Chapter 6 - Statins: Rationale, Mode of Action, and Side Effects

Abstract

Cholesterol is an essential lipid molecule that maintains the structural integrity and fluidity of all cell membranes over varying physiological conditions. Cholesterol interacts with phospholipid fatty acid chains in the cell membrane and increases membrane packing, which alters membrane fluidity and maintains membrane integrity. In 1976, Akira Endo at the Sankyo Company, Tokyo, identified the first inhibitor of the HMG-CoA reductase, which drives down the levels of intracellular cholesterol, thereby embarking on the long journey of evolution of statin drugs. Studies have shown that statin use has induced diabetes mellitus, cancer, early premature cataracts, hearing loss, suicidal ideation, peripheral neuropathy, depression, benign intention tremors and Parkinson's disease, pulmonary interstitial pneumonitis and dysfunctional breathing, interstitial cystitis and bladder wall instability, herpes zoster, impotency, and cognitive impairments. One of the most interesting findings was that elderly people with the highest LDL cholesterol levels lived longer than elderly people on statin treatment. A reasonable question is therefore: Why should we lower the bad cholesterol if those with the highest values live the longest? There are many factors that contribute to the development of heart disease. Statin treatment will ultimately offer little protection against risk. While results from trials are positive, the trials in their totality must always be taken into account as they are often powered by drug companies. These results can be full of statistical deception with raw data that is obscured from any scrutiny, they can have inadequate methodologies, and they can be biased in reprehensive outcomes.