of sugar to replace what they lost in their urine. While the logic seemed reasonable at the time, it was not a successful strategy. A diabetic colleague unfortunate enough to follow this advice later died, and history now only laughs at the good Dr. Piorry.3 However, this outcome foretold the grim shades of our own highly ineffective advice to follow a high-carbohydrate diet in the treatment of type 2 diabetes.
Apollinaire Bouchardat (1806–1886), who is sometimes called the founder of modern diabetology, established his own therapeutic diet based on the observation that periodic starvation during the Franco-Prussian War of 1870 reduced urinary glucose. His book, De la Glycosurie ou diabète sucré (Glycosuria or Diabetes Mellitus) laid out his comprehensive dietary strategy, which forbade all foods high in sugars and starches.
In 1889, Dr. Josef von Mering and Oskar Minkowski at the University of Strasbourg experimentally removed a dog’s pancreas, the comma-shaped organ between the stomach and intestine. The dog began to urinate frequently, which Dr. von Mering astutely recognized as a symptom of underlying diabetes. Testing the urine confirmed the high sugar content.
In 1910, Sir Edward Sharpey-Schafer, sometimes regarded as the founder of endocrinology (the study of hormones), proposed that the deficiency of a single hormone he called insulin was responsible for diabetes. The word insulin came from the Latin insula, which means “island,” as this hormone is produced in cells called the islets of Langerhans in the pancreas.
By the turn of the twentieth century, prominent American physicians Frederick Madison Allen (1879–1964) and Elliott Joslin (1869–1962) became strong proponents of intensive dietary management for diabetes, given the lack of other useful treatments.
Dr. Allen envisioned diabetes as a disease in which the overstrained pancreas could no longer keep up with the demands of an excessive diet.4 To give the pancreas a rest, he prescribed the “Allen starvation treatment,” which was very low in calories (1000 calories per day) and very restricted in carbohydrates (<10g per day). Patients were admitted to hospital and given only whiskey and black coffee every two hours from 7 a.m. to 7 p.m. This regime continued daily until the sugar disappeared from the urine. Why was whiskey included? It was not essential, but was administered simply because it “keeps the patient comfortable while he is being starved.”5
The response of some patients was unlike anything seen previously. They improved instantly and almost miraculously. Others, however, starved to death, which was euphemistically called inanition.
A lack of understanding of the difference between type 1 and type 2 diabetes severely hampered the usefulness of Allen’s treatment. Type 1 diabetic patients were usually dramatically underweight children, whereas type 2 diabetic patients were mostly overweight adults. This ultra-low calorie diet could be deadly for the very malnourished type 1 diabetic (more on the differences between these two types of diabetes below and in chapter 2). Given the otherwise fatal prognosis of untreated type 1 diabetes, this was not the tragedy it may at first have appeared to be. Allen’s detractors pejoratively called his treatments starvation diets, but they were widely considered the best therapy, dietary or otherwise, until the discovery of insulin in 1921.
Dr. Elliott P. Joslin opened his practice in 1898 in Boston after receiving his medical degree from Harvard Medical School, becoming the first American doctor to specialize in diabetes. Harvard University’s eponymous Joslin Diabetes Center is still considered one of the foremost diabetes institutes in the world, and the textbook Joslin wrote, The Treatment of Diabetes Mellitus, is considered the bible of diabetes care. Joslin himself is likely the most famous diabetologist in history.
Although Dr. Joslin had lost many patients to diabetes, he had also saved many by applying Dr. Allen’s treatments. In 1916, he wrote: “That temporary periods of under-nutrition are helpful in the treatment of diabetes will probably be acknowledged by all after these two years of experience with fasting.”6 He felt the improvements were so obvious to everybody involved that studies would not even be necessary to prove the point.
THE DISCOVERY OF THE CENTURY
FREDERICK BANTING, CHARLES Best, and John Macleod made the breakthrough discovery of insulin at the University of Toronto in 1921. They isolated insulin from the pancreases of cows and, with James Collip, found a way to purify it enough to administer it to the first patient in 1922.7 Leonard Thompson, a fourteen-year-old boy with type 1 diabetes, weighed only sixty-five pounds when he started insulin injections. His symptoms and signs rapidly disappeared and he immediately regained a normal weight. They quickly treated six more patients with equally stunning success. The average lifespan of a ten-year-old at diagnosis increased from about sixteen months8 to thirty-five years!
Eli Lilly and Company partnered with the University of Toronto to commercially develop this revolutionary new drug, insulin. The patent was made freely available so the entire world could benefit from the medical discovery of the century. By 1923, 25,000 patients were being treated with injected insulin, and Banting and Macleod received the Nobel Prize for Physiology or Medicine.
Euphoria ensued. With the momentous discovery of insulin, it was widely believed diabetes had finally been cured. British biochemist Frederick Sanger determined the molecular structure of human insulin, which garnered him the 1958 Nobel Prize in Chemistry and paved the way for the biosynthesis and commercial production of this hormone. Insulin’s discovery overshadowed the dietary treatments of the previous century, essentially throwing them into general disrepute. Unfortunately, the story of diabetes did not end there.
It soon became clear that different types of diabetes mellitus existed. In 1936, Sir Harold Percival Himsworth (1905–1993) categorized diabetics based on their insulin sensitivity.9 He’d noted that some patients were exquisitely sensitive to the effects of insulin, but others were not. Giving insulin to the insulin-insensitive group did not produce the expected effect: instead of lowering blood glucose efficiently, the insulin seemed to have little effect. By 1948, Joslin speculated that many people had undiagnosed diabetes due to insulin resistance.10
By 1959, the two different types of diabetes were formally recognized: type 1, or insulin-dependent diabetes, and type 2, or non-insulin dependent diabetes. These terms were not entirely accurate, as many type 2 patients are also prescribed insulin. By 2003, the terms insulin-dependent and non-insulin dependent were abandoned, leaving only the names type 1 and type 2 diabetes.
The names juvenile diabetes and adult-onset diabetes have also been applied, to emphasize the distinction in the age of patients when the disease typically begins. However, as type 1 is increasingly prevalent in adults and type 2 is increasingly prevalent in children, these classifications have also been abandoned.
THE ROOTS OF THE EPIDEMIC
IN THE 1950s, seemingly healthy Americans were developing heart attacks with growing regularity. All great stories need a villain, and dietary fat was soon cast into that role. Dietary fat was falsely believed to increase blood cholesterol levels, leading to heart disease. Physicians advocated lower-fat diets, and the demonization of dietary fat began in earnest. The problem, though we didn’t see it at the time, was that restricting dietary fats meant increasing dietary carbohydrates, as both create a feeling of satiety (fullness). In the developed world, these carbohydrates tended to be highly refined.
By 1968, the United States government had formed a committee to look into the issue of hunger and malnutrition across the country and recommend solutions to these problems. A report released in 1977, called Dietary Goals for the United States, led to the 1980 Dietary Guidelines for Americans. These guidelines included several specific dietary goals, such as raising carbohydrate consumption to 55–60 percent of the diet and decreasing fat consumption from approximately 40 percent of calories to 30 percent.
Although the low-fat diet was originally proposed to reduce the risk of heart disease and stroke, recent evidence refutes the link between cardiovascular disease and total dietary fat. Many high-fat foods, such as avocados, nuts, and olive oil, contain mono- and polyunsaturated fats that are now believed to be heart-healthy.