I just got my first opportunity to listen to the audio version of my new book, which I read myself. The experience of recording it was interesting: I had fun, but I’ll also try to write shorter sentences in the future! I recorded the audio in the first week of January, over three days of five or six hours each. When I went home afterward, I didn’t want to talk to anyone. During each day of recording, I think I spoke more than my usual allotment of words for a week.
I’m excited to announce the upcoming publication of my new book, Why Diets Make Us Fat: The Unintended Consequences of Our Obsession with Weight Loss, which explains the research behind my TED talk in detail. It will be released by the Current imprint of Penguin Random House on June 7th.
We talk a lot about weight loss, in the media and around the dinner table, but scientific research is largely absent from these discussions. This book answers the questions you probably didn’t know enough to ask. Why do dieters have to cut more calories to lose weight than they had to add in order to gain the same number of pounds? Why is cutting 3500 calories unlikely to cause anyone to lose one pound? Why might one person lose ten times as much weight as another person on the exact same diet? (No, it’s not cheating.) Why does trying to micromanage weight often backfire? Why is teasing a teenage girl about her weight likely to make her fatter? Plus the most important question: what should you do about your weight, and how do you make it work?
Welcome, TED viewers! My talk from TEDGlobal in June 2013 was posted today. For those who came here looking for the details, I’ve got you covered. Start with the three posts explaining the science behind the talk: Weight and health – show me the data!, Long-term effects of dieting, and Early dieting predicts weight gain. Then move on the my favorite post on the site, How obesity is like nearsightedness, which explains how genes and environment interact to control body weight.
These ideas didn’t originate with me, of course. This research represents decades of work by many scientists, much of it old enough to be found in physiology textbooks. But since most people don’t read textbooks, here are some good places to look for more information.
Much of the work on fitness versus fatness comes from Steven Blair of the University of South Carolina. Here’s an interview containing his recommendations for a healthy life. Just 30 minutes a day of moderate exercise is enough to provide most of the benefits.
The Fat Nutritionist has a good recent round-up of the science on why people have a strong tendency to regain the weight lost by dieting.
Arya Sharma is an obesity specialist who takes a realistic view of the difficulties associated with weight loss. Most relevant to my talk, see his blog posts Will losing weight make you fat? and Will losing weight make you sick? [links to his site are failing intermittently, but they’re correct]
Here’s a nice summary of the original study by Rudy Leibel, Jules Hirsch and colleagues showing that weight loss reduces metabolism.
If I’ve missed anything that you wanted to know about, tell me in the comments, and I’ll update the post later on.
In classic #slatepitch fashion, Emily Oster argues that calls for people to exercise to improve their health ignore the problem that most of us find exercise unpleasant. As an economist, she feels that public policy should factor in the costs of exercise, not just in gym memberships but in time that we could spend on more enjoyable activities.
She’s responding to media coverage of a recent meta-analysis showing that exercise and drug treatments are equally effective for preventing diabetes or heart attacks. Exercise was more effective than drugs for stroke patients, but less effective for patients with heart failure.
The Slate headline is golden clickbait (“Taking a Pill While Watching TV Just as Good as Exercise, Study Finds”). I fell for it, even though I’d already seen the study. But it’s wrong in one important way: no single pill can substitute for the broad benefits of exercise. Instead we’re talking about different medications to prevent or treat heart attacks, diabetes, high blood pressure, depression, and so on. Most of the seniors I know are taking handfuls of pills every day. Not to mention that exercise lowers the risk of getting some diseases of aging that can’t be cured, like Alzheimer’s disease. There’s no pill for that.
Two recent meta-analyses have reignited the public debate about whether it’s possible to be both fat and healthy. Neither publication changes the scientific picture much – and their findings are surprisingly similar, considering that the authors of the two papers drew opposite conclusions. The media coverage is what I found interesting, as it illustrates the deep cultural biases in the way we talk about these issues.
Let’s start with the facts. Cardiovascular fitness is well known to predict people’s risk of dying within a certain number of years of follow-up. “Risk of death” is the common shorthand for that lengthy concept, and I’ll use the term here (though it sounds weird to me because we’re all going to die eventually).
The first paper combined the results of ten studies that looked at whether obesity predicts some additional risk of death beyond the known risk associated with low fitness. All the studies used objective measures of weight, height, and fitness, rather than unreliable self-report. Participants were followed for 7.7 to 16 years afterward. The authors of the meta-analysis concluded that the risk of death depended only on fitness, not on fatness.
The second paper combined the results of eight studies of a related question, whether obesity predicts any additional risk of death beyond the known risks of poor metabolic health. That’s a fancy way of describing the set of risk factors that your doctor might monitor at check-ups: blood pressure, HDL (good) cholesterol, triglycerides, waist circumference, and fasting glucose. Those authors concluded that among people with good metabolic health, obesity was still associated with an increased risk of death, though only in studies with at least a ten-year follow-up.
