Why We Get Fat: And What to Do About It

We don't get fat because we overeat; we overeat because we're getting fat

The simple answer as to why we get fat is that carbohydrates make us so; protein and fat do not

In other words, the science itself makes clear that hormones, enzymes, and growth factors regulate our fat tissue, just as they do everything else in the human body, and that we do not get fat because we overeat; we get fat because the carbohydrates in our diet make us fat. The science tells us that obesity is ultimately the result of a hormonal imbalance, not a caloric one—specifically, the stimulation of insulin secretion caused by eating easily digestible, carbohydrate-rich foods: refined carbohydrates, including flour and cereal grains, starchy vegetables such as potatoes, and sugars, like sucrose (table sugar) and high-fructose corn syrup. These carbohydrates literally make us fat, and by driving us to accumulate fat, they make us hungrier and they make us sedentary. This is the fundamental reality of why we fatten, and if we’re to get lean and stay lean we’ll have to understand and accept it, and, perhaps more important, our doctors are going to have to understand and acknowledge it, too.

Of all the dangerous ideas that health officials could have embraced while trying to understand why we get fat, they would have been hard-pressed to find one ultimately more damaging than calories-in/calories-out. That it reinforces what appears to be so obvious - obesity as the penalty for gluttony and sloth - is what makes it so alluring. But it's misleading and misconceived on so many levels that it's hard to imagine how it survived unscathed and virtually unchallenged for the last fifty years. It has done incalculable harm. Not only is this thinking at least partly responsible for the ever-growing numbers of obese and overweight in the world - while directing attention away from the real reasons we get fat - but it has served to reinforce the perception that those who get fat have no one to blame but themselves. That eating less invariably fails as a cure for obesity is rarely perceived as the single most important reason to make us question our assumptions, as Hilde Bruch suggested half a century ago. Rather, it is taken as still more evidence that the overweight and obese are incapable of following a diet and eating in moderation. And it put the blame for their physical condition squarely on their behavior, which couldn't be further from the truth.

The simplest way to look at all these associations, between obesity, heart disease, type 2 diabetes, metabolic syndrome, cancer, and Alzheimer's (not to mention the other the conditions that also associate with obesity and diabetes, such as gout, asthma, and fatty liver disease), is that what makes us fat - the quality and quantity of carbohydrates we consume - also makes us sick.

What I tried to make clear in Good Calories, Bad Calories was that nutrition and obesity research lost its way after the Second World War with the evaporation of the European community of scientists and physicians that did pioneering work in those disciplines. It has since resisted all attempts to correct it. As a result, the individuals involved in this research have not only wasted decades of time, and effort, and money but have done incalculable damage along the way. Their beliefs have remained imperious to an ever-growing body of evidence that refutes them while being embraced by public-health authorities and translated into precisely the wrong advice about what to eat and, more important, what not to eat if we want to maintain a healthy weight and live a long and healthy life.

It may be easier to believe that we remain lean because we're virtuous and we get fat because we're not, but the evidence simply says otherwise. Virtue has little more to with our weight than our height. When we grow taller, it's hormones and enzymes that are promoting growth, and we consume more calories than we expend as a result. Growth is the cause - increased appetite and decreased energy expenditure (gluttony and sloth) are the effects. When we grow fatter, the same is true as well. We don't get fat because we overeat; we overeat because were fat.

Even if these researchers do see the need to address the problem immediately, though they have obligations and legitimate interests elsewhere, including being funded for other research. With luck, the ideas discussed in Good Calories, Bad Calories may be rigorously tested in the next twenty years. If confirmed, it will be another decade or so after that, at least, before our public health authorities actively change their official explanation for why we get fat, how that leads to illness, and what we have to do to avoid or reverse those fates. As I was told by a professor of nutrition at New York University after on of my lectures, the kind of change I'm advocating could take a lifetime to be accepted.

The obvious question is, what are the “conditions to which presumably we are genetically adapted”? As it turns out, what Donaldson assumed in 1919 is still the conventional wisdom today: our genes were effectively shaped by the two and a half million years during which our ancestors lived as hunters and gatherers prior to the introduction of agriculture twelve thousand years ago. This is a period of time known as the Paleolithic era or, less technically, as the Stone Age, because it begins with the development of the first stone tools. It constitutes more than 99.5 percent of human history—more than a hundred thousand generations of humanity living as hunter-gatherers, compared with the six hundred succeeding generations of farmers or the ten generations that have lived in the industrial age. It’s not controversial to say that the agricultural period—the last .5 percent of the history of our species—has had little significant effect on our genetic makeup. What is significant is what we ate during the two and a half million years that preceded agriculture—the Paleolithic era. The question can never be answered definitively, because this era, after all, preceded human record-keeping. The best we can do is what nutritional anthropologists began doing in the mid-1980s—use modern-day hunter-gatherer societies as surrogates for our Stone Age ancestors.

Referring to obesity as a “form of malnutrition” comes with no moral judgments attached, no belief system, no veiled insinuations of gluttony and sloth. It merely says that something is wrong with the food supply and it might behoove us to find out what.

Researchers have reported that the brain and central nervous system actually run more efficiently on ketones than they do on glucose.

The most fattening foods are the ones that have the greatest effect on our blood sugar and insulin levels.

