A Century of Obesity Epidemic

Why We Get Fat
by Gary Taubes

In 1934, a young German pediatrician named Hilde Bruch moved to America, settled in New York City, and was “startled,” as she later wrote, by the number of fat children she saw—“ really fat ones, not only in clinics, but on the streets and subways, and in schools.” Indeed, fat children in New York were so conspicuous that other European immigrants would ask Bruch about it, assuming that she would have an answer. What is the matter with American children? they would ask. Why are they so bloated and blown up? Many would say they’d never seen so many children in such a state.

Today we hear such questions all the time, or we ask them ourselves, with the continual reminders that we are in the midst of an epidemic of obesity (as is the entire developed world). Similar questions are asked about fat adults. Why are they so bloated and blown up? Or you might ask yourself: Why am I?

But this was New York City in the mid- 1930s. This was two decades before the first Kentucky Fried Chicken and McDonald’s franchises, when fast food as we know it today was born. This was half a century before supersizing and high- fructose corn syrup. More to the point, 1934 was the depths of the Great Depression, an era of soup kitchens, bread lines, and unprecedented unemployment. One in every four workers in the United States was unemployed. Six out of every ten Americans were living in poverty. In New York City, where Bruch and her fellow immigrants were astonished by the adiposity of the local children, one in four children were said to be malnourished. How could this be?

Fat in the Fifties
by Nicolas Rasmussen

Obesity burst into the public consciousness in the years immediately following the Second World War. Around 1950, the US Public Health Service (PHS) issued a brochure on “the greatest problem in preventive medicine in the USA”: obesity. The life insurance industry, working in collaboration with the PHS and the American Medical Association (AMA), launched a national drive, proclaiming “Overweight: America’s No. 1 Health Problem.” And no wonder, given that insurance company data and some local health surveys suggested that more than a quarter of the American population was significantly overweight or obese. By the typical measure of the day, anyone 10 percent above the “ideal weight” for a given height fell into the category of overweight—the ideal weight being that which the insurance industry found to predict maximum longevity. Those 20 percent overweight were classified as obese. The danger of excess weight was grave, because it was the leading predictor of heart disease, the nation’s top killer. […]

Stroke, cancer, and, most of all, heart disease leaped to the forefront as causes of death.20 By 1920 heart disease had taken the lead as the top cause of death; by the end of the decade, based mainly on evidence developed by Dublin and other insurance industry statisticians, health policy analysts came to believe that heart disease was also catching up with tuberculosis in terms of its total financial burden on the nation (despite the fact that heart disease tended to kill its victims later in their wage-earning years). Imposing double the economic burden of cancer, which would soon become the second greatest cause of death, heart disease had unquestionably become Public Health Enemy Number 1 by 1930. […] The [early 20th century] findings indicated a clear association between overweight and excess mortality. […] In 1930, Louis Dublin used this type of information as the basis for a groundbreaking actuarial study that specifically correlated overweight with heart disease.

Gary Taubes On Biological Homeostasis

Gary Taubes wrote, “This is Curt Richter talking about his diabetic rat experiments published in 1941. It raises an obvious question: Could Richter’s rats have been smarter than the expert committees of the American Diabetes Association? I’m just saying….”

We found that when pancreatectomized rats with marked diabetes were offered a carbohydrate, a fat, and a protein in separate containers, in place of the mixed diet, they refused the carbohydrate and ate large amounts of fat and protein (7). As a result they lost their symptoms of diabetes, i.e., their blood sugar fell to its normal level, they gained weight, ate less food, and drank only normal amounts of water.

More from the same paper:

“When placed on a self-selection diet, the rats were no longer forced to take carbohydrate, except for the small amount contained in the yeast. They stopped eating sucrose and ate large amounts of olive oil; and as a consequence, the water was no longer drained from the tissues. The thirst disappeared, energy from the sugar was no longer lost; so the food intake decreased to its normal level again. With the return to the McCollum diet, the symptoms were reversed again.

“The dietary selections made by the diabetic rats closely agree with the diets determined empirically by clinicians from human diabetics in the preinsulin period. It was generally agreed that patients did much better on a high fat than on a low fat diet. Since the insulin increases the ability to utilize carbohydrate, the need for a high fat diet is no longer present. In preliminary experiments we have found that, when treated with insulin, our diabetic rats stop taking olive oil in such large amounts and eat sucrose.”

* * *

Increased Fat and Decreased Carbohydrate Appetite of Pancreatectomized Rats
by Curt P. Richter and Edward C. H. Schmidt, Jr.

