Neurobiological plausibility of prenatal nutritional deprivation as a risk factor for schizophrenia

J Nerv Ment Dis. 1996 Feb;184(2):71-85. doi: 10.1097/00005053-199602000-00003.

Abstract

Emerging evidence indicates that schizophrenia may in some cases be a neurodevelopmental disorder, resulting in part from the effects of prenatal exposures. Studies by our group have focused attention on the potential role of prenatal nutritional deficiency as a potential etiological factor. Therefore, we sought to examine the biological plausibility of prenatal nutritional deprivation in the etiopathogenesis of schizophrenia. We conducted a review of the pertinent literature. Four lines of evidence support prenatal nutritional deficiencies as a plausible set of risk factors for schizophrenia: a) their effects are not incompatible with the epidemiology of schizophrenia; b) they have adverse effects on brain development; c) general malnutrition results in neuropathological anomalies of brain regions implicated in schizophrenia; and d) prenatal malnutrition affects maternal systems critical to the developing fetal nervous system. There is sufficient evidence to warrant further studies of prenatal nutritional deficits as risk factors for schizophrenia. A strategy for testing these hypotheses is outlined.

Publication types

  • Review

MeSH terms

  • Brain / embryology
  • Brain / growth & development
  • Female
  • Folic Acid Deficiency / complications
  • Humans
  • Infant, Newborn
  • Iodine / deficiency
  • Maternal Exposure
  • Nutrition Disorders / complications
  • Nutrition Disorders / epidemiology*
  • Pregnancy
  • Pregnancy Complications / epidemiology*
  • Prenatal Exposure Delayed Effects*
  • Risk Factors
  • Schizophrenia / epidemiology
  • Schizophrenia / etiology*
  • Stress, Psychological / complications
  • Stress, Psychological / epidemiology
  • Thyroid Hormones / deficiency
  • Zinc / deficiency

Substances

  • Thyroid Hormones
  • Iodine
  • Zinc