Tuesday, March 29, 2022

Obesity and the Regulation of Weight: Part 2

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.


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.


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.

Tuesday, March 22, 2022

Obesity and the Regulation of Weight: Part 1

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.

Tuesday, March 15, 2022

The Carbohydrate Hypothesis: Part 2

 The Carbohydrate Hypothesis: Part 2: 

In Part 2, we will discuss Sugar, Insulin, and Cholesterol.

Sugar and Insulin:

With the modernization of western diets came more and more processed foods and with those came added sugar. The increase in sugar consumption was the one noteworthy difference that might explain the increased incidence of diabetes, coronary heart disease, hypertension, and high cholesterol. The higher the sugar intake in different nations, the higher both the incidence of and mortality from cancer of the colon, rectum, breast, ovary, uterus, prostate, kidney, nervous system, and testicles. One researcher fed high sugar diets to college students and reported that it raised their cholesterol and particularly their triglycerides; their insulin levels rose, and their blood cells became stickier, which he believed could explain the blood clot that seemed to precipitate heart attacks. The higher the insulin levels the greater risk of heart disease. Both diabetes and metabolic syndrome are associated with an elevated incidence of virtually every chronic disease, not just heart disease. Elevated blood sugar, hyperinsulinemia, and insulin resistance may also cause these complications and the associated chronic disease. Let’s dive into the Insulin-Atherogenesis Hypothesis. This hypothesis states that the excessive secretion of insulin accelerates atherosclerosis and perhaps other vascular complications, any dietary factor, refined carbs in particular, that increases insulin secretion will increase risk of heart disease. In particular raising blood sugar will increase the production of what are known technically as reactive oxygen species and advanced glycation end products, both potentially toxic. Reactive oxygen species are generated primarily by the burning of glucose (blood sugar) for fuel in the cells, in a process that attaches electrons to oxygen atoms, transforming the oxygen from a relatively inert molecule into one that is avid to react chemically with other molecules. This is not an ideal situation biologically. One form of these are free radicals and all of them known together are called oxidants because they oxidize other molecules (the same chemical that causes iron to rust). The object of oxidation slowly deteriorates, called oxidative stress. Antioxidants neutralize reactive oxygen species. Advanced glycation end products, AGEs, can take years to form but begin with the attachment of a sugar (glucose) to a protein without the benefit of an enzyme to orchestrate the reaction. The role of enzymes in living organisms is to control chemical reactions to ensure that they conform to their programming. Without these enzymes the sugar sticks to the protein haphazardly and sets the stage for unintended and unregulated chemical reactions. If blood sugar levels are low enough the sugar and protein will disengage and no damage will be done. If blood sugar is elevated then the process continues. AGEs and the glycation process causes the oxidation of LDL particles and so causes the LDL and its accompanying cholesterol to become trapped in the artery wall. This means that anything that raises blood sugar, by the logic of the carb hypothesis, will lead to more atherosclerosis and heart disease, more vascular disorders, and an accelerated pace of physical degeneration, even in those of us who never become diabetic. If you have heard sugar and diabetes then you have also heard of the glycemic index. The lower the glycemic index, the less insulin pumps out and the more your blood sugar stays stabilized. The glycemic index of sucrose is lower than flour and starches and fructose is the reason why. The carbs in starches are broken down upon digestion first to maltose and then to glucose which moves directly from the small intestine into the bloodstream. Table sugar (i.e. sucrose) is both glucose and fructose, the bond is broken up by digestion. The glucose moves into the bloodstream and raises blood sugar and the fructose has little immediate effect on blood sugar. If sugar is the evil in the diet it would be the fructose that endows it with that singular distinction because fructose barely registers in the glycemic index it appears to be the ideal sweetener for diabetics. High Fructose Corn Syrup (HFCC-55) is effectively identical to sucrose upon digestion, the industry treated it and the public perceived it as a healthy additive whereas sucrose carried controversy. Because fructose is the primary sugar in fruit, HFCC is often referred to as fruit sugar and appears healthier by virtue of association. By defining carb food as good or bad on the basis of their glycemic index, health officials effectively misdiagnosed the impact of fructose on human health. The key is the influence of glucose or fructose not on blood sugar but on the liver. Fructose passes directly to the liver where it is metabolized almost exclusively, and the liver responds by converting it into triglycerides and then shipping it out on lipoproteins for storage. The more fructose in the diet the higher the subsequent triglyceride levels in the blood. Glucose, however, is the least reactive of all sugars, the one least likely to attach itself without an enzyme to a nearby protein which is the first step in the formation of AGEs. Investigators studying AGEs have proposed that Alzheimer’s starts with glycation, the haphazard binding of reactive blood sugars to these brain proteins. Because these sugars stick randomly to the fine filaments of the proteins, this in turn causes the proteins to stick to themselves and to other proteins. This impairs their function and occasionally leaves them impervious to the usual disposal mechanisms causing them to accumulate in the spaces between neurons. Sugar intake in international comparisons is positively correlated with both the incidence of and mortality from colon, rectal, breast, ovarian, prostate, kidney, nervous system, and testicular cancer. Let’s go a little deeper into how insulin affects our bodies. Insulin-like growth factor (IGF) is sufficiently similar in structure to insulin that it can mimic its effects. Add the necessary food and IGF levels increase and so will the rate of growth. IGF and its receptors appear to play a critical role in cancer. Anything that increases insulin levels will therefore increase the availability of IGF to the cells and so increase the strength of the IGF proliferation signals (insulin has been shown to affect estrogen this way too). The extra insulin receptors will cause cancerous cells to receive more than their share of insulin from the environment which will convey to the cell more blood sugar for fueling growth and proliferation; the extra IGF receptors will assure that these cells are supplied with particularly forceful commands to proliferate. Another critical role of IGF in the development of cancer may be its ability to inhibit or override the cell suicide program that serves as the ultimate fail safe mechanism to prevent damaged cells from proliferating. IGF accelerates the process by which a cell becomes cancerous and then they work to keep the cells alive and multiplying. Diet changes the nurturing of those cells.