BERNARD, who in 1859 first stated his concept of the constancy of the internal environment, described various physiological mechanisms, part responses of the organism, responses of individual organs, which contribute to the maintenance of this constancy. We have recently found that behavior mechanisms, responses of the total organism, may also serve to maintain the constancy of the internal environment. The existence of these behavior mechanisms became established in experiments in which certain physiological mechanisms had been excluded. Thus, after adrenalectomy had removed the chief physiological means of regulating sodium metabolism, it was found that the animal itself made an effort to maintain the sodium balance by seeking and ingesting large amounts of sodium chloride (1). Similarly, after parathyroidectomy had removed the physiological mechanisms for the maintenance of a constant calcium balance, the animals themselves made an effort to correct the calcium loss by ingesting large amounts of calcium solution (2).

Catching Up On Lost Time – The Ancestral Health Symposium, Food Reward, Palatability, Insulin Signaling and Carbohydrates… Part II(C)
by Gary Taubes

It was well known at the time (although it may have been forgotten since then), as I discussed in Good Calories, Bad Calories, that animals can be made to like one food more than another, and so eat more of the one than the other, by interventions that influenced their underlying physiologic/metabolic/hormonal states. Here’s how I illustrated this in GC,BC:

Throughout the first half of the twentieth century, a series of experimental observations, many of them from [Curt] Richter’s laboratory [at Johns Hopkins University], raised questions about what is meant by the concepts of hunger, thirst and palatability, and how they might reflect metabolic and physiological needs. For example, rats in which the adrenal glands are removed cannot retain salt and will die within two weeks on their usual diet from the consequences of salt depletion. If given a supply of salt in their cages, however, or given the choice of drinking salt water or pure water, they will chose to either eat or drink the salt and, by doing so, keep themselves alive indefinitely. These rats will develop a “taste” for salt that did not exist prior to the removal of their adrenal glands. Rats that have had their parathyroid glands removed will die within days of tetany, a disorder of calcium deficiency. If given the opportunity, however, they will drink a solution of calcium lactate rather than water—not the case with healthy rats—and will stay alive because of that choice. They will appear to like the calcium lactate more than water. And rats rendered diabetic voluntarily choose diets devoid of carbohydrates, consuming only protein and fat. “As a result,” Richter said, “they lost their symptoms of diabetes, i.e., their blood sugar fell to its normal level, they gained weight, ate less food and drank only normal amounts of water.

In short, change underlying physiologic/hormonal conditions and it will affect what an animal chooses to eat and so seems to like or find rewarding. The animal’s behavior and perceptions will change in response to a change in homeostasis – in the hormonal milieu of the cells in the body.

It’s quite possible that all those foods we seem to like, or even the ones we find rewarding but don’t particularly like, as Dr. Guyenet argues, and that subsequently cause obesity (not necessarily the same thing) are those foods that somehow satisfy an underlying metabolic and physiological demand. This in turn might induce our brains to register them as more palatable or rewarding, but the initial cause would be the effect in the periphery. The nutrient composition of the food, in this case, would be the key—what it’s doing in the body, not necessarily the brain.

Good Calories, Bad Calories
by Gary Taubes
pp. 331-332

This idea that energy expenditure increases to match consumption, and that the ability to do this differs among individuals, also serves to reverse the cause-and-effect relationship between weight and physical activity or inactivity. Lean people are more active than obese people, or they have, pound for pound, a higher expenditure of energy, *89 because a greater proportion of the energy they consume is made available to their cells and tissues for energy. By this conception, lean people become marathon runners because they have more energy to burn for physical activity; their cells have access to a greater proportion of the calories they consume to use for energy. Less goes to making fat. That’s why they’re lean. Running marathons, however, will not make fat people lean, even if they can get themselves to do it, because their bodies will adjust to the extra expenditure of energy, just as they would adjust to calorie-restricted diets.

