The Hungry Brain: Outsmarting the Instincts That Make Us Overeat by Stephan Guyenet Ph.D.
While a calorie-seeking brain is an asset when calories are hard to come by, it’s a liability when we’re drowning in food. Scientists call this an evolutionary mismatch; in other words, a situation in which once-useful traits become harmful once they’re dragged into an unfamiliar environment.
they found something truly remarkable: Prior to the turn of the twentieth century, fewer than one out of seventeen middle-aged white men was obese.
between 1999 and 2000 using data from the US Centers for Disease Control and Prevention. They found that it started at 24 percent in early middle age and increased sharply to 41 percent by retirement age.
Clothing is now available in staggering sizes such as XXXXXXXXL.
The new, evidence-based rule of thumb is that you must eat ten fewer Calories per day for every pound you want to lose. Yet it takes several years to arrive at a new stable weight, so most people will want to start with a larger calorie deficit to reach their target weight more quickly and then use the ten-Calorie rule of thumb to maintain the loss.
Sclafani went to the supermarket and bought a variety of calorie-dense “palatable supermarket foods,” including Froot Loops, sweetened condensed milk, chocolate chip cookies, salami, cheese, bananas, marshmallows, milk chocolate, and peanut butter. When Sclafani placed these foods into the rats’ cages, along with the obligatory standard rodent pellets and water, the rats immediately gorged on the human food, losing interest in their boring pellets. On this diet, they gained weight at an unprecedented rate.
This leads us to a disturbing conclusion: Palatable human food is the most effective way to cause a normal rat to spontaneously overeat and become obese, and its fattening effect cannot be attributed solely to its fat or sugar content.
In a seminal research paper published in 1999, University of Sheffield researchers brought together evidence from neuroscience and computer modeling to argue that selection is precisely the function of an ancient group of structures deep within the human brain called the basal ganglia.
In humans, the brain eats up one-fifth of our total energy usage, even though it accounts for only 2 percent of our body weight. The fact that evolution allowed us to bear this energy-hogging ball and chain is a testament to its importance. Making smart decisions is a good evolutionary strategy, and no animal does it better than humans.
But if the decision-making capacity of a human and a lamprey are so different, why are the basal ganglia of lampreys and humans so strikingly similar? Grillner and Stephenson-Jones propose an explanation: an evolutionary process called exaptation. As opposed to adaptation, which is the process of developing new traits—such as air-breathing lungs or a four-chambered heart—exaptation takes something that already exists and finds a new function for it; for example, expanding the basal ganglia’s decision-making jurisdiction to govern other, more advanced types of decisions.
In humans, the most numerous inputs to the striatum come from the cerebral cortex, which evolved from the pallium (similar to the one found in today’s lampreys).
As it turns out, several disorders affect the basal ganglia. The most common is Parkinson’s disease, which results from the progressive loss of cells in a part of the basal ganglia called the substantia nigra. These cells send connections to the dorsal striatum, where they produce dopamine, a chemical messenger that plays a very important role in the function of the striatum.
High levels of dopamine essentially make the basal ganglia more sensitive to incoming bids, lowering the threshold for activating movements.
In fact, common side effects of L-dopa treatment include heightened emotional states, hypersexuality, and compulsive and addictive behaviors, such as gambling, shopping, drug abuse, and binge eating. These are called impulse control disorders because people lose the ability to keep their basic impulses in check.
Learning shapes all three levels of our decision-making process: motivational, cognitive, and motor. Reinforcement strengthens them all, because they’re all required for effective goal-directed behaviors.
Most researchers believe the brain’s teaching signal is the fascinating molecule dopamine.34
On a cellular level, this happens because dopamine acts on basal ganglia loops that were recently active, increasing the likelihood that they will be activated again in the future. So whatever you’re doing when the dopamine hits, you’re more likely to repeat it when the same situation arises again.
Dopamine is the “learning chemical” rather than the “pleasure chemical.”
Your average lab rat likes cherry-flavored water about as much as grape-flavored water. So if you place a bottle of each into its cage, it will drink about the same amount from each. However, in a groundbreaking study published in 1988, Sclafani’s team showed that when they infused partially digested starch directly into the rats’ stomachs while they drank cherry-flavored water, the rats developed a preference for that flavor over the grape flavor.35 And the opposite preference developed when they repeated it with the grape flavor. Even though the starch never entered their mouths, after four days, the rats displayed a near-total preference for the starch-paired flavor. Sclafani called this phenomenon conditioned flavor preference.36
Further experiments showed that the rats weren’t detecting the starch itself but the sugar glucose that’s released as starch is broken up in the digestive tract. And the critical location for detection was the upper small intestine. Somehow, the intestine was sensing the glucose and sending a signal to the brain that said, “Something good just happened. Do that again!”
the food is rich in starch or sugar, a large spike in dopamine causes the rat to increase its preference for the flavors and aromas of the food it just ate—and become more motivated to seek foods with those flavors and aromas in the future. In this way, the rat becomes better at identifying and seeking foods that contain carbohydrate.
Sclafani’s team has also been able to condition flavor preferences using fat and protein, demonstrating that rats respond to all three major classes of calorie-containing nutrients: carbohydrate (starches and sugars), fat, and protein.38 Sclafani’s work also revealed that the more concentrated the caloric load of a food—or the higher its calorie density—the more reinforcing it is.
Calories don’t just drive flavor preferences; they also drive preferences for the aromas, sights, sounds, and even locations that predict the availability of calories. It turns out that rats like to hang out in places where good things happen, and calories in the belly is definitely a good thing. This is how we learn to respond to our surroundings in a way that gets us what we want.
When you examine this list, you’ll find it apparent that the human brain is extremely preoccupied with calories. Other than salt, every innate preference is a signal that indicates a concentrated calorie source.
every known addictive drug either increases dopamine levels in the ventral striatum or stimulates the same signaling pathway in a different manner.
We now have extremely calorie-dense, carefully engineered combinations of sugar, fat, salt, and starch that would have been inconceivable to our hunter-gatherer ancestors, who had no choice but to eat simple wild foods.
addictive naturally occurring substances. For example, the leaves of the coca plant are widely chewed in South America as a mild stimulant and appetite suppressant reminiscent of caffeine. However, when we extract and concentrate the active ingredient of the coca leaf, this results in a much more addictive substance: cocaine. A secondary chemical process called freebasing transforms cocaine into the extremely addictive drug crack cocaine.
Human technology has allowed us to concentrate and enhance the property of the coca plant that increases dopamine release and reinforces behavior, transforming it from a useful herb into a life-destroying drug.
modern food technology has allowed us to concentrate the reinforcing “active ingredients” in food to an unprecedented degree, and addiction-like behavior in a subset of people is the predictable result.
cacao tree, a plant native to tropical South America, are naturally extremely calorie dense, due to their high fat content. When fermented, roasted, and ground into a paste, these seeds become chocolate: a magical substance that’s solid at room temperature and melts in the mouth. To mask the naturally bitter flavor of chocolate, we add a generous dose of refined sugar, and sometimes dairy. The calorie density, fat content, carbohydrate content, and sweet taste of chocolate are a powerfully reinforcing combination, but chocolate has another trick up its sleeve that makes it the king of cravings: a habit-forming drug called theobromine.