Any diet can be made healthy or at least healthier—from vegan to meat-heavy—if the high-glycemic-index carbohydrates and sugars are removed, or reduced significantly.

Because the insulin level in the bloodstream is determined primarily by the carbohydrates that are consumed—their quantity and quality, as I’ll discuss—it’s those carbohydrates that ultimately determine how much fat we accumulate. Here’s the chain of events: 1. You think about eating a meal containing carbohydrates. 2. You begin secreting insulin. 3. The insulin signals the fat cells to shut down the release of fatty acids (by inhibiting HSL) and take up more fatty acids (via LPL) from the circulation. 4. You start to get hungry, or hungrier. 5. You begin eating. 6. You secrete more insulin. 7. The carbohydrates are digested and enter the circulation as glucose, causing blood sugar levels to rise.§ 8. You secrete still more insulin. 9. Fat from the diet is stored as triglycerides in the fat cells, as are some of the carbohydrates that are converted into fat in the liver. 10. The fat cells get fatter, and so do you. 11. The fat stays in the fat cells until the insulin level drops. If

The science tells us that obesity is ultimately the result of a hormonal imbalance, not a caloric one—specifically, the stimulation of insulin secretion caused by eating easily digestible, carbohydrate-rich foods: refined carbohydrates, including flour and cereal grains, starchy vegetables such as potatoes, and sugars, like sucrose (table sugar) and high-fructose corn syrup. These carbohydrates literally make us fat, and by driving us to accumulate fat, they make us hungrier and they make us sedentary.

The point to keep in mind is that you don't lose fat because you cut calories; you lose fat because you cut out the foods that make you fat-the carbohydrates.

Carbohydrates are not required in a healthy human diet. Another way to say this (as proponents of carbohydrate restriction have) is that there is no such thing as an essential carbohydrate. Nutritionists will say that 120 to 130 grams of carbohydrates are required in a healthy diet, but this is because they confuse what the brain and central nervous system will burn for fuel when diets are carbohydrate rich—120 to 130 grams daily—with what we actually have to eat. If there are no carbohydrates in the diet, the brain and central nervous system will run on molecules called “ketones.” These are synthesized in the liver from the fat we eat and from fatty acids, mobilized from the fat tissue because we’re not eating carbohydrates and insulin levels are low, and even from some amino acids. With no carbohydrates in the diet, ketones will provide roughly three-quarters of the energy that our brains use. And this is why severely carbohydrate-restricted diets are known as “ketogenic” diets. The rest of the energy required will come from glycerol, which is also being released from the fat tissue when the triglycerides are broken down into their component parts, and from glucose synthesized in the liver from the amino acids in protein. Because a diet that doesn’t include fattening carbohydrates will still include plenty of fat and protein, there will be no shortage of fuel for the brain.

For some of these populations, the word for “hunger” in their native dialects translated to “when we have to eat plants.

You don’t get fat because your metabolism slows; your metabolism slows because you’re getting fat.

The bottom line is something that’s been known (and mostly ignored) for over forty years. The one thing we absolutely have to do if we want to get leaner—if we want to get fat out of our fat tissue and burn it—is to lower our insulin levels and to secrete less insulin to begin with.

Fructose actually has unhealthy effects—including making us fat—that have little to do with its lack of vitamins or antioxidants and far more to do with how our bodies process it.

we get fat because the carbohydrates in our diet make us fat.

Those who ran the most tended to weigh the least, but all these runners tended to get fatter with each passing year, even those who ran more than forty miles a week—eight miles a day, say, five days a week.

If there are no carbohydrates in the diet, the brain and central nervous system will run on molecules called “ketones.

This is not a diet book, because it’s not a diet we’re discussing. Once you accept the fact that carbohydrates—not overeating or a sedentary life—will make you fat, then the idea of “going on a diet” to lose weight, or what the health experts would call a “dietary treatment for obesity,” no longer holds any real meaning.

Battle of Weight Loss Diets: Is Anyone Winning (at Losing)?

sugar appears to be addictive in the brain in the same way in which cocaine, nicotine, and heroin are.

In 2007, Jeffrey Flier, dean of Harvard Medical School and his wife and colleague in obesity research, Terry Maratos-Flier, published an article in Scientific American called “What Fuels Fat.” In it, they described the intimate link between appetite and energy expenditure, making clear that they are not simply variables that an individual can consciously decide to change with the only effect being that his or her fat tissue will get smaller or larger to compensate. An animal whose food is suddenly restricted tends to reduce its energy expenditure both by being less active and by slowing energy use in cells, thereby limiting weight loss. It also experiences increased hunger so that once the restriction ends, it will eat more than its prior norm until the earlier weight is attained. What the Fliers accomplished in just two sentences is to explain why a hundred years of intuitively obvious dietary advice—eat less—doesn’t work in animals. If we restrict the amount of food an animal can eat (we can’t just tell it to eat less, we have to give it no choice), not only does it get hungry, but it actually expends less energy. Its metabolic rate slows down. Its cells burn less energy (because they have less energy to burn). And when it gets a chance to eat as much as it wants, it gains the weight right back. The

the fatter we are, the more likely we are to get cancer and the more likely we are to become demented as we age.