Lifetime marijuana use and epigenetic age acceleration: A 17-year prospective examination

This study was designed to assess links between lifetime levels of marijuana use and accelerated epigenetic aging. Prospective longitudinal study, following participants annually from age 13 to age 30. A community sample of 154 participants recruited from a small city in the Southeastern United Stat...

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Veröffentlicht in:Drug and alcohol dependence 2022-04, Vol.233, p.109363-109363, Article 109363
Hauptverfasser: Allen, Joseph P., Danoff, Joshua S., Costello, Meghan A., Hunt, Gabrielle L., Hellwig, Amanda F., Krol, Kathleen M., Gregory, Simon G., Giamberardino, Stephanie N., Sugden, Karen, Connelly, Jessica J.
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container_issue
container_start_page 109363
container_title Drug and alcohol dependence
container_volume 233
creator Allen, Joseph P.
Danoff, Joshua S.
Costello, Meghan A.
Hunt, Gabrielle L.
Hellwig, Amanda F.
Krol, Kathleen M.
Gregory, Simon G.
Giamberardino, Stephanie N.
Sugden, Karen
Connelly, Jessica J.
description This study was designed to assess links between lifetime levels of marijuana use and accelerated epigenetic aging. Prospective longitudinal study, following participants annually from age 13 to age 30. A community sample of 154 participants recruited from a small city in the Southeastern United States. Participants completed annual assessments of marijuana use from age 13 to age 29 and provided blood samples that yielded two indices of epigenetic aging (DNAmGrimAge and DunedinPoAm) at age 30. Additional covariates examined included history of cigarette smoking, anxiety and depressive symptoms, childhood illness, gender, adolescent-era family income, and racial/ethnic minority status. Lifetime marijuana use predicted accelerated epigenetic aging, with effects remaining even after covarying cell counts, demographic factors and chronological age (β’s = 0.32 & 0.27, p’s 
doi_str_mv 10.1016/j.drugalcdep.2022.109363
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Prospective longitudinal study, following participants annually from age 13 to age 30. A community sample of 154 participants recruited from a small city in the Southeastern United States. Participants completed annual assessments of marijuana use from age 13 to age 29 and provided blood samples that yielded two indices of epigenetic aging (DNAmGrimAge and DunedinPoAm) at age 30. Additional covariates examined included history of cigarette smoking, anxiety and depressive symptoms, childhood illness, gender, adolescent-era family income, and racial/ethnic minority status. Lifetime marijuana use predicted accelerated epigenetic aging, with effects remaining even after covarying cell counts, demographic factors and chronological age (β’s = 0.32 & 0.27, p’s < 0.001, 95% CI’s = 0.21–0.43 & 0.16–0.39 for DNAmGrimAge and DunedinPoAm, respectively). Predictions remained after accounting for cigarette smoking (β’s = 0.25 & 0.21, respectively, p’s < 0.001, 95% CI’s = 0.14–0.37 & 0.09–0.32 for DNAmGrimAge and DunedinPoAm, respectively). A dose-response effect was observed and there was also evidence that effects were dependent upon recency of use. Effects of marijuana use appeared to be fully mediated by hypomethylation of a site linked to effects of hydrocarbon inhalation (cg05575921). Marijuana use predicted epigenetic changes linked to accelerated aging, with evidence suggesting that effects may be primarily due to hydrocarbon inhalation among marijuana smokers. Further research is warranted to explore mechanisms underlying this linkage. •Lifetime levels of marijuana use predicted accelerated epigenetic aging.•Predictions remained even after accounting for cigarette smoking and a wide range of potential confounding variables.•Dose-response and recency of use effects were both observed.]]></description><identifier>ISSN: 0376-8716</identifier><identifier>EISSN: 1879-0046</identifier><identifier>DOI: 10.1016/j.drugalcdep.2022.109363</identifier><identifier>PMID: 35231715</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Acceleration ; Adolescent ; Adult ; Age ; Aging ; Blood tests ; Cannabis ; Child ; Childhood ; Children ; Cigarette smoking ; Cigarettes ; Demography ; Dosage effects ; Dose-response effects ; Epigenesis, Genetic ; Epigenetic aging ; Epigenetics ; Ethnic factors ; Ethnic groups ; Ethnicity ; Humans ; Hydrocarbons ; Inhalation ; Lifetime cannabis exposure ; Longitudinal Studies ; Marijuana ; Marijuana Smoking - epidemiology ; Marijuana Smoking - genetics ; Marijuana Use - epidemiology ; Mental depression ; Minority &amp; ethnic groups ; Minority Groups ; Prospective longitudinal assessment ; Prospective Studies ; Respiration ; Smoking</subject><ispartof>Drug and alcohol dependence, 2022-04, Vol.233, p.109363-109363, Article 109363</ispartof><rights>2022 Elsevier B.V.