Obesity and the regulation of weight is the final chapter in Good Calories, Bad Calories. In these chapters we go over the science, the hypotheses, and the clinical trials. Next week we will dive into fat, diets, hunger, and metabolism.
The Science:
The trouble with the science of obesity, as it has been practiced for the last 60 years, is that it begins with a hypothesis that overweight and obesity result from excess calorie consumption and/or inadequate physical activity. Obesity can conveniently be blamed on fast food by association. Any hypothesis that tries to explain how obesity is caused should explain the emergence of obesity in any population and at any time not just the past few decades. Most studies comparing normal and overweight people suggest that those who are overweight eat fewer calories than those of normal weight. The first international conference on obesity in 1974 would reveal that obesity is extremely common and that it is probably the most widespread form of malnutrition. Anthropologists have reported that both nutrition and health declined rather than improved with the adoption of agriculture. Obesity is an iceberg topic. Not one thing causes it, but it comes as a result of many things changing our homeostasis. The association between physical activity and weight change is more complex than assumed. The importance of exercise in weight control is less than might be believed because increases in energy expenditure due to exercise also tend to increase food consumption. Consistently high or low energy expenditures result in consistently high or low levels of appetite. Talking about hunger as though it were a phenomenon that was exclusive to the brain, a question of willpower rather than the natural consequence of a physiological drive to replace whatever calories may have been expended, is where we are now with talks on obesity to the public. The evidence suggests that this physiological drive is true for both the fat and the lean. It is one of the fundamental observations we have to explain if we are to understand why we gain weight and how to lose it. If you have ever heard of IIFYM (macro counting) then you know that the different macronutrients (carb, protein, and fat) all have different kcal of 4,4, and 9 respectively. This distribution on metabolism and hormone secretion is radically different from those numbers and makes the 4,4,9 kcal irrelevant to why we gain weight. A fundamental requirement of any living organism is to provide a steady and reliable supply of fuel to its cells regardless of the circumstances aka keeping homeostasis. Life is dependent on homeostatic systems that exhibit the same relative constancy as body weight and none of them require a set point like the temperature setting on a thermostat. It is always possible to create a system that exhibits set-point-like behavior or a settling point without actually having a set-point mechanism involved. Disturbances in body weight regulation like obesity could be caused by pathological changes in certain parts of the nervous system, endocrine system, and depot organs. For decades, it has been insisted that dietary fat, not carbs, fattens most effectively and causes obesity. This is why low fat, low calorie diets are recommended for weight loss as well as prevention of heart disease. But, there is no evidence linking obesity to dietary fat consumption neither between populations nor in the same population. The crucial factor is not how much is eaten or how much is expended, but how those nutrients or the energy they contain is ultimately distributed, how those calories are utilized and made available when needed. It’s not the energy balance driving this system but the distribution of that energy, the demand for energy at the cellular level.
The Hypotheses:
There are multiple different hypotheses regarding why we gain weight and why we stay with the weight we gain. The Thrifty Genotype Hypothesis describes how we suck up calories when they are abundant and store them as fat until they are called upon in their time of need. Gaining weight during prosperity but having a difficult time losing it due to the modern era. Obesity hypothesis number two is strictly for self gratification. Number three is because something biological is going on (i.e. a hormone or enzyme). We see this in women when they gain weight during pregnancy and after menopause which suggests the sex hormones are involved as much or more than eating behavior and physical activity. We then have the body type hypothesis; there are three different physical types: (1) an ectomorph who is long and lean, (2) mesomorph who is broad and muscular, and (3) endomorph who is round and fat. You cannot change from one category to another. We are all endowed with the ability to adapt our metabolism and energy expenditure to both over and under nutrition. Some of us do it better than others.
