Taubes Why We Get Fat Quotes & Sayings

If you're predisposed to get fat and want to be as lean as you can be without compromising your health, you have to restrict carbohydrates and so keep your blood sugar and insulin levels low. — Gary Taubes

we are driven to get fat by "primary metabolic or enzymatic defects," as Hilde Bruch phrased it, and this fattening process induces the compensatory responses of overeating and/or physical inactivity. We eat more, move less, and have less energy to expend because we are metabolically or hormonally driven to get fat. — Gary Taubes

Does being "thin" ensure optimal "health"? No. It's now well accepted that many lean individuals have the condition known as metabolic syndrome, which is a step along the progression from health to heart disease, diabetes, cancer, and possibly Alzheimer's disease as well. The likely scenario is that these individuals, despite being lean, have what's called visceral fat - fat around the organs, and particularly the liver - and that this is exacerbating or causing the metabolic syndrome. The argument I'm making is that this visceral fat, too, is caused by the quality and quantity of the carbohydrates in the diet. 8. — Gary Taubes

A more rational form of treatment," Pennington suggested, would be one that makes fat once again flow readily out of the fat cells, that directs "measures primarily toward an increased mobilization and utilization of fuel" by the muscles and organs. — Gary Taubes

Insulin works to deposit calories as fat and to inhibit the use of that fat for fuel. Dietary carbohydrates are required to allow this fat storage to occur. Since glucose is the primary stimulator of insulin secretion, the more carbohydrates consumed - or the more refined the carbohydrates - the greater the insulin secretion, and thus the greater the accumulation of fat. "Carbohydrate is driving insulin is driving fat," as the Harvard endocrinologist George Cahill recently summed it up. — Gary Taubes

If insulin fattens those who receive it, as the evidence suggests, then how does it work? The prewar European clinicians who used insulin therapy to treat anorexics accepted the possibility, as Falta suggested, that the hormone can directly increase the accumulation of fat in the fat tissues. Insulin was "an excellent fattening substance," Erich Grafe wrote in Metabolic Diseases and Their Treatment. — Gary Taubes

The one fundamental requirement to increase the flow of fatty acids out of adipose tissue - to increase lipolysis - and so decrease the amount of fat in our fat tissue, is to lower the concentration of insulin in the bloodstream. — Gary Taubes

But if sedentary behavior makes us fat and physical activity prevents it, shouldn't the "exercise explosion" and the "new fitness revolution" have launched and epidemic of leanness rather than coinciding with an epidemic of obesity? — Gary Taubes

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. — Gary Taubes

This half century of research unequivocally supported the alternative hypothesis of obesity. It established that the relevant energy balance isn't between the calories we consume and the calories we expend, but between the calories - in the form of free fatty acids, glucose, and glycerol - passing in and out of the fat cells. If more and more fatty acids are fixed in the fat tissue than are released from it, obesity will result. — Gary Taubes

extra calorie either be consumed or conserved. As a result, anyone driven to put on fat by such a metabolic or hormonal defect would be driven to excessive eating, physical inactivity, or some combination. Hunger and indolence would be side effects of such a hormonal defect, merely facilitating the drive to fatten. — Gary Taubes

Which of us would not be preoccupied with thoughts of food if we were suffering from internal starvation? Hunger is such an awful thing that it is classically cited with pestilence and war as one of our three worst burdens. Add to the physical discomfort the emotional stresses of being fat, the taunts and teasing from the thin, the constant criticism, the accusations of gluttony and lack of "will power," and the constant guilt feelings, and we have reasons enough for the emotional disturbances which preoccupy the psychiatrists. — Gary Taubes

Anything that works to transport more glucose into the fat cells - insulin, for example, or rising blood sugar - will lead to the conversion of more fatty acids into triglycerides, and the storage of more calories as fat. — Gary Taubes

These investigators, too, concluded that differences in cancer rates could be explained by differences in fat consumption and animal-fat consumption, particularly between Japan and the United States. They did not serve science well by ignoring sugar consumption and the difference between refined and unrefined carbohydrates. — Gary Taubes

Eating carbohydrates, for example, not only elevates insulin but inhibits growth-hormone secretion; both effects lead to greater fatty-acid storage in the fat tissue. — Gary Taubes

The idea that obesity in humans is caused, as it is in animals, by a defect in the homeostatic maintenance of energy distribution and fat metabolism - that we overeat because we're getting fat, and not vice versa - barely survived into the second half of the twentieth century, although the evidence has always supported it. — Gary Taubes

