The Hungry Brain: Outsmarting the Instincts That Make Us Overeat

by Stephan Guyenet

We got fatter. Between 1980 and today, the US obesity rate more than doubled.

Certain diet contrarians have seized on this correlation, suggesting that the Guidelines themselves made us fat by recommending that we replace dietary fat with carbohydrate, leading us to eat too much refined starch and sugar. Yet the evidence has never supported such speculation, in part because Americans who actually follow these recommendations tend to be leaner than Americans who don’t.

we replaced some of our beef intake with chicken,

:< one of the consequences of the dietray guidelines was an invcrease in chicken farming to the reduction of beef. another negtive externality.

Yet they do point to a fundamental aspect of human nature: Information alone isn’t always an effective way to change behavior.

re ewan.

After completing a BS in biochemistry at the University of Virginia and a Ph.D. in neuroscience at the University of Washington,

Prior to the turn of the twentieth century, fewer than one out of seventeen middle-aged white men was obese.

Clothing is now available in staggering sizes such as XXXXXXXXL.

this looks like the begibinning of a puzzle in GOdel Escher Bach.

Atwater and his colleagues also constructed a giant live-in calorimeter to measure the combustion of food by the human body. This calorimeter was large enough to provide a modest living space for experiments lasting multiple days. Atwater’s system was so effective that it was able to demonstrate with greater than 99 percent accuracy that the energy entering a weight-stable person as food is equal to the energy leaving the body. In other words, in a person neither gaining nor losing weight, the number of calories consumed is equal to the number burned.

This undermines the commonly held belief that certain nutrients, like carbohydrate or fat, are more fattening than what their calorie content would suggest. Some foods are nevertheless more fattening than others, but this appears to be primarily because they coax us to eat more calories, not because they have a special effect on our metabolic rate.

Some foods are nevertheless more fattening than others, but this appears to be primarily because they coax us to eat more calories, not because they have a special effect on our metabolic rate.

I’ve graphed calorie intake estimates from all three methods in figure 3. As you can see, the methods yield different estimates, but they all agree that our calorie intake has increased substantially over the period of time that we gained weight the most rapidly

218 Calories. Remarkably, this increase is single-handedly sufficient to explain the obesity epidemic that developed over the same period of time, without having to invoke changes in physical activity or anything else.

as your body size changes, your body’s energy needs change too. To illustrate the principle, think of your adipose tissue as a bank account. If you start out with $10,000 in savings, an income of $1,000 a month, and expenditures of $1,000 a month, in a year, your account will still contain $10,000. Now, imagine you get a raise and your earnings climb to $2,000 a month. At first, your lifestyle remains the same and you only spend $1,000 a month, saving the extra $1,000 per month. But gradually, you start to think it would be nice to have that new computer or fancy pair of shoes. You move into a nicer apartment. Your lifestyle expands, and your expenditures creep up. Six months after your raise, you’re spending $1,500 per month, and after a year, you’re spending the full $2,000 a month. Over this year, your bank account has been accumulating money, but at a gradually slowing rate, until accumulation stops when your expenditures match your income. Your account balance plateaus at about $16,000, and it remains there until your income or expenditures change.

And so it is for adiposity. When your calorie intake increases, your body weight increases, and this extra tissue burns calories.

What are the practical implications of this? An important one is that it takes a larger change in calorie intake to gain—or lose—weight than most people realize. Making small changes to your diet, such as cutting out one slice of toast per day, will lead to correspondingly small changes in adiposity that don’t continue to accrue indefinitely. 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.

Obesity research has a long, rich history of fattening rodents for science. In the 1970s, researchers were looking for a better way to fatten their rats so they could study the development and impacts of obesity more efficiently. In the early days, researchers would simply add fat to standard rodent chow. This worked, but it often took months to produce a portly rat—making rodent obesity research a costly and time-consuming endeavor.

One fateful day when Anthony Sclafani, now the director of the Feeding Behavior and Nutrition Laboratory at Brooklyn College, was a graduate student, he happened to place a rat onto a lab bench where a fellow student had left a bowl of Froot Loops cereal. The rat waddled over and began to eat it heartily. This was surprising because rats are typically cautious with unfamiliar foods. Watching the rat greedily devouring human food, it occurred to Sclafani that foods marketed for people might be more fattening than the high-fat rodent chow he was currently using.