Cholesterol is only one of several fatlike substances that circulate through the blood and are known collectively as lipids or blood lipids. These include free fatty acids and triglycerides, the molecular forms in which fat is found circulating in the bloodstream. Both cholesterol and triglycerides are shuttled through the circulation in particles called lipoproteins. The amount of cholesterol and triglycerides varies in each type of lipoprotein. When physicians measure total cholesterol levels, they have no way of knowing how the cholesterol itself is apportioned in individual lipoproteins. It is possible that in heart disease the problem may be caused not by cholesterol but by a defect in one of these lipoproteins or an abnormal concentration of the lipoproteins themselves. Low density lipoproteins: LDL “bad”, HDL “good”, very low density lipoproteins: VLDL play a critical role in heart disease this is where more of the triglycerides are found. Carbohydrates elevate VLDL. If a physician put a patient with high cholesterol on a low fat high carb diet that may lower LDL but it would raise VLDL. Triglycerides shoot up on low fat and fall on high fat diets. High triglycerides were considerably more common in heart disease victims than high cholesterol. There are four categories of lipoproteins: (1) LDL carries most of the cholesterol, (2) VLDL carries most of the triglycerides, (3) HDL, and (4) chylomicrons which carry dietary fat from the intestine to the fat tissue. By far the most common of the 5 lipoproteins disorders was type 4 characterized by elevated VLDL, synonymous with carb induced hyperlipemia. The higher the HDL, the lower the triglycerides and the risk of heart disease. Lipid profiles provided the rationale for physicians to keep measuring total cholesterol even though it was confirmed that this was an unreliable predictor or risk. Saturated fats raise both HDL and LDL, carbs lower LDL and HDL, monounsaturated fats like oleic acid found in olive oil lower LDL and raise HDL: this principle is also found in red meat, eggs, and bacon. There are two patterns to LDL: pattern A is large, fluffy LDL low risk, pattern B is small, dense LDL high risk. The lower the fat in the diet and the higher the carb the smaller and denser the LDL and more likely for pattern B and the greater risk for heart disease.

