Dr. Ludwig is a Professor of Pediatrics at Harvard Medical School and Professor of Nutrition at Harvard TH Chan School of Public Health. He wrote the article below where he provides his hypothesis that its not how much you eat, its what you eat that’s important for weight loss. ~ Dr. Broussard
— The carbohydrate-insulin model of obesity offers a new way to conceptualize energy balance
by David S. Ludwig, MD, PhD October 18, 2021
The First Law of Thermodynamics, formulated in the 1800s, says that energy can neither be created nor destroyed. For the human body, this principle of physics means that if you consume more calories than you burn (or excrete), the excess is stored in the body (mainly as fat).
Variations on this “energy balance” principle form the foundations for how we think about, and treat, obesity. For example, the Dietary Guidelines for Americans 2020-2025 advises that “Losing weight…requires adults to reduce the number of calories they get from foods and beverages and increase the amount expended through physical activity.” The American Diabetes Association concluded in a standards of care report this year, “Behavioral changes that create an energy deficit, regardless of macronutrient composition, will result in weight loss.”
But there’s an obvious problem. The obesity pandemic shows no signs of abating, despite incessant focus on calorie balance. Quite the opposite, according to CDC data from just before and during the COVID-19 pandemic. Currently, more than 70% of U.S. adults have high BMI, putting them at risk for diabetes, heart disease, and numerous other chronic conditions — including severe illness from COVID-19.
Maybe we need to focus on energy balance even harder. Or maybe the problem is how we think about energy balance in the first place. Let’s consider three ways of translating this principle of physics to obesity.
The Uninformative View
One interpretation is with an equal sign:
Energy intake – Energy expenditure = Energy stored (body fat)
That is, weight gain can only occur with a positive energy balance and weight loss can only occur with a negative energy balance.
Although true, this common assertion provides virtually no meaningful information about the medical problem of obesity. It’s like conceptualizing fever as a problem of “heat balance.” Of course, an increase in temperature can only occur if the body generates more heat than it dissipates. This fact is so obvious that textbooks on fever needn’t restate it and patients needn’t be told it. And at risk of the absurd, gastroenterology texts don’t conceptualize constipation as a problem of “stool balance” — too much stool into the colon, not enough out.
Equating a positive energy balance with weight gain is a tautology — another way of saying what we have known from physics for 150 years. The relevant biological issue is to distinguish cause from effect. Does “overeating” (energy in > energy out) drive fat storage? Or does increasing fat storage drive overeating? Neither possibility violates any physical law, but they have fundamentally different implications to understanding obesity and designing more effective treatment.
The Conventional View
Overeating drives excess fat storage:
Energy intake – Energy expenditure → Energy stored (body fat)
This view underpins the usual explanation for the obesity epidemic. Surrounded by inexpensive, energy dense, highly processed, tasty (“hyperpalatable”) foods, people in the modern environment tend to consume more calories than they require, with the excess deposited into fat. According to this way of thinking, all calories are alike to the body. So, the only way to lose weight is to consume fewer of them (“eat less”) and increase physical activity to burn off the excess (“move more”).
Clearly, calorie restriction produces weight loss initially. However, predictable biological responses — increased hunger and reduced metabolic rate — make ongoing weight loss progressively more difficult over time, predisposing people to weight regain. Consequently, few people successfully maintain weight loss for more than a few weeks or months, as demonstrated by the notoriously poor long-term success rate of low-calorie diets.
A central conundrum of the obesity pandemic is to understand why the so-called “body weight set-point” has increased among genetically stable populations. In the 1960s, an average man in the U.S. weighed about 165 lbs. Force-feeding him to produce a 30-lb weight gain would have caused intense discomfort, and his metabolism would have sped up in the body’s attempt to burn off the extra calories. Today, the average man weighs about 195 lbs. Restricting food intake to produce a 30-lb weight loss would have the opposite effects, with intense hunger and slowing metabolism. What environmental factors have pushed so many people’s set points so much higher than they were a generation or two ago? The conventional view provides no compelling answers.
The Carbohydrate-Insulin Model
Excess fat storage drives overeating:
Energy intake – Energy expenditure ← Energy stored (body fat)
The carbohydrate-insulin models proposes that the hormonal and metabolic responses to diet, not simply calorie content, cause the body to store excess fat. After consumption of a high-glycemic load meal with lots of fast-digesting carbohydrates (e.g., processed grains, potato products, refined sugar), insulin levels rise excessively, and glucagon is suppressed. This anabolic hormonal response directs too many incoming calories from the meal into fat tissue, leaving fewer available for the rest of the body. Consequently, hunger increases, and we tend to eat more. If we try to ignore hunger and restrict calories, then metabolism slows down, producing a positive energy balance either way.
Thus, the model attributes the rapid increase in BMI across the population in large part to the processed carbohydrates that flooded the food supply during the low-fat diet era (although other dietary and environmental factors can also affect fat storage through related mechanisms).
This reversal in causal direction, although provocative regarding obesity, seems intuitively obvious in other physiological states. Does the increased hunger and food intake of an adolescent cause his growth spurt? Or does the growth spurt, with deposition of calories into new body tissue, cause the adolescent to become hungrier and eat more? Clearly the latter.
Although not commonly appreciated, the carbohydrate-insulin model is supported by extensive evidence, from bench research through clinical trials, dating back almost a century. In a new paper in The American Journal of Clinical Nutrition, my coauthors and I summarize the evidence and present a full formulation of this model.
If this model is substantially correct, then calorie restriction amounts to symptomatic treatment, destined to fail for most people because it disregards the underlying predisposition to excess fat storage. Instead, a focus on what you eat, rather than how much, would be more effective over the long term.
Toward a Consolidated View
Energy intake – Energy expenditure ⇄ Energy stored (body fat)
There is a fourth possibility, in which causal pathways operate in both directions, perhaps to synergistic effect. As one example, a hardwired preference for sweetness may cause people to overeat sugary foods. And high intakes of sugar might then augment fat storage through metabolic actions, leading to a vicious cycle.
Whether one causal view or the other is correct or the truth lies in the middle, development of more effective dietary treatment requires that we reconceptualize the physics of energy balance with a biological perspective.
David S. Ludwig, MD, PhD, is co-director of the New Balance Foundation Obesity Prevention Center at Boston Children’s Hospital. He holds the rank of Professor of Pediatrics at Harvard Medical School and Professor of Nutrition at Harvard TH Chan School of Public Health.
Disclosures – Ludwig received royalties for books that recommend a carbohydrate-modified diet; his spouse owns a nutrition education and consulting business.