PEOPLE who subject themselves to a diet of muesli, brown bread and bran to avoid bowel disease might soon be able to save themselves the trouble. In future, a simple urine test could show whether they were at risk of cancer of the colon, and, if they were not, they could give up fibre and start living.

The principle of the test is based on an intriguing theory by Robin Phillips and a team of scientists at St Mark's Hospital, London, which is renowned for its pioneering work into diseases of the colon and rectum. In his review of London hospitals, Sir Bernard Tomlinson has proposed that St Mark's moves to Northwick Park Hospital, Harrow. But its work will continue.

Mr Phillips, who is a consultant surgeon, has spent the past nine years trying to forward the cause of prevention. Research that he started in 1983 on an intuitive hunch has led him to the startling conclusion that people at risk of developing cancer of the colon do not have anything wrong with their colon, but suffer from a faulty liver.

He believes that people with the disease have an inborn error of metabolism, which means that their livers do not detoxify cancer- causing agents in the normal way. These carcinogens, which we unwittingly take in with our food, pass through the liver unchanged and end up in the bile, which can produce tumours in the colon, small intestine and rectum. Bowel cancer affects more than 24,000 people a year and kills more than 17,000. It is the second-biggest cancer killer after cancer of the lung.

'Previously, people thought that abnormal colon cells were responsible for bowel cancer,' says Mr Phillips. 'Most modern cancer research involves looking at cancer cells and trying to understand the mechanisms that occur when cells start to proliferate. Some switch turns these cells on and they start multiplying. Molecular biologists are looking at what happens after the switch is thrown. We are looking at what throws the switch.'

While diet undoubtedly plays a part in the disease - certain populations who eat a low meat and high-fibre diet have a much lower incidence than those eating a typically Western diet - Mr Phillips does not believe it is the whole story. His hypothesis is that people develop the disease when two factors are present: the inborn error of liver metabolism and the 'wrong' diet.

'We propose that some people do not have an inborn error and are not at risk, so for them it does not matter whether they eat a lot of beef and too little fibre. Some are at risk, but they eat the right diet and do not get cancer. The unlucky ones are those people who are at risk for genetic reasons. If they combine this with the wrong diet, they develop cancer.'

The villain of his scenario is bile, the green viscous liquid produced by the liver to enable the body to digest fat. Mr Phillips postulated the theory that if victims of the disease have an inborn error of metabolism and cannot detoxify carcinogens properly, their bile will be different from that of the rest of the population and will be likely to develop polyps or tumours where the bile is present.

The people they chose for their research were a group with a genetic disorder called familial adenomatous polyposis, as everyone who has it develops cancer of the colon unless the organ is removed at an early age. They also develop tumours in the duodenum, the upper part of the small intestine.

Mr Phillips's first discovery, one that immediately supported his theory, was that these patients develop the highest concentration of their duodenal tumours at the exact place where the bile duct enters the small intestine - where bile is present in large amounts and in its most concentrated form.

He next hypothesised that if bile was implicated in the production of tumours, those patients with tumours in the stomach (a place where bile is not normally present) would presumably have higher rates of reflux - flowing back - from the intestine into the stomach than those without.

With the consent of many long-suffering patients, he compared the levels of reflux in patients with stomach tumours to those without, and found that they were much higher in the first group than in the second.

Step three was to compare the bile of people with polyposis to that of a control group. Using high-performance liquid chromatography, the team discovered significant differences between the bile of polyposis patients and that of the control group.

Further work using advanced molecular biology was able to detect the genetic fingerprints of a cancer-forming agent in tissues maximally exposed to polyposis bile. After seven years of exhaustive research, Mr Phillips had proved four points of his hypothesis.

Finally, the theory had to be returned to the start - that colon cancer was due to a liver metabolism abnormality. If this was true, it would show up in a simple test that is often used to assess one aspect of people's metabolic function. This acetylation test assesses how fast or how slowly people metabolise their food.

It consists of giving patients a coffee tablet and testing their urine six hours later. If a great deal of broken-down coffee is present, they are fast acetylators; if not, they are slow. The normal population is divided equally between the two categories.

The team used 250 controls, 44 polyposis patients and 11 patients with colo-rectal cancer. To their relief, while the controls fell equally into slow and fast acetylators, an amazing 10 out of the 11 cancer patients fell into the slow category. Seventy-five per cent of the polyposis patients were also slow acetylators.

Mr Phillips now wants to try out the test on another group of people at risk of developing colon cancer - patients with ulcerative colitis. He plans to take such a group and compare those who have developed cancer with those who have not.

'If we can show that those who have developed cancer are slow acetylators, it would add considerable weight to the hypothesis that colon cancer results from an error of metabolism,' he says.

Mr Phillips claims that the significance of his work is two-fold: it will change the way that scientists look at colo-rectal cancer and could result in a simple predictive test that would determine who was at risk of the disease.

'We could test children at birth for their acetylator status and put them on the correct diet to minimise their risks. Adults could have themselves tested and similarly adopt the correct diet if they were in the risk category,' he says. For the lucky majority, the test would mean dietary freedom. For those at risk of the country's third commonest cancer, it could mean life itself.

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