This week in Good Calories, Bad Calories we are going to dive a little deeper into appetite, hunger, metabolism, diets, and fat. Next week will be the final installation of this series where we will discuss hormones, carbs and sugar, and the main book takeaways.
Appetite, Hunger, and Metabolism:
Why do we eat? How much do we eat? When do we feel hungry or satiated or stuffed? All of these play into metabolism, hunger, and appetite and when it comes to different body types plays a bigger role than we think. There is a natural assumption that obese people eat more than lean people. This is not the case. We should not confuse association with causation. The metabolism of fat patients seemed to run as fast if not faster than anyone else's. The obese tend to expend more energy than lean people of comparable nature which means their metabolism is typically burning off more calories because when people grow fat their lean body mass also increases. An obese person who maintains their weight indefinitely is in caloric equilibrium the same as any person of normal weight at maintenance. Again, it is all about finding and keeping homeostasis. Overeating, though it is observed with great regularity is not the cause of obesity, it is a symptom of an underlying disturbance. The need for overeating and the changes in weight regulation and fat storage are the essential disturbances. The first law of thermodynamics dictates that weight gain, the increase in energy stored as fat and lean muscle tissue, will be accompanied by or associated with positive energy balance, but it does not say that it is caused by a positive energy balance. But children do not grow because they eat voraciously, they eat voraciously because they are growing. They require the excess calories to satisfy the requirements of growth, resulting in a positive energy balance. The growth is induced by hormones particularly growth hormone. Both hunger and sedentary behavior can be driven by a metabolic hormonal disposition to grow fat, just as lack of hunger and the impulse to engage in physical activity can be driven by a metabolic hormonal disposition to burn calories rather than store them. A spendthrift metabolism that wastes excess calories as heat or superfluous physical activity and was assumed to be a critical factor in the genesis of obesity or leanness. The ability to burn up small excesses they observed on the order of a few hundred calories a day is well within the capacity of the ordinary person but in the obese individual the power of flexibility is much less evident. The more protein digested over the amount necessary to maintain tissues and organs the greater the heat generation. Excessive calories lost as heat in the process of digesting and utilizing protein can’t then be stored as fat or used for fuel. We have thrifty metabolisms when we are undernourished and so need to use efficiently every calorie we consume and we have spendthrift metabolisms when we’re over nourished so as to avoid excessive weight gain and obesity. An effort to conserve enough energy to maintain a constant internal balance. When well nourished, the individual tends to become more energetic and it is quite possible that they will soon burn up their stored fat by extra work or exercise which would not have been undertaken had it not been for the overfeeding. If we consume less food than we might require to replenish our reserves then the amount of heat generated in response to a meal is minimized and the stores of carb, fat, and protein are used to make up the difference. Should the caloric deficit continue the result is a gradual lowering of metabolism and a tendency toward restriction of activities due to a lack of energy and initiative. Let’s get into more on the topic of hunger. The notion that hunger can be relieved or eliminated simply by limiting choice of food is exceedingly difficult to embrace. Weight loss can be largely independent of calories, hunger can also be. An obese individual will spend much of his life in an energy balance in the static phase of obesity just as the lean do. When obese individuals try consciously to eat less when they go on a low calorie diet their metabolism and energy expenditure inevitably decrease just as they do when lean individuals are semi-starved. On a calorie restricted diet regardless of weight status their tissues are not receiving enough nutriment. Another way to phrase this is that anything that induces fatty acids to escape from the fat tissue and then be burned as fuel will promote satiety by providing fuel to the tissues.
The physiological notion of hunger is a response to the availability of internal fuels and to the hormonal mechanisms of fuel partitioning. Weight stability is nothing more than an equilibrium between the fatty acids flowing into the energy buffer of the fat tissue and the fatty acids flowing out. What the body regulates is the fuel flow to the cells. Satiety and weight loss will be promoted by factors that increase the release of fatty acids from the fat tissue and direct them to the cells of the tissues and organs to be oxidized anything that lowers insulin levels. Foods that supply calories and other nutritional requirements quickly and efficiently will come to be perceived as tasting good and so we learn to prefer them over others. It’s not so much that fat fills us up as that carbs prevent satiety and so we remain hungry. Carb craving associated with obesity, chronic hyperinsulinemia, the insulin induces hunger or prevents satiety even between meals. As far as the body is concerned, the elevated insulin is the indication that you’ve just eaten.