Theobromine is a mild stimulant that’s moderately reinforcing, like its cousin caffeine.48 Although theobromine on its own may not be the bee’s knees, when added to a substance that’s already highly reinforcing, it puts many of us over the edge. It may come as no surprise that chocolate addiction is a legitimate topic of scientific research.
The key is to control food cues in your personal environment. Ultimately, a little bit of wise planning can go a long way.
Food variety has a powerful influence on our calorie intake, and the more variety we encounter at a meal, the more we eat.
When a stimulus is new, we tend to be very interested in it because it might be important. Once we’ve seen it many times in a short period of time, it’s less likely to be important, and we stop paying attention. As it turns out, this habituation process operates each time we sit down to a meal.
This shows that we can eat our fill of a specific food and feel totally satisfied, but that doesn’t mean we won’t eat other foods if they’re available. Rolls called this phenomenon sensory-specific satiety. Satiety is the sensation of fullness we get after we eat food, and sensory-specific means this fullness only applies to foods that have similar sensory properties (sweet, salty, sour, fatty) to the ones we just ate.
Sensory-specific satiety also helps explain why we’re happy to eat dessert even after a large meal. We’re no longer hungry for savory food at all, yet when the dessert menu appears, we suddenly grow a “second stomach.” We’re satiated of savory foods, but we aren’t satiated of sweets. A novel sensory stimulus with an extremely high reward value makes it easy to pack away an additional 200 Calories of dessert. So it makes sense that the converse is also true, as we saw with the potato diet: When food reward and variety decrease, so does food intake.
Epstein’s team to calculate a personal characteristic called the relative reinforcing value of food (RRVfood). RRVfood is a measure of how hard a person is willing to work for food, relative to a nonfood reward such as reading material—and people differ greatly in this regard.
RRVfood asks: When faced with a choice, are you more likely to eat or to do something else? These studies have produced very provocative results: first, that sweet foods are exceptionally motivating, especially to youths.
A second provocative conclusion is that people who are overweight or obese tend to have a higher RRVfood than people who are lean. In particular, children who are overweight or obese are much more willing to work for highly rewarding foods like pizza or candy than lean children, even if their baseline level of hunger is the same.
Their results were remarkably consistent: RRVfood not only predicts weight gain in children, but in every age group they examined. In one study, adults with a high RRVfood gained more than five pounds over the course of a year, whereas adults with a low RRVfood only gained half a pound.
Heightened food reward sensitivity does seem to contribute to overeating and fat gain over time.
Drug abuse research suggests that a person’s susceptibility to addiction depends not only on how reinforcing the drug is for him but also on his ability to control his behavior in response to a craving—in other words, his impulsivity. Impulsivity describes a person’s ability—or lack thereof—to suppress or ignore basic urges that are beyond conscious control. It’s the opposite of what we commonly call self-control.
Epstein coined the term reinforcement pathology to describe the dangerous combination of high reinforcement sensitivity and high impulsivity. He explains that it’s like having a “lead foot and worn brakes.”
On the other hand, people who have a high RRVfood but who aren’t impulsive (lead foot and good brakes) aren’t at an increased risk of overeating or weight gain.
Epstein is quick to point out that there’s a third important factor in addition to RRVfood and impulsivity: the presence of highly rewarding food in your personal environment.
The deadliest combination, therefore, occurs when an impulsive person with a high food reward sensitivity lives in an environment that’s bursting at the seams with highly rewarding foods.57 And as we will soon see, the United States qualifies as such an environment.
Of the 2.6 million years since our genus Homo emerged, we were hunter-gatherers for 99.5 percent of it, subsistence-level farmers for 0.5 percent of it, and industrialized for less than 0.008 percent of it. Our current food system is less than a century old—not nearly enough time for humans to genetically adapt to the radical changes that have occurred. Our ancient brains and bodies aren’t aligned with the modern world, and many researchers believe this evolutionary mismatch is why we suffer from such high rates of lifestyle-related disorders, such as coronary heart disease, diabetes, and obesity.
If we can identify these commonalities, we may be able to understand what the diets of our ancestors were like, and in turn, what our bodies and brains are adapted to. Here are three prominent characteristics these diets have in common: First, they include a limited variety of foods.
Second, they have a limited ability to concentrate the reinforcing properties of food. With only the most basic processing methods at their disposal, nonindustrial cultures—and presumably our distant ancestors—are forced by necessity to eat food in a less calorie-dense, less refined, less rewarding state. Most don’t have the ability to add refined starch, sugar, salt, or concentrated fat to their meals. The glutamate they eat comes from cooking meat and bones rather than from crystalline MSG.
Third, they use few cooking methods. The cooking methods of nonindustrial cultures are extremely limited by modern standards, with most cultures only using two or three methods.
In 1889, Americans spent 93 percent of their food expenditures on food to be eaten at home, and only 7 percent eating out. Today, we spend about half of our food expenditures on food to be eaten at home, and the other half eating out (see figure 17). Much of the recent increase has come from fast-food spending, which has increased ninefold since 1960.
Examining the trajectory of food processing over human history, it’s clear that we’ve gradually purified these reinforcing attributes to their most concentrated states to satisfy our own palates. In nonindustrial diets, fat, starch, sugar, salt, and free glutamate rarely exist in highly concentrated form.
Thanks to government-subsidized corn, it’s so cheap that food manufacturers can use it to beef up the reward value of their foods at virtually no cost, tickling the brain circuits that make us reach for the cookies.
In 1822, we consumed the amount of added sugar in one twelve-ounce can of cola every five days, whereas today we consume that amount every seven hours.
This optimal concentration is called the sugar “bliss point,” and it’s the subject of much industry research, as detailed in the excellent books Salt Sugar Fat and The End of Overeating, by Michael Moss and David Kessler, respectively.
Rather than getting our fat from whole foods like meat, dairy, and nuts, we now get it primarily from oils that are mechanically and chemically extracted from seeds.
Free glutamate, responsible for the meaty umami flavor, occurs naturally—in small amounts—in cooked meats and bone stock. Today, the food industry uses highly concentrated crystalline MSG to give food the savory, meaty flavor our brains crave.
To get around the health concerns that surround MSG, companies have developed alternative sources of glutamate that slip under our radar, such as hydrolyzed yeast and soy protein extracts. The purpose of these substitutes is the same: satisfy the brain’s innate preference for glutamate that keeps people coming back to flavored tortilla chips, salad dressing, soups, and many other foods.
In particular, the combination of concentrated sugar and fat in the same food is a deadly one for our food reward system. It’s also a pairing that rarely occurs in nature, so it’s tempting to speculate that it’s more than our brains are equipped to handle constructively.
