Advice to Fat Men Is To 'Go Primitive'

Dr. Blake Donaldson insists that his weight reducing ideas are simultaneously 20 years ahead of the times and 8,000 years old. 

Donaldson, a trim 70 years old, is impressed by evidence that primitive man, for all his troubles, did not suffer from overweight. So Donaldson advises his patients to go primitive. Results, they shed a total of 4,000 pounds of fat per year. 

"The human animal " said Donaldson, while eating a big steak at a New York restaurant, "for millions of years lived just one way. He dwelled in forests and on the banks of streams. "He hunted and ate fat meat. His life was one of constant exercise. He had to be able to jump seven feet into a tree to escape a saber-toothed tiger. 

"We are fairly sure--from examining old German burial grounds and skulls found in the Arctic--that he had excellent vision, good teeth, no  arthritis or skin problems. Chances are he usually avoided the crippling and killing diseases aggravated by overweight." 

"People just refuse to believe that a ginger snap or a soda cracker is starch.

For the past four decades Donaldson has advised his overweight patients personally or through his book "Strong Medicine," to hold to the following regimen:

Do not retire before 10 p.m.; up by 6 a.m. Never sleep more than eight hours per day.

Before breakfast take a half-hour brisk walk. ("This is the most important medical advance in 8,000 years.")

For breakfast, lunch and dinner eat the same thing: one-half pound of fresh fat meat. A demitasse of black coffee three times daily is permissible.

Drink six glasses of water per day, none after 5 p.m.

Abstain from every other food, including seasoning. "It's so simple it's difficult," complained the good doctor.

"People just refuse to believe that a ginger snap or a soda cracker is starch. This is not an extreme diet. But if anybody is content to peel off three pounds of fat a week--and keep it off--my plan does it. 

"I don't object to smoking. People must have a few vices or they aren't worth talking to. They become plants.

"But I do object to flour addiction. This is a worse vice than heroin in terms of the physical damage it can do."

As Donaldson polished off his steak he confessed that being fat is not enough inducement to reduce. "It has to hurt you--either your pride or your body," he said. 

"And it's impossible to slim down some people. They simply do not obey orders. I don't think the devil himself could take fat off an opera singer."

The Heritage of Corpulence

E. B. ASTWOOD, M.D.

Endocrinology, Volume 71, Issue 2, 1 August 1962, Pages 337–341, https://doi.org/10.1210/endo-71-2-337

OBESITY is a disorder which, like venereal disease, is blamed upon the patient. The finding that treatment doesn’t work is ascribed to lack of fortitude. Corpulence in America is regarded along with narcotic addiction as something wicked, and I shall not be surprised if soon we have a prohibition against it in the name of national security. The condition is referred to in disparaging terms, including the most impolite references to the appetite. Appetite is held to be the cause, but I say it is hunger. I wish to propose that obesity is an inherited disorder and due to a genetically determined defect in an enzyme; in other words, that people who are fat are born fat, and nothing much can be done about it. I would like further to propose that the more serious of the consequences of being fat are not due to the corpulence but to the inherited defects; if this be so and we like food, we might as well eat up and be happy.

Gary Taubes. The Case for Keto: Rethinking Weight Control and the Science and Practice of Low-Carb/High-Fat Eating (Kindle Locations 345-351). Knopf. Kindle Edition. 

