Genetics, environment and psychopathology / editors, Sarnoff A. Mednick [and others].
- Date:
- 1974
Licence: Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
Credit: Genetics, environment and psychopathology / editors, Sarnoff A. Mednick [and others]. Source: Wellcome Collection.
33/364 page 17
![Research on etiology of schizophrenia 17 associative variables that markedly distinguish the premorbid state of a group that later suffered breakdown, but we cannot be sure that any of these variables are, or are closely related to, primary causal agents. They certainly help define areas which should be further studied. But correcting all or any of these deviances in our breakdown subjects [. . . ] may not have circumvented their eventual breakdown if the breakdown sprang from inherited or acquired biochemical anomalies, early behavioral experiences, interim life experiences [...], or ля interaction of all or some of these factors. The maternal, physiological, and associative variables may only be epiphenomena of the primary etiological factors or epiphenomena of a very early undetected stage of schizophrenia. Again we must face the fact that research which does not involve experimental manipulation is correlative and has difficulty producing conclusions relating to causation. The high-risk-group method does provide us with suggestion re¬ garding areas worthy of exploration. A key to the exploitation of these suggestive leads lies in the italicized sentence above. The same moral code which bars scientists from attempting to experimentally mani¬ pulate the lives of humans so as to cause them to become schizophrenic would only encourage and support reasonable attempts at experimental manipulations which were aimed at reducing the incidence of break¬ down. Positive results in such research would certainly warrant the construction of conclusions concerning the causes of reduction of inci¬ dence of schizophrenia. These results, however, would not by themselves warrant conclusions concerning the etiology of schizophrenia. (We may be able to pinpoint the administration of penicillin as a cure for an illness without detailed and specific knowledge of the cause of the illness.) However, if preventive research tells us that administration of a given drug or a given mothering experience (or combination of the two) will materially reduce the incidence of schizophrenia, we can begin to deduce causes of schizophrenia with more precision and under¬ take more focused and discriminating preventive research eventually leading to firmly based etiological conclusions. The great conceptual problem facing the prospective research worker in the area of prevention is, What justification can be found for choice of mode of intervention? It is in this area that the high-risk- group method can make its contribution. Premorbid and experiential or personal deviancies detected in high-risk samples which have suffered](https://iiif.wellcomecollection.org/image/b18032618_0034.JP2/full/800%2C/0/default.jpg)