The first source of glutamate, perhaps hundreds of thousands of years old, was simply cooked meat. Once we invented cooking vessels, we began boiling bones to make a meaty, glutamate-containing broth—something we’ve probably done since before recorded history. The next step was to develop fish sauce, which is very high in glutamate as a result of the decomposition of naturally occurring fish proteins. Primarily associated with traditional Asian cuisine today, the ancient Romans used a similar sauce called garum more than two thousand years ago. Soy sauce, another concentrated source of glutamate, has been popular in parts of Asia since the same era.
The isolation of pure glutamate by Tokyo Imperial University researcher Kikunae Ikeda in 1908 and the subsequent commercial production of MSG were the culmination of a long historical process that gave us access to increasingly concentrated forms of glutamate.
The Dutch biologist Nikolaas Tinbergen coined the term supernormal stimulus to describe the phenomenon whereby, as he put it, “it is sometimes possible to offer stimulus situations that are even more effective than the natural situation.” Whatever a species’ innate preferences are, they can often be overstimulated by presenting a cue that’s more powerful than what the species has evolved to expect—and this can sometimes lead to highly destructive behavior.
Likewise, our own innate food preferences are commercially exploited by concentrating and combining the properties we find most rewarding, resulting in foods that are more seductive than what our ancestors would have encountered. Creating an obesity epidemic wasn’t the objective; it was just an unfortunate side effect of the race to make money.
The 2010 USDA Dietary Guidelines for Americans reported that the following six foods are the top calorie sources for US adults, in descending order of the number of calories that each contributes to our diet: 1. Grain-based desserts 2. Yeast breads 3. Chicken and chicken mixed dishes 4. Soda/energy/sports drinks 5. Alcoholic beverages 6. Pizza
Here are the top six sources of calories for children and adolescents: 1. Grain-based desserts 2. Pizza 3. Soda/energy/sports drinks 4. Yeast breads 5. Chicken and chicken mixed dishes 6. Pasta and pasta dishes
Yet food reward isn’t the only thing that drives us to overeat. It goes hand in hand with convenience—another factor that titillates the brain circuits that determine our food intake,
“Life is a game of turning energy into kids,”
discipline called optimal foraging theory (OFT). OFT assumes that animals have been crafted by natural selection to acquire food from their environment efficiently, and researchers have successfully applied it to a variety of different species, including human hunter-gatherers. Given the bewildering complexity of human behavior, the basic math of OFT is disarmingly simple: The value of a food item, and hence whether or not it’s worth pursuing, depends on the number of calories it contains, minus the number of calories required to obtain and process it, divided by the amount of time required to obtain and process it.71 In other words, a food’s value is roughly determined by its calorie return rate.
One surprising implication is that hunter-gatherers don’t often collect or eat vegetables—that is, low-calorie plant foods such as leaves.72 If you’re a hunter-gatherer, it doesn’t make a lot of sense to burn 200 Calories collecting 50 Calories’ worth of salad.
The idea of moderation in eating is totally foreign to hunter-gatherers. In fact, Wood, Hill, and Pontzer explain that hunter-gatherer eating habits can be downright gluttonous.
Pontzer adds that the Hadza also drink honey “like a glass of milk.”
“They fully embrace the idea of ‘eat as much pure fat as you can possibly eat,’” explains Wood, adding, “there’s no hint of moderation whatsoever in their drive and motives with eating food.”
“Their brains are designed to want more food because more food converts into higher fertility and higher survivorship, and those things lead to higher [reproductive success].” This leads us to a key conclusion about life as a hunter-gatherer: Gluttony is good for them.
Participants with candy bowls on their desks ate an average of nine Kisses per day. Those with candy bowls in their desk drawers ate six Kisses per day, and those who had to hike all the way across the room only ate four Kisses.
lazy, in fact, that even taking a few steps across the cage to eat and drink aren’t worth the effort. How do we know? Because Salamone’s research shows that dopamine plays a key role in motivation. When he reduces dopamine signaling in the ventral striatum of rodents, they become less willing to work for a reward.
In other words, reducing their dopamine signaling makes them lazy.
Dopamine seems to play a similar role in humans. Increasing dopamine levels using amphetamine makes people more willing to work for rewards, even if the reward is small or uncertain. Dopamine turns us into go-getters.
Dopamine tunes your motivation level to be proportional to the value of the reward you’re pursuing—and it does so beyond your conscious awareness.
Ranson adapted it for use in rats and quickly discovered that the critical location for obesity was not the hypothalamus as a whole but rather a subregion of the hypothalamus called the ventromedial hypothalamic nucleus (VMN).
Researchers dubbed the VMN the satiety center, because disrupting it seemed to cause animals to lose the ability to feel full—and rapidly eat themselves to obesity.
Dubbed the obese mouse, it was extremely fat and had an appetite to match (see figure 30). It also had a low energy expenditure for its size and metabolic disturbances reminiscent of human obesity. The inheritance pattern of its obesity suggested that the effect was caused by a single gene,91 which they called the ob gene.
Theodore Zucker identified a strain of obese rats very similar to the obese mouse. The obesity-causing gene had the same inheritance pattern as the ob gene, and the rats became enormously fat, mostly (but not entirely) due to their prodigious appetites. In fact, they closely resembled rats with VMN lesions, with some animals exceeding two pounds. This strain was named the Zucker fatty rat.
other genetically obese rodent models would be identified, including diabetes and agouti mice.
Gradually, researchers converged on a remarkable conclusion: Even though each obesity model had been developed independently, VMN lesions, the obese mutation, the Zucker fatty mutation, and overfeeding all appeared to impact the same fat-regulating system. Obese mice are unable to produce the satiety factor; VMN-lesioned animals and Zucker fatty rats are unable to respond to it; and overfed animals overproduce it. These independent models all supported the fundamental importance of the same fat-regulating system Hervey had hypothesized in 1959: the lipostat.
In further studies, they found that weight loss, both in people who are lean and obese, triggers a powerful suite of biological and psychological responses that work together to restore the lost fat. To do this, the brain curtails the activity of the sympathetic nervous system and reduces thyroid hormone levels, both of which slow the metabolic rate, accounting for the cold and sluggish feeling some people experience after weight loss. The brain cuts back the number of calories a muscle burns during a given contraction, reducing the calories expended in physical activity. And most important, the brain ramps up hunger and increases the response to food cues that signal high-calorie, high-reward foods.
In effect, substantial weight loss triggers a starvation response, whether a person is lean, overweight, or obese—and this response continues until the fat comes back.
It turns out that people with garden-variety obesity—as opposed to obesity caused by a rare genetic mutation—already have high levels of leptin. And researchers have found that leptin isn’t the miraculous obesity cure the pharmaceutical industry hoped it would be. While leptin therapy does cause some amount of fat loss, it requires enormous doses to be effective (up to forty times the normal circulating amount).
have always thought, and continue to believe,” explains Leibel, “that the leptin hormone is really a mechanism for detecting deficiency, not excess.” It’s not designed to constrain body fatness, perhaps because being too fat is rarely a problem in the wild.
