In a perfect world, we'd have clear answers to all of our most pressing questions about health and nutrition. Research findings would be unassailable, doctors would have absolute confidence in the recommendations they make and treatments they prescribe, and the general public would rest assured that the latest scientific study being reported on says exactly what it claims to say.
But unfortunately we don't live in a perfect world -- we live in the real world. And in the real world, the science that informs our beliefs about nutrition and health is not black and white, but decidedly gray. The messy process of scientific inquiry is at odds with the desires of policy makers, clinicians, the media, and the general public, all of whom -- quite understandably -- crave certainty and unequivocal guidance. Yet "what is never stressed enough," according to Dr. Richard Sharpe in a recent Forbes magazine interview, "is that scientists work 'at the borders of ignorance' ... This means we are wrong most of the time, and because of this, scientists have to be very cautious about interpretations that are based on our projected ideas about what is in front of us."
I was reminded of this as I read the recent news stories about two new studies from Dr. Stanley Hazen's team at the Cleveland Clinic. These studies have been widely and uncritically reported as new evidence that meat and other animal products like eggs increase the risk of cardiovascular disease. But are the results really as clear cut as the researchers and media reports have claimed, or is there more "gray" in the story?
The fascinating premise of the two studies is that the bacteria in our gut play a significant role in converting nutrients in the food we eat to potentially harmful substances. In the first study, they showed that gut bacteria transform carnitine (found predominantly in red meat) into a chemical called TMAO. In the second study, they showed exactly the same thing -- except in this case the bacteria converted choline (found in eggs, beef liver, and other animal foods) into TMAO. In both studies, they also presented evidence that high levels of TMAO are associated with increased risk of cardiovascular disease. They proposed that TMAO might be a better explanation for the link observed in some (but not all) studies between red meat and heart disease, because recent research has cast doubt on the longstanding theory that saturated fat and cholesterol in animal foods are to blame.
But while at first glance the papers from Dr. Hazen's group might appear to be the final nail in the coffin for the omnivorous among us, a closer inspection of their data reveals some troubling questions. First, a study back in 1999 found that seafood generates much higher levels of TMAO than red meat, eggs, or any of the other 46 foods tested. One species of fish, halibut, produced 107 times as much TMAO as beef, and 53 times as much TMAO as eggs. If high TMAO levels cause cardiovascular disease, and eating fish increases TMAO more than any other food, we'd expect to see high rates of heart disease in people who eat the most fish. Yet that is the opposite of what research shows. In fact, some studies have found eating more fish (particularly cold-water, fatty fish like salmon) reduces the risk of heart attack by a greater margin than statin drugs!
Likewise, research hasn't shown a link between eating eggs and cardiovascular disease. One huge study in the British Medical Journal that followed almost half a million people for up to 20 years found no association between higher egg consumption (up to one per day) and heart attack or stroke. On the contrary, an analysis of data from the National Health and Nutrition Examination Study found that those who ate more eggs had lower rates of stroke. Some studies have even suggested that eating eggs may protect against cardiovascular disease. Eggs are an important source of heart-healthy nutrients, like vitamins C, E, B12, and B9 (folate).
In their second paper, Dr. Hazen's team raises the possibility that the foods we eat aren't the primary driving force behind our TMAO levels, because most people are able to excrete excess TMAO that accumulates in the blood via the urine. This suggests that something else may be to blame for high TMAO. What could that be? One possibility, which the researchers themselves demonstrated in the first paper, is that differences in our gut bacteria could account for the higher TMAO levels observed in some people. They showed that those with greater amounts of a type of bacteria called Prevotella in their gut generated more TMAO after eating carnitine. And what might lead to a higher concentration of Prevotella in the gut? Ironically, previous research has shown that the people who eat large amounts of whole grains are the most likely to fit this pattern. This would suggest that a diet high in whole grains -- and not red meat or eggs -- could increase the risk of heart disease by elevating TMAO in the blood.
Most of us don't tolerate uncertainty very well. We want unambiguous guidance we can act on. But ultimately this desire for certainty works against us in the realm of science and medicine. Scientific progress requires us to continually challenge our beliefs and revise even our most cherished hypotheses. "As scientists," Dr. Sharpe said in the Forbes article, "we all like our ideas and hypotheses to be proved correct; yet, there is equal merit in being proved wrong."
Dr. Hazen's group has made an important contribution to the understanding of how our gut bacteria may contribute to cardiovascular disease, but they have not implicated animal foods as the culprit. For more than half a century we were told that red meat and eggs are bad for us because they raise our cholesterol, only to find that the evidence supporting this hypothesis is weak at best. Let's not make TMAO the new cholesterol.
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