levels of omega-3 DPA.

Acute DHA treatment rescued DHA-deficient females from exaggerated dry eye disease (DED). After 12 weeks of administration of the dietary supplement, all dry eye symptoms improved significantly (P<0.001) (mean 1.3 vs 0.6 for scratching, 1.4 vs 0.7 for stinging sensation, 1.6 vs 0.7 for grittiness, 1.0 vs 0.4 for tired eyes, 1.1 vs 0.5 for grating sensation, and 0.8 vs 0.3 for blurry vision).

Glaucoma: At day 90, IOP was reduced to 13.6 ± 0.3 mm Hg in the omega-3 group; controls had a slight IOP increase to 14.2 ± 0.4 mm Hg (P < 0.05).

SanGiovanni 2005: Our general conclusion is that there is consistent evidence to suggest that omega-3 LCPUFAs may act in a protective role against ischemia-, light-, oxygen-, inflammatory-, and age-associated pathology of the vascular and neural retina.

 

 

Hearing loss and Homocysteine

Omega-3 fatty acids, particularly DHA, play crucial roles in the maintenance and function of the nervous system, including the auditory nerve, which is responsible for transmitting sound information from the ears to the brain. The protective effect of omega-3s on hearing likely stems from several mechanisms:

  1. Anti-inflammatory Effects: Chronic inflammation can damage the delicate structures of the ear and lead to hearing loss. Omega-3 fatty acids can reduce inflammation, potentially helping to preserve hearing.

  2. Improved Blood Flow: Omega-3 fatty acids can improve blood flow by making the blood less sticky and reducing blood vessel inflammation. This may enhance the supply of oxygen and nutrients to the inner ear, which could improve and preserve hearing.

  3. Reduction of Homocysteine Levels: High levels of homocysteine, an amino acid in the blood, have been associated with many health problems, including heart disease and hearing loss. Omega-3 fatty acids may help reduce homocysteine levels, providing a potential protective effect on hearing.

  4. Protecting Against Oxidative Damage: The high metabolic activity of the inner ear makes it susceptible to oxidative stress and damage. DHA, being a major component of nerve cell membranes, can enhance the function and survival of these cells, reducing the chances of hearing loss.

In summary, by reducing inflammation, improving blood flow, lowering homocysteine levels, and protecting against oxidative damage, omega-3 fatty acids may help to preserve hearing.

Curhan 2014: the relative risk of hearing loss in fresh fish eating people was reduced by up to 22% after 1,038,093 person-years of follow-up.
 
Given the fact that over 30% of elderly have to deal with severe hearing loss, this is a staggering result. How does omega3 reduce inflammation in the hearing organ? Homocysteine levels are clearly reduced by omega3 and this also affects cardiovascular disease.
 
Martínez-Vega 2015: High levels of plasma homocysteine (tHcy), a key metabolite of the folate and methionine cycles are considered an independent risk factor for cardiovascular disease and, more recently, also of human hearing loss. Genes involved in homocysteine metabolism showed decreased expression during aging of control animals, and  the changes in genetically altered mice could be significantly prevented by omega-3 feeding. 
 
It turns out that homocysteine is a major marker for general inflammation and the health of your arteries. Hyperhomocysteinemia is a possible risk factor for coronary atherosclerotic plaque which block blood flow to the coronary arteries suppling the heart. This risk factor concerns also the cochlea in the ear or glomeruli in the kidneys, in other words any crucial capillaries with highly oxygenated blood. Unlike the heart these organs are highly developed and once damaged can likely not recover and damage is permanent. In the case of kidney damage life threatening.
 
Homocysteine is a ‘non-functional’ amino acid and In the body, homocysteine can be recycled into methionine or converted into cysteine with the aid of certain B-vitamins. Homocysteine is a significant biomarker for overall health status and, although it is not clear whether this represents an indicator rather the etiology of disease including bone health, neurodegenerative disease, renal dysfunction cognitive impairments and congenital defect development is widely recognized in the literature.
 
Again, the point here is is that many studies show how omega3 reduces homocysteine. A synergistic action between polyunsaturated fatty acids and B vitamins may play a key role in regulating several metabolic pathways responsible for lowering homocysteine.

 

 

Rizzo et al. 2020 shows the various pathways that omega3 influences homocysteine pathways. Many of these enzymes involved in amino acid conversion are dependent on PUFA and B vitamins.

 

 

Testosterone, Growth Hormone and more

 

You can safely increase normal testosterone levels with omega3!

There is evidence suggesting that testosterone levels in men have been gradually decreasing over the past few decades. Several studies have shown that testosterone levels have been declining in men across different age groups and populations.

A notable study published in the Journal of Clinical Endocrinology & Metabolism in 2007 analyzed data from the Massachusetts Male Aging Study (MMAS). This study found that testosterone levels in men had declined by about 1% per year from the 1980s to the early 2000s.

Another study published in the journal Human Reproduction Update in 2017 reported a significant decline in sperm concentration and total sperm count among men from Western countries between 1973 and 2011. If the average levels of the male hormone dropped by 1 percent a year, Dr. Thomas Travison and colleagues from the New England Research Institutes in Watertown, Massachusetts, found. This means that, for example, a 65-year-old man in 2002 would have testosterone levels 15 percent lower than those of a 65-year-old in 1987. This also means that a greater proportion of men in 2002 would have had below-normal testosterone levels than in 1987.

The reasons behind the decline in testosterone levels are complex and not entirely understood. Various factors have been proposed, including:

  1. Aging population: As men age, testosterone levels naturally decline. With the overall population aging, the average testosterone levels may also decrease.
  2. Obesity: Testosterone levels are often lower in men with obesity, and the prevalence of obesity has increased significantly in recent decades.
  3. Environmental factors: Exposure to certain chemicals, such as endocrine-disrupting chemicals (EDCs), may negatively impact testosterone levels.
  4. Lifestyle factors: Poor diet and omega3 deficiency, lack of physical activity, stress, and sleep disturbances can all contribute to lower testosterone levels.

 

Here are some Studies on testosterone and Omega3:

Dietary supplementation with docosahexaenoic acid rich fish oil increases circulating levels of testosterone in overweight and obese men

“In parallel, dietary flaxseed oil (FO) improved the sex steroid hormone disturbance (luteinizing hormone/follicle-stimulating hormone, estrogen, [normalizes] testosterone, and progesterone), body weights, dyslipidemia, and insulin resistance. Moreover, FO treatment improved plasma and ovary inflammatory interleukin (IL)-1β, IL-6, IL-10, and IL-17A, tumor necrosis factor-α, and monocyte chemoattractant protein-1.” (keep in mind that flax seed oil only contains ALA and the conversion to EPA in humans is very minimal) 

“Overall, the co-administration of vitamin D and omega-3 fatty acid for 12 weeks had beneficial effects on mental health parameters, serum total testosterone, hs-CRP, plasma TAC and MDA levels, and gene expression of IL-1 and VEGF among women with PCOS.”

“Changes in testosterone levels in males were positively associated with changes to omega-3 PUFAs EPA and DHA and inversely correlated with omega-6 PUFA, arachidonic acid and dihomo-gamma-linolenic acid content in erythrocyte membranes, and was associated with beneficial changes to fasting insulin and HOMA-IR across the course of the study. DHA-enriched fish oil supplementation increases testosterone levels in overweight and obese men.”

“Safarinejad, M. R., Hosseini, S. Y., Dadkhah, F., & Asgari, M. A. (2011). Relationship of omega-3 and omega-6 fatty acids with semen characteristics, and anti-oxidant status of seminal plasma: A comparison between fertile and infertile men. Clinical Nutrition, 30(3), 359-364. “

This study examined the association between omega-3 fatty acids and semen characteristics in fertile and infertile men. It found that higher omega-3 fatty acid levels were associated with improved semen quality, but it did not specifically investigate testosterone levels.

We conclude that there are strong evidences supporting ω-3 PUFA administration and/or supplementation for the treatment and management of MOSH patients.

In summary, testosterone levels in men may be declining (age related but but also generation related) because of our systematic omega-3 deficiency. Omega-3 is a safe way to building these levels back up.

 

Thyroid disease

  1. Hyperthyroid omega-3 treated group showed significantly increased final body weight and body weight gain, decreased liver weight to body weight ratio, decreased serum triiodo-l-thyronine level, increased serum thyroid stimulating hormone level, decreased serum levels of alanine transaminase, aspartate transaminase and tumor necrosis factor-alpha.

 

Benvenga 2022: Benefits of the omega-3 polyunsaturated fatty acids (PUFA) on a number of clinical disorders, including autoimmune diseases, are widely reported in the literature. One major dietary source of PUFA are fish, particularly the small oily fish, like anchovy, sardine, mackerel and others. Taking into account (i) the anti-autoimmunity and anti-cancer properties of the omega-3 PUFA, (ii) the increasing incidence of both autoimmune thyroiditis and thyroid cancer worldwide, (iii) the predisposing role for thyroid cancer exerted by autoimmune thyroiditis, and (iv) the risk for developing metabolic and cardiovascular disorders conferred by both elevated/trendwise elevated serum TSH levels and thyroid autoimmunity, then there is enough rationale for the omega-3 PUFA as measures to contrast the appearance and/or duration of Hashimoto’s thyroiditis as well as to correct the slightly elevated serum TSH levels of subclinical hypothyroidism.

 

Graves Disease: McCoy 2011 : Within eight weeks of beginning flaxseed oil supplements, TSH levels normalized, but fell somewhat when flaxseed was decreased and PTU discontinued. Omega-3 fatty acids should be investigated as a potential treatment for autoimmune thyroid disease.

 

 

Hashimoto’s thyroiditis

Diagnosing Hahimoto’s has to be done properly. A very high TSH does not assume a positive TPO.

Thyroid peroxidase (TPO) is an enzyme normally found in the thyroid gland. TPO plays an important role in the production of thyroid hormones. A TPO test measures the amount of thyroid peroxidase antibodies in your blood.

The TPO test is primarily used to help diagnose autoimmune conditions related to the thyroid gland, such as Hashimoto’s disease and Graves’ disease. Both conditions can cause similar symptoms, such as fatigue, weight gain, and depression. These symptoms can be vague and can be caused by other conditions, making them difficult to diagnose without further testing.

In Hashimoto’s disease, the immune system mistakenly attacks the thyroid gland, causing inflammation and impaired function of the gland. People with Hashimoto’s disease often have an elevated level of TPO antibodies.

A positive TPO test indicates that an autoimmune disease may be damaging your thyroid. However, some people with autoimmune thyroid disease may not have high levels of thyroid peroxidase antibodies, and some people with high levels may never develop thyroid disease.

Inflammation plays a major role in Hashimoto and the makers are reduced with omega3:

Resolvins are a family of bioactive products that are created in the body from omega-3 fatty acids, specifically eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). They have potent anti-inflammatory effects and can help to resolve inflammatory processes. Omega-3 fatty acids have been shown in various studies to have beneficial effects on autoimmune disorders, including Hashimoto’s disease, which is an autoimmune condition of the thyroid.

There’s growing interest in the potential role of omega-3 fatty acids and their metabolites in autoimmune thyroid diseases. Studies suggest that the anti-inflammatory actions of omega-3 fatty acids could potentially modulate the autoimmune response in diseases like Hashimoto’s, helping to control inflammation and possibly even altering the course of the disease.

Song 2021: Conclusions: Decreased RVE1 levels might be a sign that HT is associated with inflammatory resolution dysfunction. RVE1 may serve as a protective factor against increased TgAb levels.

 

Recent research supports a role for nutritional approaches. This case report describes the management of a 34-y-old female with HT who declined thyroid replacement therapy and was successfully managed for a period of 5 mo. The patient was advised to follow a phytonutrient rich diet (eg, berries); avoid sensitive foods (gluten and soy); and consume quality fats, fermented foods, and filtered water. Nutritional supplementation of vitamins (B complex, D3), α-lipoic acid, coenzyme Q10, magnesium, omega-3 oil (DHA/EPA), and probiotics were used in conjunction with an herbal tincture. (Altern Ther Health Med.

 

Skin disease and Skin Aging 

Everyone knows: “give your dog omega3 for skin problems”. Humans are no exception. Skin problems (other than contact eczema) are of internal inflammatory nature. You could say the blood in the capillaries is overheating and produces little volcanoes. Essentially, eczema and pustules etc. are small wounds that do not heal. This is attributed to the high inflammatory omega6/3 index. Inflammation signals persist regardless of the trigger (food, toxins, etc) and never get turned off! Skin problems are a form of malnutrition.

Balic 2020: Omega-3 (ω-3) and omega-6 (ω-6) polyunsaturated fatty acids (PUFAs) are very desirable components of oils with special dietary and functional properties. Their therapeutic and health-promoting effects have already been established in various chronic inflammatory and autoimmune diseases through various mechanisms, including modifications in cell membrane lipid composition. PUFA-based supplementation should be encouraged in a targeted manner for individuals in need to provide better management of skin

In eczema, apart from using an elimination diet, the adequate content of fatty acids from foods (saturated, monounsaturated, and polyunsaturated fatty acids) plays an important role as an immunomodulatory agent.

The problem already starts in the mothers womb – due to the mother being highly omega3 deficient. This problem becomes worse with each additional pregnancy. The fetus is very demanding because the needs to grow its own nervous system always has priority. We can see in our tests how the baby literally “sucks the mother dry of DHA”.

The studies reported the relation between human milk fatty acids docosahexaenoic acid (C22:6n-3, DHA), eicosapentaenoic acid (C20:5n-3, EPA), alpha-linolenic acid (C18:3n-3, ALA), arachidonic acid (C20:4n-6, AA), and linoleic acid (C18:2n-6, LA) with three domains of health outcomes: neurodevelopment, body composition, and allergy, skin & eczema. Results from the 21 studies consistently suggested better health outcomes across the three domains for infants consuming milk with higher concentrations of total n-3, DHA, EPA, and ALA. 

Omega-3 fatty acids and specific amino acids were linked to enhanced wound-healing and immune function. 

Soyun Cho 2014: Anti-aging functional foods exert their influence mostly through their anti-oxidant and anti-inflammatory effects, thereby abrogating collagen degradation and/or increasing procollagen synthesis. Clinical evidence supporting a role in preventing cutaneous aging is available for oral supplements such as carotenoids, polyphenols, chlorophyll, aloe vera, vitamins C and E, red ginseng, squalene, and omega-3 fatty acids. Collagen peptides and proteoglycans are claimed to provide building blocks of the dermal matrix. 

Furthermore, omega-3 PUFA metabolites, including resolvins, are known to demonstrate strong anti-inflammatory effects during allergic and inflammatory diseases; however, little is known regarding the actual impact of these metabolites on skin diseases. In this review, we focused on metabolites that have strong anti-inflammatory actions in various inflammatory diseases, as well as those that present antitumor actions in malignancies, in addition to the actual effect of omega-3 PUFA metabolites on various cells.

Huang 2018: The major mechanisms of PUFAs for attenuating cutaneous inflammation are the competition with the inflammatory arachidonic acid and the inhibition of proinflammatory eicosanoid production. On the other hand, PUFAs in fish oil can be the regulators that affect the synthesis and activity of cytokines for promoting wound healing. A systemic review was conducted to demonstrate the association between fish oil supplementation and the benefits to the skin.

Acne

We know that inflammatory foods cause acne to be worse. Vs versa, foods rich in omega-3 fatty acids suppress the production of inflammatory cytokines with therapeutic effect. Additionally, docosapentaenoic acid and γ-linolenic acid have demonstrated improved acne lesions.

A total of 38 studies met eligibility for review, reporting benefits for O3FA supplementation in the treatment of psoriasis, atopic dermatitis, acne, and skin ulcers. 

 

 

Addiction and Alcohol

Elevated omega-3 intake may reduce distress symptoms and basal cortisol secretion in abstinent alcoholics, thus providing a valid subsidiary measure to increase the efficacy of rehabilitation programs in ethanol addicts.

 

 

Depression and Mood

Depression is one of the most difficult to measure diseases and studies are challenging as there are few biomarkers involved, however Cortisol and Inflammation play a big role as they correlate with symptoms. Cortisol reduction:

60 patients suffering from depression aged 11–18 years were followed for 12 weeks. Morning cortisol decreased in response to omega-3 but not omega-6 fatty acids at 12 weeks compared to baseline. Supplementation improves potentially disrupted daily rhythm of stress hormones and stress hormone concentrations correlate with values of selected markers of oxidative stress.

Meta-analysis of 11 and 8 trials conducted respectively on patients with a DSM-defined diagnosis of major depressive disorder (MDD) showed this Conclusions: The use of omega-3 PUFA is effective in patients with diagnosis of MDD and on depressive patients without diagnosis of MDD.

 

Lipid Rafts: Membranes are not uniform. Far from it. Their local environment depending on the membrane proteins and cellular interaction are crucial. Lipid rafts rely on omega3: Burhani 2017 Fish oil contains omega-3 polyunsaturated fatty acids (PUFA), and there are several mechanisms by which PUFAs are thought to induce an antidepressant effect, including anti-inflammatory action and direct effects on membrane properties.

Source

 

 

Dental Health

Dental teeth health and the health of your teeth is not only dependent on hygiene and the amount of sugar your eat. There is a direct link between leaky gut and the anti-inflammatory action of Omega-3.

  1. Leaky Gut:

    • Also known as increased intestinal permeability, it’s a phenomenon wherein the tight junctions of the intestinal wall become compromised, allowing undigested food particles, bacteria, and other foreign substances to cross into the bloodstream.
    • This can lead to inflammation, immune responses, and a variety of symptoms and conditions, including food sensitivities, autoimmune disorders, and more.
    • Various factors can contribute to a leaky gut, including stress, infections, certain medications, and dietary components like alcohol, gluten (in those with sensitivity), and excessive sugar.

  2. Leaky Teeth:

    • This isn’t a widely recognized or conventional term in the same way “leaky gut” is. However, oral health is crucial, and any compromise in the teeth or gums’ integrity can have systemic implications.
    • Periodontal disease, cavities, root infections, and abscesses can lead to the spread of bacteria and toxins into the bloodstream, potentially contributing to inflammation and other systemic issues.

  3. Health of Roots:

    • The roots anchor teeth to the jawbone and contain the tooth’s nerve. The health of the roots is essential for overall tooth vitality.
    • Root infections or abscesses can be painful and harmful. They can arise from untreated cavities, trauma, or periodontal disease. Such infections can spread to surrounding tissues and even become systemic.

  4. Omega-3 and Leaky Gut:

    • Omega-3 fatty acids, particularly EPA and DHA, have anti-inflammatory properties that might benefit gut health.
    • Some research suggests that omega-3s can help modulate the immune response and reduce inflammation in the gut, potentially benefiting conditions like inflammatory bowel disease.
    • By reducing inflammation, omega-3s might indirectly help maintain the integrity of the gut lining, although direct evidence on omega-3s preventing or treating leaky gut is still emerging.

  5. Omega-3 and Oral Health:

    • Omega-3s have been studied for their potential benefits in oral health. Their anti-inflammatory properties can potentially benefit periodontal health.
    • Some studies suggest that omega-3 supplementation can reduce symptoms of periodontal disease, such as reducing pocket depth and gum inflammation.
    • While omega-3s show promise in supporting oral health, it’s essential to combine their intake with good oral hygiene practices.

In summary, both the gut and oral health are intricately linked to systemic health. Omega-3 fatty acids, with their anti-inflammatory properties, show potential in supporting both gut and oral health. However, they should be seen as part of a holistic approach to health that includes a balanced diet, proper oral hygiene, regular dental check-ups, and other healthy lifestyle practices.

 

More EPA means more anti-inflammatory Lipoxins, resolvins, protectins, and maresins. Muralidharan 2023: They are families of mediators that are under SPM. In recent years it has become evident that periodontitis is a multifactorial inflammatory disease initiated by oral microbial biofilm. 

Kujur 2020: The present study showed that adjunctive use of ώ-3 fatty acids proved to be beneficial over scaling and root planing alone in the treatment of chronic moderate periodontitis. Statistical analyses demonstrated a significant reduction in probing pocket depth (t = 65.56, P = 0.000) and (t = 51.69, P = 0.000) at 1 and 3 months, respectively, in test group compared to baseline and control group. 

Castro Dos Santos 2022: 10 RCTs were selected for qualitative analysis, and of these, 8 RCTs were included in meta-analysis. RCTs showed a significant PPD reduction/CAL gain associated with the use of omega-3 fatty acids. The pooled estimates revealed significant overall PPD reduction of 0.42 mm (95% CI 0.15, 0.68) and CAL gain 0.58 mm (95% CI 0.24, 0.92). 

 

Metabolic Syndrome

The root of metabolic syndrome is Omega3 deficiency causing cardiovascular disease (CVD). Metabolic syndrome is a cluster of conditions that occur together and increase the risk of developing heart disease, stroke, kidney disease and type 2 diabetes. These conditions include:

  1. Abdominal obesity (excessive fat around the waist)
  2. High blood pressure (hypertension)
  3. Elevated blood sugar levels (insulin resistance or hyperglycemia)
  4. High triglyceride levels (a type of fat found in the blood)
  5. “Low levels of high-density lipoprotein (HDL) cholesterol, also known as “good” cholesterol”
  6. In addition, ‘Diabetes-3 is now coined’ as the mechanism for onset of dementia!

Having one of these conditions doesn’t necessarily mean you have metabolic syndrome. However, the presence of at least three of these conditions typically qualifies as a diagnosis of metabolic syndrome. Very likely all these modern civilization diseases including cancer are related to each other and can be explained in the context of omega3 inflammatory index, cortisol, stem cell health and energy metabolism.

Metabolic syndrome is where many modern chronic disease patterns come together. The cause of metabolic syndrome is not well understood, but it is believed to be related to a combination of toxic inflammation, lifestyle, and environmental factors. Insulin resistance is a major factor, a condition in which the body’s cells don’t respond properly to insulin, plays a significant role in the development of metabolic syndrome. 

Risk factors for metabolic syndrome include:

  1. Age: The risk of developing metabolic syndrome increases with age.
  2. Obesity: Being overweight or obese significantly raises the risk of metabolic syndrome.
  3. Sedentary lifestyle: A lack of physical activity contributes to the development of obesity and insulin resistance, both of which are risk factors for metabolic syndrome.
  4. Family history and epigenetics: A family history of type 2 diabetes or heart disease may increase the risk of metabolic syndrome.
  5. Ethnicity: Certain ethnic groups, such as Hispanics and Asians, may have a higher risk of developing metabolic syndrome.

Prevention and management of metabolic syndrome primarily involve lifestyle modifications, including:

  1. Regular physical activity: Engaging in at least 150 minutes of moderate-intensity aerobic exercise or 75 minutes of vigorous-intensity aerobic exercise per week can help reduce the risk of metabolic syndrome.
  2. Healthy diet: Consuming a balanced diet rich in omega3, fruits, vegetables, protein, and healthy fats can help prevent and manage metabolic syndrome.
  3. Weight loss: Losing weight, especially around the waist, can significantly reduce the risk of metabolic syndrome and its associated health issues.
  4. Smoking cessation: Quitting smoking can help lower blood pressure and improve overall heart health, thereby reducing the risk of metabolic syndrome.

While some lifestyle changes remain the cornerstone of prevention and management there does not seem to be a solution to this civilization problem and as you will see below medications make the problem worse. They never fix the root.

Omega-3 fatty acids, particularly EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), are essential nutrients that play a crucial role in maintaining overall health. They are primarily obtained through the diet, with fatty fish, such as salmon, mackerel, and sardines, being rich sources. Omega-3 fatty acids have been shown to have multiple health benefits, including anti-inflammatory, cardioprotective, and neuroprotective effects.

Research has suggested that omega-3 deficiency may be linked to the development and progression of metabolic syndrome and its associated conditions, including autoimmunity, diabetes, obesity, hypertension, and cardiovascular disease. Here is a brief overview of how omega-3 deficiency can contribute to these conditions:

  1. Autoimmunity: Omega-3 fatty acids have anti-inflammatory properties that can help modulate the immune response. A deficiency in omega-3 fatty acids can contribute to a pro-inflammatory state, which may increase the risk of developing autoimmune diseases.

  2. Diabetes: Omega-3 fatty acids can improve insulin sensitivity and glucose metabolism. A deficiency in omega-3 fatty acids has been associated with a higher risk of developing insulin resistance and type 2 diabetes.

  3. Obesity: Omega-3 fatty acids may help regulate metabolism and appetite, which can aid in weight management. A deficiency in omega-3 fatty acids may contribute to weight gain and obesity.

  4. Hypertension: Omega-3 fatty acids have been shown to have blood pressure-lowering effects. A deficiency in these fatty acids can contribute to the development of hypertension.

  5. Cardiovascular disease: Omega-3 fatty acids have cardioprotective effects, including reducing inflammation, improving blood lipid profiles, and preventing blood clot formation. A deficiency in omega-3 fatty acids can increase the risk of developing cardiovascular diseases, such as atherosclerosis, heart attack, and stroke.

Omega-3 deficiency has been implicated in all of the development of metabolic syndrome and its associated conditions, it is essential to recognize that these conditions are multifactorial and involve complex interactions among genetic, environmental, and lifestyle factors. Ensuring adequate intake of omega-3 fatty acids through a balanced diet or supplementation, when necessary, is an important aspect of maintaining overall health and may help prevent or mitigate the risk of metabolic syndrome and its related complications.

In summary, lifestyle interventions are not enough, medications never treat the root of the problem and have massive side effects!

->You have to reduce your omega6/3 index below 4:1 to avoid metabolic syndrome!

Lets break down the mechanism of Omega-3 in metabolic syndrome:

The relationship between triglycerides, glucose metabolism, and fatty acid composition is multifaceted. As discussed below at the center of this problem is the liver metabolism. 

  1. Triglycerides and Glucose: Elevated triglycerides in the blood can be due to various reasons. In the context of metabolic syndrome and insulin resistance, the liver continues to produce glucose via gluconeogenesis even in the presence of high blood glucose levels. This leads to increased insulin secretion. High insulin levels stimulate the liver to produce more triglycerides. Additionally, insulin resistance at the level of the fat cell can lead to increased breakdown of stored fat, releasing more free fatty acids into the bloodstream, which the liver can then use to produce even more triglycerides.

  2. Omega-3 and Fat Metabolism: Omega-3 fatty acids, particularly EPA and DHA, have been shown to have beneficial effects on lipid metabolism. They can reduce liver fat and reduce triglyceride levels in the blood. A deficiency in omega-3 fatty acids could potentially contribute to dyslipidemia (abnormal lipid levels), although it’s just one piece of a much larger metabolic picture.

  3. Fat Catabolism vs. Anabolism in Metabolic Syndrome: In metabolic syndrome, there’s an imbalance between fat storage (anabolism) and fat breakdown (catabolism). Insulin, which normally promotes fat storage and inhibits fat breakdown, becomes less effective in doing so due to insulin resistance. This leads to increased fat breakdown from adipose tissue and increased free fatty acids in the blood, which, as mentioned earlier, can contribute to increased triglyceride synthesis in the liver.

