Kevin Tracey, a neurosurgeon based in New York, is a man haunted by personal events – a man with a mission. “My mother died from a brain tumor when I was five years old. It was very sudden and unexpected,” he says. “And I learned from that experience that the brain – nerves – are responsible for health.”
This background made him a neurosurgeon who thinks a lot about inflammation. He believes it was this perspective that enabled him to interpret the results of an accidental experiment in a new way.
In the late 1990s, Tracey was experimenting with a rat’s brain. “We’d injected an anti-inflammatory drug into the brain because we were studying the beneficial effect of blocking inflammation during a stroke,” he recalls. “We were surprised to find that when the drug was present in the brain, it also blocked inflammation in the spleen and in other organs in the rest of the body. Yet the amount of drug we’d injected was far too small to have got into the bloodstream and traveled to the rest of the body.”
After months puzzling over this, he finally hit upon the idea that the brain might be using the nervous system – specifically the vagus nerve – to tell the spleen to switch off inflammation everywhere.
It was an extraordinary idea – if Tracey was right, inflammation in body tissues was being directly regulated by the brain. Communication between the immune system’s specialist cells in our organs and bloodstream and the electrical connections of the nervous system had been considered impossible. Now Tracey was apparently discovering that the two systems were intricately linked.
The first critical test of this exciting hypothesis was to cut the vagus nerve. When Tracey and his team did, injecting the anti-inflammatory drug into the brain no longer had an effect on the rest of the body. The second test was to stimulate the nerve without any drug in the system. “Because the vagus nerve, like all nerves, communicates information through electrical signals, it meant that we should be able to replicate the experiment by putting a nerve stimulator on the vagus nerve in the brainstem to block inflammation in the spleen,” he explains. “That’s what we did and that was the breakthrough experiment.”
By Gary Taubes, author of Nobel Dreams (1987), Bad Science (1993), Good Calories, Bad Calories (2007), and Why We Get Fat (2011). Taubes is a former staff member at DISCOVER. He has won the Science in Society Award of the National Association of Science Writers three times and was awarded an MIT Knight Science Journalism Fellowship for 1996-97. A modified version of this post appeared on Taubes’ blog.
The last couple of weeks have witnessed a slightly-greater-than-usual outbreak of extremely newsworthy nutrition stories that could be described as bad journalism feasting on bad science. The first was a report out of the Harvard School of Public Health that meat-eating apparently causes premature death and disease (here’s how the New York Times covered it), and the second out of UC San Diego suggesting that chocolate is a food we should all be eating to lose weight (the Times again).
Both of these studies were classic examples of what is known technically as observational epidemiology, a field of research I discussed at great length back in 2007 in a cover article for in the New York Times Magazine. The article was called “Do We Really Know What Makes Us Healthy?” and I made the argument that this particular pursuit is closer to a pseudoscience than a real science.
As a case study, I used a collaboration of researchers from the Harvard School of Public Health, led by Walter Willett, who runs the Nurses’ Health Study. And I pointed out that every time that these Harvard researchers had claimed that an association observed in their observational trials was a causal relationship—that food or drug X caused disease or health benefit Y—and that this supposed causal relationship had then been tested in experiment, the experiment had failed to confirm the causal interpretation—i.e., the folks from Harvard got it wrong. Not most times, but every time.
Now it’s these very same Harvard researchers—Walter Willett and his colleagues—who have authored the article from two weeks ago claiming that red meat and processed meat consumption is deadly; that eating it regularly raises our risk of dying prematurely and contracting a host of chronic diseases. Zoe Harcombe has done a wonderful job dissecting the paper at her site. I want to talk about the bigger picture (in a less concise way).
This is an issue about science itself and the quality of research done in nutrition. Science is ultimately about establishing cause and effect. It’s not about guessing. You come up with a hypothesis—force x causes observation y—and then you do your best to prove that it’s wrong. If you can’t, you tentatively accept the possibility that your hypothesis might be right. In the words of Karl Popper, a leading philosopher of science, “The method of science is the method of bold conjectures and ingenious and severe attempts to refute them.” The bold conjectures, the hypotheses, making the observations that lead to your conjectures… that’s the easy part. The ingenious and severe attempts to refute your conjectures is the hard part. Anyone can make a bold conjecture. (Here’s one: space aliens cause heart disease.) Testing hypotheses ingeniously and severely is the single most important part of doing science.
The problem with observational studies like the ones from Harvard and UCSD that gave us the bad news about meat and the good news about chocolate, is that the researchers do little of this. The hard part of science is left out, and they skip straight to the endpoint, insisting that their causal interpretation of the association is the correct one and we should probably all change our diets accordingly.