Long-term associations of cigarette smoking in early mid-life with predicted brain aging from mid- to late life.
Aging
PBAD
alcohol
imaging
longitudinal
smoking
Journal
Addiction (Abingdon, England)
ISSN: 1360-0443
Titre abrégé: Addiction
Pays: England
ID NLM: 9304118
Informations de publication
Date de publication:
Apr 2022
Apr 2022
Historique:
revised:
03
09
2021
received:
09
02
2021
accepted:
15
09
2021
pubmed:
5
10
2021
medline:
28
4
2022
entrez:
4
10
2021
Statut:
ppublish
Résumé
Smoking is associated with increased risk for brain aging/atrophy and dementia. Few studies have examined early associations with brain aging. This study aimed to measure whether adult men with a history of heavier smoking in early mid-life would have older than predicted brain age 16-28 years later. Prospective cohort observational study, utilizing smoking pack years data from average age 40 (early mid-life) predicting predicted brain age difference scores (PBAD) at average ages 56, 62 (later mid-life) and 68 years (early old age). Early mid-life alcohol use was also evaluated. Population-based United States sample. Participants were male twins of predominantly European ancestry who served in the United States military between 1965 and 1975. Structural magnetic resonance imaging (MRI) began at average age 56. Subsequent study waves included most baseline participants; attrition replacement subjects were added at later waves. Self-reported smoking information was used to calculate pack years smoked at ages 40, 56, 62, and 68. MRIs were processed with the Brain-Age Regression Analysis and Computation Utility software (BARACUS) program to create PBAD scores (chronological age-predicted brain age) acquired at average ages 56 (n = 493; 2002-08), 62 (n = 408; 2009-14) and 68 (n = 499; 2016-19). In structural equation modeling, age 40 pack years predicted more advanced age 56 PBAD [β = -0.144, P = 0.012, 95% confidence interval (CI) = -0.257, -0.032]. Age 40 pack years did not additionally predict PBAD at later ages. Age 40 alcohol consumption, but not a smoking × alcohol interaction, predicted more advanced PBAD at age 56 (β = -0.166, P = 0.001, 95% CI = -0.261, -0.070) with additional influences at age 62 (β = -0.115, P = 0.005, 95% CI = -0.195, -0.036). Age 40 alcohol did not predict age 68 PBAD. Within-twin-pair analyses suggested some genetic mechanism partially underlying effects of alcohol, but not smoking, on PBAD. Heavier smoking and alcohol consumption by age 40 appears to predict advanced brain aging by age 56 in men.
Sections du résumé
BACKGROUND AND AIMS
OBJECTIVE
Smoking is associated with increased risk for brain aging/atrophy and dementia. Few studies have examined early associations with brain aging. This study aimed to measure whether adult men with a history of heavier smoking in early mid-life would have older than predicted brain age 16-28 years later.
DESIGN
METHODS
Prospective cohort observational study, utilizing smoking pack years data from average age 40 (early mid-life) predicting predicted brain age difference scores (PBAD) at average ages 56, 62 (later mid-life) and 68 years (early old age). Early mid-life alcohol use was also evaluated.
SETTING
METHODS
Population-based United States sample.
PARTICIPANTS/CASES
METHODS
Participants were male twins of predominantly European ancestry who served in the United States military between 1965 and 1975. Structural magnetic resonance imaging (MRI) began at average age 56. Subsequent study waves included most baseline participants; attrition replacement subjects were added at later waves.
MEASUREMENTS
METHODS
Self-reported smoking information was used to calculate pack years smoked at ages 40, 56, 62, and 68. MRIs were processed with the Brain-Age Regression Analysis and Computation Utility software (BARACUS) program to create PBAD scores (chronological age-predicted brain age) acquired at average ages 56 (n = 493; 2002-08), 62 (n = 408; 2009-14) and 68 (n = 499; 2016-19).
FINDINGS
RESULTS
In structural equation modeling, age 40 pack years predicted more advanced age 56 PBAD [β = -0.144, P = 0.012, 95% confidence interval (CI) = -0.257, -0.032]. Age 40 pack years did not additionally predict PBAD at later ages. Age 40 alcohol consumption, but not a smoking × alcohol interaction, predicted more advanced PBAD at age 56 (β = -0.166, P = 0.001, 95% CI = -0.261, -0.070) with additional influences at age 62 (β = -0.115, P = 0.005, 95% CI = -0.195, -0.036). Age 40 alcohol did not predict age 68 PBAD. Within-twin-pair analyses suggested some genetic mechanism partially underlying effects of alcohol, but not smoking, on PBAD.
CONCLUSIONS
CONCLUSIONS
Heavier smoking and alcohol consumption by age 40 appears to predict advanced brain aging by age 56 in men.
Identifiants
pubmed: 34605095
doi: 10.1111/add.15710
pmc: PMC8904283
mid: NIHMS1764817
doi:
Types de publication
Journal Article
Observational Study
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
1049-1059Subventions
Organisme : NIA NIH HHS
ID : R01 AG059329
Pays : United States
Organisme : NIA NIH HHS
ID : P01 AG055367
Pays : United States
Organisme : NIA NIH HHS
ID : R56 AG037985
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG060470
Pays : United States
Organisme : NIA NIH HHS
ID : K01 AG063805
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG062483
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG037985
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG022381
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG050595
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2021 Society for the Study of Addiction.
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