The Cholesterol Hypothesis Epic Fail
This 2015 Japanese study had a few things to say about the idea that high cholesterol causes heart disease, about the so called benefits of low cholesterol, and about cholesterol lowering drugs…and they aren’t particularly complimentary.
And in fact it isn’t just this one study, and it doesn’t just apply to Japan. The truth of the matter is that the popular belief system, which suggests that high cholesterol is one of the main drivers of cardiovascular disease (and other related metabolic illnesses), and that lowering cholesterol is a big part of the answer, is problematic and misleading, and seems to disregard a large body of scientific evidence.
But this is not to suggest that high levels of cholesterol in the blood, never occur as a result of metabolic health issues, are never associated with an increased risk of susceptibility to illness, and can never be involved in the development and progression of disease. That’s a slightly different issue, and unfortunately without a little discussion about context, yes and no answers are rarely enough to provide a clear picture.
The truth of the matter is that, no matter where you are from, it’s normal for cholesterol levels to rise under certain conditions or circumstances, and this is not necessarily a bad thing, and it isn’t something to be afraid of per se.
And yet, that is not the same as saying, I never want to bring my cholesterol levels down. Nor is it the same as saying, I always want my cholesterol levels to be high. It’s the way that things work together that matters, and without a look at the big picture, it can be hard to see how something can be both good and bad at the same time. The thing is, it depends on why cholesterol is high or low, and it also depends on what is being compared to what.
From a physiological perspective, cholesterol – alongside glucose – plays a fundamental role in the protection against biochemical stress, as well as protection from degeneration and disease in general.
When a healthy person is exposed to stress, the production of cholesterol – which also happens to be the precursor to the protective ‘anti-stress’ steroid hormones (pregnenolone, progesterone, and DHEA) – increases defensively.
Ongoing exposure to stress (and the cumulative effects of aging), interfere with thyroid metabolism and energy system function, inhibiting the ability of the body to convert cholesterol into the more specialized anti-inflammatory hormones mentioned above, and so it becomes common for circulating cholesterol to rise.
Under these circumstances, cholesterol is still highly protective, however that does not mean that metabolic health is optimal. Unfortunately, it also does not mean that interfering with the production of cholesterol is the right solution.
“Mortality from infection is low in subjects with high cholesterol levels. This is because low density lipoprotein (LDL) and other lipoprotein particles stick to bacteria (and their toxic fragments) and viruses, decreasing their toxicity.”
In fact, there are a number of biologically valid reasons why low cholesterol is not something to aim for, especially when achieved via methods which interfere with the production of cholesterol, rather than methods which decrease cholesterol requirements, or increase conversion of cholesterol into other even more protective substances.
Interfering with cholesterol production, thereby preventing the supply of cholesterol needed for proper metabolic function (including protection from increased levels of metabolic stress), is not a good idea, even if it’s also true that high cholesterol is generally not a sign of optimal health.
Actually, arguably one of the worst things to do when metabolic stress is high and overall function is sub-optimal, is to get in the way of the production of something which exists as a big part of normal function, and which rises to deal with worsening issues, or as a kind of last line of defense.
“Liver disease seems to show the most marked association with cholesterol. Liver cancer incidence, liver cirrhosis mortality, and liver disease mortality have been found to be null in subjects with the highest cholesterol levels…”
The importance of cholesterol, when it comes to proper cellular and energy metabolism function (including protection from inflammation and infection, as well as biochemical stress in general), cannot be overstated. This is why interference with the production and metabolism of cholesterol, has the potential to be involved in the development of so many different metabolic conditions, including cancer and diabetes.
Inhibiting the ability to produce cholesterol with the use of cholesterol lowering drugs (statins), has been shown to have limited effectiveness, and has been demonstrated to have many potentially serious ‘side effects’, including nervous system disorders (peripheral neuropathy, diminished sexual pleasure and memory impairment), serious birth defects, musculoskeletal disorders, as well as liver dysfunction. There is also evidence suggesting that long term statin use promotes cancer, heart disease, diabetes and other serious illnesses.
“If liver damage by statins is serious, cholesterol levels may be markedly decreased by a compounding effect, namely, reduced cholesterol synthesis through the primary pharmacological effect of statins and liver damage, which also decreases cholesterol synthesis, as a side effect. And this compounding effect may start a vicious cycle.”
