Epidemiological research has been one of the mainstays of our understanding of nutrition.
There is a real worry thqt epidemiology can and may well bring our science into redicule. Valid statistically identified risk factors are pumped up into “well known facts”. So often one will hear a nutritionist being interviewed on the media and say, “my study shows that an excess of ********** , is a real aetiological factor in the development of a condition”. Maybe. What are the probabilities or risk. Equal to smokig and cancer of the lung or sufficiently modest for most people to make a note and ignore with no health consequences.
There are three objectives for epidemiology:
• to describe the distribution and extent of disease problems in human populations
• to elucidate the aetiology of diseases
• to provide the information necessary to manage and plan services for the prevention, control and treatment of disease
What is being studied must be carefully defined and the interpretation of the results of the study be within the framework of the original definition.
Nutritional epidemiology, in addition to the study of the nutritional determinants of disease, measures nutritional status in relation to environment and dietary intake. Most clinical measurements of nutritional status are used to identify deficiencies in overall intake or intake of individual nutrients.
The great nutritional studies of the 19th and early part of the 20th century led to the discovery of dietary deficiencies in the form of beri-beri, goitre, pellagra, rickets, scurvy and xerophthalmia. These spectacular discoveries led to the concept of single dietary factors in the aetiology of disease. There is an understandable desire to identify simple and singular causes of contemporary diseases. However, it is now apparent that the system is complex, with groups vulnerable to multiple other predisposing factors in addition to nutritional factors, for example infection, activity levels and individual genetic variation. Furthermore, only a proportion of individuals who are at risk develop the particular nutritional problems under study.
Reaching rapid conclusions on the basis of epidemiological associations all too frequently mars the reputation of nutrition as a science, and delays identification of processes. Many recorded associations may not be causative of the condition ; instead, they are markers for the net effect of many variables that influence morbidity and mortality ( post hoc, non ergo propter hoc : after this, not therefore on account of this, the tendency to confuse sequence with consequences)

Bradford Hill suggested nine points which may suggest causality:
1. strength of association
2. consistency
3. specificity
4. relationship in time
5. biological gradient
6. biological plausibility
7. coherence of evidence
8. experimental evidence
9. analogy
He set out the conditions which had to be met before it could be concluded that an association observed, in a case-controlled study could be interpreted as indicating cause and effect:
• there should be no bias in the selection of subjects and controls, in the way that subjects and controls reported their histories or in the way that interviewers recorded data
• that there is an appropriate time interval between exposure to the suspected agent and the development of the disease
• the lack of any other distinction between the affected subjects and their controls that could account for the observed association or of any common factor that could lead both to the specific exposure and the development of the disease.
The proof of the pudding must be confirmation by clinical trials. The observation that protection from cancer was given by fruit and vegetables lead to large scale clinical trials using fibre, vitamin and trace element supplements. The benefits were negligible if at all. This still leaves the evidence that fruit and vegetables are helpful and why has still to be explained.

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www.nutrition-nutritionists.com

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Martin Eastwood

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