To see if he could design a faster and more effective way to fatten rats, 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. In a few short weeks, the rats were obese, and neither exercise nor an enriched envir...

Sclafani’s study was published in 1976, and to this day, the cafeteria diet remains the most effective way to get a normal rat or mouse to overeat—far more effective than diets that are simply high in fat and/or sugar.

explain to ewan

Ravussin and his team wanted an intermediate method, one that had the accuracy of the metabolic ward but allowed people to select their own diets, replicating everyday life as much as possible. Their solution was to install enormous U-Select-It 3007 vending machines inside a metabolic ward, each containing a variety of entrées, snacks, and beverages. The foods in the vending machines were not chosen at random—“We were screening what people liked and disliked,” explains Ravussin—and only included foods that were tempting. The menu included things like french toast and sausages with syrup, chicken pot pie, chocolate-vanilla swirl Jell-O pudding, cheesecake, nacho cheese Doritos, M&M’s, Shasta cola, and a few apples for the health nuts (no Froot Loops, sadly)—in other words, mostly “palatable human foods” similar to those Sclafani used in his rat study. Ten male volunteers were locked up with the vending machines for seven days with the freedom to select when and what they ate. To monitor their food intake, each person had to enter an ID code when he withdrew food and return all uneaten food to the research staff for weighing. The experiment was a success: Ravussin’s team was able to accurately measure food intake in people who were selecting their own food, and at the same time take a number of other informative metabolic measurements. Yet during the course of the study, something remarkable dawned on Ravussin: The volunteers were overeating tremendously. “People were on ave...

Over the next three years, Ravussin’s team published two additional “human cafeteria diet” studies. These studies tested the vending machine setup with men, women, lean people, people with obesity, Caucasians, and Native Americans. In each case, volunteers locked in a metabolic ward with a variety of free, tasty foods overate substantially, without being asked to overeat. Ravussin named this phenomenon opportunistic voracity.

These findings are particularly remarkable because it’s normally quite difficult to get people to overeat substantially for more than a few days (imagine yourself eating twice as much food at each meal!). In other settings, researchers coax their volunteers to overeat using enticements such as money, and even then, volunteers have to force down the extra food against a growing sense of queasiness and impending stomach rupture. Yet in Ravussin’s study, his volunteers overate cheerfully without eve...

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. Today, this idea is accepted by most neuroscientists.

i should read this.

Within the lamprey basal ganglia lies a key structure called the striatum, which is the portion of the basal ganglia that receives most of the incoming signals from other parts of the brain.20 The striatum receives “bids” from other brain regions, each of which represents a specific action.

Despite being separated by a 560-million-year evolutionary chasm, the basal ganglia of lampreys and mammals (including humans) are strikingly similar. They contain the same regions, organized and connected in the same way. Within these regions lie neurons with the same electrical properties, communicating with one another using the same chemical messengers. These findings led Grillner and Stephenson-Jones to the stunning conclusion that “practically all details of the basal ganglia circuitry had developed some 560 million years ago.”

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. Grillner and Stephenson-Jones propose that the early vertebrate basal ganglia were already very good at making decisions, and there was no need for evolution to fix what wasn’t broken. We only needed to build on it.

it is not obvious to me why there needs to be a distinction between adaptation and exaptation.

This is part of the reason why lampreys don’t have mortgages.

more like speciesist discrimination.

These reciprocal connections also form loops that travel to and from specific regions of the cortex, each of which is an option generator.

if the cortex is an option generator and the basal ganglia is the decider, that seems to relocate the idea of executive control.

Dopamine is a fascinating and widely misunderstood molecule that we’ll discuss further in the next chapter, but for now, its most relevant function is to increase the likelihood of engaging in any behavior.

When dopamine levels in the striatum are increased—for example, by cocaine or amphetamine—mice (and humans) tend to move around a lot. High levels of dopamine essentially make the basal ganglia more sensitive to incoming bids, lowering the threshold for activating movements.

hmm. i do not know whether this is evidence for or aginst my theory that this is an adaptive foraging response.