A brief lesson in the history of obesity research 

On June 22, 1962, a Tufts University Medical School professor named Edwin Astwood tried and failed to correct how we think about the cause of obesity. We have been living with that failure ever since. Astwood was presenting a counterargument to what had become since the end of the Second World War the dominant thinking among medical authorities and researchers on why we get fat. Astwood called this thinking “the conviction of the primacy of gluttony,” by which he meant the unshakable belief that virtually all cases of obesity, child or adult, mild or extreme, are caused ultimately by the overconsumption of calories; that is, people get fat because they eat too much. Astwood considered this belief system—for that’s what it is—to be almost willfully naïve and perhaps the primary reason so little progress had been made in understanding obesity, let alone preventing and treating it. It is also the reason those who have the misfortune to suffer from obesity are held responsible for their condition. “Obesity is a disorder,” he said in opening his presentation, “which, like venereal disease, is blamed upon the patient,” the direct consequence of their failing. Astwood was an endocrinologist; his medical expertise and the subject of his research were hormones and hormone-related disorders. The venue for his talk was the forty-fourth annual meeting of the Endocrine Society. Astwood was its president that year, and his talk, titled “The Heritage of Corpulence,” was his presidential address. Astwood was also a member of the prestigious National Academy of Sciences. According to his NAS biographical essay, his peers considered him “a brilliant scientist” who had contributed more to our understanding of thyroid hormones and how they work than anyone alive. (He won the Lasker Award, considered one step below the Nobel Prize, for the thyroid work.) Of the young men and women who learned to do their medical research in Astwood’s Boston-area laboratory, thirty-five would go on to become full professors by the time Astwood passed away in 1976. He was “not only driven by an insatiable curiosity,” the NAS biography says of Astwood, “but by a curiosity that sought answers with willful determination.” Although Astwood was known among his friends and colleagues for having little interest in food or eating—he considered meals only “a necessary intervention in the day’s activities solely for the purpose of bodily nutrition”—much of his laboratory work in the latter years of his research career was dedicated to understanding obesity, specifically the influence of hormones on fat accumulation and the use of fat to fuel our metabolism. In the small world of 1960s-era obesity research, Astwood was something of a throwback to the pre–World War II years. While he had a profound understanding of the research literature on obesity and was a serious if not indeed brilliant scientist, he had been a physician also who treated patients in his clinic. In this he was like the physician researchers in Germany and Austria before the war who had dominated thinking on obesity and had also come to their conclusions on the nature of the obese condition by observing it closely in their human patients, taking their histories and coming to understand what they were going through and living with. Doctors would do that with any other disorder—why not do it with such a seemingly intractable disorder as obesity? Many of the most influential of those prewar European authorities had become convinced that obesity must be the result of a hormonal or metabolic dysfunction, not caused by overeating, a concept that they recognized as circular logic. (“To attribute obesity to ‘overeating,’ ” the Harvard nutritionist Jean Mayer had aptly commented eight years before Astwood’s presentation, “is as meaningful as to account for alcoholism by ascribing it to ‘overdrinking.’ ” It’s saying the same thing in two different ways, at best describing the process, not explaining why it’s happening.) Rather, it’s somehow programmed into the very biology of the fat person, a disorder of fat accumulation and fat metabolism, these German and Austrian clinical researchers concluded. They believed, as Astwood came to believe, that obesity is neither a behavioral issue nor an eating disorder, not the result of how much we choose to eat consciously or unconsciously. That German-Austrian research community had evaporated, beginning in 1933 with the rise of the Nazi Party. By the time the war was over, European thinking on obesity, grounded in decades of clinical experience and observation, had evaporated with it. The very lingua franca of medicine shifted from German prewar to English postwar. German-language medical literature was considered of little interest, even unreadable by the new generation of young American physicians and nutritionists, who repopulated the field and found the conventional, simplistic thinking on obesity all too easy to believe. With just a few exceptions, these newly minted experts weren’t burdened with actually having to help obese patients achieve a relatively healthy weight for life. They were guided instead by a theory—technically, a hypothesis—that they believed in unconditionally. They believed the truth was obvious, which is always an impediment to making progress in any scientific endeavor. Their truth was the subject of Astwood’s presentation: a “conviction in the primacy of gluttony,” the notion that obesity is almost invariably caused by eating too much, consuming more calories than we expend, and so is ultimately a behavioral or eating disorder. That conviction implied that the only meaningful difference between lean people and people who struggled with obesity is that the lean can control their food intake and hence their appetites—consume only as many calories as they expend—while people with obesity could not, or at least not once they started to get fat. The idea that the fat tissue of those who become obese might have some physiological drive to accumulate fat that the tissues of lean people don’t, some subtle hormonal disruption, was dismissed by the authorities as nothing more than “lame excuses” (quoting the Mayo Clinic’s leading 1960s-era obesity expert) for fat people not to do what came naturally to lean people—eat in moderation. If anything, the supposedly learned postwar authorities came to consider obesity the result of a psychological defect, not a physiological one. They were not shy in stating that people got fat primarily because of “unresolved emotional conflicts” or because they had “turned toward food to relieve some of the nervous tensions of life.” These authorities counseled those with obesity to embrace a lifetime of walking away from their meals still hungry, of semistarvating themselves, ideally after consulting a psychiatrist first. This is the thinking that Astwood hoped to overturn with his presidential address. He enumerated with elegance and occasional humor the reasons why obesity was surely a genetic disorder, which implied that it almost assuredly had to be a hormonal or endocrinological one. Yes, he acknowledged, this was the implication every time someone afflicted with obesity made a comment along the lines of “everything I eat turns to fat.” It was anything but a lame excuse, according to Astwood; it was a reality. It was true, he said, not just for the kind of extreme obesity that he occasionally saw in patients in his practice, but for “the common or garden varieties … the kind that we see every day.” One thing that seemed to mystify Astwood was that there was nothing subtle about the evidence arguing for a genetic, and so hormonal, influence in obesity and fat accumulation. Obesity ran in families, Astwood said, as the authorities all agreed, but not because fat parents overfed their children. It did so because of a strong genetic component. Identical twins don’t just have the same faces; they have identical body types. If one twin is obese, so almost assuredly will the other one be. Even the distribution of obesity in families suggested genetics were involved. Astwood told his audience about one of his patients who was twenty-four years old, five feet four inches tall, and weighed 457 pounds. This young man had seven siblings, three of whom also suffered from extreme obesity: “His brothers, aged 10, 15, and 21, weighed respectively 275, 380, and 340 pounds.” The four other siblings “were of normal proportions.”

