Popular health and nutrition articles often posit the essential omega–6 and omega–3 fatty acids simplistically as the "good fats." Rarely, however, is any mention given to the actual amounts and ratios of these lipids required for good health. As we've seen in previous editions of the Integrated Supplements Newsletter, a gross excess of the omega–6 essential fatty acid, linoleic acid in the modern diet may be a major contributing factor to obesity and related chronic diseases such as diabetes, cancer, and heart disease. For all practical purposes, therefore, it's clear that linoleic acid is anything but a "good fat."
Similar confusion currently surrounds the omega–3 fatty acids. As a delicate balance exists between omega–6 and omega–3 fatty acids, studies have begun to find that the ratio of the two in the diet may be an important factor in mediating inflammation and the development of chronic disease. The excess of omega–6 linoleic acid in our modern diet has led many researchers and product marketers to advocate increased intakes of the omega–3 fatty acids to balance the ratio of the two classes of lipids. As omega–3 fatty acids have garnered a steadily–increasing amount of mainstream acceptance, numerous sources of omega–3 fatty acids have been aggressively marketed in recent years, including fish oil, flax oil (and flaxseeds), krill oil, hemp oil, and many others.
But, with omega–3 supplements, we again find that the recommendations of the supplement marketers leave much to be desired. Many people currently consuming omega–3 fatty acid supplements aren't emulating the fatty acid intakes of healthy cultures, and are instead unwittingly consuming fatty acid intakes with no historical precedent, and with no scientific backing. The dangers of excess omega–3 consumption have now become a very real concern for millions of people who have been influenced by the widespread advice of health authorities and product sellers.
What's desperately needed is rational perspective on the amounts and ratios of fatty acids which are likely to offer protection against metabolic disruption and chronic disease. As it turns out, the optimal dose of omega–3 fatty acids is far lower than is often implied by supplement marketers. Supplements of omega–3 fatty acids are almost never advisable, and, in fact, common supplemental doses of omega–3 fatty acids are likely to be harmful when consumed over extended periods of time.
An excess of omega–3 fatty acids has been shown to result in profound suppression of the immune system which may lead to increased incidence of infection in the short term, and possibly the development of autoimmune disorders and even cancer in the longer–term. In addition, the tendency of fragile omega–3 fatty acids to spontaneously (i.e., non–enzymatically) oxidize is partly responsible for their potential toxicity. Oxidized metabolites of omega–3 fatty acids may cause widespread metabolic disruption as they impair metabolism on a fundamental cellular level. Inhibition of thyroid function, weight gain, accelerated skin aging, digestive disturbances, mood disorders, joint disorders, and liver damage are just a few of the potential detriments of omega–3 excess.
As is so often the case in the marketing of nutritional supplements, the potential benefits of omega–3 fatty acids have been wildly overstated, while little to no mention has been made of the potential risks.
A Brief Overview of Essential Fatty Acid Metabolism
Omega–6 linoleic acid and omega–3 alpha–linolenic acid are considered essential to human nutrition. These essential fatty acids (and the fatty acids derived from them) are involved in metabolic cascades which produce various inflammatory (and anti–inflammatory) chemicals. Linoleic acid is metabolized largely into the inflammatory mediator, arachidonic acid, while alpha–linolenic acid is (ideally) metabolized largely into the anti–inflammatory long–chain omega–3 fatty acids such as EPA and DHA.
The term: "essential," however, can be a bit misleading when used to describe nutrients like the essential fatty acids. First off, linoleic and alpha–linolenic acids are merely parent chemicals for fatty acids which can easily be consumed through food. Meats, eggs, and dairy, for example, are well–known sources of arachidonic acid, while seafood is the richest source of EPA and DHA. Consuming these "ready–made" fatty acid metabolites is likely to significantly reduce the requirements for their parent chemicals. In addition, an outright deficiency of either essential fatty acid is nearly impossible to achieve on any whole–food diet. Only in laboratory and hospital settings have such deficiencies manifested, owing to poorly–constructed artificial diets.
But, though outright essential–fatty–acid deficiency is rare, imbalances between the omega–6 and omega–3 fatty acids are common.
The metabolism of omega–6 linoleic acid into arachadonic acid, and omega–3 alpha–linolenic acid into the long–chain omega–3s (e.g., EPA and DHA), both require some of the same metabolic enzymes. This is why, as we've seen in previous Integrated Supplements Newsletters, an excess of omega–6 linoleic acid in the modern diet can dramatically interfere with the production of long–chain omega–3s, and their incorporation into tissues.