Tuesday, March 8, 2022

The Carbohydrate Hypothesis: Part 1

The Carbohydrate Hypothesis Part 1: From Good Calories, Bad Calories by Gary Taubes

The carbohydrate hypothesis goes though why we label carbs as either good or bad and how certain carbs are linked to many diseases due to the western diet. We will dive into the science, carbs and salt and blood pressure. Next week, we’ll touch on sugar and insulin as well as a bit more on cholesterol. Get ready, you’re in for a doozy. 

The Science:

Investigators starting in the 1900’s were led to believe that many western diseases such as obesity, diabetes, cardiovascular disease, hypertension, stroke, cancer, cavities, periodontal disease, appendicitis, peptic ulcers, diverticulitis, gallstones, hemorrhoids, varicose veins, and constipation had a single common cause: the consumption of easily digestible, refined carbs. By the late 1920’s, the meat eating hypothesis had given way to the notion that it was overnutrition in general, in conjunction with modern processed foods, lacking the vital elements necessary for health that were to blame. These are foods that need conservation or refrigeration, artificial preservation and coloring, or processing to keep from spoiling. As a result of these modern processed foods, far reaching changes in bodily function and metabolism are introduced which, extending over many years, can be detrimental to your health. The nutritional debate over the excessive refining of flour and sugar had always been about whether the benefits of digestibility and the pleasing white color outweighed any potential disadvantages of removing the protein, vitamins, and minerals. This led to the suggestion that even diseases like cancer could be a kind of deficiency disease caused by vitamin deficiencies. At least 70-80% of cancers in the US might be avoidable with appropriate changes to diet and lifestyle. But what about fiber? The results of the 49,000 women dietary modification trial of the women's health initiative published in 2006 confirmed that increasing the fiber in the diet by eating more whole grains, fruits, and veggies had no beneficial effect on colon cancer, nor did it prevent heart disease or breast cancer or induce weight loss. It still holds up in relation to constipation, but as far as a major factor in the common diseases of the developed world, no, fiber is not the answer. The two most important conclusions in their analysis were that  (1) man-made chemicals in pollution, food additives, and occupational exposure, play a minimal role in human cancers and that diet played the largest role and (2) clinical trials and large scale studies had demonstrated that the dietary fat and fiber hypotheses of cancer were wrong and similar investigations had repeatedly failed to confirm that red meat played any role. Healthy individuals would be expected to increase their risk of all these conditions by the consumption of refined and easily digestible carbs which inflict their damage first through their effects on blood sugar and insulin and then indirectly through triglycerides, lipoproteins, fat accumulation, and other factors. I’m sure you have all seen on your food labels like “prevents” or “protects against” or “lowers the risk of” but the reality of those claims is just that, claims. These words are used when discussing evidence that is suggestive and hypothesis generating as well as when they are discussing evidence that is as firm as science can make it and you (the public) don’t know which one it is.


