“The ingestion of a quantity of food greater than that required by the body, leads to an accumulation of fat and to obesity… (Carl von Noorden, MD, 1907).”
This dietary concept of “calorie counting” has been the dominant dietary theory for generations. As will be explained, unfortunately, this dietary theory proves to be a malicious hoax.
Before I explain why this dietary theory is a hoax, let’s first explore the theory of caloric imbalance. Calorie represents a form of energy. Therefore, this dietary theory is completely based on thermodynamic principles. It completely ignores other aspects of physiology, biochemistry, and nutrition.
Calorie can be spelled with a “small c” or a “large c”. The “small c” calorie is abbreviated cal. The “large C” Calorie is abbreviated kcal. A “calorie” is the energy required to raise the temperature of 1 gram of water 1 degree Celsius. A Calorie is the amount of energy required to raise the temperature of 1 kilogram of water 1 degree Celsius.
The calorie counting dietary theory relies on the differences between macronutrients in terms of how many calories they contain per unit size. Carbohydrates can be converted to energy in the ratio of 4 Calories per gram of carbohydrate. In a similar way, protein can be converted into energy in the ratio of 4 Calories per gram of protein. In contrast, fats are converted into energy in the ratio of 9 Calories per gram of fat.
This dietary theory of calorie counting requires the presumption that a calorie of carbohydrate will respond the same way as a calorie of protein or a calorie of fat. In other words, a calorie is a calorie is a calorie, no matter what the source. Obviously, if that was the only factor to be considered, then fat should be avoided, as it has over twice the amount of energy compared to carbohydrates or proteins. More energy per gram translates into more energy storage, which translates into larger fat cells and obesity. This was certainly part of the driving force which gave us low fat food products over the last several decades.
In truth, not all calories are equal. In fact, calories from carbohydrates are metabolized much differently than calories from protein or fat. Carbohydrates and proteins are absorbed from our small intestine and taken by the portal vein to our liver. In contrast, fats are absorbed in our small intestine and delivered to our vascular system by way of the lymphatic system. In other words, fats do not pass through the liver after absorption.
At this point, let me introduce the concept of “glycemic index.” The glycemic index is a scale from 0-100 that descn”bes how quickly carbohydrate products are absorbed. A glycemic index closer to 100 would mean th.at the carbohydrates are absorbed very quickly. Pure glucose has a glycemic index of I00. A glycemic index ofless than 25 represents carbohydrate products that are absorbed much more slowly. The “glycemic load” is determined by the glycemic index of a particular carbohydrate food combined with the total amount of carbohydrate in the food consumed.
These principles, glycemic index and glycemic load, determine how fast the liver will be receiving a load of carbohydrate. If the liver receives a large carbohydrate load, then it will begin converting carbohydrates to fat in a process called lipogenesis. Therefore, if we consume food products with a large glycemic load, then glucose will be quickly converted into fat in the liver. This fat will then be redistributed to fat cells.
The liver can only take-up so much glucose as it comes in by way of the portal vein. The remainder of the glucose load passes through the liver, into the systematic circulation.
Thus blood glucose rises, reaches the pancreas, and stimulates the pancreas to release insulin. Insulin is our storage hormone. It stores energy for us. Insulin is vitally important. Lack of insulin causes type 1 diabetes mellitus. However, having our insulin level rise too many times per day will lead to too much storage. Therefore, our goal should be to limit the number of insulin spikes per day.
As I hope I have made clear, lipogenesis in the liver and the endocrinologic effects of insulin are completely ignored in the dietary theory of “expend more calories than consumed.”
Insulin proves to be quite an interesting hormone. When insulin levels are high, the glucose from the blood is taken up in muscle cells and fat cells. Increased glucose in fat cells causes lipogenesis. In other words, the glucose that is going into a fat cell largely becomes fat.
