Saturday, July 17, 2010

Overview of Chris Masterjohn's report on EFAs

I have recently finished reading Chris Masterjohn’s wonderful report “How Essential Are the Essential Fatty Acids?”, available here for a nominal fee of $15. In this article I’m going to summarize what are the main points as I understood them and then what I think that implies in terms of diet. Overall, I find Chris Masterjohn to be an excellent and well-researched source of information. I’m in pretty solid agreement with Masterjohn’s conclusions but others may feel otherwise. I’m always open to a good debate.

Relevant points from the article concerning essentiallity of EFAs:

The discussion on essential fatty acids (EFAs) and poly-unsaturated fatty acids (PUFAs) in general is becoming a pretty heavy topic of late in the blogosphere. The topic is a complex one and I’m going to do my best to give a Layman’s overview.

Masterjohn identifies only two truly essential fatty acids: arachidonic acid (AA) in the Omega-6 family, and docosahexaenoic acid (DHA) in the Omega-3 family. Both are requisite constituents of cell membranes, but only up to a certain limit. Furthermore, they need to be balanced relative to each other. Eicosapentaenoic acid (EPA), found in fish oil, is not an EFA. Excess EPA can exacerbate some EFA deficiency symptoms.

The requirements for EFAs as a constituent of the diet are extremely low. They are at most 0.5% of calories during growth or recovery periods. At other times, they are even lower. Since most fats, saturated or not , contain an array of various fatty acids, it would be almost impossible to induce an EFA deficiency through dietary modification.

AA can be synthesized in the body from linoleic acid (LA) and DHA can be synthesized from alpha-linoleic acid (ALA). Therefore, it would presumably be sufficient to supply only AA and ALA in the diet. However, the Omega-3 and Omega-6 families compete for the same enzymes in the conversion process. The body has no regulatory mechanism to control this competition. Therefore, an excess in one family can cause a deficiency in the other. Furthermore, overcomsumption of PUFAs in general decrease the production of these enzymes and exacerbates the problem of competition. DHA and AA supplied directly in the diet do not require enzymes for conversion and thus do not lead to competition.

Although the body has no regulatory mechanism to control competition for enzymes between the Omega-6 and Omega-3 fatty acids, it is capable of controlling cell tissue ratios. This is only true as long as PUFAs remain a small percentage of the diet. As PUFAs percentage of the diet increases, the ratio at which an abundance of one fatty acid family induces a deficiency in the other decreases.

In the modern diet, especially the American diet, it is the overconsumption of Omega-6 fats we are concerned about (especially LA, which is rich in most nuts and vegetable oils). A diet overly rich in Omega-6 fats increases the tissue concentration of highly unsaturated fatty acids. The Omega-6 HUFAs are generally known to be pro-inflammatory whereas the Omega-3 HUFAs are known to be anti-inflammatory. Normally these are supposed to be balanced. When there is a dominance of Omega-6 HUFAs, in general this is associated with more inflammation. Since the degenerative diseases are are associated with inflammation and oxidative stress, we should seek to counter such an imbalance.

Oxidative stress operates in chain reactions. An oxidized PUFA becomes a peroxyl radical which can go on to oxidize another PUFA. This is normally countered by an anti-oxidant, which reacts with the free radical but does not become reactive itself. However, this consumes the anti-oxidant. Therefore it is important to maintain a diet low in oxidative stress and high in anti-oxidant nutrients.

An excess of PUFA in the diet will become stored in the adipose tissue (fat cells). Excess PUFA in adipose tissue draws down serum levels of vitamin E, further exacerbating oxidative stress.
Other relevant points:

Low density lipoprotein is known as bad cholesterol because it is typically the lipoprotein molecule to become damaged and trigger atherosclerosis. I’m not going to get into the details of how or why, but part of the process involves triggering a macrophage to become a foam cell. The specific components of an oxidized LDL particle that turn on the foam cell genes are the oxidized derivatives of LA.

PUFAs themselves contribute to oxidative stress in the body. This is because the typical oxidation reaction requires two double-bonds (thus excluding mono-unsaturated and saturated fats). The body cannot completely mitigate this, even with an abundance of antioxidants such as vitamin E. Therefore, excess dietary PUFA contributes to oxidation and inflammation within the body. CoQ10 slows lipid peroxidation in LDL up to 35 times.

