In the first part I talked about the problems of conventional wisdom, and the energy balance hypothesis in overweight and obesity. Now it’s time to get down to the nitty-gritty of how our bodies actually work when it comes to storage and use of nutrients.
One thing missing from the conventional hypothesis (Change in weight = Calories IN – Calories OUT) is the arrow of causality. Even if we’d believe this formula to be correct, it doesn’t tell us anything about what causes people to eat too much and expend too little of their energy. In this light, what should be said about obesity – and when I talk about obesity I’m talking about things that can be applied to any amount of overweight – is that it is a disorder of excess fat accumulation.
We don’t assume that people eating too much and exercising too little results in obesity, and at this point we don’t even say that specific foods such as saturated fats or sweets cause obesity. We’re just saying, that something causes the fat tissue to store excessive amounts of fat in obese and overweight people.
When looked from this point of view, overeating is not a weakness of character and the “cure” is not to live our lives constantly battling hunger and the desire to eat. This starting point also allows us to ask different kinds of questions. One extremely important one that has been missing from the caloric balance hypothesis is; if obesity is a disorder of excess fat accumulation then what regulates fat accumulation?
The nutrient cycle
Before we get to the storage of fat, it’s necessary to talk a bit about how our cells use food for energy. Basically the cells have two forms of fuel available; glucose and fatty acids (glycogen, the glucose stored in muscles for rapid need of energy is not relevant to this discussion). Our bodies first burn all available glucose for energy, and then fatty acids cover the rest.
What the body needs is a steady source of energy, and due to this after you eat 50-70% of that energy goes into the adipose tissue (body fat), from where it is then steadily released into the bloodstream as free fatty acids. Carbohydrates in food are converted into glucose and used as a primary source of fuel, but in the modern low-fat carbohydrate-rich diets this means that a significant portion of carbohydrates will also be stored as fat in adipose tissue.
The storage form of both glucose and fatty acids is a triglyceride, consisting of 3 fatty acids (tri) on a glycerol backbone (glyceride). Inside fat cells, triglycerides are continuously broken down and recomposed, releasing fatty acids into the bloodstream. This process ensures that there is a continuous supply of energy available for cells. Any excess fatty acids in the blood are converted again to triglycerides and shipped back to adipose tissue for storage.
How this system should be working is in a homeostasis, a dynamic equilibrium, where the flow of fatty acids in and out of fat cells works freely and the rest of our body is ensured a constant supply of fuel. When blood sugar (please note, that I am using the terms glucose and blood sugar interchangeably, as it’s easier to understand) gets low, more fatty acids are released, and cells stop burning glucose in favor of fatty acids.
In this context, hunger is not a psychological phenomenon, but instead a physiological sign that the fuel supply for our cells is failing and more energy is needed. That’s why we get hungrier after exercise and after a period of fasting, and that’s why in reduced-calorie diets the body starts conserving energy.
What drives fat accumulation?
I’ll repeat it here because it’s important: Fat is stored in the form of triglycerides. The glycerol molecules which form the backbone of triglycerides come from glycerol-3-phosphate, which is a byproduct of glucose metabolism. A small quantity of g-3-p is made via glyceroneogenesis in the fat tissue, but the primary source by far is dietary carbohydrates. The more there is glucose in fat cells, the more g-3-p is available, the more the body creates triglycerides, and the more the rate of fat deposition in adipose tissue increases.
In other words the arrow of causality would go like this: Carbohydrates > glucose > g-3-p > triglycerides > fattening. In fact, it is impossible to accumulate fat without the presence of g-3-p. This explains why overweight and obesity are non-existent in isolated populations such as the Inuit who rely solely on an all-meat diet, and why it has been impossible to inflict weight gain in experiments where excess calories have been fed to the test subjects without those excess calories coming from carbohydrates.
With a diet low on carbohydrates, there is less glucose for cells to burn, and thus less g-3-p to keep fatty acids bound up in the adipose tissue.
The role of hormones
The caloric balance hypothesis states that people gain weight because they eat too much and exercise too little. However, in order for this to make at least some logical sense it is implied to apply only for the overweight people. Let me explain: By this logic a child who is growing year-by-year and thus gaining weight is considered to eat too much and exercise too little. It is also presupposed, that the child is gaining weight because she’s eating too much, not for any other reason. But I doubt anyone would take this seriously. It’s much more reasonable to say that the child is overeating because she is growing.
The important thing here is to notice the causality: The child is growing, therefore she overeats. Not the child overeats, therefore she is growing. And even if you put the child on a calorie restricted diet she will keep on growing. Not as much if she could eat freely, but she would grow nonetheless. The body would simply conserve energy elsewhere in order to fuel the growth. Same applies to pregnant women. If they don’t eat enough their bodies conserve energy elsewhere in order to supply enough fuel for the growing fetus.