“…Are statins actually effective for preventing coronary heart disease in type 2 diabetes mellitus….the answer is unfortunately ‘No’…In fact, statins deteriorate glucose metabolism and increase…diabetes…”
The polyunsaturated fats (PUFAs), which are also well known to have cholesterol lowering effects, interact with circulating cholesterol in a manner which promotes the oxidation of cholesterol, and oxidized cholesterol is directly involved in the development of inflammation and cardiovascular disease, and other inflammatory illnesses including Alzheimer’s. Of course, this does not mean that cholesterol is the fundamental issue.
Even if statins can to some degree reduce exposure to oxidized cholesterol, it is more logical to limit exposure to the substances which are responsible for the damage to cholesterol, namely PUFAs and some other inflammatory things.
Apart from interfering with the production of cholesterol in the liver, the PUFAs are known to cause damage to the liver, to powerfully suppress thyroid energy metabolism, and to drive chronic and systemic inflammation. Reducing inflammation, has been shown to protect against heart disease, diabetes and cancer. This has been shown to be effective, even whilst cholesterol remains high.
“Because the liver is the major organ that synthesizes cholesterol, its dysfunction may reduce the available supply of cholesterol for hepatocyte reconstruction. If cholesterol is abundant in the blood from the beginning of liver disease, secondary damage to the liver due to cholesterol insufficiency might be avoided.”
So things can get a little confusing. Because cholesterol can be high because of stress and interference with thyroid energy systems, and this can be a bad thing in the sense that stress and metabolic suppression leads to inflammation and disease. But it’s also a good thing in the sense that high cholesterol is protective under these circumstances. If however, there is ongoing exposure to PUFAs and other inflammatory things, high cholesterol can itself become part of the problem. Again, that does not mean that the situation would be improved if cholesterol production was brought down, whilst stress and inflammation, and exposure to PUFAs, remains high. In fact this would potentially lead to far worse results.
Lowering stress and inflammation, whilst improving thyroid function, can, on the other hand, lower cholesterol levels (from both less production and increased conversion), and this can be beneficial. The answers are not always clear-cut, which can be a serious problem in a world where black and white, one size fits all simple solutions, are seen as preferable and are heavily promoted. This approach however, has been known to lead to ‘mistakes’.
“…The biggest mistake made by medical science in the previous century….the cholesterol hypothesis relies on very weak data—and sometimes considerably distorted data….cholesterol plays a very positive role in health.”
I’m not a doctor or a scientist, but it does seem clear that doctors have little choice but to accept the dominant view, and the dominant view is not always the right view. Science continues to provide conflicting results and opinions, but the more biology you read, the clearer it seems that the protective role of cholesterol is being largely ignored, and the so called causative role of high cholesterol in the promotion of heart disease, is exaggerated at best.
“The fact that the effects of cholesterol on CHD mortality decrease with age strongly suggests that high cholesterol is not a causative factor of CHD, and that high CHD mortality in the high total cholesterol groups reflects only their high proportion of FH [familial hypercholesterolemia] cases.”
It’s difficult to ignore the evidence showing that high cholesterol is protective, and low cholesterol is harmful, and continue believing that the problem is cholesterol, simply because there is some association between high cholesterol and heart disease. It’s even more difficult once you see that lowering cholesterol doesn’t fix things, but often makes everything much worse.
In order to do so, you really have to ignore all of the biological evidence regarding the metabolic effects of ongoing stress and chronic inflammation. And you have to completely disregard the science which shows the stress promoting inflammatory dangers of the breakdown products of the PUFAs, when they interact with normal physiological processes. You really have to just ignore everything except the ‘science’ which pushes the official hypothesis.
Because if you don’t, you’ll quickly start to realize that biological science has known what cholesterol is for a very long time, and that it makes complete sense for cholesterol to rise under stress. It will also start to be obvious that if stress can interfere with cholesterol turnover, and if lowering stress and improving thyroid function can bring cholesterol levels back to a reasonably optimal level, that the problem was always the ongoing exposure to biochemical stress, not cholesterol.
When you consider the many stress protective, anti-inflammatory, pro-metabolic effects of sugar, in light of the traditional ‘diet-heart hypothesis’, and in light of the positive role that sugar plays in relation to liver function, cholesterol production and cholesterol conversion, everything starts to fall into place.
Is your doctor aware of the biological significance of cholesterol, and the many ways that it can defend against stress and the onset or progression of disease?
Has your doctor read this study (Annals of Nutrition & Metabolism 2015;66(suppl 4):1–116) and other related studies questioning the validity of the cholesterol or lipid hypothesis?
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Dietary cholesterol oxidation products accelerate plaque destabilization and rupture associated with monocyte infiltration/activation via the MCP-1-CCR2 pathway in mouse brachiocephalic arteries: therapeutic effects of ezetimibe.
Image: David Hammerstein
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