4. Diet, nutrition and chronic diseases in context:
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4.3 Interactions between early and later factors throughout the life course
Low birth weight, followed by subsequent adult obesity, has been shown to impart a particularly high risk of CHD (120, 121), as well as diabetes (18). Risk of impaired glucose tolerance has been found to be highest in those who had low birth weight, but who subsequently became obese as adults (18). A number of recent studies (12, 13, 25, 59-61, 120) have demonstrated that there is an increased risk of adult disease when IUGR is followed by rapid catch-up growth in weight and height. Conversely, there is also fairly consistent evidence of higher risk of CHD, stroke, and probably adult onset diabetes with shorter stature (122, 123). Further research is needed to define optimal growth in infancy in terms of prevention of chronic disease. A WHO multicentre growth reference study (124) currently under way may serve to generate much needed information on this matter.
4.3.1 Clustering of risk factors
Impaired glucose tolerance and an adverse lipid profile are seen as early as childhood and adolescence, where they typically appear clustered together with higher blood pressure and relate strongly to obesity, in particular central obesity (76, 78, 125, 126). Raised blood pressure, impaired glucose tolerance and dyslipidaemia also tend to be clustered in children and adolescents with unhealthy lifestyles and diets, such as those with excessive intakes of saturated fats, cholesterol and salt, and inadequate intake of fibre. Lack of exercise and increased television viewing add to the risk (10). In older children and adolescents, habitual alcohol and tobacco use also contribute to raised blood pressure and to the development of other risk factors in early adulthood. Many of the same factors continue to act throughout the life course. Such clustering represents an opportunity to address more than one risk at a time. The clustering of health-related behaviours is also a well described phenomenon (127).
4.3.2 Intergenerational effects
Young girls who grow poorly become stunted women and are more likely to give birth to low-birth-weight babies who are then likely to continue the cycle by being stunted in adulthood, and so on (128). Maternal birth size is a significant predictor of a child’s birth size after controlling for gestational age, sex of the child, socioeconomic status, and maternal age, height and pre-pregnant weight (129). There are clear indications of intergenerational factors in obesity, such as parental obesity, maternal gestational diabetes and maternal birth weight. Low maternal birth weight is associated with higher blood pressure levels in the offspring, independent of the relation between the offspring’s own birth weight and blood pressure (7). Unhealthy lifestyles can also have a direct effect on the health of the next generation, for example, smoking during pregnancy (9, 130).
4.4 Gene-nutrient interactions and genetic susceptibility
There is good evidence that nutrients and physical activity influence gene expression and have shaped the genome over several million years of human evolution. Genes define opportunities for health and susceptibility to disease, while environmental factors determine which susceptible individuals will develop illness. In view of changing socioeconomic conditions in developing countries, such added stress may result in exposure of underlying genetic predisposition to chronic diseases. Gene-nutrient interactions also involve the environment. The dynamics of the relationships are becoming better understood but there is still a long way to go in this area, and also in other aspects, such as disease prevention and control. Studies continue on the role of nutrients in gene expression; for example, researchers are currently trying to understand why omega-3 fatty acids suppress or decrease the mRNA of interleukin, which is elevated in atherosclerosis, arthritis and other autoimmune diseases, whereas the omega-6 fatty acids do not (131). Studies on genetic variability to dietary response indicate that specific genotypes raise cholesterol levels more than others. The need for targeted diets for individuals and subgroups to prevent chronic diseases was acknowledged as being part of an overall approach to prevention at the population level. However, the practical implications of this issue for public health policy have only begun to be addressed. For example, a recent study of the relationship between folate and cardiovascular disease revealed that a common single gene mutation that reduces the activity of an enzyme involved in folate metabolism (MTHFR) is associated with a moderate (20%) increase in serum homocysteine and higher risk of both ischaemic heart disease and deep vein thrombosis (132).
Although humans have evolved being able to feed on a variety of foods and to adapt to them, certain genetic adaptations and limitations have occurred in relation to diet. Understanding the evolutionary aspects of diet and its composition might suggest a diet that would be consistent with the diet to which our genes were programmed to respond. However, the early diet was presumably one which gave evolutionary advantage to reproduction in the early part of life, and so may be less indicative of guidance for healthy eating, in terms of lifelong health and prevention of chronic disease after reproduction has been achieved. Because there are genetic variations among individuals, changes in dietary patterns have a differential impact on a genetically heterogeneous population, although populations with a similar evolutionary background have more similar genotypes. While targeted dietary advice for susceptible populations, subgroups or individuals is desirable, it is not feasible at present for the important chronic diseases considered in this report. Most are polygenic in nature and rapidly escalating rates suggest the importance of environmental change rather than change in genetic susceptibility.
4. Diet, nutrition and chronic diseases in context:
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