This “looked more like the work of genes,” said Astwood, not the “product of a groaning family board,” an antiquated phrase that refers to a dining table overloaded with food. We know that genes determine stature and hair color, said Astwood, and they determine the size of our feet and a “growing list of metabolic derangements, so why can’t heredity be credited with determining one’s shape?” If we had doubts that this was the case, we only had to look at animals. “Consider the pig,” he said: “His corpulence and gluttony resulted from man’s artificial selection; selective breeding provided us with this hulk with his hoggish ways, and no one will convince me that his gourmandizing is provoked by parental oversolicitude.” A reasonable picture of how those genes might be expressing themselves, Astwood explained, had been worked out since the 1930s. A series of laboratory researchers had generated an enormous amount of information about how our bodies regulate the fat we store and the fat we use for energy. “To turn what is eaten into fat, to move it and to burn it requires dozens of enzymes and the processes are strongly influenced by a variety of hormones,” he explained. Sex hormones clearly play a role in where fat is stored. Men and women, after all, tend to fatten differently: men above the waist, women below it. Thyroid hormones, adrenaline, and growth hormones all play a role in releasing fat from its depots, as does a hormone known as glucagon, secreted by the pancreas. “The reverse process,” Astwood said, “reincorporation of fat into the depots and the conversion of other food to fat, tends to be reduced by these hormones, but to be strongly promoted by insulin.” All this demonstrated “what a complex role the endocrine system plays in the regulation of fat.” An important clue to what might be happening, he added, is the fact that the numerous chronic disorders associated with obesity—“particularly those involving the arteries”—resemble arteries”—resemble those that come with diabetes so closely, it implies “a common defect in the two conditions.” Now imagine, Astwood suggested to his audience, what would happen if just one of these mechanisms went awry, impeding the release of fat from fat cells or promoting its storage. It was all too easy to imagine a slow, gradual accumulation of fat that could lead to extreme obesity if continued over years and decades. As the fat inexorably accumulated, a likely result would be what Astwood described as “internal starvation,” as the body hoarded calories in fat cells that it would otherwise need for fuel, while simultaneously increasing the weight that had to be carried around, day in and day out, requiring the expenditure of more and more energy to move and fuel that bulk. In other words, the same subtle hormonal disruption that could cause fat to accumulate to excess would also make a fat person hungry while it was happening. This would be exacerbated by the advice given to the fat person

