Cholesterol and Vascular Disease Part 4: The Great Statin Debate

It has been unequivocally established that high levels of LDL can lead to heart attacks and strokes. Parts 1- 3 of this blog described the history of cholesterol, the superiority of LDL particles over LDL cholesterol, and the pathophysiology associated with an overabundance of LDL particles. In addition to our understanding of the biological process whereby LDL particles cause vascular disease, we also have a plethora of clinical trials demonstrating the efficacy of lowering LDL.

Everyone–lay people, physicians, and scientists–is plagued by the overabundance of clinical trials involving all aspects of health and medicine, many of which clearly contradict one another. In order to practice medicine in a fashion that appropriately considers the outcomes of these clinical trials, one must find a way to make sense of them. My approach has been to evaluate the clinical trials not just individually, but as a whole. I look for trends. When studies repeatedly reach the same conclusions (especially when they pathophysiologically “make sense”) I feel much more comfortable concluding that they are correct. In the case of LDL we find a commonality that is indisputable. The studies repeatedly demonstrate that statins–a class of cholesterol lowering medications I will momentarily describe–uniformly decrease the risk of cardiovascular events by about 30%. This event reduction is consistent among patients in the setting of both primary and secondary prevention. And so we must listen to the studies and lower our patients’ LDLs accordingly.

Statins are the class of medication for cholesterol management that unequivocally possess the greatest amount of science supporting their use. These medications work by blocking a critical enzyme in our body’s production of cholesterol. In response to lower levels of cholesterol within our cells, the cells increase surface receptors to bring in more LDL particles. The result is a diminution in the number of LDL particles – as well as the LDL cholesterol – in our bloodstream. This cholesterol-lowering can clearly translate into fewer heart attacks and strokes, as well as a prolonged life span. Unfortunately statins have taken quite a beating in the lay press. Naysayers point to the possible side effects of statins and decry their use. By doing so I believe these individuals cause far more harm than good. I have personally witnessed patients discontinuing the statins because of the severe in stilled in them by lay writers. Some of these patients have such severe coronary artery disease that the discontinuation of their medication can lead to an imminent threat to their lives. The cynics’ criticism is also quite misleading. All medications have potential side effects and statins are no different. Read any package insert and you will likely be very reluctant to take any medication. It is true that statins can cause weakness, fatigue, muscle pain, short term memory loss, blood sugar abnormalities, and in the worst case scenario, death. It is also true that statins can decrease our body’s store of the critical energy producing coenzyme, but let’s be accurate about the CoQ10 issue.

Our bodies “burn through” about 3.4 mg of CoQ10 daily. Approximately a half of this is endogenously produced (we make it); the other half is consumed. So in the worst case scenario (which is grossly exaggerated) the entire 1.7 mg of CoQ10 is lost through statin use, and must be replaced by increasing our CoQ10 ingestion. As CoQ10 is poorly absorbed – only about 3 to 8% of what we ingest makes it into our bloodstream – we need to ingest much more than 1.7 mg. But how much do we really need in this situation? Let’s do the math using the lowest absorption possible, 3%. 3% of how much will give us our missing 1.7 mg? The answer, a mere 56.7%! That’s right, in a worst-case scenario to replace your statin-induced missing CoQ10 you need to take only about 50 mg. To be undeniably safe, you can take 100 mg. But why, I ask you, would you spend so much of your hard-earned money on 200, 300, or even 400 mg of CoQ10 when you need so much less? In an attempt to remain healthy, please don’t be fooled by misleading nutritional supplement marketing!

Let’s examine the other side effect possibilities. As cardiovascular disease remains the leading cause of death in the Western world these side effect possibilities (which occur only infrequently) are greatly outweighed by the well-documented benefits of statins. Therefore a medication that can decrease this risk will have a huge impact on an enormous number of people. That is why statins are so important. One final criticism should be examined – can statins lower LDL to such a great degree that our cells become starved for cholesterol? For two reasons the answer to this question is an unequivocal no. First, every cell in our body has the capacity to make cholesterol. Therefore, in the setting of low LDL, cells that need more cholesterol simply make it. Second, recently people have been identified with genetic abnormalities resulting in LDL C levels as low as 2 mg/dl. These individuals not only function completely normally (there is not issue with their extraordinarily low LDL) they also don’t get heart disease.

In sum, the bottom line when it comes to statins: Please understand that doctors go to medical school in order to help their patients.  When they prescribe statins they’re doing so for no reason other than to try to improve and prolong your life.  That does not mean that you shouldn’t raise any concerns or questions you may have.  Having open and honest discussions with your physician is paramount in achieving the optimal patient-doctor relationship. Next week we’ll look at some other cholesterol altering medication your doctor might want to prescribe.

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