Overeating not the primary cause of obesity, scientists claim
A perspective in The American Journal of Clinical Nutrition challenges the ‘energy balance model’, which says weight gain occurs because individuals consume more energy than they expend. The authors instead argue for the ‘carbohydrate-insulin model’, which explains obesity as a metabolic disorder driven by what we eat, rather than how much.
The energy balance model states that weight gain is caused by consuming more energy than we expend. Indeed, in a world surrounded by highly palatable, cheap processed foods, it’s easy for people to eat more calories than they need — an imbalance that is further exacerbated by today’s sedentary lifestyles. By this thinking, overeating, coupled with insufficient physical activity, is driving the obesity epidemic. On the other hand, despite decades of public health messaging exhorting people to eat less and exercise more, rates of obesity and obesity-related diseases have steadily risen.
The authors of ‘The Carbohydrate-Insulin Model: A Physiological Perspective on the Obesity Pandemic’ point to fundamental flaws in the energy balance model, arguing that the carbohydrate-insulin model — whose origins date to the early 1900s — better explains obesity and weight gain. According to lead author Dr David Ludwig, an endocrinologist at Boston Children’s Hospital and professor at Harvard Medical School, the energy balance model doesn’t help us understand the biological causes of weight gain.
“During a growth spurt, for instance, adolescents may increase food intake by 1000 calories a day,” he said. “But does their overeating cause the growth spurt or does the growth spurt cause the adolescent to get hungry and overeat?”
In contrast to the energy balance model, the carbohydrate-insulin model boldly claims that overeating isn’t the main cause of obesity. Instead, it lays much of the blame for the current obesity epidemic on modern dietary patterns characterised by excessive consumption of foods with a high glycaemic load: in particular, processed, rapidly digestible carbohydrates. These foods cause hormonal responses that fundamentally change our metabolism, driving fat storage, weight gain and obesity.
When we eat highly processed carbohydrates, the body increases insulin secretion and suppresses glucagon secretion. This in turn signals fat cells to store more calories, leaving fewer calories available to fuel muscles and other metabolically active tissues. The brain perceives that the body isn’t getting enough energy, which leads to feelings of hunger. In addition, metabolism may slow down in the body’s attempt to conserve fuel. Thus, we tend to remain hungry, even as we continue to gain excess fat. With its assertion that all calories are alike to the body, the energy balance model misses this critical piece of the puzzle.
Adoption of the carbohydrate-insulin model over the energy balance model has radical implications for weight management and obesity treatment. Rather than urge people to eat less, a strategy which usually doesn’t work in the long run, the carbohydrate-insulin model suggests another path that focuses more on what we eat. According to Dr Ludwig, “reducing consumption of the rapidly digestible carbohydrates that flooded the food supply during the low-fat diet era lessens the underlying drive to store body fat. As a result, people may lose weight with less hunger and struggle”.
The authors acknowledge that further research is needed to conclusively test both models and, perhaps, to generate new models that better fit the evidence. Toward this end, they call for constructive discourse and “collaborations among scientists with diverse viewpoints to test predictions in rigorous and unbiased research”.
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