The strong interrelationships between weight issues and diabetes have been given the name “diabesity,” to emphasize how the epidemic of diabetes around the world has paralleled the growth in prevalence of overweight and obesity. The graph shows the remarkable 50% increase in the percentage of adults in the United States from 1990 to 2000 that was accompanied by an increase in mean body weight of more than 4 kg.
A crucial question, though, is this: why is it so hard to lose fat but so easy to gain it? As my grandmother may have said, “a minute on the lips, forever on the hips!” There is a remarkable asymmetry in the mechanisms that the body has evolved that underlie weight gain and weight loss.
Weight loss normally occurs in situations of stress. We lose weight with famine, with infection, with injury. All of this is undesirable, and nature has evolved a series of interrelated defenses against weight loss to defend against it. When the body senses a reduction in energy availability during low-calorie diet, then, neural and hormonal pathways are turned in a direction which aims to prevent weight loss. Circulating levels of the catecholamine hormones of the sympathetic nervous system decrease.
Leptin is a hormone produced by what until a few years ago would have been considered an unusual tissue. Rather than one of the traditional hormone producing glands located in a single location in the body, leptin is produced by fatty tissue. The more fat, the more leptin. Leptin appears to have its major effect on energy balance, though, when we start to lose weight. Then, leptin levels fall, and this sets into motion further adaptations to reduce energy requirements. Increases in leptin with more food intake, in contrast, do little to restrain the degree of increase in weight gain, as the brain essentially sets up resistance systems to dampen this effect of the hormone.
With weight loss from eating less, then, our bodies set up a series of processes to reduce calorie usage both at rest and during exercise. It is not, then, that diet is useless, but we have to recognize that our physiology is designed to minimize weight loss when food is less available.
Should we give up? Is it really “forever on the hips?” With weight gain, high levels of leptin and other factors produced by fatty tissue act in a second role, as what are called “cytokines,” in essence to increase inflammation. Inflammation is not inherently bad. With infection, inflammatory cells act as essential agents to protect us. But with overweight and obesity, inflammation acts on the joints to cause arthritis, on the arteries to cause blood clots and vascular disease, and, crucially, on the tissues that produce insulin and the tissues that respond to insulin – and this is one of the fundamental causes of diabetes.
Next month: How exercise acts in conjunction with healthy diet to protect against obesity and diabetes.
Why don’t you specify which type of diabetes you’re talking about? It makes it very confusing for people who don’t know the difference when they aren’t separated.
Thank you for this. It’s very helpful to get a clear and compelling scientific perspective on this topic.