Could statins be adding to the epidemic of ‘heart failure’?

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Statins are drugs that reduce cholesterol by inhibiting an enzyme in the liver known as ‘HMG-CoA reductase’ which ‘drives’ cholesterol production (most of the cholesterol in the bloodstream is made in the liver and does not come directly from the diet). But HMG-CoA reductase also facilitates the production of a substance known as ‘coenzyme Q10’ which itself participates in the production of what is known as ‘adenosine triphosphate’ (ATP) – the most basic unit of energy ‘fuel’ in the body. The major biochemical process which involves CoQ10 that drives ATP and energy production in the body is known as ‘oxidative phosphorylation’.

Now that we have the potted biochemistry lesson over, we can see that statins have the potential, by lowering CoQ10 levels, to put a break on oxidative phosphorylation and ATP production in the muscles. The end result may be fatigue? Muscle pain is another potential consequence.

In a study published this week in the Journal of the American College of Cardiology (JACC), Danish researchers measured CoQ10 levels in individuals taking simvastatin (a commonly-prescribed statin), and compared them with those not taking statins [1]. The levels in those taking the statin were significantly lower.

Now, studies such as this one are what is termed ‘epidemiological’ in nature, which means it looks at associations between things, but cannot prove that one thing is causing another. However, of relevance here is other evidence which finds that giving statins to people does indeed have the capacity to lower levels of CoQ10 in the body [2].

What was also interesting about the JACC study is that it found that those treated with statins had lower levels of oxidative phosphorylation than those not taking them. They also had reduced ‘insulin sensitivity’. This is relevant for a number of reasons, including the fact that insulin facilitates the uptake of nutrients such as glucose into the cells. Lowered insulin sensitivity can therefore ‘starve’ the cells of essential nutrients. Reduced insulin sensitivity is also the underlying fault in type 2 diabetes. It is perhaps worth bearing in mind that statin use has been proven to increase the risk of type 2 diabetes.

Another thing worth bearing in mind here, I think, is the fact that the heart is a muscle, and depleting it of CoQ10 may be hazardous for cardiac health. Specifically, it may weaken the heart and lead to what is known as ‘heart failure’ (also known as ‘congestive cardiac failure’). I think the ‘benefits’ of statins are vastly overstated, generally speaking. However, if someone is to take statins, I think it’s a reasonable safeguard to take CoQ10 on a daily basis. 100 mg a day is a decent dose, I think, though higher doses are likely to better when symptoms of statin toxicity are present.

In researching this article, I came across an interesting review of the evidence for statin-inducted CoQ10 depletion in both humans and animals [3]. Here’s what the authors of this review have to say in their concluding remarks:

Statin-induced CoQ10 deficiency is completely preventable with supplemental CoQ10 with no adverse impact on the cholesterol lowering or anti-inflammatory properties of the statin drugs. We are currently in the midst of a congestive heart failure epidemic in the United States, the cause or causes of which are unclear. As physicians, it is our duty to be absolutely certain that we are not inadvertently doing harm to our patients by creating a wide-spread deficiency of a nutrient critically important for normal heart function.


1. Larsen S, et al. Simvastatin Effects on Skeletal Muscle – Relation to Decreased Mitochondrial Function and Glucose Intolerance. J Am Coll Cardiol. 2013;61(1):44-53

2. Passi S, et al. Statins lower plasma and lymphocyte ubiquinol/ubiquinone without affecting other antioxidants and PUFA. Biofactors 2003;18(1-4):113-24.

3. Langsjoen PH, et al. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications. Biofactors 2003;18(1-4):101-11.

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