</rights><rights>Copyright © 2022 Elsevier B.V. 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Prospective longitudinal study, following participants annually from age 13 to age 30. A community sample of 154 participants recruited from a small city in the Southeastern United States. Participants completed annual assessments of marijuana use from age 13 to age 29 and provided blood samples that yielded two indices of epigenetic aging (DNAmGrimAge and DunedinPoAm) at age 30. Additional covariates examined included history of cigarette smoking, anxiety and depressive symptoms, childhood illness, gender, adolescent-era family income, and racial/ethnic minority status. Lifetime marijuana use predicted accelerated epigenetic aging, with effects remaining even after covarying cell counts, demographic factors and chronological age (β’s = 0.32 & 0.27, p’s < 0.001, 95% CI’s = 0.21–0.43 & 0.16–0.39 for DNAmGrimAge and DunedinPoAm, respectively). Predictions remained after accounting for cigarette smoking (β’s = 0.25 & 0.21, respectively, p’s < 0.001, 95% CI’s = 0.14–0.37 & 0.09–0.32 for DNAmGrimAge and DunedinPoAm, respectively). A dose-response effect was observed and there was also evidence that effects were dependent upon recency of use. Effects of marijuana use appeared to be fully mediated by hypomethylation of a site linked to effects of hydrocarbon inhalation (cg05575921). Marijuana use predicted epigenetic changes linked to accelerated aging, with evidence suggesting that effects may be primarily due to hydrocarbon inhalation among marijuana smokers. Further research is warranted to explore mechanisms underlying this linkage. •Lifetime levels of marijuana use predicted accelerated epigenetic aging.•Predictions remained even after accounting for cigarette smoking and a wide range of potential confounding variables.•Dose-response and recency of use effects were both observed.]]></description><subject>Acceleration</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Age</subject><subject>Aging</subject><subject>Blood tests</subject><subject>Cannabis</subject><subject>Child</subject><subject>Childhood</subject><subject>Children</subject><subject>Cigarette smoking</subject><subject>Cigarettes</subject><subject>Demography</subject><subject>Dosage effects</subject><subject>Dose-response effects</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetic aging</subject><subject>Epigenetics</subject><subject>Ethnic factors</subject><subject>Ethnic groups</subject><subject>Ethnicity</subject><subject>Humans</subject><subject>Hydrocarbons</subject><subject>Inhalation</subject><subject>Lifetime cannabis exposure</subject><subject>Longitudinal Studies</subject><subject>Marijuana</subject><subject>Marijuana Smoking - epidemiology</subject><subject>Marijuana Smoking - genetics</subject><subject>Marijuana Use - epidemiology</subject><subject>Mental depression</subject><subject>Minority &amp; ethnic groups</subject><subject>Minority Groups</subject><subject>Prospective longitudinal assessment</subject><subject>Prospective Studies</subject><subject>Respiration</subject><subject>Smoking</subject><issn>0376-8716</issn><issn>1879-0046</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>7QJ</sourceid><recordid>eNqFUU1P3DAQtVARbIG_UFnqOVt_JLbTQyWKoEVaiQscOFmz9mRxtOsEJ1mVf1_D8nliLiPNvHkzbx4hlLM5Z1z9aOc-TStYO4_9XDAhcrmWSu6RGTe6Lhgr1RcyY1KrwmiuDsnXYWhZDlWzA3IoKyG55tWM3C5Cg2PYIN1ACu0EEeg0IIXoKfZhhTF3HYVVLjmHa0wwhi7-pKeU6-IBIdE-dUOPbgxbpPgPNiE-QY7JfgPrAU-e8xG5uTi_PvtbLK7-XJ6dLgpXMT0WwnNhvOSqriQvHa8RG6jrhjXlUpuyWhoPwpQaoXHgUSw9Gml8KbSHpsw6jsivHW8_LTfoHcYxwdr2KWRFD7aDYD92Yrizq25rTW2E0joTfH8mSN39hMNo225KMd9shaqklMoYmVFmh3JZ7pCwed3AmX00xbb2zRT7aIrdmZJHv72_8HXwxYUM-L0DYP7TNmCygwsYHfqQ8mOt78LnW_4DYm-kvA</recordid><startdate>20220401</startdate><enddate>20220401</enddate><creator>Allen, Joseph P.</creator><creator>Danoff, Joshua S.</creator><creator>Costello, Meghan A.</creator><creator>Hunt, Gabrielle L.</creator><creator>Hellwig, Amanda F.</creator><creator>Krol, Kathleen M.</creator><creator>Gregory, Simon G.</creator><creator>Giamberardino, Stephanie N.</creator><creator>Sugden, Karen</creator><creator>Connelly, Jessica J.