FAAH and CNR1 Polymorphisms in the Endocannabinoid System and Alcohol-Related Sleep Quality
Sleep disturbances are common among individuals with alcohol use disorder (AUD) and may not resolve completely with short-term abstinence from alcohol, potentially contributing to relapse to drinking. The endocannabinoid system (ECS) is associated with both sleep and alcohol consumption, and genetic...
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| Published in | Frontiers in psychiatry Vol. 12; p. 712178 |
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| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
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09.09.2021
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| Abstract | Sleep disturbances are common among individuals with alcohol use disorder (AUD) and may not resolve completely with short-term abstinence from alcohol, potentially contributing to relapse to drinking. The endocannabinoid system (ECS) is associated with both sleep and alcohol consumption, and genetic variation in the ECS may underlie sleep-related phenotypes among individuals with AUD. In this study, we explored the influence of genetic variants in the ECS (Cannabinoid receptor 1/
CNR1
: rs806368, rs1049353, rs6454674, rs2180619, and Fatty Acid Amide Hydrolase/
FAAH
rs324420) on sleep quality in individuals with AUD (
N
= 497) and controls without AUD (
N
= 389). We assessed subjective sleep quality (from the Pittsburgh Sleep Quality Index/PSQI) for both groups at baseline and objective sleep efficiency and duration (using actigraphy) in a subset of individuals with AUD at baseline and after 4 weeks of inpatient treatment. We observed a dose-dependent relationship between alcohol consumption and sleep quality in both AUD and control groups. Sleep disturbance, a subscale measure in PSQI, differed significantly among
CNR1
rs6454674 genotypes in both AUD (
p
= 0.015) and controls (
p
= 0.016). Only among controls, neuroticism personality scores mediated the relationship between genotype and sleep disturbance. Objective sleep measures (sleep efficiency, wake bouts and wake after sleep onset), differed significantly by
CNR1
rs806368 genotype, both at baseline (
p
= 0.023, 0.029, 0.015, respectively) and at follow-up (
p
= 0.004,
p
= 0.006,
p
= 0.007, respectively), and by
FAAH
genotype for actigraphy recorded sleep duration at follow-up (
p
= 0.018). These relationships suggest a significant role of the ECS in alcohol-related sleep phenotypes. |
|---|---|
| AbstractList | Sleep disturbances are common among individuals with alcohol use disorder (AUD) and may not resolve completely with short-term abstinence from alcohol, potentially contributing to relapse to drinking. The endocannabinoid system (ECS) is associated with both sleep and alcohol consumption, and genetic variation in the ECS may underlie sleep-related phenotypes among individuals with AUD. In this study, we explored the influence of genetic variants in the ECS (Cannabinoid receptor 1/CNR1: rs806368, rs1049353, rs6454674, rs2180619, and Fatty Acid Amide Hydrolase/FAAH rs324420) on sleep quality in individuals with AUD (N = 497) and controls without AUD (N = 389). We assessed subjective sleep quality (from the Pittsburgh Sleep Quality Index/PSQI) for both groups at baseline and objective sleep efficiency and duration (using actigraphy) in a subset of individuals with AUD at baseline and after 4 weeks of inpatient treatment. We observed a dose-dependent relationship between alcohol consumption and sleep quality in both AUD and control groups. Sleep disturbance, a subscale measure in PSQI, differed significantly among CNR1 rs6454674 genotypes in both AUD (p = 0.015) and controls (p = 0.016). Only among controls, neuroticism personality scores mediated the relationship between genotype and sleep disturbance. Objective sleep measures (sleep efficiency, wake bouts and wake after sleep onset), differed significantly by CNR1 rs806368 genotype, both at baseline (p = 0.023, 0.029, 0.015, respectively) and at follow-up (p = 0.004, p = 0.006, p = 0.007, respectively), and by FAAH genotype for actigraphy recorded sleep duration at follow-up (p = 0.018). These relationships suggest a significant role of the ECS in alcohol-related sleep phenotypes.Sleep disturbances are common among individuals with alcohol use disorder (AUD) and may not resolve completely with short-term abstinence from alcohol, potentially contributing to relapse to drinking. The endocannabinoid system (ECS) is associated with both sleep and alcohol consumption, and genetic variation in the ECS may underlie sleep-related phenotypes among individuals with AUD. In this study, we explored the influence of genetic variants in the ECS (Cannabinoid receptor 1/CNR1: