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.
THE DIFERENCES BETWEEN TYPE 1 AND TYPE 2 DIABETES
DIABETES MELLITUS COMPRISES a group of metabolic disorders characterized by chronically elevated blood glucose, or hyperglycemia.
The prefix hyper means “excessive,” and the suffix emia means “in the blood,” so this term literally means “excessive glucose in the blood.” There are four broad categories of diabetes mellitus: type 1, type 2, gestational diabetes (high blood glucose associated with pregnancy), and other specific types.1 Type 2 diabetes is by far the most common, making up an estimated 90 percent of cases.
Gestational diabetes, by definition, is not a chronic disease, though it increases the future risk of developing type 2 diabetes.
If hyperglycemia persists after pregnancy, it must be reclassified as type 1, type 2, or another specific type.
Other specific types of diabetes, listed in Table 2.1, are rare.
We will not discuss these types of diabetes or gestational diabetes any further in this book.
Table 2.1 Classifications of diabetes mellitus
Type 1 Type 2 Gestational
Other specific types: - Genetic defects - Pancreatic disease - Drug or chemical induced - Infections - Endocrinopathies