DIET AND CANCER
It is now 30 years since Richard Doll and Richard Peto (Doll and Peto, 1981) estimated that diet may contribute to one-third of all cancers. While this figure is still widely accepted, we’ve seen that there is direct chemical the action of specific food components to cancer. Part of the problem is that many foods contain agents that, either directly or indirectly, can exert DNA damaging (genotoxic) effects. The link between eating red or processed meat and bowel cancer, shown by a number of large and seemingly well-conducted studies, arises from the fact that cooked meat can release agents in the stomach that, on reaching the circulation, undergo enzymatic conversion to carcinogens. Compounds added to give colour and flavour and to stop Clostridium botulinum growing can have similar effects. It is scarcely surprising, therefore, that epidemiological studies of the association between diet and cancer are often inconclusive and contradictory. Fortunately, making sense of the data has been considerably helped by the establishment of the Cochrane Collaboration (www.cochrane.org), a non-profit consortium dedicated to analysing and summarising the literature on healthcare interventions. Its aim is to explain, briefly but in ‘plain English’, why a question is being asked, how the trials were set up, the main results and the conclusions. From its files, the most recent conclusions for dietary calcium are that, although there is evidence that calcium supplementation might make a modest contribution to the prevention of bowel cancer, there is not sufficient evidence to recommend its general use. A corresponding report on dietary fibre concludes that there is currently no evidence to suggest that increased intake will reduce the incidence or recurrence of bowel cancer within a two- to four-year period. The collective advice of the World Cancer Research Fund and the American Institute for Cancer Research on food and cancer is to eat a ‘balanced diet’ with plenty of fibre, vegetables, fruits, lentils, beans and whole grains such as brown rice and wholemeal pasta, less than 500 grams per week of red meat, ‘very little if any’ of that being processed (i.e. preserved by smoking or by the addition of salt, sugar, nitrate or nitrite) and, of course, no alcohol. Over 300 million people in the world are obese, that is, are more than 25% overweight. Obesity dramatically increases chances of developing a wide range of life-threatening conditions including diabetes (in the USA more than one person in three ends up with adult-onset diabetes), arteriosclerosis, hypertension, heart disease, age-related degenerative disease, sleep apnoea, gallstones and some cancers. Obesity specifically promotes cancers of the colon, kidney, liver, oesophagus, pancreas, endometrium and breast and there is evidence that it may also contribute to the gallbladder and ovarian cancers. The risk of breast cancer is particularly significant in post-menopausal women. Before menopause, the ovaries produce most of a woman’s oestrogen, and fat tissue makes the rest. After menopause, the ovaries stop making oestrogen and it comes mainly from fat tissues. Having more fat tissue after menopause can increase oestrogen levels and thereby the likelihood of developing breast cancer. The risk is greater for women who put on weight as adults by comparison with those who have been overweight since childhood. Furthermore, there are differences between fat cells in different regions of the body so that waist fat appears to be worse than hip or thigh fat in terms of breast cancer risk. Despite the fact that obesity is linked to breast cancer, it is also associated with a lower density of breast tissue, whereas increased tissue density is a significant risk factor for breast cancer.
While the upsurge in obesity is a relatively recent trend, there is evidence dating back 100 years for a link between the amount one eats and cancer. In rats and mice dietary restriction, which means being fed between 10% and 50% fewer calories, reduces the incidence of at least some types of cancers – and extends lifespan. Note that it’s total calorie intake rather than the nature of the food that counts. Does this apply to humans? That’s a bit more difficult to be sure about but, certainly some human tumour cells when grown in mice are very sensitive to dietary restriction. The explanation may be that when a diet is restricted to the levels of key metabolic hormones decrease, particularly insulin. As well as being a major metabolic regulator, insulin is also a very potent promoter of cell growth – and hence, potentially a driving force for cancer. Sustained low levels of such a factor may, therefore, be protective.