rs806368, rs1049353, rs6454674, rs2180619, and Fatty Acid Amide Hydrolase/FAAH rs324420) on sleep quality in individuals with AUD (N = 497) and controls without AUD (N = 389). We assessed subjective sleep quality (from the Pittsburgh Sleep Quality Index/PSQI) for both groups at baseline and objective sleep efficiency and duration (using actigraphy) in a subset of individuals with AUD at baseline and after 4 weeks of inpatient treatment. We observed a dose-dependent relationship between alcohol consumption and sleep quality in both AUD and control groups. Sleep disturbance, a subscale measure in PSQI, differed significantly among CNR1 rs6454674 genotypes in both AUD (p = 0.015) and controls (p = 0.016). Only among controls, neuroticism personality scores mediated the relationship between genotype and sleep disturbance. Objective sleep measures (sleep efficiency, wake bouts and wake after sleep onset), differed significantly by CNR1 rs806368 genotype, both at baseline (p = 0.023, 0.029, 0.015, respectively) and at follow-up (p = 0.004, p = 0.006, p = 0.007, respectively), and by FAAH genotype for actigraphy recorded sleep duration at follow-up (p = 0.018). These relationships suggest a significant role of the ECS in alcohol-related sleep phenotypes. Sleep disturbances are common among individuals with alcohol use disorder (AUD) and may not resolve completely with short-term abstinence from alcohol, potentially contributing to relapse to drinking. The endocannabinoid system (ECS) is associated with both sleep and alcohol consumption, and genetic variation in the ECS may underlie sleep-related phenotypes among individuals with AUD. In this study, we explored the influence of genetic variants in the ECS (Cannabinoid receptor 1/ : rs806368, rs1049353, rs6454674, rs2180619, and Fatty Acid Amide Hydrolase/ rs324420) on sleep quality in individuals with AUD ( = 497) and controls without AUD ( = 389). We assessed subjective sleep quality (from the Pittsburgh Sleep Quality Index/PSQI) for both groups at baseline and objective sleep efficiency and duration (using actigraphy) in a subset of individuals with AUD at baseline and after 4 weeks of inpatient treatment. We observed a dose-dependent relationship between alcohol consumption and sleep quality in both AUD and control groups. Sleep disturbance, a subscale measure in PSQI, differed significantly among rs6454674 genotypes in both AUD ( = 0.015) and controls ( = 0.016). Only among controls, neuroticism personality scores mediated the relationship between genotype and sleep disturbance. Objective sleep measures (sleep efficiency, wake bouts and wake after sleep onset), differed significantly by rs806368 genotype, both at baseline ( = 0.023, 0.029, 0.015, respectively) and at follow-up ( = 0.004, = 0.006, = 0.007, respectively), and by genotype for actigraphy recorded sleep duration at follow-up ( = 0.018). These relationships suggest a significant role of the ECS in alcohol-related sleep phenotypes. Sleep disturbances are common among individuals with alcohol use disorder (AUD) and may not resolve completely with short-term abstinence from alcohol, potentially contributing to relapse to drinking. The endocannabinoid system (ECS) is associated with both sleep and alcohol consumption, and genetic variation in the ECS may underlie sleep-related phenotypes among individuals with AUD. In this study, we explored the influence of genetic variants in the ECS (Cannabinoid receptor 1/ CNR1 : rs806368, rs1049353, rs6454674, rs2180619, and Fatty Acid Amide Hydrolase/ FAAH rs324420) on sleep quality in individuals with AUD ( N = 497) and controls without AUD ( N = 389). We assessed subjective sleep quality (from the Pittsburgh Sleep Quality Index/PSQI) for both groups at baseline and objective sleep efficiency and duration (using actigraphy) in a subset of individuals with AUD at baseline and after 4 weeks of inpatient treatment. We observed a dose-dependent relationship between alcohol consumption and sleep quality in both AUD and control groups. Sleep disturbance, a subscale measure in PSQI, differed significantly among CNR1 rs6454674 genotypes in both AUD ( p = 0.015) and controls ( p = 0.016). Only among controls, neuroticism personality scores mediated the relationship between genotype and sleep disturbance. Objective sleep measures (sleep efficiency, wake bouts and wake after sleep onset), differed significantly by CNR1 rs806368 genotype, both at baseline ( p = 0.023, 0.029, 0.015, respectively) and at follow-up ( p = 0.004, p = 0.006, p = 0.007, respectively), and by FAAH genotype for actigraphy recorded sleep duration at follow-up ( p = 0.018). These relationships suggest a significant role of the ECS in alcohol-related sleep phenotypes. Sleep disturbances are common