  4. Omega-3 Deficiency’s Role: While omega-3 deficiency can have implications on lipid metabolism and inflammation, it’s important not to pin the entire blame for metabolic syndrome or elevated triglycerides on omega-3 deficiency alone. Many factors, including overall diet quality, physical activity, genetics, and other lifestyle factors, play roles in the development and progression of metabolic syndrome.

In summary, elevated triglycerides in metabolic syndrome can arise due to disturbed glucose and fat metabolism. Omega-3 fatty acids play a role in lipid metabolism and can influence triglyceride levels, but they are just one factor among many in the broader context of metabolic syndrome.

In this context, Omega-3 fatty acids have a plethora of beneficial effects on the body, encompassing a range of mechanisms. One of the effects of omega-3 fatty acids is their potential role in modulating the stress response, specifically cortisol levels which is discussed below.

  1. Omega-3 and Cortisol: There’s some evidence to suggest that omega-3 supplementation might help attenuate the cortisol response to stress. Cortisol is a glucocorticoid hormone released by the adrenal glands in response to stress, and it plays a central role in glucose metabolism, immune function, and the inflammatory response.

  2. Cortisol and Muscle Protein Breakdown: One of the functions of cortisol is to promote the breakdown of protein in muscles, releasing amino acids into the bloodstream. These amino acids can then be used as substrates for gluconeogenesis in the liver (the production of glucose from non-carbohydrate sources) and other metabolic processes.

  3. Omega-3, Cortisol, and Liver Metabolism: If omega-3 fatty acids reduce the cortisol response, this could theoretically lead to less muscle protein breakdown and fewer amino acids being sent to the liver for gluconeogenesis. However, it’s essential to note that the liver’s metabolic processes are highly complex and regulated by multiple factors, not just amino acid availability. The central role of the liver in glucose and lipid metabolism, especially in conditions like metabolic syndrome, cannot be narrowed down to one single pathway or mechanism.

  4. Anti-inflammatory Omega3:  Omega-3s are also known for their anti-inflammatory effects, their role in improving lipid profiles, their potential benefits for brain health, and more. As systemic inflammation comes down so are average cortisol level. Research shows that average cortisol levels are reduced but up to 20%.

Nonalcoholic fatty liver disease (NAFLD)

Here is the relationship between omega-3 fatty acids and NAFLD:

  1. Anti-Inflammatory Effects: One of the hallmarks of NASH, the more severe form of NAFLD, is liver inflammation. Omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have anti-inflammatory properties. By reducing inflammation, omega-3s could theoretically attenuate the progression of NAFLD to NASH.

  2. Improving Lipid Metabolism: Omega-3 fatty acids can modulate lipid metabolism. They can reduce triglyceride levels, which is particularly relevant since elevated liver triglycerides are a defining feature of NAFLD.

  3. Modulation of Liver Fat Content: Some clinical studies have shown that supplementation with omega-3 fatty acids can reduce liver fat content in individuals with NAFLD. This effect, combined with their ability to improve lipid profiles, suggests a potential therapeutic role for omega-3s in NAFLD management.

  4. Effects on Insulin Sensitivity: Insulin resistance is closely associated with the development and progression of NAFLD. Omega-3 fatty acids may improve insulin sensitivity, thereby offering another avenue through which they might benefit those with NAFLD.

  5. Clinical Trials: Several clinical trials have investigated the potential benefits of omega-3 supplementation in NAFLD. While many studies have shown positive results, such as reduced liver fat and improved liver enzyme levels, the evidence is not entirely consistent across all trials.

  6. Recommendations: Due to the potential benefits and the generally low risk associated with omega-3 supplementation, some clinicians recommend omega-3 fatty acids as a complementary approach for NAFLD patients, especially those with elevated triglyceride levels. However, it’s essential to view omega-3 supplementation as part of a broader therapeutic strategy, which should include weight management, dietary changes, and increased physical activity. Fish oil supplements are a common source of EPA and DHA. Eating fatty fish like salmon, mackerel, sardines, and trout is also a good way to increase omega-3 intake.

In conclusion, Omega-3 fatty acids show promise in managing NAFLD, but they are not a standalone cure. A holistic approach that includes dietary modifications, weight management, physical activity, and potentially medications (as advised by a healthcare provider) remains the primary strategy for addressing NAFLD.

Nobili2015 based on the known pathogenesis of NAFLD, several clinical trials with different nutritional supplementation and prescribed drugs have been undertaken or are currently underway. Experimental evidence has emerged about the health benefits of omega-3 fatty acids, a group of polyunsaturated fatty acids that are important for a number of health-related functions.

Parker 2012: A benefit of PUFA vs. control was also observed for AST (effect size=-0.97, 95% CI: -0.13 to -1.82, p=0.02).  Sub-analyses of only randomised control trials (RCTs) showed a significant benefit for PUFA vs. control on liver fat (effect size=-0.96, 95% CI: -0.43 to -1.48, p<0.001)

This article below shows how excessive omega6 intake and not saturated fat is the problem. Once your omega3 intake is balanced your body can handle much more omega6!

Henkel 2018: The current study demonstrated that liver damage caused by dietary cholesterol in mice was strongly enhanced by a high fat diet containing soybean oil-derived ω6-poly-unsaturated fatty acids (ω6-PUFA), but not by a lard-based high fat diet containing mainly saturated fatty acids. 

Diabetes type 2 and Obesity

Obesity is a growing public health concern in many industrialized countries. According to data from the World Health Organization (WHO) and various studies, obesity rates in eg. Germany have been steadily increasing over the years. As of September 2021, it is estimated that over 25% of adults in Germany are obese (with a BMI ≥ 30), while more than 50% of the adult population is considered overweight (with a BMI ≥ 25).

Several factors contribute to the increasing rates of obesity in Germany:

  1. Unhealthy dietary habits: The consumption of high-calorie, low-nutrient foods, such as processed foods, fast food, and sugar-sweetened beverages, has contributed to weight gain among the population.

  2. Sedentary lifestyle: A decrease in physical activity levels due to the growing use of technology, increased screen time, and more sedentary jobs has played a role in the rise of obesity.

  3. Socioeconomic factors: Lower socioeconomic status is often linked to higher rates of obesity due to limited access to healthier food options, lack of time for physical activity, and limited access to resources for weight management.

  4. Genetic and environmental factors: Genetic predisposition, along with environmental influences such as stress, pollution, and disrupted sleep patterns, can also contribute to the development of obesity.

Obesity and type 2 diabetes (DM2) are closely linked, as obesity is one of the most significant risk factors for the development of type 2 diabetes. The connection between obesity and diabetes can be explained by several mechanisms:

  1. Insulin resistance: Obesity, particularly excess visceral fat (fat around the abdominal organs), is associated with insulin resistance. Insulin is a hormone that helps regulate blood sugar levels by enabling cells to take up glucose from the bloodstream. In insulin resistance, cells become less responsive to insulin, leading to higher blood sugar levels. Over time, this can result in type 2 diabetes, as the pancreas struggles to produce enough insulin to compensate for the resistance.

  2. Inflammation: Obesity is associated with chronic low-grade inflammation, as adipose (fat) tissue can produce inflammatory cytokines and other molecules that contribute to systemic inflammation. This inflammation can impair insulin signaling in cells, leading to insulin resistance and an increased risk of type 2 diabetes.

  3. Hormonal changes: Obesity can also lead to changes in the levels of various hormones, such as leptin and adiponectin, which play roles in regulating metabolism and insulin sensitivity. Imbalances in these hormones can contribute to the development of insulin resistance and type 2 diabetes.

  4. Impaired glucose metabolism: Excess body fat can impair the body’s ability to metabolize glucose, leading to higher blood sugar levels and an increased risk of type 2 diabetes.

  5. Genetic and environmental factors: Both obesity and type 2 diabetes have genetic and environmental components that can interact to increase the risk of developing the conditions. For example, individuals with a genetic predisposition to obesity and diabetes may be more susceptible to the effects of an unhealthy diet and sedentary lifestyle.

Losing weight and maintaining a healthy lifestyle, including regular physical activity and a balanced diet, can help improve insulin sensitivity, reduce inflammation, and lower the risk of developing type 2 diabetes in people with obesity. In some cases, even modest weight loss can lead to significant improvements in blood sugar control and reduce the need for diabetes medications.

 

 

Type 2 diabetes (DM2) is a complex metabolic disorder characterized by high blood sugar levels resulting from insulin resistance and insufficient insulin production. While DM2 is not initially considered a liver disease, the liver does play a significant role in the development and progression of the condition, along with other organs such as the pancreas, skeletal muscles, and adipose tissue.

In the early stages of DM2, the liver is involved in several ways:

  1. Hepatic insulin resistance: The liver is an important site of insulin action and plays a critical role in glucose homeostasis. In individuals with insulin resistance, the liver becomes less responsive to insulin, resulting in increased gluconeogenesis (the production of glucose from non-carbohydrate sources) and reduced glycogen synthesis. This leads to higher blood sugar levels and contributes to the development of type 2 diabetes.

  2. Fat accumulation: Non-alcoholic fatty liver disease (NAFLD) is commonly associated with obesity and insulin resistance. Excess fat accumulation in the liver can further exacerbate insulin resistance and increase the risk of developing type 2 diabetes. In some cases, NAFLD can progress to non-alcoholic steatohepatitis (NASH), cirrhosis, and even liver failure.

  3. Inflammation: Chronic low-grade inflammation, which is often present in individuals with obesity and insulin resistance, can also affect liver function. Inflammatory cytokines and other molecules produced by adipose tissue and the liver itself can impair insulin signaling, contributing to the development of type 2 diabetes.

Although the liver is involved in the development of type 2 diabetes, it is essential to consider the complex interplay between multiple organs and factors that contribute to the condition. Pancreatic insulin resistance also plays a crucial role in DM2, as the pancreas struggles to produce enough insulin to compensate for the resistance in target tissues. Over time, this can lead to pancreatic beta-cell dysfunction and eventually type 2 diabetes.

In summary, type 2 diabetes is a multifactorial disease involving several organs and factors, including the liver, pancreas, skeletal muscles, and adipose tissue. It is crucial to address these various aspects when managing and treating the condition.

DM2 initially presents as a liver disease and pancreatic insulin resistance has only a causal relationship. DM2 also is related to the fat metabolism in your liver. Omega-3 fatty acids are essential polyunsaturated fatty acids that have diverse functions in normal metabolism and health and are used as nutritional supplements for general health and for disease prevention and as prescription drugs for treatment of hypertriglyceridemia.

As the mechanism for adult onset insulin resistance is poorly understood, the fact that liver fat metabolism is essential in this process is often overlooked. It is clear, that Obesity and type 2 diabetic (T2DM) patients have a high prevalence of nonalcoholic fatty liver disease. So it its the arrival rate of your fatty acid molecules that influences the gluconeogenesis in the liver (the liver makes sugar molecules for survival in fasting state). This overproduction of sugar in the liver will eventually wear out the pancreas and in addition the cellular resistance to absorbing excess sugar the devastating effects of insulin and resulting inflammation will lead to a destruction of peripheral nerves, vision loss, kidney problems and heart disease. Here you can see that all of these chronic civilization problems including the above ‘auto-immune’ diseases are related to each other through this deficiency of omega3.

 

Shi 2023: mice were fed with high-fat diet enriched with saturated fat (HSF), or omega-6 polyunsaturated fat (n6HUSF), or omega-3 polyunsaturated fat (n3HUSF) with 42% of calories derived from the fat. 

The Findings: 

  1. – HSF and n6HUSF fed mice developed obesity. HSF fed mice exhibited severe hepatic steatosis associated with hepatomegaly and liver injury.
  2. – n6HUSF fed mice were characterized with moderate hepatic steatosis, accompanied with hypertriglyceridemia and hyperlipidemia
  3. – Excess energy from HSF intake results in fat storage in the liver, likely due to impaired triglyceride secretion; whereas excess energy from n6HUSF diet is stored in the periphery. Both effects are exacerbated by fructose supplementation.
  4. – n3HUSF(omega3) is beneficial, even consumed with fructose.

 

As there is clearly a link between obesity and DM2: this study shows how rats fed a high PUFA diet had less markers for obesity. The TLR4 protein and mRNA levels were markedly down-regulated by PUFA.. The TLR4 signaling pathway has been recognized as one of the main triggers in increasing the obesity-induced inflammatory response. The study concludes:

A low ratio of dietary n-6/n-3 (or reverse hi 3/6 ratio) polyunsaturated fatty acids improves obesity-linked inflammation and insulin resistance through suppressing activation of TLR4 in SD rats.

In summary, high food intake of omega6 foods and deficiency of omega3 foods in combination with high sugar causes inflammation which further spurs the mechanisms of obesity, diabetes type 2, insulin resistance and in turn heart disease and stroke risk. 

Omega3 reduces insulin resistance via Triglycerides

Hi Triglycerides are associated with Diabetes type 2. As insulin resistance grows so does fat metabolism. Excess sugar not taken up by cells gets converted to saturated fat and Triglycerides stored in adipose tissue. Sugar intake over the 20-year period was related to fat volumes later in life. Higher intakes of both sugar-sweetened beverages and added sugar were related to greater fat stores around organs in a stepwise fashion.

However this is only half the picture. Some Asian cultures eat just as much or more sugar as westerners but have little gain in Triglycerides and adipose tissue. These cultures consume more omega3 throughout their life which regulates this problem. The metabolism changes are directly related to proper omega3 intake. The mechanism is not well understood but here is a clue:

Shearer 2012: “At the pharmaceutical dose, 3.4 g/day, omega-3 fatty acids reduce plasma Triglycerides by about 25–50% after one month of treatment, resulting primarily from the decline in hepatic very low density lipoprotein (VLDL-TG) production.” Reducing the delivery of non-esterified Fatty Acids (NEFA) to the liver would be a likely locus of action for omega3. The key regulator of plasma NEFA is intracellular adipocyte lipolysis via hormone sensitive lipase (HSL), which increases as insulin sensitivity worsens. Omega3s in fish oil counteracts intracellular lipolysis in adipocytes by suppressing adipose tissue inflammation. In addition, they increases extracellular lipolysis by lipoprotein lipase (LpL) in adipose, heart and skeletal muscle and enhances hepatic and skeletal muscle β-oxidation which contributes to reduced FA delivery to the liver.” In addition, LDLs are formed from VLDLs so as omega3 is reducing VLDL so is the formation of “bad” cholesterol…

Adopted from Shearer et al: A: Triglyceride production in the cell showed no difference

B: EPA and DHA reduced Triglyceride secretion by up to 57% compared to oleic acid.

It is also likely that omega3 inhibit the assembly of VLDL. Compared to oleic acid alone (omega9), EPA and DHA significantly impaired the secretion of both molecular weight forms of apoB. The concordant decrease in the secretion of both triglyceride and apoB suggests that fish oil fatty acids impair VLDL assembly and/or secretion.

Elevated triglyceride levels have been identified as a significant risk factor for both type 2 diabetes and cardiovascular disease (CVD). 

Several studies and meta-analyses have reported a consistent association between high triglyceride levels and increased risk for these conditions.

  1. Diabetes: A high triglyceride level is often observed in individuals with insulin resistance, a hallmark of type 2 diabetes. Insulin resistance can impair the body’s ability to properly metabolize triglycerides, leading to their accumulation in the bloodstream.

A study by Tirosh et al. (2008) found that high fasting triglyceride levels were an independent risk factor for the development of type 2 diabetes in young adults. The study suggested that individuals with elevated triglyceride levels had a higher risk of developing type 2 diabetes compared to those with normal levels.

  1. Cardiovascular Disease: High triglyceride levels are considered a significant risk factor for the development of atherosclerosis, which can lead to cardiovascular events such as heart attack and stroke. Elevated triglycerides contribute to the formation of atherogenic lipoprotein particles, promoting inflammation, and endothelial dysfunction.

A meta-analysis by Hokanson and Austin (1996) concluded that high triglyceride levels were independently associated with an increased risk of coronary artery disease, especially among women. Another meta-analysis by Sarwar et al. (2007) found that elevated triglyceride levels were associated with an increased risk of coronary heart disease.

It is essential to maintain healthy triglyceride levels through lifestyle modifications, such as a balanced diet, regular exercise, and maintaining a healthy body weight, to reduce the risk of developing type 2 diabetes and cardiovascular disease.

References:

  • Tirosh, A., et al. (2008). “Changes in triglyceride levels and risk for coronary heart disease in young men.” Annals of Internal Medicine, 149(6), 377-385.
  • Hokanson, J. E., & Austin, M. A. (1996). “Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies.” Journal of Cardiovascular Risk, 3(2), 213-219.
  • Sarwar, N., et al. (2007). “Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies.” Circulation, 115(4), 450-458.

Omega-3 fatty acids have been shown to effectively lower triglyceride levels. 

Omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are commonly found in fatty fish like salmon, mackerel, and sardines. They can also be obtained through fish oil supplements and algae-based supplements.

The American Heart Association (AHA) recommends consuming at least two servings of fatty fish per week to maintain heart health. For individuals with high triglyceride levels, higher doses of omega-3s may be recommended under the guidance of a healthcare professional.

Several mechanisms have been proposed to explain the triglyceride-lowering effects of omega-3 fatty acids:

  1. Reduced hepatic production of triglycerides: Omega-3 fatty acids can decrease the synthesis of triglycerides in the liver, which reduces their overall production and release into the bloodstream.

  2. Increased clearance of triglycerides: Omega-3 fatty acids can increase the activity of lipoprotein lipase, an enzyme that helps break down triglycerides in the blood and promotes their clearance from circulation.

  3. Improved insulin sensitivity: Omega-3 fatty acids can help enhance insulin sensitivity, which may indirectly lower triglyceride levels by improving glucose metabolism.

Numerous clinical trials and meta-analyses have demonstrated the triglyceride-lowering effects of omega-3 fatty acids. For example, a meta-analysis by Eslick et al. (2009) found that omega-3 supplementation significantly reduced triglyceride levels in a dose-dependent manner.

It is important to consult with a healthcare professional before starting omega-3 supplementation, particularly at higher doses, as it may interact with medications or cause side effects in some individuals.

Reference:

  • Eslick, G. D., et al. (2009). “Benefits of fish oil supplementation in hyperlipidemia: a systematic review and meta-analysis.” International Journal of Cardiology, 136(1), 4-16.

Metabolic Disease, Diabetes-3 and Dementia

“Diabetes Type 3” is a term that has been used informally and somewhat controversially to refer to various conditions related to insulin resistance or metabolic dysfunction, but it’s not yet officially recognized as a distinct type of diabetes in the same way as Type 1 and Type 2 diabetes. One common use of the term “Diabetes Type 3” refers specifically to Alzheimer’s disease, highlighting the potential link between insulin resistance in the brain and this form of dementia.

Diabetes Type 3 and Alzheimer’s Disease

  1. Insulin Resistance in the Brain: Some researchers have proposed that Alzheimer’s disease could be termed “Type 3 diabetes” due to evidence suggesting that insulin resistance in the brain plays a role in this neurodegenerative condition.
  2. Brain Glucose Metabolism: Alzheimer’s disease is characterized by a decline in brain glucose metabolism. This impairment is somewhat similar to how muscle and fat cells in Type 2 diabetes respond inadequately to insulin.
  3. Research: Ongoing research is examining the link between glucose metabolism in the brain and Alzheimer’s, exploring treatments that address insulin sensitivity as a potential therapeutic avenue.
Metabolic Disease and dementia

In summary of the above Science it is now understood how Metabolic diseases, encompass a broader range of disorders that affect the body’s ability to process and use nutrients effectively. Common examples include:

  1. Type 2 Diabetes: Characterized by insulin resistance and high blood sugar levels.
  2. Metabolic Syndrome: A cluster of conditions including high blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol levels, increasing the risk of heart disease, stroke, and Type 2 diabetes.
  3. Obesity: Often linked with metabolic syndrome and can lead to various health problems.
  4. Cardiovascular Diseases: Can be a result of or exacerbated by metabolic disorders.
  5. Polycystic Ovary Syndrome (PCOS): A condition in women characterized by hormonal imbalances that can affect metabolic processes.

In summary, while “Diabetes Type 3” is not an officially recognized or uniformly defined medical term, it’s sometimes used to draw attention to the potential metabolic aspects of Alzheimer’s disease. Metabolic diseases broadly encompass various conditions related to the body’s metabolism, including well-recognized forms of diabetes. Omega-3 deficiency plays the essential role in this disease process!

Zinzino balance oil is stabilized with natural polyphenols. In the same context of reducing insulin resistance please also visit here!

Obesity and Cancer:

Please check the entire discussion of diabetes above as Obesity, Diabetes and cancer are ultimately linked to inflammatory index of omega6/3.

Prospective studies clearly show an increase in the risk of obesity as the level of omega-6 fatty acids and the omega-6/omega-3 ratio increase in red blood cell (RBC) membrane phospholipids, whereas high omega-3 RBC membrane phospholipids decrease the risk of obesity. 

 

What do Omega 3 fatty acids actually do? Well that is a loaded question but in short:

  1. – Omega-3 is required to keep every cell membrane (and interior membranes) fluid. PUFA (polyunsaturated fatty acids) are incorporated into lipids and perform many functions such as keeping essential membrane proteins such as channels, pumps and receptors happy.
  2. – Without Omega-3 cells are unable to divide and grow!
  3. – Without Omega-3 cells are unable to make endo- and exo-somes to excrete and intake hormones’ and other vital cellular components! This is especially vital in for proper brain function.
  4. – Omega-3 is required for nerve function because K-channels need to open and close based on the stretching of a membrane.
  5. – Omega-3 fatty acids have an anti-inflammatory effect and by creating ‘good’ eicosanoids that balance out the inflammatory effect of Omega-6 fatty acids (arachidonic acids). After consumption, n-3 PUFAs can be incorporated into cell membranes and reduce the amount of arachidonic acid available for the synthesis of proinflammatory eicosanoids (e.g., prostaglandins, leukotrienes). Likewise, n-3 PUFAs can also reduce the production of inflammatory cytokines, such as tumor necrosis factor alpha, interleukin-1, and interleukin-6. Considerable research has been conducted to evaluate the potential therapeutic effects of fish oils in numerous conditions, including arthritis, coronary artery disease, inflammatory bowel disease, asthma, and sepsis, all of which have inflammation as a key component of their pathology.

 

  1. Cancer risk in obesity, excess free fatty acids are initially stored predominately in subcutaneous adipocytes and as these depots fill, in visceral adipose. These Hypertrophied adipocytes with the wrong fatty acids then become stressed and inflammatory!
  2. The impact of long chain n-3 polyunsaturated fatty acid supplementation on inflammation, insulin sensitivity and CVD risk in a group of overweight women with an inflammatory phenotype; the raised inflammatory status group had significantly higher body mass index and area under the curve (AUC) insulin than the reference group. With LC n-3 PUFA supplementation, both groups showed significantly higher plasma eicosapentaenoic acid and docosahexaenoic acid at 4 and 12 weeks (p < 0.001), and lower triacylglycerols (4 weeks p < 0.01 and 12 weeks p < 0.05).
  3. ->>The difference in AUC insulin between the two treatment phases at 12 weeks was significantly greater in the raised inflammatory status group compared to the reference group (p < 0.05). Inflammatory markers were significantly lower after 12 weeks LC n-3 PUFA supplementation compared to baseline (C-reactive protein p < 0.05 and interleukin-6 p < 0.01) L M Browning 1, J D Krebs, C S Moore, G D Mishra, M A O’Connell, S A Jebb https://pubmed.ncbi.nlm.nih.gov/17199721/

 

Hypertension and Kidney Health

There is probably nothing more important than keeping your kidneys healthy. All other organs have a significant regenerative function but the kidney is so highly specialized that once it is damaged the situation becomes life threatening and dialyses or a transplant is required.

 

The results of this study show that ω-3 rich diet in combination with the sEH inhibitor lowered Ang-II increased blood pressure, further increased renal levels of EPA and DHA epoxides, reduced renal markers of inflammation. How does this work? Epoxy products (essentially the omega3 double bond is becoming oxidized) from PUFAs are producing local electrical signals synthesized or generated in and released from the vascular endothelium that hyperpolarize nearby vascular smooth muscle cells. This causes these cells to relax and thereby lowers blood pressure. This mechanism is very important for a healthy kidney and not just a systemic blood pressure. In other words if there is no omega3 present a local hypertensive effect in the Kidney can permanently destroy the glomeruli. Glomeruli are a very complex structures that are nearly impossible to be renewed. Eating the enriched foods resulted in clinically relevant reductions in diastolic blood pressure (− 3.1 mmHg [− 5.8, − 0.3])

This dose‐response meta‐analysis demonstrates that the optimal combined intake of omega‐3 fatty acids for BP lowering is likely between 2 g/d and 3 g/d. Doses of omega‐3 fatty acid intake above the recommended 3 g/d may be associated with additional benefits in lowering BP among groups at high risk for cardiovascular diseases.

 

Langelier 2010: Long chain-polyunsaturated fatty acids modulate membrane phospholipid composition and protein localization in lipid rafts of neural stem cell cultures  Glomerular filtration rate (GFR) and connexin 43 contents in the rafts were increased by DHA supplementation. The restoration of DHA levels in the phospholipids could profoundly affect protein localization and, consequently, their functionalities.

 

Multiple Sclerosis, DM1, Lupus, RA, Kidney disease

There is growing interest in the potential role of omega-3 fatty acids in the prevention and management of multiple sclerosis (MS), a chronic autoimmune disease that affects the central nervous system. Omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are known for their anti-inflammatory properties and potential benefits for overall brain health.

Some studies have investigated the effects of omega-3 supplementation on MS, with mixed results: Despite these mixed results, there is evidence that omega-3 fatty acids may have potential benefits for general brain health and in reducing inflammation, which could be relevant for people with MS.

Swanson, D., Block, R., & Mousa, S. A. (2012). Omega-3 fatty acids EPA and DHA: health benefits throughout life. Advances in Nutrition, 3(1), 1-7.

Aristotelous 2021: Polyunsaturated fatty acids (PUFAs) have been found to improve MS patients’ clinical outcomes. The dietary supplement significantly improved the single support time and the step and stride time (p < 0.05), both spatiotemporal gait parameters. In addition, while GDI of the placebo group decreased by about 10% at 24 months

In conclusion, the current evidence on the role of omega-3 fatty acids in the prevention and management of MS is mixed but the author could not find exact studies looking at the omega6/3 index development before and after supplementation. As usual it is questionable if the studies used proper non-rancid omega3 without keeping track of the omega6/3 index.

Li 2019: Mounting evidence generated from genetic mouse models and clinical studies has shed new light on the functions and the underlying mechanisms of ω-3 PUFAs and their metabolites in the prevention and treatment of rheumatoid arthritis, systemic lupus erythematosus (SLE), multiple sclerosis, and type 1 diabetes. Such amelioration of autoimmune disease was mainly attributed to the elevation of transforming growth factor β1 (TGF-β1) and IL-4 as well as the reduction of pro-inflammatory cytokines IL-2 from the splenocytes of B/W F1. 

