'Miracle' cure for fatness has slim chance of success

A MIRACLE treatment for fat mice, trumpeted last week as a possible cure for human obesity and provoking a multi-million-dollar share price surge, has one unpublicised drawback - preliminary research indicates it will fail to work on humans.

Three separate groups of scientists have shown that mice suffering from inherited obesity dramatically lost weight when injected with a genetically engineered hormone.

But humans do not always react in the same way as mice. Other work, which was not mentioned in the mountain of scientific reports and press releases published last week by companies financing the research, indicates that obese people already have higher-than-average levels of the same hormone. Daily injections, therefore, will not work on them in the dramatic way they worked on mice, whose bodies lack the hormone.

Some obesity scientists believe drug companies have hyped the latest research on obese mice, published on Friday in the journal Science, by suggesting that clinical trials of the hormone may begin as early as next year, with a clinical product on the market by the end of the decade.

The scientist at the centre of the latest research is Jeffrey Friedman of the Howard Hughes Medical Institute at Rockefeller University in New York. Dr Friedman unravelled the chemical nature of the ''ob'' gene for obesity in mice last December and Rockefeller has since established a $20m (pounds 12.5m) deal with Amgen, a Californian biotechnology company, to develop the research into a human drug.

When news of last week's research was leaked prematurely to Wall Street by financial analysts, shares in Amgen rose 10 per cent.

According to scientists close to the Institute, Dr Friedman has given private seminars showing that the ob protein, a hormone, can be detected in all humans. But obese people probably have higher levels compared to lean people. Nobody knows why the hormone, so effective in helping mice lose weight, seems to be associated with the opposite effect in humans. One very speculative possibility is that in the bodies of some obese people, it does not work properly.

When questioned about this work, however, Dr Friedman refused to give details. ''Those experiments are under way,"he said, "and I don't want to give you any information until we know it is correct, so the results are not final yet. The data are too preliminary for me to talk about.''

Dr Friedman and his researchers did, however, release details in their research paper, showing that they were able to measure the ob protein in six members of his own lab. He said these volunteers were all lean and therefore could not be used to compare obese people with slim people.

Developing a drug to ''cure'' obesity has important financial ramifications. In Britain alone an estimated pounds 4bn a year is spent on weight-reducing products and on treating illnesses, such as heart disease, indirectly linked to obesity. Americans spend about $40bn a year on efforts to trim the fat.

Despite the intense interest in the ob gene, however, less than a quarter of the cases of serious obesity are the result of genetic defects. Medical researchers stressed that the biggest culprits behind the doubling of obesity cases in the past 10 years are poor diet and lack of exercise.

Even Dr Friedman said research on obesity in mice could not replace current advice to overweight people: ''Diet and exercise are the mainstays of current treatment, and I would imagine even if this thing were to develop into a useful clinical tool in some circumstances, it would be a supplement to that, and not a replacement.''

See Business section, page 2

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