Cholesterol is made by the liver, predominantly in the evening hours of the day. Statins (Crestor, Lipitor, etc.) are one of the most widely prescribed medications in the world and are used to lower cholesterol levels. However, their use in patients is often inappropriate because these medications have some unique properties not seen in other pharmaceuticals. Today, I would like to discuss some misconceptions about statins.
Statins work in the liver to reduce cholesterol levels. They inhibit the enzyme HMG CoA reductase, a key enzyme in the cholesterol synthesis pathway. Consequently, by reducing cholesterol levels, they also reduce levels of LDLc, aka “bad cholesterol,” but by what is known as a downstream process. The liver has LDLc receptors that remove LDLc from the blood. Lowering cholesterol levels raises the number of LDLc receptors, thereby removing more LDLc. Two researchers won the Nobel Prize in 1985 for discovering this process. When statins were first introduced, they had short half-lives (survival time in the bloodstream), which meant they had to be taken in the evening to be effective. Newer, high-potency statins were introduced (Crestor, Lipitor), which have much longer half-lives. In fact, Lipitor has active metabolites (breakdown products) that make its half-life effectively nearly 30 hours. This means that these high-potency statins do not need to be taken at night but can be taken in the morning with other medications. This patient convenience factor is a significant reason to use only high-potency statins. Another factor favoring their use is that high doses of lower-potency statins like simvastatin (i.e. 80 mg) can lead to a life-threatening muscle breakdown condition called rhabdomyolysis.
Statins reduce coronary events as well, but not just because they lower cholesterol levels. They are also strong anti-inflammatory agents and they lower inflammation markers like C-reactive protein. By reducing inflammation, they stabilize existing blood vessel plaques (deposits in arteries) and prevent them from breaking off and causing a heart attack or stroke. Also, statins impair glucose tolerance, meaning they may cause small elevations in hemoglobin A1c and may cause someone with pre-diabetes to become an overt diabetic. This diabetogenic effect is dose-related and is not seen in doses under 20 mg, another reason to use high-potency statins. At any rate, most pre-diabetics progress to diabetes on their own anyway, and the cardioprotective effects of statins, especially in diabetics, is too great to be ignored.
Many patients are convinced that statins give them muscle aches (myalgias) and therefore refuse to take them. This is called a nocebo effect and has been shown in many studies. The nocebo effect, which is believing that you have a known side effect of a medication, is the opposite of the placebo effect, which is believing that you received an expected positive result of taking a drug despite taking the placebo and not the drug. As we age, most of us, me included, get lots of muscle aches and soreness. Studies have shown that when given a series of medications including a statin, most self-proclaimed statin intolerant subjects were unable to identify which drug was the statin. True statin-related myalgia is rare and occurs in about 1 out of 1000 statin users. Statins are safe and effective medications to prevent cardiovascular events. If you are not on one and think you should be, speak to your doctor.