What Do We Know About Atkins Diet

The Atkins diet was immensely popular in the early 2000s and is often credited as being one of the forefathers to the Paleo diet and other recent low-carb diet programs. Anecdotally, many have sworn by low-carb diets, but is there any concrete science to support the idea that consuming less carbohydrates leads to weight loss and improved health? The general idea is that carbohydrate intake increases insulin levels, which promotes the storage of fat. There is some truth to the insulin hypothesis, but the hard science paints a much more complicated picture.

The prevailing belief behind low-carb diets is that carbohydrate consumption leads to the release of insulin, which is a hormone that is secreted by the pancreas. All carbohydrates, whether it is fructose found in fruits or complex starchy carbohydrates found in beans or grains, are broken down into glucose molecules in the body by the intestines and the liver. Insulin binds to cell receptors and helps transport glucose into cells. Excess carbohydrates, broken down into glucose inside the body, gets stored as fat, therefore eating too many carbohydrates leads to weight gain. Using this baseline insulin hypothesis, low-carb diets restrict the amount of carbohydrates eaten and encourage more consumption of fats and proteins. Basically, insulin is the real villain here operating in the shadows and is fueled by carbohydrates. In order to suppress insulin production, you restrict carbohydrate consumption and as a result, excess carbs cannot be stored as fat and then the weight comes off.

The issue with the insulin hypothesis is that fat and protein also stimulate an insulin response. Essentially, the role of insulin in your body is to regulate the various nutrients, primarily glucose, fatty acids, and amino acids in your bloodstream. Dietary fats and proteins are broken down in the body into fatty acids and amino acids. While the fat you already have stored is burned as a last resort by your body, insulin will direct circulating protein, fat, and carbohydrates to be burned for energy in equal amounts. If you were to consume 100 calories of either protein, fat, or carbs, insulin would suppress fat burning and use any one of the circulating fuels. Since they are all in equal amounts, theoretically, consuming 100 calories of protein over 100 calories of carbohydrates should not make any difference in terms of fat storage.

In accordance with the first law of thermodynamics, the low-carb/insulin hypothesis must prove that insulin is somehow leading to a decrease in energy intake with lower carbohydrate consumption. Studies have shown that high-protein meals can stimulate insulin production equal or greater than high-carbohydrate meals. Other studies have observed that the higher degree of insulin release, the increased levels of satiety. This contradicts the idea that high-carb intake causes increased food consumption as a result of dramatic insulin spikes. Furthermore, despite high-carb meals causing a higher insulin response than meals rich in fat, satiety has been observed to be more or less the same. In animal studies, subjects injected with insulin did not show any increase in food intake or weight increases. Contrary to the insulin hypothesis, insulin was more correlated to less food intake and decreased weight gain.

Anecdotal evidence should not be dismissed when it comes to people that have found tremendous success with low-carb diets. Like many other diets, the results may be positive, but the idea driving the diet remains up to debate. The insulin hypothesis for low-carb diets is not supported by the current science that is available. Lower consumption of carbohydrates may very well be the source of the weight loss, but insulin does not appear to be one of the main factors.