The leptin system functions by the same principle as the thermostat in your home, which measures the ambient temperature and compares it to the temperate set point you’ve programmed. If the temperature dips too low, your thermostat engages the heating system; if it rises too high, it engages the air conditioner. This feedback system serves to maintain the stability, or homeostasis, of your home’s interior temperature.
Similarly, the hypothalamus (and other brain regions, to a lesser extent) is the body’s lipostat—the brain region that regulates appetite and body fatness. It receives information about the size of fat stores from signals, including leptin, and coordinates the physiological and behavioral responses necessary to maintain adiposity (see figure 33
As Leibel and Hirsch observed in their weight-loss studies, if a person loses fat, the lipostat engages a coordinated suite of responses that work to increase energy intake, reduce energy expenditure, and thereby regain the lost fat.
In humans, the lipostat isn’t as good at preventing fat gain, as if your home thermostat has very good heat to prevent the temperature from dropping, but weak air conditioning to prevent the temperature from rising.
Leibel and Hirsch’s findings suggest that the lipostat isn’t broken in garden-variety obesity—it simply regulates adiposity around a higher set point, analogous to turning up the thermostat in your home.104
In other words, for the brain of a person with obesity, obese is the new lean. Researchers call this phenomenon leptin resistance, because the brain seems to have a hard time “hearing” normal levels of leptin.
The first is that once a person develops obesity, it becomes a self-sustaining state, and the person has to overeat to feel the same satisfaction that a lean person feels after eating a smaller meal.
A second key implication is that weight loss is hard because it requires us to fight deeply wired impulses. Long-term diet trials suggest that the hypothalamus is remarkably good at undermining fat-loss efforts.
The good news is that the lipostat responds to the cues we give it through our diet and lifestyle, and we can use this to our advantage.
Again, it seemed as if the diets were not just passively causing weight gain but actually changing the set point of the lipostat. Levin ascribed much of this effect to the diet’s palatability, in part because the rats would only overeat and gain weight on chocolate-flavored Ensure—not vanilla or strawberry!106
Something about the bland diet was allowing their bodies to feel comfortable at a lower weight, suggesting that just as with Levin’s rats eating plain old rat pellets, the low reward value of the diet may have lowered their adiposity set point.
Cabanac found that the portion control group developed the expected hunger response to weight loss—but the bland diet group didn’t. He reported that the bland diet volunteers “reduced their intake voluntarily and were always in good spirits,” while the portion control group “had to continually fight off their hunger and would spend the night dreaming of food.”
On the bland diet, the starvation response never kicked in. Cabanac concluded that diet palatability influences the set point of the lipostat in humans.
RESTRICTING REWARD High-reward foods tend to increase food intake and adiposity, while lower-reward foods tend to have the opposite effect. This suggests a weight management “secret” you’ll rarely find in a diet book: eat simple food.
some practical conclusions. First, calorie-dense, highly rewarding food may favor overeating and weight gain not just because we passively overeat it but also because it turns up the set point of the lipostat.
Second, focusing the diet on less rewarding foods may make it easier to lose weight and maintain weight loss because the lipostat doesn’t fight it as vigorously.
It appears that exercise helps keep the lipostat happy at a lower set point.
The problem with many of the human studies is that they simply offer people exercise advice, without having any way to enforce the advice, and often without even accurately measuring how much exercise was actually performed. In contrast, when we only consider studies in which volunteers had to regularly report to a research gym and exercise under supervision—ensuring compliance—a different picture emerges. In these studies, fat loss is often substantial, and it increases with the intensity and duration of the exercise regimen. So it appears that many of us in the research world, including myself at one time, may have misjudged exercise: It really does cause fat loss.
What’s remarkable is what happened in people who lost as much, or more, weight than expected: They actually decreased their calorie intake in response to the exercise regimen. In the end, about half of the volunteers ate more as a result of the exercise, and half didn’t. Presumably, this reflects the effects of exercise on the lipostat,
It turns out that exercise helps preserve muscle mass during weight loss. Although slow progress on the scale may be frustrating, changes in the mirror and in health as a result of exercise can be better than what the scale suggests.108
evidence suggests that if you can maintain a high level of physical activity, it will probably help you prevent fat gain, accelerate fat loss, and maintain that loss. But it only works if you actually do it—and even then, the degree of fat loss depends on how effectively your brain compensates for the lost calories by increasing your appetite.
When people go on a low-carbohydrate diet, their spontaneous calorie intake drops substantially—even though they usually aren’t making any deliberate effort to eat fewer calories. Why? As you may have noticed, this effect looks a whole lot like what happens when the adiposity set point goes down. If we take a closer look at the diets of people who eat a low-carbohydrate diet, what we see is that when they reduce their carbohydrate intake, the proportion of protein in the diet tends to go up. As it turns out, amino acids, the building blocks of protein, act directly in the hypothalamus, influencing the lipostat system. Although most of the direct evidence comes from rodent studies, a substantial amount of indirect evidence suggests that a high intake of protein may be able to lower the adiposity set point in humans too.
Rather, advice to eat a low-carbohydrate diet may be effective simply because it’s an easy way to get people to eat high-protein foods and reduce major food reward culprits.
Satya Kalra discovered that a small protein called neuropeptide Y (NPY) causes massive overeating when it’s injected into the brain of a rat. Adding to the excitement, researchers discovered that NPY is naturally produced by neurons in the arcuate nucleus, a tiny region of the hypothalamus near the VMN satiety center, and it became more abundant after fasting, suggesting that it could be involved in hunger (see figure 34).
His team was able to show that injecting insulin into the brains of rats reduces the production of NPY in the hypothalamus and also reduces food intake.
Leptin reduced hunger-promoting NPY levels exactly as predicted, supporting the idea that leptin controls food intake (in part) by reducing NPY levels in the brain.
Schwartz published a paper showing that the hypothalamus, and particularly the arcuate nucleus, contains high levels of the receptor for leptin. Even more tantalizing was the accumulating evidence that another group of proteins, called melanocortins, play the opposite role of NPY in the brain: When injected into the brains of rodents, melanocortins powerfully suppressed food intake.111 Like
Schwartz’s group showed that melanocortin levels are also regulated by leptin—yet in the opposite direction of NPY. NPY and melanocortins are key cellular pathways by which leptin regulates food intake and adiposity via the brain.
remarkably logical explanation for how leptin regulates the lipostat: It turns off neurons that drive eating, and it turns on neurons that inhibit eating. And, by implication, when leptin levels decline, neurons that drive eating turn on and neurons that inhibit eating turn off, increasing the drive to eat. This “push-pull” system is redundant and extremely robust, and only disrupting major nodes in the signaling pathway can derail it.