Diets:
There are many, many diets consistently marked to the public and every year there seems to be one in particular that stands out against the grain. The main diets involve calorie restriction of the restriction of certain food groups. The effect of weight loss diets changes over time. Modest benefits of semi starvation slowly diminish with time as the calorie restriction induces a compensatory inhibition of energy expenditure. Most of the weight loss is water, not fat. Diets were promoted not because they were effective but because they were supposedly least harmful. Patients are simply encouraged to eat as much as is necessary to avoid feeling hungry, but to avoid carbs in doing so. Carb restricted diets performed at least as well and usually better even when the caloric content of the carb restriction was significantly greater. A healthy diet, it is said, must contain fats, protein, and carbs because of the misconception that our system requires dietary glucose to function and to prevent deficiency diseases. Almost all studies of deficiency diseases the diets were high in refined carbs and low in meat, fish, eggs, and dairy. When physicians talked about lean meat as the basis of a weight-reducing diet they didn’t mean chicken without the skin but instead meant meat, fish, and poultry in which the visible fat had been trimmed away. Semi-starvation diets would inevitably fail because they work not by selective reduction of adipose deposits but by wasting of all body tissues and therefore any success obtained must be maintained by chronic undernourishment. Until recently, few nutritionists or clinicians considered it worth their time and effort to test weight reducing diets. Instead, they spent their careers study the physiological and psychological abnormalities associated with the condition of obesity comparing food consumption and physical activity in obese and lean individuals amd studying obesity in animals. They tried to induce fat people to endure semi starvation by behavioral modification. They studied pharmacological methods of suppressing hunger or surgical methods of reducing the amount of food that could be consumed or digested. Testing diets or even treating obese patients was regarded as lesser work.
Fat:
Many studies have been done on fat: on mice, on humans, or on whether a low fat or a high fat diet works better. It was found to be a difficult assignment of gaining weight by increasing only the fat. The rate at which fatty acids were released from the fat deposits of congenitally obese mice was significantly slower than it was in lean mice. If energy goes into the fat tissue faster than it comes out the energy stored in the fat tissue has to increase. As the adipose tissue accumulates fat its expansion will increase the rate at which fat calories are released back into the bloodstream and this could eventually compensate for the initial defect itself. We will continue to accumulate fat and so continue to be in positive energy balance until we reach a new equilibrium and the flow of fat calories out of the adipose tissue once again matches the flow of calories in. Obesity is simply the body’s way of compensating for a defect in the storage and metabolism of fat. The compensation occurs homeostatically without any conscious intervention. This defect in fat metabolism would explain the sedentary behavior typically associated with obesity and why all of us fat or lean will become easily fatigued when we restrict calories for any length of time. As long as obese individuals have this metabolic defect and their cells are not receiving the full benefit of the calories they consume their tissues will always be conserving energy and so expending less than they otherwise might. If fatty acid is needed for energy a deficit could indeed promote lethargy and indolence. A disorder of fat accumulation, not a disorder of overeating. The release of fat or its combustion is impeded or the deposition or synthesis of fat is promoted and the result is obesity. That in turn will cause a deficit of calories elsewhere in the body, internal starvation, and thus a compensatory hunger and sedentary behavior. All 3 major constituents of food supply carbon atoms for combustion (Krebs cycle). Fat tissues contain the ready cash for all the expenditures of the organism. Only when the organism does not or cannot draw on the ready cash for its daily business is it put into depots, and excessive replenishment, through overeating, takes place. The concentration of fatty acids in the circulation is surprisingly low immediately after a meal, when blood-sugar levels are highest, but then increases steadily in the hours that follow as the blood sugar ebbs. It's as though our cells have the option of using fatty acids or glucose for fuel, but when surplus glucose is available, as signaled by rising insulin or blood sugar levels, the fatty acids are swept into the fat tissue for later use. While the fat is stored as triglycerides it enters and exits the fat cells in the form of fatty acids. As triglycerides, the fat is locked into the fat cells, because triglycerides are too big to slip through the cell membranes. They have to be broken down into fatty acids before the fat can escape into the circulation. Inside the fat cells, triglycerides are continuously broken down into their component fatty acids and glycerol (lipolysis), and fatty acids and glycerol are continuously reassembled into triglycerides, a process known as the triglyceride/fatty acid cycle. Any fatty acids that are not immediately repackaged back into triglycerides will slip out of the fat cell and back into the circulation. Anything that works to transport more glucose into the fat cells, insulin for example or rising blood sugar will lead to the conversion of more fatty acids into triglycerides and the storage of more calories as fat.
The one fundamental requirement to increase the flow of fatty acids out of adipose tissue to increase lipolysis and so decrease the amount of fat in our fat tissue is to lower the concentration of insulin in the bloodstream. The more LPL activity on a particular cell type the more fatty acids it will absorb, which is why LPL is known as the gatekeeper for fat accumulation. When insulin levels drop the LPL activity on the fat cells decreases and the LPL activity on the muscle cells increases, the fat cells release fatty acids and the muscle cells take them up and burn them. During exercise, LPL activity increases in muscle tissue, enhancing the absorption of fatty acids into the muscles to be burned as fuel. But when the workout is over, LPL activity in the fat tissue increases. The sensitivity of fat cells to insulin will also be sufficiently altered.
