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      Alcohol use and misuse during the COVID-19 pandemic: a potential public health crisis?

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      a , b
      The Lancet. Public Health
      The Author(s). Published by Elsevier Ltd.

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          Abstract

          In an attempt to control the 2019 coronavirus disease (COVID-19) pandemic, governments across the world have implemented distancing measures during the search for medical countermeasures, resulting in millions of people being isolated for long periods. Alcohol misuse is one of the leading causes of preventable mortality, contributing annually to about 3 million deaths worldwide. 1 In some individuals, long term, excessive alcohol misuse might escalate into an alcohol use disorder. The potential public health effects of long-term isolation on alcohol use and misuse are unknown. Stress is a prominent risk factor for the onset and maintenance of alcohol misuse. For example, chronic alcohol use results in neuroadaptations in stress and reward pathways, which lead to dysfunctional hypothalamic pituitary adrenocortical and sympathetic adrenomedullary axes, characterised by dysregulation of the cortisol response and deficits in emotional regulation. 2 In turn, these neuroadaptations lead to increased cravings for alcohol in response to stress. The effects of long-term social isolation on stress levels, including increased neuroendocrine responses and stress reactivity, have been described in non-human animals. 3 However, the ongoing lockdowns across many countries are unique and little is known of the effects on the general population of chronic isolation (with respect to health and wellbeing) in these circumstances A risk factor for the onset and maintenance of alcohol misuse and alcohol use disorder is trait impulsivity (ie, the tendency to take risks or act without adequate forethought or reflection). Impulsivity can moderate stress-induced consumption of alcohol 4 and is also associated with relapse in addicted individuals. 5 Thus, this period of isolation might lead to a spike in alcohol misuse, relapse, and potentially, development of alcohol use disorder in at-risk individuals, therefore placing further strain on addiction and drug and alcohol services, and the health service in general, during and after the pandemic. Most governments, including the UK Government, have responded to the COVID-19 pandemic by advising the public to remain indoors, avoid unnecessary social contact, to protect themselves and health-care systems, and to save lives. We suggest that, as well as this important public health advice, governments should give public health warnings about excessive alcohol consumption during isolation to protect vulnerable individuals.

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          Most cited references4

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          Genetic influences on impulsivity, risk taking, stress responsivity and vulnerability to drug abuse and addiction.

          Genetic variation may partially underlie complex personality and physiological traits--such as impulsivity, risk taking and stress responsivity--as well as a substantial proportion of vulnerability to addictive diseases. Furthermore, personality and physiological traits themselves may differentially affect the various stages of addiction, defined chronologically as initiation of drug use, regular drug use, addiction/dependence and potentially relapse. Here we focus on recent approaches to the study of genetic variation in these personality and physiological traits, and their influence on and interaction with addictive diseases.
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            Stress, dysregulation of drug reward pathways, and the transition to drug dependence.

            This review provides a neuroadaptive perspective regarding the role of the hormonal and brain stress systems in drug addiction with a focus on the changes that occur during the transition from limited access to drugs to long-term compulsive use of drugs. A dramatic escalation in drug intake with extended access to drug self-administration is characterized by a dysregulation of brain reward pathways. Hormonal studies using an experimenter-administered cocaine binge model and an escalation self-administration model have revealed large increases in ACTH and corticosterone in rats during an acute binge with attenuation during the chronic binge stage and a reactivation of the hypothalamic-pituitary-adrenal axis during acute withdrawal. The activation of the hypothalamic-pituitary-adrenal axis with cocaine appears to depend on feed-forward activation of the mesolimbic dopamine system. At the same time, escalation in drug intake with either extended access or dependence-induction produces an activation of the brain stress system's corticotropin-releasing factor outside of the hypothalamus in the extended amygdala, which is particularly evident during acute withdrawal. A model of the role of different levels of hormonal/brain stress activation in addiction is presented that has heuristic value for understanding individual vulnerability to drug dependence and novel treatments for the disorder.
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              Effect of social isolation on stress-related behavioural and neuroendocrine state in the rat.

              The present study investigated the effects of post-weaning social isolation (SI) on behavioural and neuroendocrine reactivity to stress of male and female rats. Innate aspects of fear and anxiety were assessed in the open field and elevated plus maze tests. Spontaneous startle reflex and conditioned fear response were further investigated. The neuroendocrine response of isolates was examined by measuring basal and stress release of ACTH and corticosterone and by evaluating the mRNA expression of mineralocorticoid (MR) and glucocorticoid (GR) receptors using in situ hybridization. Locomotor activity in the open field was not modified by chronic SI. In males, but not females, SI produced an anxiogenic profile in the elevated plus maze. Male isolates showed a trend towards increased startle reflex amplitude relative to socially-reared controls. Moreover, SI in males produced alterations of the HPA axis functioning as reflected by higher basal levels of ACTH, and enhanced release of ACTH and corticosterone following stress. In contrast, startle response or HPA axis functioning were not altered in female isolates. Social isolates from both genders showed reduced contextual fear-conditioning. Finally, the mRNA expression of MR and GR was not modified by SI. The results of the present study suggest that chronic SI increases emotional reactivity to stress and produces a hyperfunction of the HPA axis in adult rats, particularly in males. Copyright 2003 Elsevier B.V.
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                Author and article information

                Contributors
                Journal
                Lancet Public Health
                Lancet Public Health
                The Lancet. Public Health
                The Author(s). Published by Elsevier Ltd.
                2468-2667
                8 April 2020
                8 April 2020
                Affiliations
                [a ]School of Psychology, University of Portsmouth, Portsmouth PO1 2DT, UK
                [b ]School of Pharmacy and Biomedical Science, University of Portsmouth, Portsmouth PO1 2DT, UK
                Article
                S2468-2667(20)30088-8
                10.1016/S2468-2667(20)30088-8
                7195126
                32277874
                9e0ca19e-a7c4-42fa-9e53-a9efb5379631
                © 2020 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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