On April 8, a story was widely disseminated in the news media claiming that carnitine, a nutritional supplement that has been shown to be effective for preventing and treating cardiovascular disease, might actually cause heart disease. The news stories referred to a study published the previous day in the journal Nature Medicine. However, as is often the case with negative media reports about vitamins, minerals, herbs, or other natural substances, the conclusions grossly misrepresented what the research actually showed. These reports were more than simply irresponsible; they were actually harmful to the public health, because they inappropriately scared people out of taking a safe substance that can relieve heart-disease-related symptoms, and in some cases, prolong life.
Carnitine is manufactured by the human body and also occurs in various animal foods, particularly red meat. Its chief function in the body is to facilitate the transport of fatty acids into mitochondria, where they are metabolized to produce energy. Double-blind clinical trials have shown that carnitine supplements can increase exercise capacity in people with heart disease-related chest pain (angina). In addition, people with intermittent claudication (a condition caused by atherosclerosis of the lower extremities) were able to walk farther without pain after they were treated with carnitine for six months. In patients with congestive heart failure, carnitine supplementation increased exercise capacity, improved heart function, and increased survival times. And in a randomized controlled trial, patients started on carnitine supplements shortly after suffering a heart attack had a 90 percent decrease in mortality over the next 12 months, compared with people who did not receive carnitine.
So, what about the study that claimed carnitine is bad for the heart? That conclusion was based on two main points. First, supplementation of a particular strain of mice with carnitine promoted the development of atherosclerosis, apparently because it was converted by intestinal bacteria to a heart-damaging compound, trimethylamine-N-oxide (TMAO). Second, in an observational study of 2,595 human subjects undergoing evaluation for possible heart disease, higher blood levels of carnitine were associated with a higher incidence of "cardiac events" such as heart attacks, strokes, and heart disease-related deaths. Neither of these points warrants the conclusion that carnitine is harmful to the human cardiovascular system.
Regarding to the first point, mouse biochemistry differs in many ways from that of humans, and findings in mice do not necessarily apply to humans. Moreover, the mice that were used in this research were genetically engineered so that they lacked a key enzyme involved in fat metabolism, and were therefore especially susceptible to developing atherosclerosis. While the new research found that intestinal bacteria in humans can also convert carnitine to TMAO, a vast body of previous clinical research (mentioned above) suggests that the beneficial effects of carnitine outweigh any potential deleterious effect of its breakdown product, TMAO.
With regard to the observational study of 2,595 subjects that linked higher blood carnitine levels to heart disease, the researchers were able to demonstrate such an association only after manipulating the data. Normally, statisticians are supposed to adjust their numbers to account for "multiple comparisons." For example, five heads in a row when flipping a coin five times would be considered a statistically significant event. In contrast, it would be easy to find five heads in a row when searching through 100 consecutive coin flips, and that finding would not be considered statistically significant. The researchers acknowledged that their supposed carnitine-heart-disease link was not statistically significant, according to commonly accepted criteria. It only became significant when they used "less stringent" (i.e., mathematically inappropriate) criteria.
Even if a true association did exist between blood levels of carnitine and heart disease, there would be no reason to assume that such an association indicates cause-and-effect. Cardiovascular disease is often associated with impaired kidney function, and weak kidneys have a reduced capacity to excrete carnitine. Consequently, higher carnitine levels might be a consequence, rather than a cause, of heart disease. It is noteworthy that the observed association between heart disease and carnitine levels disappeared completely when the researchers corrected for differences in kidney function. That key point was not mentioned in the media reports, and the researchers themselves were apparently unaware of its importance.
The bulk of the scientific evidence indicates that carnitine is beneficial for the heart, and the conclusion circulated by the media that carnitine is harmful is unwarranted. One wonders why natural-medicine-bashing junk science so often makes its way into the news.
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