Diet, genes and disease: implications for nutrition policy

There is extensive evidence to show that there is considerable variation in diet and disease patterns in Europe and that many of the dietary patterns are predictive of chronic disease. Increasingly, there is evidence that this dietary effect is mediated by genetic background. The present paper examines the role of polymorphisms within three genes, those responsible for the synthesis of apoE, 5,10-methylenetetrahydrofolate reductase (MTHFR) and PPARgamma. There is clear evidence to support the concept that the diet-disease link is moderated by genetic variation. The paper then considers whether this moderating effect will have implications for dietary recommendations. In the formulation of dietary reference values it has long been recognized that these values cannot cover the needs of all individuals. By setting the upper level at the mean value +2 sd, the needs of 97.5% of the population are covered. Setting a hypothetical scenario of a nutrient requirement of 200 mg/d and a polymorphism with an allelic frequency in the general population in the range of 0, 10, 20 and 30% that causes an increased nutrient requirement of 25%, there was no evidence that the traditional approach requires revision. Whilst it is recognized that genetic variability may not influence population goals, genetic variability will have to be taken into account in the clinical nutrition management of disease. To knowingly assign a patient to life-long treatment with a diet that for genetic reasons will have no success is both unethical and uneconomical. Once accepted in clinical nutrition, the diet-gene interaction will filter into the prevention of disease in public health nutrition.