Gary Taubes Quotes

Though more strenuous exercise would burn more calories, it would also lead to a significant increase in appetite. This is the implication of the phrase "working up an appetite." "Vigorous muscle exercise usually results in immediate demand for a large meal,

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.

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.

For every 5 percent of saturated-fat calories that replaced carbohydrates in the diet, the risk of breast cancer decreased by 9 percent. This certainly argued against the hypothesis that excessive fat consumption caused breast cancer.

All those who have insisted (and still do) that overeating and/or sedentary behavior must be the cause of obesity have done so on the basis of this same fundamental error: they will observe correctly that positive caloric balance must be associated with weight gain, but then they will assume without justification that positive caloric balance is the cause of weight gain. This simple misconception has led to a century of misguided obesity research.

By 1980, this link between cancer and low cholesterol was appearing in study after study. The most consistent association was between colon cancer and low cholesterol in men. In the Framingham Study those men whose total cholesterol levels were below 190 mg/dl were more than three times as likely to get colon cancer as those men with cholesterol greater than 220; they were almost twice as likely to contract any kind of cancer than those with cholesterol over 280 mg/dl.

British physician Cyril Donnison in 1938 in Civilization and Disease, hypertension was already among the best-documented examples of a disease that seemed specific to Western societies and the more affluent social classes elsewhere.

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.

First of all, the carbohydrates restricted are sugar, refined flour, and starchy vegetables, not the green leafy vegetables, so there should still be significant fiber in the diet, although it's not actually necessary. In fact, a likely scenario is that you'll eat more green vegetables when you're carb-restricting than not, because you're likely to substitute more green leafy vegetables and salads for the starchy vegetables, pasta, and bread that you're not eating. A restaurant meal might be a dish of meat, fish, or fowl with green vegetables or salad substituted for the potatoes (or rice or pasta or the hamburger bun).

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.

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.

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.

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.

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

Fructose, and fructose is uniquely fattening as carbohydrates go.

Yudkin also fed high-sugar diets to college students and reported that it raised their cholesterol and particularly their triglycerides; their insulin levels rose, and their blood cells became stickier, which he believed could explain the blood clots that seemed to precipitate heart attacks.

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.

Though the traditional response to the failure of semi-starvation diets to produce long-term weight loss has been to blame the fat person for a lack of willpower, Bruch, Rony, and others have argued that this failure is precisely the evidence that tells us positive caloric balance or overeating is not the underlying disorder in obesity.

It is my belief that when all the evidence is taken into account, rather than just a prejudicial subset, the picture that emerges will be more revealing of the underlying reality.

Excess weight and obesity, like all diseases of civilization, are caused by the singular hormonal effects of a diet rich in refined and easily digestible carbohydrates. The fattening of our adult years, after all, is not just associated with chronic diseases of civilization, it is a disease of civilization, and so it, too, may be a symptom of an underlying disorder. In this hypothesis, it is the quality of the calories consumed that regulates weight, and the quantity - more calories consumed than expended - is a secondary phenomenon.

The obvious implication is that obesity and Type 2 diabetes are two sides of the same physiological coin, two consequences, occasionally concurrent, of the same underlying defects - hyperinsulinemia and insulin resistance.

McGovern's Dietary Goals had turned the dietary-fat controversy into a political issue rather than a scientific one,

Dreadful science can pass for seminal research in the field of obesity.

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.

By the 1960s hypertension and high cholesterol were two of the three major risk factors associated with premature coronary heart disease (the third was smoking), so it was difficult to imagine that eating carbohydrates might be beneficial for one risk factor, cholesterol, while being detrimental for another, blood pressure.

In 1975, Richard Doll and Bruce Armstrong published a seminal analysis of diet and cancer, in which they noted that, the higher the sugar intake in different nations, the higher both the incidence of and mortality from cancer of the colon, rectum, breast, ovary, uterus, prostate, kidney, nervous system, and testicles.

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.

Jared Diamond to describe agriculture as "the worst mistake in the history of the human race.")

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.

It's tempting to suggest that one reason why the obesity-research community has paid little attention to the logical and scientific deficiencies of the overeating/sedentary-behavior hypothesis is that it becomes difficult even to discuss the subject without constantly tripping over the solecisms it engenders.

…Sugar has become an ingredient avoidable in prepared and packaged foods only by concerted and determined effort, effectively ubiquitous. Not just in the obvious sweet foods (candy bars, cookies, ice creams, chocolates, sodas, juices, sports and energy drinks, sweetened iced tea, jams, jellies, and breakfast cereals both cold and hot), but also in peanut butter, salad dressings, ketchup, BBQ sauces, canned soups, cold cuts, luncheon meats, bacon, hot dogs, pretzels, chips, roasted peanuts, spaghetti sauces, canned tomatoes, and breads. From the 1980's onward manufacturers of products advertised as uniquely healthy because they were low in fat…not to mention gluten free, no MSG, and zero grams trans fat per serving, took to replacing those fat calories with sugar to make them equally…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 was removed from candy bars sugar added, or at least kept, so that they became health food bars. Fat was removed from yogurts and sugars added and these became heart healthy snacks, breakfasts, and lunches.

