2412. The Problem with Food and Exercise Studies

By Gina Kolata, The New York Times, August 11, 2016

Nearly everything you have been told about the food you eat and the exercise you do and their effects on your health should be met with a raised eyebrow.

Dozens of studies are publicized every week. But those studies hardly slake people’s thirst for answers to questions about how to eat or how much to exercise. Does exercise help you maintain your memory? What kind? Walking? Intense exercise? Does eating carbohydrates make you fat? Can you prevent breast cancer by exercising when you are young? Do vegetables protect you from heart disease?

The problem is one of signal to noise. You can’t discern the signal — a lower risk of dementia, or a longer life, or less obesity, or less cancer — because the noise, the enormous uncertainty in the measurement of such things as how much you exercise or what exactly you eat, is overwhelming. The signal is often weak, meaning if there is an effect of lifestyle it is minuscule, nothing like the link between smoking and lung cancer, for example.

And there is no gold standard of measurement, nothing that everyone agrees on and uses to measure aspects of lifestyle.

The result is a large body of studies whose conclusions are not reproducible. “We don’t know how to measure diet or exercise,” said Dr. Barnett Kramer, director of the National Cancer Institute’s division of disease prevention.

His division is working on ways to sort out inconsistencies in research used to generate health advice, hoping to improve what has become a real mess: “You can ask people how many times a week or how many times a month they eat bread or berries or ask them to keep a diary of what they ate in the last 24 hours.” But, he said, it should be no surprise that people misremember or give researchers an answer they think makes them sound good.

“I can’t remember what meals I ate a week ago,” Dr. Kramer said. “Now ask me what meals I had as an adolescent, or how much I exercised.”

David Allison, director of the nutrition obesity research center at the University of Alabama at Birmingham, says the same problems plague obesity research, with only two things known with certainty. All other things being equal, if you eat more calories, you will gain weight. And all other things being equal, if you exercise enough, you will lose a small amount of weight.

Adding to the confusion is a cacophony of poorly designed research, the tendency for different researchers studying the same effect to use different measurements and report outcomes differently, and researchers’ tendency to selectively report positive or “interesting” results.

The result is what Dr. Kramer calls whipsaw literature. “One week drinking coffee is good for you, and the next week it is lethal,” he says.

The situation is so bad that what gets published tends to be what the scientists believe ahead of time, says Dr. John Ioannidis, a professor of medicine and of health research and policy at Stanford University’s medical school. “There are so many nutrients and so many diets,” he said. “So many outcomes — heart disease, cancer, stroke. What kind of data do you collect? A follow-up at two months, six months, two years, 10 years? You end up having millions of choices.”

And the scientists get to pick the one they want. “I can get you any result you want in any observational data set,” he said.

There have been rigorous lifestyle studies, but they are few and far between. A large diet study in Spain found that a Mediterranean diet, with fruits, vegetables, fish and olive oil or nuts, decreased the risk of heart attacks and strokes. Two large federal studies looked at a high-fiber diet but failed to find evidence it protects against colon cancer.

Then there are the seemingly contradictory but well-done studies. One large federal study found that — contrary to all assumptions — diet and weight loss did not prevent heart attacks and strokes in people with Type 2 diabetes. Another large federal study found that people at risk for Type 2 diabetes could stave it off by losing a modest amount of weight and exercising.

A few years ago, two researchers decided to ask just how crazy the cancer and diet literature was. They began with a cookbook, “The Boston Cooking-School Cookbook,” and randomly selected recipes, listing the ingredients, until they had 50 distinct ingredients. Then they did a literature search asking if those ingredients were associated with cancer.

Four out of five were linked to cancer, the researchers reported, either increasing or decreasing the risk. Often the same ingredient that increased risk in one study decreased it in another. Those ingredients not associated with cancer risk tended to be odd, like terrapin, and had not been studied by nutrition researchers.

But when the authors, Dr. Jonathan Schoenfeld, a radiation oncologist at the Dana-Farber Cancer Institute, and Dr. Ioannidis, looked at meta-analyses of the ingredients, which combined data from all the studies, the effects generally went away.

They titled their paper, “Is everything we eat associated with cancer?”

