High cholesterol runs in my husband’s family. After being prescribed a statin medication to bring down her cholesterol numbers, however, my mother-in-law suffered debilitating pain and muscular dysfunction, prompting her to prefer the risks of foregoing it to losing the freedom to run, walk, and use her two hands. So when The Atlantic reported this week that scientists have discovered a possible explanation for the statin muscular problem, I was immediately intrigued. 

The widespread use of statins to treat high cholesterol has been growing since the early 2000s. U.S. government data from the Medical Expenditure Panel Survey (MEPS) showed that, between 2000 and 2010, purchases of statin cholesterol medications rose from 3.4 million to 9.5 million prescriptions, an increase of 179 percent. The statin sales rate outpaced the growth of two other fast-growing pharmaceutical markets, those of antidiabetics and antihypertensives. And while antidiabetics in the form of semaglutides like Ozempic and Wegovy have skyrocketed in popularity in the last few years, changing guidelines on what healthy cholesterol levels look like have continued to expand the circle of Americans deemed in need of prescription medication, while Americans struggle to keep up.

Muscular pain, aches, and weakness are fairly common side effects of these medications. While clinical trials only found muscular dysfunction in 5 percent of statin-using patients, observational studies recorded a much higher 30 percent, which is consistent with anecdotal evidence. Still, enough users have no trouble with the drug that the connection has remained baffling.

That is, until recently, when two groups of scientists stumbled upon a potential explanation while studying an unrelated muscular disease. What these Mayo Clinic doctors found was that patients with the muscular disease had mutations in a gene encoding in an enzyme: HMG-CoA reductase, the same enzyme that statins block in the process of halting cholesterol production. In other words, problems with this enzyme, whether caused by a genetic disease or by a cholesterol-reducing drug, seem to signal problems for healthy muscular function as well. 

Surprisingly to absolutely no one, this discovery has arrived hand-in-hand with a brand new drug to treat the problem. Mevalonolactone, as it is called, has shown promise in treating statin-induced limb weakening in mice, and increased limb control for one bedridden Bedouin woman with a genetic disease. And so, we are told, “problem solved.” For every problem, a pill; for every pill, a side effect; for every side effect, another encapsulated solution. Rinse and repeat.

A few steps removed from the granular level of mutated genes, HMG-CoA reductase, and cholesterol standards that your grandfather could never have met, however, is the broader question of what it means to be healthy. Why, in other words, is cholesterol considered to be bad enough that doctors would prescribe more drugs for the side effects of statins rather than returning to the root? 

The history of high cholesterol as a medical bogeyman is a long one, too long to be chronicled here. It is enough, for now, to note that standard medical practice today links high cholesterol to heart disease and stroke. 

But one of the few long-term, controlled studies on the health effects of vegetable oils done in 1968–73, the Minnesota Coronary Experiment, casts doubt on this bedrock belief, as I have previously reported. The experiment was one of the most rigorous ever conducted on vegetable oils and cholesterol in the human diet, and included 9,423 participants in state mental hospitals and nursing homes, between the ages of 20 and 97 years old. Participants were studied for 56 months, both groups eating the same healthy diet, with the exception of fats: one group’s fats came exclusively from corn oil, the others from animal fats. 

What the experimenters found was remarkable: While substituting vegetable oils for animal fats lowered the total level of cholesterol in the participants’ blood, this lowered cholesterol did not result in longer life. In fact, as cholesterol fell lower, the risk of death increased—22 percent for each thirty-point fall. Incidence of heart attacks, most notably, was unchanged in the first group, despite their eating what is still today considered to be the gold standard of a “heart healthy” diet. (Fifty-five years later, five of the seven oils on the American Heart Association’s list of recommended, “heart healthy” fats are still vegetable oil.)

It is enough, in short, to say that there is more to the story here than what we have been told. While scientists’ understanding of cholesterol, its purpose in the body, and the effects of blocking its production, is incomplete, their eagerness to sell pharmaceutical solutions to the perceived problems is nevertheless unabated. Their Baconian belief in nature as a machine, in which there’s always a technical—or pharmaceutical—solution, suggests that every part is interchangeable, that one cog can be added or removed and the others will still hold constant.

But this is not the way that nature works. The fabric of the human body is deeply integrated, and the discovery of the enzyme linking two seemingly unrelated parts—cholesterol production and muscular function—could not more beautifully depict that. The mere fact of our not understanding it should inspire a reverence for the processes as they exist, rather than an eagerness to stick our fingers in the holes.