Sometimes researchers provide valuable insights; many times their data and/or message gets manipulated into something that is hard to fathom, let alone understand.
Take, for instance, a recent news story about a study looking at the link between red meat consumption and heart disease. The story tries to make a case that consuming meat per se doesn’t increase the risk of cardiovascular disease (red flags should start shooting up if you do any research at all on the interaction between diet and health) but that a chemical called carnitine, that just happens to be found in red meat is really to blame. What’s ironic about this statement is that the CBS cover story goes on to supply most of the arguments needed to punch holes in this theory, almost to the point of being laughable.
A quick digression – carnitine is a chemical that is known to help shuttle fats into the cells where they can be used for energy. The heart uses a lot of carnitine to help supply all the energy it needs to run smoothly and many studies have been done that show cardiovascular benefits with carnitine use.(1-3) Red meat and dairy products are the highest dietary sources of carnitine, but many people take carnitine in supplemental form to avoid all the negative complications from consuming meat and dairy.
The study mentioned in this article shows that diets high in red meat promote the growth of a gut bacteria that breaks down carnitine into a compound called trimethylamine-N-oxide (TMAO). TMAO may promote the growth of plagues in the arteries by preventing the breakdown of cholesterol, which can increase the risk of heart disease. The researchers, and the person that wrote this story, somehow concluded that the carnitine was to blame for the increased heart disease risk, completing missing the point that consuming red meat led to the gut bacteria changes that created the environment where carnitine could be a problem.
To further illustrate this point, these same researchers showed that only those people that consumed red meat regularly had high levels of TMAO, which in turn could lead to atherosclerosis. Vegans and vegetarians did not have high levels of TMAO, even with carnitine supplementation. Clearly, something was very different between these two study groups – red meat consumption. Therefore, the common sense conclusion would be that consuming red meat is the problem, not the carnitine.
By trying to focus their spotlight on carnitine, these researchers (and whoever paid for this study) are spinning their conclusions to an extent I have rarely seen outside of politics. One of the researchers was even quoted “We need to examine the safety of chronically consuming carnitine supplements as we’ve shown that, under some conditions, it can foster the growth of bacteria that produce TMAO and potentially clog arteries.” What he failed to mention is that eating red meat is the ‘condition’ he is referring to.
References
- Cacciatore L, Cerio R, Ciarimboli M, Cocozza M, Coto V, D’Alessandro A, D’Alessandro L, Grattarola G, Imparato L, Lingetti M (1991). “The therapeutic effect of L-carnitine in patients with exercise-induced stable angina: a controlled study”. Drugs Exp Clin Res 17 (4): 225–235. PMID 1794297.
- Bartels GL, Remme WJ, Pillay M et al. (July 1994). “Effects of L-propionylcarnitine on ischemia-induced myocardial dysfunction in men with angina pectoris”. The American Journal of Cardiology 74 (2): 125–130. doi:10.1016/0002-9149(94)90084-1. PMID 8023775. \
- Michael A. Arsenian (November – December 1997). “Carnitine and its derivatives in cardiovascular disease”. Progress in Cardiovascular Diseases 40 (3): 265–286. doi:10.1016/S0033-0620(97)80037-0. PMID 9406679
