Television show questions statins to boost ratings, Dutch doctors claim

BMJ 2007; 334 doi: (Published 22 March 2007) Cite this as: BMJ 2007;334:604

Statins - public debate long overdue

The public debate over statins is long overdue.
Doctors and patients should realize that statins do not extend lives in women or elderly, and the results in men are all but clear. The
bad news first:

Atorvastatin, Lipitor[tm], for example, has shown (versus placebo) not to reduce infarct in women [ASCOT] or fatal myocardial infarct in men [SPARCL], not to reduce mortality in anyone, not to slow calcification [Medline 16415377 and 15944423] and to cause the ubiquinone [CoQ10] lowering detriment [mitochondrial function, myalgia] a mevalonate production reducer is expected to cause [it takes 10 mevalonate molecules to make CoQ10, 6 to make cholesterol]. Top-dose atorvastatin lowers both blood CoQ10 and LDL-cholesterol levels by 50% [Medline 15210526].

The good news is that one can consider atorvastatin as mild antiinflammatory, or as a 'nitroglycerin mimic' [promoting the NO-synthase pathway and thus arterial compliance] with a 40% reduction in angina [ASCOT]. However, just like the pain reduction from a COX-2 inhibitor would keep people away from a knee surgeon, a reduction in angina pain would be expected to keep patients away from cath-labs, explaining fewer 'interventions' in some combined-endpoint 'event' studies.

Atorvastatin reduces angioplasty incidence but so does going to a non-cathlab hospital FIRST after acute coronary syndrome and when the chances to eventually wind up with a balloon or by-pass intervention are both reduced by 90% -- while the chance of being alive at 6 months was found to be not less but in fact 14% greater [Medline 1566006]. Atorvastatin lowers 'interventions' by possibly 40%, your choice of first hospital by 90%. The lack of any mortality benefit from atorvastatin suggests that we are treating and affecting symptoms, not the fundamental cause of arterial decline and deaths.

A mevalonate synthesis inhibitor lowers the amount of LDL since it takes ~48% cholesterol to create a stable LDL particle but it does not alter LDL composition (quality) for the better -that could be effected by reducing homocysteine, by lowering trans-fat intake and by healthy levels of carotenoids, tocopherols, CoQ10 and omega-3 content of the LDL particles, avenues that need urgent exploration.

The simplified picture and the core of the debate is here:

Competing interests:
None declared

Competing interests: No competing interests

25 March 2007
Eddie Vos
Sutton (Qc) Canada J0E 2K0