among individuals with alcohol use disorder (AUD) and may not resolve completely with short-term abstinence from alcohol, potentially contributing to relapse to drinking. The endocannabinoid system (ECS) is associated with both sleep and alcohol consumption, and genetic variation in the ECS may underlie sleep-related phenotypes among individuals with AUD. In this study, we explored the influence of genetic variants in the ECS (Cannabinoid receptor 1/CNR1: rs806368, rs1049353, rs6454674, rs2180619, and Fatty Acid Amide Hydrolase/FAAH rs324420) on sleep quality in individuals with AUD (N = 497) and controls without AUD (N = 389). We assessed subjective sleep quality (from the Pittsburgh Sleep Quality Index/PSQI) for both groups at baseline and objective sleep efficiency and duration (using actigraphy) in a subset of individuals with AUD at baseline and after 4 weeks of inpatient treatment. We observed a dose-dependent relationship between alcohol consumption and sleep quality in both AUD and control groups. Sleep disturbance, a subscale measure in PSQI, differed significantly among CNR1 rs6454674 genotypes in both AUD (p = 0.015) and controls (p = 0.016). Only among controls, neuroticism personality scores mediated the relationship between genotype and sleep disturbance. Objective sleep measures (sleep efficiency, wake bouts and wake after sleep onset), differed significantly by CNR1 rs806368 genotype, both at baseline (p = 0.023, 0.029, 0.015, respectively) and at follow-up (p = 0.004, p = 0.006, p = 0.007, respectively), and by FAAH genotype for actigraphy recorded sleep duration at follow-up (p = 0.018). These relationships suggest a significant role of the ECS in alcohol-related sleep phenotypes. |
| Author | Hodgkinson, Colin A. Brooks, Alyssa T. Soundararajan, Soundarya Schwandt, Melanie L. Krumlauf, Michael Wallen, Gwenyth R. Ramchandani, Vijay A. Kazmi, Narjis George, David T. |
| AuthorAffiliation | 3 Office of the Clinical Director, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health , Bethesda, MD , United States 4 Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health , Bethesda, MD , United States 2 National Institutes of Health Clinical Center , Bethesda , MD, United States 1 Human Psychopharmacology Laboratory, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health , Bethesda, MD , United States |
| AuthorAffiliation_xml | – name: 4 Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health , Bethesda, MD , United States – name: 1 Human Psychopharmacology Laboratory, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health , Bethesda, MD , United States – name: 2 National Institutes of Health Clinical Center , Bethesda , MD, United States – name: 3 Office of the Clinical Director, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health , Bethesda, MD , United States |
| Author_xml | – sequence: 1 givenname: Soundarya surname: Soundararajan fullname: Soundararajan, Soundarya – sequence: 2 givenname: Narjis surname: Kazmi fullname: Kazmi, Narjis – sequence: 3 givenname: Alyssa T. surname: Brooks fullname: Brooks, Alyssa T. – sequence: 4 givenname: Michael surname: Krumlauf fullname: Krumlauf, Michael – sequence: 5 givenname: Melanie L. surname: Schwandt fullname: Schwandt, Melanie L. – sequence: 6 givenname: David T. surname: George fullname: George, David T. – sequence: 7 givenname: Colin A. surname: Hodgkinson fullname: Hodgkinson, Colin A. – sequence: 8 givenname: Gwenyth R. surname: Wallen fullname: Wallen, Gwenyth R. – sequence: 9 givenname: Vijay A. surname: Ramchandani fullname: Ramchandani, Vijay A. |
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| Copyright | Copyright © 2021 Soundararajan, Kazmi, Brooks, Krumlauf, Schwandt, George, Hodgkinson, Wallen and Ramchandani. Copyright © 2021 Soundararajan, Kazmi, Brooks, Krumlauf, Schwandt, George, Hodgkinson, Wallen and Ramchandani. 2021 Soundararajan, Kazmi, Brooks, Krumlauf, Schwandt, George, Hodgkinson, Wallen and Ramchandani |
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| Keywords | Pittsburgh Sleep Quality Index alcohol use disorder actigraphy endocannabinoids sleep phenotypes |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors have jointly supervised the work These authors have contributed equally to this work This article was submitted to Addictive Disorders, a section of the journal Frontiers in Psychiatry Reviewed by: Maciej Salaga, Medical University of Lodz, Poland; Patrizia Romualdi, University of Bologna, Italy Edited by: Bolanle Adeyemi Ola, Lagos State University, Nigeria |
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| Title | FAAH and CNR1 Polymorphisms in the Endocannabinoid System and Alcohol-Related Sleep Quality |
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