That study is no surprise to a group that puts together an authoritative guide, the Physicians Data Query, for the National Cancer Institute. The group’s screening and prevention board wants to make some sort of statement about whether diet affects cancer risk. But the studies are just so unreliable that it is hard to draw conclusions. The board’s feelings about whether diet has any link to cancer “are pretty consistently negative,” said Dr. Donald Berry, a biostatistician at M. D. Anderson Cancer Center in Houston, who is a member of the board.

“Were I to write a paper on the subject, I might use this variant of their title: ‘Is anything we eat associated with cancer?’” Dr. Berry said. “And my answer would be ‘No. The preponderance of the evidence is either negative or unreliable and subject to false-positive conclusions.’”

Some medical experts say the problems with lifestyle studies are so overwhelming — and the chance of finding anything reproducible and meaningful so small — that it might be best to just give up on those questions altogether.

“They may not be worth studying,” said Dr. Vinay Prasad, a cancer researcher at Oregon Health and Science University. “People want certainty, but, boy, we have no good answers.”

As for Dr. Kramer, he has not given up on rigorous research. What is needed at this point, he says, is a little more humility among researchers in interpreting and reporting the implications of their own evidence.

1588. Food: How Meat Advocates Skewer Science

By The Physicians Committee for Responsible Medicine, Good Medicine, Autumn 2014

In 1974, a new book titled We Never Went to the Moon: America’s Thirty Billion Dollar Swindle alleged that NASA faked the lunar landing. In 2001, the Fox network broadcasted a documentary on the subject, and a follow-up survey showed that as many as one in five Americans doubted that Neil Armstrong’s boots had ever touched the moon’s surface.

Fast-forward to June 23, 2014. Time magazine’s cover proclaimed in large type “Eat Butter” and featured a big artistic swirl of the stuff. Several other publications—the New York Times, the Wall Street Journal, the New Scientist, and others—ran similar stories. The experts have been wrong all this time, the articles exclaimed. Fat isn’t unhealthy after all. Steak and pork chops won’t hurt you. Go ahead, dig in!

Of course, meat and dairy products are strongly linked to all manner of health problems, from heart disease to cancer, diabetes, obesity, and hypertension. So what is behind the contrarian stories?

Eskimos and Maasai

Some of the articles were based on a new book called The Big Fat Surprise: Why Butter, Meat, and Cheese Belong in a Healthy Diet. Its author, Nina Teicholz, aimed to rehabilitate meat’s image, starting with Eskimo and Inuit populations of the far north. They have almost no heart disease, she held, despite a diet heavy on fish and blubber. Was she right or wrong? 

Wrong. A study from the University of Ottawa Heart Institute published in the Canadian Journal of Cardiology showed that cardiovascular disease has been at least as frequent among northern native populations as for others.1 Strokes have been particularly common, and life expectancy overall was found to be about a decade shorter. Heart disease seemed rare among northern native populations mainly because reporting of medical problems has been spotty.

Teicholz then invoked the Maasai, an African population who are supposedly free of heart disease, despite a diet of meat, milk, and blood. Right or wrong? 

Wrong. Researcher George V. Mann wrote in 1978, “We have collected hearts and aortae from 50 authenticated Maasai men who died of trauma and we found extensive atherosclerosis.”2

Okay, so the Maasai’s arteries are clogged with atherosclerotic plaques. But they don’t have heart attacks, Teicholz maintained; so meat and milk must be safe. Right or wrong? 

Wrong. Plaques that form in arteries can rupture, sparking the formation of a clot that blocks blood flow like a cork in an artery, causing a heart attack. Teicholz’s notion was that the Maasai have plaques, but the plaques somehow never rupture, like time bombs that never explode. This is highly unlikely. A better explanation for the lack of reported heart attacks among the Maasai comes from their tragically short life expectancy. If life is cut short in one’s 40s by an accident or an infection, plaques have not had enough time to produce a heart attack. Moreover, in a rural population with limited medical care and poor medical records, heart attacks may not be recognized or reported.

Ancel Keys and the Seven Countries Study 

Teicholz and other fat-backers zeroed in especially on Ancel Keys, the University of Minnesota researcher who identified the dangers of fatty foods in the 1950s. Looking at six countries with reliable dietary and medical records, Keys found a clear association between fat intake and heart disease deaths.3

But as Teicholz tells it, the rug was pulled out from under Ancel Keys by University of California at Berkeley statistician Jacob Yerushalmy.4 If Keys had zeroed in on more countries than just six, Yerushalmy held, the relationship between saturated fat and heart disease would have been weakened. In Teicholz’s words, it “nearly disappeared.” Right or wrong? 

