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Effect of illness expression and liability on familial associations of clinical and subclinical psychosis phenotypes

Authors

  • T. Lataster,

    Corresponding author
    1. South Limburg Mental Health Research and Teaching Network, Maastricht University Medical Centre, Maastricht, the Netherlands
    • Tineke Lataster, Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University Medical Centre, PO BOX 616, Maastricht, 6200 MD, the Netherlands.

      E-mail: t.lataster@maastrichtuniversity.nl

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    • These authors contributed equally to this work.
  • K. Verweij,

    1. Department of Psychiatry, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, Utrecht, the Netherlands
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    • These authors contributed equally to this work.
  • W. Viechtbauer,

    1. South Limburg Mental Health Research and Teaching Network, Maastricht University Medical Centre, Maastricht, the Netherlands
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  • GROUP

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    • GROUP authors are: René S. Kahn[2], Don H. Linszen[3], Jim van Os[1], Durk Wiersma[4], Richard Bruggeman[4], Wiepke Cahn[2], Lieuwe de Haan[3], Lydia Krabbendam[1], Inez Myin-Germeys[1].

Abstract

Objective

Given the familial influences on schizophrenia, it may be hypothesized that specific symptom domains also cluster within families, and that this applies to both clinical and subclinical levels of expression. This hypothesis was put to the test in a group of patients with a DSM-IV diagnosis of psychotic disorder together with their unaffected siblings, and a group of healthy sib-pairs.

Method

Subclinical positive, negative and depressive symptoms in relatives and healthy controls were assessed with the Community Assessment of Psychic Experiences (CAPE). Positive and negative schizotypy in relatives and controls was measured with the Structured Interview for Schizotypy–Revised. Multilevel linear regression analyses were conducted to investigate clustering of symptom dimensions within patient–relative sib-pairs (N = 811 pairs), healthy sib-pairs of affected families (N = 136 pairs) and healthy control sib-pairs (N = 58 pairs).

Results

Familial clustering of symptoms was found in all three groups. Effect sizes were largest in healthy control sib-pairs, smallest in patient–relative sib-pairs and intermediate in healthy sib-pairs of affected families.

Conclusion

Studies of sibling associations in genetic studies of psychometric expression of psychosis liability need to take into account the fact that the higher levels of background genetic risk and presence of diagnosed illness are inversely associated with sibling associations.

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