Reifen 1998: SLE mice fed linseed oil (a reminder here that many of older adults are unable to convert linseed oil to DHA even if it is non-rancid) showed lower titers of antibodies to DNA and to cardiolipin and less severe kidney damage than mice fed other diets, including fish oil.

PUFA consumption prevents proteinuria onset and reduces weight gain.

Pestka et al. 2014 found that ω-3 PUFAs-enriched diets delayed the onset and markedly attenuated the severity of autoimmune glomerulonephritis (leading to kidney failure). Elevated plasma autoantibodies, proteinuria and glomerulonephritis were evident in mice fed either the n-6 PUFA or n-9 MUFA diets, however, all three endpoints were markedly attenuated in mice that consumed the n-3 PUFA diet until 34 wk of age.

 

More on Auto-immunity, Rheumatoid Arthritis, Diabetes and Inflammatory disease

Autoimmunity can be summarized: If your body is in a high alert inflammatory state, the immune system is compromised and the body starts to attack its own cells. At an inflammatory index of over 20:1 your cell membrane will release 20x inflammatory message into the cell. These are called inflammatory eicosanoids such as prostaglandins made from omega6 arachidonic acid. These in turn will tell the cell start a destructive cycle.

NSAIDS, leaky gut and inflammatory markers:

NSAIDs (non steroidal anti inflammatory drugs) work by inhibiting the activity of cyclooxygenase enzymes, the very enzyme that converts omega6 arachidonic acid to inflammatory prostaglandins. So by increasing your omega3 message rather than reducing omega6 you can bring down the inflammatory response initiated by omega6:

Lee 2012: Ten RCTs (Random placebo controlled trials) involving 183 RA patients and 187 placebo-treated RA controls were included in this meta-analysis. The analysis showed that omega-3 PUFAs clearly reduced nonsteroidal anti-inflammatory drug (NSAID) consumption.

NSAIDS never ‘fix’ anything and have been shown to be dangerous when used long term. Typically by blocking the COX enzymes, all they can do is inhibit the downstream eicosanoid inflammatory response over and over. It is much more effective to catch the problem at its source which is the ratio of omega6/3 in the membrane.

Over the past decade, mounting evidence generated from genetic mouse models and clinical studies has shed new light on the functions and the underlying mechanisms of ω-3 PUFAs and their metabolites in the prevention and treatment of RA (rheumatoid arthritis), systemic lupus erythematosus (SLE), multiple sclerosis, and type 1 diabetes. There is a strong relationship between the excess of carbohydrate consumption and the lack of omega3 in your diet. These metabolic relationships are all related to your liver fat metabolism. 

Li 2019: how omega3 fatty acids in the membrane affect the gene expression of anti-inflammatory markers.

There is evidence that the continuous use of ibuprofen causes cancer over time. While some studies have suggested a potential association between long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and an increased risk of certain types of cancer, such as colorectal cancer, other studies have reported a slight reduction in cancer risk for eg breast cancer which maybe linked to the blocking non-selectively COX-2 inflammatory process.

Both rheumatoid and osteo- arthritis are long term effects of inflammation of the the period of years and decades. The inflammatory process also known as “leaky gut” and “leaky joints” is directly related to the level of inflammatory omega6 attacks the cartilage and other synovial joint tissue. In other words Auto-immunity, diabetes and arthritis are related to each other as discussed under Metabolic Syndrome above and contribute to the slow destruction of functional tissue.

Once again fish eaters have better arthritis outcomes Tadeshi 2018 and 2016 findings suggest that higher intake of fish may be associated with lower disease activity in RA patients.: In an adjusted linear regression model, subjects consuming fish ≥2 times/week had a significantly lower markers. Disease Activity Score in 28 Joints with CRP (DAS28-CRP) compared with subjects who ate fish never to <1/month (difference −0.49). For each additional serving of fish per week, DAS28-CRP was significantly reduced by 0.18!   

NSAIDs inhibit inflammation resolving effects of omega3

Cyclooxygenase (COX) inhibitors, which are commonly used as anti-inflammatory medications (e.g., nonsteroidal anti-inflammatory drugs or NSAIDs), primarily target the COX enzymes (COX-1 and COX-2) that are involved in the conversion of arachidonic acid (AA) into pro-inflammatory eicosanoids, such as prostaglandins and thromboxanes.

Eicosapentaenoic acid (EPA), an omega-3 fatty acid, can also be metabolized by COX enzymes to produce eicosanoids, but these are generally considered less inflammatory (series 3 prostaglandins and thromboxanes) or even anti-inflammatory compared to those derived from AA. Here’s how COX inhibitors may affect the metabolism of EPA:

  1. Non-Selective COX Inhibitors: These drugs inhibit both COX-1 and COX-2 enzymes. While they effectively reduce the production of pro-inflammatory eicosanoids from AA, they can also inhibit the formation of anti-inflammatory eicosanoids derived from EPA. This is because the same COX enzymes are involved in metabolizing both AA and EPA.

  2. Selective COX-2 Inhibitors: These drugs are designed to selectively inhibit the COX-2 enzyme, which is primarily associated with inflammation and pain. They may have a lesser impact on the COX-1-mediated formation of anti-inflammatory eicosanoids from EPA, but can still affect the balance of eicosanoids in the body.

  3. Impact on Anti-Inflammatory Eicosanoids: By inhibiting COX enzymes, COX inhibitors can potentially reduce the production of anti-inflammatory eicosanoids derived from EPA, such as series 3 prostaglandins and thromboxanes. However, the overall impact on inflammation and health depends on the balance between different types of eicosanoids and other factors.

  4. Alternative Pathways: It’s also worth noting that EPA can be metabolized through other pathways to DHA, such as the lipoxygenase (LOX) pathway, to produce anti-inflammatory mediators like resolvins, which are not directly affected by COX inhibitors.

In summary, while COX inhibitors are effective in reducing the production of pro-inflammatory eicosanoids from AA, they can also impact the formation of anti-inflammatory eicosanoids from EPA. The net effect on inflammation and health depends on the specific COX inhibitor, its selectivity, and the overall balance of eicosanoids and other inflammatory mediators in the body.

Selective COX-2 inhibitors increase the risk of myocardial infarction and stroke that is attributed to their ability to inhibit prostacyclin (PGI2), lipoxins, resolvins, and endothelial nitric oxide (eNO) but not platelet COX-1 derived thromboxane A2 (TXA2). 

Conclusions: Our results mirror other controlled studies that compared ibuprofen and omega-3 EFAs demonstrating equivalent effect in reducing arthritic pain. omega-3 EFA fish oil supplements appear to be a safer alternative to NSAIDs for treatment of nonsurgical neck or back pain in this selective group.

Stress

Biomarkers of stress response in humans, including:

  1. Cortisol: This hormone is released by the adrenal gland in response to stress and helps to regulate blood sugar levels, blood pressure, and the immune system.

  2. Heart rate variability (HRV): This refers to the variation in time between heartbeats and is a measure of the activity of the autonomic nervous system, which regulates the body’s response to stress.

  3. Alpha-amylase: This enzyme is produced by the salivary gland in response to stress and helps to break down carbohydrates in the mouth.

  4. C-reactive protein (CRP): This is a marker of inflammation and is released in response to stress and other stimuli that cause inflammation.

  5. Brain-derived neurotrophic factor (BDNF): This protein is involved in the growth and survival of neurons in the brain and has been linked to stress and depression.

  6. Interleukin-6 (IL-6): This cytokine is produced by the immune system in response to stress and is involved in the regulation of inflammation.

  7. Adrenocorticotropic hormone (ACTH): This hormone is released by the pituitary gland in response to stress and stimulates the adrenal gland to release cortisol.

These biomarkers can be measured through various methods such as blood tests, saliva tests, and heart rate monitoring to assess an individual’s stress response. So these biomarkers can be measured after your 9 month period of taking balance oil omega3. Most of these markers are discussed here in the context of inflammation and autoimmunity. Just search eg. crtl. F- “crp” and you will find your studies related to omega3 improvements on stress!

 

Cortisol and other hormones

 

-> Omega3 lowers cortisol levels! But only at higher dosages!

 

Madison 2021: Omega-3 supplementation reduced total cortisol levels throughout the stressor. The high dose of omega-3 (2.5 g/d), but not the low dose (1.25 g/d), produced a significant (19%) reduction in total cortisol release compared to the placebo group. 

 

Source Madison 2021; at the same time cortisol levels go significantly down, so do IL-6 inflammatory markers and IL-10 anti-inflammatory stay level.

 

One has to distinguish between endogenous (body synthesized) and exogenous drug cortisol. Cortisol is a steroid hormone, in the glucocorticoid class of hormones made from cholesterol in the adrenal glands. Cortisol is generally seen as an inflammatory marker within your body.  So most studies using omega3 show how overall average cortisol levels decrease as inflammation decreases. Circadian levels are typically very high in the morning and decline rapidly in the afternoon. 

-> Cortisol enhances the sympathetic (fight or flight) nervous systems

-> Cortisol purpose is to provide glucose for the brain and muscles and raise the blood pressure

-> acts on nuclear receptors to break down proteins and the free amino acids in turn then activate gluconeogenesis in the liver

-> indirectly activates the breakdown of glycogen storage to provide even more glucose in the blood stream

-> acts vasoconstrictive to bring more blood into the muscles, brain and other organs by enhancing the receptor sensitivity for norepinephrine

-> indirectly depresses your immune response by activating a negative feedback system through cytokines because in a flight of flight state the body wants to conserve the energy it takes to run an immune response 

-> increases gastric acid 

-> Cortisol is the reason why a constant state of stress will lower your immunity and cause “adrenal fatigue” and a multitude of other problems.

 

https://www.saintjohnscancer.org/

 

Endogenous cortisol is an important messenger within your your own body and there is a balance throughout the day to regulated blood sugar among many things. There is an integrate balance between omega3 and your cortisol regulation telling your body what metabolic state it resides in. Cortisol is best known for producing the “fight or flight” response and it will raise blood sugar for brain functions further complemented by a decrease in the sensitivity of peripheral tissue to insulin, thus preventing this tissue from taking the glucose from the blood. In addition it will stop protein synthesis. Prolonged Elevated levels of cortisol can lead to the breakdown of proteins and muscle wasting.

When used as a medication, it is known as hydrocortisone and prevents the release of substances in the body that cause the very inflammation we have been talking about above because it downregulates immunity. It is used to treat conditions resulting from overactivity of the B-cell-mediated antibody response in rheumatoid diseases, as well as allergies.

Cortisone drug use and injections have major side effects:

Bathena 2006: Lipogenesis and lipolysis, which modulate fatty acid concentrations in plasma and tissues, are under hormonal control. The principal hormones involved in lipid metabolism are insulin, glucagon, catecholamines, cortisol and growth hormone. The concentrations of these hormones are altered in chronic degenerative conditions such as diabetes and cardiovascular disease, which in turn leads to alterations in tissue lipids.

 

But in turn Cortisol can weaken the activity of the immune system. It downregulates the interleukins and other cytokines involved in regulating an immune response. This is a complex and balanced system. In other words you want some inflammation but not too much once the immune threat is over. Using Cortisol continuously as a drug thus has devastating effects on your immunity and the general health of your cells particularly the hypothalamus:

Singh 2012: Hence, ω-3 fatty acids, which are also known to enhance parasympathetic activity and increase the secretion of anti-inflammatory cytokines interleukin (IL)-4 and IL-10 as well as acetylcholine in the hippocampus and may be protective. Therefore, treatment with ω-3 fatty acids may be applied for the prevention of metabolic syndrome.

In Addition, stress also causes a higher telomerase activity through inflammation which causes apoptosis (cell death). This is discussed above.

McAuley 2009: This is likely the reason why long-term exposure to cortisol damages cells in the hippocampus and this damage results in impaired learning and memory. This in turn will cause depression and long term increase in stress response.

 

 

 

How does omega3 affect cortisol levels?

The main mechanism is likely via eicosanoids, however there are multitude of effects involved as discussed above.

-> Omega3s, EPA and DHA lower the inflammatory response by replacing inflammatory omega-6 arachidonic acid response directly in the cell membrane! “EPA and DHA are able to partly inhibit a number of aspects of inflammation including leukocyte chemotaxis, adhesion molecule expression and leukocyte-endothelial adhesive interactions, production of eicosanoids like prostaglandins and leukotrienes from the n-6 fatty acid arachidonic acid, production of inflammatory cytokines, and T-helper 1 lymphocyte reactivity” Calder 2014

-> DHA and EPA inhibit cortisol synthesis and neurological brain damage by regulating apoptosis (Brosini 2020) The level of glucocorticoids in blood are regulated by the negative feedback loop of the hypothalamic-pituitary-adrenal. “Overall, the presence of a cell population in the hippocampus that is highly sensitive to EPA and DHA, responding with a significant activation of n-3 PUFAs-induced genes, “

 

Now you can see how cortisol is often regarded as a central player of other hormones because it can regulate their balance e.g. insulin vs glucagon. It is very important to understand that all hormones are messengers within the body to create a balanced homeostasis. Adding “hormonal drugs” such as thyroid hormone continuously to the body (synthetic or not) is not beneficial because they overrides the delicate balances between all metabolic processes and never really fix anything. Omega3 actually naturally regulates your internal hormone production.

Wound Healing and recovery from surgery

Omega-3 fatty acids have been shown to play a role in the wound healing process due to their anti-inflammatory properties and ability to modulate the immune response. They are polyunsaturated fatty acids that include eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are mainly found in fish oil, as well as alpha-linolenic acid (ALA), which is found in plant-based sources like flaxseed and walnuts.

Some of the ways in which omega-3 fatty acids may contribute to wound healing include:

  1. Reducing inflammation: Omega-3 fatty acids have been found to decrease the production of pro-inflammatory substances and increase the production of anti-inflammatory substances. This can help reduce inflammation at the wound site, which can be beneficial for the healing process.

  2. Modulating immune response: Omega-3 fatty acids can influence the function of immune cells involved in wound healing, such as macrophages and neutrophils. They can help regulate the immune response, promoting the removal of damaged tissue and preventing excessive inflammation that can hinder the healing process.

  3. Promoting angiogenesis: Omega-3 fatty acids have been found to promote the growth of new blood vessels (angiogenesis) in the wound area, which is crucial for supplying oxygen and nutrients to the healing tissues.

  4. Improving skin barrier function: Omega-3 fatty acids are essential components of the skin’s lipid barrier and can help maintain the integrity and function of the skin, which is important for wound healing.

There is no doubt incorporating omega-3-rich foods or supplements into one’s diet may potentially support the body’s natural healing process. However, it’s essential to consume proper non-rancid supplements and deal with the underlying health conditions or other medications involved to speed up the healing process.

Several studies have investigated the role of omega-3 fatty acids in wound healing. Here are a few notable examples:

  1. Tissue repair and inflammation reduction: A study published in the journal Wound Repair and Regeneration in 2014 found that supplementation with omega-3 fatty acids could promote tissue repair and reduce inflammation in the healing process. The study concluded that omega-3 fatty acids might have potential therapeutic applications in wound healing

  2. Diabetic wound healing: A 2017 study published in the journal BioMed Research International investigated the effects of omega-3 fatty acids on diabetic wound healing in rats. The results suggested that omega-3 supplementation could improve wound healing in diabetic animals by enhancing angiogenesis (formation of new blood vessels) and reducing inflammation; 

  3. Pressure ulcers: A 2015 study published in the journal Advances in Skin & Wound Care found that omega-3 fatty acid supplementation might have a positive effect on the healing of pressure ulcers in critically ill patients 

  4. Burn wound healing: A 2012 study published in the Journal of Burn Care & Research examined the effects of omega-3 fatty acid supplementation on burn wound healing in rats. The researchers observed that omega-3 fatty acid supplementation improved the healing of burn wounds by reducing inflammation and promoting collagen synthesis 

  5. Long-chain Omega-3 polyunsaturated fatty acids (Omega-3 PUFAs) are widely recognized as powerful negative regulators of acute inflammation. 

Several studies have examined the effects of omega-3 fatty acids on recovery from surgery. Here are a few notable examples:

  1. Postoperative recovery: A systematic review and meta-analysis published in the journal Nutrients in 2020 examined the effects of omega-3 polyunsaturated fatty acids on postoperative recovery. The analysis of 33 studies concluded that omega-3 supplementation might improve the recovery process after surgery, including reducing inflammation, shortening hospital stays, and lowering the risk of postoperative complications

  2. Colorectal cancer surgery: A 2017 study published in the British Journal of Nutrition investigated the effects of omega-3 fatty acid supplementation on postoperative complications and recovery in patients undergoing surgery for colorectal cancer. The researchers found that omega-3 fatty acids might help reduce the risk of postoperative complications and shorten hospital stays 

  3. Cardiac surgery: A 2018 meta-analysis published in the journal Critical Care examined the impact of omega-3 fatty acids on outcomes after cardiac surgery. The study found that omega-3 supplementation might help reduce postoperative inflammation, shorten the duration of mechanical ventilation, and decrease the length of stay in the intensive care unit 

  4. Orthopedic surgery: A 2018 study published in the Journal of Clinical Orthopaedics and Trauma investigated the effects of omega-3 supplementation on recovery after total knee arthroplasty (knee replacement surgery). The results suggested that omega-3 fatty acid supplementation could improve knee function, reduce pain, and decrease the use of pain medications after surgery 

Although these studies indicate that omega-3 fatty acids may play a role in recovery from surgery, it is crucial to consult with a healthcare professional before using omega-3 supplements in the context of surgical recovery. The optimal dosage, duration, and potential interactions with other medications or treatments must be considered.

 

Weight loss

 

Studies suggest that omega-3 fatty acids may have a positive effect on weight loss, particularly when combined with exercise and a healthy diet. Omega-3 fatty acids may also improve insulin sensitivity, reduce adiposity, and improve cardiovascular disease risk factors. As discussed above weight loss depends on your cortisol levels, general inflammation and the proper sugar metabolism! Please also check the obesity section above.

 

  1. Thorsdottir I, Tomasson H, Gunnarsdottir I, Gisladottir E, Kiely M, Parra MD. Randomized trial of weight-loss-diets for young adults varying in fish and fish oil content. An average man in the study (95 kg at baseline receiving 1600 kcal/day) was estimated to lose 3.55 kg (95% CI, 3.14-3.97) (1); 4.35 kg (95% CI, 3.94-4.75) (2); 4.50 kg (95% CI, 4.13-4.87) (3) and 4.96 kg (95% CI, 4.53-5.40) on diet (4) in 4 weeks, from baseline to midpoint.  Int J Obes (Lond). 2007;31(10):1560-1566. doi:10.1038/sj.ijo.0803639 https://pubmed.ncbi.nlm.nih.gov/17502874/

  2. Flachs P, Rossmeisl M, Kopecky J. The effect of n-3 fatty acids on glucose homeostasis and insulin sensitivity. Most animal experiments document beneficial effects of omega-3 on insulin sensitivity and glucose metabolism even under conditions of established obesity and insulin resistance.  Physiol Res. 2014;63 Suppl 1:S93-118. doi: 10.33549/physiolres.932410 https://pubmed.ncbi.nlm.nih.gov/24564669/

  3. Kabir M, Skurnik G, Naour N, et al. Treatment for 2 mo with n 3 polyunsaturated fatty acids reduces adiposity and some atherogenic factors. Subcutaneous adipocyte diameter (P < 0.0018) were lower in the fish oil group than in the placebo group. a randomized controlled study. Am J Clin Nutr. 2007;86(6):1670-1679. doi: 10.1093/ajcn/86.5.1670 https://pubmed.ncbi.nlm.nih.gov/18065585/

  4. Hill AM, Buckley JD, Murphy KJ, Howe PR. Combining fish-oil supplements with regular aerobic exercise improves body composition and cardiovascular disease risk factors.  FO supplements and regular exercise both reduce body fat and improve cardiovascular and metabolic health. Increasing intake of n-3 FAs could be a useful adjunct to exercise programs aimed at improving body composition and decreasing cardiovascular disease risk. Am J Clin Nutr. 2007;85(5):1267-1274. doi: 10.1093/ajcn/85.5.1267 https://pubmed.ncbi.nlm.nih.gov/17490962/

  5. Krebs JD, Browning LM, McLean NK, et al. Additive benefits of long-chain n-3 polyunsaturated fatty acids and weight-loss in the management of cardiovascular disease risk in overweight hyperinsulinaemic women. Ninety-three women completed the study (35 WLFO, 32 WLPO and 26 control), with significant weight-loss in WLFO (10.8+/-1.0%) and WLPO (12.4+/-1.0%) compared to the control group (P<0.0001) Int J Obes (Lond). 2006;30(10):1535-1544. doi: 10.1038/sj.ijo.0803291 https://pubmed.ncbi.nlm.nih.gov/16552404/

 

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Stroke

There are over 800 publications listed on ncbi on this topic. Approximately 50 percent of strokes are caused by common CVD factors, such as uncontrolled high blood pressure. However, the remaining 50 percent are caused by other conditions, such as inherited stroke disorders! 

Omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been extensively studied for their potential effects on stroke risk and outcomes. Here’s a detailed look at how omega-3s might influence stroke:

Omega-3 Fatty Acids and Stroke Prevention

  1. Blood Pressure Reduction: Omega-3 fatty acids can help lower blood pressure, a major risk factor for stroke. By reducing vascular resistance and improving endothelial function, omega-3s contribute to better cardiovascular health.

  2. Anti-inflammatory Effects: Chronic inflammation is associated with atherosclerosis, which can lead to strokes. Omega-3 fatty acids have anti-inflammatory properties that may help reduce the development and progression of arterial plaque.

  3. Antiplatelet Effects: Omega-3 fatty acids can inhibit platelet aggregation, reducing the formation of blood clots that can block arteries and cause ischemic strokes.

  4. Improvement in Lipid Profiles: Omega-3s can lower triglycerides and may alter other lipid parameters, such as increasing HDL (good) cholesterol and possibly lowering LDL (bad) cholesterol. Improved lipid profiles are associated with reduced atherosclerosis risk.

  5. Plaque Stability: By reducing inflammation and improving lipid profiles, omega-3 fatty acids may help stabilize atherosclerotic plaques, making them less likely to rupture and cause a stroke.

Omega-3 Fatty Acids and Stroke Recovery

  1. Neuroprotection: Omega-3 fatty acids, particularly DHA, are crucial components of neuronal membranes and play roles in neuroprotection. They can influence brain recovery mechanisms and potentially improve outcomes after a stroke.

  2. Reduction of Secondary Inflammation: Following a stroke, inflammation can exacerbate neuronal damage. Omega-3 fatty acids can modulate the immune response and potentially reduce secondary damage due to inflammation.

Research and Evidence

  • Clinical Trials and Studies: Several large-scale epidemiological studies and clinical trials have examined the relationship between omega-3 intake and stroke risk. While results are somewhat mixed, many studies suggest a protective effect, particularly for ischemic stroke. For example, the GISSI-Prevenzione trial, which involved individuals with a history of cardiovascular disease, found that omega-3 supplementation led to a significant reduction in the risk of stroke.

  • Dietary Sources vs. Supplements: While eating fatty fish (a rich source of EPA and DHA) has been consistently associated with reduced stroke risk, the evidence for omega-3 supplements is less clear. Some studies show benefits, while others do not show a significant effect.

Recommendations

  • Dietary Intake: Health organizations generally recommend eating at least two servings of fatty fish per week to obtain protective levels of EPA and DHA.

  • Supplementation: Omega-3 supplements might be considered for individuals who do not consume fish, following consultation with healthcare providers, especially for those at high risk of cardiovascular diseases or stroke.

In summary, omega-3 fatty acids have potential benefits in reducing the risk of stroke through multiple mechanisms, including lowering blood pressure, reducing inflammation, and improving lipid profiles. They may also help improve recovery outcomes after a stroke. Further research, particularly into the optimal dosages and the relative benefits of dietary sources versus supplements, continues to refine our understanding of these relationships.

Our analysis indicates that any fish consumption confers substantial relative risk reduction compared to no fish consumption (12% for the linear model), with the possibility that additional consumption confers incremental benefits (central estimate of 2.0% per serving per week).

OKeefe 2024: Among 183 291 study participants, there were 10 561 total strokes, 8220 ischemic strokes, and 1142 hemorrhagic strokes recorded over a median of 14.3 years follow-up. For eicosapentaenoic acid, comparing quintile 5 (Q5, highest) with quintile 1 (Q1, lowest), total stroke incidence was 17% lower (HR, 0.83 [CI, 0.76–0.91]; P<0.0001), and ischemic stroke was 18% lower (HR, 0.82 [CI, 0.74–0.91]; P<0.0001). For docosahexaenoic acid, comparing Q5 with Q1, there was a 12% lower incidence of total stroke (HR, 0.88 [CI, 0.81–0.96]; P=0.0001) and a 14% lower incidence of ischemic stroke (HR, 0.86 [CI, 0.78–0.95]; P=0.0001). Neither eicosapentaenoic acid nor docosahexaenoic acid was associated with a risk for hemorrhagic stroke. 

 

 

 

 

Lower Back Pain and Degenerative Disc Disease

The results of this and many studies suggest that n-3 FA dietary supplementation reduces systemic inflammation by lowering AA/EPA ratios in blood serum and has potential protective effects on the progression of spinal disc degeneration. In this study a lowering of the AA/EPA ratio reduction of blood AA/EPA ratios from 40 to 20 was demonstrated which resulted in a significant recovery of injured rat center discs NP (no change in the control group).

NaPier et. al. 2019 showed disc regeneration with omega-3 diet in this rat experiment.

Causal Effects of Omega-3 Fatty Acids on Low Back Pain; this study finds that there is a causal link between genetically increased plasma omega-3 levels and the reduced risk of low back pain in European ancestries. In other words if your omega 3 level in your blood is high for genetic or other reasons: you reduce your low back pain probability by over 55%. (note: in this study the index ratio of AA/DHA was reduced from 42:1 to 20:1; we typically are looking for 4:1 or less).

Omega3 and back pain

Maroon 2006: Results: Of the 250 patients, 125 returned the questionnaire at an average of 75 days on fish oil. Seventy-eight percent were taking 1200 mg and 22% were taking 2400 mg of EFAs. Fifty-nine percent discontinued to take their prescription NSAID medications for pain. Sixty percent stated that their overall pain was improved, and 60% stated that their joint pain had improved. Eighty percent stated they were satisfied with their improvement, and 88% stated they would continue to take the fish oil. There were no significant side effects reported.

Furthermore, a positive correlation was observed between the omega-6:3 ratio [IVW, OR 95% CI: 1.057 (1.014, 1.101), p = 0.009] with abdominal and pelvic pain. Additionally, we found a negative correlation between omega-3 FAs [IVW, OR 95% CI: 0.947 (0.902, 0.994), p = 0.028] and lower back pain or sciatica.

Dai 2023: Conclusion: Our analysis suggests that higher circulating concentrations of omega-3 FAs and DHA and a lower omega-6:3 ratio are associated with a reduced risk of abdominal and pelvic pain. Additionally, a higher concentration of circulating omega-3 FAs is linked to a reduced risk of lower back pain and/or sciatica. 

