Addiction as a Coping Response: Hyperkatifeia, Deaths of Despair, and COVID-19

Abstract

Back to table of contents Previous article Next article Reviews and OverviewsFull AccessAddiction as a Coping Response: Hyperkatifeia, Deaths of Despair, and COVID-19George F. Koob, Ph.D., Patricia Powell, Ph.D., Aaron White, Ph.D.George F. Koob, Ph.D., Patricia Powell, Ph.D., Aaron White, Ph.D.Published Online:1 Nov 2020https://doi.org/10.1176/appi.ajp.2020.20091375AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail Neuroadaptations that occur in response to repeated substance use diminish the euphoria that is produced by the acute use of a drug and increase levels of physical and emotional stress between drug use episodes. An individual who struggles with addiction can be tempted to return to drug use to reduce misery that is caused by use of the drug itself. Recent developments, including an increase in "deaths of despair" in the United States, increases in alcohol use by some individuals as a result of the 2019 coronavirus disease (COVID-19) pandemic, and limited availability of in-person treatment and recovery support, raise concerns about the use of alcohol and other drugs in an effort to cope with distress. In this article, we examine the role of negative reinforcement in the development of addiction, discuss neuroadaptations that lead to increases in emotional and physical misery between episodes of drug use, and explore how using substances to cope with the emotional strain of social isolation and financial uncertainty during the COVID-19 pandemic could contribute to deaths of despair.Conceptual Framework of AddictionAlcohol Use Disorder as a Prototype AddictionAlcohol use disorder (AUD) can be defined as a chronically relapsing disorder that is associated with compulsive alcohol drinking, the loss of control over intake, and the emergence of a negative emotional state when alcohol is no longer available. Patterns of alcohol use in AUD can range from intermittent episodes of binge alcohol intake to prolonged heavy drinking over longer periods that progresses to continual drinking for fear of withdrawal. Comorbid affective disorders, a history of trauma, and exposure to stressors increase the likelihood of developing AUD (1, 2). Abstinence from such alcohol binges or chronic high alcohol intake is characterized by a withdrawal syndrome with severe emotional and somatic symptoms and intense craving for alcohol. Negative emotional states commonly trigger relapse (3, 4), and such negative emotional states can be driven by excessive alcohol consumption itself. Like other substance use disorders, AUD is now considered a spectrum disorder, as described in DSM-5 (5), which provides a framework for determining the intensity of the disorder based on the number of symptoms the individual presents.Heuristic Framework for AddictionA heuristic framework for studying addiction, characterized by a three-stage cycle—binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation—provides a starting point for exploring our theme in this article, namely, the intersection between alcohol addiction, deaths of despair, and social isolation that are caused by the COVID-19 pandemic (6, 7). Under this framework, dysregulation occurs in three functional domains that reflect the three stages of the addiction cycle: incentive salience/pathological habits in the binge/intoxication stage, negative emotional states in the withdrawal/negative affect stage, and executive function deficits in the preoccupation/anticipation stage. These three domains and stages are hypothesized to be mediated by three major neurocircuitry elements: basal ganglia, extended amygdala, and prefrontal cortex, respectively (6). An individual can enter the addiction cycle at any of these three stages (6) (Figure 1).FIGURE 1. Conceptual framework for the neurobiological basis of substance use disordersaa The framework involves a three-stage cycle—binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation. These three stages involve dysregulations in three functional domains (incentive salience/habits, negative emotional states, and executive function) that are mediated by three major neurocircuitry elements (basal ganglia, extended amygdala, and prefrontal cortex, respectively). The negative emotional state of drug withdrawal, termed hyperkatifeia, can be facilitated and exacerbated by non-drug-related allostatic loads, such as genetics, epigenetics, childhood trauma, and psychiatric comorbidity, in addition to excessive drinking. Hyperkatifeia in turn drives the negative reinforcement source of motivation for compulsive-like alcohol seeking and using. Hyperkatifeia can drive impulsivity via negative urgency that is associated with relapse in the preoccupation/anticipation stage and then a return to the binge/intoxication stage. Hyperkatifeia can also drive the malaise of protracted abstinence that sets up a return to the binge/intoxication stage via cravi