How epidemiologists think

We can now look back on the strategies used to find causes of mental disorders and how epidemiologists go about the task. To find aetiological clues, they looks for links. This is best done by working not with individual patients, nor even with series of patients in one clinic. Instead it is better to have data that represent all cases of a disorder in a defined population. Anything short of that could well be biased, in that the data would fail to represent all occurrences. Then one can start to ask questions that may throw light on aetiology.

1. Is there a gender difference in prevalence, or if the data are available, in incidence? If there is, one gender may carry greater biological susceptibility; or may be exposed to more of some environmental factor.

2. Does incidence vary regionally, or between contrasted environments, or between different socioeconomic groups? If there is little variation, it suggests that environmental factors may play little part in the aetiology.

3. If persons who have the disorder are compared with those who do not, have the cases been exposed to some environmental factor more often than the controls?

Each of these questions leads to a testable hypothesis.

The way in which a candidate risk factor comes to be proposed is itself very interesting. There are three types.

1. The inspired hypothesis A sharp-eyed clinician develops the idea that some factor—in any of the three domains—is present more often than by chance in a certain disorder; and that that factor may contribute to the onset of the disorder. This is exactly what happened to the ophthalmologist Sir Norman Gregg in Sydney when he noticed that many disabled children had mothers who had contracted rubella during the pregnancy. The association was later confirmed and shown to be causal. So here a hypothesis arising in the course of clinical work was taken out of the clinic and tested by epidemiological methods, then the knowledge applied in prevention.

2. A coarse observation A second pathway to a hypothesis starts with a coarse observation of a link between a disorder and, say, some demographic variable. In the aetiology of schizophrenia, a slight excess in winter birthdates was noticed in persons who later developed schizophrenia. This has led to others over the years, such as the possible excess of schizophrenia in the offspring of women who had influenza during the second trimester of their pregnancy. One study reported an increased risk in the female offspring of women who were pregnant during the Dutch Famine of 1944 to 1945. (96) Work on the 1946 birth cohort in Britain has yielded the important finding that persons who later developed schizophrenia had been recorded as children to have had more speech and educational problems, more social anxiety, and a preference for solitary play. (97> From the simple observation of a slight excess of winter births in schizophrenia, a series of other studies have followed, all based on a neurodevelopmental hypothesis. These are far removed from the hypothesis about 'schizophrenogenic' families so seriously espoused only three decades ago.

3. The enquiry is theory driven A good example is what came from attachment theory. The hypothesis was that if a close affectional relationship were not experienced in childhood, the individual would be vulnerable to depression and anxiety in adult life. In epidemiological research on Alzheimer's disease, it was theory that led to a search for putative risk factors such as a family history of Down syndrome, aluminium in drinking water, maternal age at the patient's birth, and a history of previous head injury. It was also theory that led Jenkinson et al.(98) to find an inverse association between Alzheimer's disease and rheumatoid arthritis. This subsequently led to studies of people who had been treated with long-term anti-inflammatory drugs. Breitner's conclusion is that they probably have a lower probability of developing Alzheimer's disease.(99)

4. A matrix All these three approaches can be brought together, then used as the building material to construct a matrix. This can then drive a systematic search. In Ia.bJe..4, the main categories of mental disorders are listed across the top to form the columns, while the rows are made up of those variables that may contribute to the onset or course of morbidity. The matrix proves to be a tidy way of organizing what information is already available; but it also acts heuristically by proposing associations that call for investigation but might not otherwise have been considered. The variables can be placed in categories: sociodemographic, experiential, intrapersonal (psychological), and biological. The alert observer will notice that the matrix has one limitation: it is in only two dimensions and therefore does not display the interactions between two or more variables, yet these can be of the greatest importance. Basic examples are the indisputable interaction between age and gender in the onset of schizophrenia; or the possible interaction between head injury and having the apolipoproteinE e4 allele. To think about such interactions, users of the matrix need to select their own combinations in, or expand it by adding other disorders or putative risk factors.

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