 

 

Fertility, Pregnancy and Fetus development

 

-> Studies show that omega3 significantly increases fertility in men and women; stem cells as well as sperm and oocytes simply cannot function and divide without proper omega3

-> Your growing baby is trying to develop its nervous system and needs every DHA molecule available for that task. Our tests show that both mother and baby usually end up deficient on omega3

-> your hormonal regulation depends on proper omega3 fat metabolism; your inflammatory index determines how receptive your body is to new life

->   Studies show Your baby’s IQ depends on the proper availability of omega3

 

Omega-3 fatty acids, particularly EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), are known to have numerous health benefits, including potential positive effects on fertility in both men and women. Here are some studies and reviews that have investigated the role of omega-3 fatty acids in fertility:

  1. Gaskins, A. J., & Chavarro, J. E. (2018). Diet and fertility: a review. American Journal of Obstetrics and Gynecology, 218(4), 379-389. 

This review article discusses the effects of diet on fertility, including the role of omega-3 fatty acids. The authors report that higher intake of omega-3 fatty acids has been associated with better semen quality in men and improved embryo quality in women undergoing assisted reproductive treatments.

  1. Safarinejad, M. R. (2011). Effect of omega-3 polyunsaturated fatty acid supplementation on semen profile and enzymatic anti-oxidant capacity of seminal plasma in infertile men with idiopathic oligoasthenoteratospermia: a double-blind, placebo-controlled, randomised study. Andrologia, 43(1), 38-47. 

In this double-blind, placebo-controlled, randomized study, omega-3 supplementation led to significant improvements in sperm parameters, such as sperm concentration, motility, and morphology, in men with idiopathic oligoasthenoteratospermia (a condition characterized by low sperm count, poor sperm motility, and abnormal sperm morphology).

  1. Jungheim, E. S., Frolova, A. I., Jiang, H., & Riley, J. K. (2013). Relationship between serum polyunsaturated fatty acids and pregnancy in women undergoing in vitro fertilization. The Journal of Clinical Endocrinology & Metabolism, 98(8), E1364-E1368. 

This study found that women with higher serum levels of omega-3 fatty acids had a higher probability of pregnancy after in vitro fertilization (IVF). The authors suggest that omega-3 fatty acids may have a positive impact on fertility by modulating inflammation and improving oocyte and embryo quality.

  1. Nassan, F. L., Chavarro, J. E., & Tanrikut, C. (2018). Diet and men’s fertility: does diet affect sperm quality? Fertility and Sterility, 110(4), 570-577. 

This review article highlights the potential role of diet in modulating sperm quality and male fertility, with a particular focus on omega-3 fatty acids. The authors note that several studies have found a positive association between higher omega-3 fatty acid intake and improved sperm quality.

 

Men:

Safarinejad 2010 Conclusions: Infertile men had lower concentrations of omega-3 FAs in spermatozoa than fertile men. The ratio of serum omega-6/omega-3 fatty acids was significantly higher in infertile (14.8+/-4.3) patients compared to fertile controls (6.3+/-2.2) (P=0.001).

Long chain omega 3 fatty acids appear to improve male and female fertility. Safarinejad 2011:  

A significant improvement of sperm cell total count (from 38.7 ± 8.7 ‘ 10⁶ to 61.7 ± 11.2 ‘ 10⁶, P = 0.001) and sperm cell concentration (from 15.6 ± 4.1 ‘ 10⁶ per ml to 28.7 ± 4.4 ‘ 10⁶ per ml, P = 0.001) was observed in the omega-3 group. 211 men were observed in a randomized study in in only 32 weeks!

 

Women and Baby:

Middleton 2018: In the overall analysis, preterm birth < 37 weeks and early preterm birth < 34 weeks were reduced in women receiving omega-3 LCPUFA compared with no omega-3. There was a possibly reduced risk of perinatal death and of neonatal care admission, a reduced risk of LBW babies;

Higher levels of serum long-chain ω3-PUFA were associated with higher probability of clinical pregnancy and live birth. Specifically, after multivariable adjustment, the probability of clinical pregnancy and live birth increased by 8%! – Chiu 2018

Omega-3 PUFAs are essential for the growth and development of the central nervous system during pregnancy, infancy, and childhood! A sufficient dietary supply of these compounds [pufa] is essential for normal brain development –

Bourre 2007: Omega-3 fatty acids could play a positive role in the prevention of menstrual syndrome and postmenopausal hot flushes. The normal western diet contains little ALA (less than 50% of the RDA). The only adequate sources are rapeseed oil (canola), walnuts and so-called “omega-3” eggs (similar to wild-type or Cretan eggs). The amounts of EPA and DHA in the diet vary greatly from person to person.

 

Maternal seafood intake during pregnancy of less than 340 g per week was associated with increased risk of their children being in the lowest quartile for verbal intelligence quotient (IQ) (no seafood consumption, odds ratio [OR] 1.48!

 

We have collected preliminary evidence from testing mothers during pregnancy how the growing baby is literally “depriving” the mother of omega-3s and after birth a previously supplemented woman and the baby are testing highly deficient. Therefore we now recommend a double/triple dosage of balance oil for pregnant women. Most important goal is to provide the baby with missing vital DHA for brain development and and reducing the baby’s arachidonic inflammatory index.

Sebastini 2019 concludes: A review of the scientific literature in this field was performed, focusing specifically on observational studies in humans, in order to investigate protective effects elicited by maternal diets enriched in plant-derived foods and possible unfavorable outcomes related to micronutrients deficiencies and their impact on fetal development. A design of pregestational nutrition intervention is required in order to avoid maternal undernutrition and consequent impaired fetal growth.

Men: ω3 fatty acids, can improve some degree of sperm parameters in infertile men. 

Amirani 2020: Conclusion:  Based on the results of this meta-analysis omega-3 PUFA supplementation during pregnancy has a significant beneficial effect on HDL-cholesterol, and C-reactive protein.

 

Sinclair 2022: Docosahexaenoic acid (DHA) is a major constituent of neural and visual membranes and is required for optimal neural and visual function. DHA is derived from food or by endogenous synthesis from α-linolenic acid (ALA), an essential fatty acid. Low blood levels of DHA in some westernised populations have led to speculations that child development disorders and various neurological conditions are associated with sub-optimal neural DHA levels, a proposition which has been supported by the supplement industry. 

 

Don’t forget to check the IQ development section!

 

General Immune System Function

Shakoor 2021: Undoubtedly, nutrition is a key determinant of maintaining good health. Key dietary components such as vitamins C, D, E, zinc, selenium and the omega 3 fatty acids have well-established immunomodulatory effects, with benefits in infectious disease. Some of these nutrients have also been shown to have a potential role in the management of COVID-19. 

 

Shakoor 2021: Omega-3 downregulates inflammation and possibly viral replication

 

Rogero 2020: EPA and DHA replace arachidonic acid (ARA) in the phospholipid membranes. When oxidized by enzymes, EPA and DHA contribute to the synthesis of less inflammatory eicosanoids and specialized pro-resolving lipid mediators (SPMs), such as resolvins, maresins and protectins. This reduces inflammation.

Rogero 2020: If the cell membrane has sufficient omega-3, DHA and EPA it can directly act to prevent a cytokine storm in the infected cells.

 

 

Heavy metal poisoning, caused by excessive exposure to metals like lead, mercury, arsenic, cadmium, and chromium, can have detrimental effects on the immune system, among other bodily systems. The impact on the immune system can be varied and complex, as different heavy metals may exert their effects through different mechanisms. Here’s a general overview of how heavy metals can affect the immune system:

  1. Immunosuppression: Some heavy metals can suppress the immune system, making the body more susceptible to infections. For instance, lead exposure can lead to decreased numbers of circulating white blood cells and can disrupt the function of natural killer cells, T cells, and other lymphocytes.

  2. Inflammation: Chronic exposure to certain heavy metals can lead to a state of low-grade inflammation, as the immune system is constantly activated to try to deal with the persistent presence of these toxins.

  3. Autoimmunity: Some heavy metals can modify self-proteins, making them appear foreign to the immune system and potentially triggering autoimmune reactions, where the body’s immune system attacks its own cells and tissues. Mercury, for example, has been associated with autoimmune effects in susceptible individuals.

  4. Altered Cytokine Production: Heavy metals can influence the production of cytokines, which are signaling proteins that mediate and regulate immunity, inflammation, and hematopoiesis. This can disrupt normal immune responses and signaling pathways.

  5. Oxidative Stress: Many heavy metals induce oxidative stress by generating free radicals, which can damage cells, including immune cells. This oxidative stress can also lead to the activation of signaling pathways that affect immune function.

  6. Functional Impairment: Heavy metals can directly impair the function of immune cells. For example, they can affect the ability of macrophages to engulf and destroy pathogens, or they can inhibit the proliferation of lymphocytes necessary for an adequate immune response.

  7. Developmental Effects: Exposure to heavy metals, especially in critical developmental periods like childhood, can have long-lasting effects on the immune system, potentially leading to increased risk of infections and diseases later in life.

Omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are known for their anti-inflammatory and antioxidant properties, which may play a role in the body’s defense against the oxidative stress caused by heavy metals.

Here are some ways through which omega-3 fatty acids might confer protection against heavy metal toxicity:

  1. Antioxidant Support: Omega-3 fatty acids can enhance the body’s antioxidant defense system. Since heavy metal exposure can increase oxidative stress, omega-3s may help mitigate this by boosting the levels of antioxidants, which can neutralize free radicals and reduce oxidative damage.

  2. Anti-inflammatory Effects: Chronic exposure to heavy metals can lead to inflammation. Omega-3 fatty acids are known to have anti-inflammatory properties by giving rise to anti-inflammatory eicosanoids and resolvins, potentially countering the inflammatory response triggered by heavy metals.

  3. Membrane Integrity: Omega-3 fatty acids are important components of cell membranes and may help maintain membrane fluidity and function. This could potentially protect cells from the uptake of heavy metals or help maintain cellular function in the face of metal-induced damage.

  4. Neuroprotection: Some heavy metals, like mercury and lead, are neurotoxic. Omega-3 fatty acids, particularly DHA, are vital for brain health and may offer some protection against the neurotoxic effects of heavy metals.

  5. Chelation and Excretion: While omega-3 fatty acids themselves do not chelate heavy metals, their anti-inflammatory and antioxidant properties might support the overall health of organs like the liver and kidneys, which are involved in detoxification and excretion processes.

  6. Modulation of Gene Expression: Omega-3 fatty acids can influence gene expression related to metabolism, stress responses, and detoxification pathways, possibly providing a cellular mechanism to cope with toxic insults.

While these mechanisms suggest potential benefits and will benefit the immune system, it’s important to stress that omega-3 fatty acids are not a treatment for heavy metal poisoning and they do not replace the conventional methods of detoxification, such as chelation therapy.

 

5. Saturated Fat and more

First of all, we need to understand that digestion of fats is a complicated process involving the liver/gallbladder, pancreatic enzymes, small intestine and ultimately the whole body. In short, fats need to be emulsified then broken down into its fatty acids and transported within the bloodstream in specific vesicles and then reassembled or metabolized. Fat does not mix with water or blood for that matter and it always needs to be incorporated into membranes or vesicles such as LDL or chylomicrons.

Bile Salts and the Gallbladder

Bile salts play a critical role in the digestion and absorption of fats in the small intestine. Bile is produced by the liver and stored in the gallbladder, and is released into the small intestine when fat is present.

When bile salts come into contact with fat molecules in the small intestine, they emulsify the fat, which means they break it down into smaller droplets. This increases the surface area of the fat, allowing digestive enzymes to more effectively break it down into smaller components that can be absorbed by the body.

Bile salts also help to solubilize fatty acids and other fat-soluble compounds, which allows them to be absorbed into the bloodstream and transported to the liver for further processing.

In addition to their role in fat digestion, bile salts also play a role in the elimination of waste products from the body, including excess cholesterol and other fat-soluble toxins.

Overall, bile salts are essential for the efficient digestion and absorption of dietary fats, and their absence, such as in individuals who have had their gallbladder removed, can lead to difficulty digesting and processing fats. This can result in symptoms such as abdominal pain, bloating, and diarrhea, which may be alleviated by taking pancreatic enzymes or modifying the diet as previously mentioned.

 

Short summary on what fats should or should not be included in your diet

1.>Saturated fats and Cholesterol:

Saturated fats have gotten a bad reputation for no evident reason. Saturated fats are starting point for the formation of higher fatty acid and thus for the formation of the triglycerides as energy stores and phospholipids as the main component of cell membranes of cell membranes.


Above all, they cause the demarcation of cells from the intercellular space. the intercellular space, so that important biochemical important biochemical processes can take place undisturbed within the cells.


However an excessive diet of carbohydrates produces palmitic acid, which leads to a disturbance in the ratio of ratio of saturated to unsaturated fatty acids. As a consequence, insulin resistance develops, toxic
effects on the pancreas, slowing down of fat burning and slowing down of fat burning and pro-inflammatory processes emerge.

Many people do not eat enough saturated fats and an improper keto diet can also lead to vital lack of saturated fats. Research shows that saturated fats are not related to disease development. Again it is the excess consumption of carbohydrates that produces a high saturated fatty acid metabolism leading to insulin resistance. A keto diet rich in saturated fats can oppose this mechanism.

This study shows that saturated fats and cholesterol have no effect on heart health.

The age old question: Are humans carnivores or vegetarian? Is there a difference in saturated fats in our food?

You can break down the answer to what fats do Humans really need?

  1. Omega-3 is essential and only found in grazing animals or algae consuming cold water fish
  2. Stearic acid is usually only found in animal products. Most plants contain very little and mostly Palmitic acid which is not supplying omega-9 in the human body.
  3. Humans are omnivores however the protein and fatty acid compositions in animal food sources resemble much more closely our needs compared to plant sources.

Saturated fat consisting of mainly Palmitic (PA) and Stearic acid (SA) are a major source for energy storage in Adipose tissue and other organs as well as vital fatty acids for membrane lipids. However studies show that SA is very important for human heart health. Now, the main dietary source of stearic acid is animal fat. The levels of stearic acid are usually very low in plants, with the exception of coconut oil, cocoa butter, and palm kernel oil. Many people now test low in stearic acid with often negative values indicating the lack of animal fat meat consumption. In this study A stearic acid-rich diet improves thrombogenic and atherogenic risk factor profiles in healthy males . Our balance test often shows that people are deficient (negative value) in SA probably because they don’t eat enough red meat: animal meat is rich in stearic acid, plants contain less than 7% (except coconut), you need large amounts of SA for heart health and other organs rather than PA; this is not well understood but one of the reasons maybe that SA is Carbon-18 and you can make oleic acid from it omega9. you cannot do that from PA (cabon-16). Omega-9 is plays a vital role in membrane health.

 

 

Why do we need to cook meat?

Source: “Cooking was unquestionably a revolution in our dietary history. Josephine Joordens of Leiden University and her colleagues proposed in 2014 that eating fatty fish could have significantly increased the availability of certain long-chain polyunsaturated fatty acids (LC-PUFA), which helped to support the initial moderate increase in brain size of early humans about 2 million years ago.

Four years earlier, David Braun of the George Washington University and his colleagues announced that they had discovered the earliest evidence of human butchery of aquatic animals. At a 1.95-million-year-old site in Koobi Fora, Kenya, they found evidence that early humans were butchering turtles, crocodiles, and fish, along with land-dwelling animals. Aquatic animals are rich in nutrients needed in human brain growth, such as DHA (docosahexaenoic acid), one of the most abundant LC-PUFAs in our brains.

Cooking makes food both physically and chemically easier to chew and digest, enabling the extraction of more energy from the same amount of food. It can also release more of some nutrients than the same foods eaten raw and can render poisonous plants palatable. Important components of meat include not only vitamins A and K, calcium, sodium, and potassium, but also iron, zinc, vitamin B6, and vitamin B12; the latter, although necessary for a balanced primate diet, is present only in small quantities in plants.”

 

 

So, is Cholesterol dangerous or not?

Cholesterol and especially LDL is always discussed as the “bad guy” in the context of saturated fat, arteriosclerosis, heart disease and stroke. Is that really true? 

1> The presence of LDL-cholesterol containing vesicles in in arterial plaques does not prove any relationship to cardiovascular disease. 

2> LDLs are the transport vesicles to all the peripheral cells. Cholesterol is naturally predominant in these vesicles because every cell in the body needs large amounts of cholesterol to function; for that purpose at any given time 0.2% of the blood consists of cholesterol and up to several kg of the human body mass consist of cholesterol!

3> Cholesterol is an important precursor to many hormones!

4> Cholesterol is so important that The liver produces cholesterol regardless of the amount of cholesterol consumed in the diet. If your diet is low in cholesterol, the liver will increase cholesterol production to ensure that the body has enough to meet its needs. Statins interfere with this natural process in the liver.

5> When you remove Cholesterol cell-cell communication eg. brain synapses cease to function, cells cannot make vesicles, membrane proteins become impaired and cell division is affected. 

6> 30+ years of statin use teaches us that there is no relationship of lowering cholesterol and heart disease or stroke. In other words, taking statins does not protect you from heart attack or stroke. On the contrary, recent studies now show that cholesterol below 150mg/dl is dangerous and increases your mortality significantly.

Why do we need Cholesterol?

The cholesterol molecule is unique due to its distinct structure, properties, and the various functions it performs within the body. Here are a few aspects that make cholesterol unique:

  1. Chemical structure: Cholesterol is a lipid molecule classified as a sterol, which is a combination of steroid and alcohol. Its structure consists of a hydrocarbon tail, a four-ring steroid nucleus, and a hydroxyl group. The hydroxyl group makes cholesterol an amphipathic molecule, meaning it has both hydrophilic (water-loving) and hydrophobic (water-fearing) properties. This characteristic allows cholesterol to interact with both lipids and proteins in cell membranes.

  2. Cell membrane function: Cholesterol is an essential component of cell membranes, providing stability and regulating membrane fluidity. Its amphipathic nature enables cholesterol to be embedded within the phospholipid bilayer, helping to maintain the proper balance between rigidity and flexibility.

  3. Precursor to essential molecules: As mentioned in the previous response, cholesterol is a precursor to various crucial hormones and molecules, such as cortisol, aldosterone, sex hormones, and vitamin D. These molecules play important roles in regulating metabolism, inflammation, blood pressure, reproduction, and bone health.

  4. Lipoprotein transport: Cholesterol is transported through the bloodstream by lipoproteins, such as low-density lipoprotein (LDL) and high-density lipoprotein (HDL). These lipoproteins have different roles in cholesterol transport and metabolism, and their balance is important for maintaining cardiovascular health.

  5. Bile acid synthesis: Cholesterol is also a key component in the synthesis of bile acids, which are produced in the liver and stored in the gallbladder. Bile acids are essential for the digestion and absorption of dietary fats and fat-soluble vitamins.

Due to its unique structure and properties, cholesterol plays a vital role in numerous physiological processes within the body. Maintaining appropriate cholesterol levels through a balanced diet is crucial for all metabolic cellular functions.

 

How much Cholesterol is in the human body?

First of all you need to know that about 40% of a cellular mass consists of lipids made with fatty acids. According to a study published in the Journal of Lipid Research, lipids constitute about 40% of the dry weight of a typical mammalian cell!

According to previous studies published in the Journal of Lipid Research, the average cholesterol content of human tissues is only about 5-10 mg/g of tissue?, or about 0.5-1% by weight?  This means that if you take the total mass of all the tissues in the human body (excluding water), the amount of cholesterol would be at least 0.5-1% of that mass. The fact is that nobody actually seems to know the exact numbers and a literature searches merely mention the blood cholesterol levels of 200 mg/dL x 50 dL = 10,000 mg or 10g in the blood stream of an average 80kg male or 0.2%w/w. 

Zhang 2018: Comprising 30 mol % of the lipids in cell membranes, cholesterol plays vital biophysical roles in monolayer and bilayer membranes. It increases the lipid-packing density and maintains high membrane fluidity.

Zuckerman 2004: Cholesterol (or other higher sterols such as ergosterol and phytosterols) is universally present in large amounts (20-40 mol%) in eukaryotic plasma membranes, whereas it is universally absent in the membranes of prokaryotes. 

If we assume that cholesterol makes up about 10% (30% of 40% lipids) of the dry weight of a typical mammalian cell, and that cells make up about 60% of the total body weight of an average male (=48 kg), we can estimate the total amount of cholesterol in the body as follows:

Total cholesterol in the body = (~10% of cell mass) x (total cell mass in the body); Total cell mass in the body = 0.6 x body weight = 0.6 x 80 kg = 48 kg

Therefore, the total amount of cholesterol in the body would be approximately: Total cholesterol in the body = 0.10 x 48 kg = 4.8 kg

Note that this is a rough estimate and the actual amount of cholesterol in the body can vary widely depending on a variety of factors, including age, sex, diet, and underlying health conditions.

So in summary, if at any given time 0.2% of the blood consists of cholesterol and up to several kg of the human mass are cholesterol, don’t you think this is an important molecule?

Given the fact that lipids far outnumber protein (~20:3 million) or other cellular molecules this makes cholesterol a very important component of a functional cell. Not only does it keep the membranes fluid, flexible and functional… Cholesterol also serves as a precursor for the biosynthesis of  steroid hormones, bile acid and vitamin D. Cholesterol also plays a vital part in the innate immune system. These are all required for vital body functions and allow for a healthy digestion, immunity and hormonal regulation.

What happens when you remove cholesterol?

Regardless of the above discussion studies show the detrimental effects of low cholesterol especially on the ability to form vesicles and communicate which is essential for synaptic function:

–Wasser 2007: Cholesterol is a major lipid component of cellular membranes and regulates the degree of membrane fluidity. The presence of cholesterol is thought to be important for proper synapse structure and function in the brain. Experiments in which cholesterol levels are altered have revealed several roles for cholesterol in neurones including promotion of synaptogenesis, maintenance of synapse organization, and enablement of synaptic vesicle (SV) fusion and endocytosis (; ; ; ). During development, glia-derived cholesterol enhances the formation of synapses (; ; ). In neuroendocrine cells, cholesterol depletion disrupts syntaxin clusters and decreases evoked catecholamine release (; ; ; ). In addition, cholesterol depletion with methyl-β-cyclodextrin (MCD) inhibits clathrin-dependent endocytosis in multiple preparations (; ). In nerve terminals, cholesterol interacts with several SV proteins (). In addition, cholesterol is a prominent component of SV membranes () and has been proposed as a spatial organizer of synaptic vesicle recycling ().

–Rau 2007: Cholesterol is a major constituent of plasma cell membranes and influences the functions of proteins residing in the membrane. We conclude that cholesterol depletion … does affect the trafficking and consequently the MHC class I antigen-processing pathway.”

–Levitan 2010: “maintaining membrane cholesterol level is required for coupling ion channels to signalling cascades.” depletion shows effects (i) specific interactions between cholesterol and the channel protein, (ii) changes in the physical properties of the membrane bilayer and (iii) maintaining the scaffolds for protein-protein interactions.

Functional dependence of the Potassium channel on the availability of cholesterol. The channel is only fully functional with proper cholesterol. Partial substitution of native cholesterol by epicholesterol resulted in significant increase in Kir2 current suggesting that it is a specific lipid-channel interaction rather than changes in the physical properties of the membrane that is responsible for cholesterol-induced suppression of Kir2 channels.

In summary, Cholesterol is biosynthesized by all animals because all cells require it as an essential structural component of animal cell membranes. Your liver makes most of the cholesterol your body needs if cells require additional supply. Cholesterol and other fats are carried in your bloodstream as spherical particles called lipoproteins. The two most commonly known lipoproteins are low-density lipoproteins (LDL) and higha-density lipoproteins (HDL). LDL constitute the highest portion of “cholesterol vesicles” in the blood and are responsible to shuttle their content to the cells. 75% of the LDL content is cholesterol and ApoB, the responsible receptor target protein. Cells express an LDL receptors when they require more supply and can then endocytose/uptake these vesicles. LDLs can vary significantly in size and content. They also contain triglycerides, proteins and omega6.

LDL vs HDL

  1. Size: LDL particles are smaller and denser than HDL particles. This makes them more likely to penetrate the walls of arteries and deposit cholesterol, while HDL particles are less likely to do so.

  2. Composition: LDL particles contain more cholesterol than HDL particles. LDL particles also contain a higher proportion of saturated and trans fats, which are more likely to contribute to atherosclerosis.

  3. Function: LDL particles carry cholesterol to the cells in the body, while HDL particles carry cholesterol away from the cells and back to the liver for processing.

Once again, the primary job of LDL is to carry cholesterol and other vital lipids to the peripheral target cell. The simple fact that LDLs are predominant and loaded with ‘fat’ means that a small percentage also can become oxidized into so-called foam cells and stick to the blood vessels infiltrated with macrophages. The oxidation process is complex and poorly understood but a deficiency of omega-3 will contribute to this process. This Nature article clearly shows 2 facts: 1) fresh fish diets lower cholesterol and LDL; 2) supplementation elevated LDL levels showing that most supplement are rancid and causing more harm. Below you will also see that E-EPA drug has the same effect as statin drugs in lowering cholesterol naturally without most of the side effects.

But inherently there is nothing bad about LDLs and naturally you will find a natural correlation of plaques and LDL. If your diet is high in cholesterol containing foods you will naturally also contain more LDL in your blood. Soliman 2018; The assumption: The relationship between dietary cholesterol and total plasma cholesterol has been reported to be linear based on observational cohort studies [,]. However, the limitation of the observational studies is the presence of confounding variables that may amplify positive or negative correlations as well as the existence of selection biases []. Additionally, the intake of dietary cholesterol is usually associated with an increased intake of saturated fatty acids which is documented to increase LDL Cholesterol and the risk of cardiovascular disease []. 

Statins:

Statins actually did us the biggest favor in deciding the issue weather cholesterol is dangerous: There are a lot of assumptions that go into the science of statin pharmacology. Simply lowering the LDL cholesterol levels by inhibiting vital production in the liver (which statins do) does not mean heart disease risks are lowered. After 30 years we know that taking these drugs only lowers your chance of a heart attack or stroke by less than 2%.

“Notwithstanding the success of statin treatment for reaching treatment goals, the residual cardiovascular risk being about 70% remains remarkably high [–].”

Statins lower LDL but so what?

To the contrary this group found that the oxidized LDLs actually proved to be beneficial. Instead of increasing the amount of cholesterol uptake and accumulation in the macrophage foam cells, mildly oxidized LDL almost completely prevents increases in cholesterol!

This entire foam cell process maybe a protective mechanism to repair inflamed and damaged arteries. The effect of human CRP (normally an inflammation marker) was shown to be atheroprotective, and the importance of CRP-LDL interactions in this protection was noted.

In summary, Cholesterol is vital for every cellular function and most of the supply comes from your food in the first place. Otherwise it is made in the liver and intestines by a very complicated 50+ enzymatic process using massive energy and metabolic resources. In essence, the cholesterol factory is complicated but so vital to the body, if cholesterol is not available from food sources. 

