Birth Weight, Schizophrenia, and Adult Mental Disorder

Abel, Kathryn M.; Wicks, Susanne; Süsser, Ezra; Dalman, Christina; Pedersen, Marianne Bruus; Mortensen, Preben Bo; Webb, Roger T.

doi:10.1001/archgenpsychiatry.2010.100

Cited by 191 publications

(204 citation statements)

References 44 publications

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“…Because many of the frontotemporal regions where SA appears to be most sensitive to BW variation within MZ twins have been separately implicated in multiple common psychiatric disorders (42,43), our data also propose a potential neurodevelopmental mechanism for the observed association between normative BW variation in fullterm pregnancies and later risk for psychopathology (7).…”

Section: Modeling Prenatal Environmental Influences On Brain Developmentmentioning

confidence: 63%

Prenatal growth in humans and postnatal brain maturation into late adolescence

Raznahan

Greenstein²,

Lee³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

177

179

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Prenatal life encompasses a critical phase of human brain development, but neurodevelopmental consequences of normative differences in prenatal growth among full-term pregnancies remain largely uncharted. Here, we combine the power of a withinmonozygotic twin study design with longitudinal neuroimaging methods that parse dissociable components of structural brain development between ages 3 and 30 y, to show that subtle variations of the in utero environment, as indexed by mild birth weight (BW) variation within monozygotic pairs, are accompanied by statistically significant (i) differences in postnatal intelligence quotient (IQ) and (ii) alterations of brain anatomy that persist at least into late adolescence. Greater BW within the normal range confers a sustained and generalized increase in brain volume, which in the cortical sheet, is specifically driven by altered surface area rather than cortical thickness. Surface area is maximally sensitive to BW variation within cortical regions implicated in the biology of several mental disorders, the risk for which is modified by normative BW variation. We complement this near-experimental test of prenatal environmental influences on human brain development by replicating anatomical findings in dizygotic twins and unrelated singletons. Thus, using over 1,000 brain scans, across three independent samples, we link subtle differences in prenatal growth, within ranges seen among the majority of human pregnancies, to protracted surface area alterations, that preferentially impact later-maturing associative cortices important for higher cognition. By mapping the sensitivity of postnatal human brain development to prenatal influences, our findings underline the potency of in utero life in shaping postnatal outcomes of neuroscientific and public health importance.P renatal life encompasses a foundational and universally critical phase of human brain development. Consequently, research aimed at understanding how prenatal influences play out in later life cannot only illuminate mechanisms of fundamental importance to basic developmental neuroscience, but may also have public health implications.Exquisite sensitivity of the developing brain to prenatal environmental insults has been well established through experimental animal models (1). In humans, where experimental approaches are not feasible, numerous observational studies have linked frank insults during prenatal life [as indexed by premature delivery (2); abnormally low birth weight for gestational age (3); and maternal exposure to radiation (4) or starvation (5)], to altered postnatal brain development. However, by virtue of their relative rarity, such frank prenatal insults may be less impactful at the population level than more subtle variations of the in utero environment occurring among the uncomplicated pregnancies from which most people are born (6). Evidence that subtle alterations of the prenatal environment may have meaningful consequences for postnatal development in humans can be found in large-scale epidemiolog...

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Section: Modeling Prenatal Environmental Influences On Brain Developmentmentioning

confidence: 63%

Prenatal growth in humans and postnatal brain maturation into late adolescence

Raznahan

Greenstein²,

Lee³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

177

179

View full text Add to dashboard Cite

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“…In terms of schizophrenia risk, maternal infection such as influenza (where vaccination is available and safe), maternal malnutrition, anemia, smoking, and other factors that affect fetal growth are all potential avenues of primary prevention for many illnesses. Low birth weight and developmental delays have been associated with a range of poor outcomes over the life course, 89 not limited to psychoses, 90,91 but including hypertension, 92 diabetes mellitus, 93 poorer educational performance, 94 poorer employment prospects, and increases in common mental disorders. 95,96 None of these is specific to schizophrenia, though some may play an independent role in increasing risk.…”

Section: From the Crossroads To The Skies: Putative Prevention Stratementioning

confidence: 99%

The Prevention of Schizophrenia--What Can We Learn From Eco-Epidemiology?

Kirkbride

Jones

2010

Schizophrenia Bulletin

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The search for the causes of schizophrenia has predominantly originated from 2 research paradigms; genetics and epidemiology. While each approach has made important contributions to etiological understanding, neither has fully resolved the exact milieu of risk factors for schizophrenia, and there is growing recognition that several pathways to the onset of such disorders may exist. Eco-epidemiology offers an integrative framework to study schizophrenia etiology, incorporating multiple, interactive levels of causation, including genetic, epigenetic, individual, familial, community, and societal domains over the life course. In this article, we review the current evidence base, through the lens of eco-epidemiology, to determine whether it warrants the design and implementation of putative prevention strategies for schizophrenia. We argue that while there are potentially large public health gains available, we do not currently have sufficient empirical data to design effective prevention strategies. It will be important for the research community to more fully elucidate the likely multifactorial, multilevel, polygenetic, and ecoepidemiological basis of schizophrenia before we can design useful prevention strategies. We conclude by speculating on the forms effective strategies might take.

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“…Jones et al, 2 in a follow-up of the Northern Finland birth cohort, found a greater than 2-fold increased risk of schizophrenia for subjects with birth weight below 2500 g. In the largest such study to date, in which Abel et al 3 combined Danish and Swedish national population-based cohorts, a dose-response relationship between birth weight and schizophrenia spectrum disorders (SSD) was reported. Other studies, however, have been less conclusive, 2,4,5 with some effects either becoming attenuated or disappearing following control for potential confounders.…”

Section: Introductionmentioning

confidence: 99%