foods in such small quantities that nutritionists have considered it insufficient and the question is whether this quantity is indeed sufficient for good health. Once James Lind demonstrated that scurvy could be prevented and cured by eating fresh fruits and vegetables, nutritionists assumed that these foods are an absolutely essential dietary source of vitamin C. What had been demonstrated, they will say, is that scurvy is “a dietary deficiency resulting from lack of fresh fruit and vegetables.” To be technically accurate, however, Lind and the nutritionists who followed him in the study of scurvy demonstrated only that the disease is a dietary deficiency that can be cured by the addition of fresh fruits and vegetables. As a matter of logic, though, this doesn’t necessarily imply that the lack of vitamin C is caused by the lack of fresh fruits and vegetables. Scurvy can be ameliorated by adding these to the diet, but the original lack of vitamin C might be caused by other factors. In fact, given that the Inuit and those Westerners living on the Inuit’s vegetable-and fruit-free diet never suffered from scurvy, as Stefansson observed, then other factors must be involved. This suggested another way of defining a balanced diet. It’s possible that eating easily digestible carbohydrates and sugars increases our need for vitamins that we would otherwise derive from animal products in sufficient quantities.

This was the issue that Stefansson was raising in the early 1920s. If the Inuit thrived in the harshest of environments without eating carbohydrates and whatever nutrients exist in fruits and vegetables, they, by definition, were consuming a balanced, healthy diet. If they did so solely because they had become evolutionarily adapted to such a diet, which was a typical rejoinder to Stefansson’s argument, then how can one explain those traders and explorers, like Stefansson himself and the members of his expeditions, who also lived happily and healthfully for years at a time on this diet?

Nutritionists of the era assumed that all-meat diets were unhealthy because (1) excessive meat consumption was alleged to raise blood pressure and cause gout; (2) the monotony of eating only meat—or any other single food—was said to induce a physical sense of revulsion; (3) the absence of fresh fruit and vegetables in these diets would cause scurvy and other deficiency diseases, and (4) protein-rich diets were thought to induce chronic kidney damage, a belief based largely on early research by Louis Newburgh.

None of these claims were based on compelling evidence. Newburgh, for instance, had based his conclusions largely on experiments in which he fed excessive quantities of soybean, egg whites, and beef protein to rabbits, which, as critics would later observe, happen to be herbivores. Their natural diet is buds and bark, not their fellow animals, and so there was little scientific value in force-feeding them meat or animal protein. Nonetheless, the dangers of an all-meat diet were considered sufficiently likely that even Francis Benedict, as Stefansson told it, claimed that it was “easier to believe” that Stefansson and all the various members of his expeditions “were lying, than to concede that [they] had remained in good health for several years on an exclusive meat regimen.”

In the winter of 1928, Stefansson and Karsten Anderson, a thirty-eight-year-old Danish explorer, became the subjects in a yearlong experiment that was intended to settle the meat-diet controversy. The experiment was planned and supervised by a committee of a dozen respected nutritionists, anthropologists, and physicians.*95 Eugene Du Bois and ten of his colleagues from Cornell and the Russell Sage Institute of Pathology would oversee the day-to-day details of the experiment.

For three weeks, Stefansson and Anderson were fed a typical mixed diet of fruits, cereals, vegetables, and meat while being subjected to a battery of tests and examinations. Then they began living exclusively on meat, at which point they moved into Bellevue Hospital in New York and were put under twenty-four-hour observation. Stefansson remained at Bellevue for three weeks, Anderson for thirteen weeks. After they were released, they continued to eat only meat for the remainder of one year. If they cheated on the diet, according to Du Bois, the experimenters would know it from regular examinations of Stefansson’s and Anderson’s urine. “In every individual specimen of urine which was tested during the intervals when they were living at home,” Du Bois wrote, “acetone [ketone] bodies were present in amounts so constant that fluctuations in the carbohydrate intake were practically ruled out.”