So after reading this, ask yourself if it is a good idea to inhibit a vital production of an important cholesterol molecule or restrict the intake of cholesterol in our food. A chicken egg contains 180-375mg of cholesterol in the yoke of 18g. A steak of 100g contains 78mg cholesterol. Why have we been told to restrict these foods if there is at any given time there is already 10,000 mg of cholesterol floating in those so called HDL and LDL lipid transport vesicles in the blood? At a low average an 80kg body of which 60% is water = 32kg cell mass = 12.8kg lipids = roughly ~1kg of Cholesterol (assuming 20% by moles but cholesterol only weighs half of the average lipid). 1kg is likely a high estimate because not all intra-cellular lipid membranes contain that much cholesterol, however it is even found in mitochondria and other organelles. But even a very very low estimate of a few hundred grams of cholesterol in the body shows how important this molecule is and below you see that studies show if your blood cholesterol goes below 200mg/dl or 10g of total blood circulating cholesterol your mortality is going up significantly. 

In addition, Against all teaching saturated stearic acid actually lowers cholesterol: Fasting HDL-cholesterol concentrations were lower after the stearic acid diet than the palmitic acid and oleic acid diets Unlike oleic acid, the hypocholesterolemic effect of stearic acid may be mediated by inhibition of intestinal hydrophobic [cholic acid] synthesis! The consumption of fatty red meats of course increases your overall cholesterol but studies show how a large amount of cholesterol is necessary in our diets. The longstanding argument of good vs bad cholesterol or LDL vs HDL is largely fabricated by statin manufactures because everyone knows that the body needs massive amounts of cholesterol. HDLs are the vesicles that are found to deliver cholesterol from the liver to cells and LDLs simply return it in the form of esterified cholesterol so it can be excreted. The fact that artery foam cells contain more LDL and are part of plaques does not mean that cholesterol is causing plaque, atherosclerosis, heart disease or stroke. It is now believed that excess sugar and the resulting production of excess Triglyceride levels are inexorably linked to heart disease risk. Triglycerides are packaged into very low-density lipoprotein, which are then converted into low-density lipoprotein, LDL. Increased sugar intake, therefore, leads to increased VLDL production, which in turn leads to increased production of LDL particles which are then found naturally in excess in arterial plaques. But is is the excess sugar which is causing the inflammatory foam cells ultimately destroying the circulation not the cholesterol. 

Inflammation causes Plaques not Cholesterol: There is now overwhelming experimental and clinical evidence that atherosclerosis is a chronic inflammatory disease. Lessons from genome-wide association studies, advanced in vivo imaging techniques, transgenic lineage tracing mice, and clinical interventional studies have shown that both innate and adaptive immune mechanisms can accelerate or curb atherosclerosis.

 

Statins and what they teach us!

 

The flawed JUPITER study: 

The JUPITER study was the hallmark of the argument that LDL reduction actually reduces heart disease…”The rate of the primary end point, a composite of five conditions (nonfatal myocardial infarction, nonfatal stroke, hospitalization for unstable angina, arterial revascularization, or confirmed death from cardiovascular causes) was only 0.77% per year in the rosuvastatin arm and 1.36% in the placebo arm. These rates translate into an absolute risk reduction of about a half percentage point per year (0.59%), or 1.2% over the approximately 2-year total duration of the trial. This figure is obviously much less impressive to the casual reader than the relative risk reduction of 44%.” “Based on an absolute risk reduction of 0.59% per year for the primary endpoint, 169 persons need to be treated for one year to prevent one combination of clinical events measured in JUPITER. For more unambiguous major coronary events, including fatal or non-fatal myocardial infarction, 500 persons need to be treated for one year to prevent one event (NNT of 1:500). These are large numbers, considering that the persons being treated were deemed to be healthy at the start of the study. Therefore, the safety and costs associated with treating such patients need to be carefully considered.”

This is actually a typical example of how major conclusions are drawn from miniature patient numbers! 0.77% vs 1.36% – a very common problem – Many scientist agree that there is no relationship between LDL and heart disease and we know that now after 30 years of prescribing statins. 

Short duration of studies: “In a meta-analysis including 90,056 patients with hypercholesterolemia of whom 47% had pre-existing CHD, there was a 23% relative risk reduction of nonfatal or fatal myocardial infarction {first year}, but only a 2.4% absolute risk reduction over a mean of 5 years, or approximately 0.48% per year (number needed to treat: 208)” (and 5 years is not really a long time either).

This kind of sums up how small the effect is “among the sick” to begin with: the overall reduction of about 20% per mmol/L LDL cholesterol reduction translated into 48 (95% CI 39-57) fewer participants having major vascular events per 1000 among those with pre-existing CHD at baseline, compared with 25 (19-31) per 1000 among participants with no such history. Understand, that out of those ‘90,000 participants’ in 5 years, there were 8186 deaths, 14,348 individuals had major vascular events, and 5103 developed cancer.

In summary: The arguments of good versus bad cholesterol is largely futile. In fact, the 35years of cholesterol statin drug prescription has only lowered heart disease or stroke but about 2%, statistically insignificant!

YI et. al. showed that your mortality is increasing rapidly below about 150mg/dL cholesterol!

The consensus here is, that your body needs large amounts of cholesterol and there is no obvious relationship between cholesterol and heart disease or stroke. Cholesterol is essential for membrane fluidity and it actually compensates for the lack of omega-3. It is also essential for steroid hormone production. That is why your liver synthesizes cholesterol if your diet is deficient. Inhibiting this important mechanism with statins makes no physiological sense. The mere fact that despite the ca. 80 pts reduction of cholesterol by statins and the lack of disease improvement outcomes proves this point.

Statin-induced myopathies

Hydroxyl-methylglutaryl coenzyme A reductase inhibitors or statins interfere with the production of mevalonic acid, which is a precursor in the synthesis of coenzyme Q10. Q10 is one of the most important anti-oxidants that in combination with omega-3 keep your mitochondria healthy. Statins can reduce the internal production of Q10 by up to 40% and this cannot be rectified by taking supplements. The sad thing is this has been know for over 15 years. This is likely the mechanism why statins do not improve your chance of heart disease.

Statin side effects are severe including headache dizziness, feeling sick, fatigue, physically weakness digestive problems, constipation, diarrhea, indigestion or gas., muscle pain, insomnia. low blood platelet counts. 1 in 21 experience severe muscle pain and 1:200 develop diabetes type 2 This also shows us that there the resulting lack of vital Cholesterol is important for cellular function, particularly energy metabolism and inflammation levels only go up.

STATIN induced Diabetes:

Casula 2017: Overall, NOD (new onset diabetes) risk was higher in statin users than nonusers (RR 1.44; 95% CI 1.31-1.58). High between-study heterogeneity (I2 = 97%) was found. Estimates for all single statins showed a class effect, from rosuvastatin (RR 1.61; 1.30-1.98) to simvastatin (RR 1.38; 1.19-1.61).

 

 

Here is a list of the long term potential long-term risks of taking statin drugs:

  1. Muscle damage: Statin drugs can cause muscle damage, including myopathy (muscle weakness) and rhabdomyolysis (a more severe form of muscle damage that can lead to kidney damage). While these side effects are rare, they can be serious.

  2. Liver damage: Statin drugs can cause liver damage, although this is also rare. Liver function tests are usually monitored periodically to detect any signs of liver damage.

  3. Cognitive decline: Some studies have suggested that long-term use of statin drugs may be associated with an increased risk of cognitive decline, including memory loss and confusion. However, other studies have found no such association.

  4. Diabetes: Some studies have suggested that long-term use of statin drugs may be associated with an increased risk of developing diabetes. This risk appears to be highest in people who already have risk factors for diabetes, such as obesity or insulin resistance.

  5. Nutrient deficiencies: Statin drugs may interfere with the body’s production of coenzyme Q10 (CoQ10), which is important for energy production and muscle function. Some studies have also suggested that statin drugs may interfere with the absorption of vitamin D.

 

A discussion with the narrative about statins:

“It’s important to note that the benefits of statin drugs typically outweigh the risks, especially in people with high cholesterol levels or a history of cardiovascular disease. However, it’s also important to talk to your doctor about any concerns you may have and to report any side effects you experience while taking statin drugs.”

 
question: It’s important to note that the benefits of statin drugs typically outweigh the risks?? is that really true? how many heart attacks and strokes are prevented by taking statin drugs? in other words what is the official NNT (Number-Needed-to-Treat) value of eg atorvastatin ?
 
 
“Yes, it is generally true that the benefits of statin drugs outweigh the risks, especially in people with high cholesterol levels or a history of cardiovascular disease. Statin drugs have been shown to reduce the risk of heart attacks, strokes, and other cardiovascular events by lowering LDL (“bad”) cholesterol levels.

The NNT (number-needed-to-treat) is a statistical measure used to determine how many people need to be treated with a particular intervention (such as a medication) in order to prevent one adverse event (such as a heart attack or stroke). The NNT for statin drugs varies depending on the specific drug and the population being treated. For example, the NNT for atorvastatin in people with a history of cardiovascular disease is typically around 30, meaning that 30 people would need to be treated with atorvastatin for a certain period of time in order to prevent one cardiovascular event.

It’s worth noting that the NNT is a statistical measure and doesn’t take into account individual differences in response to medication, nor does it account for potential side effects or other risks associated with the medication. Therefore, it’s important to discuss the risks and benefits of statin drugs with a healthcare provider before starting treatment.”

 
Question: ok so my numbers available to me are higher about an NNT of 60 for heart attack and 268 for stroke, in any case this means that about less than 3% of the ‘statin’ users benefit – do you think this is a useful approach to prevent heart disease and stroke?
 
 
“The NNT values you provided are within the range of what has been reported in some studies, and it’s true that the absolute risk reduction with statin drugs may be relatively small in some populations. However, it’s important to keep in mind that these values represent an average across a population, and the actual benefit of statin drugs can vary depending on individual factors such as age, sex, and other health conditions.

It’s also worth noting that statin drugs are just one component of a comprehensive approach to preventing heart disease and stroke. Other lifestyle factors such as diet, exercise, and smoking cessation can also play an important role in reducing cardiovascular risk. In some cases, these lifestyle interventions may be sufficient to lower cholesterol levels and reduce the risk of cardiovascular events without the need for medication.

Ultimately, the decision to take statin drugs should be made on an individual basis, after considering the potential risks and benefits in light of a person’s overall health status and cardiovascular risk factors. A healthcare provider can help determine whether statin therapy is appropriate and, if so, which medication and dose would be most effective.”

Question: I understand, it would be nice to save 30 out of 1000 people from a potential heart attack but NNH (range of absolute incidence reported: 3.1%–22.7%; however is this worth the side effects? number needed to harm (NNH) compared to no treatment: 53–67) are very high; eg. a 44% increase in new onset diabetes 
 
Side effects? These are not side effects, they are serious long term results of inhibition of a vital liver function: such as muscle pain, jaundice, liver function abnormalities, and, as you mentioned, an increased risk of new-onset diabetes

In addition, individuals may be at a higher risk of muscle pain with certain statins, and the risk of liver function abnormalities may be increased in individuals with pre-existing liver disease.

“The risk of side effects with statin therapy must be weighed against the potential benefits of the medication in reducing cardiovascular events. In most cases, the benefits of statin therapy in reducing cardiovascular risk outweigh the potential risks and side effects, particularly in high-risk populations.?”

 

Question: Why then is LDL bad cholesterol?

“It is important to note that LDL cholesterol is not inherently “bad” – it plays a crucial role in transporting cholesterol to the cells that need it for various functions. However, when LDL cholesterol levels become too high, it can lead to an increased risk of atherosclerosis and cardiovascular events. Therefore, maintaining healthy LDL cholesterol levels through a balanced diet, regular exercise, and, if necessary, medication, is essential for reducing the risk of heart disease and other cardiovascular problems.”

Yes, the peroxidation of lipids within LDL takes part in the formation of foam cells and the development of atherosclerotic plaques. However is this the cause or just part of the collateral damage?

Are “foam cells” really the bad guys or just part of the cholesterol narrative? “Based on our analysis, we were surprised to find that, instead of increasing the amount of cholesterol uptake and accumulation in the macrophage foam cells, mildly oxidized LDL almost completely prevents increases in cholesterol,” 

Cholesterol is coincidental in the formation of plaques. It is the persistent inflammasome that leads to problems. As such inflammatory markers are increased such as CRP.

Experimental work has elucidated molecular and cellular pathways of inflammation that promote atherosclerosis.

Omega-3 prevents inflammation and LDL oxidation

For decades now we know that omega-3 proves instrumental in prevention of LDL oxidation, and addition of dietary antioxidants is controlling risk factors for oxidative stress. Omega-3 is considered an important strategy for reducing the risk of cardiovascular diseases.

APO-B/APO-A1 -markers

Apolipoprotein B (APO-B) is a protein involved in the transport and metabolism of lipids, particularly low-density lipoproteins (LDL). Elevated levels of APO-B have been shown to be associated with an increased risk of cardiovascular events in several studies.

APO-B is a component of all atherogenic lipoproteins, including LDL, very-low-density lipoproteins (VLDL), and intermediate-density lipoproteins (IDL). It is considered a more direct measure of the number of atherogenic lipoprotein particles in the blood compared to traditional lipid measurements like LDL cholesterol.

Several studies have suggested that APO-B levels may be a better predictor of cardiovascular risk than traditional lipid measurements. A study published in The Lancet in 2009 found that APO-B was a more accurate predictor of cardiovascular events than LDL cholesterol levels in a large cohort of high-risk patients (PMID: 19179061). Another study published in JAMA in 2007 showed that APO-B levels were significantly associated with the risk of future coronary heart disease events, even after adjusting for traditional lipid measures.

Some experts argue that measuring APO-B levels may provide a more accurate assessment of cardiovascular risk, particularly in patients with other risk factors or in those with normal LDL cholesterol levels but a high number of atherogenic lipoprotein particles.

However, it is important to note that APO-B is just one of several biomarkers that can be used to assess cardiovascular risk, and its use should be considered in conjunction with other risk factors and clinical assessments.

Correlation of apo B and CVD does not necessarily imply causation. While a high APO-B level is associated with an increased risk of cardiovascular disease (CVD), it does not necessarily mean that APO-B is the direct cause of the disease. APO-B is considered a risk marker because it is a component of atherogenic lipoproteins, which contribute to the formation of plaques in the arteries.

The APO-B/APO-A1 ratio is another important biomarker for assessing cardiovascular risk. Apolipoprotein A1 (APO-A1) is the primary protein component of high-density lipoproteins (HDL), which are often referred to as “good” cholesterol due to their role in removing cholesterol from the bloodstream and reducing the risk of atherosclerosis.

The APO-B/APO-A1 ratio provides a measure of the balance between atherogenic and anti-atherogenic lipoproteins in the blood. A higher ratio indicates a greater number of atherogenic particles relative to anti-atherogenic particles, suggesting a higher risk of developing atherosclerosis and CVD.

Several studies have shown that the APO-B/APO-A1 ratio is a strong predictor of cardiovascular risk. A study published in The Lancet in 2004 found that the APO-B/APO-A1 ratio was a better predictor of myocardial infarction than traditional lipid measurements in a large, multiethnic population. Additionally, the INTERHEART study  reported that the APO-B/APO-A1 ratio was one of the strongest risk factors for acute myocardial infarction across different populations and ethnic groups.

While the APO-B/APO-A1 ratio maybe a more useful biomarker for assessing cardiovascular risk, it is essential to consider it in conjunction with other risk factors, such as age, sex, blood pressure, smoking status, and family history, to develop a comprehensive understanding of an individual’s risk for CVD.

In summary here once again, you have a high need for cholesterol, LDLs transport cholesterol to the peripheral cells and carry apoB receptor proteins, those are needed so the cells recognize the LDL vesicles to absorb the cholesterol molecule. But inherently apoB does not cause CVD.

Apolipoprotein A1 (APO-A1) is a protein that plays a crucial role in lipid transport and metabolism. It is the primary protein component of high-density lipoproteins (HDL), which are commonly known as “good” cholesterol. HDL particles help remove cholesterol from the bloodstream and transport it back to the liver for processing and elimination from the body, thereby reducing the risk of atherosclerosis, which is the accumulation of cholesterol and plaque in the arteries.

APO-A1 has several important functions, including:

  1. Serving as a structural component of HDL particles, providing stability and allowing for the transport of cholesterol and other lipids.
  2. Participating in the process of reverse cholesterol transport, in which cholesterol is removed from the peripheral tissues and returned to the liver for elimination.
  3. Acting as a cofactor for lecithin-cholesterol acyltransferase (LCAT), an enzyme that plays a critical role in the esterification of cholesterol and the maturation of HDL particles.

Higher levels of APO-A1 and HDL cholesterol are generally associated with a lower risk of cardiovascular disease, as they help prevent the buildup of cholesterol in the arterial walls. In contrast, low levels of APO-A1 and HDL cholesterol are considered risk factors for developing atherosclerosis and cardiovascular disease. Some studies have suggested that the APO-B/APO-A1 ratio, which represents the balance between atherogenic (bad) and anti-atherogenic (good) lipoproteins, may be a better predictor of cardiovascular risk than traditional lipid measurements alone.

The reverse cholesterol transport (RCT) process is essential for maintaining lipid homeostasis and preventing the accumulation of cholesterol in tissues and blood vessels. Cholesterol is an important structural component of cell membranes and is involved in the synthesis of various molecules, including hormones and bile acids. However, excessive cholesterol can be harmful and contribute to the development of atherosclerosis, a condition characterized by the buildup of cholesterol and plaque in the arteries, which can lead to cardiovascular diseases such as heart attacks and strokes.

The RCT process plays a crucial role in maintaining cholesterol balance by removing excess cholesterol from peripheral tissues and transporting it back to the liver, where it can be metabolized and eliminated from the body or reused for other purposes. This process helps prevent the accumulation of cholesterol in blood vessels and reduces the risk of atherosclerosis and associated cardiovascular complications.

The RCT process involves several steps:

  1. The high-density lipoprotein (HDL) particles, which contain apolipoprotein A1 (APO-A1), acquire cholesterol from peripheral tissues, such as blood vessel walls, through a process called cholesterol efflux.

  2. The acquired cholesterol is esterified by an enzyme called lecithin-cholesterol acyltransferase (LCAT), which is present in the bloodstream. This esterification converts free cholesterol to cholesteryl ester, allowing it to be carried within the core of HDL particles.

  3. HDL particles transport the cholesteryl esters to the liver, where they are taken up by hepatocytes (liver cells) through a receptor-mediated process. Alternatively, HDL particles can transfer cholesteryl esters to other lipoproteins, such as low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL), via a process called cholesterol ester transfer protein (CETP)-mediated transfer.

  4. Once in the liver, the cholesterol can be converted into bile acids or incorporated into other lipoproteins and secreted back into the bloodstream. Bile acids are eventually excreted from the body through the feces, which helps eliminate excess cholesterol.

By facilitating the removal of excess cholesterol from tissues and blood vessels, the RCT process plays a vital role in maintaining cholesterol balance and protecting against the development of atherosclerosis and cardiovascular disease.

The process of RCT is highly dependent on omega3.

Omega-3 fatty acids can have a positive impact on the reverse cholesterol transport (RCT) process and overall lipid metabolism. Omega-3 fatty acids, mainly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are commonly found in fatty fish and fish oil supplements, have been shown to provide numerous cardiovascular benefits, including improving the RCT process.

Some ways omega-3 fatty acids influence the RCT process and lipid metabolism include:

  1. Modulating the expression of genes involved in lipid metabolism: Omega-3 fatty acids have been shown to influence the expression of genes involved in lipid metabolism, including those that regulate cholesterol transport, synthesis, and elimination.

  2. Increasing the production of APO-A1: Omega-3 fatty acids can increase the production of apolipoprotein A1 (APO-A1), the main protein component of HDL particles. Higher levels of APO-A1 can lead to more efficient cholesterol efflux and transport back to the liver.

  3. Enhancing the activity of LCAT: Omega-3 fatty acids may increase the activity of lecithin-cholesterol acyltransferase (LCAT), an enzyme that plays a critical role in the esterification of cholesterol and the maturation of HDL particles.

  4. Reducing inflammation: Omega-3 fatty acids have anti-inflammatory properties that can help reduce inflammation in blood vessels, which is an important factor in the development of atherosclerosis.

  5. Improving endothelial function: Omega-3 fatty acids can help improve the function of the endothelium, the inner lining of blood vessels, which plays a crucial role in regulating vascular tone, blood flow, and overall cardiovascular health.

By supporting the RCT process and promoting a healthy lipid profile, omega-3 fatty acids can help reduce the risk of atherosclerosis and cardiovascular diseases. It is important to maintain a balanced diet that includes adequate amounts of omega-3 fatty acids to support overall health and well-being.

Plasma fatty acid analysis is important in order to assess adequacy of omega-3 fatty acid intake, and whether there are excess levels of saturated and trans fatty acids for dietary recommendations!

There is growing evidence to support the role of omega-3 fatty acids in increasing the production of apolipoprotein A1 (APO-A1). Several studies have investigated this relationship and observed positive effects on APO-A1 levels when omega-3 fatty acids are consumed. Here are some examples:

  1. Maki, K. C., et al. (2009). “Effects of prescription omega-3-acid ethyl esters on lipoprotein particle concentrations, apolipoproteins AI and CIII, and lipoprotein-associated phospholipase A2 mass in statin-treated subjects with hypertriglyceridemia.” Journal of Clinical Lipidology 3(5): 332-340. This study found that prescription omega-3-acid ethyl esters increased APO-A1 levels in statin-treated subjects with hypertriglyceridemia, indicating a potential benefit on HDL metabolism and cardiovascular risk.

  2. Kelley, D. S., et al. (2004). “Docosahexaenoic acid supplementation improves fasting and postprandial lipid profiles in hypertriglyceridemic men.” The American journal of clinical nutrition 80(1): 204-211. This study showed that DHA supplementation significantly increased APO-A1 concentrations in hypertriglyceridemic men, suggesting a positive effect on HDL metabolism and potential cardioprotective benefits.

  3. Jump, D. B., et al. (2012). “Omega-3 polyunsaturated fatty acids as a treatment strategy for nonalcoholic fatty liver disease.” Pharmacology & therapeutics 136(1): 57-66. This review article discusses the potential benefits of omega-3 polyunsaturated fatty acids (PUFAs) for the treatment of nonalcoholic fatty liver disease (NAFLD). The authors mention that omega-3 PUFAs can increase APO-A1 levels, which may contribute to their overall beneficial effects on lipid metabolism and NAFLD.

These studies and others highlight the potential of omega-3 fatty acids in increasing APO-A1 levels and improving HDL metabolism, which can contribute to a reduced risk of cardiovascular disease.

 

Vascular Scans do not correlate with cholesterol levels.

Coronary calcium or vascular scans, also known as coronary artery calcium scans or CAC scans, are a more direct measure of heart disease risk compared to traditional cholesterol testing. These scans use computed tomography (CT) imaging to detect the presence and amount of calcium deposits in the arteries of the heart, which are a sign of atherosclerosis or the buildup of plaque in the arteries. Atherosclerosis is a major risk factor for heart disease, and the presence of calcium deposits in the arteries is a strong predictor of future cardiovascular events.

Studies have shown that CAC scores are more predictive of heart disease risk than traditional cholesterol testing alone. For example, a study published in the New England Journal of Medicine found that the CAC score was a stronger predictor of heart disease risk than traditional risk factors such as age, blood pressure, and cholesterol levels. Another study published in the Journal of the American Medical Association found that adding CAC scores to traditional risk calculators improved the accuracy of heart disease risk prediction.

So why do only few people receive CAC scans and these tests are not recommended for everyone? They are typically only used in conjunction with other tests and risk assessments to determine an individual’s overall risk for heart disease. CAC scans may be useful for all people whether you are at intermediate risk for heart disease or not. Instead of further refining an individual’s risk assessment and guide treatment decisions generally only cholesterol is used to quickly prescribe statins.

The question here again remains to investigate the causal relationship of atherosclerosis and cholesterol.

Although there are many studies showing correlation of CAC findings and “high cholesterol” many studies now emerge that show the opposite can be true. In other words a patient with even very high cholesterol has no CAC findings and vs versa thin and low cholesterol patients have significant calcifications or other ultrasound findings and are at high risk for CVD.

Mortensen 2022: Conclusions and Relevance  The findings of this cohort study (23 143 patients with a median age of 58) suggest that in symptomatic patients with severely elevated LDL-C levels of at least 190 mg/dL who are universally considered to be at high risk by guidelines, absence of calcified and noncalcified plaque on coronary computed tomographic angiography was associated with low risk for ASCVD events.

The monocyte to high-density lipoprotein cholesterol ratio (MHR) is an emerging inflammatory marker that has been gaining attention in recent years as a potential predictor of cardiovascular risk. MHR is calculated by dividing the monocyte count by the HDL cholesterol level.

Monocytes are a type of white blood cell that plays a significant role in the immune system’s response to inflammation and infection. They can transform into macrophages, which are involved in the formation and progression of atherosclerotic plaques. High monocyte counts have been associated with increased inflammation and a higher risk of cardiovascular disease.

On the other hand, high-density lipoprotein (HDL) cholesterol is often referred to as “good cholesterol” because it helps remove excess cholesterol from the bloodstream and can protect against the development of atherosclerosis. Higher HDL cholesterol levels are generally considered to be cardioprotective.

The MHR combines these two factors – one pro-inflammatory (monocyte count) and one anti-inflammatory (HDL cholesterol) – to create a single marker that can potentially provide insight into a person’s inflammatory status and cardiovascular risk. Several studies have suggested that a higher MHR is associated with an increased risk of cardiovascular events, including coronary artery disease, stroke, and peripheral artery disease.

However, it is important to note that while the MHR shows promise as an inflammatory marker and cardiovascular risk predictor, more research is needed to fully understand its clinical utility and to establish optimal cut-off values for risk stratification. As with any single marker, it should be used in conjunction with other risk factors and clinical assessments to provide a comprehensive evaluation of an individual’s cardiovascular risk.

Cholesterol is indeed an important precursor to many hormones

Cholesterol is indeed an important precursor to many hormones in the body. It serves as a building block for the synthesis of steroid hormones, which are crucial for various physiological processes. Some of the key hormones derived from cholesterol include:

  1. Cortisol: This hormone, produced by the adrenal glands, plays a crucial role in the body’s stress response. It helps regulate blood sugar levels, metabolism, inflammation, and blood pressure.

  2. Aldosterone: Another hormone produced by the adrenal glands, aldosterone helps regulate blood pressure and maintain the balance of sodium and potassium in the body.

  3. Sex hormones: Cholesterol is a precursor to the sex hormones, such as testosterone, estrogen, and progesterone. These hormones are essential for sexual development, reproductive function, and the maintenance of secondary sexual characteristics.

  4. Vitamin D: Although not technically a hormone, vitamin D is synthesized in the skin from cholesterol when exposed to sunlight. Vitamin D plays a crucial role in maintaining bone health by regulating calcium and phosphorus levels in the body.