These processes are controlled by hormones, and the most important of them when it comes to accumulation of fat is insulin. The primary role of insulin is to direct the flow of glucose from blood into cells, for use as energy or storage as triglycerides. Therefore it can be said that insulin is also controlling fattening by causing the body to form more triglycerides. Another effect of insulin is that it inhibits fat cells from releasing free fatty acids into the bloodstream.
When the body works in harmony, or homeostasis, we would be getting a steady supply of energy from the food we eat. Our cells would first use glucose from the diet as energy, store the rest in adipose tissue, and then gradually release the stored energy as free fatty acids. In this model eating is followed by an increase in insulin levels, as a response to the carbohydrates in diet, driving fat accumulation. When all glucose from the bloodstream is either used for energy or stored, insulin levels would go down and the adipose tissue would then start releasing free fatty acids.
The real problem is that our bodies were not evolved to handle such high spikes in blood sugar that are common when eating modern diet high in sugar and carbohydrates. An increase in blood sugar is followed by an increase in insulin levels, and when this keeps going on for a long time cells start to become resistant to insulin, meaning that more and more insulin is needed to keep the blood sugars steady.
However, because fat tissue is extremely sensitive to insulin, muscles and other parts of our body start to lose their sensitivity – or become resistant – much sooner than the fat tissue. This causes less glucose to be used as fuel, and instead fat cells soak up all the excess blood sugar to prevent it from reaching toxic levels. Since insulin also inhibits the release of free fatty acids from fat tissue into the bloodstream, suddenly the body is in a situation where muscles and other tissues cannot use all the glucose in bloodstream for energy, more and more of it is being directed into the fat tissue for storage, and yet the fat tissue is not releasing its energy stores.
In this unbalanced situation when people are kept on calorie restricted diets, their fat deposits may actually be increasing even though the rest of their bodies are starving for energy: insulin directs the flow of nutrients into adipose tissue, and prevents them from being released back into the bloodstream. Now when all the glucose from the bloodstream is gone, irresistibly strong cravings for sweets occur as the body needs energy, but fat tissue is unable to release it.
This inability to release free fatty acids and therefore provide a steady supply of energy is a result of chronically elevated insulin levels, which is a result of insulin resistance. Both the obese and overweight people, as well as type II diabetics, all have elevated insulin levels. They also have a greatly exaggerated insulin response to dietary carbohydrates – meaning that their bodies secrete significantly more insulin when carbohydrates are consumed compared to a healthy person.
In this sense it is idiotic to the point of insanity to “treat” type II diabetics by giving them more insulin and recommending them to eat high-carbohydrate diets. This is yet another example of modern medicine treating a symptom, not the cause of the disorder. When type II diabetes patients are treated with insulin for up to 12 months, weight can be expected to go up by 2.0 – 4.5 kg. This weight gain then leads to the often-cited vicious cycle of increased insulin resistance, leading to the need for more exogenous insulin and to further weight gain, which increases the insulin resistance even more.
When it comes to the role of glycerol-3-phosphate in fat accumulation, or how insulin drives blood sugar into cells and inhibits the use of fatty acids for energy, and even the development of insulin resistance and obese people having chronically elevated insulin levels, none of this research is particularly controversial. Yet it is rejected out-of-hand in the mainstream obesity field. One reason – as I mentioned in the part 1 – is that so much has been invested in the current dogma that it’s very difficult change course now. The other reason is that the field of medicine has become overspecialized, and most nutrition researchers do not have e.g. sufficient knowledge of biochemistry to see the necessary connections.
I originally thought this topic would be covered in two articles, but after writing all this I feel a third one is needed; one that puts together practical advice and what all this science talk actually means when it comes to losing weight and staying healthy. After all, obesity is just one part of metabolic syndrome which is also associated with cancer, heart disease, and Alzheimer’s. All of which may have the same underlying cause described above.
Meanwhile, if you want to know more I’d recommend spending an hour to watch this lecture by Gary Taubes: Why we gain weight: Adiposity 101 and the Alternative Hypothesis of Obesity.
It may be stated categorically that the storage of fat, and therefore the production and maintenance of obesity, cannot take place unless glucose is being metabolized. Since glucose cannot be used by most tissues without the presence of insulin, it may also be stated categorically that obesity is impossible in the absence of adequate tissue concentrations of insulin… Thus an abundant supply of carbohydrate food exerts a powerful influence in directing the stream of glucose metabolism into lipogenesis, whereas a relatively low carbohydrate intake tends to minimize the storage of fat.
– Edgar Gordon, JAMA, 1963