Obesity: Food kills, flab protects

OBESITY kills, everyone knows that. But is it possible that we've been looking at the problem in the wrong way? It seems getting fatter may be part of your body's defence against the worst effects of unhealthy eating, rather than their direct cause.

This curious insight comes at the same time as several studies distancing obesity itself from a host of diseases it has long been blamed for, including heart disease and diabetes.

Instead, these studies point the finger at excess fat in the bloodstream, either when the fat cells of obese people finally get overloaded or when lean people who can't store a lot of fat eat too much. This seems to have a destructive effect by provoking the body's immune response.

None of this changes the fact that too much rich food and too little exercise is bad for you. But viewing obesity as a symptom of an unhealthy diet, rather than the direct cause of disease and death, plus a better appreciation of the immune system's reaction to fat, should radically change our understanding of what is shaping up to be one of modern society's biggest health scourges. The findings also point to new ways to treat diabetes, heart disease and other diet-linked conditions.

In recent years, most rich countries, and some poorer ones, have seen a massive rise in so-called "metabolic syndrome", whose symptoms can include insulin resistance, high blood cholesterol and an increased risk of diabetes, heart disease and stroke. That the syndrome goes hand in hand with obesity is well known, but exactly how all these conditions are linked is unclear.

In an attempt to determine the effects of obesity itself, diabetes researchers Roger Unger and Philipp Scherer, both at the University of Texas Southwestern Medical Center in Dallas, reviewed several recent studies of the role of fat cells in humans and mice.

In particular, the pair looked at the fates of people with a genetic condition that means they can't make their own fat cells and mice genetically engineered to have low supplies of these cells and fed a diet that would make normal mice obese. They found that, despite not being obese, both tend to develop metabolic syndrome earlier on in life than their overweight, overfed counterparts.

This led Unger and Scherer to conclude that obesity protects the body from the effects of overeating by providing somewhere safe to deposit the dietary deluge of fat and sugar, which in excess is toxic to many body tissues (Trends in Endocrinology and Metabolism, DOI: 10.1016/j.tem.2010.01.009).

Only when the body's fat cells, or adipocytes, are crammed to capacity do the problems of metabolic syndrome begin. The fully engorged adipocytes begin to die and leak their contents into the bloodstream, including saturated fatty acids such as palmitic acid. Such fats then accumulate in tissues such as the liver, pancreas and heart, where they may prompt the symptoms of metabolic syndrome.