The efficient incorporation of long–chain omega–3 fatty acids (e.g., DHA) into tissues is thought to be required for the health benefits of omega–3s to manifest. The question then becomes: how do we ensure that omega–3s are metabolized safely and efficiently so as to optimize tissue levels of long–chain omega–3s? Consuming additional alpha–linolenic acid (e.g., plant–based omega–3 sources such as oils from soybeans, canola, flax, hemp, chia, et al.) doesn't seem to be the answer – especially if the diet contains excess linoleic acid. Alpha–linolenic acid simply doesn't seem to be metabolized into the long–chain omega–3s efficiently in the presence of linoleic acid:
Study Link – Can adults adequately convert alpha–linolenic acid (18:3n–3) to eicosapentaenoic acid (20:5n–3) and docosahexaenoic acid (22:6n–3)?
Quote from the above study:
The use of ALA labelled with radioisotopes suggested that with a background diet high in saturated fat conversion to long–chain metabolites is approximately 6% for EPA and 3.8% for DHA. With a diet rich in n–6 PUFA, conversion is reduced by 40 to 50%.
Knowing this, it probably makes sense to consume some long–chain omega–3s from seafood, but consuming significant (supplemental) amounts of additional long–chain omega–3s from fish/marine oils, is a practice which should be questioned. The long–chain omega–3s are very chemically fragile, and are well–documented to undergo spontaneous oxidation in the body when consumed in excess. Worse yet, adding fish oils (and the like) to a diet high in linoleic acid will only increase overall polyunsaturated fatty acid (PUFA) intake to one likely to cause widespread oxidative damage over time.
This is why we've previously advocated that the linoleic acid content of the diet (and overall PUFA intake) be kept low (~2% of calories). Not only does a low linoleic acid intake facilitate the incorporation of long–chain omega–3s into tissue, but low overall levels of PUFA make oxidative damage of PUFA less likely (with low linoleic acid intake, only trace amounts of omega–3 fatty acids are needed to optimize tissue levels of long–chain omega–3s, so lipid peroxidation is not a major concern).
Healthy Intakes of Omega–3 and Omega–6 Fatty Acids
Where overt essential fatty acid deficiency is rare, the recommendations of public health authorities for essential–fatty–acids are geared towards achieving optimal tissue levels resulting in reduced risk of chronic disease. Many researchers have noted a correlation between the level of long–chain (e.g., EPA, DHA) omega–3 fatty acids in tissue, and protection from various chronic and/or degenerative disorders. Achieving healthy tissue levels of omega–3, however, is only partly determined by dietary omega–3 intake. Because the metabolism of the two classes of fatty acids is so intertwined, a healthy intake of omega–3 fatty acids simply cannot be derived without also looking at the background level of omega–6 fats in the diet.
Studies have found that when the level of omega–6 fats in the diet is low, the level of omega–3s needed to ensure healthy tissue omega–3 levels is low as well. When the level of omega–6 fats in the diet is high (as it is in the United States and many other industrialized countries), the level of omega–3s needed to ensure healthy tissue levels of omega–3s is commensurately high.
Along these lines, researchers have calculated the dietary levels of long–chain omega–3s which would be needed to ensure what they believe to be healthy tissue levels of these fatty acids. In countries with low linoleic acid intake, healthy omega–3 intakes would be miniscule. In the Philippines, for example, where a mere 0.8% of calories come from linoleic acid, a paltry 278 milligrams of long–chain omega–3s per day would be sufficient to achieve what were deemed to be healthy omega–3 tissue levels.
By contrast, in the United States, where 7% to 9% of dietary calories come from linoleic acid, 3,667 milligrams of long–chain omega–3s would be necessary to achieve healthy tissue levels:
Study Link – Healthy intakes of n–3 and n–6 fatty acids: estimations considering worldwide diversity.
Quote from the above study:
n–3 LCFA intakes needed to meet a tissue target representative of Japan (60% n–3 in LCFA) ranged from 278 mg/d (Philippines, with intakes of 0.8% of energy as linoleate, 0.08% of energy as a–linolenate, and 0.06% of energy as arachidonic acid) to 3667 mg/d (United States, with 8.91% of energy as linoleate, 1.06% of energy as a– linolenate, and 0.08% of energy as arachidonic acid).
The safety of such high doses of EPA and DHA is questionable, however. Even the US FDA has stated that the combined dose of EPA and DHA from supplements should not exceed 3 grams (3,000 mg) per day.
Importantly, the researchers of the above study noted that the long chain omega–3 content needed to ensure healthy tissue levels in Americans could be reduced to one–tenth of this dose if intake of linoleic acid was lowered. Clearly, then, the ideal answer is to lower linoleic acid intakes – not to dramatically increase intakes of EPA and DHA:
Quote from the above study:
This allowance for n–3 LCFAs can likely be reduced to one–tenth of that amount by consuming fewer n–6 fats.