 from all sides: Eat less, exercise more. Starve yourself, if necessary. If the proposed treatment for a fat accumulation problem that itself caused internal starvation—that is, hunger—was to starve even more, we can imagine all too easily why it would fail, if not in the short run, certainly eventually. “This theory,” Astwood said, “would explain why dieting is so seldom effective and why most fat people are miserable when they fast. It would also take care of our friends, the psychiatrists, who find all kinds of preoccupation with food, which pervades dreams among patients who are obese. Which of us would not be preoccupied with thoughts of food if we were suffering from internal starvation? 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.”

In 1963, Sir Stanley Davidson and Dr. Reginald Passmore wrote in the textbook Human Nutrition and Dietetics, the definitive source of nutritional wisdom for a generation of British medical practitioners, that “the intake of foods rich in carbohydrate should be drastically reduced since over-indulgence in such foods is the most common cause of obesity.” They didn’t understand yet why physiologically this was the case—it was just then being worked out in laboratories—but the fact seemed undeniable. That same year Passmore coauthored an article in the British Journal of Nutrition that began with the declaration: “Every woman knows that carbohydrate is fattening: this is a piece of common knowledge, which few nutritionists would dispute.”

Gary Taubes. The Case for Keto: Rethinking Weight Control and the Science and Practice of Low-Carb/High-Fat Eating (Kindle Locations 479-484). Knopf. Kindle Edition. 

This observation about the physiological nature of obesity was made decades ago, perhaps centuries ago. The most conspicuous examples are animals (as Astwood noted with his “consider the pig” point) and the animal models of obesity that nutritionists and obesity researchers have studied since the late 1930s. Indeed, researchers would occasionally admit that it’s clearly true about animals and animal models of obesity—that some animals get fat effectively independent of how much they eat and even when they eat no more than lean animals—but then somehow reject its relevance to humans on the basis that everyone knows that humans get fat because they eat too much. Their devotion to their energy balance thinking and to its implications was so great that they couldn’t escape it. 

Take, for instance, Jean Mayer, the most influential American nutritionist in the 1960s and into the ’70s. Mayer started his research career at Harvard in the late 1940s and then moved on to become dean of Tufts University. The nutrition school at Tufts was later named after him. As a nutritionist, Mayer got some things right and many things wrong, as scientists often do, even the best of them. He spent the later years of his life arguing that people with obesity get that way because they don’t exercise enough. Our current obsession with physical activity is largely rooted in Mayer’s proselytizing in the 1970s. But at the beginning of his career in the 1950s, he studied a strain of obese mice. “These mice,” he wrote, “will make fat out of their food under the most unlikely circumstances, even when half starved.” 