Feinstein examined the efficacy of various obesity treatments in a lengthy review in the Journal of Chronic Diseases, he dismissed exercise in a single paragraph. "There has been ample demonstration that exercise is an ineffective method of increasing energy output," Feinstein noted, "since it takes far too much activity to burn up enough calories for a significant weight loss. In addition, physical exertion may evoke a desire for food so that the subsequent intake of calories may exceed what was lost during the exercise.

Diabetologists implicitly take the same tack whenever they discuss the need for their diabetic patients to "normalize" blood sugar, while recommending that this be accomplished primarily with "intensive insulin therapy" rather than restricting the carbohydrate content of their diets.

By the 1830s, when the British emancipationists finally put an end to the slave trade, some twelve and a half million Africans had been shipped off as slaves to the New World; two-thirds of them worked and died growing and refining sugar.

When I was lecturing recently to a group of cardiologists at the Mayo Clinic I said ...
Why is it that from the moment you enter medical school to the moment you retire, the only disorder that you will ever diagnose with a physics textbook is obesity? This is biology folks, it's endocrinology, it's physiology - physics has nothing to do with it. The laws of thermodynamics are always true, the energy balance equation is irrelevant.
If someone's getting fatter I guarantee you they're taking more energy than they expend (as long as they're getting heavier). And if they're getting leaner I guarantee they're expending more than they're taking in. [It's] given, let's never discuss it again. And if you say it to your patients you're telling them nothing
(University Of Colorado Medical School, May 9th 2013 - via YouTube)

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.

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?

There is a theory that creativity arises when individuals are out of sync with their environment. To put it simply, people who fit in with their communities have insufficient motivation to risk their psyches in creating something truly new, while those who are out of sync are driven by the constant need to prove their worth.

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.

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.

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.

If we consider the last forty years of research as a test of Mayer's hypothesis that physical activity induces weight loss or even inhibits weight gain, it's clear the hypothesis leads nowhere meaningful. What Mayer initially insisted had to be true, so much so that he publicly accused the "enemies of exercise" of propagating "pseudo-science," had devolved over the intervening decades into an analysis of whether the prescription of an exercise program would inhibit weight gain by three ounces each month or accelerate it by two.

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

Some regulatory phenomenon could drive us to gain weight, which would in turn cause a positive energy balance - and thus overeating and/or sedentary behavior.

pressure in school-age children. The NIH has funded subsequent

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.

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.

As this research had now made clear, the critical molecules determining the balance of storage and mobilization of fatty acids, of lipogenesis and lipolysis, are glucose and insulin - i.e., carbohydrates and the insulin response to those carbohydrates.

To be a dissenter was to be unfunded because the peer-review system rewards conformity and excludes criticism,

First, it led to overconsumption, because of what he called the deception of the appetite-control apparatus by the density of the carbohydrates.

Obese patients who try to reduce their weight by semi-starvation, as Rony noted, will always be fighting what he called their "spontaneous impulses of eating and activity." Once they give in to these impulses, which is effectively preordained, they will get fat again.

It's the effect of these carbohydrates on insulin that would explain the dietary observations - the futility of calorie restriction, the relative ease of weight loss when carbohydrates are restricted, and perhaps two centuries of anecdotal observations that sweets, starches, bread, and beer are uniquely fattening.

The hypothesis was based on decades of eyewitness testimony from missionary and colonial physicians and two consistent observations: that these "diseases of civilization" were rare to nonexistent among isolated populations that lived traditional lifestyles and ate traditional diets, and that these diseases appeared in these populations only after they were exposed to Western foods - in particular, sugar, flour, white rice, and maybe beer.

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.

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.

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.

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.

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.

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.

Obesity is caused by the kind of calories we consume and not the quantity, and so if we avoid carbohydrates our bodies function correctly and shed any excess weight.

Making LDL the "bad cholesterol" oversimplified the science considerably, but it managed to salvage two decades' worth of research, and to justify why physicians had bothered to measure total cholesterol in their patients.

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.

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

What constitutes a healthy diet? What should we eat if we want to live a long and a healthy life? To address this question, we'll examine the evidence supporting both the prevailing wisdom and this alternative hypothesis, and we'll confront the strong possibility that much of what we've come to believe is wrong.

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.

[T]he salient question is whether the increasing awareness of [heart] disease beginning in the 1920s coincided with the budding of an epidemic or simply better technology for diagnosis.

It's the fructose in these sweeteners that makes them sweet, just as it makes fruit sweet, and it appears to be the fructose that makes them so fattening and, in turn, so bad for our health.

In 1960, fewer than 13 percent of Americans were obese, and diabetes had been diagnosed in 1 percent. Today, the percentage of obese Americans has almost tripled; the percentage of Americans with diabetes has increased sevenfold.

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

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.

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,

For those who would immediately dismiss the possibility that sugar itself may be responsible for more premature deaths than cigarettes, we have to consider the fact that cigarettes themselves would have been far less harmful and far less addictive had it not been for sugar. "Were it not for sugar," Wightman Garner,