The usual way of thinking considers obesity a problem of energy balance. Take in more calories than you expend—in other words, “overeat”—and weight gain will inevitably result. The simple solution, according to the prevailing Energy Balance Model (EBM), is to eat less and move more.
Variations on this recommendation have been advocated to the public by government and professional health organizations for decades. For instance, the USDA Dietary Guidelines for Americans state, “Losing weight …requires adults to reduce the number of calories they get from foods and beverages and increase the amount expended through physical activity.” Health care providers almost invariably prescribe low-calorie diets (typically restricted in fat, the most calorie dense nutrient) and exercise to their patients.
In a new Perspective article in American Journal of Clinical Nutrition, my 16 coauthors and I argue that viewing body weight control as an energy balance problem is fundamentally wrong, or at least not helpful, for three reasons:
1. It hasn’t worked
The obesity pandemic continues to worsen worldwide despite an incessant focus on calorie balance. Of particular concern is an emerging pandemic vicious cycle. Obesity is among the most important risk factors for COVID-19 susceptibility and severity, after advanced age. Conversely, the COVID-19 pandemic may exacerbate obesity, at least according to preliminary data in children. We need a more effective approach to weight control, now more than ever.
2. It doesn’t consider biology
The relationship between energy balance and body fat reflects a law of physics (conservation of energy), providing no information about biology. It’s like considering fever a problem of “heat balance”—too much heat being generated by the body, not enough heat dissipated. Although technically true, this view doesn’t address the critical questions: what’s causing the fever and how we can cure it?
3. It can’t distinguish cause from effect
The law of energy conservation holds that the relationship between energy balance and body weight is inseverable but provides no information about the direction of cause and effect. During the growth spurt, an adolescent may consume hundreds of calories more than he burns. But does this “overeating” make him grow taller, or does the rapid growth make him hungry and eat more? Clearly, the latter … as no amount of “overeating” will make an adult grow any taller.
The Carbohydrate-Insulin Model (CIM), an alternative obesity paradigm considered in our Perspective, makes a bold claim: we’ve had it backwards all along! Overeating doesn’t cause obesity; rather, increasing body fatness—resulting from the effects of diet on hormones and metabolism—drives overeating.
The processed, rapidly digestible carbohydrates that flooded the food supply during the low-fat diet craze (think Fat-Free Snackwells Cookies) have raised insulin and suppressed glucagon levels. This highly anabolic hormonal state after a meal directs an excessive amount of incoming calories toward storage in fat tissue. As a result, too few calories are available to fuel the needs of metabolically active organs, like muscle. The brain responds by increasing hunger in an attempt to solve this “energy crisis”—driving us to consume extra calories to replace those being diverted into fat tissue. If we try to resist hunger, and cut back calories, energy expenditure (calorie burn) may slow down, explaining why so few people succeed on low-calorie diets over the long term. Eventually, biology trumps willpower.
If the CIM is right, then a focus on what you eat will be more effect than on how much. By replacing processed carbohydrates (white bread, white rice, potatoes, cookies, cakes, sugary beverages) with healthy high-fat foods (nuts and nuts butters, full fat dairy, avocado, oil olive, even dark chocolate), we can lessen the drive to “overeating” at the source, by shifting calories away from deposition in fat tissue. As a result, hunger naturally decreases, and weight loss may occur more easily, like the reduction in body temperature that follows treatment of fever with aspirin. For individuals with more severe metabolic dysfunction, such as type 2 diabetes, more intensive carbohydrate restriction (such as a ketogenic diet) may be optimal.
Although rapidly digestible carbohydrates (technically, high-glycemic load) play a key role in the CIM, the model provides a way of understanding how many dietary factors (amount and type of protein, type of fat, micronutrients fiber, pre- and probiotics) and other environmental factors can influence body fat storage, other than directly through “overeating.”
Although the CIM is not proven, our Perspective highlights the extensive supportive basic and clinical research that already exists. We argue that the CIM better reflects a century of accumulated knowledge on the biology of obesity than the EBM. And we call for better funding to conduct the definitive research. As highlighted in our Perspective, versions of this debate have raged for a century!
Featured image by Rod Long via Unsplash