The problems with “malevolent cholesterol” hypothesis keep stacking up. They do not end with criticisms of the idea that lowering LDL (or cholesterol) will lower cardiovascular risk. Consider the main target of drugs like Lipitor – LDL – what everyone calls “the bad cholesterol.” As we have discussed, LDL is not cholesterol but rather a transport vehicle for cholesterol.
So why is LDL considered “bad”?
Dr. Ronald Krauss, a metabolism specialist based in San Diego, has studied cholesterol biochemistry in depth. Science journalist Gary Taubes quoted Krauss at length in his 2008 bestselling book, Good Calories, Bad Calories: “if you look at the literature and just look at the average coronary patients … their LDL cholesterol levels are often barely discernibly elevated compared to patients who do not have coronary disease.”
As Taubes put it, high LDL is “only a marginal risk factor.”
While working at Berkeley, Krauss discovered that LDL was actually heterogeneous – i.e., it came in different classes. Krauss came to believe that the number and sizes of those LDL classes might be far more important in terms of determining risk for cardiovascular disease than the total amount of LDL.
Drugs like Lipitor treat LDL as if it is some monolithic entity that is “bad” — a boogeyman that needs to be reduced by any means necessary.
But Krauss and other elite lipid researchers have shown that LDL is a much more complex entity. A large, fluffy kind of LDL may be benign — even helpful. A small, denser variant of LDL, also known as VLDL (or “very low density lipoprotein”), may be the one that’s the real troublemaker.
One theory suggests how VLDL particles might do their dirty work. McGill University cardiologist, Allan Sniderman, came up with a metaphor for VLDL, calling these particles “little bits of sand.” These gritty molecules may damage artery walls and lead to the formation of plaques — initiating a process that ultimately clogs arteries and causes heart disease and death. As Taubes notes in Good Calories, Bad Calories, VLDL particles may also cause structural changes in certain proteins that make them easier to adhere to artery walls. Because small, dense LDL remains in the blood stream longer than larger and fluffier LDL, it has more time and greater opportunities to do damage. Finally, it could be that LDL must be oxidized (i.e. “rusted”) before it can damage arteries: VLDL oxidizes much more easily than does regular sized LDL.
Biochemistry aside, if you have questions about a potential Lipitor case, connect with the attorneys at Davis & Crump now at 800-277-0300.
