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by
Jason Fung
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March 21 - March 25, 2020
Among the most consistent findings was the constant feeling of cold experienced by the participants. As one explained, “I’m cold. In July I walk downtown on a sunny day with a shirt and sweater to keep me warm. At night my well fed room mate, who isn’t in the experiment, sleeps on top of his sheets but I crawl under two blankets.”
Eating less does not result in lasting weight loss.
Published in 2006, this randomized controlled trial was called the Women’s Health Initiative Dietary Modification Trial.
Do caloric-reduction diets work? No. The Women’s Health Initiative Dietary Modification Trial was the biggest, baddest, most kick-ass study of the Eat Less, Move More strategy that has ever been or ever will be done—and it was a resounding repudiation of that strategy.
Reduced metabolism and the increased hunger are not the cause of obesity—they are the result.
Yet nutritional authorities continue to preach that caloric reduction will lead to nirvana of permanent weight loss. In what universe do they live?
Let me state it as plainly as I can: “Eat Less” does not work. That’s a fact. Accept it.
The Women’s Health Study, the most ambitious, expensive and comprehensive diet study ever done, also looked at exercise.14 The 39,876 women were divided into three groups representing high (more than one hour per day), medium and low levels of weekly exercise. Over the next ten years, the intense exercise group lost no extra weight. Furthermore, the study noted, “no change
in body composition was observed,” meaning that muscle was not replacing fat.
Exercise represents a stress on the body. Small amounts are beneficial, but excessive amounts are detrimental.17
He followed a low-carbohydrate, high-fat diet of natural foods for twenty-one days. Feltham believed, based on clinical experience, that refined carbohydrates, not total calories, caused weight gain. The macronutrient breakdown of his diet was 10 percent carbohydrate, 53 percent fat and 37 percent protein.
Overeating did not, in fact, lead to lasting weight gain. In the same way, undereating does not lead to lasting weight loss.
Our body also responds in a similarly smart manner. Increased caloric intake is met with increased caloric expenditure. With the increase in total energy expenditure, we have more energy, more body heat and we feel great. After the period of forced overeating, the increased metabolism quickly sheds the excess pounds of fat.
Since losing weight reduces total energy expenditure, many obese people assume that they have a slow metabolism, but the opposite has proved to be true.
The fundamental biological principle at work here is homeostasis.
No wonder it is so hard to keep the weight off! Diets work well at the start, but as we lose weight, our metabolism slows. Compensatory mechanisms start almost immediately and persist almost indefinitely. We must then reduce our caloric
intake further and further simply to maintain the weight loss.
The reason diets are so hard and often unsuccessful is that we are constantly fighting our own body. As we lose weight, our body tries to bring it back up. The smarter solution is to identify the body’s homeostatic mechanism and adjust it downward—and there lies our challenge. Since obesity results from a high body set weight, the treatment for obesity is to lower it.
It would be later confirmed that hypothalamic damage resulted in intractable weight gain in humans.
Metformin decreases the amount of glucose13 produced by the liver and increases glucose uptake by the muscles.14
metformin does not increase insulin at all.
Patients in the metformin group did not gain any more weight than those on diet alone.
The crucial point to understand, however, is not how insulin causes obesity, but that insulin does, in fact, cause obesity.
I CAN MAKE YOU fat. Actually, I can make anybody fat. How? I prescribe prednisone, a synthetic version of the human hormone cortisol.
Like insulin, it makes you fat.
Prolonged cortisol stimulation will raise glucose levels and, subsequently, insulin.
CORTISOL IS THE so-called stress hormone, which mediates the flight-or-fight response, a set of physiological responses to perceived threats.
Under conditions of chronic stress, glucose levels remain high and there is no resolution to the stressor. Our blood glucose can remain elevated for months, triggering the release of insulin.
Prednisone increases glucose levels by 6.5 percent and insulin levels by 20 percent.4
Long-term use of prednisone leads to an insulin-resistant state in a patient or even to full-blown diabetes.
Cortisol is produced in the adrenal gland. When the adrenal gland is damaged, cortisol levels in the body can drop very low. The hallmark of Addison’s disease is weight loss. Up to 97 percent of patients exhibited weight loss.19 (Cortisol levels went down. People lost weight.)
Stress contains neither calories nor carbohydrates, but can still lead to obesity. Long-term stress leads to long-term elevated cortisol levels, which leads to extra pounds. Reducing stress is difficult, but vitally important. Contrary to popular belief, sitting in front of the television or computer is a poor way to relieve stress. Instead, stress relief is an active process.
A single night of sleep deprivation increases cortisol levels by more than 100 percent.
In another study, shortened sleep duration increased the risk of type 2 diabetes.
Dr. William Davis, author of Wheat Belly, a New York Times bestseller, suggests that the dwarf wheat that we eat today may be far different from the original wheat.
Since the body doesn’t want to die (and neither do we), it protects itself by developing insulin resistance—demonstrating homeostasis.
Obesity drives itself. A long-standing obesity cycle is extremely difficult to break, and dietary changes alone may not be sufficient.
By alternating periods of high drug effect and low drug effect, there is no chance for the body to develop resistance to the nitroglycerin. If the drug patch is worn constantly, it quickly becomes useless. Our body simply develops drug resistance.
In the case of insulin resistance, it comes down to both meal composition and meal timing—the two critical components of insulin resistance.
The balance between the fed state (insulin dominant) and the fasted state (insulin deficient) has been completely destroyed. (See Figure 10.2.) We now spend most of our time in the fed state. Is it any great mystery that we’re gaining weight?
But in the development of obesity, the increase in meals is almost twice as important as the change in diet.11 We obsess about what we should eat. We eat foods that practically didn’t exist ten years ago. Quinoa. Chia seeds. Acai berries. All in the hopes of making us slim. But we spare not even a single thought as to when we should be eating.
Eating more frequent meals does not aid in weight loss.13
People have fasted for prolonged periods without low blood sugar, the world record being 382 days.15 The human body has evolved mechanisms to deal with prolonged periods without food. The body instead burns fat for energy, and blood sugar levels remain in the normal range, even during prolonged fasting, due to gluconeogenesis.
Furthermore, we cannot simply eat our usual diet and add some fat or protein or snacks and expect to lose weight. Against all common sense, weight-loss advice usually involves eating more.
Every morning, just before we wake up, a natural circadian rhythm jolts our bodies with a heady mix of growth hormone, cortisol, epinephrine and norepinephrine (adrenalin). This cocktail stimulates the liver to make new glucose, essentially giving us a shot of the good stuff to wake us up. This effect is called the dawn phenomenon, and it has been well described for decades.
The more one eats at breakfast, the higher the total caloric intake over the entire day.
Breakfast eaters averaged 539 extra calories per day compared to those that skipped breakfast—a finding consistent with other trials.
Obesity is effectively the result of government policy.