Psychiatry, genetics and pathography : a tribute to Eliot Slater / editors, Martin Roth, Valerie Cowie ; assisted by Brian Barraclough.

Date:
1979
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Licence: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)

Credit: Psychiatry, genetics and pathography : a tribute to Eliot Slater / editors, Martin Roth, Valerie Cowie ; assisted by Brian Barraclough. Source: Wellcome Collection.

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    6 PSYCHIATRY, GENETICS AND PATHOGRAPHY characteristic of children, the indicator will be an imperfect one. Some children of Huntington's patients may be fidgety for reasons other than the specific Huntington gene ... It makes sense to us to see whether a high risk hypothesis, genetic or environmental, works in schizophrenic families with¬ out arguing that it must work equally well in the general population. It is our contention that not all theories about the aetiology of schizophrenia are equally meritorious. As clinicians with a genetic bent and a Popperian conscience, we believe that the theories should be pushed to their limits and hazarded to refutation, or, at the least, made ready for testing. We are enthusiastic about, but not committed to, two different genetic theories each of which provides for important contributions from the environment broadly defined (Gottesman and Shields, 1967, 1972; Heston, 1970; Shields, 1971; Shields, Heston and Gottesman, 1975; Slater, 1958; Slater and Cowie, 1971). The balance of this paper shows the result of con¬ frontation and compromise between polygenic and monogenic orientations towards the aetiology of schizophrenia in the service of testability and refutation. Although we confidently expect our brethren in the fields of molecular biology and developmental gene¬ tics to administer the coup de grâce to the hydra-headed schizo¬ phrenia problem, their strategies will proceed most efficiently with guidance from psychiatric geneticist experienced in twin and family studies (cf Shields and Gottesman, 1973). Semantic Confusion versus Semantic Clarification Semantic and logical problems have plagued the concept of schizoidia from the beginning. Most troublesome has been the extent to which the concept implies a phenotypic resemblance to schizophrenia,* or a genotypic connection with it, or as Essen- Möller ( 1946) believed, both. We shall differentiate and define four uses of the term schizoid, three of which have no aetiological implications: Sd 1—Schizoid in the literal sense of resembling schizophrenia phenotypically but in a diluted fashion. This is how the word is used in the accepted diagnostic term schizoid personality, meaning shy, sensitive, aloof or eccentric (American Psychiatric Association, 1968; General Register Ofiice, 1968). It does not imply a genealogical or aetiological connection *It is in this sense that the concept has attracted the most attention. Scholarly reviews by Essen-Möller (1946) and by Planansky (1972) delineate much of the background against which our views should be considered. Despite the criticisms we level at the concept throughout this paper, we would not deny the heuristic value already proved for the term schizoid as a powerful explanatory variable in the hands of some investigators for some kinds of research closely related to our interests (e.g. / 0degaard, 1946, and Stevens, 1969).
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