(Dr. Arya Sharma points out that the definition of metabolic health in this paper was lenient. His work has shown no increased risk over 16 years for obese people who are metabolically healthy under a more stringent set of requirements.)
To me, the similarities between the two papers far exceed their differences. The first paper just missed finding a statistically significant effect on relative risk for obese people who are fit (average 1.13, 95% confidence interval 1.00-1.27). The second paper’s results barely achieved significance for obese people who are metabolically healthy (average 1.24, 95% confidence interval 1.02-1.55). As each paper reports on tens of thousands of participants, the problem is not a lack of statistical power but that the effect is weak, if it exists at all. At worst, the second paper suggests that the healthy obese have a 24% greater risk than healthy normal-weight people.
Compare that to the much larger risk increase for unfit or metabolically unhealthy people at any weight, reported in both papers. The relative risks ranged from 2.42 to 3.55, or roughly a threefold higher risk than healthy normal-weight people. So if obesity does present an independent risk, it’s about one-tenth as large as the risk associated with poor fitness or poor metabolic health.
What would a sensible society do with that information? Perhaps encourage everyone to concentrate on the risk factors that have a huge effect and are relatively controllable, by exercising and eating their veggies. Or worry about the many people who face a high risk of death because of unhealthy lifestyles but aren’t concerned because they’re thin.
What do we do instead? Ignore the first study and use the second to argue about whether it’s (sometimes) OK to be fat, with headlines like “Healthy Obesity is a Myth, Report Says” and “Overweight And Healthy: A Combo That Looks Too Good To Be True.” Sigh.
In July 1999, I went to Japan for the first time, to speak at the RIKEN Institute near Tokyo. At the end of the week, I had a free day, and a friend suggested that I go to Nikko National Park. From the tour boat on Lake Chuzenji, I was loving the look of the hills and sky, but it wasn’t quite a photo until the fisherman showed up. All the men who were out fishing that afternoon had brightly colored umbrellas to protect them from the sun.
In the train station on the way home, I had trouble finding the correct platform. As I stood there trying to match my notes to the characters on the signs, a guy who described himself as a salaryman offered to help locate my train. Of course I ended up riding back with him. His English was rudimentary, so I tried to stick to small words when he asked me what I did for a living. Despite my convoluted attempt to describe scientific editing at the fourth grade level, he immediately understood: “Ah, Nature!” And he meant the journal, which is apparently famous in Japan. I can’t imagine having that happen on an American train.
If your parents are nearsighted (or short-sighted, if they happen to be British), you’re likely to be nearsighted too. The heritability of this problem is as high as 90% in some twin studies. But that’s only true if you and your parents or siblings grow up in a similar environment.
When you shift to a different lifestyle, the outcomes change. In 1974, a team of researchers evaluated a community of Inuit in the Canadian Arctic soon after formal schooling was introduced. Of adults over 30, only a small fraction (4.5%) were nearsighted. In contrast, 45% of younger adults, ages 15-29, were nearsighted – a tenfold rate increase, which happened much faster than genes in the population could vary.
The increase in nearsightedness that struck the Inuit in one generation has spread all over the world. The US rate went from 25% in the early 1970s to 42% three decades later. In a few societies, nearsightedness rates are now nearly as high as they can get. Among modern Chinese students in Singapore, 90-95% are nearsighted.
Research in lab animals and epidemiology in people suggest that the culprit is too much time spent indoors. Weak artificial light does not provide the signals that the developing eye needs to grow to the right size.
Do these rapid changes mean that genes don’t matter to nearsightedness? Not at all. Children with a genetic predisposition are more likely to become nearsighted – or more severely nearsighted – than children whose parents have good vision.
Here’s one way to think about it. Picture 100 children lining up to receive their portion of nearsightedness. In an environment where kids spend all day outside, there’s only a small amount available, enough for the first three or four children in line. The rest get normal vision. In Singapore, there is a huge amount of nearsightedness, so the first few kids get a lot more, and there’s still enough left for almost everyone to get some.
In both cases, the kids line up in the same order, which is determined by their genetics. Regardless of the environment, the children at the front of the line (the most vulnerable) do worst, and those at the back of the line do best. But the amount of outdoor time determines how far down the line the problem is distributed.
Obesity has also increased in the population much faster than genes could change. Weight is as heritable as height. And like nearsightedness, weight is influenced by the environment, with the strongest effects on the genetically vulnerable.
Scientists don’t yet know which environmental changes are most important for the increase in obesity. Candidates include processed foods, antibiotics, stress, sleep loss, prescription drugs, reduced exercise, and decreased cigarette smoking, among others. Whatever has changed over the past 50 years, it probably isn’t our collective willpower.
