He described an expanding body of evidence to show that the composition of the diet directly influences the diversity of the microbes in the gut, providing the link between diet, colonic disease and colon cancer.

People eating a healthy diet containing high levels of complex carbohydrate had significant populations of micro-organisms in their gut called Firmicutes. These bacteria use the undigested residues of starch and proteins in the colon to manufacture short-chain fatty acids and vitamins such as folate and biotin that maintain colonic health. One of these fatty acids, butyrate, not only provides most of the energy to maintain a healthy gut wall, but it also regulates cell growth and differentiation. Both experimental and human studies support its role in reducing colon cancer risk.

However, gut microbes may also make toxic products from food residues. Diets high in meat will produce sulphur - this decreases the activity of 'good' bacteria that use methane and increases the production of hydrogen sulphide and other possible carcinogens by sulphur-reducing bacteria.

"Colon cancer is the second leading cause of cancer-related deaths in adults in Westernized communities." said Professor O'Keefe, "Our results suggest that a diet that maintains the health of the colon wall is also one that maintains general body health and reduces heart disease".

"A diet rich in fibre and resistant starch encourages the growth of good bacteria and increases production of short chain fatty acids which lessen the risk of cancer, while a high meat and fat diet reduces the numbers of these good bacteria." Professor O'Keefe went on. "Our investigations to date have focused on a small number of bacterial species and have therefore revealed but the tip of the iceberg, our colons harbour over 800 bacterial species and 7,000 different strains. The characterization of their properties and metabolism can be expected to provide the key to colonic health and disease".

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The researchers suspected the problem was in the traditional lab experiment design. So they reevaluated the data, picking a mouse of each strain from each environment - similar to matching pairs in human clinical trials - and found only the same number of false positives as would be expected by chance.

When mouse testing creates a false positive, leading a researcher to believe a drug has worked, the drug could be sent to further animal testing and human clinical trials at a cost of millions of dollars. Drugs that fail in clinical trials cannot be marketed, and the money is wasted. To recoup those losses, drug companies must increase the costs of marketable drugs.

"Drugs aren't expensive because they're costly to make," Garner said. "They're expensive because the company has to recoup the costs of the other drugs that have failed in human clinical trials. Numbers are hard to estimate, but for every drug that reaches the marketplace, well over 100 have been abandoned at some point in their development."

Garner said giving mice varying environments also could be better for the animals because fewer could be used. Weeding out an unsuccessful drug would eliminate an unnecessary second round of animal testing.

"The really exciting message is that we have shown how the false positives in early drug discovery can be drastically reduced without costing anything more than a change in experimental design," Garner said. "These are positive results for pharmaceutical research, patients and for mice."