Midlife alcohol consumption and later life cognitive impairment: Light drinking is not protective and APOE genotype does not change this relationship.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2022
Historique:
received: 05 10 2021
accepted: 12 02 2022
entrez: 11 3 2022
pubmed: 12 3 2022
medline: 27 4 2022
Statut: epublish

Résumé

Much debate exists about the role of light to moderate alcohol intake and subsequent cognitive function. The apolipoprotein E genotype may modify the relationship. Using data from the Honolulu-Asia Aging Study, a longitudinal population-based cohort (n = 2,416), Cox proportional hazards regression analyses were performed to measure midlife alcohol intake (average age = 52 years) and later life cognitive function (average age = 87 years) and to explore the role of apolipoprotein E genotype. No protective effect of light drinking (>1 drink/month- 1 drink/day) or moderate drinking (>1-2 drinks/day) was observed in the cohort in adjusted models (HR = 1.013, CI:0.88-1.16; HR = 1.104, CI:0.91-1.34, respectively). Heavy drinking (>2-4 drinks/day) and very heavy drinking (>4 drinks/day) increased the risk for incident moderate cognitive impairment (HR = 1.355, CI:1.09-1.68; HR = 1.462, CI:1.04-2.05, respectively). When examining the relationship by apolipoprotein E ε4 carrier status, a similar dose-response pattern was observed in both groups with higher hazard ratios for those carrying at least one copy of the apolipoprotein E ℇ4 allele. As alcohol level increased, the age at incident moderate cognitive impairment decreased, especially among those with at least one apolipoprotein E ℇ4 allele. We did not observe a significant protective effect for light to moderate drinking in midlife and subsequent cognitive impairment in this cohort. Heavy drinking increased the risk for moderate cognitive impairment and decreased the age at incidence, as did carrying at least one allele of the apolipoprotein E ℇ4 gene.

Identifiants

pubmed: 35275952
doi: 10.1371/journal.pone.0264575
pii: PONE-D-21-32089
pmc: PMC8916616
doi:

Substances chimiques

ApoE protein, human 0
Apolipoprotein E4 0
Apolipoproteins E 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0264575

Subventions

Organisme : NIA NIH HHS
ID : UF1 AG053983
Pays : United States
Organisme : NIA NIH HHS
ID : UF1 AG057707
Pays : United States
Organisme : NIA NIH HHS
ID : RF1 AG056499
Pays : United States

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

E Julia Chosy (EJ)

Pacific Health Research and Education Institute, Honolulu, Hawaii, United States of America.

Steven Edland (S)

University of California at San Diego, La Jolla, California, United States of America.

Lenore Launer (L)

National Institute on Aging, National Institutes of Health, Bethesda, Maryland, United States of America.

Lon R White (LR)

Pacific Health Research and Education Institute, Honolulu, Hawaii, United States of America.

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Classifications MeSH