The mammalian body seems geared to eliminate excess PUFA, using it preferentially for energy production (as opposed to structural purposes) even in the presence of extreme EFA deficiency.

The first and second phases of the Diet and Reinfarction Trial (DART) suggest fish-oil supplementation is only beneficial to heart attack survivors on beta-blockers or calcium-channel blockers.

Conclusions / Recommendations:

These conclusions are my own, although they are largely in line with Chris Masterjohn’s. In addition, there are some further points here that come from the EFA report that were not mentioned above.

My conclusions in order by my perception of their relevance:

Severely limit all dietary PUFA. The dietary requirements for EFA are extremely low and can be adequately met with fats that are mostly saturated: butter, lard, etc. All PUFA contributes to oxidative stress and thus to degenerative disease. Increasing dietary PUFA is also likely to exacerbate EFA deficiency. The only reason for supplementing with Omega-3 is because Omega-6 is already too high in the diet. Otherwise, such supplementation is not natural or necessary. In general, this means being on the lookout for all fried foods, processed foods, and commercial sauces or dressings. Be aware that most dressings are made with soybean or canola oil bases and most crackers and chips are also made with vegetable oils. Not only are these high in Omega-6, they are often rancid as well.

Use only fresh, non-rancid fats and use correct preservation methods. Most of the industrial processed fats in our diet are already oxidized (rancid). Your body can do nothing with these fats and must immediately try to stop the oxidative chain reactions they induce. Omega-6 fats are highly prone to rancidity. Omega-3 even more so. In fact, Omega-3 is so prone to rancidity, you will not find it in any commercially prepared food since it is simply not stable enough. Your best sources for these fats are organic grass-fed animal products such as butter, beef, and organ meats. If you can acquire fresh seafood, this is also a good source. Omega-3 fats are easily damaged by cooking so fish should be lightly cooked or raw, as with sushi. Oils should be cold-pressed and stored in dark containers in a cool place. Butter should be kept in a container that limits exposure to oxygen, such as a French butter dish. All excess fats and oils should be refrigerated.

Make sure the diet is high in nutrients. Vitamin E is important in mitigating oxidative stress. Essential vitamins and minerals are required to make the enzymes necessary in the EFA conversion process. Depletion of B6, biotin and essential minerals such as magnesium and calcium exacerbate EFA imbalances and deficiency. Supplementation may be ok, but this can sometimes lead to nutrient imbalances or certain types of toxicity. Vitamins and minerals are always best acquired through fresh, whole foods. Supplements made from whole food sources are preferable to synthetics.

If you are taking a statin, supplement with exogenous CoQ10. Statins decrease endogenous production of CoQ10 and based on my understanding of Masterjohn’s findings, this will greatly increase oxidative stress due to PUFAs.

It may not matter whether the diet is higher fat or higher starch. The human body seems to allow a lot of leeway in dietary preference towards fat or starch. Saturated and mono-unsaturated fats are easily synthesized from excess carbohydrate. In this regard, it may not matter whether one ingests more calories in the form of carbohydrates or fats such as butter and coconut oil. However, keeping dietary fat low will in general also keep PUFA intake low. Carbohydrates should preferentially come from unrefined sources. Root vegetables are best. Brown rice, corn, popcorn, and lentils are also good choices. Bread and pasta are the poorest choices. Do not follow a restrictive diet. Do not severely limit carbohydrates, fats, or calories.

Fish oil supplementation may or may not be a good strategy. The goal here, in my view, would be to overturn a high tissue concentration of Omega-6 HUFA. Once this has been achieved, following an adequate diet, there would be no reason for further Omega-3 supplementation. Any extra EFA supplementation necessarily increases oxidative stress. Note that turning over HUFA tissue concentration is a long term goal, on the order of months to years, and is difficult to measure directly.

Masterjohn recommends cod-liver oil supplementation but only in small quantities and only during healing or growth periods. These are periods such as pregnancy or recovering from an illness. It should be noted that the quality of the cod-liver oil is important in the case of supplementation. It should be properly handled to ensure preservation, have a good balance of EFAs, and also provide sufficient vitamins A and D (without those vitamins being synthetically added).



I will likely write more on this in a future post, with reference to some diagrams, but I've covered the gist of it here. I consider this a good overview for now.

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