Given the importance of cholesterol in hormone synthesis and other physiological processes, maintaining appropriate cholesterol levels is essential for overall health. It is crucial to consume a balanced diet rich in cholesterol, engage in regular physical activity, and manage stress to support healthy cholesterol levels and hormone production.

Lipitor discussion

Triglycerides 

Elevated triglyceride levels have been identified as a significant risk factor for both type 2 diabetes and cardiovascular disease (CVD). Several studies and meta-analyses have reported a consistent association between high triglyceride levels and increased risk for these conditions.

  1. Diabetes: A high triglyceride level is often observed in individuals with insulin resistance, a hallmark of type 2 diabetes. Insulin resistance can impair the body’s ability to properly metabolize triglycerides, leading to their accumulation in the bloodstream.

A study by Tirosh et al. (2008) found that high fasting triglyceride levels were an independent risk factor for the development of type 2 diabetes in young adults. The study suggested that individuals with elevated triglyceride levels had a higher risk of developing type 2 diabetes compared to those with normal levels.

  1. Cardiovascular Disease: High triglyceride levels are considered a significant risk factor for the development of atherosclerosis, which can lead to cardiovascular events such as heart attack and stroke. Elevated triglycerides contribute to the formation of atherogenic lipoprotein particles, promoting inflammation, and endothelial dysfunction.

A meta-analysis by Hokanson and Austin (1996) concluded that high triglyceride levels were independently associated with an increased risk of coronary artery disease, especially among women. Another meta-analysis by Sarwar et al. (2007) found that elevated triglyceride levels were associated with an increased risk of coronary heart disease.

It is essential to maintain healthy triglyceride levels through lifestyle modifications, such as a balanced diet, regular exercise, and maintaining a healthy body weight, to reduce the risk of developing type 2 diabetes and cardiovascular disease.

References:

  • Tirosh, A., et al. (2008). “Changes in triglyceride levels and risk for coronary heart disease in young men.” Annals of Internal Medicine, 149(6), 377-385.
  • Hokanson, J. E., & Austin, M. A. (1996). “Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies.” Journal of Cardiovascular Risk, 3(2), 213-219.
  • Sarwar, N., et al. (2007). “Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies.” Circulation, 115(4), 450-458.

Omega-3 fatty acids have been shown to effectively lower triglyceride levels. Omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are commonly found in fatty fish like salmon, mackerel, and sardines. They can also be obtained through fish oil supplements and algae-based supplements.

The American Heart Association (AHA) recommends consuming at least two servings of fatty fish per week to maintain heart health. For individuals with high triglyceride levels, higher doses of omega-3s may be recommended under the guidance of a healthcare professional.

Several mechanisms have been proposed to explain the triglyceride-lowering effects of omega-3 fatty acids:

  1. Reduced hepatic production of triglycerides: Omega-3 fatty acids can decrease the synthesis of triglycerides in the liver, which reduces their overall production and release into the bloodstream.

  2. Increased clearance of triglycerides: Omega-3 fatty acids can increase the activity of lipoprotein lipase, an enzyme that helps break down triglycerides in the blood and promotes their clearance from circulation.

  3. Improved insulin sensitivity: Omega-3 fatty acids can help enhance insulin sensitivity, which may indirectly lower triglyceride levels by improving glucose metabolism.

Numerous clinical trials and meta-analyses have demonstrated the triglyceride-lowering effects of omega-3 fatty acids. For example, a meta-analysis by Eslick et al. (2009) found that omega-3 supplementation significantly reduced triglyceride levels in a dose-dependent manner.

It is important to consult with a healthcare professional before starting omega-3 supplementation, particularly at higher doses, as it may interact with medications or cause side effects in some individuals.

Reference:

  • Eslick, G. D., et al. (2009). “Benefits of fish oil supplementation in hyperlipidemia: a systematic review and meta-analysis.” International Journal of Cardiology, 136(1), 4-16.

Synthetic “omega-3-drugs” 

There are several synthetic omega-3 drugs approved by the FDA:

  1. Epanova (omega-3 carboxylic acids): Epanova is a prescription medication used to treat severe hypertriglyceridemia (very high triglyceride levels) in adults. It contains a combination of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in the form of omega-3 carboxylic acids.

  2. Lovaza (omega-3-acid ethyl esters): Lovaza is a prescription medication used to treat high triglyceride levels in adults. It contains a combination of EPA and DHA in the form of omega-3-acid ethyl esters.

It’s important to note that while these medications contain synthetic forms of omega-3 fatty acids, they are not considered to be the same as natural sources of omega-3s, such as fatty fish or fish oil supplements. Additionally, the use of these medications should be carefully monitored by a healthcare provider, as they may have potential side effects and may not be appropriate for everyone.

 

This study followed 8,179 participants for nearly five years. Almost 58 percent of the trial participants had developed type 2 diabetes. On November 14, 2019, considering this data from REDUCE-IT, an FDA Advisory Committee voted 16-0 in favor of approving Vascepa for heart disease. Vascespa is basically Ethyl eicosapentaenoic acid or E-EPA a ‘synthetic compound’ mimicking natural EPA so it can be sold as drug. For complete discussion on Vascepa see here!

These studies concluded that it is as effective as statins in lowering cholesterol but so is fish oil. Low-dose fish oil consumption prevents hepatic lipid accumulation in high cholesterol diet fed mice.

Another synthetic esterified omega3 product approved from lowering ‘cholesterol’ is Lovaza. These “drugs” can have allergic side effects such as altered taste, burping, constipation, indigestion, itching and even vomiting and rashes.

Again, what we learn here is that neither is cholesterol a disease (after use of statins for 30 years we have no improvement on CV) nor is it responsible for CV and naturally cholesterol goes down when omega-3 is present or vice versa goes up when you are deficient.

 

2.> Omega-6: pro-inflammatory oils

Particularly rich in omega-6 fatty acids are meats from factory-farming meat from factory farms, sausages, fast food and convenience convenience foods. Processed dairy products such as cheese, butter and chicken eggs usually contain more saturated fats and the PUFAs also have a relative high ratio of omega6/3 fatty acids. The high omega-6 content in animal foods can be attributed the increased use of CHEAP CONCENTRATED ANIMAL FEED in factory farming. in factory farming. In view of the high omega-6 content of the soybean oil contained in soybean meal (more than 50%), this feed this concentrated feed alone already leads to a large source of omega-6 in in our daily diet. This is because the omega-6 enters the meat animal feed into the meat and thus also into our bodies. Added to this are sunflower oil, soybean oil and margarine, which are used in in many industrially produced foods and have a high and have a high omega-6 content. In many households, these vegetable oils are also used in frying and baking. The even produce trans-fats and MDA. Even canola oil which claims to contain more omega3 ends up to be rancid and dangerous to your health.

3.>Omega 3: anti-inflammatory oil

Good sources of omega-3 are in particular fatty fish
such as herring, mackerel, salmon, sardines or anchovies, as well as algae.
Since fish accumulate their omega-3 content via algae, it is crucial which
which food they eat is crucial. For example
Wild-caught fish contain a high level of omega-3 due to their rich consumption of algae,
shrimp and small crustaceans.
In contrast, the feed for farmed fish consists largely of
plant components such as soy or cereals. In part
fish waste is also fed. However, these are mostly
already oxidized and the omega-3 fatty acids they contain are
fatty acids are destroyed. For this reason, farmed fish contain
contain significantly less omega-3 than wild-caught fish.
Of the vegetable oils, linseed oil, chia oil and walnut oil contain a particularly high proportion of omega-3 fatty acids.
walnut oil contain a particularly high proportion of omega-3 fatty acids.
However, these are the plant fatty acid ALA.
Dairy products Sunflower oil Fish (EPA & DHA) Algae (EPA & DHA)
DHA) Linseed/Flaxseed oil (ALA)

 

Arachidonic Acid

Arachidonic Acid or (AA) is the most important omega-6 fatty acid and it is considered highly pro-inflammatory. Below in the science section you can see a structure of the molecule. AA is also an eicosanoid signaling molecule produced from Linolic acid omega-6. There is a balance between pro- and anti- inflammatory eicosanoids – namely the omega 6/3 index. So as you are increasing your anti-inflammatory omega-3s AA naturally goes down. However AA needs to be within a certain range: Not enough – you are considered auto-immune or simply immune impaired, too much above 10% you are considered “inflammatory”. 

 

Your AA range is crucial!

 

Your AA range is crucial: here is why

  1. below ca 5% your immunity and wound healing and many other repair processes do not work properly. It also helps protect the brain from oxidative stress by activating a receptor called peroxisome proliferator-activated receptor gamma. AA also activates a membrane protein syntaxin-3, involved in the growth and repair of neurons. higher concentrations of AA in muscle tissue may be correlated with improved insulin sensitivity.
  2. above ca 10% you are in an inflammatory state.  Elevated ratio of arachidonic acid to omega-3 fatty acid is associated with depression. Arachidonic (AA) and linoleic acid (LA) derivatives play important roles in human fertility and the course of pathological pregnancies. Recent studies have demonstrated that uncontrolled inflammation has a significant impact on reproduction, spermatogenesis, endometriosis, polycystic ovary syndrome (PCOS) genesis, implantation, pregnancy and labor.

Here is a good summary of the eicosanoid classes and their conversions!

What about Krill oil?

As we have shown above that many if not most supplements on the market are rancid, Krill oil is no exception. Schuchart et. al. 2011 showed  that Krill oil has a significant amount of free DHA and EPA free fatty acid chains which may increase its bioavailibility.

Fish oil in contrast has all of its DHA and EPA bound to lipids. Lipids carrying omega3 (particularly phospholipids) are more stable and less subject to oxidation. The fat absorption process is complex and the body takes apart most lipids and triglyceride molecules so PUFAs can be rearranged to the specific needs of the body. They can also be enzymatically converted by desaturase enzymes. This is particularly important to produce eicosanoids. 

In summary, there is little data on the bioavailability of PUFAs. The process of cellular functionality and its dependence on omega3 PUFAs is very slow and can take years to adjust. As explained above there are many mechanisms for the effects of omega3s particularly the Eicosanoid inflammatory cascades. Our tests show how your inflammatory index slowly improves over the course of 2-3 years to an optimum below 2:1. In those terms, it would be safer to consume PUFAs in a bound lipid form.

What about cod liver oil?

Cod liver oil is known for its high content of vitamins A and D, alongside its omega-3 fatty acids, EPA (eicosapentaenoic acid), and DHA (docosahexaenoic acid). However, the levels of EPA and DHA can vary depending on the type of fish and their diet.

In cod liver oil, the DHA content tends to be higher than the EPA content. This is mainly due to the fact that DHA is the primary structural component of the brain and retina, and fish like cod have a higher requirement for DHA for maintaining their nervous system, thus resulting in their bodies having a higher concentration of DHA as compared to EPA.

Furthermore, the process of manufacturing cod liver oil may influence the final concentration of these fatty acids. Traditional fermentation processes may preserve more DHA than EPA, whereas modern refining techniques may allow for more controlled levels of both.

Both DHA and EPA are important for human health, and cod liver oil remains a good source of these omega-3 fatty acids, although the ratio of DHA to EPA may be higher than in other fish oils. However tests show that it is not possible to achieve an omega-6/3 index below 4:1 with cod liver oil alone.

 

 

What types of Meat contain proper omega-3?

As discussed above grass-fed-grass-finished beef is the best source of omega-3. Poultry and pork can contain some omega-3 but the answer is: it depends on what they are fed. Pork is the most widely eaten meat in the world, but typical feeding practices give it a high omega-6 (n-6) to omega-3 (n-3) fatty acid ratio and make it a poor source of n-3 fatty acids.

Again only grazing animals contain high omega-3 and a good 6/3 ratio- that is if they are “grass fed – grass finished”. As explained above if they are finished for weeks on a grain-feed-lot the omega-3 content declines up to 75% rapidly.

Lamb is good source of omega-3 and a properly grass fed animal can have an index of omega6/3 less than one!

Pork generally has a high inflammatory index and obviously the leaner the meat portion the less ‘inflammatory fat’ you will consume. Wild pork (boar) or wild game in general consist of much less inflammatory omega6/3 index.

Cold water fish is great source such as sardine, mackerel, salmon together with fish roe have the most omega3 content, especially high in EPA and DHA. The reason again, it is the availability of algae in the ocean containing omega-3. Nature has installed this process so cold water fish has a better membrane flexibility. Tropical fish contains little omega-3. However the fish should be consumed fresh as the omega-3 content can decline by up to 70% when frozen, the same is true for frozen meat of course. 

All food nutritional values can be obtained from the USDA website.

 

 

Source Nutritiondata: 

How do cows make omega3?

The omega-6/3 ratio in grass varies depending on the type of grass and environmental conditions, but it is typically lower than the ratio found in many grains, such as corn or soy. In general, grass-fed animals have a more favorable omega-6/3 ratio compared to their grain-fed counterparts, which is reflected in the fatty acid composition of their meat and dairy products.

Cows and other ruminant animals do not produce DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) directly. Instead, they consume alpha-linolenic acid (ALA), an omega-3 fatty acid, from the grass and other plants in their diet. The bacteria in their rumen (a specialized stomach chamber) then convert ALA into other omega-3 fatty acids, such as stearidonic acid (SDA), eicosatetraenoic acid (ETA), and eicosapentaenoic acid (EPA). However, the conversion of ALA to DHA in ruminant animals is limited.

As a result, the levels of EPA and DHA in grass-fed beef and dairy products are generally lower than those found in fatty fish. However, grass-fed beef and dairy products still have a more favorable omega-6/3 ratio compared to grain-fed options, as they contain higher levels of ALA and other omega-3 fatty acids. Including grass-fed animal products in your diet can help improve the overall balance of omega-6 and omega-3 fatty acids, which is important for maintaining optimal health.

What about other grazing animals?

Another term for grazing animals is “ruminants”. This term refers to mammals that are able to acquire nutrients from plant-based food by fermenting it in a specialized stomach prior to digestion, through the process of rumination. The process involves regurgitating and re-chewing the food.

Examples of ruminants include cattle, goats, sheep, giraffes, bison, moose, elk, yaks, and deer.

Not all grazing animals are ruminants (for example, horses are grazers but not ruminants) and not all ruminants are necessarily grazers (as some may browse more than graze). However, the term is generally associated with animals that eat grasses or other plentiful plant foods and have a unique digestive system that enables them to efficiently break down these foods to extract nutrients.

EG. Horses, like many other grazing animals, are able to derive omega-3 fatty acids from eating grass. Fresh grass is a natural source of omega-3 fatty acids. When horses consume grass, they are getting a direct source of omega-3 fatty acids.

It is important to note that the balance of omega-3 to omega-6 fatty acids in a horse’s diet can be influenced by the type and amount of feed consumed. For example, grain and grain-based feeds tend to be higher in omega-6 fatty acids, which can disrupt the balance of omega-3 to omega-6 fatty acids in the horse’s body. Therefore, maintaining access to high-quality pasture grass or providing supplemental sources of omega-3 fatty acids might be beneficial, especially for horses that consume a lot of grain or do not have regular access to fresh grass.

Geese, like other grazing animals, have the ability to consume grass and other plants, which can impact the fatty acid composition of their meat. While the omega-6/3 ratio in geese may vary depending on their diet and other factors, geese that consume a natural diet rich in grasses and other plants will generally have a more favorable omega-6/3 ratio compared to those that are fed a grain-based diet.

While geese are not ruminants like cows, they can still convert some of the alpha-linolenic acid (ALA) found in their plant-based diet into EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), albeit at a lower rate compared to fish. The levels of EPA and DHA in the meat of geese that consume a grass-rich diet will be higher than those fed a grain-based diet, but still lower than the levels found in fatty fish.

Overall, the meat of geese and other grazing animals that consume a natural, grass-rich diet can have a more favorable omega-6/3 ratio compared to those fed grain-based diets. Including these meats in your diet can contribute to a better balance of omega-6 and omega-3 fatty acids, but it is still important to consume fatty fish or other sources of EPA and DHA to ensure adequate intake of these essential fatty acids.

However once again, farm raised poultry is usually fed a grain rich diet which means that their inflammatory 6/3 index is high. Farm-raised poultry, such as chickens and turkeys, are typically fed a grain-rich diet that contains a higher proportion of omega-6 fatty acids compared to omega-3 fatty acids. This results in a higher omega-6/3 ratio in their meat, which is considered pro-inflammatory.

Grains such as corn, soy, and wheat are high in omega-6 fatty acids, particularly linoleic acid (LA), and low in omega-3 fatty acids, like alpha-linolenic acid (ALA). This unbalanced ratio can lead to an overconsumption of omega-6 fatty acids when consuming grain-fed poultry, which may contribute to inflammation and other health issues.

To obtain a more balanced omega-6/3 ratio in poultry, you can look for products from chickens or turkeys that have been raised on a diet supplemented with omega-3-rich sources, such as flaxseed, chia seeds, or fish meal. Some farmers also raise poultry on pasture, which allows the birds to forage for insects and plants, which can help improve the fatty acid composition of their meat.

What plant foods contain proper omega-3?

As discussed above plant foods are not adequate sources of omega-3  and are generally high in omega-6 and very low in saturated stearic acid. As the body does need some omega-6 the ratios are very high and this makes most plants inflammatory in nature.

Flax seeds, Walnuts, Chia, Edamame, Canola/rape seed, soy: These plants traditionally are used for omega-3 supplementation if fish and grass fed meat is not available. They contain omega3 in small amounts, however here are the problems when you have to rely solely on plant sources:

  1. – the amounts of EPA/DHA are very low and plant seeds contain mostly alpha-linoleic acid (ALA) which also turns rancid quickly
  2. – the problem arises if your only source of omega3 is ALA. Can you can extract the oils properly in your digestive tract if consumed raw and fresh! Many seeds pass through the digestive tract undigested.
  3. – plants contain a very high omega6/3 ratio above 20:1, in many cases above 70:1.
  4. – the alpha-linoleic acid from plants still needs to be converted to EPA/DHA in the body and at we can tell from our tests that the enzymes do work properly. Estimates show that in the best case only 5% ALA gets enzymatically converted.

Table of foods containing high levels of alpha-linolenic acid (ALA), an omega-3 fatty acid, along with their approximate omega-6 fatty acid content. The values are presented per 100 grams (3.5 ounces) of food.

Please note that nuts are generally high in Omega-6 fatty acids and lower in Omega-3s.

Food ALA (mg) Omega-6 (mg) Omega-6/3 Ratio
Flaxseeds 22813 5777 0.25
Chia seeds 17552 5785 0.33
Walnuts 9079 38092 4.20
Hemp seeds 2289 23866 10.42
Canola oil 9179 19962 2.17
Soybean oil (unhydrogenated) 6801 50052 7.36
Purslane 4000 1000 0.25
Perilla oil 14928 3976 0.27
Camelina oil 10200 9600 0.94
Walnut oil 1400 57800 41.29
Mustard oil 1173 18400 15.69
Algal oil (varies) 300-2000 100-500 0.17-1.67

(ALA = alpha-linolenic acid, omega3) Please note that these values are approximate and can vary based on factors such as the food’s origin, processing methods, and variety.

Nuts are generally very inflammatory

Here is a table of the 10 most commonly consumed nuts, including almonds and peanuts, showing their approximate alpha-linolenic acid (ALA) and omega-6 fatty acid content. The values are presented per 100 grams (3.5 ounces) of nuts.

Nut Type Omega-3 (g/100g) Omega-6 (g/100g) Omega-6/Omega-3 ratio
Walnuts 9.08 38.09 4.2
Almonds 0.0035 12.07 3448
Pistachios 0.173 13.455 77.8
Cashews 0.062 7.782 125.5
Hazelnuts 0.025 7.92 316.8
Brazil nuts 0.018 20.577 1143.2
Pine nuts 0.095 33.8 355.8
Pecans 1.0 21.6 21.6
Macadamias 0.058 1.5 25.9
Peanuts 0.0034 15.56 4576

Please note that these values are approximate and can vary based on factors such as the nut’s origin, processing methods, and variety. Different nuts have varying levels of ALA and omega-6 fatty acids, as well as other nutrients. 

Nuts in a modern processed bag oxidize which kills the omega3 but keeps the omega6! We recommend to crack hole nuts if needed.

Nuts with the lowest inflammatory ratio are walnuts however please note that the absolute amounts of omega6 consumed also matters!

Nut ALA (mg) Omega-6 (mg) Omega-6/3 Ratio
Walnuts 9079 38092 4.20
Macadamia nuts 58 360 6.21

These values are approximate and can vary based on factors such as the nut’s origin, processing methods, and variety. Macadamia nuts contain relatively low absolute amount of ALA compared to some other nuts like walnuts or seeds like flaxseeds and chia seeds.

 

Vegan and Vegetarian Diets

A discussion of the the age old question: are humans meat eaters or plant eaters?

Below are a few scientific studies that may help you decide on this issue. This discussion is especially important in the light of the animal agriculture industry damaging our planet. These detrimental effects are real due to animal feed lots, habitat loss due to monocultures, overfishing, and more. There is no doubt that mass animal production for the sake of cheap meat is bad for the planet and so is the practice of monocultures, GMO, over hybridization of vegetable plant species and chemical farming! Just to be clear if we abolished agricultural animal production we estimate green house gas reduction by about 15-20%. Then there are the issues of land use, deforestation and water use, questions that are certainly beyond the scope of this website. But is the sustainable farming of grass-fed-grass-finished cattle as it has been done for thousands of years possible to satisfy human need for protein? It is certainly the practice of the developed countries relying on highly centralized megafarms for much of their food production that is at the center of the discussion here. Food production in general has been radically changed in the last 50 years, from individual small and local farmers to now only 5-10 corporations owning over 90% of the entire market. 

Source

Simply pouring concrete produces 8% of the green house gasses annually (when cement cures it releases CO2). China used more cement between 2011 and 2013 than the U.S. used in the entire 20th Century.  Then the main question remains why after 100 of electric vehicles we are still driving 99% archaic gas engines and our electricity is mainly produced from fossil fuel with all the alternative renewable source technologies we have had for over a century…

 

Here we are concerned with the question if humans need to eat meat to be healthy and the studies in relation to omega3.  Above, you have seen the evidence of detrimental effects of inflammatory plant fats and the lack of saturated fats. However the omega3 supplementation is not the only factor because we need to assume that protein intake is adequate which is also beyond the science objective of this website. The bottom line is that humans have an integrate relationship with meat consumption from the very beginning. Humas lived as hunters and gatherers for at least 100,000 years and even when we switched to farming we kept house animals as an important protein and nutritional source and there is no doubt that farm animals were necessary for proper plant farming fertilization purposes. When chemical synthetic fertilizers were invented this natural and sustainable process was interrupted and used for the greed of human mass production.

Body types: The entire discussion around what body type requires meat or plant diets is largely futile since most non-grazing animals are factual omnivores. Eg. arguments of low stomach acid, teeth or length of intestines do not really matter for omnivores, as you will see below. Omnivores adapt and obviously humans have been cooking meat for a long time, so they don’t need the fang teeth of a tiger. Humans hunt and cook meat because this is a very efficient way of satisfying your need for protein. And if you cant hunt or fish, humas developed the art of farming animals for food. Even chimpanzees can and do eat meat to satisfy their need for protein. However, you simply cannot feed a cow meat. It’s a grazing animal and it won’t touch it (actually when cows were forced to eat sheep brain, mad cow disease was the result).  Humans and other carnivores are further up the food chain because grazing herbivores and fish exist.

The important conclusion here is: only grazing animals or fish can extract omega3 from algae due to their special digestive tract. If you cannot achieve that task, you need to have a proper sources of omega3, which usually means extending the food chain. Many plant eating animals are short lived. Herbivores have different digestive systems, but as a method of extreme survival, even herbivores seem to eat small quantities of meat in a desperate attempt to survive. Humans clearly do not fall into the category of herbivores. We are along with dogs, cats or bears more adapted to eat meat. If you are an elephant for example, you have to get your omega3 through seeds, nuts, roots and fruit rich in alpha-linoleic acid. The ALA then still has to be converted to EPA and DHA, however our tests show that this process is very inefficient (less than 5%) and often does not work properly at all in older humans. To stay with the example of elephants: “A comparison with data from free-ranging African elephants or Asian work-camp elephants showed that the captive elephants had lower proportions of polyunsaturated fatty acids (PUFAs), and for several lipid fractions a higher n-6:n-3 ratio, than their counterparts in the wild.” 

Vegan omega3 oil versions made from algae are available and they constitute an adequate source of omega3. However you should know that they contains less EPA than fish oil and we don’t fully understand all of the benefits of natural fish oil ingredients. The bottom line for Zinzino customers is the balance test. If you can achieve an omega 6/3 ration below 4:1 with the vegan oil, it should be effective. Choosing the fish oil version instead is recommend for at least several month until your index is balanced. Again, we don’t have a full analyses of all the more ‘rare’ omega3 species and omega6 for that matter which are present in fish. In other words the fish is providing a source of PUFAs that are not achievable by simply consuming vegan oil. For further discussion in this matter, also look at the benefits of “butter” above.

 

Below are a few scientific studies that may help you decide. However, the omega3 supplementation or food intake is not the only decisive factor because we are assume the protein, vitamin, mineral and other nutritional intake is adequate. 

 

This study shows how Vegans have a 2.3x higher relative risk at hip fractures and overall a 1.5x higher risk at overall fractures than meat eaters. Even fish eaters did not equate to meat eaters however we don’t know much about their actual fish quality intake.

Tong et al. 2020

IQ: Mueller 2020: A vegan diet can be potentially critical for young children with risks of inadequate supply in terms of protein quality and energy as well as long-chain fatty acids, iron, zinc, vitamin D, iodine, calcium, and particularly vitamin B12. Deficiencies in these nutrients can lead to severe and sometimes irreversible developmental disorders. If such a diet is chosen for ethical, ecological, or health reasons, a well-planned, diversified diet with additional supplementation of vitamin B12, vitamin D, iodine, and potentially other micronutrients is crucial to ensure a healthy and nutritious intake during childhood.

Athletes: Rogerson 2017 “It was revealed elsewhere that veganism creates challenges that need to be accounted for when designing a nutritious diet. This included the sufficiency of energy and protein; the adequacy of vitamin B12, iron, zinc, calcium, iodine and vitamin D; and the lack of the long-chain n-3 fatty acids EPA and DHA in most plant-based sources. “

Sanders 2009: Dietary analyses show that vegan diets are devoid of DHA and vegetarian diets that included dairy food and eggs only provide about 0.02 g DHA/d. Vegetarian and especially vegan diets supply more linoleic acid (18:2n-6) than omnivore diets. The intake of alpha-linolenic acid (18:3n-3) also tends to be similar or greater but depends on culinary oils used. The proportions of DHA in plasma, blood cells, breast milk, and tissues are substantially lower in vegans and vegetarians compared with omnivores. 

Of course we have known this for a long time. Obeid 1994: This study demonstrates that vegetarians give birth to infants with less DHA in their plasma and cord artery phospholipids but this did not appear to be independently related to the outcome of pregnancy.

