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.
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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).
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
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.”
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.