So why do we treat nearsighted and obese people so differently? You wouldn’t tell a person who wears glasses, “Well, it’s your own fault. You should have played outside more as a child.” But even health care professionals tend to blame their patients for being overweight, though they should know how powerfully the body fights against weight loss.
Maybe it’s time to rethink our cultural focus on individuals and their willpower as the cause of weight gain. In addition to being more fair, concentrating on the bigger picture might give us some ideas that actually work to promote health and fitness.
Puffins in the water are shy, flipping underwater as soon as a boat gets too close. On land, not so much. The colony of Atlantic puffins breeding on Lunga Island, Scotland, seemed undisturbed by dozens of tourists within two or three feet of their nests. We had a rare sunny day to watch these birds, which were just starting to breed in late June 2013. Their day was divided between territorial squabbles and nest-building, interrupted by occasional trips to bring back some fish for their mates.
When we think about weight regulation, eating and exercise are easy to observe. Metabolism seems more abstract. You might imagine it’s a hand-waving explanation for why some people don’t weigh what you’d expect based on their behavior. In casual conversation, the concept is sometimes used that way, but metabolism has a concrete meaning to physiologists.
When you digest food, your body can do three things with the energy: use it to do work on the outside world (like lifting heavy objects), store it as fat, or turn it into heat. By far the most energy turns into heat, but that’s not as wasteful as it sounds. That heat maintains your body temperature, and some of it is a byproduct of life-sustaining activities like pumping blood through your veins. The rest (about 60%) is released because your digestion is inefficient at turning food into useable energy.
Metabolism is simply how much heat your body produces. It’s measured in calories (the kind that are listed on food labels, which scientists call “kilocalories”) by placing a person in an insulated room with water-filled walls and then measuring the change in water temperature. Or more commonly (because it’s less expensive), metabolic rate is estimated from oxygen consumption, though that approach requires some assumptions about the person’s diet.
Height, weight, age, and sex all influence metabolism. Thyroid hormone is the main regulator of metabolism, but it’s also increased by adrenaline released during the fight-or-flight reaction and by muscle activity, including shivering with cold or tensing up from anxiety.
Metabolism also changes when you move outside the weight range determined by your individual set point. If your weight is 10% below your set point, your metabolism is typically about 15% lower than someone of the same weight who’s at their set point. A similar compensation happens in the opposite direction when you eat too much – your body burns more energy for a while. That’s why you may wake up feeling too hot a few hours after a big meal. The problem for dieters is that the compensation for overeating seems to fade over time, while the low metabolism in successful dieters lasts as long as six or seven years, as long as anyone has measured it.
Teenagers who are unhappy with their weight are vulnerable to eating disorders. Big surprise. But most people probably wouldn’t guess that concerns about weight also predict which adolescents will become fatter over the next few years, as I discussed in my TEDGlobal talk.
Dr. Dianne Neumark-Sztainer heads a study at the University of Minnesota to identify risk factors for weight-related problems in teenagers. Her team studied over 2500 boys and girls in middle school or high school and again five years later.
The initial characteristics that predicted weight gain in girls during the study also predicted increases in disordered eating. The strongest predictors were a history of dieting, concerns about weight, and weight-related teasing from family. Girls whose families nagged or teased them about their weight when the study began had twice the risk of gaining weight over the next five years, compared to girls who weren’t teased.
You might imagine that the girls were already overweight, so they got teased, and then went on gaining weight. But that explanation doesn’t work because the same relationship between dieting or teasing and weight gain was found for girls who started the study at a normal weight. Similarly, a long-term follow-up of over ten thousand boys and girls born to participants in the Nurses Health Study found that frequent dieting at 9-14 years of age increased the risk of transitioning from normal weight to overweight over the next two years by a factor of 4.8 in girls and 1.7 in boys.
Why might dieting predict weight gain? One possible explanation is that food restriction leads people to binge. Indeed, teasing nearly doubled the risk of increased binge-eating among girls in the Minnesota study. Girls in the Nurses Health Study who dieted frequently were twelve times more likely to report binge eating. A third study of girls in northern California found similar results.
The deliberate cognitive control of food intake, common in dieters, may sound like a good idea, but it has several unwanted consequences. People who eat this way are heavier, on average, and more likely to gain weight over time than people who simply eat when they’re hungry and stop when they’re full. You might imagine that people adopt a controlled eating style because they have a genetic predisposition to gain weight, but that’s unlikely because the relationship holds even between identical twins.
People who ignore hunger seem to be more susceptible to external cues telling them how much to eat, such as serving size or what their friends are eating. That makes it easier for food marketers to manipulate them into overeating. And a minor dietary indulgence like eating a scoop of ice cream is more likely to set off a food binge in controlled eaters than in people who eat in response to hunger.
What’s a parent to do? By all means, talk to your kids about healthy eating. But don’t give them a hard time about their weight. Not only does that kind of talk contribute to eating disorders, but it’s also likely to make them fatter in the long run.