Rosell 2005: The proportions of plasma EPA and DHA were lower in the vegetarians and in the vegans than in the meat-eaters,  In the vegetarians and the vegans, plasma DHA was inversely correlated with plasma LA. (this means that your inflammatory index will be high)

 

Bone health and Rickets 

It has long been known how a diet without meat in adolescents years is detrimental to bone health in children which persists through lifetime. This is attributed to Vitamin D, protein and fiber in many studies. Dunnigan 2005: Meat and fibre intakes showed significant negative and positive associations respectively with rachitic and osteomalacic relative risk (RR; zero meat intake: RR 29·8 (95 % CI 4·96, 181), P<0·001; fibre intake: RR 1·53 (95 % CI 1·01, 2·32), P+0·043). The negative association of meat intakes with rachitic and osteomalacic relative risk was curvilinear; relative risk did not fall further at meat intakes above 60 g daily.

 

General Diet Studies: Now here is where it gets a little more complicated. Fish eaters or Pescovotairians are not in the same group as full vegans or even strict vegetarians. So in this study as discussed above fish eaters have a 13% lower incidence of heart disease.  By contrast, vegetarians had 20% higher rates of total stroke (hazard ratio 1.20, 95% confidence interval 1.02 to 1.40) than meat eaters, equivalent to three more cases of total stroke (95% confidence interval 0.8 to 5.4 more) per 1000 population over 10 years, mostly due to a higher rate of haemorrhagic stroke. 

 

Depression studies: Here is another example of how difficult these “diet studies” in relation to outcomes really are: Eleven (44%) of the outcomes indicated that vegetarian and vegan diets were associated with higher rates of depression, while seven (28%) outcomes revealed beneficial effects of the diets on depression. Seven (28%) outcomes found no association between vegetarian and vegan diets and depression, although two of these studies found a higher risk of depression in some groups.

Overall meta analysis shows that fish eaters or pescatarians  live longer than meat eaters because they simply get more omega3 and their inflammatory index is lower. But a full vegetarians and vegans don’t get enough “animal protein quality amino acids” and other ingredients such as B12 or omega3 or stearic acid for that matter to sustain their bones, tendons, muscles and other cellular functions in their diet. So the consensus is that a completely plant based diet is not healthy for overall longevity. 

Once again, the Mediterranean diet comes out to be beneficial, however the diet contains moderate amounts of fish and red meat as well as plant based ingredients: Crous-Bou 2019 shows how a balanced diet that provides plenty of omega3 including grass fed meat has an effect telomere length:

Telomere length is a major marker for longevity: Perez 2018 The available evidence suggests that there is no effect of diet on telomere length, but the ‘strong heterogeneity’ in the type and duration of dietary interventions does not allow any final statement on the absence of an effect of diet on telomere length. Telomere length (TL) is considered a biomarker of aging: shorter telomeres are associated with a decreased life expectancy and increased rates of age-related chronic diseases. Telomere attrition has been shown to be accelerated by oxidative stress and inflammation.

Several observational studies have reinforced the suggestive benefits of adherence to the Mediterranean diet (a plant-rich dietary pattern), consumption of seeds (and its derivatives), and dietary intake of carotenoids on TL, which further supports the research benefits of plant-rich dietary patterns and plant foods to promote health and longevity.

Rafie 2017: Except for the fruits and vegetables, which showed positive association with TL, results were inconsistent for other dietary factors. Also, certain food categories including processed meat, cereals and sugar-sweetened beverages may be associated with shorter TLs. 

 

To be fair, there are plenty of studies showing how “low meat intake” increases longevity. These studies are not meat-free and very difficult to compare in terms of heterogeneity. It maybe impossible to draw conclusions because too many factors are involved in the life style choices of ‘meat eaters’ or ‘vegetarians’ for that matter. If a meat eater or vegan eats processed foods every day and has no proper access to good protein or omega3 the outcomes of the study is not very useful. The same article concludes: ” Further investigation of meat intake in relation to survival in other cohorts is needed because the published studies summarized herein represent only a subset of the available cohort data. “

That is why we should always stick to the omega6/3 index ratio and focus on adequate omega3 supply to draw conclusions on specific health issues and diseases rather than interpreting very diverse food and life style habits. 

In summary, The omega 6/3 index does not lie, no matter what food you eat! if your vegan diet provides adequate amounts of EPA and DHA it maybe beneficial. However omega-3 is only one important neutraceutical essential in the human diet!

 

 

What about Plant Protein?

Plants can provide all nine essential amino acids, but the concentration of these amino acids can vary significantly between different plant sources. The nine essential amino acids are histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine. They are termed “essential” because the human body cannot synthesize them, so they must be obtained from the diet.

Here’s a breakdown of plant sources in relation to essential amino acids:

  1. Complete Protein Sources: Some plant foods are considered “complete” proteins because they contain adequate amounts of all nine essential amino acids in proportions suitable for human nutrition. Examples include quinoa, buckwheat, soy, and hemp seeds.

  2. Complementary Proteins: Many plant foods are deficient in one or more essential amino acids. However, by combining different plant foods, it’s possible to obtain all the essential amino acids. This practice is often referred to as protein complementation. For instance, legumes might be low in methionine but high in lysine, while grains might be high in methionine but low in lysine. By consuming both legumes and grains (like beans and rice), you can achieve a more balanced amino acid profile.

  3. Variability: Some plant foods are particularly low in specific essential amino acids. For example, most grains are lower in lysine, while legumes are typically lower in methionine.

  4. Importance of Diverse Diet: Vegetarians and vegans, who rely solely or primarily on plant sources for protein, should aim to consume a diverse range of foods to ensure they receive all essential amino acids in adequate amounts.

In summary, individual plant sources usually do not contain all nine essential amino acids in the ideal proportions and come with a hefty proportion of inflammatory omega-6. Only few plant sources contain alpha linolenic acid, but the turn rancid quickly plus the body has only a very inefficient way of converting ALA into vital EPA and DHA.

In conclusion, I would like to say that I don’t believe killing animals for the purpose of nutrition is the best way to obtain protein for our bodies, however it appears that this is the way we have been “designed” to eat. In the future, we may be able to adapt our omnivore digestive system to a purely plant based diet and even extract proper omega3. However, we simply are a long ways away from achieving a healthy plant nutrition that fully satisfies our needs over a long lifetime. Given the history of our short evolution we are currently meat eaters out of necessity of survival and convenience. The purpose of this short discussion was to have proper understanding of the science and long term effects of these diets.  Many athletes choose to be on a vegetarian or even vegan diet and they can perform well for the short time of their career. As an omnivore it is also important to do periodical fasting. That is what our ancestors were doing. Food was not always available as it is today and you had to work hard for it. Fasting renews your stem cells and regenerates your gut flora.  About 150,000 tons of food is tossed out in US households alone each day! Also don’t throw your food scraps into the landfill. Get a small composter and feed the plants around you even if you don’t grow your own garden. I want to thank “vegans and vegetarians” and meat eaters for all their efforts to save the planet from cruelty and wastefulness. At some point we have to decide what human health in the context of nature and the whole planets well being really means.

 

 

 

 

6. General Science and Supplements

 

Enzymatic PUFA conversion and age

Supplementation with plant based omega3 (eg. from Flax seed oil) is very limited. As described earlier the conversion of Alpha-linolenic acid (ALA) to EPA and DHA is possible however very inefficient. Estimates range from 0% to less than 8%. Tests show that at advanced age this process does not work at all anymore (so you show a high ALA but almost no EPA). In addition the same enzymes that make EPA for ALA also make inflammatory omega6 arachidonic acid from LA.

Here you can clearly see that supplementation with ALA sources did not deliver any significant EPA conversion.

The age-related reduction in PUFA composition was inversely correlated with SCD (desaturase) expression and activity resulting in elevations in monounsaturated fatty acid. This means that even if you have alpha linoleic acid in your diet (eg from flax seed oil) you cannot convert it to necessary DHA when you get older because you don’t have a functional desaturase enzyme activity anymore. We can see this blockage in the enzymatic activity in our balance tests.insert caption

source: https://me-pedia.org/wiki/Eicosanoid

As you can see the EPA has a special role. That is why the body can make small amounts from ALA but also reconvert DHA:

The “EPA shunt” or “EPA-to-EPA conversion” likely refers to the metabolic pathway involving the conversion of EPA (eicosapentaenoic acid) to other metabolites. However, without more context or specific details, it’s challenging to provide a more accurate or comprehensive explanation. Additionally, I am unable to provide real-time or the most up-to-date information or developments that might have occurred after my last training data in September 2021.

EPA, along with DHA (docosahexaenoic acid), is one of the omega-3 fatty acids, crucial for human health. They are found primarily in fatty fish and algae oil, and they play essential roles in inflammatory response, cardiovascular health, and neural development.

If the reference is to a specific concept, pathway, or mechanism proposed or described by a researcher or author named Sprecher, it would be helpful to have more information or a more detailed reference to the specific work or publication in question.

Please note that to give precise, accurate, and responsible information regarding scientific concepts, details, and context are crucial, especially if the information is to be used for educational or health-related decision-making.

 

Dihomo-gamma-linolenic acid (DGLA) is a fatty acid that has several roles in the body.

  1. Prostaglandin Production: One of DGLA’s most significant roles is as a precursor in the production of a type of eicosanoids called series-1 prostaglandins. These molecules have a variety of effects throughout the body, many of which are anti-inflammatory.

    For example, prostaglandin E1 (PGE1), which is produced from DGLA, has a variety of beneficial effects. It can inhibit platelet aggregation (which helps prevent blood clots), dilate blood vessels (which can help lower blood pressure), and has anti-inflammatory effects.

  2. Competes with Arachidonic Acid: DGLA competes with arachidonic acid (AA) for the enzyme that converts these fatty acids into their respective series of prostaglandins. In doing so, it can help reduce the production of series-2 prostaglandins, which are typically pro-inflammatory. This can have a modulating effect on inflammation in the body.

  3. Direct Anti-Inflammatory Effects: Some research has suggested that DGLA itself, even before it is converted into prostaglandins, has anti-inflammatory effects. This is believed to occur through a variety of mechanisms, including suppressing the production of inflammatory cytokines and chemokines.

However, it’s important to note that much of our understanding of DGLA’s roles in the body comes from in vitro (test tube) studies and animal models.

For most people tests show that the body has even established a negative feedback mechanism where the AA precursor, DGLA , accumulates because the body has already reached its limit.

Figure 2

Gamma-linolenic acid (GLA) is an omega-6 fatty acid that is found in various plant seed oils such as evening primrose oil, borage oil, and blackcurrant seed oil. GLA is not typically found in high levels in the diet, so it is often taken as a dietary supplement.

GLA plays a crucial role in the body’s inflammation response. After it’s consumed, GLA is converted into dihomo-gamma-linolenic acid (DGLA), which is one of the body’s three omega-6 derived anti-inflammatory molecules.

Some research suggests that GLA and its derivatives might help reduce symptoms of conditions like rheumatoid arthritis, eczema, and premenstrual syndrome (PMS), though more research is needed in these areas.

In addition to its potential anti-inflammatory properties, GLA also helps maintain the integrity of the skin barrier, regulate water loss, and protect the skin from injury and inflammation.

Please note that while omega-6 fats are essential for good health, they must be balanced with omega-3 fats in your diet. Most people consume too many omega-6 fats and not enough omega-3s, leading to inflammation. However, because GLA is metabolized differently than other omega-6 fats and has anti-inflammatory properties, it doesn’t contribute to this imbalance.

Gamma-linolenic acid (GLA) is metabolized in the body through a series of enzymatic reactions. Here’s an overview of this process:

  1. Desaturation: Once consumed, GLA, which is an 18-carbon omega-6 fatty acid, is acted upon by the enzyme delta-5-desaturase to produce dihomo-γ-linolenic acid (DGLA).

  2. Elongation: DGLA is then elongated by the enzyme elongase to form a 20-carbon omega-6 fatty acid known as arachidonic acid (AA).

  3. Conversion to Eicosanoids: Both DGLA and AA can be further metabolized by cyclooxygenase or lipoxygenase enzymes to form various eicosanoids. These are biologically active compounds that have diverse functions in inflammation, immune responses, and other physiological functions.

Notably, while AA-derived eicosanoids are generally pro-inflammatory, DGLA can give rise to anti-inflammatory compounds. This makes GLA unique among omega-6 fatty acids, as it can potentially lead to both pro- and anti-inflammatory compounds, depending on its metabolic pathway.

  1. Conversion to Prostaglandins: AA can also be converted into various types of prostaglandins, thromboxanes, and leukotrienes, which have wide-ranging effects on inflammation, blood clotting, and other physiological processes.

It’s important to note that the process of GLA metabolism is complex and influenced by many factors, including the presence of other dietary fats, individual genetic factors, overall health status, and more. For example, the activity of delta-5-desaturase can be inhibited by factors such as aging, stress, alcohol, and certain medical conditions, which can affect the efficiency of GLA metabolism.

The body try’s to downregulate inflammation!

Arachidonic acid (AA) is a polyunsaturated omega-6 fatty acid that plays a vital role in the body and is generally highly inflammatory as discussed. In the order of eicosanoid conversion AA is made from dihomo-gamma-linolenic acid (DGLA), but it’s one of the pathways. Here’s a brief overview of how AA can be synthesized:

  1. From Linoleic Acid (LA): The most common pathway for the synthesis of arachidonic acid in the human body starts with linoleic acid (LA), an essential omega-6 fatty acid. LA is first converted to gamma-linolenic acid (GLA) by the enzyme delta-6-desaturase.

  2. Conversion to DGLA: GLA is then elongated to form dihomo-gamma-linolenic acid (DGLA). This step is catalyzed by an elongase enzyme.

  3. Formation of Arachidonic Acid: Finally, DGLA can be converted to arachidonic acid by the enzyme delta-5-desaturase. This conversion adds a double bond to DGLA, producing AA.

However, it’s important to note that not all DGLA is destined to become arachidonic acid. DGLA can also be a substrate for the production of anti-inflammatory eicosanoids. The balance between DGLA and AA, and the metabolic pathways they enter, can be influenced by various factors, including diet, the presence of other fatty acids, and the activity of specific enzymes.

In summary, DGLA is a precursor for the synthesis of arachidonic acid, it’s part of a sequence of metabolic transformations that begin with linoleic acid. So very often AA can appear balanced but DGLA is very high trying to downregulate inflammation.

 

How can I increase my desaturase activity?

The activity of desaturase enzymes is influenced by a variety of factors, including age, diet, and overall health. While it’s true that aging can affect enzyme activity, certain strategies can potentially optimize the function of these enzymes.

  1. Nutrient-dense diet: Essential fatty acids, vitamins, and minerals support various bodily functions, including enzyme activity. For example, a diet rich in zinc, magnesium, and B vitamins can potentially boost desaturase activity.

  2. Limit Alcohol and Unhealthy Fats: Excessive alcohol and consumption of unhealthy fats (trans fats, for instance) can impair the activity of desaturase enzymes.

  3. Regular exercise: Regular physical activity is associated with better overall health and may support enzyme function.

  4. Adequate Sleep: Poor sleep can impact various bodily functions, including enzyme activity. Prioritizing good sleep hygiene may contribute to optimal enzyme function.

  5. Manage Stress: Chronic stress can negatively affect body’s biochemical processes, including enzymatic reactions. Implementing stress management strategies like meditation, yoga, or other relaxation techniques could be beneficial.

Remember, the ability to convert ALA to EPA and DHA decreases with age, and it’s typically not efficient even in young individuals. Therefore, for most people, especially as they age, it’s advisable to obtain EPA and DHA directly from dietary sources like fatty fish or from high-quality supplements if necessary. Always consult a healthcare professional or a dietitian before making significant changes to your diet or starting a supplement regimen.

What are lipids?

Lipids are your building blocks of your cellular membrane. But they also include fats, waxes, oils, hormones, and certain components of membranes and function as energy-storage molecules and chemical messengers. There are a vast amount of over 1000 species involved in many different tissue variations. Lipids contain fatty acids, saturated and omega-6 and -3 chains. That is what alters and varies their function. For example cardiolipin is prevalent to up to in heart muscle containing large amounts of omega-3! Again Omega3 PUFA are incorporated into membrane lipids and are most stable in that form!

Source: Atlas of plant and animal histology
Read more Studies

 

Vitas labs does independent anonymous fatty acid testing!

READY TO BALANCE!
Interpret your Balance Test

 

Other Zinzino supplements and their Science

 

Not your average Multi-Vitamin!

Xtend+

All ingredients are derived from natural sources. – Vitamin C from acerola, B-vitamins from buckwheat, Magnesium from seawater The B vitamins (B1-B12) and also a number of minerals in Xtend+ such as copper, magnesium, iodine and manganese have health claims stating that they are important for normal energy-yielding metabolism. Xtend+ contains several vitamins and minerals with approved health claims related to bones and muscles. These are Vitamin D, C, K and magnesium, manganese and zinc. Xtend+ contains 1-3, 1-6 beta glucans. These nutrients, derived from the cell walls of highly purified, proprietary strains of baker’s yeast, have been proven to enhance the immune system.

Several of the compounds (for example folate, iron, B6, copper) also con­tribute to this crucial health benefit. In addition to the vitamins and minerals, Xtend+ also contains carotenoids, xanthophylls and a group of polyphenols from a basket of fruits, spices and vegetables. To get the same amount of all these nutrients from foods, you would have to eat more than 3 000 calories of the most nutrient-dense foods every day.

All the ingredients combined in Xtend+ offer over a hundred health benefits as confirmed by EFSA (the European Food Safety Authority). These affect every cell, organ and tissue in the body. Xtend+ is the perfect complement to BalanceOil products, providing you with a complete nutritional support program.

 

Zinzinogen+

Curcumin extract
With its bright yellow color, curcumin is the cornerstone in the ZinoGene+ formulation. As a member of the ginger family, curcumin is produced by plants of the Curcuma longa species. Historically, curcumin has been used in India for thousands of years, both as a spice and as part of their Ayurvedic traditions. Today, it is widely used all around the globe in supplements, cosmetics, food flavoring, and food coloring. There are many different curcumin extracts on the market, but there is a considerable variance when it comes to their bioavailability, and as such they differ a lot when it comes to how much of the ingredient wields an active effect. The curcumin extract that makes it into our products is very carefully selected and provides a full spectrum of curcuminoids. We have chosen the global award-winning ingredient HydroCurc®, which is the world´s most bioavailable curcumin. This means enhanced absorption, and consequently improved efficacy and functionality.

Data shows evidence for curcumin-mediated DNA methylation alterations as a potential mechanism of colon cancer chemoprevention. In contrast to non-specific global hypomethylation induced by 5-aza-CdR, curcumin-induced methylation changes occurred only in a subset of partially-methylated genes, which provides additional mechanistic insights into the potent chemopreventive effect of this dietary nutraceutical.

Curcumin clearly changes gene expression in 3 cancer cell lines compared to control.

Quercetin
Quercetin is a natural pigment present in many fruits, vegetables and grains. It has antioxidant properties and belongs to a subgroup of polyphenols called flavonoids. It is estimated that the average person consumes 10–100 mg of it daily through food sources such as onions, apples, capers, berries, broccoli, citrus fruits, cherries, coffee, grapes, green tea, and red wine.
Important to note, is that the amount of quercetin in foods may depend on the conditions in which the food was grown. As such, in order to optimize bioavailability and functionality, we have made our own proprietary blend of quercetin using three different ingredients from two different plant sources: the pagoda tree, and onions. As always, the quality of our ingredients is every bit as important as the quantity, and this has remained our priority when it comes to the sources of quercetin we have selected for this formulation.

Fucoidans
Fucoidan-containing seaweeds have a rich history of medicinal and therapeutic use. Brown seaweed contains an element called fucoidan. Fucoidans from seaweed are non-stick compounds (think of them as the biological equivalent of Teflon). They are found in various species of brown algae and are located in the cell walls of the seaweed plant serving to protect it from external stress.
The nutritional properties of fucoidans are nothing new. Historically, fucoidan-containing seaweed have been used in ancient traditions for thousands of years. In fact, the earliest records of its use are dated back to 12000BC, where archaeological digs at Monte Verde in Chile have uncovered evidence of their use.
Today, fucoidans are being incorporated as high value ingredients in nutritional products. We know that quality and price vary considerably among the different suppliers and have chosen to apply an exclusive fucoidan ingredient in our ZinoGene+.

Active research into the health benefits of fucoidan continues across a range of health indications including anti-cancer, immune modulation, anti-viral, digestive health, anti-inflammation, wound healing and anti-ageing applications.

Orally administered Synergy and DPF, but not intraperitoneal DPF treatment, significantly ameliorated symptoms of colitis based on retention of body weight, as well as reduced diarrhoea and faecal blood loss, compared to the untreated colitis group.

Fucoidans can stimulate multi potent stem-like cells. We found that fucoidan induced hABM-MSC proliferation. It also significantly increased ALP activity, calcium accumulation and the expression of osteoblast-specific genes

Treatment of senescent MSCs with fucoidan significantly reversed this cellular senescence.

 

Bowel Health: Dietary fucoidans provide small but constant amounts of FCSPs to the intestinal tract, which can reorganize the composition of commensal microbiota altered by FCSPs, and consequently control inflammation symptoms in the intestine. 

Source: Yang 2021

Order Zinogen+ here

Order Zinogen+ here

 

 

Zinoshine+ Vitamin D and Magnesium – Deficiency

Immunity: patients who turn critical with viral infections including ‘covid‘ are very low on Vitamin D levels typically below 35ng/l. Above the 36th parallel north you do not get sufficient sunshine to make your own D. Most people do not realize that you really need to spend 20min+ in full sun exposure on your back skin to make proper levels of D. To the contrary, we choose to spend most of our day indoors because we are afraid of the sun and also use sun blockers. The result is that we are all testing low in Vitamin D levels!

Recommended Vitamin D levels:

Your Vitamin D demands fluctuate and depend on injury, stress, immune response, pollution, toxicity and your ability to absorb and make natural D!  30 ng/mL (75 nmol/L) is now defined as sufficiency in western medicine standards;

->however levels of 20ng/mL have been show to have many detrimental effects on health, so 30ng/mL are clearly set too low. We like to see levels between 40-80ng/ml (above 90 there maybe a danger of overdose).

 

Order your at home VITAMIN D TEST HERE

What is Vitamin D?

“Vitamin D3 (cholecalciferol)” is actually a steroid-like hormone not a ‘cofactor’ to enzymes, as most other vitamins. Vitamin D3 is fat soluble and gets converted to its active form calcitriol and can pass into the cell to dock onto a receptor to control nuclear DNA transcription of eg. calcium transport proteins. This has great implications for Muscle and Bone health but also the immune system: Vitamin D has many effects on the immune system as vitamin D receptors are present in many cell types including various immune cells such as antigen-presenting-cells, T cells, B cells and monocytes.  You should be aware that this mechanism cannot be functional if your omega3 levels are low and the membrane fluidity and functionality is not properly established. In addition you need large amounts of Magnesium for Vitamin D3 to be absorbed. Humans can synthesize D3 with the help of UV radiation in the skin. It is generally accepted that above the 36th degree latitude people become Vitamin D deficient quickly. But even below 36 degrees most people avoid the sun nowadays and are deficient.

Bone Health: Daylight outdoor exposure showed a significant negative association with combined relative risk against rickets and osteomalacia (RR 0·33 (95 % CI 0·17, 0·66), P<0·001).

167 Studies revealed: There was fair evidence from studies of an association between circulating 25(OH)D concentrations with some bone health outcomes (established rickets, PTH, falls, BMD). 

 

 

Vitamin D analyses of covid severity MaryamVasheghani 2021

 

Zinzino balance oil already contains some Vitamin D, however as discussed above your demands for Vitamin D fluctuate and we recommend that a supplementation of simultaneous Vitamin D and Magnesium. Magnesium is a necessary cofactor for enzyme function in fat and steroid metabolism!

 

 

Vitamin D and Magnesium deficiency go together and symptoms may include:

  • Fatigue.
  • Bone pain.
  • Muscle weakness, muscle aches, or muscle cramps.
  • Mood changes, like depression.

Vitamin D is actually a hormone involved in important functions within the body, helping to regulate the absorption of calcium and phosphorus, but perhaps the most vital is that it assist with facilitating normal immune system function. Further, getting a sufficient amount of vitamin D is important for normal growth and development of bones and teeth*. Like most nutritional and health factors, there is a significant amount of individuality when it comes to addressing our vitamin D needs. Many social and behavioral influences affect our ability to get sufficient amounts of vitamin D through sunshine alone. Factors such as being in an area with high pollution, using sunscreen, the amount of time spent indoors, living and working in big cities where buildings block sunlight, all play a part in how our bodies respond to the sun and produce this essential ‘sunshine vitamin’. In addition, your body weight needs to be taken into consideration. Vitamin D is a fat-soluble vitamin and as such the more excess body weight we have, the more we need to produce and consume in order for us to reach and maintain sufficient levels in our blood*. About 1 billion people have vitamin D deficiency worldwide. That is why it is important to both monitor your vitamin D levels and adjust with extra sources of vitamin D besides sunlight whenever necessary.

The source of vitamin D we use is lichen. It is a small unique plant species consisting of a symbiotic association of algae and fungus. It is found on mountainsides, rocks, and trees, in an abundance, and this natural source of Vitamin D3 is a conscious choice made for the sake of our environment.

Magnesium is very important in this enzymatic immune function metabolism. It is very important in the process of D3 absorption! However even Magnesium absorption depends on the quality of the supplement, its chemical form and most of all on omega3! So omega3, D3 and Magnesium go together. It is now recommended that you supplement with >250mg Magnesium per day.


There are many sources to vitamins and minerals out there. Zinzino strives to find the best and most efficient sources available on the market. ZinoShine+ features 4 different magnesium salts: magnesium hydroxide from seawater, magnesium citrate, magnesium malate and magnesium bisglycinate. Together, these four sources provides a broad spectrum approach for enhanced absorption and utilization in our body*.

Vitamin K note: Vitamin K is only needed for Vitamin D absorption in very high dosages. That is why Zinzino does not include it. We always recommend to get your Vitamin K levels tested as well to ensure that you have adequate levels.

 

Order your Vitamin D test here:
Order your Zinoshine Vitamin D + Magnesium

 

 

TOTOX test

Many commercial fish oils can be harmful if not properly tested.

Here are the test results for Zinzino:

7. General Science

 

OR, RR, HR, What does the statistical study lingo mean?

Statics can be mathematical gibberish. So here are a few explanations as to understand what is published.

The main objective of a study is that you are looking for a relationship between a ‘question and the outcome’ of the study and how likely this probability of a relation is. EG. what is the IQ of kids from fish eating mothers. As discussed above there are so many life-style factors involved and the study try to correct for the ‘outliers” .  But in any case many data points are collected (so look for studies with many participants). So if your study says there is a 0.5% chance of getting sick after taking this vaccine and the study only involves 5000 people that means we are talking about 25 people getting sick after vaccination; that is not a significant pool of participants. If on the other hand they studied 100 mothers eating 5 servings of fish per week vs no-fish and 50 kids (50%) had an IQ increase of 7 points: that is significant. However to make sure the data is not just randomly scattered and data points are actually following a curve, linear or polynomial (many events in nature are logarithmic) we have statistical analyses:

  1. The famous ‘p-value’ = p < 0.05, which means that there is less than a 5% chance that the difference in the outcome variable is due to chance.
  2. confidence interval = A 95% CI, on the other hand, is a range of values that are likely to include the true value of the effect being studied with a probability of 95%. It is a measure of the precision of the estimate. For example, if a study finds that the 95% CI for the effect of a treatment is (2, 4), it means that if the study were repeated many times, 95% of the time the true effect of the treatment would fall between 2 and 4.

