Scientists propose a rethink of the role of carbs in obesity
- A favorite theory asserts that carbohydrates in food cause a spike in insulin, which promotes fat storage and increases appetite, resulting in overeating.
- However, recent research shows that this “carbohydrate-insulin model” could be an oversimplification.
- In an article in the journal Science, researchers argue that while low carbohydrate, high fat diets might help some persons lose weight, a far more nuanced model is required to clarify how they work.
- They write that insulin levels between meals, and the hormone’s effect on multiple organs, are more very important to balancing the body’s energy budget.
- For decades, the sources of obesity - and the most effective way to lose excess weight - have been the main topic of fierce debate among scientists and healthcare professionals.
According to 1 theory, referred to as the “carbohydrate-insulin modelTrusted Source,” drink and food that contain huge amounts of carbohydrates result in a spike in circulating insulin levels.
The hormone drives fat cells, or “adipocytes,” to store the surplus calories, which reduces the option of these energy sources for all of those other body.
This, subsequently, increases hunger and slows metabolism, which contributes to weight gain as time passes.
Dietitians often cite the carbohydrate-insulin model to explain the success of high fat, low carb diets like the ketogenic diet.
Unlike carbohydrates, fat molecules does not result in a spike in insulin levels immediately after a meal.
On the far side of the debate, the energy balance modelTrusted Source makes less of a distinction between fat and carbohydrates.
This model focuses instead on the balance between total calorie consumption by eating and drinking, and total calorie expenditure through physical activity.
According to the model, if calorie consumption exceeds expenditure, the effect will be weight gain over time. But if expenditure exceeds intake, the eventual outcome will be weight loss.
Overly simplistic?
Writing in the journal Science, two scientists argue that the carbohydrate-insulin model is overly simplistic.
John Speakman, from the University of Aberdeen in britain, and Kevin Hall, of the National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, MD, usually do not dispute the success of high fat, low carbohydrate diets for a few individuals.
They also acknowledge that insulin plays a significant role in body fat regulation.
But they question if the aftereffect of insulin on adipocytes after consuming food saturated in carbohydrates is solely responsible for weight gain.
They write:
“[W]e suggest that the role of insulin in obesity may be better understood by considering its action on multiple organs that's driven by factors mostly independent of carbohydrate intake. Reconsidering the role of insulin may improve our knowledge of the causes of obesity and its treatment.”
They cite a 2020 study in mice that compared the effect of 29 different diets on surplus 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 bigger insulin levels will climb after eating.
As a result, based on the model, the mice should lay out more body fat and increase their total calorie consumption.
However, after 12 weeks - roughly equal to 9 years in humans - mice that ate high carb diets consumed fewer calories and had gained less fat and overall body weight.
This is despite having higher circulating insulin levels following eating.
Studies in humans
Acknowledging that studies in mice may not reflect what goes on in humans, the authors cite research in persons that produced similar results.
For instance, another recent studyTrusted Source compared the effect of two diets on persons with excess weight.
Each diet lasted for 2 weeks. One comprised around 10% carbohydrate and 75% fat, as the other contains approximately 75% carbohydrate and 10% fat.
Participants were permitted to eat as much or as little as they wanted.
As predicted by the carbohydrate-insulin model, the high carb diet resulted in a more substantial 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 reduced carb diet.
Only the high carb diet led to a significant lack of body fat.
Speakman and Hall argue that insulin affects many organs around your body, and not only after mealtimes.
They write that its role in regulating surplus fat “is most beneficial understood within a dynamic network of factors controlling and mediating the consequences of energy imbalance.”
For example, they state high insulin levels, coupled with signals from fat tissue, tell the mind to lessen energy intake when the amount of surplus fat rises above a crucial threshold.
Source: www.medicalnewstoday.com