Wrong. Including additional countries, as Yerushalmy suggested, did muddy the correlation between fat and heart disease deaths, because many of these countries had poor data on diet or medical care at that time. Even so, the correlation between fat and heart deaths remained high, and the correlation between animal protein and heart deaths was even higher.

Meta-analysis 

What really grabbed the headlines, however, was a meta-analysis published in early 2014 by the Annals of Internal Medicine.5 The meta-analysis combined 72 smaller studies, finding no overall effect of saturated fat on heart risks. According to the fat lobby, that proved that “bad” fat isn’t bad for your heart after all. Right or wrong?

Wrong. The Annals meta-analysis combined data from many studies. Some were designed to accurately show the dangerous effects of saturated fat. The designs of other studies did not make the hazards of saturated fat readily apparent. The net result was that the two types of studies canceled each other out, showing no risks. For example, take these two studies the Annals meta-analysis included:

The Oxford Vegetarian Study6 included 11,000 people whose diets ranged from vegan to ovolactovegetarian to nonvegetarian, with saturated fat intake ranging from a low of 6 percent of calories to more than 13 percent of calories. The study found that the fattiest diets tripled the risk of dying of heart disease, compared with diets that had very little saturated fat.

But in a Swedish study, no groups were on lower-fat diets. All of the study groups averaged more than 13 percent of their calories from saturated fat. Not surprisingly, the study could not identify any effect of avoiding saturated fat, because no groups in the study had a low fat intake.

Is Meat Safe or Not? 

Of course, no one orders saturated fat at a restaurant or puts it on a shopping list. This fat is hidden in meat, dairy products, and other foods. And here, the evidence is crystal clear. Meat-eaters are heavier than people who avoid meat. They have higher blood pressure, higher risk of diabetes, cancer, heart disease, and many other problems. And in carefully controlled studies, when people take meat out of their diets, they lose weight, and cholesterol, diabetes, and heart disease all improve. So while researchers debate the statistics on saturated fat, it pays to remember that getting away from meat is a healthy choice. 

So how could the media have been duped? As John McDougall, M.D., said, people are always looking for good news about bad habits.

1. Fodor GJ, Helis E, Yazdekhasti N, Vohnout B. “Fishing” for the origins of the “Eskimos and heart disease” story: facts or wishful thinking? Can J Cardiol. 2014;30:864-868.
2. Mann GV. The Masai, milk, and the yogurt factor: an alternative explanation. Atherosclerosis. 1978;29:265.
3. Keys A. Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp NY. 1953;20:118-139.
4. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease: a methodologic note. NY State J Med. 1957;57:2343-2354.
5. Chowdhury R, Warnakula S, Kunutsor S, et al. Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis. Ann Intern Med. 2014;160:398-406.
6. Appleby PN, Thorogood M, Mann JI, Key TJA. The Oxford Vegetarian Study: an overview. Am J Clin Nutr. 1999;70:525S-531S.
7. Wallstrom P, Sonestedt E, Hlebowicz J, et al. Dietary fiber and saturated fat intake associations with cardiovascular disease differ by sex in the Malmo Diet and Cancer Cohort: a prospective study. PLoS One. 2012;7:e31637.

1418. Always Hungry? Here Is Why

By David S. Ludwig and Mark. I. Friedman, The New York Times, May 16, 2014

For most of the last century, our understanding of the cause of obesity has been based on immutable physical law. Specifically, it’s the first law of thermodynamics, which dictates that energy can neither be created nor destroyed. When it comes to body weight, this means that calorie intake minus calorie expenditure equals calories stored. Surrounded by tempting foods, we overeat, consuming more calories than we can burn off, and the excess is deposited as fat. The simple solution is to exert willpower and eat less.

The problem is that this advice doesn’t work, at least not for most people over the long term. In other words, your New Year’s resolution to lose weight probably won’t last through the spring, let alone affect how you look in a swimsuit in July. More of us than ever are obese, despite an incessant focus on calorie balance by the government, nutrition organizations and the food industry.

But what if we’ve confused cause and effect? What if it’s not overeating that causes us to get fat, but the process of getting fatter that causes us to overeat?

The more calories we lock away in fat tissue, the fewer there are circulating in the bloodstream to satisfy the body’s requirements. If we look at it this way, it’s a distribution problem: We have an abundance of calories, but they’re in the wrong place. As a result, the body needs to increase its intake. We get hungrier because we’re getting fatter.

