Book Notes - The Hungry Brain

First, we encountered the reward system, centered in the basal ganglia, which teaches us how to get food properties—such as fat, sugar, starch, and salt—that the brain instinctively views as valuable. The reward system collects food-related cues from our external sense organs and our digestive tract, and guides us toward valuable foods by helping us learn and motivating our behavior. What we experience is that we crave and enjoy certain foods more than others, and we develop deeply ingrained eating habits around the foods we enjoy. Unfortunately, this system evolved in an ancient world where calories were hard to come by, and obtaining them required a lot of work, and therefore motivation. In the modern affluent world, where calorie-dense, highly rewarding foods are ubiquitous, our hardwired motivation to eat remains strong, and it drives us to overconsume.

Next, we explored the economic choice system, centered in the orbitofrontal cortex and the ventromedial prefrontal cortex, which integrates the costs and benefits of possible actions and selects the one that’s the best “deal.” This system contains both conscious and nonconscious elements, because it integrates costs and benefits from all parts of the brain that relate to the decision at hand. Some of the costs and benefits it considers relate to system 2 processes, such as predicting the future impact on your waistline of eating a pastry, or calculating whether you can afford to buy it. Yet much of what it considers is nonconscious, and in many animals, including humans, it appears to be wired to value calories above all other food properties. And the easier the calories are to get, the more of them we eat. Another way of saying this is that when it comes to food, its primary cues are calories and convenience. This becomes a liability in a world where calorie-dense foods are more convenient than ever to purchase, prepare, and consume.

The lipostat is a third system, located primarily in the hypothalamus, which nonconsciously regulates adiposity by influencing appetite, our responsiveness to seductive food cues, and our metabolic rate. It takes its cues primarily from the hormone leptin, which is produced by fat tissue, although it also responds to food reward, protein intake, physical activity, stress, and possibly sleep (as well as other factors that are beyond the scope of this book). The lipostat has one job: to prevent your adiposity from decreasing. And it’s very good at what it does, because in the world of our ancestors, losing weight meant having fewer offspring. This is the system that makes weight loss difficult and often temporary, and it may also be part of the reason why our weight tends to creep up over the years. It partially explains why people with obesity tend to eat more than lean people, making obesity a self-sustaining state. When the lipostat squares off with our best intentions to eat the right amount and stay slim, it usually wins in the end.

Working in parallel with the lipostat, the satiety system regulates food intake on a meal-to-meal basis by making us feel full and reducing our drive to continue eating after we’ve had enough. Located primarily in the brain stem, the satiety system takes its cues from the digestive tract, which relays how much volume we’ve eaten, and the protein and fiber content of our food. The satiety system also receives cues from the reward system, which tends to shut down the feeling of satiety when we eat highly rewarding foods, such as pizza, french fries, and ice cream. And finally, it takes important cues from the lipostat, which increases or decreases satiety to help maintain the stability of body fat stores. One of the reasons why modern food tends to be so exceptionally fattening is that it doesn’t provide the cues the satiety system needs to appropriately regulate calorie intake. We tend to use the sensation of fullness as an intuitive signal that we’ve eaten enough, so when we eat calorie-dense, low-fiber, low-protein, highly palatable foods that provide little satiety per calorie, we overeat substantially without even realizing it.

The genetic details of how each person’s lipostat and satiety system are constructed go a long way toward explaining why some of us develop obesity in the modern world, while others remain lean. Each person’s brain has a unique genetic blueprint, and this nudges us to interact differently with food and defend different levels of adiposity. Some people are naturally resistant to overeating even in a very fattening food environment, while most of us are susceptible. Certain lucky folks don’t gain weight even if they do overeat, because their lipostat just burns off the excess calories. This makes it very difficult to judge people for their weight, since we’re all born with different predispositions. At the same time, for most of us, our genetic makeup is just a predisposition—not an inevitable fate. Our ancestors four generations ago carried the same genes we do, yet they rarely developed obesity because they lived in a different context that provided profoundly different cues to the brain and body.

The sleep and circadian rhythm systems, located in the hypothalamus, the brain stem, and other brain regions, nonconsciously influence eating behavior and adiposity in large part by interacting with the reward system, the lipostat, and the economic choice system. The amount of restorative sleep we get, the timing of our sleep, the blue-wavelength light we see, and the timing of our meals are key cues that regulate these systems. When we don’t sleep enough, or don’t sleep well enough, it increases the reward system’s responsiveness to food cues, and we often end up eating more calories. It affects our economic choice system, promoting an “optimism bias” that makes us think more about the current benefits of eating a pastry than the future costs. And it nudges us to become less faithful to our rational, constructive daily goals, such as eating healthy food. When our sleeping and eating behaviors are misaligned with the day-night cycle of the sun, or with our own internal clocks, it can also cause us to gain weight and undermine our metabolic health. In the modern affluent world, with its time-consuming responsibilities, high rates of sleep disorders, abundant artificial light at night, stimulating media, rotating shift work, and travel between time zones, the sleep and circadian rhythm systems receive cues that often send our eating behavior and weight in the wrong direction.

Finally, the threat response system, rooted in many parts of the brain but coordinated in large part by the amygdala, is a largely nonconscious collection of processes that help us manage challenging situations by altering our behavior and physiology. This system takes its cues from a variety of sensory inputs that convey information about potential threats, such as vision and hearing, but also from abstract concepts, such as the possibility of being laid off. In the modern world, most of the threats it deals with are psychological, but in many ways it still reacts as if we’re fighting off wild beasts. It’s not clear that we have more to be stressed about today than our ancestors did, yet it’s possible that we cope with our stress less effectively than we did in times past. In certain people, psychological stress sharply increases cortisol levels, and this may reduce the sensitivity of the lipostat to leptin, in turn increasing food intake and the accumulation of body fat. This is particularly true when we feel like we have little control over a stressful situation. Stress also shifts our eating preferences toward comfort food—which is usually calorie dense and highly palatable—because it helps dampen the activity of the stress response system and makes us feel better.