In Parkinson’s disease, the gradual loss of substantia nigra neurons causes dopamine levels to decline in the areas of the dorsal striatum that select movements, particularly well-worn movement patterns. This makes the dorsal striatum progressively less sensitive to incoming bids from motor regions, rendering it increasingly difficult for any motor option generator to gain access to the body’s muscles. People with Parkinson’s disease develop difficulty initiating and executing movements and have a particularly hard time performing sequences of movements. In severe cases, Parkinson’s disease patients are scarcely able to initiate movements at all, a phenomenon called akinesia, Greek for “no movement.”

As with many drugs, L-dopa is a blunt tool. In Parkinson’s disease, parts of the dorsal striatum need more dopamine—but the rest of the brain doesn’t. When a person takes L-dopa, dopamine-producing neurons throughout the brain—including those located in the area that provides dopamine to the ventral striatum, the ventral tegmental area (VTA)—sponge it up and convert it to dopamine. This can lead to abnormally elevated levels of dopamine in the ventral striatum.

ventral striatum is same as nucleus accumbens.

As I mentioned earlier, the ventral striatum primarily regulates motivations and emotional states. Analogous to what happens in the dorsal striatum, elevating dopamine in the ventral striatum makes it more sensitive to incoming bids, increasing the likelihood that it will activate motivational and emotional states. 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.

These are called impulse control disorders because people lose the ability to keep thei...

The ventral striatum is so sensitive to incoming bids that inappropriate option generators are able to grab the reins. In addition, higher levels of dopamine in the striatum may cause the activity of certain loops to become abnormally strong over time, resulting in addictive and compulsive behaviors, a topic we’ll discuss in the next chapter.

finally! a popular science book that presents dopamine in an accurate way!

Jim was suffering from a rare disorder called abulia, which is Greek for “an absence of will.”31 Patients who suffer from abulia can respond to questions and perform specific tasks if prompted, but they have difficulty spontaneously initiating motivations, emotions, and thoughts. A severely abulic patient seated in a bare room by himself will remain immobile until someone enters the room. If asked what he was thinking or feeling, he’ll reply, “Nothing.” Needless to say, abulic patients have little motivation to eat. Abulia is typically associated with damage to the basal ganglia and related circuits,

Learning is the process of acquiring new knowledge, skills, movement patterns, motivations, and preferences, or reinforcing those that already exist.

When we hear the word learning, we tend to imagine ourselves poring over a textbook absorbing facts, but nearly everything we do—and think and feel—was learned at some point, whether intentionally or not. Roy Wise, a motivation and addiction researcher at the National Institute on Drug Abuse in Baltimore, Maryland, made this point in a 2004 review paper: Most goal-directed motivation—even the seeking of food or water when hungry or thirsty—is learned. It is largely through selective reinforcement of initially random movements that the behavior of the [newborn] comes to be both directed and motivated by appropriate stimuli in the environment.

this is pt churchlands point about mother nature assuming ceertain regularities in the environment.

For reinforcement to occur, there has to be a teaching signal that changes the activity of basal ganglia loops based on experience, such that good responses are reinforced and bad responses are discarded. Most researchers believe the brain’s teaching signal is the fascinating molecule dopamine.

eventually it comes to understand the remarkable significance of the little box.

dont we all.

Later, Pavlov’s team found that when they consistently rang a bell prior to feeding the dogs, the dogs eventually salivated in response to the bell alone.

false. he never used a bell. he uesd a metronome. practically speaking, this resulted in pavlov executing a random behavior from the totalset of all possible human behaviors.

You may have heard that dopamine is the “pleasure chemical,” responsible for causing the neurochemical rush that makes us feel really good as we win a race, have sex, eat chocolate, or smoke crack cocaine. Although that idea is common in popular science writing, it has long been out of date within the scientific community. As a matter of fact, dopamine release doesn’t correspond very well with the experience of pleasure. Experiments have shown that animals appear to experience pleasure without dopamine, and studies in humans back this up. Pleasure is more related to a class of chemicals called endorphins that are often released in the striatum simultaneously with dopamine, although these are probably only one component of the experience of pleasure. 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.