In the January 1 article in the Sunday Magazine, “The Fat Trap,” Tara Parker-Pope acknowledged that weight loss is very difficult and that the rate of recidivism in obesity is upsettingly high – that hard as losing weight may be, keeping it off requires near superhuman effort.





We empathize with Ms. Parker-Pope and respect her for admitting what we can only imagine was difficult – despite all of her diet- and exercise-related consciousness and erudition, she remains 60 pounds overweight. We fully agree with her assertion that obesity is not an issue of weak will, but we believe her article omits several major issues that are critical to understanding the obese condition, and its cure and prevention.





First, while Ms Parker-Pope notes that over a third of all Americans are now classified as obese, she neglects to mention that this number has increased 2.5-fold in the past fifty years. This is the obesity epidemic that we read so much about, and it’s accompanied by an equally dramatic increase in type-2 diabetes–from 5.6 million Americans diagnosed in 1980 to 17 million today.





These epidemics are critical observations in the science of obesity. They tell us that something dramatic has changed in the past fifty years, and despite all the discussion of obesity-predisposing genes in the article, it is widely accepted that whatever is driving these epidemics of obesity and diabetes, a change in our DNA is not it. The salient question is not so much why losing weight and keeping it off is so difficult – something that’s always been obvious, even if the underlying science was not well understood – but why are so many people fatter now than ever before?





The article implies that merely making too much food available and not being sufficiently physically active is sufficient to raise the amount of fat a body will defend. And it implies that this is the salient change in the state of the nation that has driven the obesity epidemic – we eat more than we did 50 years ago and we’re less active.





This assumption is based on yet another assumption about the fundamental cause of obesity that has been held by obesity researchers (and virtually everyone else) since the end of the Second World War and may have no basis in fact: that obesity is fundamentally caused merely by consuming more calories than our bodies choose to expend. For whatever reason, we fail to properly match the calories we consume with the calories we expend, and this is what drives the inexorable accumulation of fat on our bodies. And this is why Ms. Parker-Pope says she ultimately blames herself for her obesity.





This notion that obesity is what researchers in the field call an “energy balance disorder” is the context of Ms. Parker-Pope’s article and of all the research in it. Indeed, this is why the research studies discussed in her article employed semi-starvation diets (800 calories a day) or even starvation diets (500 calories) to induce weight loss in their obese subjects.





Prior to the Second World War, though, the leading authorities in the world on obesity had come to accept a different hypothesis of obesity. This vanished after the war, but not because it was shown to be wrong, but because the mostly German and Austrian clinicians who embraced it were out of favor.





The idea was that obesity is caused by a dysregulation of the hormones and enzymes that regulate the accumulation of fat in our fat tissue, just as disorders of vertical growth – dwarfism or gigantism, for instance – are known to be caused by defects in growth hormone signaling. Put simply, obesity was perceived as a disorder of fat metabolism, not of energy balance. This distinction is critical.





Despite all the discussion in Ms. Parker-Pope’s article of hormonal changes in obese and weight-reduced obese individuals – of esoteric hormones like peptide YY, and ghrelin that influence hunger and satiety – not once in over 5,000 words does she mention the hormone that directly governs the storage and oxidation of fat in our bodies–insulin. This hormone is the “principle regulator of fat metabolism,” as the Nobel Laureate Rosalyn Yalow and her colleague Solomon Berson described it almost fifty years ago.





It’s now well accepted that chronically elevated levels of insulin and a condition known as insulin resistance are the common precursors to heart disease and type-2 diabetes. Some 75 million Americans suffer from insulin resistance, according to the Centers of Disease Control; they have what’s officially called “metabolic syndrome.” That obesity, too, is considered a disorder of insulin resistance – the first symptom physicians are told to look for to diagnose metabolic syndrome is an expanding waistline–begins to explain why it is so intimately associated with both heart disease and diabetes.

These facts are not controversial, and yet the regulatory role of insulin in fat storage – despite its inclusion in endocrinology and biochemistry textbooks – is never mentioned in Ms. Parker-Pope’s article. Ms. Parker-Pope notes, for instance, that scientists have conducted studies looking at whether injecting people with the hormone leptin will lead to weight loss, but neglects to point out what is common knowledge among diabetes specialists: that when type-2 diabetics inject themselves with insulin they get fatter, and when they take drugs that lower insulin levels (metformin, for instance) they tend to lose weight.





Since this regulatory role of insulin in fat metabolism was established in the 1960s, a viable alternative explanation for the cause of obesity has been that it is caused by a dysregulation of insulin signaling. By this logic, the way to treat obesity is not by eating less and exercising more, as Ms. Parker-Pope implies, but by reducing insulin levels, perhaps as low as possible. That is accomplished most efficiently by severely restricting the carbohydrate content of the diet and removing, in particular, refined grains and sugars that have the greatest effect in stimulating insulin secretion.





The implication of this basic endocrinology is that obesity is caused not by eating too much and sedentary behavior, but by a disruption of the hormonal and enzymatic regulation of fat tissue caused by the easily digestible, refined carbohydrates and sugars that we do eat. Indeed, by this logic, calorie-restricted diets – starvation and semi-starvation diets as used in the studies Ms. Parker-Pope discusses–can be thought of as particularly counterproductive ways to reduce carbohydrate consumption and so insulin levels, starving the body, as they do, of the energy required to effectively run metabolic processes.





In the past decade, clinical trials have repeatedly demonstrated that when obese and overweight individuals consciously restrict the carbohydrates they eat, but not calories, they not only lose weight, on average, but their heart disease and diabetes risk factors improve significantly. Their insulin resistance, in effect, resolves. Those of us who have lost weight ourselves and witnessed the effect of these diets on our patients can confirm that this is exactly what happens.





This is accompanied by another well-accepted effect of carbohydrate-restriction – intrusive and obsessive thoughts of food seem to disappear on these diets. In fact, the American Medical Association has described the absence of hunger (technically “anorexia”) as a well-known side effect of diets that severely restrict carbohydrate content but otherwise allow dieters to eat as many calories (from fat and protein) as they want.





This implies that if researchers like those Ms. Parker-Pope quotes in her article had studied the metabolic and hormonal adaptations to weight loss on carbohydrate-restricted diets, rather than on calorie-restricted diets, they would have come to entirely different conclusions about the intractability of obesity, about the supposedly superhuman effort required to maintain weight loss, and about the metabolic and hormonal alterations that accompany this process.





Until the medical researchers themselves and the journalists, like Ms. Parker-Pope, who cover the field, acknowledge that there is indeed an alternative explanation for why we get fat, and that it leads to a surprisingly effective means of treating and preventing the disease, we can expect to make little progress.





Ms. Parker-Pope says she ultimately blames herself for allowing her weight to get out of control. We believe she should blame the hormones and enzymes that regulate her fat tissue, and the researchers and public health authorities who have been trying to convince her that it’s all about how much she eats and exercises, and forgot to mention that the hormone insulin is primarily responsible for storing fat in her fat tissue, and the amount of insulin her body secretes is dependent primarily on the amount and the type of carbohydrates she consumes.





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Gary Taubes Peter Attia, M.D.

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