Part V of a conversation with a low-fat zealot and statin advocate

The low-fat zealot and statin advocate says,
"Please tell us what you believe to be the true mechanism of atherosclerosis formation with references. Please tell us how to reduce the rate of heart disease with references. Thank you."

The model is given in "Uffe Ravnskov, Fat and Cholesterol are Good for You!, GB Publishing, Sweden, 2009" in the chapter titled "The Real Cause" with 40 references at the end of the chapter. This model can be reconciled with many risk factors. In most cases the model says that most vulnerable plaques are simply boils that have been generated by bacteria or viruses. The model can also explain why arteries are more afflicted with plaques than veins, unlike the model advocated by statinphiles.

He did not discuss the weak risk factor associated with higher LDL levels for younger males but I will attempt an explanation. There is a positive correlation between higher LDL levels and insulin levels. Insulin is an anabolic process and will increase anabolism. Since the body will attempt to balance the anabolic processes with the catabolic processes the growth hormone output will be decreased and the steroid output will be increased. These resulting conditions would make the body more susceptible to infections that might manifest as atherosclerosis.

I said there is a positive correlation between LDL level and insulin level but the insulin level can be lowered by a low-carb diet with, many times, little change in LDL levels. Even Dr. Ornish's diet with low caloric intake coupled with stress management might succeed in lowering the insulin levels with a probable lowering of LDL level. Nevertheless, even if the LDL levels do not decrease, as is often the situation when ingesting saturated fats, the growth hormone level will be increased and the steroid level will be decreased, which should increase one's health and immune system. One can then certainly appreciate how LDL levels might not very strongly correlate with insulin levels. Thus, this model succeeds in showing how LDL can be considered a weak risk factor but not a direct cause of atherosclerosis.

One subject not often brought up in discussions such as these is the importance of stress as a risk factor. Unremitting stress leads to an increase of cortisol production which, in turn, raises insulin levels. This combination leads to increased clotting factors production and an impaired immune system. Stress can tend to cancel out any positive effects of a particular diet choice. It is also seen that the symptoms of stress are similar to those of people with the metabolic syndrome.

Another anabolic hormone is testosterone. It has been noted that the metabolic syndrome is associated with a lowered average testosterone level. In an attempt to balance out anabolic and catabolic processes the anabolic testosterone level is lowered when the anabolic insulin levels are raised. A diet that lowered the insulin levels should then result in more desirable testosterone concentration levels.

In the context of stress one can discuss how LDL is an insignificant risk factor for women. I have read somewhere (don't ask me for the reference) that females have a much more healthy response to stress than males do. The relative absence of testosterone must at least partially explain this phenomenon. This healthy response would involve less production of clotting factors and less damage to the immune system.

I am not a physician but in my lifetime I have seen two people who contracted influenza and shortly thereafter were severely afflicted with CHD. Before the flu episode I needed to strain to keep up with one of these people while walking. Afterward he had difficulty walking until after he received a coronary bypass.