It’s like edema, a common medical condition in which fluid leaks from blood vessels into surrounding tissues. No matter how much water they drink, people with edema may experience unquenchable thirst because the fluid doesn’t stay in the blood, where it’s needed. Similarly, when fat cells suck up too much fuel, calories from food promote the growth of fat tissue instead of serving the energy needs of the body, provoking overeating in all but the most disciplined individuals.

We discuss this hypothesis in an article just published in JAMA, The Journal of the American Medical Association. According to this alternative view, factors in the environment have triggered fat cells in our bodies to take in and store excessive amounts of glucose and other calorie-rich compounds. Since fewer calories are available to fuel metabolism, the brain tells the body to increase calorie intake (we feel hungry) and save energy (our metabolism slows down). Eating more solves this problem temporarily but also accelerates weight gain. Cutting calories reverses the weight gain for a short while, making us think we have control over our body weight, but predictably increases hunger and slows metabolism even more.

Consider fever as another analogy. A cold bath will lower body temperature temporarily, but also set off biological responses — like shivering and constriction of blood vessels — that work to heat the body up again. In a sense, the conventional view of obesity as a problem of calorie balance is like conceptualizing fever as a problem of heat balance; technically not wrong, but not very helpful, because it ignores the apparent underlying biological driver of weight gain.

This is why diets that rely on consciously reducing calories don’t usually work. Only one in six overweight and obese adults in a nationwide survey reports ever having maintained a 10 percent weight loss for at least a year. (Even this relatively modest accomplishment may be exaggerated, because people tend to overestimate their successes in self-reported surveys.) In studies by Dr. Rudolph L. Leibel of Columbia and colleagues, when lean and obese research subjects were underfed in order to make them lose 10 to 20 percent of their weight, their hunger increased and metabolism plummeted. Conversely, overfeeding sped up metabolism.

For both over- and under-eating, these responses tend to push weight back to where it started — prompting some obesity researchers to think in terms of a body weight “set point” that seems to be predetermined by our genes.

But if basic biological responses push back against changes in body weight, and our set points are predetermined, then why have obesity rates — which, for adults, are almost three times what they were in the 1960s — increased so much? Most important, what can we do about it?

As it turns out, many biological factors affect the storage of calories in fat cells, including genetics, levels of physical activity, sleep and stress. But one has an indisputably dominant role: the hormone insulin. We know that excess insulin treatment for diabetes causes weight gain, and insulin deficiency causes weight loss. And of everything we eat, highly refined and rapidly digestible carbohydrates produce the most insulin.

By this way of thinking, the increasing amount and processing of carbohydrates in the American diet has increased insulin levels, put fat cells into storage overdrive and elicited obesity-promoting biological responses in a large number of people. Like an infection that raises the body temperature set point, high consumption of refined carbohydrates — chips, crackers, cakes, soft drinks, sugary breakfast cereals and even white rice and bread — has increased body weights throughout the population.

One reason we consume so many refined carbohydrates today is because they have been added to processed foods in place of fats — which have been the main target of calorie reduction efforts since the 1970s. Fat has about twice the calories of carbohydrates, but low-fat diets are the least effective of comparable interventions, according to several analyses, including one presented at a meeting of the American Heart Association this year.

A recent study by one of us, Dr. Ludwig, and his colleagues published in JAMA examined 21 overweight and obese young adults after they had lost 10 to 15 percent of their body weight, on diets ranging from low fat to low carbohydrate. Despite consuming the same number of calories on each diet, subjects burned about 325 more calories per day on the low carbohydrate than on the low fat diet — amounting to the energy expended in an hour of moderately intense physical activity.

Another study published by Dr. Ludwig and colleagues in The Lancet in 2004 suggested that a poor-quality diet could result in obesity even when it was low in calories. Rats fed a diet with rapidly digesting (called high “glycemic index”) carbohydrate gained 71 percent more fat than their counterparts, who ate more calories over all, though in the form of slowly digesting carbohydrate.

These ideas aren’t entirely new. The notion that we overeat because we’re getting fat has been around for at least a century, as described by Gary Taubes in his book “Good Calories, Bad Calories.” In 1908, for example, a German internist named Gustav von Bergmann dismissed the energy-balance view of obesity, and hypothesized that it was instead caused by a metabolic disorder that he called “lipophilia,” or “love of fat.”

