Joshua B B Garfield1, Sue M Cotton2, Nicholas B Allen3, Ali Cheetham4, Marni Kras5, Murat Yücel6, Dan I Lubman7. 1. Eastern Health Clinical School, Faculty of Medicine, Nursing, and Health Sciences, Monash University, Level 2,5 Arnold Street, Box Hill, Victoria, 3128, Australia; Turning Point, Eastern Health, 54-62 Gertrude Street, Fitzroy, Victoria, 3065, Australia. Electronic address: joshuag@turningpoint.org.au. 2. Orygen, The National Centre of Excellence in Youth Mental Health, 35 Poplar Road, Parkville, Victoria, 3052, Australia; Centre for Youth Mental Health, University of Melbourne, 35 Poplar Road, Parkville, Victoria, 3052, Australia. Electronic address: sue.cotton@orygen.org.au. 3. School of Psychological Sciences, The University of Melbourne, Victoria, 3010, Australia; Department of Psychology, 1227 University of Oregon, Eugene, OR, 97403, USA. Electronic address: nallen3@uoregon.edu. 4. Turning Point, Eastern Health, 54-62 Gertrude Street, Fitzroy, Victoria, 3065, Australia. Electronic address: alisonc@turningpoint.org.au. 5. Brain and Mental Health Laboratory, Monash Institute of Cognitive and Clinical Neurosciences, School of Psychological Sciences, Monash University, Clayton, VIC, Australia. Electronic address: marnikras@gmail.com. 6. Brain and Mental Health Laboratory, Monash Institute of Cognitive and Clinical Neurosciences, School of Psychological Sciences, Monash University, Clayton, VIC, Australia. Electronic address: murat.yucel@monash.edu. 7. Eastern Health Clinical School, Faculty of Medicine, Nursing, and Health Sciences, Monash University, Level 2,5 Arnold Street, Box Hill, Victoria, 3128, Australia; Turning Point, Eastern Health, 54-62 Gertrude Street, Fitzroy, Victoria, 3065, Australia. Electronic address: dan.lubman@monash.edu.
Abstract
BACKGROUND: Anhedonia is prevalent among substance-dependent populations. The hedonic allostasis model suggests this is due to the effects of addictive substances on neural substrates of reward processing. However, previous research may have been confounded by other factors likely to influence anhedonia, including tobacco use, psychopathology, and history of trauma and other stressors. Thus it remains unclear whether elevated anhedonia in substance-dependent populations is caused by substance use itself, or is due to other correlates of substance dependence. METHODS: Multivariate analysis of covariance was conducted to test whether opioid-dependent participants' anhedonia scores were elevated, relative to a non-dependent control group, after controlling for psychosocial factors likely to influence anhedonia. Correlational analyses within opioid-dependent participants were also conducted to examine whether anhedonia was associated with recent illicit opioid use or duration of abstinence. RESULTS: There was a modest, but significant, elevation in anhedonia in opioid-dependent participants, relative to controls (Partial η2=0.034, p=0.041) after controlling for psychosocial variables that were associated with anhedonia. Depressive symptoms and history of post-traumatic stress disorder also remained significantly associated with anhedonia in the adjusted model. Among participants on opioid pharmacotherapy, there were significant associations between frequency of recent illicit opioid use and scores on anhedonia measures (all rs>0.25, p<0.013), but among abstinent opioid-dependent participants, relationships between duration of abstinence and anhedonia were not significant (all rs<0.24, p>0.22). CONCLUSION: These findings support the hypothesis that use of opioids can cause anhedonia, although other psychosocial factors may also contribute to the high prevalence of anhedonia among opioid-dependent populations.
BACKGROUND: Anhedonia is prevalent among substance-dependent populations. The hedonic allostasis model suggests this is due to the effects of addictive substances on neural substrates of reward processing. However, previous research may have been confounded by other factors likely to influence anhedonia, including tobacco use, psychopathology, and history of trauma and other stressors. Thus it remains unclear whether elevated anhedonia in substance-dependent populations is caused by substance use itself, or is due to other correlates of substance dependence. METHODS: Multivariate analysis of covariance was conducted to test whether opioid-dependent participants' anhedonia scores were elevated, relative to a non-dependent control group, after controlling for psychosocial factors likely to influence anhedonia. Correlational analyses within opioid-dependent participants were also conducted to examine whether anhedonia was associated with recent illicit opioid use or duration of abstinence. RESULTS: There was a modest, but significant, elevation in anhedonia in opioid-dependent participants, relative to controls (Partial η2=0.034, p=0.041) after controlling for psychosocial variables that were associated with anhedonia. Depressive symptoms and history of post-traumatic stress disorder also remained significantly associated with anhedonia in the adjusted model. Among participants on opioid pharmacotherapy, there were significant associations between frequency of recent illicit opioid use and scores on anhedonia measures (all rs>0.25, p<0.013), but among abstinent opioid-dependent participants, relationships between duration of abstinence and anhedonia were not significant (all rs<0.24, p>0.22). CONCLUSION: These findings support the hypothesis that use of opioids can cause anhedonia, although other psychosocial factors may also contribute to the high prevalence of anhedonia among opioid-dependent populations.
Authors: Marie Eikemo; Philipp P Lobmaier; Mads L Pedersen; Nikolaj Kunøe; Anna Maria Matziorinis; Siri Leknes; Monica Sarfi Journal: Neuropsychopharmacology Date: 2019-03-31 Impact factor: 7.853
Authors: Andrew S Huhn; Robert K Brooner; Mary M Sweeney; Denis Antoine; Alexis S Hammond; Hasan Ayaz; Kelly E Dunn Journal: Addict Behav Date: 2020-09-28 Impact factor: 3.913