Читать книгу The Diabetes Code - Dr. Jason Fung - Страница 9

HOW TYPE 2 DIABETES BECAME AN EPIDEMIC

THE WORLD HEALTH Organization released its first global report on diabetes in 2016 and the news was not good. Diabetes was an unrelenting disaster. Since 1980—a single generation—the number of people around the world afflicted with diabetes has quadrupled. How did this ancient disease suddenly become the twenty-first-century plague?

A SHORT HISTORY OF DIABETES

THE DISEASE OF diabetes mellitus (DM) has been recognized for thousands of years. The ancient Egyptian medical text, Ebers Papyrus, written around 1550 BC, first described this condition of “passing too much urine.”¹ Around the same time, ancient Hindu writings discussed the disease of madhumeha, which loosely translated means “honey urine.”² Afflicted patients, often children, were mysteriously, inexorably losing weight. Attempts to stop the wasting were unsuccessful despite continual feeding, and the disease was almost uniformly fatal. Curiously, ants were attracted to the urine, which was inexplicably sweet.

By 250 BC, the Greek physician Apollonius of Memphis had termed the condition diabetes, which by itself connotes only excessive urination. Thomas Willis added the term mellitus, meaning “from honey” in 1675. This descriptor distinguishes diabetes mellitus from a different, uncommon disease known as diabetes insipidus. Most commonly caused by traumatic brain injury, diabetes insipidus is also characterized by excessive urination, but the urine is not sweet. Fittingly, insipidus means “bland.”

Colloquially, the non-specific term diabetes refers to diabetes mellitus since it is far, far more common than diabetes insipidus. In this book, the term diabetes only refers to diabetes mellitus, and there will be no further discussion of diabetes insipidus.

In the first century AD, the Greek physician Aretaeus of Cappadocia wrote the classic description of type 1 diabetes as a “melting down of flesh and limbs into urine.” This summary captures the essential feature of this disease in its untreated form: excessive urine production is accompanied by almost complete wasting away of all tissues. Patients cannot gain weight no matter what they eat. Aretaeus further commented that “life (with diabetes) is short, disgusting and painful” as there was no effective treatment. Once affected, patients followed a predestined, fatal course.

Tasting the urine of the stricken patient for sweetness was the classic diagnostic test for diabetes (ewww. . .). In 1776, the English physician Matthew Dobson (1732–1784) identified sugar as the substance causing this characteristic sweet taste. The sweetness was found not only in the urine, but also in the blood. Slowly, an understanding of diabetes was unfolding, but a solution was still out of reach.

In 1797, the Scottish military surgeon John Rollo became the first physician to formulate a treatment that carried any reasonable expectation of success. He had observed substantial improvement in a diabetic patient eating an all-meat diet. Given the uniformly grim prognosis of diabetes, this approach was a breakthrough. This extremely low carbohydrate diet was the first diabetic treatment of its kind.

By contrast, French physician Pierre Piorry (1794–1879) advised diabetics to eat large quantities 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. (The most recent Dietary Guidelines for Americans released in 2016 have removed restrictions on total dietary fat in a healthy diet.¹¹)

Similarly, the link between natural, saturated fat and heart disease has been proven false.¹² While artificially saturated fats, such as trans fats, are universally accepted as toxic, the same does not hold true for naturally occurring fats found in meat and dairy products, such as butter, cream, and cheese—foods that have been part of the human diet for time beyond memory.

As it turns out, the consequences of this newfangled, unproven, low-fat, high-carbohydrate diet were unintended: the rate of obesity soon turned upwards and has never looked back.

The 1980 Dietary Guidelines spawned the infamous food pyramid in all its counterfactual glory. Without any scientific evidence, the formerly “fattening” carbohydrate was reborn as a healthy whole grain. The foods that formed the base of the pyramid—foods we were told to eat every single day—included breads, pastas, and potatoes. These were the precise foods we had previously avoided in order to stay thin. They are also the precise foods that provoke the greatest rise in blood glucose and insulin.