That’s the nature of overweight and obesity. That’s what it means to have a “compulsory tendency toward marked overweight due to abnormal accumulation of fat.” Mayer’s mice did not get fat by overeating. They got fat by eating. Half-starving them didn’t make them lean. It only made them hungry and slightly less fat. So let’s redefine what we mean by obesity. People with obesity are not thin people who couldn’t control their appetites (for whatever reason, psychological or neurobiological) and therefore ate too much. They’re people whose bodies are trying to accumulate excess fat even when they’re half-starved. The drive to accumulate fat is the problem, and it’s the difference between the fat and the lean. The hunger and the cravings, and then the failures and the sins, as Astwood suggested, are the results. This observation should be blindingly obvious to anyone who has ever had a weight problem, who fattens easily. Those who fatten easily are profoundly different from those who don’t and may have been from the womb onward. Their physiology is different; their hormonal and metabolic responses to foods are different. Their bodies want to store calories as fat; the bodies of their lean friends don’t. In George Bernard Shaw’s play Misalliance, written in 1909–10, his character John Tarleton puts it this way: “It’s constitutional. No matter how little you eat you put on flesh if you’re made that way.” Shaw, via Tarleton, may have been exaggerating slightly, but that’s as good a way to capture the simplicity of the idea as any. If these people want to be relatively lean and healthy, if such a thing is possible, they have to eat differently. There may be foods they cannot eat. Foods that make them fat may not make their lean friends fat.

Gary Taubes. The Case for Keto: Rethinking Weight Control and the Science and Practice of Low-Carb/High-Fat Eating (Kindle Locations 697-700). Knopf. Kindle Edition. 

SEATTLE, Oct. 2—The American Diabetes Association has recommended that physicians encourage their diabetic patients to eat the same amount of carbohydrate foods—sugars, starches and celluloses—as people who are unaffected by the disease.

If physicians and patients follow the association's recommendation, it will mean a major change in the rationale of treating the disease, which has afflicted man since ancient times.

The association said that the recommendation to alter diabetics' diets—raising carbohydrates and thereby lowering fats—was taken to minimize the risk of diabetic patients developing hardened arteries (called arteriosclerosis), heart attacks and strokes.

Though the private association's guidelines are not binding on physicians, the recommendations are likely to influence the dietary care of many of the 2.8 million known diabetics in this country. The association said that an additional 1.6 million Americans have undetected diabetes.

The recommendations, which were made in a “special report,” were intended as a general policy. Like all other general guidelines in medicine, they may have to be tailored by a private physician to an individual patient's needs.

A Cardinal Therapy

Diet is a cardinal therapy for diabetes because weight reduction alone can control the disease in many—but not all—adult diabetics.

In the past, the association has not set limits on the amount of carbohydrates that it has recommended diabetics to eat. However, many doctors have urged their diabetic patients to limit carbohydrates to about 30 per cent of the calories in their daily diet, and thereby, to eat a disproportionately larger amount of fats.

Now, the association said that diabetics, like other Americans, can eat diets that contain about 45 per cent carbohydrates. Carbohydrates include a wide variety of sugars. Table sugar is just one of many that nature provides.

The remainder of the diet should consist of fats and proteins in a ratio geared to the patient's taste and his doctor's advice. Because the association says that most diabetics must limit their calories each day, this means that these patients would eat less fat.

Fifty years after the discovery of insulin — the hormone that among other functions controls the blood sugar level — arteriosclerosis has become the major killer of diabetics. Americans rarely die now of diabetic coma because insulin, a hormone derived inexpensively from the pancreas glands of animals, is so widely available for human use.

However, not all diabetics require insulin. Physicians generally prescribe insulin injections just for patients whose diabetes cannot be managed by special diet or pills. Such pills do not contain insulin, but rather other drugs that, by different pharmacologic actions, affect the blood sugar level.

“There no longer appears to be any need to restrict disproportionately the intake of carbohydrates in the diet of most diabetic patients,” the association said in the current issue of Diabetes, a scientific journal that the American Diabetes Association publishes in New York.

“The average proportion of calories consumed as carbohydrate in the U. S. population as a whole approximates 45 per cent. This proportion or even higher appears to be acceptable for the usual diabetic patient as well,” the report said.

Dr. Edwin L. Bierman, who was chairman of the committee that wrote the report, stressed in an interview here:

“For those adult diabetics treated by diet alone, the cornerstone of our recommendation is restriction of total caloric intake, and it doesn't make any difference how you do it.”

