Selenium, Statins and Cognitive Decline

Just having completed a piece on the importance of selenium to muscle function and the serious implications of the selenium inhibiting effects of statin drugs, I was surprised to find this article calling attention to the role of selenium in cognitive decline.

Physicians prescribing statins need only to look at a schematic of the mevalonate pathway to know at a glance what to expect. Drug companies tell us their statins work by inhibition of the reductase step in the mevalonate biochemical path thereby inhibiting cholesterol synthesis.

Far more important is what they do not tell us of the other branches of the mevalonate tree, inhibited just as surely and inevitably as cholesterol. The reductase step is at the very beginning of the mevalonate path, the very base of this many-branched tree. Any gardener knows that girding a tree at its base affects all its branches not just one. And so it is that we lose our CoQ10, dolichols, and normal phosphorylation pathways and our selenoprotein pathway, the subject of this article.

Inhibiting selenoproteins is not just a chance occurrence. It is an inevitable consequence in every statin user. Perhaps this is why Muldoon has found in two major studies, one in 2001 with Mevacor and one in 2004 with Zocor, showing 100% cognitive decline in statin users if sufficiently sensitive testing is done.

Dr. Akbaraly, of Universite Montpellier, France and colleagues reported in Epidemiology a longitudinal cohort study suggesting that selenium status decreases with age and may contribute to declines in neuropsychological functions among the elderly. The researchers recruited 1389 community-dwelling French subjects during 1991 to 1993 for a 9-year longitudinal study with 6 waves of follow-up. The participants ranged in age from 60 to 71 years at baseline when they provided information on sociodemographic factors and were tested to assess cognitive function.

Selenium levels were determined using atomic absorption spectrometry. The investigators report that cognitive decline was associated with decreases of plasma selenium over time after controlling for potential confounders. "Our results, together with information on involvement of selenoproteins in brain functions, support possible relationships between selenium status and neuropsychologic functions in aging people," Dr. Akbaraly's team concludes. "In this context, the preventive effect of selenium supplementation at a nutritional level needs to be evaluated with large-scale studies," they suggest.

I see this as yet another mechanism explaining statin's legacy of cognitive decline.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor

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