Increasing evidence points to the link between diet and disease. But why are we not taking heed, asks Kay-Tee Khaw.
The major health challenge in industrialised societies with ageing populations is chronic disability, caused by heart attacks and strokes, diabetes, cancer, dementia, osteoporosis, chronic bronchitis, glaucoma and cataracts leading to blindness.
There is now increasing evidence that diet greatly influences the development of such conditions. International differences in death rates from coronary heart disease are more than tenfold and attention has often been drawn to the high rates in Britain compared with France, Spain and Japan. But the incidence of many other conditions, including strokes, common cancers and hip fractures, varies just as much.
In Japan there has been an 80 per cent reduction in strokes among women over the past 25 years, and in the United States a 33 per cent decrease in strokes and 24 per cent decrease in coronary heart disease in ten years. On the other hand, stroke and cancer rates have nearly doubled in Hungary and in other countries in Eastern Europe and in the United Kingdom and Sweden hip fracture rates have nearly trebled over the past 30 years. If we now had in the UK the hip fracture rates of 30 years ago, two out of three fractures would not occur.
Migrant studies are suggestive: Japanese in Japan have low rates of heart disease, breast and prostate cancer but Japanese living in the US have rates more similar to those of US Caucasians. Hypertension and its sequelae, heart disease and stroke, are rare in rural Kenyan Luo but become common when Kenyans from the countryside move to urban Nairobi.
A critical question must be whether changing diet will influence health. Here randomised controlled trials provide the strongest evidence. Where these have been done, results have been variable. For instance, a trial of betacarotene and vitamin E supplementation in Finnish smokers showed no reduction in heart disease or cancer. However, a British trial reported a 30 per cent reduction in repeat heart attacks among those advised to eat fatty fish at least twice a week. Another trial of secondary prevention after a heart attack conducted in France, this time in patients advised to eat a Mediterranean diet, found a 70 per cent reduction in mortality after four years compared with those receiving standard diet advice. A French trial reported a 30 per cent reduction in hip fracture rates after 18 months in elderly women taking vitamin D and calcium supplements compared with women taking a placebo. Folic acid supplementation in high-risk women will reduce the risk of having babies with spina bifida.
Many dietary factors such as the antioxidants and bioflavonoids (found in fruit and vegetables) omega three fatty acids (found in fatty fish) and minerals such as calcium and potassium (also found in vegetables) may be protective for chronic diseases associated with ageing, such as cardiovascular disease and cancer.
Yet there are few issues more likely to generate controversy than dietary recommendations. Originally, most of these focused on daily minimum nutrient intakes for prevention of deficiency diseases such as scurvy, rickets and beriberi. These levels are relatively uncontroversial as the relationship is more or less dichotomous: deprivation of the nutrient causes the disease and supplementation cures it. However, the deficiency diseases are but an extreme of the spectrum of manifestation of diet-related disease. Low vitamin D levels and low calcium intake have been implicated in osteoporotic fractures, low levels of intake of micronutrients such as vitamin C, folate and bioflavonoids associated with increased risk of cardiovascular disease and cancer. The difficulty is that these are not all-or-none effects but appear to be related to the size of the dose.
The research and public health focus has thus shifted from the issue of minimum requirements that may prevent diseases due to nutrient deficiency to the question of what optimal amounts might be - both for the prevention of chronic disease and for optimal health, which are not the same. These requirements are much more difficult to establish.
But this is where we get to the paradox of perceived risk. Many people, including a lot of eminent scientists, stopped eating beef following the debates over the link between BSE (bovine spongioform encephalopathy) and CJD (Creutzfeld Jacob disease). While the risks of CJD are still debatable they do not in any way compare in magnitude to the likelihood of having a heart attack, stroke or cancer, which will affect at least one in four of us.
Yet suggestions, for instance, that the population should decrease its intake of saturated fat or of salt even slightly to lower the risk of heart disease or stroke lead to uproar. The argument is made that the two examples are not comparable, but it would seem that rare conditions often appear more threatening than common ones.
It is easy to forget that what we take for granted is not necessarily inevitable. Only a century ago, infectious diseases such as tuberculosis and nutrient deficiencies were rife: for example, more than 90 per cent of infants in Northern Europe and the US had evidence of rickets. Ill health and high mortality at all ages were taken as a fact of life. We would not now find this acceptable. There is no good reason why the high rates of chronic disabling conditions now experienced in Britain cannot be reduced to the low levels we know are possible in some groups.
Kay-Tee Khaw is professor of clinical gerontology at the University of Oxford.