Document Detail

Perinatal choline effects on neonatal pathophysiology related to later schizophrenia risk.
MedLine Citation:
PMID:  23318559     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Deficient cerebral inhibition is a pathophysiological brain deficit related to poor sensory gating and attention in schizophrenia and other disorders. Cerebral inhibition develops perinatally, influenced by genetic and in utero factors. Amniotic choline activates fetal α7-nicotinic acetylcholine receptors and facilitates development of cerebral inhibition. Increasing this activation may protect infants from future illness by promoting normal brain development. The authors investigated the effects of perinatal choline supplementation on the development of cerebral inhibition in human infants.
METHOD: A randomized placebo-controlled clinical trial of dietary phosphatidylcholine supplementation was conducted with 100 healthy pregnant women, starting in the second trimester. Supplementation to twice normal dietary levels for mother or newborn continued through the third postnatal month. All women received dietary advice regardless of treatment. Infants' electrophysiological recordings of inhibition of the P50 component of the cerebral evoked response to paired sounds were analyzed. The criterion for inhibition was suppression of the amplitude of the second P50 response by at least half, compared with the first response.
RESULTS: No adverse effects of choline were observed in maternal health and delivery, birth, or infant development. At the fifth postnatal week, the P50 response was suppressed in more choline-treated infants (76%) compared with placebo-treated infants (43%) (effect size=0.7). There was no difference at the 13th week. A CHRNA7 genotype associated with schizophrenia was correlated with diminished P50 inhibition in the placebo-treated infants, but not in the choline-treated infants.
CONCLUSIONS: Neonatal developmental delay in inhibition is associated with attentional problems as the child matures. Perinatal choline activates timely development of cerebral inhibition, even in the presence of gene mutations that otherwise delay it.
Randal G Ross; Sharon K Hunter; Lizbeth McCarthy; Julie Beuler; Amanda K Hutchison; Brandie D Wagner; Sherry Leonard; Karen E Stevens; Robert Freedman
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Publication Detail:
Type:  Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of psychiatry     Volume:  170     ISSN:  1535-7228     ISO Abbreviation:  Am J Psychiatry     Publication Date:  2013 Mar 
Date Detail:
Created Date:  2013-03-01     Completed Date:  2013-04-15     Revised Date:  2014-11-14    
Medline Journal Info:
Nlm Unique ID:  0370512     Medline TA:  Am J Psychiatry     Country:  United States    
Other Details:
Languages:  eng     Pagination:  290-8     Citation Subset:  AIM; IM    
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MeSH Terms
Attention / drug effects*,  physiology*
Brain / drug effects*,  physiopathology*
Child, Preschool
Choline / physiology*
DNA Mutational Analysis
Electroencephalography / drug effects
Follow-Up Studies
Genetic Predisposition to Disease / genetics
Infant, Newborn
Neural Inhibition / drug effects*,  physiology*
Nootropic Agents / administration & dosage*
Perinatal Care
Phosphorylcholine / administration & dosage*
Randomized Controlled Trials as Topic
Receptors, Nicotinic / genetics
Schizophrenia / drug therapy*,  genetics,  physiopathology*
Sensory Gating / drug effects*,  physiology*
Signal Processing, Computer-Assisted
alpha7 Nicotinic Acetylcholine Receptor
Grant Support
Reg. No./Substance:
0/Chrna7 protein, human; 0/Nootropic Agents; 0/Receptors, Nicotinic; 0/alpha7 Nicotinic Acetylcholine Receptor; 107-73-3/Phosphorylcholine; N91BDP6H0X/Choline
Comment In:
Am J Psychiatry. 2013 Mar;170(3):245-7   [PMID:  23450283 ]
Erratum In:
Am J Psychiatry. 2013 May 1;170(5):566

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