The Role of TFAs (trans fatty acids & other degenerated fatty acids)
in Disease and the Possible Effects of Fasting

Summary
In his book Enter The Zone, Barry Sears makes clear that AA-derived eicosanoids produce the histamine and inflammatory responses that typify modern medical conditions. But the one question remains: What are the AA-derived eicosanoids responding to? What is causing the excessive AA action? From my reading of Erdmann, Budwig, and Erasmus, there are appear to be several answers, all stemming from the introduction of trans fats and degenerate fatty acids (collectively: TFAs) into our diet with the advent of industrial processing methods.

Eric Armstrong
TreeLight.com/Health

Effects of Trans Fats

The trans fats and other degenerated fatty acids that result from commercial refining methods and hydrogenation (Erdmann 66-69 and 76-79, Erasmus 328-330) have been shown to act as "decoys" that the body uses in place of CIS fats it needs. Because they are not chemically active, and because they have never existed before in the history of man's evolution, the body does not how to recognize and avoid these decoys. So they act as metabolic poisons.

They have three main effects:

  1. As part of the cell membrane, they reduce cellular integrity. So the lungs, digestive tract, and internal cells wind up "admitting allergens, undigested foods, viruses, and even potential carcinogens" (Erdmann 78). Undigested proteins can then cause antibodies to form that attack similar proteins native to the body in autoimmune disease (Erasmus, 373), in addition to various forms of allergy and inflammation.

  2. The saturated fat sources the trans fats come in (hydrogenated margarine, fried foods, and partially hydrogenated anything) cause you to eat 6 times as much as you ordinarily would (Budwig 22), presumably as a result of the body's need for chemically active EFAs in cell membranes, eicosanoids, prostaglandins, hormones, brain cells, and the central nervous system. That leads to obesity and attendant cardiovascular and diabetic problems.

  3. If cellular integrity is damaged so much that the cell membranes do not interact chemically as they should (Erdmann 76-77), then it is not too farfetched to suppose that the immune system no longer recognizes them. "All cells have protein and lipid projections on their outer walls that serve as identifying markers to the immune system" (Fuhrman 145). The identification process may well be impeded by the TFAs, along with other chemical activities.

    There is some evidence that the problem with cholesterol in hardening of the arteries is not the cholesterol itself, but the result of free radical damage done to it. What causes that free radical damage. Are free radicals being generated randomly? Or is the immune system (which uses free radicals as a primary defense mechanism) attacking cellular membranes whose identify has been compromised by trans fats??? This scenario would explain the host of auto-immune diseases that are emerging in modern day society.

    Free radicals are produced in the mitochondria, where they are a normal and expected byproduct of energy metabolism. They are also produced in the eyeball, as the eye reacts to X-rays and ultraviolet light. Finally, free radicals are generated by the immune system itself, as a means for destroying invaders. So it is not hard to imagine that TFAs incorporated into bodily tissues render them unrecognizable to the immune system, and that the resulting free radical damage contributes to various forms of heart disease.

These three scenarios are realistic consequences of trans fats and degenerated fatty acids in our diet. (Erdmann gives a blood-chilling account of the processing of "cold-pressed" olive oil that would convince the most die-hard skeptic.) Pauling describes limitation of the antihistamine response with Vitamin C. Sears suggests regulating AA-derived eicosanoids through insulin-regulation. GLA supplementation has also been suggested (Graham, Kurilla). But if real cause of excessive AA action is TFA accumulation, then all of these approaches, as effective as they may be, amount to treating symptoms rather causes. If that is the case, then symptomatic relief must be regarded as an initial, stop-gap measure to buy time until the underlying condition can be cured.

The interesting question therefore remains: If the accumulation of trans fats and degenerated fatty acids in the body is the major problem, what is the best way to eliminate them?? Sears points out that with a good diet, the body will largely rebuild itself in two years. So that is clearly one method.

Effects of Fasting

Fasting is another interesting option. Budwig notes that triglyceride levels are raised at the start of fasting in subjects that have been fed saturated fats, but not in subjects that have been fed polyunsaturates. So fasting can rather rapidly restore the right balance of saturated fat and unsaturated fat in the body. Can it also help eliminate the "impostor" trans fats that have occupied positions where CIS fats are needed? This is an interesting topic for research.

If nothing else, it may be that fasting accelerates the tissue breakdown process, so that in subsequent feeding repairs are given highest priority. The overall effect may be to speed up tissue replacement by some factor which reduces the two-year replacement period to one that occurs in a matter of months. This would account for the high level of importance placed on the post-fasting diet by those who recommend fasting.

That is the only alternative I am aware of, at this time. It may be the only alternative there is for people with severe conditions of trans fat accumulation. Regardless of the method used to limit the impact of past TFA accumulation, it is imperative that we stop the intake of the dangerous TFAs found in margarine, fried foods, and partially hydrogenated anything.

Other Notes

  1. A preference for a particular substance like ALA (over LA) indicates a substance that is in short supply in the environment. This is supported by Pauling's example of the single-cell organism. ALA is obviously in short supply in even a varied plant-food diet.
  2. A tendency to retain a substance (like AA) indicates a substance that is infrequent supply. The body may have to go a relatively long period of time without.
  3. LA and ALA-mediated eicosanoids seem to provide one pathway for the control of biochemical systems. AA-mediated eicosanoids provide another. Could this be the essential fact that defines as "omnivores", capable of living on either food supply?
  4. Why does the body retain AA so tenaciously? Why does AA produce both kinds of eicosanoids? Thinking about it, it seems to me that when plant food is plentiful, animals may be strong and hard to hunt. Early in our evolution, or diets may have been largely plant based during these times. During the winter, when plant food is scarce, it could be that game is weaker and easier to hunt, although still scarce. During these times, AA would be virtually the only source for eicosanoid production. Retention of AA would therefore be protection against prolonged deprivation of dietary AA as well as plant-based EFAs.

References

Copyright © 1998, 2011 by Eric Armstrong. All rights reserved.
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