When it comes to carbs the more the refining, the whiter the product, and the lower the vitamin, mineral, protein, and fiber content. Carb foods can be transported around the world without spoiling or being devoured by rodents on the way such as sugar, molasses, white flour, white rice. Refined carbs represented the most dramatic change in human nutrition since the introduction of agriculture. Americans replaced a good portion of the whole grains they ate in the 19th century with refined carbs. In most cases, cereal grains, tubers, veggies, fruits, and white flour, sugar, rice and beer were all included under one single category of carb versus two: refined and unrefined. Refined carbs, as we know, can cause the body to lose its homeostasis resulting in disease. Anything that slowed the digestion of these carbs like eating unrefined carbs reduced the strain on the pancreas, the organ that secretes insulin in response to rising blood sugar, or anything that increased the assimilation of glucose without the need for insulin (excessive physical activity) might help prevent diseases of the pancreas. It is believed the concentration of carbs in the refining process did its damage in 3 ways; 1: it led to overconsumption because of the deception of the appetite control apparatus by the density of the carb, 2: exacerbated by the removal of protein from the original product, 3:the refining process increased the rate of digestion of carbs and so the onrush of blood sugar on the pancreas which would explain diabetes. Carb rich diets can cause the body to retain water and so raise blood pressure, it’s not just about salt. Eating carbs prompts the kidneys to hold sodium rather than excrete it, the body retains water to balance out, in doing so removing carbs works like diuretics. Treatment of obesity with very low-carb diets would be met with not complete elimination to maintain fluid balance and avoid large shifts in weight due to water. The water retaining effect of carbs was due to the insulin secreted which in turn induced the kidneys to hold sodium rather than excrete it and that insulin levels were higher in hypertensives than normal individuals. The more carbs consumed, the more insulin is needed to transport the glucose from the carbs into cells where it can be used as fuel. The insulin prompts the liver to synthesize and secrete triglycerides for storage in the fat tissue instead of excrement. If eating a carb rich diet in the presence of insulin resistance will abnormally elevate triglyceride levels, it is hard to avoid the implication that eating a carb rich diet increases the risk of heart disease as well. Carbs are disposed of in 3 sites, adipose tissue, liver, and arterial walls. Complex carbs break down into simple sugars during the process of digestion but they take awhile to do so and if the carb is bound up with fiber the digestion takes even longer. When consuming carbs with a meal the presence of fat and protein in a food decreased the blood-sugar response and so decreased the glycemic index. The more refined the carb, the greater the blood sugar and insulin response. Anything that increases the speed of digestion of carbs will increase the glycemic response (mashing, liquid form, polishing).

Salt and Blood Pressure (BP):

The salt-hypertension hypothesis concludes that when salt is consumed we retain water to balance it out and the kidney’s filter and excrete (cannot be proven). If BP is elevated in pre-hypertension or hypertension, salt reduction would only reduce by 4-5 points versus the 20 points or more BP already is which makes little difference. Eating less salt was a preventive measure that is thought to help the general public and the health organizations and companies used scare tactics to make the public believe that salt equals bad. However, as you read above, eating refined carbs raises BP due to insulin. Other hormonal mechanisms by which insulin raises BP include nervous system stimulation and the same fight or flight response normally produced by adrenaline. Insulin increases heart rate and constricts blood vessels, raising BP. The higher the insulin level the greater the stimulation of the nervous system, and if they remained high the sympathetic nervous system would constantly be working to raise BP.


Tuesday, March 1, 2022

The Fat-Cholesterol Hypothesis


This month’s blogs are a dive into the book “Good Calories, Bad Calories”. Author Gary Taubes gives an unbiased run through of many of the nutrition standards we grew up with. We will take a look into the many nutrition fads and opinions that have been passed through history with no regard to the science behind them. Today we will go through The Fat-Cholesterol Hypothesis. 

