The debate about the safety of statins continues to rage, with some researchers claiming that they are essentially no more harmful that placebo. In reality, though, the evidence on which these claims are based is flawed for several reasons. Here are just some of those reasons:
1. Commercial sponsors of clinical trials may not be motivated to search exhaustively for potential side effects..
2. Many trials do not state clearly how and how often adverse effects were assessed. Because of this, it far from certain that all adverse events have been recognised and logged appropriately.
3. Trial volunteers tend to be enthusiastic individuals, and may therefore be less likely to report side effects than patients in routine clinical practice.
4. Many trials have a ‘run-in’ period where individuals are given a placebo to help ensure adequate compliance with medication. This can cause studies to be ‘enriched’ with highly motivated individuals who, again, may be less likely to complain of side-effects.
5. One major statin trial (The Heart Protection Study) employed a run-in period which subjected all potential participants to the active drug. Individuals with evidence of adverse events were excluded, which obviously means a higher percentage of ‘statin tolerant’ individuals made it into the study proper.
6. Several studies are of short duration and, worse still, may have been subject to early termination (something which tends to downplay harm and exaggerate benefits).
7. In many trials, adverse effects are only deemed to have occurred if there’s been extreme deviation from normal biochemistry (for example, judging that myopathy has occurred only when creatinine kinase levels are 10 times the upper limit of normal or higher). Setting the bar this high obviously works to depress side effect rates.
8. Many studies exclude types of individuals who exist in the real world and may take statins, including older patients, patients with other conditions or on other drugs that may make them uniquely sensitive to adverse effects from statins.
9. Published accounts of clinical trials in medical journals generally report only a minority of adverse events compared to full ‘clinical study reports’.
Plus, it should be borne in mind that statins reduce cholesterol by inhibiting an enzyme in the liver known as ‘HMG-CoA reductase’. This enzyme ‘drives’ cholesterol production but it also facilitates the production of a substance known as ‘coenzyme Q10’ – an essential player in the production of what is known as ‘adenosine triphosphate’ (ATP) – the most basic unit of energy ‘fuel’ in the body. We know that giving statins to people does indeed have the capacity to lower levels of CoQ10 in the body .
Depletion of CoQ10 is thought to be a major reason for why statins can reduce energy production (and therefore provoke fatigue) in muscles. However, it’s worth bearing in mind 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’. Previously, researchers have noted the ability for statins to induce CoQ10 depletion in both humans and animals . In this particular review, the authors concluded that:
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.
In a recent study, the effect of supplementing individuals with CoQ10 was tested in a group of individuals who were also given statins . In this study, 62 individuals with heart failure were put on one of two regimes for 4 months.
1. a statin (atorvastatin 10 mg a day) plus 100 mg of CoQ10, twice a day
2. a statin (atorvastatin 10 mg a day) plus placebo, taken twice a day
The individuals in the study were subjected to a range of measurements including the heart’s ‘ejection fraction’ (basically, how much blood the heart pumps with each beat), and levels of the substance ‘N-terminal B-type natriuretic peptide’ (higher levels are generally found in worsened heart function). Compared to the placebo group, those taking CoQ10 were found to have better ejection fractions and lower levels of N-terminal B-type natriuretic peptide.
My conclusion, that CoQ10 depletion is a genuine potential issue in those who take statins, and that CoQ10 supplementation should at least be considered by those who take statins or have taken them (particularly if they suffer from heart failure or other symptoms linked to CoQ10 depletion).
1. Passi S, et al. Statins lower plasma and lymphocyte ubiquinol/ubiquinone without affecting other antioxidants and PUFA. Biofactors 2003;18(1-4):113-24
2. 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
3. Pourmoghaddas M, et al. Combination of atorvastatin/coenzyme Q10 as adjunctive treatment in congestive heart failure: A double-blind randomized placebo-controlled clinical trial. ARYA Atheroscler. 2014;10(1):1-5