Again, this fact is significant, as the omega–6 and, to a greater extent omega–3 fatty acids are chemically fragile. Consuming high amounts of both could lead to various forms of metabolic disruption including immune dysfunction, premature aging (most visibly premature aging of the skin), digestive and gastrointestinal disturbances, bleeding disorders, reduced blood sugar control, depression, and even cancer. The potential for these long–term effects indicates that there's more to essential fatty acid nutrition than just achieving tissue omega–3 levels which happen to correspond to those of healthy cultures. Those advocating omega–3 supplementation often fail to make any mention of the importance of lowering the omega–6 (especially linoleic acid) content of the diet to avoid an overall excess of PUFA consumption.
Which Diet Should We Emulate?
The researchers conducting the above study used Japanese tissue levels of long–chain omega–3s as the benchmark for healthy intakes. They found that the Japanese intake of long–chain omega–3s (~750 mg per day combined of EPA and DHA) would offer 98% of the worldwide population protection against numerous diet–related diseases. But even the Japanese diet may be less–than–optimal when it comes to fatty acid intake. Though the health benefits of the Japanese diet are largely attributed to the regular intake of seafood rich in long–chain omega–3s, researchers have provided convincing evidence that the linoleic acid content of the Japanese diet (though significantly lower than that of the American diet) may still be too high for optimal health.
To improve the health of the Japanese population, The Japan Society for Lipid Nutrition has recently recommended that linoleic acid intake be reduced. The authors of the scholarly article below go so far as to state that the widely–touted benefits of omega–3 fatty acids can be alternately interpreted as illustrative of the effects of linoleic acid excess – a fact which is often conveniently ignored by the sellers of omega–3 supplements:
Article Link – The Japan Society for Lipid Nutrition recommends to reduce the intake of linoleic acid. A review and critique of the scientific evidence.
Quote from the above study:
There are quite a few mechanisms of action of omega–3 fatty acids, but the competition between the omega–6 and omega–3 fatty acids at steps of elongation, desaturation, esterification into phospholipids, their release, conversion to eicosanoids (lipid mediators) and at their receptors is the major theme that explains why omega–3 fatty acids are necessary for the prevention of CHD [coronary heart disease] and other chronic diseases. Accepting the usefulness of omega–3 fatty acids is nearly equal to admitting the risk of excessive LA [linoleic acid] intake.
The authors go on to say that, for those who eat fish regularly (as the Japanese generally do) a healthy intake of linoleic acid may be below 3% of calories. The authors found no evidence to recommend that the Japanese increase their omega–3 consumption.
For all intents and purposes, therefore, the Japanese intake of long–chain omega–3 fatty acids (~ 750 mg per day) likely represents the upper limit of what healthy cultures have been shown to consume. Even this amount, however, may be higher than is optimal. Because of the metabolic instability of omega–3s, there's clearly a limit on how many can be consumed without doing harm. The few cultures consuming higher amounts of long–chain omega–3s than the Japanese simply don't seem to experience additional health benefits as a result. Likely because of their high intake of omega–3 lipids, Inuit cultures, for example, are known to exhibit bleeding disorders, and premature signs of aging:
Study Link – The bleeding tendency in Greenland Eskimos.
And in controlled trials incorporating omega–3 rich fish oils, higher omega–3 doses generally compromise the beneficial effects instead of enhancing them.
Mediterranean–style diets have been associated with reduced risk of cardiovascular disease and reduced rates of all–cause mortality. Though the omega–3 content of the Mediterranean diet may be higher than that of the standard American diet, it may be their low level of linoleic acid which is a more important health–promoting factor.
The Lyon Diet Heart Study – one of the most successful studies ever conducted on the association between diet and cardiovascular disease – found that the reduction in linoleic acid was an essential part of the Mediterranean diet's success:
Study Link – Dietary Prevention of Coronary Heart Disease The Lyon Diet Heart Study.
Quote from the above study:
...only the trials that also lowered intake of n–6 PUFAs and increased n–3 fatty acids successfully lowered cardiovascular and all–cause mortality in the experimental cohort.
The fact that the Lyon Diet Heart Study employed the use of parent alpha–linolenic acid from canola oil (and not long–chain omega–3s as would be found in fish oil) is further evidence that excess linoleic acid is likely to be a more important contributor to diet–related disease than the amount or type of omega–3s.