Next, we have the obesity hypotheses of exogenous and endogenous: an immoderate lifestyle (exo obesity driven by external forces to the body) or to the fact that some people seemed predestined to grow fat and stay fat regardless of how much they ate or exercised (endo driven by internal forces). There is also a working hypothesis that the degree of tolerance for carbs varies from patient to patient and indeed in the same patient at different periods of their life. The positive caloric balance/overeating hypothesis dictates that the primary defect is in the brain, in the regulation of ingestive behaviors, particularly at the cognitive level. This defect purportedly causes us to consume more calories than we expend and thus induces weight gain. The assumption that energy expenditure and energy intake are independent variables. By contrast, the alternative hypothesis proposes that the primary defect is hormonal and metabolic, in fat storage and/or burning of fat for fuel (oxidation) and is in the body, not the brain. Overeating and inactivity (hunger and lethargy) are side effects of this underlying metabolic defect not causes. Immoderate eating and physical inactivity do not induce obesity because the body adjusts intake to expenditure and expenditure to intake. This alternative hypothesis of obesity constitutes three distinct propositions: (1) Obesity is caused by a regulatory defect in fat metabolism, (2) That insulin plays the primary role in this fattening process, (3) Carbs, in particular refined carbs and perhaps fructose content, and the amount of sugar consumed are the prime suspects in the chronic elevation of insulin. The hypothesis is based on three fundamental propositions: (1) That the supply of fuel to all body tissues must always remain adequate for them to function during all physiological conditions and even during prolonged food deprivation, (2) Each of the various metabolic fuels, protein, fat, carbs, is equally capable of supplying energy to meet the demands of the body, (3) The body has no way of telling the difference between fuels from internal sources, the fat tissue, liver glycogen, muscle protein, and fuels that come from external sources. Finally we have the hypothesis of hunger, satiety, and weight regulation which means that obesity is caused by a hormonal environment, increased insulin or increased sensitivity to insulin, that tilts the balance of fat storage and fat burning. This hypothesis also implies that the only way to lose body fat successfully is to reverse the process to create a hormonal environment in which fatty acids are mobilized and oxidized in excess of the amount stored.
The clinical trials:
There were clinical trials done with men and with rats where they were starved or put on very low calorie diets. Here are the results. When the men were finished with their calorie deficits it was found that the men started indulging in excess amounts of food despite caution about the dangers of overindulgence, after such a strict diet all the men over-ate and gained all their weight back plus some after the calorie restriction. Behavior and complaints induced by the constant ravenous hunger that obsessed the subjects, food became the topic of all conversations, it was all they thought about which made them miserable and used disordered eating techniques like chewing gum so they would stick to the low cal diet. With obese rats it was found that if the rats were starved they would lose weight but still contain more fat than the normal rats because the weight loss was from muscle. Rats adjust their intake in response to caloric content, not volume, mass, or even taste, and this is presumably true of humans as well. What investigators failed to take into account was their own previous observation that the nutrient composition of the diet seemed to profoundly affect the desire to consume calories to excess. On the flip side, when subjects went on a diet to fatten them up it seemed almost impossible to do so on high fat, high protein diets in which the food to be eaten in excess was meat. Back to the rats. When feeding them a diet of refined carbs and sugar it was discovered they could induce deficiency diseases in the rats. It was also found that the hypothalamus regulated adiposity in rats. Damage to the ventromedial hypothalamus caused a defect that directed nutrients away from the tissues and organs where they were needed for fuel and into the fat tissue. We mentioned obesity and sex hormones in the section above and in rats it was found that the female sex hormone estrogen, without it the rats eat voraciously, dramatically decrease physical activity and quickly grow obese. The critical point is that when researchers remove the ovaries from these rats, but restrict their diets to only what they were eating before the surgery, the rats become just as obese just as quickly. The number of calories consumed makes little difference. Insulin response and malnutrition and metabolism were also studied in the rats. Weight loss increased when the subjects divided their calories into 7 meals which served to moderate the insulin response. When is came to food acceptance and the urge to eat, it was found in rats to have relatively little to do with a local condition of the gastrointestinal canal, little to do with the organs of taste and very much to do with quantitative deficiencies of currently metabolized materials, the relative presence of usable fuel in the bloodstream.
