Scientists propose a rethink of the role of carbs in obesity
09 May, 2021
For decades, the causes of obesity - and the simplest way to lose excess weight - have been the main topic of fierce debate among scientists and healthcare professionals.
According to one theory, referred to as the “carbohydrate-insulin modelTrusted Source,” food and drink that contain large 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, in turn, increases hunger and slows metabolism, which brings about weight gain as time passes.
Dietitians often cite the carbohydrate-insulin model to make clear the success of high fat, low carbohydrate diets including the ketogenic diet.
Unlike carbohydrates, dietary fat does not cause a spike in insulin levels soon 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 through eating and drinking, and total calorie expenditure through exercise.
According to this model, if calorie consumption exceeds expenditure, the result will be weight gain as time passes. 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.
In addition they acknowledge that insulin plays a crucial role in body fat regulation.
But they question whether the aftereffect of insulin on adipocytes after consuming food saturated in carbohydrates is solely in charge of weight gain.
They write:
“[W]e suggest that the role of insulin in obesity could 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 knowledge of the causes of obesity and its treatment.”
They cite a 2020 study in mice that compared the result of 29 different diets on surplus fat.
Of the, 16 diets maintained a frequent intake of protein while varying the relative contribution of fat and carbohydrate to total calorie consumption.
The carbohydrate-insulin model predicts that the more carbohydrates are in a diet, the bigger insulin levels will climb after eating.
As a result, in line with the model, the mice should lay out 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.
Studies in humans
Acknowledging that studies in mice might not reflect what happens in humans, the authors cite research in persons that produced similar results.
For instance, another recent studyTrusted Source compared the result of two diets on persons with excess weight.
Each diet lasted for 14 days. One comprised around 10% carbohydrate and 75% fat, as the other consisted of approximately 75% carbohydrate and 10% fat.
Participants were allowed to eat as much or less than 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 resulted in a significant lack of body fat.
Speakman and Hall argue that insulin affects many organs around your body, and not just after mealtimes.
They write that its role in regulating surplus 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 mind to lessen energy intake when the quantity of surplus fat rises above a crucial threshold.
Source: www.medicalnewstoday.com
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