Abstract
Accumulating evidence suggests that chronic diseases, physical as well as neuropsychiatric,
may have their origins in early life. Alterations in fetal development have been reported
to be associated with an increased risk of subsequent cardiovascular and metabolic
disorders. This has been formulated as the fetal or developmental programming hypothesis.
Schizophrenia is a severe and chronic neuropsychiatric illness of teenage and adult
life. Birth cohort studies have reported low birth weight, delays in attaining motor
milestones, and deficits in premorbid cognitive and social functioning as factors
associated with, and possible risk factors for future schizophrenia. These provide
empirical support for the currently widely accepted neurodevelopmental hypothesis
of schizophrenia, where abnormalities in early brain development contribute to the
evolution of the disorder. Interference with brain development from infections in
early life is in line with a neurodevelopmental view of schizophrenia. Prenatal maternal
infections such as influenza have been linked with increased risk of both childhood
sub-clinical psychotic symptoms and adult schizophrenia. Prenatal maternal infections
can increase fetal exposure to excessive maternal glucocorticoids. This can reprogram
the hypothalamic-pituitary-adrenal axis leading to increased risk of several chronic
diseases including schizophrenia. In this review we focus on epidemiological and preclinical
studies concerning prenatal maternal influenza and risk of both childhood psychotic
symptoms and later development of schizophrenia in the offspring. We discuss these
findings in light of the fetal programming hypothesis, which points towards common
links, in early life, between chronic diseases, physical (such as hypertension and
type-two diabetes) and neuropsychiatric (such as schizophrenia).
Keywords
Schizophrenia - influenza - pregnancy - prenatal - infection - fetal programming -
chronic disease - childhood development
