Note: This format is one that I will (hopefully) use quite often. I’ll take an article that I read and “spark-note” it for the average person. Thus, you learn the takeaway lessons with a fraction of the effort.
Carbs. Everyone is afraid of them. Eat them and, boom, that thunderclap was your thighs. Or so the conventional wisdom goes. But Stephan Guyenet, the brilliant blogger of Whole Health Source, is doing his damned best to dispel the dogma about carbohydrates and insulin as the evil geniuses behind the obesity epidemic. The following excerpts come from his excellent post “The Carbohydrate Hypothesis of Obesity: a Critical Examination“, a post which ought to be mandatory reading for everyone ever. Of course, if you’re lazy, then enjoy the spark notes version below:
I’d like to begin by emphasizing that carbohydrate restriction has helped many people lose body fat and improve their metabolic health. Although it doesn’t work for everyone, there is no doubt that carbohydrate restriction causes fat loss in many, perhaps even most obese people. For a subset of people, the results can be very impressive. I consider that to be a fact at this point, but that’s not what I’ll be discussing here.
If calories and protein are kept the same, high-carbohydrate meals cause equal or greater satiety than high-fat meals, and equal or less subsequent food intake, despite a much larger insulin response.
Therefore, if insulin doesn’t increase energy intake (if anything, the combination of insulin and amylin that the pancreas releases in response to carbohydrate decreases it), and doesn’t decrease energy expenditure (if anything, it increases it), then how exactly is it supposed to cause energy accumulation in the body as fat? There is no energy fairy. Obese people are obese despite having higher fasting insulin, not because of it. The fact is, insulin spikes after meals temporarily decrease fat release from fat cells, but if you look at total 24 hour energy balance, insulin spikes do not cause fat accumulation. This is exactly how you would expect the system to work if it were designed to constructively handle a wide variety of macronutrient ratios, which it is. Just as cholesterol did not evolve to give us heart attacks, insulin did not evolve to make us fat.
Insulin is also co-secreted with amylin, which suppresses food intake and body weight (13). This is why insulin is viewed by most obesity researchers as an anti-obesity hormone, not an obesity hormone.
Obese people do not have a defect in the ability to release fat from fat cells and burn it, to the contrary. They release more fat from fat cells than lean people, and burn more of it. However, this is compensated for by a higher energy intake, and a higher rate of fat incorporation into fat cells that counterbalances the increased expenditure.
Food reward/palatability is an alternative possibility that fits the evidence better. Another plausible hypothesis is reduced fiber and micronutrient density.
Carbohydrate consumption per se is not behind the obesity epidemic. However, once overweight or obesity is established, carbohydrate restriction can aid fat loss in some people. The mechanism by which this occurs is not totally clear, but it has nothing to do with removing the supposed suppressive effect of insulin on fat release from fat cells. Carbohydrate restriction spontaneously reduces calorie intake (as does fat restriction), suggesting the possibility that it alters body fat homeostasis, but this alteration likely occurs in the brain, not in the fat tissue itself. The brain is the primary homeostatic regulator of fat mass, just as it homeostatically regulates blood pressure, breathing rate, and body temperature.
