cells to take up the glucose (thereby halting the rise in blood glucose concentration) and to store it as glycogen or as fat, to be used for energy between meals. Other nutrients, such as amino acids, also trigger the release of insulin, and insulin has effects on food components other than sugar (such as preventing the breakdown of fat).
Many different things can go wrong in that normal course of events, and so the term “diabetes mellitus” covers a wide variety of underlying problems linked by shared symptoms arising from high levels of blood sugar. That diversity can be crudely partitioned into two groups of diseases: so-called Type-2 or non-insulin-dependent diabetes mellitus (also known as “adult-onset diabetes”), and the much less common Type-1 or insulin-dependent diabetes mellitus (also known as “juvenile-onset diabetes”). The latter is an autoimmune disease in which a person’s antibodies destroy the person’s own pancreatic cells that secrete insulin. Type-1 diabetics tend to be thin, to produce no insulin, and to require multiple daily injections of insulin. Many of them carry certain genes (certain so-called HLA alleles) that code for elements of the immune system. Type-2 diabetes instead involves increased resistance of body cells to the person’s own insulin, so that cells fail to take up glucose at normal rates. As long as the pancreas can respond by releasing more insulin, the cells’ resistance can be overcome, and blood glucose remains within a normal range. But eventually the pancreas becomes exhausted, it may no longer be able to produce enough insulin to overcome that resistance, blood glucose levels rise, and the patient develops diabetes. Type-2 diabetes patients tend to be obese. In early stages of the disease they can often control their symptoms by dieting, exercising, and losing weight, without requiring tablets or insulin injections.
However, distinguishing Type-2 and Type-1 diabetes can be difficult, because Type-2 diabetes is now increasingly appearing already in teen-agers, while Type-1 diabetes may not first appear until in adulthood. Even Type-2 diabetes (as defined by insulin resistance) is associated with many different genes and manifests itself by varied symptoms. All of my subsequent discussion in this chapter will concern the much more common (about 10 times commoner) Type-2 diabetes, which I shall henceforth refer to simply as “diabetes.”
Genes, environment, and diabetes
More than 2,000 years ago, Hindu physicians noting cases of “honey urine” commented that such cases “passed from generation to generation in the seed” and also were influenced by “injudicious diet.” Physicians today have rediscovered those deadly insights, which we now rephrase by saying that diabetes involves both genetic and environmental factors, and possibly also intra-uterine factors affecting the fetus during pregnancy. Evidence for a role of genes includes the 10-times-higher risk of getting diabetes if you have a diabetic first-degree relative (a parent or a sibling) than if you don’t. But diabetes, like hypertension, is not one of those simple genetic diseases (as is sickle-cell anemia) in which a mutation in the same gene is responsible for the disease in every patient. Instead, dozens and dozens of different genetic susceptibility factors for diabetes have been identified, many of them united only by their common feature that a mutation in any of those genes may result in high blood-glucose levels due to insulin resistance. (I mention again that these comments apply to Type-2 diabetes; Type-1 diabetes involves its own separate set of genetic susceptibility factors.)
In addition to those genetic factors in diabetes, diabetes also depends upon environmental and lifestyle factors. Even if you are genetically predisposed to diabetes, you won’t necessarily get the disease, as would be the case if you carried a pair of genes for muscular dystrophy or Tay-Sachs disease. The risk of developing diabetes increases with age, and with having diabetic first-degree relatives, and with being born of a diabetic mother, which you yourself can’t do anything about. But other risk factors that predict diabetes are factors under our control, including especially being overweight, not exercising, eating a high-calorie diet, and consuming much sugar and fat. Most diabetics (I emphasize again, most Type-2 diabetics) can reduce their symptoms by reducing those risk factors. For example, the prevalence of diabetes is 5 to 10 times higher in obese people than in those of normal weight, so that diabetes patients can often regain health by dieting, exercising, and losing weight, and those same measures can protect people predisposed to diabetes against getting the disease.