Because of this synergy of appetite-stimulating substances, released in just the right downstream brain regions, NPY neurons are the most powerful driver of eating known to science. If there is such thing as a “hunger neuron” that drives pure, visceral hunger, the NPY neuron is it.113
Sternson’s work shows that the way NPY neurons compel a mouse to seek food is by making the mouse feel bad until it eats.115
it becomes clear that eating motivates us in two distinct ways that reinforce one another: Unpleasant hunger neurons get turned off, and food reward neurons get turned on.
What this suggests is that the primary reason obese animals overeat and become tremendously fat is that their NPY neurons are in constant overdrive because there isn’t any leptin around to keep them in check. Get rid of the NPY neurons, and the animals slim down,
second, even more remarkable implication: The hunger, the obsession with food—many of the physiological and psychological effects that we see in people who are dieting, starving, or born without leptin—could be largely due to a population of hyperactive NPY neurons that is small enough to fit on the head of a pin.
There is little remaining doubt among researchers, and even many doctors, that appetite and body fatness are biologically regulated by nonconscious regions of the brain.
When Velloso’s team analyzed the data, a striking trend emerged: Many of the genes that were more active in obese mice were related to the immune system, and particularly a type of immune system activation called inflammation.
confirming that inflammation in the hypothalamus blocks leptin signaling, leading to leptin resistance and weight gain.
Much of the study focused on two types of cells in the brain called astrocytes and microglia. While neurons are the cells that do most of the information processing of the brain, astrocytes and microglia play a supporting role in keeping delicate neurons happy—protecting them from threats, helping them heal, giving them energy, and cleaning up after them.120 When the brain is injured, these cells go into overdrive, increasing in size and number to counter the threat and accelerate healing. “All conditions that damage the brain,” explains Thaler, “such as trauma, stroke, neurodegenerative disease, even infections to some extent, cause this effect.”
And we found it: Astrocytes in the hypothalami of obese rats and mice were enlarged, and their filaments were tangled together in a thick mat. Microglia had also enlarged and multiplied. Both changes were specifically located in the same area as NPY and POMC neurons (the arcuate nucleus), but not elsewhere.
Not only that, but the injury response and inflammation that developed when animals were placed on a fattening diet preceded the development of obesity, suggesting that this brain injury could have played a role in the fattening process.
Schur’s analysis showed that the more signs of damage we found in a person’s hypothalamus, the more likely he was to have obesity. What’s more, this effect was once again located in the part of the hypothalamus that harbors NPY and POMC neurons. “The scariest implication,” explains Schur, “is that the food we eat may cause damage in areas of the brain that we need to regulate our body weight and our appetite, as well as our blood sugar and, to some degree, our reproductive health.”121
However, what we can conclude is that the hypothalamus is under duress in obesity and that this is likely caused (at least in part) by the unhealthy food we eat. In response to this challenge, the hypothalamus activates a broad swath of cellular stress response pathways, and some of these have the potential to dampen leptin signaling and contribute to the fattening process.122 This likely operates in parallel with the set-point-altering effects of food reward and protein intake
Brain damage is a daunting term, and it may make the situation seem hopeless for people who would like to lose weight. Yet our research also suggests that the process is reversible—at least in mice. When we switch mice off a fattening diet and back on to a strict healthy diet, even without restricting their calorie intake, they lose their excess fat, and their astrocytes and microglia go back to normal. This is true even if they’ve been obese for a long time.
What’s so fattening about the diets we use to make rodents obese in a research setting, and how do they injure the hypothalamus? In many ways, they are similar to the diets of affluent humans. They’re made of refined ingredients; they have a high calorie density; they’re highly rewarding (to rodents); they’re high in fat and often sugar. The
We don’t know all the details yet, but we do know that easy access to refined, calorie-dense, highly rewarding food leads to fat gain and insidious changes in the lipostat in a variety of species, including humans.
In other words, repeated bouts of overeating don’t just make us fat; they make our bodies want to stay fat. This is consistent with the simple observation that in the United States, most of our annual weight gain occurs during the six-week holiday feasting period between Thanksgiving and the new year, and that this extra weight tends to stick with us after the holidays are over.
How might this happen? We aren’t entirely sure, but researchers, including Jeff Friedman, have a possible explanation: Excess leptin itself may contribute to leptin resistance. To understand how this works, I need to give you an additional piece of information: Leptin doesn’t just correlate with body fat levels; it also responds to short-term changes in calorie intake. So if you overeat for a few days, your leptin level can increase substantially, even if your adiposity has scarcely changed (and after your calorie intake goes back to normal, so does your leptin).
Yet Rudy Leibel’s group has also shown that high leptin levels alone aren’t enough—the hypothalamus seems to require a second “hit” for high leptin to increase the set point of the lipostat. This second hit could be the brain injury process we, and others, have identified in obese rodents and humans.
recap what I’ve proposed thus far. We overeat because we’re surrounded by seductive, calorie-dense food that’s a great deal. The food’s high reward value increases the set point of the lipostat, though not necessarily permanently, and this further facilitates overeating. At the same time, overeating itself spikes leptin levels and injures the hypothalamus by a mechanism we have yet to nail down (likely involving diet quality in addition to quantity).
These two simultaneous hits cause the hypothalamus to lose sensitivity to the leptin hormone, meaning that it requires more leptin, and therefore more body fat, to hold off the starvation response that drives us to overeat. This time, the increase in your set point is permanent, or at least difficult to reverse. The lower limit of your comfortable weight creeps up.
Decerebrate rats reacted to a variety of satiety-related signals in the same way as normal rats: They ate less at a meal when Grill’s team gave them a “snack” first, and they ate less in response to satiety hormones that the gut normally produces when we eat. This demonstrated, without a shadow of a doubt, that the brain stem is single-handedly capable of monitoring what’s happening in the gut and generating the satiety response that ends a meal.126
When you eat food, it enters your stomach and stretches it. After partially digesting the food, your stomach gradually releases it into the small intestine. Here, specialized cells in the intestinal lining detect the nutrient content of what you ate, for example, the amount of carbohydrate, fat, and protein. These stretch and nutrient signals are relayed to the brain, primarily via the vagus nerve, which plays a major role in bidirectional gut-brain communication (see figure 39). At the same time, incoming nutrients cause the gut and pancreas to release a number of hormones that either activate the vagus nerve or act on the brain directly.
Despite the fact that part of the hypothalamus was once called the satiety center, and leptin was dubbed the satiety factor, we now believe the brain stem is the primary brain region that directly regulates meal-to-meal satiety, while leptin and the hypothalamus primarily regulate long-term energy balance and adiposity. Grill’s research shows that although decerebrate rats take normal-sized meals, if they are underfed, they are unable to compensate normally by increasing the size of subsequent meals. In other words, their satiety system works great, but their lipostat is out of the picture, once again suggesting that the hypothalamus may be required for that function.
accurate name for the hypothalamus would be the adiposity center, and leptin, the adiposity factor.
