Maybe there’s something about obesity, about being fatter than we want to be, that we’re just not getting, that has managed to escape us completely. Yes, we can lose weight by eating less and exercising more, as virtually every public health authority tells us and The Biggest Loser certainly makes abundantly and biannually clear. That’s not the problem. But once we get lean (or at least leaner), why does it take something close to superhuman effort to stay that way?
This was the question addressed on Jan. 1—the official opening day of our annual dieting season—by a New York Times Magazine cover story, “The Fat Trap.” The author was Tara Parker Pope, who writes the Times “Well” column, and the answer she provided was that biology indeed seems to work against maintaining a leaner weight once we have first tipped the scales to obesity. So once we get fat, our bodies want to stay that way. And this has been the experience (at least so far) of Ms. Parker Pope, who acknowledged in the article that despite all her copious diet- and exercise-related erudition, she remains stubbornly 60 pounds overweight.
Ms. Parker-Pope said she ultimately blames herself for this situation, apparently because she let her weight get out of control in the first place. Had she only managed to be more vigilant when she was younger, more rigorous in her program of diet and exercise, obesity would never have crept upon her, and maintaining a healthy weight now would not be so difficult. And this is a common and understandable response.
But maybe there’s something else going on with the obese human body and the someday-to-be obese that predetermines the condition. Something other than a failure of vigilance or moral fortitude while we’re still lean, before it becomes too late. And if there is, that probably tells us something about why we get fat and how to reverse the process that is surely worth knowing.
One critical observation here that speaks directly to the underlying science is the fact that we are in the midst, of course, of an obesity epidemic. Over the past 50 years, the proportion of Americans who are clinically obese has increased by 2.5-fold. And this has been accompanied by an equally dramatic increase in Type 2 diabetes—from 5.6 million Americans diagnosed in 1980 to 17 million today.
These epidemics tell us that something dramatic has changed in the past 50 years, and that it’s not our genes. Genetic changes in humans simply don’t happen in that short a time. The change must be in our environment, and if we can figure out why so many people are fatter (and diabetic) now than ever before, that will help us understand why losing weight is so difficult, and keeping it off so seemingly impossible.
The conventional wisdom on this subject is pretty simple: we’re fatter (and more diabetic) now because we eat more than we ever did and we’re less active. And this assumption is based on another more fundamental assumption about the cause of obesity that seems intuitively obvious, if not predetermined by the very laws of physics themselves, but could indeed be wrong. The assumption is that obesity is fundamentally caused merely by consuming more calories than our bodies choose to expend.
By this logic, obesity is what researchers in the field call an “energy balance disorder.” It’s the context of virtually all research on cure and prevention of the disorder. Indeed, this is why when researchers study how our bodies seemingly adapt to weight loss and make it so difficult to maintain that loss, the researchers first semi-starve their obese subjects (allow them to eat, say, 800 or 1,200 calories a day) or even starve them (500 calories) to induce that weight loss in the first place. This just seems like the natural, if not only way, to do it.
But what if this assumption is wrong? What if the laws of physics have nothing to do with it? Prior to the Second World War, the leading authorities on obesity were Germans and Austrians and they had come to accept a different hypothesis of obesity. This hypothesis vanished after the war, but not because it was shown to be wrong, but because American researchers and clinicians were now mostly uninterested in what Germans or Austrians had to say about anything.
The pre-war assumption was that obesity is indeed a hormonal disorder, just like any other growth defect, and not an energy balance disorder. It is caused by a defective regulation 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 the hormones and enzymes that regulate our growth.
Despite all the discussion in the obesity journals these days (and in the New York Times Magazine) of hormonal changes in obese and weight-reduced obese individuals—of esoteric hormones with names like peptide YY and ghrelin—what’s considered of very little interest is the hormone that directly governs the storage and oxidation of fat in our bodies—insulin. This hormone is the “principal regulator of fat metabolism,” as the Nobel laureate Rosalyn Yalow and her colleague Solomon Berson described it almost 50 years ago and that’s still the conventional wisdom today.
Also well accepted in medical circles is the idea 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.
Since the regulatory role of insulin in fat metabolism was first established in the early 1960s, a viable alternative explanation for the cause of obesity has been that it is caused by a defect in insulin signaling. By this logic, the way to treat obesity is not by eating less and exercising more, as we’re all told to do, but by reducing insulin levels, perhaps as low as possible. And because we secrete insulin primarily in response to the carbohydrates in our diet, it means the best way to reduce insulin levels is to eliminate these carbohydrates—in particular, refined grains and sugars that have the greatest effect in stimulating insulin secretion.
The tragedy here is that this science was embraced 50 years ago by working physicians outside of academia, before it was embraced by the authority figures in the relevant fields of medical science. A few of these physicians then wrote very successful diet books based on it—beginning with Herman Taller in 1961 and, most famously, Robert Atkins, a decade later—and the authority figures responded by protecting their turf, an all too human response. They insisted it was all quackery, despite the solid grounding in science that already existed and has continued to flourish and expand ever since.
If we embrace the idea that obesity is indeed a hormonal disorder, then the reason we’ve gotten fatter in the past 50 years is because our publichealth authorities have been telling us to eat low-fat, high-carbohydrate diets—rather than the exact opposite—and we’ve been doing it, and because we’ve increased our consumptions of sugars (sucrose, the powdered white stuff we put in coffee and tea, and high fructose corn syrup) in part because they’re fat-free and we thought we could do so without paying a price in increased adiposity.
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 tend to lose significant weight, but their heart disease and diabetes risk factors improve significantly as well. Their insulin resistance, in effect, resolves. (An observation that itself suggests that it’s the quantity and quality of carbohydrates we consume that are the fundamental cause of metabolic syndrome.)
Another well-accepted effect of carbohydrate-restriction is that intrusive and obsessive thoughts of food seem to disappear on these diets. People lose weight, but they’re not hungry doing so. In fact, the American Medical Association has described the absence of hunger (technically “anorexia”) as a 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.
Clinical trials have repeatedly demonstrated that when obese and overweight individuals consciously restrict the carbohydrates they eat, but not calories, they not only tend to lose significant weight, but their heart disease and diabetes risk factors improve significantly as well.
So maybe eating less and exercising more fails to cure obesity, maybe it’s so damn hard to keep weight off when we do this because it’s simply the wrong treatment. And maybe it’s the wrong treatment because the clinicians and researchers studying obesity have misconceived the cause. Get the cause of the disorder right, and the treatment and method of prevention becomes all too obvious.
Instead of blaming ourselves for allowing our weight to get out of control, maybe we should blame the hormones and enzymes that regulate our fat tissue. Maybe we should blame the researchers and public health authorities who have been trying to convince us that getting fat is a physics problem, not a biological one, about how much we eat and exercise rather than how hormones control our fat tissue. Had they been telling us all long to pay attention to some very basic endocrinology, they’d have been telling us to stay away from these fattening carbohydrates and maybe none of this would have happened.