But such theories have been generally ignored, perhaps because they challenge entrenched cultural attitudes. The popular emphasis on calorie balance reinforces the belief that we have conscious control over our weight, and that obesity represents a personal failure because of ignorance or inadequate willpower.

In addition, the food industry — which makes enormous profits from highly processed products derived from corn, wheat and rice — invokes calorie balance as its first line of defense. If all calories are the same, then there are no bad foods, and sugary beverages, junk foods and the like are fine in moderation. It’s simply a question of portion control. The fact that this rarely works is taken as evidence that obese people lack willpower, not that the idea itself might be wrong.

UNFORTUNATELY, existing research cannot provide a definitive test of our hypothesis. Several prominent clinical trials reported no difference in weight loss when comparing diets purportedly differing in protein, carbohydrate and fat. However, these trials had major limitations; at the end, subjects reported that they had not met the targets for complying with the prescribed diets. We wouldn’t discard a potentially lifesaving cancer treatment based on negative findings, if the research subjects didn’t take the drug as intended.

There are better ways to do this research. Studies should provide participants with at least some of their food, to make it easier for them to stick to the diets. Two studies that did this — one by the Direct Group in 2008 and the other by the Diogenes Project in 2010 — reported substantial benefits associated with the reduction of rapidly digestible carbohydrate compared with conventional diets. We need to invest much more in this research. With the annual economic burden of diabetes — just one obesity-related complication — predicted to approach half a trillion dollars by 2020, a few billion dollars for state-of-the-art nutrition research would make a good investment.

If this hypothesis turns out to be correct, it will have immediate implications for public health. It would mean that the decades-long focus on calorie restriction was destined to fail for most people. Information about calorie content would remain relevant, not as a strategy for weight loss, but rather to help people avoid eating too much highly processed food loaded with rapidly digesting carbohydrates. But obesity treatment would more appropriately focus on diet quality rather than calorie quantity.

People in the modern food environment seem to have greater control over what they eat than how much. With reduced consumption of refined grains, concentrated sugar and potato products and a few other sensible lifestyle choices, our internal body weight control system should be able to do the rest. Eventually, we could bring the body weight set point back to pre-epidemic levels. Addressing the underlying biological drive to overeat may make for a far more practical and effective solution to obesity than counting calories.

David S. Ludwig directs the New Balance Foundation Obesity Prevention Center at Boston Children’s Hospital and is a professor of pediatrics at Harvard Medical School. Mark I. Friedman is vice president of research at the Nutrition Science Initiative.

1315. Why Nutrition Is So Confusing

By Gary Taubes, The New York Times, February 8, 2014

Nearly six weeks into the 2014 diet season, it’s a good bet that many of us who made New Year’s resolutions to lose weight have already peaked. If clinical trials are any indication, we’ve lost much of the weight we can expect to lose. In a year or two we’ll be back within half a dozen pounds of where we are today.

The question is why. Is this a failure of willpower or of technique? Was our chosen dietary intervention — whether from the latest best-selling diet book or merely a concerted attempt to eat less and exercise more — doomed to failure? Considering that obesity and its related diseases — most notably, Type 2 diabetes — now cost the health care system more than $1 billion per day, it’s not hyperbolic to suggest that the health of the nation may depend on which is the correct answer.

Since the 1960s, nutrition science has been dominated by two conflicting observations. One is that we know how to eat healthy and maintain a healthy weight. The other is that the rapidly increasing rates of obesity and diabetes suggest that something about the conventional thinking is simply wrong.

In 1960, fewer than 13 percent of Americans were obese, and diabetes had been diagnosed in 1 percent. Today, the percentage of obese Americans has almost tripled; the percentage of Americans with diabetes has increased sevenfold.

Meanwhile, the research literature on obesity has also ballooned. In 1960, fewer than 1,100 articles were published on obesity or diabetes in the indexed medical literature. Last year it was more than 44,000. In total, over 600,000 articles have been published purporting to convey some meaningful information on these conditions.

It would be nice to think that this deluge of research has brought clarity to the issue. The trend data argue otherwise. If we understand these disorders so well, why have we failed so miserably to prevent them? The conventional explanation is that this is the manifestation of an unfortunate reality: Type 2 diabetes is caused or exacerbated by obesity, and obesity is a complex, intractable disorder. The more we learn, the more we need to know.