The hypothalamus influences brain stem satiety circuits in response to long-term changes in adiposity. In other words, if you’re dieting and you’ve lost fat, the hypothalamus ensures that it takes more food to feel full at a meal than it did before you lost fat. Your brain dampens the feeling of satiety so you won’t feel satisfied until you’ve eaten enough calories to start regaining fat. This is why people who are dieting often seem to have a bottomless appetite and never feel full.
you’ve overeaten and gained fat, your brain enhances the feeling of satiety so your meals will be smaller for a while. This is how we think the hypothalamus and brain stem work together to regulate appetite and adiposity.
The system of gut-brain communication that governs satiety doesn’t do a perfect job of transmitting the calorie value of a meal to the brain. In other words, some foods make us feel more full than others, even if they contain the same number of calories. Because of this, we can exploit the quirks of the satiety system to help naturally reduce (or increase) our calorie intake, without discomfort.
White bread, as expected, had a low satiety index relative to other foods, meaning it delivers little satiety per unit calorie. Whole-grain bread, in contrast, had a significantly higher satiety index.
Fruit, meat, and beans tended to have a high satiety index. Plain potatoes were off the charts—far more filling than any other food. Holt and colleagues noted that “simple ‘whole’ foods such as the fruits, potatoes, steak and fish were the most satiating of all foods tested.”
sating ability of each item was largely explained by a few simple food properties. The first is calorie density; in other words, the volume of food per calorie.128
Neck and neck with calorie density was another factor we’ve encountered before: palatability. The more palatable a food, the less filling it was. Again, this makes sense. Palatable foods are those that the brain intuitively views as highly valuable, and the brain is quite good at removing barriers to their consumption.
Within the hypothalamus lies a region called the lateral hypothalamus (LH), which is a nexus between energy balance and food reward functions (among other things). Researchers have known for a long time that stimulating the LH causes animals to eat voraciously, and disrupting it makes them lean.
palatable food activates neurons in the LH. Furthermore, the LH sends fibers directly to the NTS of the brain stem, where it inhibits neurons that play a role in satiety—so it’s not much of a leap to suppose that eating palatable foods might inhibit the very NTS neurons that make us feel full.
Sticking with simple foods can help us restrain our calorie intake without feeling hungry.
The third most influential factor Holt and colleagues identified is a food’s fat content. The more fat it contained, the less filling it was per calorie.
The key to understanding this is to remember that we’re talking about fullness per unit calorie.
For these reasons, adding fat to food is a highly effective way to increase your calorie intake without increasing your satiety much, and limiting added fat helps reduce calorie intake without sacrificing satiety.
Research has shown that the reason fat makes us eat more is precisely because of its high calorie density and palatability.
What this means is that if we eat fat in the context of unrefined, filling foods like meat, fish, eggs, dairy, nuts, and avocados, a higher fat intake can be compatible with a naturally slimming diet pattern. While these foods are high in fat, they don’t have the deadly combination of calorie density and extreme palatability that characterize other high-fat foods like potato chips and cookies.
fourth critical factor that Holt’s team identified is fiber.
Finally, the protein content of a food was a major contributor to satiety.
Both the lining of the small intestine and the pancreas have the ability to detect dietary protein,
Holt and her colleagues put the pieces together for us: “The results therefore suggest that ‘modern’ Western diets which are based on highly palatable, low-fibre convenience foods are likely to be much less satiating than the diets of the past or those of less developed countries.”
Börjeson recruited forty identical and sixty-one fraternal twins and measured their body weights. He found that identical twins tended to have very similar body weights, while fraternal twins were more divergent. “Genetic factors,” he concluded, “apparently play a decisive role in the origin of obesity.” Since Börjeson’s study, many others have confirmed that genes have an outsized influence on adiposity.
Furthermore, not only did twins gain a similar amount of fat, they even gained it in the same places.
primary reason some people readily burn off excess calories is that they ramp up a form of calorie burning called “non-exercise activity thermogenesis” (NEAT). NEAT is basically a fancy term for fidgeting.
Levine’s data show that it can incinerate nearly 700 Calories per day! The “most gifted” of Levine’s subjects gained less than a pound of body fat from eating 1,000 extra Calories per day for eight weeks. Yet the strength of the response was highly variable, and the “least gifted” of Levine’s subjects didn’t increase NEAT at all, shunting all the excess calories into fat tissue and gaining over nine pounds of body fat.
Stephen O’Rahilly and Sadaf Farooqi haven’t been twiddling their thumbs since they identified humans who lack leptin; in the meantime, they’ve located a number of other single-gene mutations that cause severe obesity. As it turns out, nearly all of them are in the leptin signaling
this case, they all say in chorus: Leptin signaling in the brain is a key component of the biological control of adiposity.
The most common mutation disrupts the melanocortin-4 receptor, which is primarily responsible for the appetite-suppressing effects of melanocortins in the brain (the substances released by POMC neurons). In these children, melanocortin release triggered by their own circulating leptin fails to restrain their appetites, so they eat substantially more than typical children. However, according to Farooqi, known mutations only account for about 1 percent of adults admitted to an obesity clinic.
This suggests that genetic differences in brain function are the primary reason why some people are fatter than others.
A century ago in the United States, people carried the same genes we do today, yet few people had obesity. What has changed isn’t our genes, it’s our environment—our food, our cars, our jobs. This leads us to a critical conclusion about obesity genes: In most cases, they don’t actually make us fat, they simply make us susceptible to a fattening environment.
Francis Collins, geneticist and director of the National Institutes of Health, is fond of saying, “Genetics loads the gun, and environment pulls the trigger.” Unless you have a faulty gun, which is rare, if you don’t pull the trigger, it doesn’t discharge.
Their volunteers ate nearly 300 more Calories per day when they were sleep-deprived than when they were well-rested. “In our experience,” explains St-Onge, “sleep restriction increases food intake. It’s as simple as that.”
We now know that the arousal system has multiple component brain regions, most of which are located in the brain stem and hypothalamus (see figure 41). These regions send a broad network of fibers throughout much of the brain, releasing chemicals like dopamine, serotonin, norepinephrine, and acetylcholine, which keep us awake and alert.
We now have strong evidence that a chemical called adenosine is that signal. Adenosine builds up in the brain while we’re awake, and it builds up even faster when we exert ourselves. As it accumulates, it begins to inhibit the arousal system and activate the VLPO. Eventually, when adenosine builds up sufficiently, it triggers the flip-flop switch, and we fall asleep. During sleep, the brain clears excess adenosine, restoring our wakefulness by morning. Caffeine works by blocking adenosine’s actions.
During sleep, the brain clears waste products that accumulate during the day as a result of normal metabolism, including adenosine. It gently remodels itself, reinforcing important connections and pruning unimportant ones. And it mops up the protein amyloid-β, which is implicated in the development of Alzheimer’s disease, one of the most tragic scourges of aging.