Insulin does three things to a fat cell that we should want to avoid. First, as described above, insulin drives glucose into the fat cells. Second, insulin inhibits fat cells from releasing fat. When fat cells do not release fat into the bloodstream, then fat cannot be used as an energy source by other cells. Third, insulin stimulates hunger. In general, it is thought that insulin causes Leptin resistance. Leptin is a hormone that is released from fat cells and causes satiety. Thus Leptin is our satiety hormone that decreases appetite. As a brief aside, Ghrelin, is our hunger hormone. It is released by the stomach and acts on the hypothalamus to increase hunger and increase gastric secretions.
Further, when we expose our pancreas to years of glucose loads, which produce hyperinsulinemia, meaning more insulin in the bloodstream than there should be, we set the stage for insulin resistance. Insulin resistance represents a state where our body’s cells no longer respond properly to insulin. As the cells become unresponsive to insulin, the glucose in the bloodstream remains high and further insulin is secreted by the pancreas. This vicious cycle continues and creates type 2 diabetes mellitus. This process of insulin resistance, also leads to obesity, hypertension, heart disease and inflammation. In brief, this process of insulin resistance related to years of glucose loading, produces the metabolic syndrome described in Chapter 1.
Thus far in our discussion, we have described only glucose as the carbohydrate. There are other carbohydrates that need to be considered. Especially, fructose, the sugar found in fruits and vegetables. Additionally, we will cover sucrose, which is a disaccharide, meaning two sugars: 1 molecule of glucose and 1 molecule of fructose.
Interestingly, fructose does not cause the pancreas to secrete insulin. Therefore, some time ago, it was thought that fructose may be helpful in the management of diabetes mellitas. It is not. Fructose causes insulin resistance on its own, in a way that is unclear. In other words, fructose could worsen diabetes mellitus. Our bodies cannot convert fructose to glucose. Instead, almost all of the fructose ingested is converted to fat.
Fructose is absorbed in our intestine and delivered to our liver by the portal vein. There, the liver turns fructose into fat by way of lipogenesis.
Another sugar to consider is the milk sugar lactose. Lactose is a disaccharide with 1 molecule of glucose and 1 molecule of galactose. For all intents and purposes, galactose acts similarly to fructose. In other words, virtually all of the galactose consumed gets converted into fat.
Since the mid 1980s, Coca-Cola and Pepsi replaced sucrose with High Fructose Corn Syrup. Most of the High Fructose Com Syrup is HFCS-55. That represents a carbohydrate sweetener with 55% fructose and 45% glucose. High Fructose Com Syrup is actually sweeter than sucrose and cheaper.
Thus far, we have covered simple sugars called, monosaccharides and disaccharides. Starches are polymeric carbohydrates, meaning many sugar molecules bound together. Well known sources of starch include potatoes, wheat, com and rice.
Starches have varying glycemic indexes based on how much fiber is left on the starch food product. When it is said that the packaged food industry often ”processes” carl>ohydrates, what that means is that the fiber has been removed :from the starch. For instance, whole grain wheats have an outer “bran” and an ”inner endosperm}’ The endosperm is all starch, and the outer bran is all fiber. When whole grain wheat is processed to create white flour, the bran is simply removed from the endosperm.
Therefore, as expected, the glycemic index for white bread is higher than the glyccmic index for whole grain bread. However, all bread has significant glycemic loads.
Fruits and vegetables vary widely in the amount of carbohydrate that they contain. For instance, potatoes, sweet potatoes, yams, and com have significant carbohydrate loads.
In contrast, mushrooms, broccoli, cauliflower and asparagus have very small carbohydrate loads. The so-called tropical fruits also have a much higher carbohydrate load than blueberries, raspberries, strawberries and tomatoes.
Other carbohydrate rich foods include legumes. These include peas, beans, chickpeas, lentils, soybeans, peanuts and pulses (seeds of legumes).
Even nuts have widely varying carbohydrate counts. For instance, cashews and chestnuts have a significant amount of carbohydrate, where walnuts, macadamia nuts, Brazil nuts, and pecans have very low carbohydrate counts.
