Science; Selling the Big Issue

Article excerpt

Anyone who has spent their life counting calories knows that obesity is all about figures. But these days the important figures are no longer just the one you see reflected in the mirror, the number of calories in a grapefruit, or how many minutes of sex are needed to cancel out last night's burger, fries and thick chocolate shake.

The crucial figures are the six weight-related genes, half-a-dozen brain proteins, 12 anti-obesity drugs, a doubling in the number of obese people, pounds 2 billion pounds and rising in health costs.

Once to be fat was to be happy and also a sign of health and prosperity. Large men were envied while curvaceous women were celebrated as models of fertility and beauty. Now tubbiness is a time bomb with the fuses already lit and running to all our vital organs. Based on body-mass index (BMI) - a measurement found by dividing your weight in kilograms by your height in metres squared - the number of British people considered clinically obese has doubled in the last 10 years to 17 per cent of men and 13 per cent of woman, and 50 per cent of us are overweight. A BMI of 20 to 25 is normal or ideal and over 30 is considered obese, but recent epidemiological {population-based} studies have revealed health risks start to climb even with a small spare tyre. According to statistics compiled by the Association for the Study of Obesity, a person with a BMI of 27 has double the risk of heart disease, hypertension and gallstones and 14 times the chance of becoming diabetic. With a BMI of over 30 this soars to four times the risk of heart disease, hypertension and gallstones, 30 to 50 times the risk of diabetes and a quadrupling of the chance of degenerative arthritis. The cost of treating this ill health is huge, conservatively estimated at around pounds 2 billion a year in the UK not counting the impact of work lost, benefits paid and social disruption. But can we help it? Findings from genetic researchers over the past two years suggest we may have much less control over our expanding waistlines than we've been encouraged to think. Using information gleaned from rats and mice, researchers have discovered that our eating habits are governed by a complex series of switches and relationships that work to keep the body's energy intake and energy usage in balance. The first clue to the labyrinth was revealed two years ago when US scientist Jeffrey Friedman, and colleagues at the Rockefeller University New York, discovered that a species of chronically obese mice had a defect on what is now known as the obese or ob gene, which resulted in constantly low levels of a protein they named leptin. Mice with the defect grew rapidly to three times the size of a normal mouse, but when they were injected with leptin, lo and behold, they lost weight. Manufactured by the ob gene, leptin circulates in the blood at levels corresponding to the amount of fat in the body and appears to act as signalling system which guides the brain's control over basic metabolic functions such as heat creation, digestion and energy storage. When leptin reaches a certain level, the brain registers that enough fat has been taken in, turns off the "I need food" message, and initiates a new message to stimulate energy burning rather than conservation, and tells the ob gene to stop producing leptin. Conversely, when leptin levels in the blood fall, the brain activates the desire to eat and slows metabolic functions to conserve energy. With the arrival of fat, the ob gene switches on and leptin levels start to rise again. Exactly how all this occurred was a mystery but it looked like the ultimate diet pill. All that was needed was to find a way to artificially increase leptin and trick the brain into thinking the body had eaten enough. Unfortunately this eureka moment didn't last long. Further research found that though humans have the ob gene, the mouse mutation simply doesn't occur. …