The experimental diet included many types of meat. To test the argument that the vitamins necessary in such a diet to avoid scurvy and remain healthy could be obtained only by eating raw meat, as was incorrectly assumed to be the practice of the Inuit, all of the meat was cooked. (In fact, the Inuit only occasionally ate raw meat.) Stefansson and Anderson each consumed an average of almost two pounds of meat per day, or twenty-six hundred calories: 79 percent from fat, 19 percent protein, and roughly 2 percent from carbohydrates (a maximum of fifty calories a day), which came from glycogen contained in the muscle meat. (Glycogen is the compound that stores glucose, a carbohydrate, in the liver and the muscle.)

“The only dramatic part of the study was the surprisingly undramatic nature of the findings,” wrote Du Bois, when he later summarized the results. “Both men were in good physical condition at the end of the observation,” he reported in 1930, in one of the nine articles he and his colleagues published on the study. “There was no subjective or objective evidence of any loss of physical or mental vigor.” Stefansson lost six pounds over the course of the year, and Anderson three, even though “the men led somewhat sedentary lives.” Anderson’s blood pressure dropped from 140/80 to 120/80; Stefansson’s remained low (105/70) throughout. The researchers detected no evidence of kidney damage or diminished function, and “vitamin deficiencies did not appear.” Nor did mineral deficiencies, although the diet contained only a quarter of the calcium usually found in mixed diets, and the acidic nature of a meat-rich diet was supposed to increase calcium excretion and so deplete the body of calcium. Among the minor health issues reported by Du Bois and his colleagues was the observation that Stefansson began the experiment with mild gingivitis (inflammation of the gums), but this “cleared up entirely, after the meat diet was taken.”

When Stefansson published Not by Bread Alone, a popular treatise on fat-and-protein diets, in 1946, a New York Times reviewer wrote, “Mr. Stefansson makes the mixed-diet technicians and the nuts-and-fruits addicts look terribly silly.” Du Bois, who supervised the experiments, wrote an introduction to Stefansson’s book. After Stefansson and Anderson were living exclusively on meat, he said, “a great many dire predictions and brilliant theories faded into nothingness.” A diet that should have left Stefansson and Anderson deathly ill from scurvy had left them as healthy as or healthier than the balanced diet they had been eating in the years immediately preceding the study. “Quite evidently we must revise some of our text book statements,” Du Bois concluded.

The textbook statements on vitamins would go unrevised, however, despite laboratory research that has confirmed Stefansson’s speculations. Nutritionists would establish by the late 1930s that B vitamins are depleted from the body by the consumption of carbohydrates. “There is an increased need for these vitamins when more carbohydrate in the diet is consumed,” as Theodore Van Itallie of Columbia University testified to McGovern’s Select Committee in 1973. A similar argument can now be made for vitamin C. Type 2 diabetics have roughly 30 percent lower levels of vitamin C in their circulation than do nondiabetics. Metabolic syndrome is also associated with “significantly” reduced levels of circulating vitamin C, which suggests that vitamin-C deficiency might be another disorder of civilization. One explanation for these observations—described in 1997 by the nutritionists Julie Will and Tim Byers, of the Centers for Disease Control and the University of Colorado respectively, as both “biologically plausible and empirically evident”—is that high blood sugar and/ or high levels of insulin work to increase the body’s requirements for vitamin C.

The vitamin-C molecule is similar in configuration to glucose and other sugars in the body. It is shuttled from the bloodstream into the cells by the same insulin-dependent transport system used by glucose. Glucose and vitamin C compete in this cellular-uptake process, like strangers trying to flag down the same taxicab simultaneously. Because glucose is greatly favored in the contest, the uptake of vitamin C by cells is “globally inhibited” when blood-sugar levels are elevated. In effect, glucose regulates how much vitamin C is taken up by the cells, according to the University of Massachusetts nutritionist John Cunningham. If we increase blood-

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