Good Calories, Bad Calories

This “harmony of tissue metabolisms” is orchestrated by the hypothalamus, via the central nervous system and the endocrine system of hormones. These regulate the filling and emptying of the various storage depots in response to an environment that might require that we suddenly expend more or less energy, or store more or less fat, to accommodate seasonal variations. The hypothalamus does what the brains of insects do: it integrates sensory signals from the body and the rest of the brain, and couples them to motor reflexes that permit or restrain eating behavior. It also adjusts this filling and emptying of the fuel reserves to accommodate the immediate need for fuel and the anticipated need for fuel.

According to this hypothesis, weight stability is nothing more than an equilibrium between the fatty acids flowing into the energy buffer of the fat tissue and the fatty acids flowing out. What the body regulates, as Le Magnen suggested, is the fuel flow to the cells; the amount of body fat we accumulate is a secondary effect of the fuel partitioning that accomplishes this regulation.

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. Le Magnen himself demonstrated this in his animal experiments. When he infused insulin into rats, it lengthened the fat-storage phase of their day-night cycle, and it shortened the fat-mobilization-and-oxidation phase accordingly. Their diurnal cycle of energy balance was now out of balance: the rats accumulated more fat during their waking hours than they could mobilize and burn for fuel during their sleeping hours. They no longer balanced their overeating with an equivalent phase of undereating. Not only were their sleep-wake cycles disturbed, but the rats would be hungry during the daytime and continue to eat, when normally they would be living off the fat they had stored at night.^*134 Indeed, when Le Magnen infused insulin into sleeping rats, they immediately woke and began eating, and they continued eating as long as the insulin infusion continued. When during their waking hours he infused adrenaline—a hormone that promotes the mobilization of fatty acids from the fat tissue—they stopped eating.

If this hypothesis holds for humans, it means we gain weight because our insulin remains elevated for longer than nature or evolution intended, and so we fail to balance the inevitable fat deposition with sufficient fat oxidation. Our periods of satiety are shortened, and we are driven to eat more often than we should. If we think of this system in terms of two fuel supplies, the immediate supply in the gut and the reserve in our fat deposits, both releasing fuel into the circulation for use by the tissues, then insulin renders the fat deposits temporarily invisible to the rest of the body by shutting down the flow of fatty acids out of the fat cells, while signaling the cells to continue burning glucose instead. As long as insulin levels remain elevated and the fat cells remain sensitive to the insulin, the use of fat for fuel is suppressed. We store more calories in this fat reserve than we should, and we hold on to these calories even when they’re required to supply energy to the cells. We can’t use this fat to forestall the return of hunger. “It is not a paradox to say that animals and humans that become obese gain weight because they are no longer able to lose weight,” as Le Magnen wrote.