Some studies tell you upfront what they found eg:  intake by 100 mg/day increases child IQ by 0.13 points or kids had a verbal IQ that was 7.55 points higher (95% CI .75 to 14.4) than those whose mothers did not eat fish. 

 

But some studies give you OR, RR, HR, (odds ratio, relative risk, health ratio)

Where RR is the relative risk, OR is the odds ratio, and p is the control event rate, which leads to the following: OR = ((1 – p) * RR) / (1 – RR * p). Thus, for instance, a RR of 2.0 with a p of 0.1 would lead to an OR of 2.25, whereas if p increases to 0.2 it would lead to an OR of 2.67.

A HR (hazard ratio) of 0.5 means that participant in the experimental group had ~half the risk of experiencing a “bad” outcome (progression) than patients in the comparison group did. Or an HR of 1.2 (like in the case of asprin as a blood thinner) means that your increased risk of taking the drug is 20% (nocebo effect). The hazard ratio includes a confidence interval (CI) at the end of the value because it is an estimate.

 

The “odd” Odds Ratio

In Short, the odds ratio OR does not mean your odds are eg. 0.55 for a particular risk… it only means 0.55 compared to the control group…

Consider a study investigating the relationship between regular exercise and the risk of developing heart disease. The relative risk (RR) is found to be 0.6 (those who regularly exercise are 60% as likely to develop heart disease as those who don’t exercise), and the probability of heart disease in the non-exercising population (p) is 0.2 (20% of non-exercisers develop heart disease).

Using these values in the formula:

OR = ((1 – 0.2) * 0.6) / (1 – 0.6 * 0.2) = 0.8 * 0.6 / 0.88 = 0.48 / 0.88 = 0.55

The odds ratio would be 0.55, suggesting that those who exercise regularly are less likely to develop heart disease compared to those who don’t exercise. However the risk is not reduced by 45% here.

An odds ratio less than 1 indicates a reduction in risk, but it does not directly translate to a percentage decrease in risk. An odds ratio of 0.5, for example, would mean that the exposed group (in our example, those who exercise regularly) have half the odds of developing the outcome (heart disease) compared to the unexposed group (those who don’t exercise).

So, in the second example, the people who exercise regularly have 55% of the odds of developing heart disease compared to those who don’t exercise. This doesn’t mean their risk is reduced by 45%, but rather that their odds are 45% less compared to the non-exercising group.

To put it another way, if you were to say their risk is reduced, you could say their odds of getting the disease are 45% lower than those who don’t exercise, not that their risk is reduced by 45%. It’s a subtle but important distinction in epidemiological studies.

Eg this study  shows: Reduced risk of hyperactivity of kids in fish eating mothers was OR 0.34.

“OR .34, 95% CI .15 to .78” is a way of reporting the results of a study that used odds ratio (OR) and confidence interval (CI) to measure the strength of the association between a particular exposure or risk factor and a specific outcome.

An OR is a measure of the odds of an event occurring in one group compared to another group. In this case, the OR of .34 means that the odds of the event occurring in the group exposed to the risk factor are  0.34 times the odds or 1/3 of the event occurring in the group not exposed to the risk factor.

A 95% CI is a range of values that are likely to include the true value of the OR with a probability of 95%. In this case, the 95% CI of .15 to .78 means that there is a 95% chance that the true value of the OR falls within the range of .15 and .78.

So the statement OR .34, 95% CI .15 to .78, indicates that there is a statistically significant association between the risk factor and the outcome, with a odds ratio of 0.34, and the true odds ratio is likely to fall between 0.15 and 0.78.

>The smaller the OR, the lower the likelihood of the outcome, and the lower the CI, the more precise the estimate of the OR.

An odds ratio (OR) of 0.1 means that the odds of an event occurring in the exposed group (i.e. those who were exposed to a particular factor, such as a treatment or a risk factor) are 0.1 times the odds of the event occurring in the unexposed group (i.e. those who were not exposed to the factor).

In other words, an OR of 0.1 indicates a strong protective effect of the exposure, meaning that the odds of the event occurring are much lower in the exposed group compared to the unexposed group. For example, if the odds of developing a particular disease in a group of people exposed to a certain treatment are 0.1 times the odds of developing the disease in a group of people who did not receive the treatment, this suggests that the treatment is highly effective at reducing the risk of the disease.

It is important to note that an OR of 0.1 on its own does not provide information about the statistical significance or clinical relevance of the effect. The significance and relevance of the effect depend on a variety of factors, such as the sample size, the study design, and the clinical context. Therefore, it is always important to interpret the OR in the context of the specific study and the question being asked.

So and OR of 0.1 does not necessarily mean that only 10% of the exposed group experience the effect compared to the control group. The odds ratio is a measure of association between an exposure and an outcome, and it does not directly provide information on the proportion of individuals who experience the outcome in each group.

To calculate the proportion of individuals who experience the outcome in each group, you would need to look at the raw data, such as the number of individuals with the outcome in each group, and calculate the proportions or percentages.

An odds ratio of 0.1 means that the odds of the outcome occurring in the exposed group are one-tenth (or 10%) of the odds of the outcome occurring in the unexposed group. So, if the odds of the outcome in the unexposed group were 20%, then the odds of the outcome in the exposed group would be 2% (i.e. 10% of 20%).

It’s important to note that the odds ratio is not the same as a risk ratio or a risk difference, which are measures that directly compare the risk of an outcome between two groups. The interpretation of the odds ratio depends on the specific study design and the characteristics of the population being studied.

Statistical regression analysis determine whether the difference in the outcome variable between the two groups is statistically significant, and whether the relationship between the two variables is getting weaker or disappearing over time.

Some examples of numbers that may be used to measure statistical regression include the p-value, which represents the probability that the difference in the outcome variable between the two groups is due to chance, and the coefficient of determination (R²) which represents the proportion of the variance in the outcome variable that is explained by the predictor variable.

Again, A common threshold for statistical significance is p < 0.05, which means that there is less than a 5% chance that the difference in the outcome variable is due to chance. A low R² value, like less than 0.3, indicates a weak relationship between the predictor and outcome variables.

Study design: Always look at the study design and the methods. EG. Arthritis score is very complex but well defined = WOMAC 

But when measuring mental clarity or depression results can be difficult to put into numbers! However most studies that are peer reviewed undergo a rigorous process of making sure that numbers they get are meaningful.

Also take time to look at the plots and figures: Eg lower blood pressure readings vs time on DHA index. 

Again: This is not a true statement: “the odds of developing DM were reduced by 28% (OR 0.72, 95% CI 0.63 to 0.84, p<0.001)” = it should be: the odds of developing DM were reduced by 28% compared to the risk of the control group (not specified here)>..

 

 

Placebo

 

The famous Placebo effect was coined when it was recognized in the 18th and 19th centuries that drugs or remedies often worked best while they were still new. So the belief system of the study participant plays an important role. Or in other words a doctor telling take this you will get better already has a significant effect.

A placebo is a substance that has no therapeutic effect or it is a sham replacement procedure such as placing a surgical probe but not performing the actual procedure.

But how big is the placebo effect and how do we make sure a treatment is actually working? It is almost impossible to estimate the effect due to the study design or circumstances. Average estimates are around 50% for any treatment (even surgery) ; In this study KIrsch analyzing data from the FDA, concluded that 82% of the response to antidepressants was accounted for by placebos.

The placebo effect makes it more difficult to evaluate new treatments. For that reason clinical trials supposed to control for this effect by including a group of subjects that receives a sham treatment. The subjects in such trials are blinded as to whether they receive the treatment or a placebo. 

For more information look here.

However, simply the knowledge of the participant of being on a trial for a certain condition is a bias:

Placebo effects across trials were highly correlated (r=.60 and .77) when placebos bore the same name but were not significantly correlated when placebos had different names. Placebo effects were significantly associated with response expectancy but not with acquiescence or absorption.

Clinical trials are often double-blinded so that the researchers or doctors also do not know which test subjects are receiving the active or placebo treatment. The placebo effect in such clinical trials is weaker than in normal therapy since the subjects are not sure whether the treatment they are receiving is active. Very often treatment are staggered, eg 1st group half receive placebo and then much later receive treatment. 

Many trials such as vaccine or chemotherapy trials do not require placebos because that would be considered unethical. 

In this example there was an effect reported for patients with HER2-positive early breast cancer that taking this drug -significantly improves long-term disease-free survival  (HR 0·76, 95% CI 0·68-0·86)??.  Then the “observation groups” were crossed over so in the end only 813 out of 5100 participants were in the ‘observer group’. This renders the results non-conclusive in our opinion. However an effectivness: “Estimates of 10-year disease-free survival were 63% for observation, 69% for 1 year of trastuzumab, and 69% for 2 years of trastuzumab” – so in effect 6% more survived by taking the drug, yet the drug caused 7.3% heart failure (vs 0.9% in the observation group).

So in summary, this 10 year cancer treatment ‘study’ is an example of a ‘pretend’ placebo random controlled study. The study did not use a blinded group that received a placebo, nor was the ‘observation’ group in a comparable size, nor did they get treated by a placebo. So in other words the observer group was not given the ‘healing effect’ of knowing they are getting treated within the study. Yes Fig. 2 shows a small effect: after 10 years eg. 472 women survived vs 388 in the observation group subset F which this paper accounted for a the HR of 0.76. However are the results statistically meaningful with a CI that goes up to HR 0.86?

 

Here is a discussion on the ethics of using the placebo effect.

To evade this issue or to convolute the outcome results, trials use another “drug” that is already FDA approved as a placebo (but still call this a placebo controlled study). EG. a vaccine study uses the Meningococcal vaccine as placebo or chemo-agent is replaced by a “more benign long term supplemental treatment” such as “trastuzumab only” as the control or in this case radiation. Obviously these are ‘fake studies’ or in other words you cannot compare the side effects or outcome of your new drug to the side effects of another drug or compare ‘apples to oranges’. A placebo is a substance that has no therapeutic effect such as saline or sometimes a diluted sugar pill. In addition many of these studies show very marginal effects.

In conclusion,  we argue that If the outcome of a treatment in anything less than 80-90% effective on the condition, that simply means that 8-9 out of 10 treated persons report significant improvement the treatment is questionable. So if a study is not properly placebo controlled the results have to show at least 80% effective. If you subtract the placebo estimate of 50% this makes the treatment “30% more effective than placebo”.

 

NOCEBO: A nocebo effect is said to occur when negative expectations of the patient regarding a treatment cause the treatment to have a more negative effect than it otherwise would have. Many of these ‘not placebo controlled’ or fake-placebo controlled studies show outcome effects of less than 50%. EG the flu vaccine can be effective as low as 19% which means ~30% could be below the placebo, which means that the treatment was harmful.

Here is a history of the yearly flu effectiveness of the vaccines on the CDC website.

By its own words the CDC distinguishes ‘RCT efficacy trials’ and ‘effectiveness studies’: Vaccine effectiveness is a measure of how well flu vaccines work among different groups of people, in different settings, and in different real-world conditions (as opposed to RCTs or “clinical trials”).

However we argue here these effectiveness studies or often called ‘meta analyses’ are in-fact a large placebo control study but without subtraction of the actual effect. We have great difficult time finding any placebo RCTs. Instead another term of ‘non-inferiority’ is coined: a comparator quadrivalent inactivated influenza vaccine in a pediatric population: A phase 3, randomized noninferiority study 

Scientists in the US examined data from 12 clinical trials of Covid vaccines and found that the “nocebo effect” accounted for about 76% of all common adverse reactions after the first dose and nearly 52% after the second dose.

However just as it is difficult to “measure and absolute average of placebo” it is difficult to measure ‘nocebo’. Many times the rate of trial-dropouts is very high. These withdrawals maybe  mentioned but not taken into effective ‘placebo control data’. Data were extracted from 20 RCTs fulfilling our search criteria. Of 3049 placebo-treated patients, 57.8% (95% CI: 50.1%-66.7%) reported at least one AE and 6.6% (95% CI: 5.3%-8.4%) discontinued placebo treatment because of AEs. 

Demicheli 2018 finds: We included 52 clinical trials of over 80,000 people assessing the safety and effectiveness of influenza vaccines: Inactivated influenza vaccines probably reduce influenza in healthy adults from 2.3% without vaccination to 0.9% (risk ratio (RR) 0.41, 95% confidence interval (CI) 0.36 to 0.47; 71,221 participants; moderate-certainty evidence), and they probably reduce ILI from 21.5% to 18.1% (RR 0.84, 95% CI 0.75 to 0.95; 25,795 participants; moderate-certainty evidence; Vaccination may lead to a small reduction in the risk of hospitalisation in healthy adults, from 14.7% to 14.1%

This is also call the NNT (number of necessary targets): In other words 71 healthy adults need to be vaccinated to prevent one of them experiencing influenza! 

Summary: the flu vaccine is far from being 30-70% effective and there are no proper RCT studies, plus treatment often shows a nocebo effect instead. Use natural nutraceuticals like omega3 and vitaminD to strengthen your immunity.

 

Studies need to be repeated, analyzed in meta studies and independently verified!

A meta-analysis is a statistical method used to combine the results of multiple independent studies on a particular research question, with the aim of increasing the overall sample size and statistical power, and obtaining more reliable estimates of the effect size of a particular intervention or exposure.

In a meta-analysis of clinical studies, researchers systematically review the published literature to identify all relevant studies that have investigated a particular clinical intervention or exposure, and then pool the data from these studies to obtain an overall estimate of the treatment effect.

Meta-analyses are typically conducted using a standardized set of procedures that include:

  1. Identification of relevant studies: The first step in conducting a meta-analysis is to identify all relevant studies that have been published on the topic of interest. This is typically done using a systematic search of electronic databases such as PubMed or Embase, as well as manual searches of reference lists and conference abstracts.

  2. Selection of studies: Once relevant studies have been identified, the next step is to select those that meet pre-defined inclusion and exclusion criteria. For example, studies may be excluded if they do not meet certain quality criteria, if they are not randomized controlled trials, or if they do not report outcomes of interest.

  3. Extraction of data: Data are then extracted from each included study, typically including information on the study design, patient population, intervention or exposure, and outcomes.

  4. Statistical analysis: The data are then statistically analyzed using specialized software, with the aim of obtaining a summary estimate of the effect size of the intervention or exposure. This involves pooling the data across studies and calculating an overall effect size estimate, as well as assessing the variability of the effect size across studies.

  5. Interpretation of results: The final step is to interpret the results of the meta-analysis, taking into account the strengths and limitations of the included studies, as well as the overall quality of the evidence.

In summary, a meta-analysis of clinical studies is a statistical method used to combine the results of multiple independent studies on a particular research question, with the aim of obtaining a more reliable estimate of the treatment effect.

 
PAXLOVID example:

Paxlovid is a prescription medication used for the treatment of mild to moderate COVID-19 in adults and pediatric patients aged 12 years or older weighing at least 40 kg. It is a combination of two drugs: nirmatrelvir and ritonavir.

Nirmatrelvir is a protease inhibitor that works by inhibiting an enzyme called the main protease (Mpro) of the SARS-CoV-2 virus, which is responsible for the replication of the virus. Ritonavir is another protease inhibitor that works by inhibiting an enzyme called cytochrome P450 3A4 (CYP3A4), which breaks down nirmatrelvir in the body, allowing it to remain effective for a longer period of time.

The development of Paxlovid was a collaboration between Pfizer and the US government’s Operation Warp Speed program, which was established in 2020 to accelerate the development, manufacturing, and distribution of COVID-19 vaccines, therapeutics, and diagnostics. Clinical trials for Paxlovid began in 2020, and the drug was granted emergency use authorization (EUA) by the US Food and Drug Administration (FDA) in November 2021 (normally this process involves years of rigorous phase3 trials).

2021 study: The EUA was based on the results of a phase 2/3 clinical trial that showed Paxlovid reduced the risk of hospitalization or death by 89% in high-risk adults with mild to moderate COVID-19. The trial included more than 1,200 patients and was conducted in the US, Mexico, Brazil, and Argentina.

 

2022: However recent studies show NO EFFECT: There was no significant difference in the duration of SARS-CoV-2 RNA clearance among the two groups (mean days, 10 in Paxlovid plus standard treatment group and 10.50 in the standard treatment group; ARD, −0.62; 95% CI −2.29 to 1.05, P = 0.42). The incidence of adverse events that occurred during the treatment period was similar in the two groups (any adverse event, 10.61% with Paxlovid plus standard treatment vs. 7.58% with the standard, P = 0.39; serious adverse events, 4.55% vs. 3.788%, P = 0.76).

 

It is important to look at the absolute changes:  Rosenberg 2023: Hospitalization or death occurred in 0.55% (n = 69) of patients who received nirmatrelvir plus ritonavir compared with 0.97% (n = 310) of patients who did not receive the treatment.

Evaluating the absolute changes of “treated vs placebo” helps you to draw conclusions if small effects of a drug treatment are worth side effects. In addition possible long term safety data is often not available. In addition, always verify if the placebo used in the study was actually saline.

 

ODDs Ratio: This meta analyses shows an effect however they are using OR: Three RCTs involving 4241 patients were included. Overall, anti-viral agents were associated with a significantly lower risk of COVID-19 related hospitalization or death compared with the placebo (OR, 0.23; 95% CI: 0.06-0.96; p = 0.04) 

So treating people with paxlovid does not mean they have only a “23% chance” of eg not getting hospitalized. OD 0.23 means that the odds of the outcome occurring in the exposed group are about a quarter (or 23%) of the odds of the outcome occurring in the control group. So, if the odds of the outcome in the untreated group were 20%, then the odds of the outcome in the treated group would be 5% (i.e. 25% of 20%). Now it is important to know what are the odds or better the relative risk of the control group to evaluate this data. This number is not easily obtainable and fluctuates!

 

Lai 2022: If you look at the absolute numbers of treated vs ‘placebo’ you can see the effect is very small. 585 (treated) events vs 628 (placebo)! So out of 3 large studies 43 people had less events when treated or roughly 1%. This does not correspond to 23% reduction in events! In addition 177 vs 126 = 51 more treated people had adverse effects.

To be fair, the analyses shows 69 vs 160 people had serious adverse effects and it is not full clear to the author how 160 people ~3% receiving a placebo ended up with severe effects in these studies. Generally “adverse effects” are defined as any new symptoms, clinical or laboratory abnormalities, or complications that occurred after the start of treatment.

 

Macrophages – Their balance in the innate immune system

Macrophages are a type of white blood cell that plays an important role in the immune system. They are involved in both innate and adaptive immune responses and can polarize into different functional subtypes, depending on the cytokine environment they are exposed to.

M1 and M2 macrophages represent two different functional phenotypes of macrophages with distinct roles in the immune response. M1 macrophages are classically activated macrophages that are induced by interferon-gamma (IFN-γ) and lipopolysaccharide (LPS), which are primarily produced during bacterial and viral infections. M1 macrophages produce pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-1β, and reactive oxygen species (ROS) to promote pathogen clearance and tissue damage.

M2 macrophages, on the other hand, are alternatively activated macrophages that are induced by cytokines such as IL-4, IL-13, and IL-10, which are produced during parasitic infections, allergies, and tissue repair processes. M2 macrophages produce anti-inflammatory cytokines, such as IL-10 and TGF-β, and promote tissue remodeling and repair.

The balance between M1 and M2 macrophages is crucial for maintaining immune homeostasis and preventing chronic inflammation. Excessive M1 polarization can lead to tissue damage and autoimmune diseases, while excessive M2 polarization can lead to impaired pathogen clearance and increased susceptibility to infections. Therefore, the appropriate balance between M1 and M2 macrophages is essential for a healthy immune response.

A cytokine storm is an exaggerated and uncontrolled immune response characterized by the overproduction of pro-inflammatory cytokines, which are signaling molecules that help to regulate the immune response. Cytokine storms are most commonly associated with viral infections, such as severe cases of COVID-19, influenza, and Ebola. However, they can also occur in response to other types of infections, autoimmune diseases, and immunotherapies.

In a cytokine storm, immune cells produce large amounts of cytokines, which can lead to systemic inflammation, tissue damage, and multiple organ failure. This can result in severe and potentially life-threatening symptoms, such as high fever, respiratory distress, low blood pressure, and organ dysfunction.

The severity of a cytokine storm depends on several factors, including the type of pathogen or trigger, the individual’s immune system response, and the presence of underlying health conditions. Treatment for cytokine storms may include immunosuppressive drugs, anti-cytokine therapy, and other supportive care measures to manage symptoms and prevent complications. Chinese Medicine herbal treatments can also control the inflammatory process.

 

 

Netosis

Neutrophils are primarily responsible for the process of NETosis. NETosis is a form of programmed cell death in which neutrophils release extracellular traps (NETs) made of DNA, histones, and granule proteins to trap and kill pathogens. This process is an important part of the immune response and is triggered by various stimuli, such as microbial pathogens, inflammatory cytokines, and other inflammatory mediators. While other cell types, such as eosinophils, mast cells, and macrophages, can also undergo NETosis, neutrophils are the primary cells involved in this process.

 

 

Normal Immune response has a balance between M1 and M2 macrophages, if this balance is disturbed serious blood clots and other cardiovascular events can occur. 

 

What happens during starvation and Ketosis?

Beta-oxidation is the metabolic process where fatty acid molecules are broken down in the mitochondria and/or in peroxisomes to generate acetyl-CoA, which then enters the citric acid cycle (Krebs cycle), ultimately leading to the production of ATP through oxidative phosphorylation. This process indeed requires oxygen because the electrons removed from the fatty acids are passed down the electron transport chain and eventually combined with oxygen to form water.

In conditions of starvation, the body prioritizes the use of fats for energy through beta-oxidation because glycogen stores are limited and are depleted within about 24 hours. The liver converts some of the acetyl-CoA into ketone bodies, which can be used as an energy source by the brain and other tissues when glucose levels are low.

However, if tissue becomes anaerobic, such as during intense exercise when oxygen delivery to muscles may be insufficient, or in pathological conditions like ischemia, the following can occur:

  1. Beta-Oxidation Decreases: Since beta-oxidation requires oxygen, it cannot proceed at its normal rate without adequate oxygen supply. Instead, cells must rely more on glycolysis, the process of breaking down glucose for energy in the absence of oxygen.

  2. Lactic Acid Production: Anaerobic glycolysis results in the production of lactic acid. While muscles and other tissues can tolerate some level of lactic acid, excessive accumulation can lead to muscle fatigue and discomfort, commonly known as lactic acidosis.

  3. Ketone Body Utilization: During starvation, ketone bodies are an alternative fuel source, particularly for the brain. Ketones do not require oxygen to be used for energy, but their production through ketogenesis in the liver is initially dependent on the oxygen-requiring beta-oxidation process. Thus, if a state of anaerobiosis persists, the production of ketone bodies might be affected.

  4. Protein Catabolism: In prolonged starvation combined with anaerobic conditions, the body may increase the breakdown of proteins into amino acids, which can be used for gluconeogenesis (the generation of glucose from non-carbohydrate sources), although this is not an anaerobic process and primarily takes place in the liver and kidneys which typically remain aerobic.

In summary, beta-oxidation of fats does indeed require oxygen. If a tissue becomes anaerobic, beta-oxidation is hampered, and the cell must rely on anaerobic glycolysis for energy, which is less efficient and has byproducts like lactic acid. However, during starvation, the body can use ketone bodies that have been generated during prior aerobic conditions as an alternative energy source that does not require oxygen.

Omega-3 fatty acids, particularly EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), have several roles in cellular metabolism and cardiovascular health that could theoretically enhance beta-oxidation:

  1. Cardiovascular Health: Omega-3 fatty acids are known for their cardiovascular benefits. They can improve endothelial function, reduce triglyceride levels, lower blood pressure, and have anti-inflammatory and antithrombotic properties. By improving overall cardiovascular health, omega-3s can enhance blood flow, thereby potentially increasing oxygen delivery to tissues. Enhanced oxygen delivery could support aerobic processes, including beta-oxidation.

  2. Membrane Fluidity: DHA is an important component of cell membranes and can affect their fluidity. This can influence membrane-bound proteins, including those involved in the electron transport chain. Improved membrane fluidity can facilitate the activity of enzymes involved in beta-oxidation and oxidative phosphorylation.

  3. Regulation of Gene Expression: Omega-3 fatty acids can regulate the expression of certain genes involved in fatty acid metabolism. They can act on nuclear receptors such as PPARs (peroxisome proliferator-activated receptors), which play a role in the expression of genes involved in fatty acid transport and oxidation.

  4. Anti-inflammatory Effects: Omega-3 fatty acids have anti-inflammatory properties. Inflammation can impair endothelial function and reduce tissue oxygenation, so by reducing inflammation, omega-3s might indirectly support beta-oxidation.

  5. Cytochrome c Function: While omega-3 fatty acids are not direct activators of cytochrome c, their role in maintaining cell membrane integrity and fluidity might affect the overall function of the electron transport chain, in which cytochrome c is involved.

In summary, omega-3 fatty acids can influence these aspects of metabolism and cardiovascular function. The direct effect of omega-3 on beta-oxidation rates in humans needs to be understood in the context of a myriad of other regulatory mechanisms. It’s not solely the presence of omega-3 that dictates the rate of beta-oxidation; rather, it is a combination of nutritional status, energy demands, hormonal regulation, and the availability of substrates and oxygen. However it has become clear that without proper Omega3 levels fat metabolism and ketosis is impaired. 

 

 

 

How do your own research

Pubmed Search

We recommend to use the ‘pubmed’ option, then you turn on filters by ‘reviews’ or ‘clinical trial’

Search for your condition: eg “omega3 index and cancer”

 

NCBI PubMed and PubMed Central (PMC) are both online databases that provide access to scientific literature and research articles. However, they differ in their focus and content.

PubMed is a search engine that indexes and provides abstracts of articles from a variety of biomedical and life science journals, including those from publishers such as Elsevier, Springer, and Wiley. PubMed is operated by the National Center for Biotechnology Information (NCBI), which is part of the National Library of Medicine (NLM), a branch of the United States National Institutes of Health (NIH).

PubMed Central, on the other hand, is a digital repository that provides free access to full-text articles from a subset of the journals indexed in PubMed. The articles in PMC are primarily focused on biomedical and life sciences research, and are submitted by publishers or authors to be freely accessible to the public.

While both databases provide access to scientific literature, PubMed is a comprehensive search engine for biomedical literature and includes abstracts and citations from many different journals, while PMC provides access to full-text articles from a more limited set of journals. Additionally, PMC contains articles that have been specifically designated for open access, while PubMed includes articles from a wider range of journals that may or may not be freely accessible.

 

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