The Obesity Code. Jason Fung
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erroneous assumption is made that energy expenditure remains constant except for exercise. Total energy expenditure is the sum of basal metabolic rate, thermogenic effect of food, nonexercise activity thermogenesis, excess post-exercise oxygen consumption and exercise. The total energy expenditure can go up or down by as much as 50 percent depending upon the caloric intake as well as other factors.
Assumption 3: We exert conscious control over Calories In
Eating is a deliberate act, so we assume that eating is a conscious decision and that hunger plays only a minor role in it. But numerous overlapping hormonal systems influence the decision of when to eat and when to stop. We consciously decide to eat in response to hunger signals that are largely hormonally mediated. We consciously stop eating when the body sends signals of satiety (fullness) that are largely hormonally mediated.
For example, the smell of frying food makes you hungry at lunchtime. However, if you have just finished a large buffet, those same smells may make you slightly queasy. The smells are the same. The decision to eat or not is principally hormonal.
Our bodies possess an intricate system guiding us to eat or not. Body-fat regulation is under automatic control, like breathing. We do not consciously remind ourselves to breathe, nor do we remind our hearts to beat. The only way to achieve such control is to have homeostatic mechanisms. Since hormones control both Calories In and Calories Out, obesity is a hormonal, not a caloric, disorder.
Assumption 4: Fat stores are essentially unregulated
Every single system in the body is regulated. Growth in height is regulated by growth hormone. Blood sugars are regulated by the hormones insulin and glucagon, among others. Sexual maturation is regulated by testosterone and estrogen. Body temperature is regulated by a thyroid-stimulating hormone and free thyroxine. The list is endless.
We are asked to believe, however, that growth of fat cells is essentially unregulated. The simple act of eating, without any interference from any hormones, will result in fat growth. Extra calories are dumped into fat cells like doorknobs into a sack.
This assumption has already been proven false. New hormonal pathways in the regulation of fat growth are being discovered all the time. Leptin is the best-known hormone regulating fat growth, but adiponectin, hormone-sensitive lipase, lipoprotein lipase and adipose triglyceride lipase may all play important roles. If hormones regulate fat growth, then obesity is a hormonal, not a caloric disorder.
Assumption 5: A calorie is a calorie
This assumption is the most dangerous of all. It’s obviously true. Just like a dog is a dog or a desk is a desk. There are many different kinds of dogs and desks, but the simple statement that a dog is a dog is true. However, the real issue is this: Are all calories equally likely to cause fat gain?
“A calorie is a calorie” implies that the only important variable in weight gain is the total caloric intake, and thus, all foods can be reduced to their caloric energy. But does a calorie of olive oil cause the same metabolic response as a calorie of sugar? The answer is, obviously, no. These two foods have many easily measurable differences. Sugar will increase the blood glucose level and provoke an insulin response from the pancreas. Olive oil will not. When olive oil is absorbed by the small intestine and transported to the liver, there is no significant increase in blood glucose or insulin. The two different foods evoke vastly different metabolic and hormonal responses.
These five assumptions—the key assumptions in the caloric reduction theory of weight loss—have all been proved false. All calories are not equally likely to cause weight gain. The entire caloric obsession was a fifty-year dead end.
So we must begin again. What causes weight gain?
HOW DO WE PROCESS FOOD?
WHAT IS A calorie? A calorie is simply a unit of energy. Different foods are burned in a laboratory, and the amount of heat released is measured to determine a caloric value for that food.
All the foods we eat contain calories. Food first enters the stomach, where it is mixed with stomach acid and slowly released into the small intestine. Nutrients are extracted throughout the journey through the small and large intestines. What remains is excreted as stool.
Proteins are broken down into their building blocks, amino acids. These are used to build and repair the body’s tissues, and the excess is stored. Fats are directly absorbed into the body. Carbohydrates are broken down into their building blocks, sugars. Proteins, fats and carbohydrates all provide caloric energy for the body, but differ greatly in their metabolic processing. This results in different hormonal stimuli.
CALORIC REDUCTION IS NOT THE PRIMARY FACTOR IN WEIGHT LOSS
WHY DO WE gain weight? The most common answer is that excess caloric intake causes obesity. But although the increase in obesity rates in the United States from 1971 to 2000 was associated with an increase in daily calorie consumption of roughly 200 to 300 calories,1 it’s important to remember that correlation is not causation.
Furthermore, the correlation between weight gain and the increase in calorie consumption has recently broken down.2 Data from the National Health and Nutrition Examination Survey (NHANES) in the United States from 1990 to 2010 finds no association between increased calorie consumption and weight gain. While obesity increased at a rate of 0.37 percent per year, caloric intake remained virtually stable. Women slightly increased their average daily intake from 1761 calories to 1781, but men slightly decreased theirs from 2616 calories to 2511.
The British obesity epidemic largely ran parallel to North America’s. But once again, the association of weight gain with increased calorie consumption does not hold true.3 In the British experience, neither increased caloric intake nor dietary fat correlated to obesity—which argues against a causal relationship. In fact, the number of calories ingested slightly decreased, even as obesity rates increased. Other factors, including the nature of those calories, had changed.
We may imagine ourselves to be a calorie-weighing scale and may think that imbalance of calories over time leads to the accumulation of fat.
Calories In – Calories Out = Body Fat
If Calories Out remains stable over time, then reducing Calories In should produce weight loss. The First Law of Thermodynamics states that energy can neither be created nor destroyed in an isolated system. This law is often invoked to support the Calories In/Calories Out model. Prominent obesity researcher Dr. Jules Hirsch, quoted in a 2012 New York Times article,4 explains:
There is an inflexible law of physics—energy taken in must exactly equal the number of calories leaving the system when fat storage is unchanged. Calories leave the system when food is used to fuel the body. To lower fat content—reduce obesity—one must reduce calories taken in, or increase the output by increasing activity, or both. This is true whether calories come from pumpkins or peanuts or pâté de foie gras.
But thermodynamics, a law of physics, has minimal relevance to human biology for the simple reason that the human body is not an isolated system. Energy is constantly entering and leaving. In fact, the very act we are most concerned about—eating—puts energy into the system. Food energy is also excreted from the system in the form of stool. Having studied a full year of thermodynamics in university, I can assure you that neither calories nor weight gain were mentioned even a single time.
If we eat an extra 200 calories today, nothing prevents the body from burning that excess for heat. Or perhaps that extra 200 calories is excreted as stool. Or perhaps the liver uses the extra 200. We obsess about caloric input into the system, but output is far more important.
What determines the energy output of the system? Suppose we consume 2000 calories of chemical energy (food) in one day. What is the metabolic fate of those 2000 calories? Possibilities for their use include
•heat production,
•new protein production,
•new bone production,
•new