Starting off with some history in 1924 the American Heart Association (AHA) was founded due to the rising number of people dying from heart disease. During that time it was a “private organization of doctors” meaning that these few doctors called what was good and what was bad regarding heart health. In the 1950’s we saw premature deaths from infectious disease and nutritional deficiencies drop which left more Americans living long enough to die of chronic diseases such as cancer and heart disease. Thus, the Diet-Heart Hypothesis was born. This hypothesis stated dietary fat causes heart disease which led to low-fat diets, and their products, being introduced. The relationship between dietary fat, cholesterol, and heart disease is more complicated than just cutting out parts of your diet. The Diet-Heart hypothesis constitutes three independent propositions: 1. Lowering cholesterol prevents heart disease, 2. Eating less fat or less saturated fat not only lowers cholesterol and prevents heart disease but 3.That it also prolongs life. In the 1960’s deaths from coronary heart disease appeared to decline after peaking. This peak was due to clinicians becoming more aware in recognizing cardiac disturbances and recording them more frequently, however, authorities said it was somewhat due to the preventative benefits of eating less fat and lowering cholesterol. The AHA used scare tactics to force the public to eat low-fat so they wouldn’t die of heart disease. In the 1970’s, a study found that the vegetable oils and margarines (polyunsaturated) the AHA were recommending as replacements (because they had an alliance with the companies who made them) caused cancer in lab animals.

Now let’s get into science vs corporations and government. Establishing the dangers of cholesterol in our blood and the benefits of low fat diets has always been portrayed as a struggle between science and corporate interests. A question was asked of why so many people suffer coronary heart disease despite having low cholesterol and why multitudes of people with high cholesterol never get or die from heart disease. Any research that was not in favor of the low-fat-diet hypothesis was deemed irrelevant, misinterpreted, or based on untrustworthy data. Unfortunately, if science doesn’t fit the dogma it either gets ignored or never cited, but not invalidated. The reason we still see low fat diets being popularized is truly due to its advocates inability to recognize or acknowledge error, rather than evidence. When working for corporations or government scientists are supposed to be free of conflict and bias. Based on funding, if a group of scientists' research failed to support the government positions then the funding would go to someone whose research did. Now we have the dilemma if a study is correct and has no funding will the public take it seriously or will they listen to the scare tactics used by big corporations to make the risks of “unhealthy” behaviors seem detrimental. 

The USDA is a government funded organization. When they first came out with the Dietary Recommendations the statistics used were based on guesses not reliable evidence. They took a bunch of speculation, acknowledged the claims were science, and then decided they were fact. The Dietary Goals gave way to other government agencies giving dietary advice and the document became the end all be all. Though the Dietary Goals admitted the existence of scientific controversy, it also insisted that Americans had nothing to lose by following the advice. The question to be asked is not why should we change our diet but why not. The committee eventually published a revised edition of Dietary Goals, but with only minor revisions. Now the first recommendation was to avoid being overweight. 

Finally we dig into cholesterol. Cholesterol is a pearly white fatty substance that is found in all body tissues and is an essential component of cell membranes and physiological processes including metabolism and sex hormones. Many circumstances influence total cholesterol levels: exercise will lower it, weight gain will raise it, weight loss will lower it, stress will raise it. The levels will fluctuate seasonally and change with body position. Hormones will affect levels as well as diuretics, sedatives, tranquilizers, and alcohol. For these reasons alone, cholesterol levels can change by 20-30% over the course of weeks. The cholesterol we eat has very little effect on the amount of cholesterol in our blood. The fats we do eat (animal and vegetable) are composed of many different kinds of fats, each with its own chain length and degree of saturation, and each with a different effect on cholesterol. Our brains are 70% fat, mostly in the form of a substance known as myelin that insulates nerve cells and all the nerve endings in the body. Fat is the primary component of all cell membranes. Changing the proportion of saturated to unsaturated fats in the diet, might change the composition of the cell membranes. This could alter the permeability of cell membranes, which determines how easily they transport, among other things, blood sugar, proteins, hormones, bacteria, viruses, and tumor-causing agents into and out of the cell. The relative saturation of these membrane fats could affect the aging of cells and the likelihood that blood cells will clot in vessels and cause heart attacks. Lower cholesterol by diet might help prevent heart disease for some, but it also may raise susceptibility or even cause other conditions such as stroke and cancer. Most of the studies done on cholesterol have involved men. With the few studies involving women, it was found that the higher the cholesterol the longer they lived and this could be due to our sex hormones needing more of the fat to run our systems properly. 

 Stay tuned for Part 2!