Hopefully the above was convincing that a calorie of carbohydrate is significantly different than a calorie of protein or fat. Proteins and fats do not stimulate lipogenesis in the liver. Further, proteins and fats do not cause insulin to be released from the pancreas. Therefore, conclusively, a calorie is not a calorie is not a calorie. Carbohydrate calories are significantly different
If that is the case, then how did the concept of “expend more calories than consumed” become such a prevalent dietary theory throughout most of our lives? Well, to understand that, you have to understand “Big Sugar.” Sugar is a profitable business. Sugar has always been represented in this country with large associations: Sugar Institute (1928), Sugar Research Foundation (1943), Sugar Association Incorporated (1951), International Sugar Research Foundation (1968), and World Research Organization (1978). These powerful associations have consistently sold the deception that a calorie of sugar is no more fattening than a calorie of any other food. To them, obesity is simply the excess consumption of all calories. Big Sugar had many powerful allies. These include Fred Stare, MD, the founder of Harvantts Nutritional Department, Ancel Keys, MD, from the University of Minnesota, and Theodore Van Itallie from Columbia University.
Big Sugar basically used the same tactics that Big Tobacco used to try and convince the public that nicotine was not addictive. The nefarious behavior of Big Sugar was brought to light by Christina Kearns, DDS (JAMA 2016). Dr. Keams came across the paperwork from a sugar company called the Great Western Sugar Company. This sugar company was in business from 1893 to 1984 in Longmont, Colorado. When this sugar company shut down, it donated all of its paperwork to the library at Colorado State University.
This paperwork had many documents which were previously kept confidential and out of the public view. Dr. Keams realized that the Great Western Sugar Company along with Big Sugar had a public relations strategy to mislead the American public of the dangers of carbohydrates.
Another interesting thing to consider about carbohydrates is the following questions: Is there a carbohydrate deficiency syndrome? It is clear that when it comes to proteins there are “essential amino acids.” If we do not ingest essential amino acids in our diet, then there will be a protein deficiency syndrome. Our body cannot synthesize essential amino acids. There are also essential fats, that will be discussed further below. There is no carbohydrate deficiency syndrome.
Another concerning concept regarding carbohydrates involves Alzheimer’s disease. Carbohydrate consumption can lead to type 2 diabetes mellitus. Type 2 diabetes mellitus doubles the risk of developing Alzheimer’s disease (OIT 1996). This correlation between diabetes and Alzheimer’s disease is not well enough understood enough to characterize it as a causation. In other words, it is unclear whether or not type 2 diabetes mellitus actually causes Alzheimer’s disease or is just often associated with Alzheimer’s disease. In theory, type 2 diabetes mellitus can lead to hypertension and microvascular disease. Hypertension and microvascular disease can cause small strokes in the brain.
Many small strokes in the brain can cause dementia. In fact, sugar intake correlates with hypertension to a much greater extent than salt intake. Insulin may lead to hypertension by a couple of different paths. Insulin stimulates the kidneys to secrete antidiuretic hormone (Miller Bodgono:ff 1954). Antidiuretic hormone causes fluid retention, which can increase blood pressure. Insulin also acts on the central nervous system to increase sympathetic tone (Landsberg 1986). By definition, increased sympathetic tone causes hypertension.
Based on the above, it might be easy to conclude that sugar, in all of its form, causes obesity. Then, should we eat primarily protein? Isn’t that the Paleo Diet (Stanley Eaton 1985), which descended from the Atkin’s Diet (1970s), which descended from Dr.
Harvey’s Diet (1864)? We will discuss protein metabolism latter. For now, understand that when an excess of protein is consumed, the liver will convert the excess amino acids (proteins are made up of amino acids) into glucose. This process is termed gluconeogenesis. This newly formed glucose will then navel to the pancreas and stimulate insulin secretion.
Hopefully, the above causes you to limit carbohydrate intake, but please do not replace carbohydrates with artificial sweeteners. All brands of artificial sweeteners stimulate receptors of the tongue which sense sweet taste. These receptors stimulate Cranial Nerves VII and IX, which transmit the information that a sweet food has been tasted to the brainstem. From there, nerve transmission reaches the pancreas by way of the neuroenteric nervous system. The pancreas, which has been misled into thinking that glucose will soon enter the blood stream, releases insulin. Unnecessary insulin in the blood stream does not do anything good for our metabolism. Artificial sweeteners have another deleterious effect, which will be described below.