Figure 1.1. Obesity trends in the U.S. after introduction of the “food pyramid” ¹³

As Figure 1.1 shows, obesity increased immediately. Ten years later, as Figure 1.2 shows, diabetes began its inevitable rise. Age-adjusted prevalence is still rising precipitously. In 1980, an estimated 108 million people worldwide suffered with diabetes. By 2014, that number had swelled to 422 million.¹⁴ Even more concerning is the fact that there seems to be no end in sight.

THE TWENTY-FIRST-CENTURY PLAGUE

DIABETES HAS INCREASED significantly in both sexes, every age group, every racial and ethnic group, and all education levels. Type 2 diabetes attacks younger and younger patients. Pediatric clinics, once the sole domain of type 1 diabetes, are now overrun with an epidemic of obese adolescents with type 2 diabetes.¹⁵

This is not merely a North American epidemic, but a worldwide phenomenon, although close to 80 percent of the world’s adult diabetics live in developing nations.¹⁷ Rates of diabetes are rising fastest in the low- and middle-income nations of the world. In Japan, 80 percent of all new cases of diabetes are type 2.

Figure 1.2. The rising tide of diabetes in the United States¹⁶

China, in particular, is a diabetes catastrophe. In 2013, an estimated 11.6 percent of Chinese adults had type 2 diabetes, eclipsing even the long-time champion, the U.S., at 11.3 percent.¹⁸ Since 2007, 22 million Chinese—a number close to the population of Australia—have been newly diagnosed with diabetes. This number is even more shocking when you consider that only 1 percent of Chinese had type 2 diabetes in 1980. In a single generation, the diabetes rate has risen by a horrifying 1160 percent. The International Diabetes Federation estimates that the worldwide rate of diabetes will reach 1 in every 10 adults by the year 2040.¹⁹

The problem is not trivial. In the U.S., 14.3 percent of adults have type 2 diabetes and 38 percent of the population has prediabetes, totaling 52.3 percent. This means that, for the first time in history, more people have the disease than not. Prediabetes and diabetes is the new normal. Worse, the prevalence of type 2 diabetes has increased only in the last forty years, making it clear that this is not some genetic disease or part of the normal aging process but a lifestyle issue.

It is estimated that, in 2012, diabetes cost $245 billion in the United States due to direct health costs and lost productivity.²⁰ The medical costs associated with treating diabetes and all its complications are two to five times higher than treating nondiabetics. Already, the World Health Organization estimates that 15 percent of annual health budgets worldwide are spent on diabetes-related diseases. Those numbers threaten to bankrupt entire nations.

The combination of prohibitive economic and social costs, increasing prevalence, and younger age of onset make obesity and type 2 diabetes the defining epidemics of this century. Ironically, despite the explosion of medical knowledge and technological advances, diabetes poses an even bigger problem today than it did in 1816.²¹

In the 1800s, type 1 diabetes predominated. While almost uniformly fatal, it was relatively rare. Fast-forward to 2016, when type 1 diabetes accounts for less than 10 percent of total cases. Type 2 diabetes dominates and its incidence is growing despite its already endemic nature. Almost all type 2 diabetes patients are overweight or obese and will suffer complications related to their diabetes. Although insulin and other modern medicines can treat blood glucose efficiently, lowering blood glucose alone does not prevent the complications of diabetes, including heart disease, stroke, and cancer—leading causes of death.

That we should have a worldwide epidemic of one of the world’s oldest diseases is a bombshell. Whereas all other diseases, from smallpox to influenza to tuberculosis to AIDS, have been controlled over time, the diseases associated with diabetes are increasing at an alarming rate.

But the question still remains: Why? Why are we powerless to stop the spread of type 2 diabetes? Why are we powerless to stop the spread among our children? Why are we powerless to stop the ravages of type 2 diabetes on our bodies? Why are we powerless to prevent the heart attacks, strokes, blindness, kidney disease, and amputations that accompany it? More than 3000 years after its discovery, why is there no cure?

The answer is that we have fundamentally misunderstood the disease called type 2 diabetes. To design rational treatments that have a chance of success, we must begin again. We must understand the root causes of the disease, or in medical terms, the aetiology. What is the aetiology of type 2 diabetes? Once we understand that, we can begin. Let us begin.