In all likelihood, those seeking to prevent diet–related disorders by altering their fatty acid intake will be well served to reduce their linoleic acid intake to below 2% of daily calories. With this low linoleic acid intake, optimal intakes of EPA and DHA will likely be significantly lower than the average intake in Japan. But, as the majority of the industrialized world is likely to consume excess linoleic acid, the formal omega–3 recommendations of several countries, as well as the World Health Organization and North Atlantic Treaty Organization may therefore be slightly high. These organizations generally recommend between 300 mg and 500 mg of total EPA and DHA per day. This amount is roughly in line with the American Heart Association's recommendation to consume 1 to 2 fish meals per week.
Although 300 mg – 500 mg of EPA and DHA may be slightly higher than optimal on a diet low in linoleic acid, this intake is still reasonable and, in all likelihood, safe. Many of those who take omega–3 supplements, however, may be consuming far greater (and potentially unsafe) amounts of omega–3 fatty acids. It's not entirely uncommon to find fish oils and related sources of omega–3s recommended in doses of multiple teaspoons per day – doses which not a shred of long–term scientific evidence actually supports. A single teaspoon (or 5 capsules) of standard fish oil for example, will contain approximately 1300 mg of combined EPA and DHA – an amount almost twice that of the average Japanese intake per day. Add to this the EPA and DHA in the diet, and many supplement takers are sure to be consuming problematic amounts of long–chain omega–3s.
Alpha–Linolenic Acid – What Omega–3 Deficiency?
In addition, those consuming plant–based sources of omega–3 alpha–linolenic acid (e.g., flax oil, hemp oil) may not only be consuming a relatively inefficient source of omega–3, but may also be adding to their burden of linoleic acid as these plant–based sources invariably contain significant amounts of it.
As such, reviews of the literature have found the health benefits of omega–3 alpha–linolenic acid to be inconsistent at best – likely because many variables exist which may interfere with the proper conversion of alpha–linolenic acid into the long–chain omega–3s:
Study Link – n–3 Fatty acids from fish or fish oil supplements, but not alpha–linolenic acid, benefit cardiovascular outcomes in primary– and secondary prevention studies: a systematic review.
Quote from the above study:
Evidence suggests that increased consumption of n–3 FAs from fish or fish–oil supplements, but not of a–linolenic acid, reduces the rates of all–cause mortality, cardiac and sudden death, and possibly stroke.
Those who attribute modern diet–related disorders to an omega–3 deficiency should carefully investigate the changes in the omega–3 content of the American diet throughout the 20th Century. Largely due to increases in the consumption of soybean and canola oil, the omega–3 content of the American diet actually increased significantly between 1909 and 1999. Depending upon the type of calculations used, the omega–3 alpha–linolenic acid content of the diet during this time increased from 0.39% to up to 0.72% of calories:
Study Link – Changes in consumption of omega–3 and omega–6 fatty acids in the United States during the 20th century.
The above study notes, however, that the concomitant increase in linoleic acid consumption during this time has served to interfere with the metabolism and incorporation of omega–3 fatty acids in tissues:
Quote from the above study:
The estimated per capita consumption of soybean oil increased >1000–fold from 1909 to 1999. The availability of linoleic acid (LA) increased from 2.79% to 7.21% of energy... The apparent increased consumption of LA, which was primarily from soybean oil, has likely decreased tissue concentrations of EPA and DHA during the 20th century.
Sellers of plant–based omega–3 supplements such as flax oil and hemp oil should address the question: If adding alpha–linolenic acid to the diet were beneficial in correcting modern diet–related disorders, why did these disorders become epidemic during the time when the American public did just that? The only honest stance, of course, is that we don't need more omega–3 alpha–linolenic acid in our diet – we simply need to dramatically reduce the diet's level of omega–6 linoleic acid. This simple solution is hard to come by, however, as there's no money to be made by telling people what to avoid.
From the research that exists, we yet again find reason to believe that an excess of linoleic acid is the primary lipid–related contributor to modern chronic diseases. It's unlikely, therefore, that omega–3 fatty acids will function optimally unless linoleic acid levels are lowered. Simply adding omega–3 fatty acids to the diet is a far–riskier practice than many people imagine, and in the next Integrated Supplements Newsletter, we'll examine some of the potential problems that may arise from the consumption of supplemental doses of omega–3 fatty acids.
Articles In This Series:
A Diet For Long-Term Weight Control and Optimal Health:
Part 1- Sugars And Carbohydrates From An Addiction Perspective
Part 2 - The True Role of Sugar in Weight Gain, Diabetes, and Metabolic Syndrome
Part 3 - In Defense of Fruit
Part 4 - Fatty Acid Intake In Industrial Versus Traditional Diets
Part 5 - The Role of Modern Fats in Heart Disease, Cancer, and Obesity
Part 6 - Essential Fatty Acids and Metabolic Disruption
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These statements have not been evaluated by the FDA. No Integrated Supplements product is intended to diagnose, treat, cure or prevent any disease.