Many types of natural experiments, including ones that I mentioned at the beginning of this chapter as demonstrating the relation between the Western lifestyle and non-communicable diseases in general, specifically illustrate the role of environmental factors in diabetes. The worldwide rise in those factors underlies the current worldwide diabetes epidemic. One such type of natural experiment involves the rise and fall of diabetes prevalences accompanying the rise and fall of Western lifestyle and affluence in the same population. In Japan, graphs against time of diabetes prevalence and economic indicators are parallel, down to details of year-to-year wiggles. That’s because people eat more, hence they risk developing more diabetes symptoms, when they have more money. Diabetes and its symptoms decline or disappear in populations under starvation conditions, such as French diabetes patients under the severe food rationing imposed during the 1870–1871 siege of Paris. Groups of Aboriginal Australians who temporarily abandoned their acquired sedentary Western lifestyle and resumed their traditional vigorous foraging reversed their symptoms of diabetes; one such group lost an average of 18 pounds of body weight within seven weeks. (Remember that obesity is one of the leading risk factors for diabetes.) Decreases in diabetes symptoms and in waist circumference were also noted for Swedes who for three months abandoned their very un- Mediterranean Swedish diet (over 70% of calories from sugar, margarine, dairy products, alcohol, oil, and cereals) and adopted instead a Mediterranean diet typical of slim Italians. Swedes who adopted a “Paleolithic diet” designed to resemble that of hunter-gatherers became even healthier and developed even slimmer waists.
Another natural experiment is provided by the sky-high explosions of diabetes among groups that emigrated and thereby gave up a vigorous Spartan lifestyle to adopt sedentary high-calorie low-exercise living based on abundant supermarket food. A dramatic example involved the Yemenite Jews who were airlifted to Israel by Operation Magic Carpet in 1949 and 1950, and were thereby plunged abruptly into the 20th century from formerly medieval conditions. Although Yemenite Jews were almost free of diabetes upon reaching Israel, 13% of them then became diabetic within two decades. Other migrants who sought opportunity and instead found diabetes included Ethiopian Jews moving to Israel, Mexicans and Japanese moving to the U.S., Polynesians moving to New Zealand, Chinese moving to Mauritius and Singapore, and Asian Indians moving to Mauritius, Singapore, Fiji, South Africa, the U.S., and Britain.
Developing countries that have recently been growing more affluent and Westernized have correspondingly been growing more diabetic. In first place stand the eight Arab oil-producers and newly affluent island nations that now lead the world in national diabetes prevalences (all of them above 15%). All Latin American and Caribbean countries now have prevalences above 5%. All East and South Asian countries have prevalences above 4% except for five of the poorest countries, where prevalences remain as low as 1.6%. The high prevalences of the more rapidly developing countries are a recent phenomenon: India’s prevalence was still below 1% as recently as 1959 but is now 8%. Conversely, most sub-Saharan African countries are still poor and still have prevalences below 5%.
Those national averages conceal large internal differences that constitute further natural experiments. Around the world, urbanization results in less exercise and more supermarket food, obesity, and diabetes. Individual urban populations that thereby achieved notably high diabetes prevalences include the already mentioned Wanigela people of Papua New Guinea’s capital city (37% prevalence) and several groups of urban Aboriginal Australians (up to 33%). Both of those cases are all the more striking because diabetes was unknown among New Guineans and Australians under traditional conditions.
Thus, the Western lifestyle somehow increases the risk that those enjoying it will become diabetic. But the Western lifestyle consists of many interlinked components: which components contribute most to the risk of diabetes? While it isn’t easy to tease apart the effects of correlated influences, it appears that the three strongest risk factors are obesity and sedentary lifestyle (which you can do something about) and family history of diabetes (which you can’t do anything about). Other risk factors that you can’t control are either high or low birth weight. While diet composition surely acts at least in part by its relation to obesity, it also seems to have some independent influence: among people matched for obesity, those consuming a Mediterranean diet appear to be at lower risk than those with high intakes of sugar, saturated fatty acids, cholesterol, and triglycerides. Not exercising may create risks mainly through predisposing towards obesity, while smoking, inflammation, and high alcohol consumption appear to be independent risk factors. In short, Type-2 diabetes originates with genetic factors and possibly intra- uterine factors, which may become unmasked later in life by lifestyle factors resulting in disease symptoms.
