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.

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

Kevin S. Fansler says, "But the model would have you believe that God/evolution sent LDL down to constantly war against the epithelium of arteries. Strangely enough LDL has declared peace with the epithelium of veins. Why is that?" 

D. M. replies:
"Probably because the blood pressure is higher in the arteries. Hypertension is a risk factor for CHD, so that's a reasonable explanation."

Kevin Fansler says, "The model for atherosclerosis formation as presented by D. M. (courtesy of statin advocates) is severely deficient and so simplistic that it cannot even distinguish between arteries and veins. The statin advocate must only appeal to other risk factors while they claim that high LDL levels directly cause CHD. The emperor has no clothes."

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

The low-fat zealot and statin advocate says,
"The mechanism is known. No speculation is required. Lipoproteins that carry the apo B (LDL and VLDL) adhere to the artery walls, other lipoproteins don't. The higher the concentration in the blood of apo B lipoproteins, the more they diffuse into the artery wall. Once inside the wall they become oxidized. Oxidized LDL stimulates inflammation. In response to the inflammation macrophages are attracted, they devour the oxidized LDL and send out more inflammatory chemicals. They become foam cells which grow and eventually burst leaving cholesterol crystals in the artery wall. The crystals penetrate the artery wall causing even more inflammation."

The model presented above is very appealing to those who believe that LDL cholesterol is "bad" and is the direct cause of atherosclerosis. But the model would have you believe that God/evolution sent LDL down to constantly war against the epithelium of arteries. Strangely enough LDL has declared peace with the epithelium of veins. Why is that? Also if concentration of LDL is so important why is the correlation of atherosclerosis with LDL levels so weak? Why do many people with hypercholesterolemia live a life untouched by atherosclerosis? This simplistic model serves the statin industry and their FDA captives quite will as long as it is not examined closely. I have to laugh every-time I see this model presented on TV by a statin advertiser.

Part II of a conversation of a statin lover

This advocate of the low-fat diet and use of statins says,"In the review I cited Dr. Morrison's study and Dr. Esselstyn's study where all-cause mortality was greatly reduced. Meta-analyses of various statin studies also show a significant decrease in all-cause mortality."

Yes, there are those studies that show that people with CHD can obtain a decrease in all-cause mortality when tracked for a limited time-span. There are even studies that show apparently healthy middle-aged people with high cholesterol values receiving a very limited absolute decrease in overall mortality over a limited time span. But I wonder if there would be any advantage if the study were carried out over a time span of 15-20 years. The use of statins markedly decrease more than one substance that is needed to maintain life processes. This should be no surprise since these statins are no more than subtle rearrangements of the particular statin found in red-rice yeast, which maintains a symbiotic relationship with red rice. The statin substance in the yeast tends to protect the red rice from the predations of animals that would like to feed on red rice. In effect, people that use statins are using a substance that evolved as a poison.

Long-time users of statins would have to contend with increasing incidence of muscle weakness, depression, foggy memory, increased rate of traffic accidents and awareness that one could irreversibly damage one's liver. 

The Framingham results showed that for people over fifty, high cholesterol was not a risk factor. 

A workshop hosted by the National Heart, Lung, and Blood Institute reviewed 19 studies in 1990 and found that for women, if anything, the higher the cholesterol, the longer they lived.

Part I of a conversation with a statin advocate

The statin advocate says,
"Glucose is the energy of life. You can't live without it. If it's too low you go into a coma and die. But that doesn't mean you can't have too much. LDL is also essential but you can still have too much. Just because glucose is essential doesn't mean the body always does a good job of regulating it and just because LDL is essential doesn't mean the body always does a good job of regulating it either."

The equivalency between glucose and LDL is weak. It is well established that excessive glucose causes glycation of tissues. It is not well established what harm excessive LDL levels cause. Does it directly cause plaques to form? No experiments have ever established this. Only speculation exists. Some scientists think that the cholesterol existing in plaques are byproducts of the body fighting bacteria present in the artery and also the repair process where the endothelium is injured. Granted there may be optimum LDL levels but they vary with choice of diet, exercise, presence of infection, and stress levels. The body responds by attempting to establish those optimum levels for the environmental conditions. Sometimes the body is not successful if a poor diet or chronic stress is imposed.

The body also tries to set optimum conditions for blood sugar levels under given environmental conditions. However, a high-carb diet can force these blood-sugar levels to values that cause harm to the body. The correct approach is to change the environmental conditions to bring these levels down to the normal range. This approach would be to use a low-carb diet. One would not want to use insulin to force the blood sugar to lower levels as this would only increase insulin resistance and make the underlying problem worse. Likewise LDL levels can be forced higher than the normal range by environmental factors. Again the environmental factors should usually be changed to try to bring the LDL levels back in the normal range. Sometimes this is difficult and one can only try to optimize the VAP results where triglyceride levels, fluffiness of LDL particles, etc. are all considered.

Below is an assertion that is made by the statin advocate who obviously believes that high LDL levels are a direct cause of atherosclerosis.
"What's the best way to figure out how much LDL is normal and healthy? Look at modern hunter gatherers and free living mammals. Their LDL is 50 to 70 mg/dl and they have no heart disease. The LDL level for the average American is about twice that much. If you read peer reviewed scientific articles which try not to go beyond the evidence - instead of Dr. Ravnskov's highly biased books which completely ignore evidence that doesn't support his extreme claims - it is very clear that LDL is strongly associated with atherosclerosis, heart attacks and all-cause mortality."

The statin advocate holds up the modern hunter-gatherer's (MHG's) LDL levels as ideal. The diet of MHG's varied widely. The Masai dined mostly on meat, blood and high saturated fat milk. They had little heart disease but their kin who lived in urban areas had abundant heart disease. The traditional Inuit had little heart disease but did have appreciable incidence of hemorrhagic stroke. They ate meat and less-saturated fat. There are other MHG's who had a higher carbohydrate intake but restricted calories and they also fared well. Nevertheless, most of these MHG's are infested with parasites. Most parasites excrete substances that lower the body's inflammation response to protect them. These substances may also lower the LDL levels in the body as LDL is involved in the inflammation response. The lowered inflammation response may cause less plaque buildup when the endothelium is being repaired and thereby reduce the risk for CHD. On the other hand, the lowered immune response might be a disadvantage in fighting bacterial and viral infections.

Statins also lower the inflammation response but at what price? Muscle damage, depression, etc. can result

Even if one were on an MHG diet, one might not be able to achieve these low levels of LDL if the diet were combined with the modern way of life sans parasites or statins.

I am really interested in total mortality rates rather than CHD mortality rates. These cholesterol and statin people like to focus on CHD mortality rates. I would rather die of a heart attack than cancer.