</creator><general>Elsevier B.V</general><general>Elsevier Science Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QJ</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>5PM</scope></search><sort><creationdate>20220401</creationdate><title>Lifetime marijuana use and epigenetic age acceleration: A 17-year prospective examination</title><author>Allen, Joseph P. ; Danoff, Joshua S. ; Costello, Meghan A. ; Hunt, Gabrielle L. ; Hellwig, Amanda F. ; Krol, Kathleen M. ; Gregory, Simon G. ; Giamberardino, Stephanie N. ; Sugden, Karen ; Connelly, Jessica J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-2d128d31695314c19eefa99f0f4b7845b8da2847eafcade2bde838d427daf4523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Acceleration</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Age</topic><topic>Aging</topic><topic>Blood tests</topic><topic>Cannabis</topic><topic>Child</topic><topic>Childhood</topic><topic>Children</topic><topic>Cigarette smoking</topic><topic>Cigarettes</topic><topic>Demography</topic><topic>Dosage effects</topic><topic>Dose-response effects</topic><topic>Epigenesis, Genetic</topic><topic>Epigenetic aging</topic><topic>Epigenetics</topic><topic>Ethnic factors</topic><topic>Ethnic groups</topic><topic>Ethnicity</topic><topic>Humans</topic><topic>Hydrocarbons</topic><topic>Inhalation</topic><topic>Lifetime cannabis exposure</topic><topic>Longitudinal Studies</topic><topic>Marijuana</topic><topic>Marijuana Smoking - epidemiology</topic><topic>Marijuana Smoking - genetics</topic><topic>Marijuana Use - epidemiology</topic><topic>Mental depression</topic><topic>Minority &amp; 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Prospective longitudinal study, following participants annually from age 13 to age 30. A community sample of 154 participants recruited from a small city in the Southeastern United States. Participants completed annual assessments of marijuana use from age 13 to age 29 and provided blood samples that yielded two indices of epigenetic aging (DNAmGrimAge and DunedinPoAm) at age 30. Additional covariates examined included history of cigarette smoking, anxiety and depressive symptoms, childhood illness, gender, adolescent-era family income, and racial/ethnic minority status. Lifetime marijuana use predicted accelerated epigenetic aging, with effects remaining even after covarying cell counts, demographic factors and chronological age (β’s = 0.32 & 0.27, p’s < 0.001, 95% CI’s = 0.21–0.43 & 0.16–0.39 for DNAmGrimAge and DunedinPoAm, respectively). Predictions remained after accounting for cigarette smoking (β’s = 0.25 & 0.21, respectively, p’s < 0.001, 95% CI’s = 0.14–0.37 & 0.09–0.32 for DNAmGrimAge and DunedinPoAm, respectively). A dose-response effect was observed and there was also evidence that effects were dependent upon recency of use. Effects of marijuana use appeared to be fully mediated by hypomethylation of a site linked to effects of hydrocarbon inhalation (cg05575921). Marijuana use predicted epigenetic changes linked to accelerated aging, with evidence suggesting that effects may be primarily due to hydrocarbon inhalation among marijuana smokers. Further research is warranted to explore mechanisms underlying this linkage. •Lifetime levels of marijuana use predicted accelerated epigenetic aging.•Predictions remained even after accounting for cigarette smoking and a wide range of potential confounding variables.•Dose-response and recency of use effects were both observed.]]></abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>35231715</pmid><doi>10.1016/j.drugalcdep.2022.109363</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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ispartof Drug and alcohol dependence, 2022-04, Vol.233, p.109363-109363, Article 109363
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source Applied Social Sciences Index & Abstracts (ASSIA); MEDLINE; Elsevier ScienceDirect Journals Complete
subjects Acceleration
Adolescent
Adult
Age
Aging
Blood tests
Cannabis
Child
Childhood
Children
Cigarette smoking
Cigarettes
Demography
Dosage effects
Dose-response effects
Epigenesis, Genetic
Epigenetic aging
Epigenetics
Ethnic factors
Ethnic groups
Ethnicity
Humans
Hydrocarbons
Inhalation
Lifetime cannabis exposure
Longitudinal Studies
Marijuana
Marijuana Smoking - epidemiology
Marijuana Smoking - genetics
Marijuana Use - epidemiology
Mental depression
Minority & ethnic groups
Minority Groups
Prospective longitudinal assessment
Prospective Studies
Respiration
Smoking
title Lifetime marijuana use and epigenetic age acceleration: A 17-year prospective examination
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