Our propensity to alter our behavior in response to physiological needs is what the Johns Hopkins physiologist Curt Richter called, in a heralded 1942 lecture, “total self-regulatory functions.” Behavioral adaptation is one of the fundamental mechanisms by which animals and humans maintain homeostasis. Our responses to hunger and thirst are manifestations of this, replenishing calories or essential nutrients or fluids. Physical activity, as Richter suggested, is another example of this behavioral regulation, in response to an excess or dearth of calories. “We may regard the great physical activity of many normal individuals, the play activity of children, and perhaps even the excessive activity of many manic patients, as efforts to maintain a constant internal balance by expending excessive amounts of energy,” he explained. “On the other hand, the low level of activity seen in some apparently normal people, the almost total inactivity seen in depressed patients, again may be regarded as an effort to conserve enough energy to maintain a constant internal balance.”

p. 457-460

This is where physiological psychologists provided a viable alternative hypothesis to explain both hunger and weight regulation. In effect, they rediscovered the science of how fat metabolism is regulated, but did it from an entirely different perspective, and followed the implications through to the sensations of hunger and satiety. Their hypothesis explained the relative stability of body weight, which has always been one of the outstanding paradoxes in the study of weight regulation, and even why body weight would be expected to move upward with age, or even move upward on average in a population, as the obesity epidemic suggests has been the case lately. And this hypothesis has profound implications, both clinical and theoretical, yet few investigators in the field of human obesity are even aware that it exists.

This is yet another example of how the specialization of modern research can work against scientific progress. In this case, endocrinologists studying the role of hormones in obesity, and physiological psychologists studying eating behavior, worked with the same animal models and did similar experiments, yet they published in different journals, attended different conferences, and thus had little awareness of each other’s work and results. Perhaps more important, neither discipline had any influence on the community of physicians, nutritionists, and psychologists concerned with the medical problem of human obesity. When physiological psychologists published articles that were relevant to the clinical treatment of obesity, they would elicit so little attention, said UCLA’s Donald Novin, whose research suggested that the insulin response to carbohydrates was a driving force in both hunger and obesity, that it seemed as though they had simply tossed the articles into a “black hole.”

The discipline of physiological psychology was founded on Claude Bernard’s notion of the stability of the internal environment and Walter Cannon’s homeostasis. Its most famous practitioner was the Russian Ivan Pavlov, whose career began in the late nineteenth century. The underlying assumption of this research is that behavior is a fundamental mechanism through which we maintain homeostasis, and in some cases—energy balance in particular—it is the primary mechanism. From the mid-1920s through the 1940s, the central figure in the field was Curt Richter of Johns Hopkins. “In human beings and animals, the effort to maintain a constant internal environment or homeostasis constitutes one of the most universal and powerful of all behavior urges or drives,” Richter wrote.

Throughout the first half of the twentieth century, a series of experimental observations, many of them from Richter’s laboratory, raised questions about what is meant by the concepts of hunger, thirst, and palatability, and how they might reflect metabolic and physiological needs. For example, rats whose adrenal glands are removed cannot retain salt, and will die within two weeks on their usual diet, from the consequences of salt depletion. If given a supply of salt in their cages, however, or given the choice of drinking salt water or pure water, they will choose either to eat or to drink the salt and, by doing so, keep themselves alive indefinitely. These rats will develop a “taste” for salt that did not exist prior to the removal of their adrenal glands. Rats that have had their parathyroid glands *132 removed will die within days of tetany, a disorder of calcium deficiency. If given the opportunity, however, they will drink a solution of calcium lactate rather than water—not the case with healthy rats—and will stay alive because of that choice. They will appear to like the calcium lactate more than water. And rats rendered diabetic voluntarily choose diets devoid of carbohydrates, consuming only protein and fat. “As a result,” Richter said, “they lost their symptoms of diabetes, i.e., their blood sugar fell to its normal level, they gained weight, ate less food and drank only normal amounts of water.”

The question most relevant to weight regulation concerns the quantity of food consumed. Is it determined by some minimal caloric requirement, by how the food tastes, or by some other physical factor—like stomach capacity, as is still commonly believed? This was the question addressed in the 1940s by Richter and Edward Adolph of the University of Rochester, when they did the experiments we discussed earlier (see Chapter 18), feeding rats chow that had been diluted with water or clay, or infusing nutrients directly into their stomachs. Their conclusion was that eating behavior is fundamentally driven by calories and the energy requirements of the animal. “Rats will make every effort to maintain their daily caloric intake at a fixed level,” Richter wrote. Adolph’s statement of this conclusion still constitutes one of the single most important observations in a century of research on hunger and weight regulation: “Food acceptance and the urge to eat in rats are found to have relatively little to do with ‘a local condition of the gastro-intestinal canal,’ little to do with the ‘organs of taste,’ and very much to do with quantitative deficiencies of currently metabolized materials”—in other words, the relative presence of usable fuel in the bloodstream.

