Because conventional thinking usually rests on years (sometimes centuries) of research, scientists are naturally skeptical of radical new ideas. But occasionally, problems with normal science arise, such as a persistent failure to solve important puzzles and anomalies that can’t be easily explained away. Science may then enter what the famous philosopher Thomas Kuhn called a “crisis,” when competing paradigms emerge to clash with the old ones.
Writing in the European Journal of Clinical Nutrition, my coauthors and I argue that the field of obesity research is entering a crisis. To stem the rising tide of obesity-related disease, we must embrace, not resist, paradigm clash.
When calorie restriction keeps failing — and rates of obesity keep going up — we need to test new approaches.
For the past century, thinking about obesity has been based on the notion of energy balance, comparing the number of calories we consume to those that we burn. Surrounded by delicious, energy-dense foods, the surplus calories we take in are deposited into body fat, and we gain weight. In other words, overeating causes obesity.
In this view, the body treats all calories the same, so the only way to lose weight is to reduce our calorie intake or exercise more to burn calories off. This notion is behind the last century’s calorie-counting and, later, low-fat diets targeting the most calorie-dense nutrient.
But consider this paradox. Since 2000, calorie consumption in the U.S. has plateaued or decreased, according to an analysis by Dariush Mozaffarian, MD, DrPH of Tufts University. Americans have also become somewhat more physically active. Yet obesity rates have risen by more than a third, to almost half of the U.S. population.
Another puzzle is why the so-called “body weight set-point” has risen so much among genetically stable populations. In 1960, an average man in the U.S. was able to maintain a weight of about 165 pounds without constant dieting. Today, that average man weighs about 195 pounds.
The carbohydrate-insulin model
A competing paradigm, also dating back a century, argues that we’ve reversed cause and effect. Overeating isn’t the primary cause of obesity. Rather, the process of gaining weight causes us to overeat.
Consider the adolescent growth spurt. During their most rapid stages of growth, teens may increase food intake by hundreds of calories a day. But does this “overeating” cause the growth spurt? Or does the growth spurt itself, with rapid storage of those extra calories in new body tissues, cause the adolescent to get hungry and eat more?
Our recently proposed carbohydrate-insulin model helps explain this phenomenon. It focuses on the processed, quickly digested carbs — think white bread, white rice, sugary breakfast cereals, and potato products — that flooded our diet during the low-fat diet craze. These carbs cause a spike in blood sugar, raise insulin levels too high, and induce other hormonal changes that tell our body to store the calories as fat.
This model of obesity sees the real problem as one of calorie distribution. Too many calories are being sequestered in fat tissue and too few remain in the blood to satisfy our energy needs. Sensing starvation, our brain sends hunger signals to prompt us to eat. In other words, overeating is a symptom of a poor diet.
Coaxing fat out
Instead of cutting back calories, which merely prompts body metabolism to slow down and sets the stage for weight regain, weight-loss efforts should focus on reducing the surge of blood glucose and insulin after meals. That can be accomplished with a higher-fat diet low in processed carbs. (Slow-digesting “low glycemic load” carbs like whole fruits, non-starchy vegetables, beans, and minimally processed grains don’t cause such large glucose and insulin surges.)
Without the hormonal signals driving us to store excessive calories, fat tissue can be coaxed to release calories into the blood, reducing hunger and supporting metabolism. This way, you can lose weight without restricting calories and are more likely to succeed long term.
Does this mean the carbohydrate-insulin model should replace the energy-balance paradigm? Unfortunately, the research needed to provide a definitive answer has never been done. The National Institutes of Health has invested in many major low-fat diet trials, all failing to show any benefit for the main outcomes. But the agency has yet to fund a major, long-term low-carb trial.
In papers we published in 2018 and 2021, in addition to our new paper, we have aimed to build the carbohydrate-insulin model from the available scientific evidence. Yet critics claim to have disproven the model based on weak evidence, such as small trials lasting two weeks or less.
Energy balance bias
One reason energy balance thinking still dominates may be cultural. Obesity has long been blamed on a weakness of character and a lack of self-control. Despite decades of research into the genetic and biological influences on body weight, obesity is still surrounded by stigma, unlike almost any other chronic disease. Even healthcare professionals may harbor this bias.
But when calorie restriction keeps failing — and rates of obesity keep going up — we need to test new approaches. It may even be possible for competing paradigms to combine, providing deeper insights than from either alone. Given that the costs of type 2 diabetes, just one weight-related complication, are almost $1 billion a day, we can’t afford to dismiss new thinking on obesity’s causes.
Another version of this piece was published in The Washington Post on July 28.
Learn more about the New Balance Foundation Obesity Prevention Center.
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