Back to the topic of carbohydrates, insulin, and obesity for a moment. This time we’ll discuss satiety as it relates to variations in these three things. We’ll primarily be using material from Gary Taubes’ Good Calories Bad Calories, as it has some of the most substantive discussion on satiety and insulin that I’ve seen. Besides insulin’s effect on one’s ability to burn fat, its next most important (and related) trait is its strong effect on satiety.
After page 427 of the book, Taubes’ first discusses two popular hypothesis related to diet and satiety. The first is called the glucostat hypothesis and was developed by Jean Mayer. “Receptors in the hypothalamus, said Meyer, metabolize glucose, initiating the sensation of hunger when the available supply of glucose falls, and provoking satiety when it rises.” So, he thought that if the body sensed a lack of supply (of calories), it would burn the remaining glucose in the blood to make one hungry, and thus cause one to up the supply through eating. Taubes (and even Mayer) explain, however, that this hypothesis is lacking an explanation of the body’s fine adjustment knob when it comes to weight (i.e., when one recovers from illness, they quickly achieve their former weight as people often do after ending a diet). Taubes doesn’t offer the hypothesis much treatment, perhaps because of its lack of breadth.
The second hypothesis explaining weight and satiety is what’s called the lipostatic regulation of the lipostat (thus named by Gordon Kennedy). It would “evolve in the 1970’s into the remarkably durable notion that we are all endowed with a certain set point of body weight or adiposity that we defend against both caloric deprivation and […] caloric surplus.” The main thinking here is that the body has a set point (or weight), above which the hypothalamus will suppress hunger, and below which it will induce hunger. Taubes’ dismisses this theory because it simply failed to explain how the brain manages to monitor our fat stores. He also thought that simply explaining that our brain monitored our fat stores and regulated hunger appropriately was just another way of saying that our weight is usually stable because of “a mysterious mechanism in the brain whose function is to achieve this stability.” Thus this one was killed cause of its black boxyness.
Taubes later gets to his insulin-based hypothesis, which appears grounded in a mountain of research. He cites several studies and then explains “that anything that induces fatty acids to escape from the fat tissue and then be burned as fuel will promote satiety by providing fuel to the tissues. Anything that induces lipogenesis, or fat synthesis and storage, will promote hunger by removing the available fuel from the circulation.” So, essentially, those foods that promote the burning of fats instead of glucose will promote satiety. Cue wikipedia: “Since insulin is the primary hormonal signal for energy storage into fat cells, which tend to retain their sensitivity in the face of hepatic and skeletal muscle resistance, [insulin resistance] stimulates the formation of new fatty tissue and accelerates weight gain.” Connecting the dots then, not only do carbohydrates raise our insulin levels which leads to the uptake of fat, but they also trigger hunger because they promote the burning of glucose almost exclusively (i.e., our ready energy stores are depleted).
Taubes concludes (pp. 435):
“The implication of this hypothesis is that both weight gain and hunger will be promoted by factors that work to deposit fatty acids in the fat tissue and inhibit their mobilization—i.e., anything that elevates insulin. Satiety and weight loss will be promoted by factors that increase the release of fatty acids from the fat tissue and direct them to the cells of the tissues and organs to be oxidized—anything that lowers insulin levels.”
Inasmuch as Taubes has done his research, and it appears that he has, it looks as if it all boils down to insulin. Next in this series we’ll talk about the glycemic index.