Tuesday, April 5, 2022

Obesity and the Regulation of Weight: The Final Part

 In our final blog edition of Good Calories, Bad Calories we are going to discuss how your hormones play a role in obesity, more on carbs and sugar, and the main takeaways from the book.


Hormones:

Common obesity is the only manifestation of an endocrine disturbance, so slight that it upsets the balance of intake and output by less than .1 of 1%. Neither eating less or exercising more will lead to long term weight loss as the body naturally compensates. We get hungry and if we can’t satisfy that hunger we’ll get lethargic and our metabolism will slow down to balance our intake. This happens whether we are lean or obese. As food intake drops, the level of thyroid hormone falls and metabolic rate is lowered. Food intake has to be reduced even further to drop below the level of energy expenditure. Hunger mechanisms, including the feeling of an empty stomach lead us to search for food. Obesity may be caused by a hormonal or metabolic defect determined primarily by genetic inheritance but the epidemiology tells us that this defect is triggered by environmental factors. The likely explanation is the effect of diet on this regulation of fat metabolism and energy balance. Since insulin is the hormone responsible for promoting the incorporation of fat into our adipose tissue and the conversion of carbs into fat, the obvious suspects are refined carbs and easily digestible starches which have well documented effects on insulin. In obesity, the cause is an excess of insulin or an inordinate sensitivity to insulin by the fat cells; the result is an overstock of fuel in the adipose tissue and so internal starvation but now the symptoms are weight gain and hunger. Insulin seemed to have a dramatic effect on hunger, that insulin was the primary regulator of fat deposition in the adipose tissue, and that obese patients had chronically high levels of insulin. Other hormones such as adrenaline have been shown to increase the mobilization of fat from the fat cells. Virtually anything that increases the secretion of insulin will also suppress the secretion of hormones that release fat from the fat tissue. Sex hormones determine where fat is stored as evidence by the differences in fat distribution between men and women. Thyroid hormones, adrenaline, and growth hormone accelerate the release of fatty acids from fat depots, as does a hormone known as glucagon, secreted by the pancreas. Female sex hormones do not appear to play a major role in determining where fat appears on the body, women who have their ovaries removed put on fat very much like other women. These hormones do however seem to affect the quantity of fat which would explain the tendency of women to gain weight after menopause. The hormones that promote fat mobilization include: epinephrine, norepinephrine, ACTH, glucagon, TSH, Melanocyte stimulating hormone, vasopressin, and GH;  the hormones that promote fat accumulation include: insulin.


Carbs and Sugar:

