The Crucial Statin Decision

One of the most crucial and often agonizing medical decisions people have to make these days, as well as one of the main reasons people consult with me, is whether to take statin drugs prescribed by either their family doctor or their cardiologist.

Statin drugs are a family of chemicals that has been in use since the 1960s that work in the same way: They inhibit the action of the HMG- CoA reductase enzyme in the liver, which prevents the liver from synthesizing cholesterol, particularly the so-called “bad” cholesterol, LDL. As a result, the level of cholesterol and LDL in the blood drops, often precipitously, and the patient is often told that they now have less of a risk of either having a heart attack or dying from a cardiac event.

Plaque in the coronary arteries has been the presumed cause of heart attacks for a long time. And cholesterol deposition has been the presumed cause of the plaque itself. As the years have gone by, however, this theory has been discredited in favor of more complex explanations involving inflammation and other factors, in addition to LDL. Because statin drugs have a mild anti-inflammatory effect, they are seen to have benefits even in this more complex scenario.   Patients are routinely told that the studies linking statin drugs to prevention of myocardial infarction (MI) are “slam-dunks,” that the doctor him or herself takes statin drugs to prevent an MI, or that the patient will be dismissed if they refuse to take the medication. The side effects of statins -- primarily digestive issues, muscle weakness and pain, and congestive heart failure -- are grudgingly acknowledged with a “yes, but they are rare,” or, “I rarely see this.”

Against this backdrop, a new study about statin drugs has emerged, which is why I wanted to highlight it in this blog post.

In the study[1], which was published in a peer-reviewed journal in 2015 by Okuyama et al, the authors claim that, contrary to widely held beliefs, the primary toxicity of statin drugs is on their inhibition of CoQ10 and “Heme A” biosynthesis, which are compounds required for energy generation (in the form of ATP) and mitochondrial maintenance and repair.  As a result, the body’s cells, particularly of the heart, are unable to obtain the energy they need for normal cellular metabolism and repair. The result of this energy-starved state (ATP is the energy “currency” in mammalian cells) is impaired muscle function, including function of the heart, which, after all, is a type of muscle. This drug-induced energy deficit explains the common side-effects from statins, which are muscle weakness and congestive heart failure.

Other results of the lowering of available energy include heart and blood vessel dysfunction, decreased anti-oxidant protection and crucially accelerated arterial calcification. In addition, statins inhibit the conversion of vitamin K1 into the active form of the vitamin, K2, whose main function is to prevent calcification of the various blood vessels of the body. As a result, statin users have increased coronary artery plaques than nonusers in clinical trials.[2]

Yes, you read that correctly: According to this study, statin use increases the rate and amount of coronary artery lesions as compared to controls, the very situation they are meant to prevent and treat. This outcome is in addition to the well-recognized side effect of congestive heart failure, which has been confirmed by studies showing that statin use results in a predictable increase in the level of natriuretic peptide in the brain, a recognized marker for the presence of congestive heart failure.[3] The Okuyama study reports 130 cases of statin cardiomyopathy (leading to heart failure – often the cause of death in “heart” patients”) within four years of commencing statin therapy in a single cardiology practice in Japan. [4]

In an interview following the publication of this article, Okuyama was asked whether there was any safe and effective use of statin drugs – including those with familial hypercholesterolemia. His response: “I can propose no safe and effective means to protect from the side effects of statins. Instead, I recommend those taking statins to start discussing with their doctors that they replace their statins with safer omega-3 fatty acids.”[5] In other words, eat wild fish, grass-fed butter and eggs instead of taking drugs that actually accelerate the very disease you are trying to prevent.

But what about the plethora of evidence cardiologists refer to when they talk about the benefits of statin drugs? What about the JUPITER trial, the AFCAPS/TEXCAPS, CORONA, GISSI PREV and other trials that demonstrate that statin drugs are and should be our primary weapon in the prevention of coronary heart disease? Without getting into a long and boring dissection of the flaws of each of these studies, suffice to say the primary characteristic they all share is that they were 100 percent financed by statin manufacturers.   One major study on statins that was not industry funded, the 2011 Nilsson study,[6] was funded by a government agency. It looked at the results over five years of 4 million statin users. This is the largest study, by far, of statin drugs ever done, and it found NO evidence that statin use reduced cardiovascular events or risk. The study also pointed out that during the five-year period studied, the use of statin drugs tripled, yet the number of heart attacks and deaths from heart attacks did not change. In fact, according to the study, within the subgroup of men between ages 50 and 59, the primary statin users in the U.S., the rate of cardiac events increased by 19.5% in spite of a 310 percent increase in statin use. The study authors also postulated that statin use increased the likelihood of developing diabetes, a well-accepted risk factor for the development of coronary heart disease.

Looking at all this information, one wonders how statin drugs actually achieved their “wonder drug” status in the eyes of such a preponderance of both conventional and alternative practitioners, many of whom prescribe Red yeast rice as a “natural” statin alternative.   Perhaps it is time for a re-evaluation of statin therapy and even a re-evaluation of the entire heart-disease theory.

For more information on this topic, please check out my article “What Causes Heart Attacks,” as well as my forthcoming book on all things heart-related, Human Heart, Cosmic Heart, to by published this fall by Chelsea Green Publishing.

Be well.


[1]   Okuyama H., Langsjoen PH, Hamazaki T, et. Al Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms. Exper Rev Clin Pharmacol. March 2015; 8(2): 189-199.

[2] ibid

[3] ibid

[4] ibid Hamilton K, Okuyama, H., Atherosclerosis and heart failure stimulated by statins (interview). December 2015. Available at

[5] Hamilton K, Okuyama, H., Atherosclerosis and heart failure stimulated by statins (interview). December 2015. Available at

[6] Nilsson S., Molstad S., Karlberg C., et. Al. No connection between the level of exposition to statins in the population and the incidence/mortality of acute myocardial infarction. An Ecological study based on Sweden’s municipalities. J. Negat Results Biomed. 2011; 10:6.