While doctors and researchers often issue soothing reassurances about the potential for statins to cause harm, this is at odds with numerous reports that they can cause side effects such as fatigue and muscle pain.
Now, a recent study claims to provide evidence that, for the most part, statin side effects are ‘imagined’ [1].
In this research, the adverse effect rates from statins was compared with those seen in individuals taking placebo (dummy) pills in a total of 29 studies. Their conclusion was that apart from increasing the risk of diabetes, statins don’t have any more adverse effects than placebo. The actual words the authors use in their conclusion are: “Only a small minority of symptoms reported on statins are genuinely due to the statins: almost all would occur just as frequently on placebo.”
Confident, reassuring stuff, indeed. Yet how do these findings explain how a significant number of people who take statins seem to have side-effects that resolve (albeit, sometimes slowly) on discontinuation of their medication? Of course, as the authors of this most recent study allude to, these side-effects are due to the opposite of the placebo response – sometimes referred to as the ‘nocebo response’.
However, is there anything about the way statin studies (and other trials) may be designed and conducted that might jeopardize our ability to get accurate data on the adverse effects of drugs?
Several explanations are possible. First, commercial sponsors of clinical trials may not be motivated to search exhaustively for potential side effects. One pointer towards this is that, although evidence of liver damage is documented in the majority of trials, new cases of diabetes being diagnosed was only documented in three of the 29 trials assessed in the recent study.
Second, many trials do not state clearly how often adverse effects were assessed.
Third, some trials’ inclusion criteria narrow the population spectrum by excluding patients with severe diabetes, kidney failure or high blood pressure. In reality, though, these individuals may come to be prescribed and take statins.
Fourth, trial volunteers tend to be enthusiastic, and may therefore be less likely to report side effects than patients in routine clinical practice.
Fifth, 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.
Finally, many trials exclude patients on medication sharing the same liver metabolic pathway as statins (e.g. fibrates and macrolide antibiotics). Patients on such drugs might well suffer higher rates of pharmacologically mediated effects.
I make no secret of the fact that I think the benefits of statins are over-hyped and that the adverse effects are generally downplayed. As a result, a cynical observer might read my reservations here and think ‘well, he would say that’.
But, here’s the kicker: those six issues I detail above were plucked from the study in question (much of what I wrote was actually taken verbatim).
So, by their own admission, there are many reasons why the adverse effect rates seen in studies do not accurately reflect the rates seen in the real world. Then, how can the authors conclude that: ““Only a small minority of symptoms reported on statins are genuinely due to the statins: almost all would occur just as frequently on placebo.” The reality is the deficiencies of the studies do not allow them (or anyone) to conclude that at all. The authors’ conclusion is actually totally at odds with their own admissions about the untrustworthiness of the study data.
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