tween identifying dietary risk factors for single diseases and determining how these risk factors influence the spectrum of chronic diseases and conditions, including atherosclerotic cardiovascular diseases, hypertension, obesity, cancer, osteoporosis, diabetes mellitus, hepatobiliary disease, and dental caries. The report complements and extends past efforts of government agencies and voluntary health and other scientific organizations by presenting an in-depth analysis of the overall relationship between diet and the major chronic diseases (e.g., AHA, 1988; DHHS, 1988; NRC, 1982; USDA, 1985; USDA/DHHS, 1980).
In the foregoing chapters, the committee reviews the evidence on all major public health conditions in which diet is believed to play an important role. In this chapter, it presents its overall conclusions about the effect of nutrients, foods and food groups, and dietary patterns on chronic diseases.
In Chapter 2, the committee presents criteria for assessing the data from single studies and explains the process for evaluating the cumulative evidence. The committee first considers the special strengths and weaknesses of each kind of epidemiologic and laboratory study on diet and chronic diseases and then evaluates the total evidence against the commonly used criteria for assessing causality, i.e., strength of association, dose-response relationship, temporally correct association, consistency of association, specificity of association, and biologic plausibility. It emphasizes, however, that these criteria alone do not define acceptability of the evidence.
Special attention is given to dietary interactions and competing risks, which are important considerations both for arriving at conclusions and for formulating dietary recommendations. For example, although diets containing high levels of plant foods have been associated with a lower risk of certain cancers, such diets, because of their high fiber content, could in principle initially inhibit the absorption of essential minerals such as calcium, thereby possibly enhancing other risks. Such potential competing risks and dietary interactions were considered in drawing the conclusions presented in this chapter.
The committee recognizes that genetically dependent variability among individuals and variability due to age, sex, and physiological status may affect physiological requirements for nutrients as well as responses to dietary exposures and, thus, the risk of chronic diseases. Therefore, to the extent possible, it addresses not only the risk to the general population, but also the feasibility of defining risks to subpopulations and individuals that may differ in susceptibility. Recognizing the limitations of the data on diet-disease relationships, the committee wishes to emphasize the necessarily interim nature of its conclusions.
Chapter 2 explains the many limitations to drawing conclusions about the association between dietary factors and chronic diseases. The term insufficient data could perhaps be applied to most issues concerning nutrition and health. In particular, it characterizes many of the relationships between diet and certain chronic diseases. The lack of certainty about causal associations and mechanisms of action is common and stems in part from attempts to relate a complex mixture such as diet to complex, multifactorial chronic diseases for which the pathophysiological, environmental, and genetic predisposing factors are imprecisely understood. Although this is a cause for concern, and therefore warrants further research (see Directions for Research in Chapter 28), it is not unusual in questions pertaining to human health.
In some cases, there is conclusive evidence that a particular dietary factor plays a role in the etiology of a particular chronic disease, but that is the exception rather than the rule. Despite such limitations, a large body of evidence has emerged in the past four decades concerning chronic diseases and their relationship to general dietary patterns or specific dietary components.
The strengths and limitations of different types of studies in humans and the methods of assessing dietary intake in such studies are described in Chapter 2. In general, the accuracy of assessing dietary intake is limited by the need to rely on the subjects' memories, the potential for misclassification, the bias of the subject or the investigator, the difficulty of precisely quantifying dietary exposure in years past (which would reflect the long latency period of most chronic diseases), the difficulty of standardizing the methodology of data collection, variation in accuracy of recall between subjects and controls, the likelihood of dietary modification by subjects over time, and the limitations of food composition data.