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by
Jason Fung
There’s a problem, though. All this activity had no effect on obesity at all. Obesity increased relentlessly, even as we sweated to the oldies. Just take a look at Figure 4.1,2 on the next page.
The phenomenon is global. A recent eight-country survey revealed that Americans exercised the most—135 days per year compared to a global average of 112 days.
Glad you asked. The Dutch and Italians, with their low exercise rates, experienced less than one-third the obesity of those iron-pumping Americans.
Pontzer discusses the surprising results in a New York Times article: “We found that despite all this physical activity, the number of calories that the Hadza burned per day was indistinguishable from that of typical adults in Europe and the United States.”6
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.
The increase in nonexercise activity thermogenesis may account for up to 70 percent of the increased energy expenditure.5
The paper concluded “that there was evidence that a physiological sensor was sensitive to the fact that body weight had been perturbed and was attempting to reset it.”
The theory of obesity that’s been dominant for the last half century—that excess calories inevitably lead to obesity—the theory that’s assumed to be unassailably true, was simply not true. None of it was true.
YOU CAN TEMPORARILY force your body weight higher than your body wants it to be by consuming excess calories. Over time, the resulting higher metabolism will reduce your weight back to normal.
Since losing weight reduces total energy expenditure, many obese people assume that they have a slow metabolism, but
The fundamental biological principle at work here is homeostasis. There appears to be a “set point” for body weight and fatness, as first proposed in 1984 by Keesey and Corbett.
The problem in obesity is that the set point is too high.
Eating more is not the cause of weight gain but instead the consequence. Eating more does not make us fat. Getting fat makes us eat more.
Our body is not a simple scale balancing Calories In and Calories Out. Rather, our body is a thermostat.
As subjects’ body weight increased by 10 percent, their daily energy expenditure increased by almost 500 calories.
The mistake here is to focus on the proximate and not the ultimate cause. The ultimate cause of the cold was the low setting of the thermostat.
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.
The search for answers would lead to the discovery of leptin.
DR. ALFRED FROHLICH from the University of Vienna first began to unravel the neuro-hormonal basis of obesity in 1890;
This established the hypothalamic region as a key regulator of energy balance, and was also a vital clue that obesity is a hormonal imbalance.
The hypothalamus integrates incoming signals regarding energy intake and expenditure.
The race to find this satiety factor was on. Discovered in 1994, this factor was leptin, a protein produced by the fat cells.
Rare human cases of leptin deficiency were soon found. Treatment with exogenous leptin (that is, leptin manufactured outside the body) produced dramatic reversals of the associated massive obesity.
Exogenous leptin was administered to patients in escalating doses,13 and we watched with breathless anticipation as the patients . . . did not lose any weight. Study after study confirmed this crushing disappointment. The vast majority of obese people are not deficient in leptin. Their leptin levels are high, not low. But these high levels did not produce the desired effect of lowering body fatness. Obesity is a state of leptin resistance.
This leaves us with much the same question that we began with. What causes leptin resistance? What causes obesity?
Blame the patient, of course! Doctors and dieticians berated, ridiculed, belittled and reprimanded. They were drawn irresistibly to caloric reduction because it transformed obesity from their failure to understand it into our lack of willpower and/or laziness.
What causes weight gain? Contending theories abound: •Calories •Sugar •Refined carbohydrates •Wheat •All carbohydrates •Dietary fat •Red meat •All meat •Dairy products •Snacking •Food reward •Food addiction •Sleep deprivation
•Stress •Low fiber intake •Genetics •Poverty •Wealth •Gut microbiome •Childhood obesity
This approach is wrong, since these theories all contain some element of truth. Let’s look at an analogy. What causes heart attacks? Consider this partial list of contributing factors: •Family history •Age •Sex •Diabetes •Hypertension •Hypercholesterolemia •Smoking •Stress •Lack of physical activity
The other major problem with obesity research is that it fails to take into account that obesity is a time-dependent disease.
Given the time it takes for obesity to develop, short-term studies are of limited use.
But this mistake is made in human obesity studies all the time. Obesity develops over decades. Yet hundreds of published studies consider only what happens in less than a year. Thousands more studies last less than a week. Still, they all claim to shed light on human obesity. There is no clear, focused, unified theory of obesity. There is no framework for understanding weight gain and weight loss.
OBESITY IS NOT caused by an excess of calories, but instead by a body set weight that is too high because of a hormonal imbalance in the body.
Leptin, a key regulator of body fat, did not turn out to be the main hormone involved in setting the body weight. Ghrelin (the hormone that regulates hunger) and hormones such as peptide YY and cholecystokinin that regulate satiety (feeling full or satisfied), all play a role in making you start and stop eating, but they do not appear to affect the body set weight.
This hormonal theory of obesity avoids making these false assumptions. Consider the following: Assumption 1: Calories In and Calories Out are independent of each other. The hormonal theory explains why Calories In and Calories Out are tightly synchronized with each other. Assumption 2: Basal metabolic rate is stable. The hormonal theory explains how hormonal signals adjust basal metabolic rate to either gain or lose weight. Assumption 3: We exert conscious control over Calories In. The hormonal theory explains that hunger and satiety hormones play a key role in determining whether we eat.
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BEFORE DISCUSSING INSULIN, we must understand hormones in general. Hormones are molecules that deliver messages to a target cell.
Both leptin and ghrelin, key hormones in the control of body fatness and appetite, show a daily rhythm and are disrupted by sleep disturbance.
The most obvious candidate is the refined carbohydrate—highly refined grains and sugars.
Highly refined carbohydrates are the most notorious foods for raising blood sugars. High blood sugars lead to high insulin levels. High insulin levels lead to weight gain and obesity. This chain of causes and effects has become known as the carbohydrate-insulin hypothesis. The man who found himself at the center of the controversy was the infamous Dr. Robert Atkins.
In 1972, he published his original book, Dr. Atkins’ Diet Revolution. It was an immediate bestseller and one of the fastest-selling diet books in history.
However, by the mid 1950s, the caloric-reduction theory of obesity was gaining ascendency.
Since it takes extra energy to metabolize dietary protein (the thermogenic effect of food), eating more protein could theoretically cause more weight loss.
Dr. Atkins argued in his 1972 bestseller that severely restricting carbohydrates would keep insulin levels low, thus reducing hunger and eventually leading to weight loss.
The AHA admitted that the reduced-fat diet was unproven over the long term. It also conceded that the Atkins diet evidenced a superior cholesterol profile and yielded a more rapid initial weight loss. Despite these benefits, the AHA maintained its concerns with atherogenicity—the rate at which plaques would form in the arteries. There was, of course, no evidence to support this concern. Regarding its own recommended but scientifically unsupported low-fat diet, the AHA had no concerns at all!
New England Journal of Medicine in 2003,5 confirmed greater short-term weight loss with the Atkins diet. In 2007, the Journal of the American Medical Association published a more detailed study.6 Four different popular weight plans were compared in a head-to-head trial. One clear winner emerged—the Atkins diet. The
However, in comparing the Atkins to the Ornish, it became clear that not only was weight loss better, but so was the entire metabolic profile. Blood pressure, cholesterol and blood sugars all improved to a greater extent on Dr. Atkins’s diet.
While the Mediterranean diet held its own against the powerful, fat-reducing Atkins diet, the low-fat AHA standard was left choking in the dust—
Dr. David Ludwig from Harvard University9 found that the low-fat diet slowed body metabolism the most. What was the best diet for maintaining metabolism? The very-low-carbohydrate diet.
are highly refined carbohydrates. There is evidence that these foods activate the reward systems in our brains, which gives us “comfort.”