Their conclusion should serve as a caution to people who think sleep is a waste of time: “Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks.”
these deficits grew with each additional night of short sleep.
Importantly, volunteers felt sleepier for the first few days of sleep restriction, but after that, “subjects were largely unaware of these increasing cognitive deficits.” This suggests that people who short themselves on sleep may not even be aware of how poorly they’re performing.
The results of these brain scans suggest that sleep restriction increases the brain’s responsiveness to food—particularly calorie-dense junk food like pizza and doughnuts. The parts of the brain associated with food reward, including the ventral striatum, were more active in sleep-restricted volunteers, perhaps explaining why they ate more.
This suggests that lack of sleep doesn’t just impair our cognitive functions; it may also impair the lipostat that senses the body’s energy status and sets our motivation for food.
“The brain is basically telling you that you’re in a food-deprived state when you really are not,”
St-Onge and her team have shown that limiting sleep to four hours a night does indeed increase calorie expenditure, but only by about 100 Calories per day. Since her sleep-deprived volunteers ate nearly 300 excess Calories daily, that still leaves 200 Calories to accumulate around their midsections at the end of the day—enough to turn a susceptible person overweight over time.
It’s also worth noting that the association between short sleep and weight gain is particularly strong in children.
Short sleepers are not only more likely to have obesity than people who sleep more; they’re also more likely to develop chronic diseases, such as cardiovascular disease and diabetes, and more likely to die overall.
Yet sleep loss doesn’t just affect the lipostat—it also undermines our ability to control the very impulses it activates.
Sleep loss also favors overeating by affecting how we perceive risks and rewards.
Chee’s results showed that pulling an all-nighter causes people to become less concerned about potential losses and more attracted to potential gains—basically, they become risk takers.
“Generally, with sleep loss you have a shifting of your economic preferences,” explains Dan Pardi, a graduate student in the lab of Stanford sleep researcher Jamie Zeitzer. Researchers call this effect an optimism bias, and Pardi wondered if it might also apply to eating behavior.
“When you have inadequate sleep,” explains Pardi, “you’re probably less likely to live in accordance with your own health goals. You’re less likely to get into bed on time, you’re less likely to go to the gym, and you’re less likely to have your eating behaviors align with your long-term health goals.”
When Siffre emerged from the Abyss of Scarasson and analyzed his results, he realized something remarkable: the length of his wake-sleep cycle had remained close to twenty-four hours for his entire two-month séjour in the cave. Yet because his cycle was slightly longer than twenty-four hours, it gradually desynchronized from the day-night cycle of the sun. This suggested that the human body must quite literally contain a twenty-four-hour(ish) clock.
If we think of the cellular clocks in the body as a giant orchestra, the SCN is the conductor.137 The master clock, in turn, takes its cues from the retina, the light-sensitive film of cells in the back of the eye, which detects the day-night cycle of the sun (see figure 43). But due to the characteristics of the retinal cells that transmit this information, the SCN only responds to blue light, which happens to be most abundant at midday.
Rotating shift work is associated with an alarming array of health problems, including obesity, type 2 diabetes, cancer, and cardiovascular disease.
Not only can the master clock desynchronize from the day-night cycle of the sun, but individual organ clocks can desynchronize from one another.
Yet when we disrupt the circadian rhythm by eating late at night, traveling to a faraway time zone, or doing shift work, some of our organ clocks can fall out of sync with others. What would normally be a harmonious performance is reduced to a disorganized cacophony. Researchers call this circadian desynchrony and hypothesize that it leads to metabolic problems and weight gain.
This suggests that what is really fattening in these experiments is not simply fattening food but the combination of fattening food and circadian desynchrony.
threat response system that responds to external and psychological threats, including the everyday psychological stressors we commonly call “stress.” In broad strokes, here’s how it works:
The amygdala cooperates with many different brain regions, both conscious and nonconscious, to scan for signs of a threat. Some of these regions process concrete sensory information, such as objects moving rapidly toward you, things that look like spiders, or loud sounds, while others process abstract concepts like being laid off, carrying debt, or arguing with a loved one. When the amygdala detects a threat, it communicates with other brain regions to activate a coordinated suite of threat responses designed to minimize the potential damaging consequences of the situation.
increases your level of arousal by activating many of the same brain regions that are involved in regulating the sleep/wake cycle (see figure 41). This bathes broad swaths of your brain in dopamine, serotonin, noradrenaline, and other chemicals that focus your mind on the problem and motivate you to do what it takes to resolve it. That’s why it’s hard to sleep when you’re stressed.
amygdala may send signals to your brain stem that activate fast defensive reflexes, such as startling, freezing, protecting your head, or closing your eyes. These signals can also instinctively generate facial expressions of fear or anxiety—recognizable across all human cultures.
amygdala sends signals to activate your sympathetic nervous system. The sympathetic nervous system is a network of nerve fibers that runs throughout the body and participates in the fight-or-flight response (see figure 46). Your pulse and breathing rate quicken, and your blood pressure rises. Your palms begin to sweat. Digestion slows, and in extreme cases, your bladder and rectum may expel their contents.
Blood flow to your muscles increases. The levels of sugar and fat in your bloodstream begin to climb, providing your muscles with more energy for fight or flight. This process prepares your body for vigorous action, but it happens even in response to psychological threats that don’t require you to meet physical challenges. Your body is preparing to fight off a grizzly bear, even if the actual threat is an Excel spreadsheet.
amygdala activates a critical part of the threat response system called the hypothalamic-pituitary-adrenal axis (HPA axis). It does so by sending a signal that causes the hypothalamus to release a chemical called corticotropin-releasing factor (CRF).144 CRF and a few related molecules turn out to be key players in the threat response.145
Some of the effects of cortisol, such as increasing blood levels of sugar and fat, are similar to those of the sympathetic nervous system, but on a slower, longer time scale. These sustain the high metabolic demands of dealing with a stressor for a long time. Other effects of cortisol include suppressing immune function and, as we will soon see, increasing food intake. Because of its slow kinetics, cortisol is a key player in the long-term response to chronic stress.
CRF stimulates the brain as a whole to shift from normal, everyday behaviors like eating and socializing, to threat response behaviors like running away and (perhaps) thinking about how you’ll pay the bills.
The final act of the brain’s threat response is learning. Once you’ve survived a threatening situation, your amygdala learns how to recognize and respond to similar situations more effectively in the future.
This lack of control is a key factor in modeling the most harmful types of human psychological stress. In the modern world, we’re often subjected to stressful events we can’t easily control, like traffic, bullying, nagging, illness, deadlines, and debt.147 Research in psychology and neuroscience suggests that uncontrollable stressors have a stronger effect on the threat response system, and are much more harmful to our health and mental state, than stressors we believe we can control.
How do these uncontrollable, often social, stressors affect food intake? Remarkably, it depends entirely on the food that’s available.
