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Genetic and environmental influences on premenstrual symptoms in an Australian twin sample

Published online by Cambridge University Press:  05 February 2002

S. A. TRELOAR ,
A. C. HEATH  and
N. G. MARTIN
S. A. TRELOAR
Affiliation:
From Queensland Institute of Medical Research and Joint Genetics Program, University of Queensland, Brisbane, Queensland, Australia; and Missouri Alcoholism Research Center, Department of Psychiatry, Washington University School of Medicine, St Louis MO, USA
A. C. HEATH
Affiliation:
From Queensland Institute of Medical Research and Joint Genetics Program, University of Queensland, Brisbane, Queensland, Australia; and Missouri Alcoholism Research Center, Department of Psychiatry, Washington University School of Medicine, St Louis MO, USA
N. G. MARTIN
Affiliation:
From Queensland Institute of Medical Research and Joint Genetics Program, University of Queensland, Brisbane, Queensland, Australia; and Missouri Alcoholism Research Center, Department of Psychiatry, Washington University School of Medicine, St Louis MO, USA
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Abstract

Background. We aimed to explore the prevalence and factor structure of premenstrual symptoms in a sample of Australian twins; to investigate phenotypic associations between reported premenstrual symptoms, personality and reproductive dimensions; and to identify the relative contributions of genes and environment to premenstrual symptoms and the extent of genetic and environmental covariation with the personality trait Neuroticism and lifetime major depression.

Method. Seven hundred and twenty female twin pairs (454 monozygotic and 266 dizygotic) from the Australian National Health and Medical Research Council Twin Register reported on experience of 17 premenstrual symptoms during the previous 12 months. In the same questionnaire twins also responded to questions on symptom states, and personality dimensions including neuroticism. Interview data enabling diagnosis of lifetime history of DSM-IV major depression were also available. We fitted univariate and multivariate genetic models to the data.

Results. Most frequently reported symptoms were breast tenderness/pain and bloating/weight gain, followed by affective symptoms. Twelve-month prevalence was 2·4% for the combination of symptoms and functional interference meeting a very rough approximation of DSM-III-R criteria for late luteal dysphoric disorder. Principal factor analysis identified a single premenstrual (PMS) factor. Additive genetic influences (44% of total variance) were identified for PMS. Although we found genetic correlations of 0·62 between reported PMS and neuroticism, and 0·70 with lifetime major depression, 39% of the genetic variance of PMS was not explained by these factors.

Conclusions. Our findings support the existence of genetic influences on premenstrual symptoms, but we were unable to distinguish between liability to symptom experience and symptom reporting. Retrospective reporting may have contributed to our finding that PMS genes were shared in part with neuroticism and liability to lifetime major depression.

Type
Original Article
Information
Psychological Medicine , Volume 32 , Issue 1 , January 2002 , pp. 25 - 38
Copyright
© 2002 Cambridge University Press

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