Though the obese did not appear to eat more calories on average than the lean they did consume more carbs. There is something about carbs that allows the consumption of such enormous quantities of food and yet still induces hunger as the night approaches. The implication is that there is a direct connection between carbs and our experience of hunger, or between fat and protein and our experience of satiety. In early weight loss diets only a minimal amount of carbs and added fats would be allowed in the diet due to being considered nonessential. The idea was to keep the body in what is called nitrogen equilibrium. Though glucose is a primary fuel for the brain it’s not the only fuel, the body can also use ketones produced in the liver the rest come from glucose synthesized from the amino acids in protein either from the diet or from the breakdown of muscle. This suggested another way of defining a balanced diet, it’s possible that eating easily digestible carbs and sugars increases our need for vitamins that we would otherwise derive from animal products in sufficient quantities. The uptake of vitamin C by cells is globally inhibited when blood sugar levels are elevated. In every case the weight loss after 3-6 months was 2-3x greater on the low carb unrestricted calorie than calorie restricted low fat. Four facts had been established beyond a reasonable doubt: 1. Carbs are singularly responsible for prompting insulin secretion, 2. Insulin is singularly responsible for inducing fat accumulation, 3. Dietary carbs are required for excess fat accumulation, 4. Both type 2 diabetes and obese have abnormally elevated levels of circulating insulin and a greatly exaggerated insulin response to carbs in the diet. Just a few more details are necessary to understand why we get fat. The first is that the amount of glycerol phosphate available to the fat cells to accumulate fat to bind the fatty acids together into triglycerides and lock them into adipose tissue also depends directly on the carbs in the diet. Dietary glucose is the primary source of glycerol phosphate. It may be impossible to store excess body fat without at least some carbs in the diet and without ongoing metabolism of these dietary carbs to provide glucose and the necessary glycerol phosphate. The storage of fat and therefore the production and maintenance of obesity cannot take place unless glucose is being metabolized. Fructose is converted more efficiently into glycerol phosphate than glucose. Fructose is considered the most lipogenic carb. However it does not stimulate the pancreas to produce insulin so glucose is still needed. The 50/50 glucose/fructose table sugar or HFCS does this. The longer the insulin remains elevated the longer the fat cells will accumulate fat and the longer they’ll go without releasing it. There is great biological variation in what they called the insulin-secretory responses. This causes us to secrete more or less insulin to the same amount of carb ingested, could be more or less effective at lowering blood sugar or at promoting fat accumulation, or it remains elevated in the circulation for longer or shorter periods of time. And because variations of less than 1% in the partitioning of calories either for fuel or for storage as fat could lead to the accumulation of tens of pounds of excess fat over over a decade it would take only infinitesimal variations in these insulin-secretory responses to mark the difference between leanness and obesity, between health and diabetes. We can also talk about the supply of nutrients from mom to baby. The nutrient supply from mother to developing child passes the placenta in proportion to the nutrient concentration in the mother’s bloodstream. If the mother has high blood sugar then the developing pancreas in the fetus will respond to this stimulus by overproducing insulin secreting cells. It suggests that once a generation of adolescents and adults start eating the highly refined carbs and sugars now ubiquitous in our diets even their children will feel the effect and perhaps their children’s children.


Main Takeaways:

  1. Dietary fat, whether saturated or not, is not a cause of obesity, heart disease, or any other chronic disease of civilization.

  2. The problem is the carbs in the diet, their effect on insulin secretion, and thus hormonal regulation of homeostasis, the more easily digestible and refined the carb the greater the effect on our health, weight, and well-being.

  3. Sugars, sucrose and HFCS are harmful, because the combination of fructose and glucose simultaneously elevates insulin levels while overloading the liver with carbs.

  4. Through their direct effect on insulin and blood sugar, refined carbs, starches, sugars are the dietary cause of coronary heart disease and diabetes. They are most likely the dietary causes of cancer, Alzheimer's, and other chronic diseases of civilization.

  5. Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.

  6. Consuming excess calories does not cause us to grow fatter anymore than it causes a child to grow taller. Expanding more energy than we consume does not lead to long-term weight loss, it leads to hunger.

  7. Fattening and obesity are caused by an imbalance in the hormone regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses this balance.

  8. Insulin is the primary regulator of fat storage. When insulin levels are elevated, either chronically or after a meal, we accumulate fat in our fat tissue. When insulin falls we release fat from our fat tissue and use it for fuel.

  9. By stimulating insulin secretion, carbs make us fat and ultimately cause obesity. The fewer the carbs we consume the leaner we will be.

  10. By driving fat accumulation, carbs also increase hunger and decrease the amo9unt of energy we expend in metabolism and physical activity.

  11. Evolution should be our best guide for what constitutes a healthy diet. It takes time for a population or a species to adapt to any new factor in its environment; the longer we’ve been eating a particular food as a species, and the closer that food is to its natural state the less harm it is likely to do.

  12. The most dramatic alterations in human diets in the past 2 million years are 1. The transition from carb poor to carb rich diets that came with the invention of agriculture, 2. The increasing refinement of those carbs, 3. The dramatic increases in fructose consumption.

  13. Can take the necessary steps to prevent these disorders rather than trying to cure them or ameliorate them after the fact.

  14. We don’t get fat because we’re sedentary, we become sedentary because we’re getting fat. And we’re not lean because we’re active, rather we’re active because we’re lean and our bodies are predisposed to burn off the calories we consume rather than stash them away in our fat tissue.