Should we lower cholesterol as much as possible?

Editor—As Ravnskov et al state,¹ any revision of targets needs to be evidence based and responsible, taking into account the risks and benefits of such a measure. However, some of the authors' assertions are unclear and potentially misleading.

They do not explain in what way lowering coenzyme Q10 is harmful. The study of Rundek et al, one of the few that measured Q10 values, did so in insufficient numbers of patients, and the authors still conclude significance despite failing to show anything statistically solid.²

In one of the largest studies to date, the heart protection study, no evidence was found for neuropsychiatric and pulmonary side effects above placebo level.³ With regards to cancer, Ravnskov et al disregard recent evidence that statins seem to protect against several forms of cancer,⁴ not least colorectal cancer; instead, they favour older evidence. The heart protection study had cancer incidence (including various subtypes) as an end point, and no increased cancer risk was found in that trial.³

With respect to the authors' competing interests, three of them dispute the very association between hypercholesterolaemia and heart disease. In familial hypercholesterolaemia, in which young adults with no other risk factors may develop accelerated atherosclerosis, the underlying biochemical abnormality is well known (defects in low density lipoprotein receptors), thus making the authors' hypothesis almost completely untenable.

That a large proportion of the population may require pharmacological prophylaxis for cardiovascular disease seems counterintuitive. However, dietary patterns have deteriorated, we are in the middle of an obesity epidemic, and dietary measures are generally insufficient to mitigate cardiovascular risk in both hypercholesterolaemia and obesity. With the benefits of statins documented in several large studies, why deny statin treatment on the basis of comparatively inconclusive evidence?