Wilson’s team feeds its monkeys healthy, unrefined, high-fiber chow, stressed subordinate monkeys eat less and lose weight while dominant monkeys maintain weight. Yet when the researchers give the monkeys a choice between standard chow and a very rewarding high-fat, high-sugar diet, the monkeys’ eating behavior changes dramatically.
Yet the dominant animals keep eating the same amount of food as before. In contrast, the stressed subordinates double their daily calorie intake. So in the context of a strict healthy diet, stress makes monkeys undereat, whereas when they have a choice between healthy fare and junk food, they overeat spectacularly.
Wilson’s research suggests that the magic formula for overeating is the combination of chronic uncontrollable stress and a choice of highly rewarding food.149
Over a four-day period, Ravussin’s team found that the methylprednisolone group ate a whopping 1,687 Calories more per day than the placebo group.
why overeating and obesity are key features of Cushing’s syndrome: Cortisol and related compounds cause leptin resistance in the hypothalamus.
As it turns out, uncontrollable stress—like being hassled all day by four rhesus monkeys or your boss—has a particularly potent cortisol-raising effect. In contrast, when you’re facing a challenge but you have a chance to determine your own fate, the situation feels less threatening, and your cortisol response is proportionally smaller. This may be part of the reason why uncontrollable stress is the most effective at driving overeating and adiposity.
Yet there’s another, more common-sense reason why some of us overeat when we’re stressed, and research is increasingly suggesting that it could be important: Junk food simply makes us feel better emotionally.
As predicted by Dallman’s comfort food hypothesis, the group that drank sugar water showed a smaller stress response than the group that drank plain water. It appeared that sugar helped them feel better in the face of stress.152 Yet it’s not just sugar: Dallman and others have since shown that giving rats access to a high-fat food does the same thing.
She hypothesized that sugar’s stress-busting effect is due to its metabolic impact on the body, not its rewarding effects in the brain, and therefore that saccharin would be ineffective. “The result,” explains Ulrich-Lai, “was completely opposite my hypothesis. The saccharin worked just as well as sugar.” Subsequent experiments confirmed that the sweet taste itself was responsible.
Then they tested the rats’ stress responses to restraint stress. The sex worked. In fact, according to Ulrich-Lai, it was a little bit more effective than the sugar.
natural rewards may attenuate stress by changing how the amygdala processes stress-related information.
The reward value itself helps us feel better by dampening the activity of the threat response system. It may also explain why stress only causes overeating when there’s highly rewarding food around: When we want to self-medicate our stress, bland food just doesn’t cut it.
As Daniel Kahneman relates in his book Thinking, Fast and Slow, the brain’s thought processes can be roughly divided into two systems. System 1 is fast, effortless, intuitive, and nonconscious, while system 2 is slow, effortful, rational, and conscious. System 2 understands the long-term consequences of our choices and represents our rational intentions: it wants you to eat the right amount of nutritious food, get plenty of exercise and sleep, and stay lean, fit, and healthy to a ripe old age.
Unfortunately, system 1 isn’t so rational.
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.
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.”
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
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.
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.
Clearly, something about weight loss surgery alters how the brain nonconsciously regulates food intake and adiposity.
Kevin Hall’s research shows that Americans would have to reduce our average calorie intake by at least 218 Calories per day to return to our 1978 body weights, a reduction of nearly 10 percent. Alternatively, we’d have to burn 218 extra Calories exercising—which represents almost half an hour of jogging every day—and hope we don’t work up an appetite.
The following six steps translate the research I detailed throughout this book into practical steps you can take in your daily life.
1. Fix your food environment Tempting food cues in your personal environment are powerful drivers of overeating due to their impact on brain areas that govern motivation and economic choice. Fortunately, one of the most effective tools in our arsenal is also one of the simplest: Reduce your exposure to food cues.
Here are three measures you can take to do so.
First, get rid of all tempting, calorie-dense foods that are easy to grab and eat in your home and work environment—particularly those that are readily visible on counters and tables.
Second, reduce your exposure to food cues in general. It’s possible to overeat even healthy foods, so don’t tempt yourself too much. Limit the amount of visible food in your personal food environment at home and at work,
Third, create effort barriers to eating. These barriers don’t have to be large to be effective. For example, if you have to peel an orange to eat it, you probably won’t go for it unless you’re genuinely hungry.
2. Manage your appetite If your brain thinks you’re starving, it will eventually wear you down, no matter how strong your resolve. The solution is to give it the cues it needs to realize you aren’t starving.
The most straightforward way to do this is to choose foods that send strong satiety signals to the brain stem but contain a moderate number of calories. These are foods that have a lower calorie density, higher protein and/or fiber content, and a moderate level of palatability. This tends to include simple foods that are closer to their natural state, such as fresh fruit, vegetables, potatoes, fresh meats, seafood, eggs,
the lipostat comfortable with your target weight.
Regular physical activity, restorative sleep, and stress management may also support a leaner adiposity set point, facilitating weight loss and maintenance.
3. Beware of food reward The brain values foods that contain calorie-dense combinations of fat, sugar, starch, protein, salt, and other elements, and it sets your motivation to eat those foods accordingly.
When we eat simple foods that are less dense in calories and closer to their natural states, they’re still enjoyable but they don’t have that intensely rewarding edge that drives us to overdo it.
4. Make sleep a priority I hope I’ve already dispelled the myth that sleep is a waste of time. Restorative sleep is an important cue for the nonconscious brain that has a major impact on performance and eating behavior—even if we aren’t directly aware of it.
5. Move your body Regular physical activity can help manage your appetite and weight in at least two ways. First, it increases the number of calories you use, making it less likely you’ll overeat.
Second, physical activity may also help maintain the lipostat in the brain, encouraging a naturally lower level of adiposity in the long run.
6. Manage stress The threat response system evolved to protect us, but sometimes in the modern world it can undermine our quality of life and our best intentions to eat the right amount of food.
five actions you can take to identify the problem and manage stress eating by giving your threat response system the right cues.
first action is simply to identify whether or not you’re a stress eater.
second action is to identify the stressor(s)—particularly chronic stressors you don’t feel you can control. These often include work stress, money, health problems, prolonged caregiving, interpersonal conflict, and/or a lack of social support.
third action is to try to mitigate the stressor. There are multiple ways to do this. Can you fix it or avoid it? If not, is there a way you can turn what seems like an uncontrollable stressor into a controllable stressor?
Another way to mitigate stress is by practicing mindfulness meditation.
Most of what stresses us has little to do with what’s happening right now—it’s usually about what might happen in the future.
There are many ways to meditate, but here’s a simple technique that works: Find a comfortable seat where you can maintain a straight but relaxed spine. Keep your eyes open and your gaze slightly downward. Then just pay attention to the rise and fall of your abdomen as you breathe. You’ll notice things happening around you, and your mind will wander, but just keep gently bringing your attention back to your breath.
The fourth action is to replace stress eating with more constructive coping methods.
fifth action is to remove calorie-dense comfort food from your personal surroundings at home and at work.