Manual Nutrition and Alcohol: Linking Nutrient Interactions and Dietary Intake

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If special dietary requirements affect only very few people with an inborn error of metabolism, policy recommendations could legitimately ignore such outliers, since such people can be identified and treated by physicians. In many instances, however, the true extent of genetic variation is unknown. The frequency of genetic variants in enzymes and proteins and their effect on enzyme activity suggest that there may be great variations in nutritional requirements or in gene-nutrition interaction.

Genetic factors as they relate to nutrition must be considered individually.

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The role of genetics in relation to dietary lipids and CHD is one example. Many coronary events could be prevented if the entire population would reduce its cholesterol levels by decreasing saturated fat intake.

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Although individual risk reduction for those with "normal" cholesterol levels is relatively small, the total effect on the population would be considerable, because even small reductions in risk lead to a large public health benefit when the entire population is considered. This phenomenon of small effects in individuals, but a large impact on the population, has been termed the prevention paradox. A double-pronged strategy of case detection and individual management of those at high risk, together with a public health strategy to reduce cholesterol levels in the population as a whole, could therefore have large effects.

Currently, the adverse public health effects of obesity are well known. Thus it is appropriate to advise everyone to avoid obesity. In the future, it may be possible to identify those at particular risk of obesity from excess caloric intake and to focus special preventive efforts on this group i. For many diseases, there are substantial racial or ethnic differences in frequencies. Thus, a recommendation for a population subgroup may need to differ from that for the racial majority, though this may raise difficult policy questions because the recommendation can be easily misunderstood.

However, there are precedent examples unrelated to nutrition including greater screening for Tay-Sachs disease among Ashkenazi Eastern European Jews, thalassemia among Mediterranean and Southeast Asian populations, and sickle-cell disease among blacks. Problems can arise when a small group of persons is placed at high risk by a policy decision that would benefit the majority.

An especially poignant example relates to iron supplementation and its effect on people with hemochromatosis see section on Hemochromatosis. Public health policy designed to benefit the population without discernible risk to certain individuals or subgroups has many merit it is simple to implement, may cost less to society, and may benefit many people. As knowledge of genetic variation and its impact grows, it may be possible to direct recommendations to individuals, and it may no longer be necessary to assume the existence of an average person who can respond to general recommendations.

A more sophisticated form of disease prevention based on biologic variation will then be desirable. Genetic variability in biochemical processes is ubiquitous; every person is genetically unique.

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The relevance of this genetic individuality for nutrition and for the role of certain nutrients in disease causation requires much greater understanding. Their rarity makes them medical problems; they are not usually viewed as problems of nutrition that affect public health. Heterozygotes, or carriers, of these inborn errors are much more common in the population. The possible role of the carrier state in causing clinically manifest disease during periods of stress, infection and malnutrition, for example, requires more study. Most chronic diseases whose etiology and pathogenesis are influenced by nutritional factors have genetic determinants.

High blood pressure, obesity, hyperlipidemia, atherosclerosis, and various cancers appear to aggregate in families for genetic reasons rather than merely because of a common environment. Recommendations to avoid nutrient excesses that predispose to these diseases are therefore unlikely to apply to everyone in the same way, and poorly understood interactions between genetics and the environment often govern the outcome of suboptimal nutrition.

For most diseases, we lack the knowledge needed to identify susceptible genotypes by appropriate tests. For other conditions, however, such as the hyperlipidemias, we can already identify persons at high risk and concentrate specific medical efforts on this subpopulation. For conditions where specific tests are lacking but there is a strong family history of a given disease, appropriate preventive approaches can be tried for family members who have not yet been affected. With advances in knowledge, an increasing number of population subgroups will be found to be at higher, or lower, risk for one or another chronic disease because of their genetic makeup.

Specific recommendations directed at high-risk populations therefore will become possible and desirable. In the meantime, dietary recommendations directed at the entire population are appropriate for many conditions, even though different people will benefit unequally from such advice. As an example, a diet low in both fat and salt is likely to reduce disease incidence in the general population even though the beneficial effects for a given person may be small or nil.

This paradox explains some of the controversies between those who promote an approach based on attention to persons at high risk and those who support a more global public health approach.

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Both approaches are needed. The high-risk approach is most appropriate in medical practice. The population approach requires support by the media, the food industry, nutritionists and dietitians, the public health profession, and the medical profession. When using the population approach, however, one must guard against harming certain genetically variant persons. As we acquire a better understanding of genetics and it becomes increasingly possible to investigate genetic phenomena at a fundamental level, we will be able to conduct better studies to elucidate the exact role of genetic factors for each nutrient and.

As these roles become understood, the associations between genetic factors and the interactions between heredity and the environment will become clearer and may lead to the modification of current policies. For example, the basis of salt sensitivity in hypertension, hyperlipidemia, osteoporosis, hemochromatosis, NIDDM, alcoholism, and obesity are currently amenable to further study. Annest, J.

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