The British Journal of Psychiatry (2007) 190: 156-161. doi: 10.1192/bjp.bp.106.024943
© 2007 The Royal College of Psychiatrists
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Cancer risk among parents and siblings of patients with schizophrenia

ITZHAK LEVAV, MD, MSc

Mental Health Services

IRENA LIPSHITZ, MA

Cancer Registry, Ministry of Health, Jerusalem

ILYA NOVIKOV, PhD

Gertner Institute, Tel Hashomer Hospital, Tel Hashomer

INNA PUGACHOVA, BSc

Department of Information and Evaluation, Mental Health Services, Ministry of Health, Jerusalem, Israel

ROBERT KOHN, MD, MPhil

Department of Psychiatry and Human Behavior, Brown University, Providence, Rhode Island, USA

MICHA BARCHANA, MD, MPH

Cancer Registry

A. PONIZOVSKY, MD, PhD

Mental Health Services, Ministry of Health, Jerusalem

HAIM WERNER, PhD

Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel

Correspondence: Dr Itzhak Levav, Ministry of Health, 2 Ben Tabai Street, Jerusalem 91010, Israel. Tel: +972 2 568 1429; fax: +972 2 672 5822; email: Itzhak.Levav{at}moh.health.gov.il

Declaration of interest None. Funding detailed in Acknowledgements.

Background A reduced risk of cancer has been noted among people with schizophrenia. Given that genetic causes have been proposed as an explanation of this finding, one would expect that the risk of cancer among first-degree relatives would be equally reduced.

Aims To investigate the risk of cancer among the biological parents and full siblings of people receiving in-patient care for schizophrenia.

Method Linkage analysis was conducted between national population, psychiatric and cancer databases. Standardised incidence ratios for all cancer sites were calculated by comparing the incident rates among first-degree relatives with national incidence rates.

Results A reduced cancer risk was found across all groups examined. Among parents, whose numbers were adequately large, the findings reached statistical significance. For index cases and siblings – a markedly younger population – only a trend was elicited.

Conclusions The genetic hypothesis – namely, the presence of a gene with the dual effect of reducing the cancer risk and disrupting neurodevelopment – is a plausible explanation for these findings.


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