Have we got the science of obesity back to front?


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Michelle D’urbano

IN PRINCIPLE, it sounds simple: eat less and move more. This dietary advice for tackling obesity has been around for decades. Yet, despite all the calorie counting, dieting and exercising, worldwide obesity rates just keep ticking up. People in the US, for example, were heavier in 2021 than they were in 2020, placing many more people at risk from diabetes and other serious chronic diseases. So why hasn’t this approach to weight control worked?

One possibility is that we haven’t tried hard enough. Perhaps we have lacked the discipline and willpower to maintain healthy dietary and exercise habits – a challenge made more difficult today for those surrounded by inexpensive, tasty, highly processed foods.

Or perhaps the problem is the focus on “calorie balance” itself. In a recent paper, my colleagues and I question the basic assumption of whether taking in more calories than you burn really is the primary cause of obesity. We argue that the evidence actually points the other way: we are driven to overeat because we are getting fatter (The American Journal of Clinical Nutrition, doi.org/gmtn3z).

This may seem incredible, but consider the adolescent growth spurt. As their growth rate speeds up, teenagers may eat hundreds of calories more each day than they used to. Does this “overeating” cause the rapid growth? Or does the rapid growth, which requires more calories to build new body tissues, make teens hungrier so they eat more? Clearly the latter, as adults won’t grow taller, no matter how much they eat.

The key to how this works in obesity is hormones, especially the fat-storage hormone insulin. Processed, rapidly digestible carbohydrates – foods like sweetened breakfast cereals, potato chips and sugary beverages – raise our insulin level too high. This causes our fat cells to take in and store too many calories, leaving fewer available for the rest of the body. A few hours after eating a high-carb meal, the number of calories in the bloodstream plummets, so we get hungrier sooner after eating.

Consider another example: oedema, in which excess fluid builds up in body tissues, such as the legs. People with oedema tend to become thirsty, despite the excess, because the fluid doesn’t stay in the blood where it is needed. From this perspective, the difficulty resisting hunger that so many dieters have isn’t a sign of poor discipline, but rather a biological problem involving how our bodies distribute the calories we consume.

The two opposing views of cause and effect in obesity have radically different implications for how to prevent and treat weight problems. Whereas the usual approach focuses on how much to eat, with prescriptions for daily calorie intake, in our view, the emphasis should be placed on what to eat.

Replacing processed carbs with high-fat foods – such as nuts, full-fat dairy, olive oil, avocado and dark chocolate – lowers insulin levels, making more calories from the meal available for the rest of the body. Counter-intuitively, higher-fat foods may help shed body fat, a possibility supported by clinical trials comparing high-fat diets with low-fat ones.

This way of thinking might help explain why calorie restriction usually fails long before a person with obesity approaches an ideal body weight. A low-calorie, low-fat diet further restricts an already limited supply of energy to the body, exacerbating hunger without addressing the underlying predisposition to store too many calories in body fat. Consequently, weight loss becomes a battle between mind and metabolism that most people will probably lose.

Although much more research will be needed to test this provocative idea, it is time to question the basic assumptions about cause and effect, calories and weight gain that have dominated our thinking for decades.

David S. Ludwig is a researcher at Boston Children’s Hospital @davidludwigmd

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