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Schizophrenia - Twin studies

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There have been a large number of studies of varying quality that have looked at the incidence of schizophrenia in twins.

Gottesman and Shields (1976)reviewed the results of 5 twin studies. They found that in monozygotic (MZ) twins there was a concordance rate of 35-58% compared with 9-26% amongst dizygotic (DZ) twins. They also found a concordance rate in MZ twins of 75-91% when the sample was restricted to the most severe form of schizophrenia. The milder forms had concordance rates of 17-33% suggesting there may be greater genetic loading with severe forms of schizophrenia.

Moldin (1998) reviewed twin studies published between 1920 and 1987 and found that concordance rates for monozygotic twins averaged 46%, even when reared in different families, whereas the concordance rates for dizygotic twins averaged only 14%

A recent review of the genetic evidence from twin studies has suggested a more than 28% chance of one identical twin obtaining the diagnosis if the other already has it[1] (see twin studies), but such studies are not noted for pondering the likelihood of similarities of social class and/or other socio-psychological factors between the twins.

The estimates of heritability of schizophrenia from twin studies varies a great deal, with some notable studies[2][3] showing rates as low as 11.0%–13.8% among monozygotic twins, and 1.8%–4.1% among dizygotic twins.

CautionsEdit

AssumptionsEdit

The twin studies have all assumed that the shared environmental effects for MZ and DZ twins are equal which may be incorrect.

Potential confounds in schizophrenia twin studiesEdit

It has been suggested that the shared life in the womb, in terms of chorionic status and placentation, may be a significant sources of biases in interpretation of twin data in concordance studies, resulting in possible overestimates of twin concordance and the heritability of schizophrenia.

For example, monochorionic MZ twins may be at additional risk for obstetric difficulties due to shared blood circulation,[ such as exposure to pathogens, abnormalities in cortisol or glucose levels,arteriovenous shunting, hypoxia, or excitotoxicity, all of which may impact on neural functioning and development. Such mechanisms provide ways in which such concordance could arise as a result of nongenetic factors

Methodological criticismsEdit

Some scientists criticize the methodology of the twin studies, and have argued that the genetic basis of schizophrenia is still largely unknown or open to different interpretations, for example see The Gene Illusion by Jay Joseph.


See alsoEdit

References & BibliographyEdit

  1. Torrey, E.F., Bowler, A.E., Taylor, E.H. & Gottesman, I. I (1994) Schizophrenia and manic depressive disorder. New York: Basic books. ISBN 0-465-07285-2
  2. Koskenvuo M, Langinvainio H, Kaprio J, Lonnqvist J, Tienari P (1984) Psychiatric hospitalization in twins. Acta Genet Med Gemellol (Roma), 33(2),321-32.
  3. Hoeffer A, Pollin W. (1970) Schizophrenia in the NAS-NRC panel of 15,909 veteran twin pairs. Archives of General Psychiatry, 1970 Nov; 23(5):469-77.

Key textsEdit

BooksEdit

  • Gottesman II & Shields J. (1982) .Schizophrenia, The Epigenetic Puzzle. New York: Cambridge University Press,
  • Torrey, E. F., Bowler, A. E.; Taylor, E. H.; and Gottesman, I. I. (1994). Schizophrenia and Manic-Depressive Disorder: The Biological Roots of Mental Illness as Revealed by the Landmark Study of Identical Twins. New York: Basic Books.

PapersEdit

  • Gottesman II & Shields J. (1976). A Critical review of recent adoption, twin and family studies of schizophrenia: Behavioural genetics perspectives. Schizophrenia Bulletin 2: 360-401.
  • Kety SS, Wender PH, Jacobsen B, Ingaham LJ, Jansson L, Faber B, Kinney DK. Mental illness in the biological and adoptive relatives of schizophrenic adoptees. Archives of General Psychiatry 1994 June; 51: 442-455.
  • Moldin, S. O. (1998).Sponsoring initiatives in the molecular genetics of mental disorders.In: Genetics and Mental Disorders : Report of the NIMH Genetics Workgroup. Bethesda, Md.: NIH 98-4268 1998. Note: Table 4.


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