Here’s another possibility: The 600,000 articles — along with several tens of thousands of diet books — are the noise generated by a dysfunctional research establishment. Because the nutrition research community has failed to establish reliable, unambiguous knowledge about the environmental triggers of obesity and diabetes, it has opened the door to a diversity of opinions on the subject, of hypotheses about cause, cure and prevention, many of which cannot be refuted by the existing evidence. Everyone has a theory. The evidence doesn’t exist to say unequivocally who’s wrong.

The situation is understandable; it’s a learning experience in the limits of science. The protocol of science is the process of hypothesis and test. This three-word phrase, though, does not do it justice. The philosopher Karl Popper did when he described “the method of science as the method of bold conjectures and ingenious and severe attempts to refute them.” 

In nutrition, the hypotheses are speculations about what foods or dietary patterns help or hinder our pursuit of a long and healthy life. The ingenious and severe attempts to refute the hypotheses are the experimental tests — the clinical trials and, to be specific, randomized controlled trials. Because the hypotheses are ultimately about what happens to us over decades, meaningful trials are prohibitively expensive and exceedingly difficult.  It means convincing thousands of people to change what they eat for years to decades. Eventually enough heart attacks, cancers and deaths have to happen among the subjects so it can be established whether the dietary intervention was beneficial or detrimental.

And before any of this can even be attempted, someone’s got to pay for it. Since no pharmaceutical company stands to benefit, prospective sources are limited, particularly when we insist the answers are already known. Without such trials, though, we’re only guessing whether we know the truth.

Back in the 1960s, when researchers first took seriously the idea that dietary fat caused heart disease, they acknowledged that such trials were necessary and studied the feasibility for years. Eventually the leadership at the National Institutes of Health concluded that the trials would be too expensive — perhaps a billion dollars — and might get the wrong answer anyway. They might botch the study and never know it. They certainly couldn’t afford to do two such studies, even though replication is a core principle of the scientific method. Since then, advice to restrict fat or avoid saturated fat has been based on suppositions about what would have happened had such trials been done, not on the studies themselves.

Nutritionists have adjusted to this reality by accepting a lower standard of evidence on what they’ll believe to be true. They do experiments with laboratory animals, for instance, following them for the better part of the animal’s lifetime — a year or two in rodents, say — and assume or at least hope that the results apply to humans. And maybe they do, but we can’t know for sure without doing the human experiments.

They do experiments on humans — the species of interest — for days or weeks or even a year or two and then assume that the results apply to decades. And maybe they do, but we can’t know for sure. That’s a hypothesis, and it must be tested.

And they do what are called observational studies, observing populations for decades, documenting what people eat and what illnesses beset them, and then assume that the associations they observe between diet and disease are indeed causal — that if people who eat copious vegetables, for instance, live longer than those who don’t, it’s the vegetables that cause the effect of a longer life. And maybe they do, but there’s no way to know without experimental trials to test that hypothesis.

The associations that emerge from these studies used to be known as “hypothesis-generating data,” based on the fact that an association tells us only that two things changed together in time, not that one caused the other. So associations generate hypotheses of causality that then have to be tested. But this hypothesis-generating caveat has been dropped over the years as researchers studying nutrition have decided that this is the best they can do.  

One lesson of science, though, is that if the best you can do isn’t good enough to establish reliable knowledge, first acknowledge it — relentless honesty about what can and cannot be extrapolated from data is another core principle of science — and then do more, or do something else. As it is, we have a field of sort-of-science in which hypotheses are treated as facts because they’re too hard or expensive to test, and there are so many hypotheses that what journalists like to call “leading authorities” disagree with one another daily.

It’s an unacceptable situation. Obesity and diabetes are epidemic, and yet the only relevant fact on which relatively unambiguous data exist to support a consensus is that most of us are surely eating too much of something. (My vote is sugars and refined grains; we all have our biases.) Making meaningful inroads against obesity and diabetes on a population level requires that we know how to treat and prevent it on an individual level. We’re going to have to stop believing we know the answer, and challenge ourselves to come up with trials that do a better job of testing our beliefs.

Before I, for one, make another dietary resolution, I’d like to know that what I believe I know about a healthy diet is really so. Is that too much to ask?

Gary Taubes is a health and science journalist and co-founder of the Nutrition Science Initiative.