For decades, the causes of obesity and the most effective way to lose weight have been the subject of fierce debate among scientists and healthcare professionals.
According to one theory, known as the carbohydrate-insulin model, food and drink that contain large amounts of carbohydrates cause a spike in circulating insulin levels.
The hormone drives fat cells, or adipocytes, to store the excess calories, which reduces the availability of these energy sources for the rest of the body.
This, in turn, increases hunger and slows metabolism, which leads to weight gain over time.
Dietitians often cite the carbohydrate-insulin model to explain the success of high fat, low carbohydrate diets such as the ketogenic diet.
Unlike carbohydrates, dietary fat does not cause a spike in insulin levels immediately after a meal.
On the other side of the debate, the energy balance model makes less of a distinction between fat and carbohydrates.
This model focuses instead on the balance between total calorie intake through eating and drinking, and total calorie expenditure through physical activity.
According to this model, if calorie intake exceeds expenditure, the result will be weight gain over time. But if expenditure exceeds intake, the eventual outcome will be weight loss.
Writing in the journal Science, two scientists argue that the carbohydrate-insulin model is overly simplistic.
John Speakman, from the University of Aberdeen in the United Kingdom, and Kevin Hall, of the National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, MD, do not dispute the success of high fat, low carb diets for some individuals.
They also acknowledge that insulin plays an important role in body fat regulation.
But they question whether the effect of insulin on adipocytes after eating food high in carbohydrates is solely responsible for weight gain.
They write:
[W]e propose that the role of insulin in obesity may be better understood by considering its action on multiple organs that is driven by factors mostly independent of carbohydrate intake. Reconsidering the role of insulin may improve our understanding of the causes of obesity and its treatment.
They cite a 2020 study in mice that compared the effect of 29 different diets on body fat.
Of these, 16 diets maintained a constant intake of protein while varying the relative contribution of fat and carbohydrate to total calorie intake.
The carbohydrate-insulin model predicts that the more carbohydrates are in a diet, the higher insulin levels will climb after eating.
As a result, according to the model, the mice should lay down more fat and increase their total calorie intake.
However, after 12 weeks roughly equivalent to 9 years in humans mice that ate high carb diets consumed fewer calories and had gained less fat and overall body weight.
This was despite having higher circulating insulin levels following eating.
Acknowledging that studies in mice may not reflect what happens in humans, the authors cite research in people that produced similar results.
For example, another recent study compared the effect of two diets on people with excess weight.
Each diet lasted for 2 weeks. One comprised around 10% carbohydrate and 75% fat, while the other consisted of approximately 75% carbohydrate and 10% fat.
Participants were allowed to eat as much or as little as they wanted.
As predicted by the carbohydrate-insulin model, the high carb diet resulted in a larger spike in insulin levels following meals.
However, participants on the high carb diet consumed fewer calories and reported that they felt just as satisfied after eating compared with those on the low carb diet.
Only the high carb diet resulted in a significant loss of body fat.
Speakman and Hall argue that insulin affects many organs around the body, and not just after mealtimes.
They write that its role in regulating body fat is best understood as part of a dynamic network of factors controlling and mediating the effects of energy imbalance.
For example, they say high insulin levels, combined with signals from fat tissue, tell the brain to reduce energy intake when the amount of body fat rises above a critical threshold.
David Ludwig, M.D., Ph.D., professor of nutrition at Harvard School of Public Health in Boston, MA, a leading proponent of the carbohydrate-insulin model, questioned the research cited in the article by Speakman and Hall.
He told Medical News Today that the study in mice was strongly biased because the low carb diets contained large amounts of saturated fat.
In rodents, saturated fat causes severe inflammation and metabolic dysfunction, precluding a meaningful test of the [carbohydrate-insulin model], he said.
He added that other studies have found that rodents on high carb diets rapidly develop obesity.
He also challenged the validity of relatively short studies in humans, such as the 2-week study cited by Speakman and Hall, which he said do not give the body sufficient time to adapt to the change in nutrients.
His own meta-analysis suggests that longer studies consistently show higher energy expenditure on low carb diets.
Several reviews of clinical trials have shown that low carb, high fat keto diets promote weight loss.
Prof. Naveed Satar from the Institute of Cardiovascular and Medical Science at the University of Glasgow in the U.K. told Medical News Today that low carb diets can help people lose weight.
He believes the diets owe their success to lower total calorie intake as a result of reduced appetite, but not from how some experts envisioned the workings of the carbohydrate-insulin model.
People who go on low carb diets tend to eat less as they increase protein intake, which tends to suppress appetite a little, he explained.
He added that his own research suggests that the excess calorie intake of individuals with excess weight tends to come from fat rather than sugar.
This suggests that, along with reduced calorie intake, reduced fat intake should remain an important component of weight-loss diets.
Continued here:
Should we rethink the role of carbs in obesity? - Medical News Today
