Statins can certainly reduce cholesterol, and by as much as 60%, so you would expect the clinical results to be dramatic, especially if they are the world’s number one bestseller worth many billions of dollars annually.¹ Unfortunately the results are not dramatic, and whether a reduction in cholesterol leads to improved mortality is still apparently a subject for hot debate decades after dietary cholesterol and saturated fats were declared ‘villains’ by Dr Ancel Keys.

A key problem with the hypothesis, that lowering serum cholesterol is protective against heart disease, is the lack of efficacy in a dose-response relationship when using these powerful drugs. In these terms, you would expect more drug to produce more lowering and therefore more benefit. In fact, these drugs have no significant effect on people with no cardio-vascular disease history (primary prevention),^2,3 while for those with existing cardiovascular disease (secondary prevention), statins achieve a mere 1-2% absolute risk reduction. Furthermore, this is the case whether or not they are used conservatively or intensively.^4–6

This marginal benefit is routinely inflated in the research by using results stated in terms of relative risk, a practice which turns a small drug effect of a few percent into something much larger and marketable. In fact, nearly all of the data set from roughly 200,000 patients is of dubious quality due to direct funding by the pharmaceutical industry, a serious conflict of interest because of the potential for exaggeration of benefit and simultaneous under-reporting of side-effects.

This cannot, however, be quantified because declarations of a conflict of interest in scientific papers is only a recent innovation designed to bring credibility to a tarnished archive which contains many distortions and manipulations. Not least is the problem of publication bias, which means a large part of the data set containing negative or insignificant results for statin use is purposely missing. We can add to this the problem of ghost authorship, where an unknown percentage of papers are prepared by pharmaceutical industry writers and statisticians for experts to sign off. Nevertheless, it is obvious that we are not in credible scientific territory when we find, for example, in the summary of the important CTT Collaborators meta-analysis of 14 trials, the statement that, ‘most of the trials in this report were supported by research grants from the pharmaceutical industry. Some members of the writing committee…have had the costs of participating in scientific meetings reimbursed by the pharmaceutical industry.’⁷

This kind of influence has successfully stalled the development of the science for decades while these very profitable drugs are still covered by patents. The drug companies even know that the mechanism that produces a marginal benefit in secondary prevention trials—and inconsistent results—is not actually via cholesterol lowering, but are reluctant to admit this. This is because physicians will then prescribe more appropriate medicines that don’t interfere with cholesterol synthesis, an intervention which produces unnecessary side-effects.

And the side-effects are legion: muscle pain is the most common side-effect reported, which is a category that includes myalgia, myositis and rhabdomyolysis;^1,8 and there is also a possible increase in LDL cholesterol—that’s right, an increase in LDL with statin use!⁹

The reference list for all the common side-effects is actually quite extensive even if you do a cursory search on PubMed: digestive disorders,^2,10 nerve damage,^11,12 insulin resistance,¹³ diabetes,¹⁴ endocrine disruption,¹⁵ erectile dysfunction,¹⁶ a decline in free testosterone,¹⁷ cardiovascular system damage,^18,19 herpes zoster,²⁰ a reduction in measures of cognition,²¹ cancer (colorectal, bladder, lung), ²² breast cancer,⁷ and liver toxicity,²³ just to pick out a few papers.

Statin use also causes an imbalance of key nutrients which are, ironically, necessary for cardiovascular system health. For example, we can see a decline in CoQ10,²⁴ zinc and copper,²⁵ and sadly a decrease in omega-3 fatty acid, which is a heart protective nutrient.²⁶

The slight benefit associated with statin use, the lack of dose-response, and the routine data manipulation should be enough to concern most readers who have the time to look beyond the brash journal abstracts. However, a cause of deeper concern is the research that demonstrates elevated cholesterol is actually protective, especially for women, which obviously means that attempting to lower cholesterol is counterproductive.

For example, epidemiological data from Japan indicates that elevated cholesterol (total or LDL) is protective in all age groups in terms of all-cause mortality.²⁷ Elevated cholesterol is also apparently protective for elderly people living in Finland, in an age group 75 years and older.²⁸

This kind of finding, running contrary to the ‘lipid hypothesis’, compels us to ask what it actually is that statins do to achieve a treatment effect that is apparent in some trials, if it is not by lowering cholesterol? It turns out that scientists have for a long time been aware that statins have antioxidant and anti-inflammatory properties, and that this might actually be responsible for the marginal benefit in using them to treat patients with cardiovascular disease. This discovery has actually been steadily reinventing the rather staid class of anti-cholesterol drugs into an anti-inflammatory panacea for treating conditions as varied as epilepsy and asthma.^29–31 They may even turn out to be useful antimicrobial drugs,³² or even anticancer agents.³³

Interestingly, the staunch proponents of the out-dated lipid hypothesis have now also begun to take on board the possible role of inflammation in heart disease, but characteristically, without abandoning their existing strategy of  intensive cholesterol lowering with statins. As a result, the new recommendations not only include a need to reduce the dietary intake of saturated fats and cholesterol, a statin to lower serum cholesterol, adjunct drugs such as ezetimibe (cholesterol absorption inhibitor) or PCSK91(monoclonal antibody), but also a prescription for anti-inflammatory medicines. This new class of medicines potentially includes the chemotherapy agent methotrexate and the immune system inhibitor canakinumab—an impressive line-up to fortify the position of our chameleon bestseller in the battle against cardiovascular disease.^34,35

While this article gives absolutely no advice about pharmaceutical drugs, alternative medicine has plenty to offer the reader who is concerned about elevated cholesterol. You can start by avoiding high-fructose corn syrup, sucrose or trans fats, and begin eating plenty of fibre derived from organic wholefoods. Added to this is the necessity to drink clean water, do regular exercise, check thyroid function, stop smoking and effectively manage stress. A more clinical approach involves taking key phytonutrients and medicinal herbs, a strategy supported by an extensive evidence-base, but this is the subject of a much longer eBook called Cholesterol, Statins, Herbs And Nutritionism.

Disclaimer: this article is intended for the purpose of general education only, and is not a substitute for diagnosis, treatment advice, or a prescription that is given in a consultation with a qualified physician.

References:

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