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Prenatal nutritional deficiency and risk of adult schizophrenia.
Schizophr Bull 2008; 34(6):1054-63SB

Abstract

Converging evidence suggests that a neurodevelopmental disruption plays a role in the vulnerability to schizophrenia. The authors review evidence supporting in utero exposure to nutritional deficiency as a determinant of schizophrenia. We first describe studies demonstrating that early gestational exposure to the Dutch Hunger Winter of 1944--1945 and to a severe famine in China are each associated with an increased risk of schizophrenia in offspring. The plausibility of several candidate micronutrients as potential risk factors for schizophrenia and the biological mechanisms that may underlie these associations are then reviewed. These nutrients include folate, essential fatty acids, retinoids, vitamin D, and iron. Following this discussion, we describe the methodology and results of an epidemiologic study based on a large birth cohort that has tested the association between prenatal homocysteine, an indicator of serum folate, and schizophrenia risk. The study capitalized on the use of archived prenatal serum specimens that make it possible to obtain direct, prospective biomarkers of prenatal insults, including levels of various nutrients during pregnancy. Finally, we discuss several strategies for subjecting the prenatal nutritional hypothesis of schizophrenia to further testing. These approaches include direct assessment of additional prenatal nutritional biomarkers in relation to schizophrenia in large birth cohorts, studies of epigenetic effects of prenatal starvation, association studies of genes relevant to folate and other micronutrient deficiencies, and animal models. Given the relatively high prevalence of nutritional deficiencies during pregnancy, this work has the potential to offer substantial benefits for the prevention of schizophrenia in the population.

Authors+Show Affiliations

College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, Mailman School of Public Health, New York, NY, USA. asb11@columbia.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18682377

Citation

Brown, Alan S., and Ezra S. Susser. "Prenatal Nutritional Deficiency and Risk of Adult Schizophrenia." Schizophrenia Bulletin, vol. 34, no. 6, 2008, pp. 1054-63.
Brown AS, Susser ES. Prenatal nutritional deficiency and risk of adult schizophrenia. Schizophr Bull. 2008;34(6):1054-63.
Brown, A. S., & Susser, E. S. (2008). Prenatal nutritional deficiency and risk of adult schizophrenia. Schizophrenia Bulletin, 34(6), pp. 1054-63. doi:10.1093/schbul/sbn096.
Brown AS, Susser ES. Prenatal Nutritional Deficiency and Risk of Adult Schizophrenia. Schizophr Bull. 2008;34(6):1054-63. PubMed PMID: 18682377.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prenatal nutritional deficiency and risk of adult schizophrenia. AU - Brown,Alan S, AU - Susser,Ezra S, Y1 - 2008/08/04/ PY - 2008/8/7/pubmed PY - 2009/2/4/medline PY - 2008/8/7/entrez SP - 1054 EP - 63 JF - Schizophrenia bulletin JO - Schizophr Bull VL - 34 IS - 6 N2 - Converging evidence suggests that a neurodevelopmental disruption plays a role in the vulnerability to schizophrenia. The authors review evidence supporting in utero exposure to nutritional deficiency as a determinant of schizophrenia. We first describe studies demonstrating that early gestational exposure to the Dutch Hunger Winter of 1944--1945 and to a severe famine in China are each associated with an increased risk of schizophrenia in offspring. The plausibility of several candidate micronutrients as potential risk factors for schizophrenia and the biological mechanisms that may underlie these associations are then reviewed. These nutrients include folate, essential fatty acids, retinoids, vitamin D, and iron. Following this discussion, we describe the methodology and results of an epidemiologic study based on a large birth cohort that has tested the association between prenatal homocysteine, an indicator of serum folate, and schizophrenia risk. The study capitalized on the use of archived prenatal serum specimens that make it possible to obtain direct, prospective biomarkers of prenatal insults, including levels of various nutrients during pregnancy. Finally, we discuss several strategies for subjecting the prenatal nutritional hypothesis of schizophrenia to further testing. These approaches include direct assessment of additional prenatal nutritional biomarkers in relation to schizophrenia in large birth cohorts, studies of epigenetic effects of prenatal starvation, association studies of genes relevant to folate and other micronutrient deficiencies, and animal models. Given the relatively high prevalence of nutritional deficiencies during pregnancy, this work has the potential to offer substantial benefits for the prevention of schizophrenia in the population. SN - 0586-7614 UR - https://www.unboundmedicine.com/medline/citation/18682377/Prenatal_nutritional_deficiency_and_risk_of_adult_schizophrenia_ L2 - https://academic.oup.com/schizophreniabulletin/article-lookup/doi/10.1093/schbul/sbn096 DB - PRIME DP - Unbound Medicine ER -