A dose-response analysis of the effects of prenatal alcohol exposure on cognitive development.

cognitive function dose‐response fetal alcohol spectrum disorders fetal alcohol syndrome prenatal alcohol exposure

Journal

Alcohol, clinical & experimental research
ISSN: 2993-7175
Titre abrégé: Alcohol Clin Exp Res (Hoboken)
Pays: United States
ID NLM: 9918609780906676

Informations de publication

Date de publication:
30 Mar 2024
Historique:
revised: 01 02 2024
received: 16 05 2023
accepted: 07 02 2024
medline: 30 3 2024
pubmed: 30 3 2024
entrez: 30 3 2024
Statut: aheadofprint

Résumé

Most studies of the effects of prenatal alcohol exposure (PAE) on cognitive function have assumed that the dose-response curve is linear. However, data from a few animal and human studies suggest that there may be an inflection point in the dose-response curve above which PAE effects are markedly stronger and that there may be differences associated with pattern of exposure, assessed in terms of alcohol dose per drinking occasion and drinking frequency. We performed second-order confirmatory factor analysis on data obtained at school age, adolescence, and early adulthood from 2227 participants in six US longitudinal cohorts to derive a composite measure of cognitive function. Regression models were constructed to examine effects of PAE on cognitive function, adjusted for propensity scores. Analyses based on a single predictor (absolute alcohol (AA)/day) were compared with analyses based on two predictors (dose/occasion and drinking frequency), using (1) linear models and (2) nonparametric general additive models (GAM) that allow for both linear and nonlinear effects. The single-predictor GAM model showed virtually no nonlinearity in the effect of AA/day on cognitive function. However, the two-predictor GAM model revealed differential effects of maternal drinking pattern. Among offspring of infrequent drinkers, PAE effects on cognitive function were markedly stronger in those whose mothers drank more than ~3 drinks/occasion, and the effect of dose/occasion was strongest among the very frequent drinkers. Frequency of drinking did not appear to alter the PAE effect on cognitive function among participants born to mothers who limited their drinking to ~1 drink/occasion or less. These findings suggest that linear models based on total AA/day are appropriate for assessing whether PAE affects a given cognitive outcome. However, examination of alcohol dose/occasion and drinking frequency is needed to fully characterize the impact of different levels of alcohol intake on cognitive impairment.

Sections du résumé

BACKGROUND BACKGROUND
Most studies of the effects of prenatal alcohol exposure (PAE) on cognitive function have assumed that the dose-response curve is linear. However, data from a few animal and human studies suggest that there may be an inflection point in the dose-response curve above which PAE effects are markedly stronger and that there may be differences associated with pattern of exposure, assessed in terms of alcohol dose per drinking occasion and drinking frequency.
METHODS METHODS
We performed second-order confirmatory factor analysis on data obtained at school age, adolescence, and early adulthood from 2227 participants in six US longitudinal cohorts to derive a composite measure of cognitive function. Regression models were constructed to examine effects of PAE on cognitive function, adjusted for propensity scores. Analyses based on a single predictor (absolute alcohol (AA)/day) were compared with analyses based on two predictors (dose/occasion and drinking frequency), using (1) linear models and (2) nonparametric general additive models (GAM) that allow for both linear and nonlinear effects.
RESULTS RESULTS
The single-predictor GAM model showed virtually no nonlinearity in the effect of AA/day on cognitive function. However, the two-predictor GAM model revealed differential effects of maternal drinking pattern. Among offspring of infrequent drinkers, PAE effects on cognitive function were markedly stronger in those whose mothers drank more than ~3 drinks/occasion, and the effect of dose/occasion was strongest among the very frequent drinkers. Frequency of drinking did not appear to alter the PAE effect on cognitive function among participants born to mothers who limited their drinking to ~1 drink/occasion or less.
CONCLUSIONS CONCLUSIONS
These findings suggest that linear models based on total AA/day are appropriate for assessing whether PAE affects a given cognitive outcome. However, examination of alcohol dose/occasion and drinking frequency is needed to fully characterize the impact of different levels of alcohol intake on cognitive impairment.

Identifiants

pubmed: 38554140
doi: 10.1111/acer.15283
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NIAAA NIH HHS
ID : R01-AA025905
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA06966
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA09524
Pays : United States
Organisme : NIAAA NIH HHS
ID : P50 AA07606
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA06390
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA06666
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA14215
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA18116
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA08105
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA10108
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA13272
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA001455
Pays : United States
Organisme : NIDA NIH HHS
ID : R21 DA021034
Pays : United States

Informations de copyright

© 2024 Research Society on Alcohol.

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Auteurs

Joseph L Jacobson (JL)

Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan, USA.

Tugba Akkaya-Hocagil (T)

Department of Statistics and Actuarial Science, University of Waterloo, Waterloo, Ontario, Canada.

Sandra W Jacobson (SW)

Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan, USA.

Claire D Coles (CD)

Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia, USA.

Gale A Richardson (GA)

Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.

Heather Carmichael Olson (HC)

Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington, USA.

Nancy L Day (NL)

Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.

R Colin Carter (RC)

Department of Emergency Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York City, New York, USA.
Department of Pediatrics, Columbia University Vagelos College of Physicians and Surgeons, New York City, New York, USA.
Institute of Human Nutrition, Columbia University Vagelos College of Physicians and Surgeons, New York City, New York, USA.

Neil C Dodge (NC)

Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan, USA.

Khue-Dung Dang (KD)

School of Mathematics and Statistics, University of Melbourne, Parkville, Victoria, Australia.

Richard J Cook (RJ)

Department of Statistics and Actuarial Science, University of Waterloo, Waterloo, Ontario, Canada.

Louise M Ryan (LM)

School of Mathematical and Physical Sciences, University of Technology Sydney, Sydney, New South Wales, Australia.
ARC Centre of Excellence for Mathematical and Statistical Frontiers, University of Melbourne, Parkville, Victoria, Australia.

Classifications MeSH