The authors of a paper in the journal Expert Review of Clinical Pharmacology didn’t hold back in their scathing condemnation of statin drugs (intended to reduce cholesterol levels). The abstract alone is quite an indictment of these drugs: “In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis we present a perspective that statins may be causative in coronary artery calcification […] the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs.”
Controversy over the use of statin drugs is nothing new. The Food and Drug Administration (FDA) acknowledges that these agents increase the risk for elevated blood sugar and development of type 2 diabetes. This is alarming considering statins are often prescribed in lock-step with a diagnosis of type 2 diabetes owing to the cardiovascular complications that typically result from this condition. If statins come with a risk for elevated blood sugar—and the prestigious Mayo Clinic informs the public that they do—then it seems counterproductive for people trying to lower chronically elevated blood sugar to take a drug that does the opposite.
Moreover ironically frequent statin use is associated with acceleration of coronary artery calcification among type 2 diabetics with advanced atherosclerosis. This finding fits in with numerous studies showing that while statins are effective for lowering LDL cholesterol (LDL-C) a reduction in LDL-C doesn’t automatically translate into improved cardiovascular outcomes or reduced mortality. For example use of torcetrapib a drug that demonstrably raised HDL and lowered LDL “resulted in an increased risk of mortality and morbidity of unknown mechanism.” (Emphasis added.) Yes a drug that raised the “good” cholesterol and lowered the “bad” cholesterol actually led to worse health outcomes. But this isn’t news either. Data pooled from many studies show that while statins are effective for lowering LDL-C there are often no significant benefits for prevention of coronary heart disease. And if the point of statin drugs is to reduce cholesterol in order to protect cardiovascular health—but there’s evidence that statins might actually exacerbate existing damage and trigger new pathologies—then it’s hard to understand why they’re still so widely prescribed.
Other alarming “side effects” of statins that Mayo Clinic and FDA cite are cognitive impairment confusion fuzzy thinking memory loss and forgetfulness that “span all statin products and all age groups.” FDA acknowledges that “the symptoms were not serious and were reversible within a few weeks after the patient stopped using the statin” – but how often do physicians advise patients to discontinue statin use?
The potential neurological and cognitive effects of statins are especially troubling considering that higher cholesterol later in life is associated with reduced risk for dementia. Older individuals with higher serum cholesterol have better cognitive function than those with lower cholesterol leading researchers to write “low cholesterol may serve [as] a clinical indicator of risk for cognitive impairment in the elderly.” This seeming “paradox” is not limited to cognitive function. High LDL-C is inversely associated with mortality in most people over 60 years which has researchers questioning the validity of the cholesterol hypothesis and calling for a re-evaluation of guidelines that recommend reduction of LDL-C in the elderly.
After decades of low fat diets and demonization of dietary fat we now understand that the “French paradox” and “Spanish paradox” aren’t paradoxes at all and that fat—including saturated fat—is not the enemy of good health. So perhaps higher cholesterol being protective later in life is not a paradox either. Maybe we have simply been very wrong about cholesterol all along—at least in some ways.
The Expert Reviews paper discusses additional mechanisms by which statins may directly contribute to cardiovascular damage such as inhibiting the synthesis of vitamin K2. This little-known and underappreciated vitamin is required for activating enzymes that control calcium trafficking in the body—that is depositing it into bones and teeth (where we want it) and keeping it out of soft tissues such as arterial walls (where we don’t want it). Another key mechanism is impairment of the electron transport chain that produces energy (ATP) inside the mitochondria. This may be responsible for the well-known symptoms of fatigue and muscle pain and weakness frequently reported among statin users. The implications are not trivial. According to the authors of the paper “Statins have been demonstrated to decrease the concentration of mitochondria in muscle. In view of this obvious skeletal muscle toxicity it would be naive to assume that statins would not likewise negatively impact the much harder working heart muscle cells which have exceedingly high ATP requirements.”
This is not intended as an across-the-board condemnation of statin drugs. These medications may be warranted in some cases and there are people for whom they are beneficial. But the increasingly worrisome “side effects” – which are not really side effects at all but are direct consequences of disrupting the cholesterol synthesis pathway which affects a host of other systems in the body – warrants caution. As always work with your physician to monitor your cardiovascular health and determine appropriate courses of action.