What makes this shift all the more perplexing is that it occurred immediately after the science of fat metabolism evolved to explain why carbohydrates were uniquely fattening, and it followed a six-year period in which carbohydrate-restricted diets achieved unprecedented credibility among clinicians. — Gary Taubes

When researchers looked at trends between diet and disease, as Himsworth and Joslin had done with diabetes and Keys and a later generation of researchers would do with heart disease and even cancer, they would measure only fat, protein, and total carbohydrate consumption and fail to account for any potential effect of refined carbohydrates. — Gary Taubes

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

Yudkin blamed heart disease exclusively on sugar, and he was equally adamant that neither saturated fat nor cholesterol played a role. He explained how carbohydrates and specifically sugar in the diet could induce both diabetes and heart disease, through their effect on insulin secretion and the blood fats known as triglycerides. — Gary Taubes

If we replace five pounds of fat with five pounds of muscle, which is a significant achievement for most adults, we will increase our energy expenditure by two dozen calories a day. — Gary Taubes

Even low levels of insulin, far below those considered the clinical symptom of hyperinsulinemia (chronically high levels of insulin), will shut down the flow of fatty acids from the fat cells. Elevating insulin even slightly will increase the accumulation of fat in the cells. The longer insulin remains elevated, the longer the fat cells will accumulate fat, and the longer they'll go without releasing it. — Gary Taubes

Just as animal research tells us that gluttony and sloth are side effects of a drive to accumulate body fat, it also says that eating in moderation and being physically active (literally, having the energy to exercise) are not evidence of moral rectitude. Rather, they're the metabolic benefits of a body that's programmed to remain lean. — Gary Taubes

From the 1980s onward, manufacturers of products advertised as uniquely healthy because they were low in fat or specifically in saturated fat (not to mention "gluten free, no MSG & 0g trans fat per serving") took to replacing those fat calories with sugar to make them equally, if not more, palatable, and often disguising the sugar under one or more of the fifty-plus names by which the fructose-glucose combination of sugar and high-fructose corn syrup might be found. Fat — Gary Taubes

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. — Gary Taubes

Despite the depth and certainty of our faith that saturated fat is the nutritional bane of our lives and that obesity is caused by overeating and sedentary behavior, there has always been copious evidence to suggest that those assumptions are incorrect, and that evidence is continuing to mount. — Gary Taubes

Studying many obese people in great detail and following them over a long period of time, I have come to the conclusion that ... overeating, though it is observed with great regularity, is not the cause of obesity; it is a symptom of an underlying disturbance ... . Food, of course, is essential for obesity - but so is it for the maintenance of life in general. The need for overeating and the changes in weight regulation and fat storage are the essential disturbances. — Gary Taubes

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. — Gary Taubes

The hypothesis simply failed to explain how the brain manages to monitor our fat stores, and then raise or lower food intake and energy expenditure in response. Saying that we're all endowed with a lipostat that monitors our adiposity and then regulates hunger appropriately is just another way of saying that our weight remains remarkably stable, whether we're lean or obese, and then assigning the cause to a mysterious mechanism in the brain whose function is to achieve this stability. — Gary Taubes

Even though fructose has no immediate effect on blood sugar and insulin, over time -maybe a few years-it is a likely cause of insulin resistance and thus the increased storage of calories as fat. The needle on our fuel-partitioning gauge will point toward fat storage, even if it didn't start out that way, — Gary Taubes

These preliminary studies then prompted hundreds of millions of dollars of studies that failed to confirm the initial hypothesis that fat or animal fat led to cancer. — Gary Taubes

An obvious example of this reverse causation would be pregnant women, who are driven to fatten by hormonal changes. This hormonal drive induces hunger and lethargy as a result. In the context of evolution, these expanded fat stores would assure the availability of the necessary calories to nurse the infants after birth and assure the viability of the offspring. — Gary Taubes

In 2002, a Cochrane Collaboration review of the evidence concluded that low-fat diets induced no more weight loss than calorie-restricted diets, and in both cases the weight loss achieved "was so small as to be clinically insignificant." A similar analysis was published in 2001 by the U.S. Department of Agriculture. In this case, the authors identified twenty-eight relevant trials of low-fat diets, of which at least twenty were also calorie-restricted. The overweight subjects consumed, on average, less than seventeen hundred calories a day for an average weight loss of not quite nine pounds over six months. — Gary Taubes

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. — Gary Taubes