In 1976, the Japanese biochemist Akira Endo isolated a novel substance from the fungus Penicillium citrinum, one that displayed a remarkable ability to inhibit cholesterol synthesis by cells (1). The substance, which he called compactin, was the first of the statins, a class of drugs that now stands in the midst of considerable controversy within the realm of medicine.
Since the 1990s, medical doctors have been prescribing statins copiously to their patients. This is best demonstrated by the rise of the drug atorvastatin, which during 1996 to 2012 became the best-selling pharmaceutical of all time (2). Today, statins are among the most widely prescribed drugs in existence, a behaviour that is endorsed by most cardiologists around the world (3).
Yet despite their meteoric rise and seal of approval from the medical mainstream, many members of the public are wary of these drugs. They prefer to turn to other health sources such as the alternative medicine proponent Dr Joseph Mercola, who openly argues against taking statins (4). Despite hordes of cardiologists recommending statins, many people reject this advice; they would rather go with Dr Mercola.
Alternative medicine proponent, Dr Mercola, is anti-statin.
Many medical doctors remain genuinely perplexed by this trend - why would anyone disregard the advice of numerous prestigious cardiologists and turn to other less reputable alternatives? The answer is quite simple, but before we address it, let's take a balanced look at statins, at how they work and their effects on human health.
How Statins Work
Mechanistically, statins work on two levels. First, they inhibit cell cholesterol formation. Second, they exert pleiotropic effects (multiple additional effects unrelated to the inhibition of cholesterol formation). It is necessary to understand both of these processes if we are to know how statins work.
Cholesterol is a lipid (fat) molecule synthesized by all animal cells. In addition to being a vital component of cell membranes, cholesterol is essential for the synthesis of steroid hormones, bile acids, and vitamin D. Statins inhibit the enzyme HMG-CoA reductase, the rate-limiting step in cell cholesterol formation (3). Since HMG-CoA reductase is the rate-limiting step, statins have broad and potent effects on the cholesterol profile - but there's a lot more to statins than that.
Cell cholesterol formation is a multi-step pathway; the step involving HMG-CoA reductase (top of diagram) is but one of many.