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Jack M. McClellan, MD; Ezra Susser, MD, DrPH; Mary-Claire King, PhD

JAMA. 2006;296:582-584.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Schizophrenia is a debilitating neuropsychiatric disorder that likely stems from multiple genetic and environmental factors.¹ Identifying molecular mechanisms underlying schizophrenia offers the promise of improved treatment and prevention strategies. Finding culprit mutations and the genes that harbor them is therefore one of the great challenges of human genomics.

Studying populations who survived in utero exposure to maternal starvation may reveal clues regarding the genetic bases of schizophrenia. For example, epidemiological investigations of 2 famines in the 20th century—the Nazi-induced 1944-1945 Dutch Hunger Winter² and the Chinese famine of 1959-1961 following the failure of the Great Leap Forward³—demonstrated an increased risk for schizophrenia among offspring conceived in famine conditions. A possible molecular basis for this risk may be the occurrence of new mutations in genes critical for brain development. Furthermore, folate deficiency, which could occur in famine, may be . . . [Full Text of this Article]

Famine and Schizophrenia

Author Affiliations: Department of Psychiatry, University of Washington, Seattle (Dr McClellan); Department of Epidemiology, Mailman School of Public Health, Columbia University, and New York State Psychiatric Institute, New York (Dr Susser); and Departments of Genome Sciences and Medicine (Medical Genetics), University of Washington, Seattle (Dr King).

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