THAT a healthy way of life can prevent cancer is well known. It is also becoming clear that clean living can help those who already have tumours to survive, and may even prevent the disease from coming back. A number of studies have shown these effects in breast cancer and colon cancer. But how they work at a molecular level remains a mystery.

One person keen to know what is going on is Dean Ornish of the University of California, San Francisco. Besides his academic job, he is the founding president of the Preventive Medicine Research Institute, a charitable foundation based in Sausalito, California—and, as he freely admits in the interests of full disclosure, an author of general-interest books on preventive medicine and a consultant for large food companies on how to make “more healthful foods”. He was also one of the first to show scientifically that healthy living (a low-fat vegetarian diet, plenty of exercise and—of course—no smoking) can not merely stop, but also reverse the progress of coronary heart disease. He and his colleagues therefore decided to look at gene activity in a group of people with cancer who had chosen to change their ways rather than undergo medical treatment, to see if that would illuminate the nature of the health-giving processes in question.

The team chose men with prostate cancer for their study. They picked this cancer because it is slow-growing. When such a cancer has been diagnosed early, doing nothing is a reasonable alternative to the trauma of surgery, radiation or hormone therapy. Dr Ornish enrolled 30 such early-stage patients into a programme of “comprehensive lifestyle changes”. These included a low-fat, whole-food, plant-based diet, stress management, moderate exercise and plenty of “psychosocial group support”. Patients' prostates were sampled at the start of the study, and then three months later to see what had changed.

For a gene to do its work, it has to be transcribed into a molecular messenger. This messenger, a molecule of a substance called RNA, carries instructions to the protein-making parts of a cell, telling them what to make. The more RNA messengers that have been transcribed from a gene, the more active that gene is assumed to be. Count the shifting number of messengers, then, and you can see the effects on the genes of a course of treatment. And that, using so-called gene-chip technology, is what Dr Ornish did.

He and his colleagues found that after three months, the activity of more than 500 genes was altered in the prostate in a way that might be expected to help fight cancer. The good life turned off tumour-promoting genes (known as oncogenes)—including several that are the target of efforts to develop anti-cancer drugs. Meanwhile, disease-preventing genes, including one for a protein that may help the immune system to recognise tumour cells, were switched on. Exactly how changes in lifestyle have this effect on the genes is unclear. But the study suggests the process reaches deep into the body's molecular biology.

Before anyone rushes out for a quick glass of wheatgrass juice, though, there are a few caveats. First, 30 patients is quite a small sample, so the results should be treated cautiously. Second, there was no control group. Though a “before and after” comparison like this does have some value, it is better to conduct a study in which half the participants do not receive the treatment under test, and then compare the two halves.

Nevertheless, the results are intriguing. As far as Dr Ornish is concerned, the message is that it is wrong to be nihilistic about cancer and assume that nothing can be done because “it is in the genes”. As for how much prevention is necessary, he says his earlier work showed a correlation between the degree to which patients adhere to the kind of changes he proposes and the level of improvement they make. “It is”, he adds, “all in my book.”