Fat Doesn’t Mean Not Fit

Eric “Butterbean” Esch, having weighed 425 lbs at his heaviest, was one of the best boxers of the 1990s. He regularly knocked out his competitors in under a minute. He didn’t look impressive, besides being obese. He wasn’t the best trained nor did he fight with much style. But he was a powerhouse. He could take punches and give them in return. And when he landed a punch, it was devastating.

As with many others, Butterbean’s obesity was not an indicator of a lack of muscle, stamina, and aerobic health. Even in later fights when his power was decreased, he still could hold his own for many rounds. In 2002, he remained on his feet for 10 rounds with one of the greatest fighters of all time, Larry Holmes, before finally knocking him back against the ropes with the fight ending after the referee did a standing 8 count. He expanded his career into professional wrestling and MMA matches, winning many more fights. As late as 2011 in his mid-40s, he was still knocking out opponents and he was still fat.

This is why so few people can lose weight through exercise alone. All that more exercise does for most, specifically on a high-carb diet, is to make them hungrier and so leading to them eating more (exercise on a ketogenic diet is a bit different, though). And indeed, many athletes end up focusing on carbs in trying to maintain their energy, as glucose gets used up so quickly (as opposed to ketones). Long-distance runners on a high-carb diet have to constantly refuel with sugary drinks provided along the way.

Americans have been advised to eat more of the supposedly healthy carbs (whole grains, vegetables, fruit, etc) while eating less of the supposedly unhealthy animal foods (red meat, saturated fats, etc) and the data shows they are doing exactly that, more than ever before since data was kept. But telling people that eating lots of carbs, even if from “whole foods”, is part of a healthy diet is bad advice. And when they gain weight, blaming them for not exercising enough is bad advice stacked upon bad advice.

Such high-carb diets don’t do any good for long-term health, even for athletes. Morally judging fat people as gluttonous and slothful simply doesn’t make sense and it is the opposite of helpful, a point that Gary Taubes has made. It’s plain bullshit and this scapegoating of the victims of bad advice is cruel.

This is why so many professional athletes get fat when they retire, after a long career of eating endless carbs, not that it ever was good for their metabolic health (people can be skinny fat with adipose around their internal organs and have diabetes or pre-diabetes). But some like Butterbean begin their athletic careers fat and remained fat. Many football players are similarly overweight. William Perry, AKA The Fridge, was an example of that, although he was a relative lightweight at 335-350 lbs. Even more obvious examples are seen with some gigantic sumo wrestlers who, while grotesquely obese, are immensely strong athletes.

Sumo wrestlers are also a great example of the power of a high-carb diet. They will intentionally consume massive amounts of starches and sugars in order to put on fat. That is old knowledge, the reason people have understood for centuries the best way to fatten cattle is to feed them grains. And it isn’t as if cattle get fat by being lazy while sitting on the couch watching tv and playing on the internet. It’s the diet alone that accomplishes that feat of deliciously marbled flesh. Likewise, humans eating a high-carb diet will make their own muscles and organs marbled.

I speak from personal experience, after gaining weight in my late 30s and into my early 40s. I topped out at around 220 lbs  — not massive, but way beyond my weight in my early 20s when I was super skinny, maybe down in the 140 lbs range (the result of a poverty diet and I looked gaunt at the time). In recent years, I had developed a somewhat protruding belly and neck flabs. You could definitely tell I was carrying extra fat. Could you tell that I also was physically fit? Probably not.

No matter how much I exercised, I could not lose weight. I was jogging out to my parent’s place, often while carrying a backpack that sometimes added another 20-30 lbs (books, water bottle, etc). That jog took about an hour and I did it 3-4 times a week and I was doing some weightlifting as well, but my weight remained the same. Keep in mind I was eating what, according to official dietary guidelines, was a ‘balanced’ diet. I had cut back on my added sugars over the years, only allowing them as part of healthy whole foods such as in kefir, kombucha, and fruit. I was emphasizing lots of vegetables and fiber. This often meant starting my day with a large bowl of bran cereal topped with blueberries or dried fruit.

I was doing what Americans have been told is healthy. I could not lose any of that extra fat, in spite of all my effort and self-control. Then in the spring of last year I went on a low-carb diet that transitioned into a very low-carb diet (i.e., keto). In about 3 months, I lost 60 lbs and have kept it off since. I didn’t do portion control and didn’t count calories. I ate as much as I wanted, but simply cut out the starches and sugars. No willpower was required, as on a keto diet my hunger diminished and my cravings disappeared. It was the high-carb diet that had made me fat, not a lack of exercise.