Dr. Bierman, who is considered one of the nation's leading researchers on diabetes and arteriosclerosis, treats patients with such diseases at the Seattle Veterans Administration Hospital and teaches medical students at the University of Washington.

“Most adult diabetics are obese,” he said, citing statistics from the Metropolitan Life Insurance Company, which show that two‐thirds of the female diabetics and half of the male diabetics in this country are more than 20 per cent overweight. Obesity does not cause diabetes, but it does tend to bring out the disease in those patients who are genetically susceptable.

Advice for Obese and Lean

Accordingly, the Diabetes Association stressed in its report that doctors should advise their overweight diabetic patients to reduce and their leaner diabetics to avoid weight gains with advancing age.

A calorie is a unit measurement of the amount of heat energy that a specific food can yield for muscular and other bodily activity when it is chemically changed in the tissues lof man. Though the need varies with each individual, depending in such factors as age, activity, weight and height, American men generally use about 2,500 calories per day and women about 1,800 calories.

Diabetes, depending on its severity, can produce weakness, weight loss and fatigue among other symptoms. These symptoms result from the biochemical changes that scientists think result from production of an insufficient amount of insulin to meet the body's needs.

Lack of insulin impairs the body's metabolism, or biochemistry, of carbohydrates. As a result of the complex interlocking relationship of the body's biochemical reaction, diabetes also disturbs the metabolism of protein, chemicals, water and fats.

“Today many diabetologists believe that blood fat is as important to a diabetic as is blood sugar,” Dr. Bierman said, meaning that abnormal blood fat levels are now considered one of the several factors associated with a high risk for arterosclerosis.

The Diabetes Association's action comes at a time when experts are expressing a growing appreciation and concern about the role of nutrition in health.

“The basic nutritional requirement for patients with diabetes are in general the Isame as those for all individuals,” the association said. Such needs include adequate quantities of protein, vitamins, minerals and essential fatty acids.

However, the association stressed that physicians should write dietary prescriptions for diabetic patients whenever necessary as part of their broader general health care that includes:

¶Periodic medical examination.

¶Regular exercise.

¶Avoidance of cigarette smoking.

¶ Attention to personal hygiene.

¶Prevention of infection.

For many decades, physicians have noted that diabetic patients handle infections poorly. This is true despite the proper use of antibiotic drugs when infection occurs in a diabetic patient.

The reason for this phenomenon mystifies scientists who still do not know what causes the incurable, yet treatable disease, diabetes. Though most doctors say they believe diabetes is a heredetary disease, scientists do not know the precise pattern of such proposed inheritance.

Until insulin was discovered, starvation diets were doctors' best therapy for the disease.

A half‐century ago when Dr. Frederick G. Banting and Dr. Charles H. Best, working in Dr. John J. R. Macleod's laboratory at the University of Toronto, discovered insulin, physicians began prescribing regular diets for diabetes patients.

“Thereafter, somehow, carbohydrate restriction began to hold sway as the cornerstone of treatment of diabetes,” Dr. Bierman said.

Though evidence began mounting in the late nineteentwenties that diabetics could eat diets higher in carbohydrates without apparent untoward effects, results of such observations caused few physicians to change their dietary prescription habits for their diabetic patients.

Now, those earlier observations are being confirmed with more sophisticated laboratory techniques by investigators like Dr. Bierman.

Earlier this year, for example, Dr. Bierman and his colleagues, Dr. John D. Brunzell, Dr. Roger L. Lerner, Dr. William R. Hazzard and Dr. Daniel Porte Jr., reported in the New England Journal of Medicine scientific evidence that showed high carbohydrate diets lowered blood sugar in the mild diabetic and normal humans studied.

“Diets high in carbohydrates do not raise the blood sugar,” Dr. Bierman said, adding, “That's the misconception that most physicians have had during the last 30 years.”