By David S. Segal, Joel Yager and John L Sullivan (Auth.)
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Extra resources for Foundations of Biochemical Psychiatry
This factor might help to ex plain an all too frequent phenomenon in schizophrenia research—the failure of dif ferent investigators, using the same research design, to obtain the same, or even similar, results. Another significant problem in this re search area is that of attempting to mea sure changes in brain biochemistry through the analysis of peripheral tissue or body fluids. Although the presumed site of origin of the schizophrenic process is in the brain, the biochemist usually can only measure secondary (plasma) or tertiary (urine) parameters as an index of what is occur ring in brain tissue.
E. W. Reed and S. C. Reed, Mental Retardation: A Family Study (Saunders, Philadelphia, 1965). 18. P. E. Meehl, Amer. Psychol. 17, 827 (1962). 19. E. , Suppl. No. 23 (1941). 20. P. , Suppl. No. 171 (1963). 21. W. Pollin, J. R. Stabenau, J. Tupin, Psychiatry 28, 60 (1965). 22. T. Lidz, S. Fleck, A. Cornelison, Schizophrenia and the Family (International Universities Press, New York, 1966). 23. I. I. Gottesman and J. Shields, Brit. J. Psychiat. 112,809 (1966). 24. Ö. , Suppl. No. 169 (1963), p. 94.
Pol ygenic modifiers of a single main gene ex plain the same facts, and indeed would yield the same mathematical results as sim ple additive polygenic theory per se. A multitude of genes summating to produce schizophrenia directly or a single main gene plus groups of genes summating to produce modifying traits account equally well for findings such as the tendency of monozygotic twins to be concordant with respect to severity of illness. Conclusion A main gene of large effect modified by multiple factors, including polygenic traits, suggests a number of testable hypotheses.