Cognition and Addiction

A Researcher's Guide from Mechanisms Towards Interventions

Antonio Verdejo García

• Publisher: Academic Press
• Year: 2019
• ISBN:
  9780128152997
• Topic: Psicología
• Subtopic: Neuropsicología

Cognition and Addiction: A Researcher's Guide from Mechanisms Towards Interventions provides researchers with a guide to recent cognitive neuroscience advances in addiction theory, phenotyping, treatments and new vistas, including both substance and behavioral addictions. This book focuses on "what to know" and "how to apply" information, prioritizing novel principles and delineating cutting-edge assessment, phenotyping and treatment tools. Written by world renowned researcher Antonio Verdejo-Garcia, this resource will become a go-to guide for researchers in the field of cognitive neuroscience and addiction.

• Examines cognitive neuroscience advances in addiction theory, including both substance and behavioral addictions
• Discusses primary principles of cutting-edge assessment, phenotyping and treatment tools
• Includes detailed chapters on neuro-epidemiology and genetic imaging

Chapter 1

Cognition

the interface between nature and nurture in addiction

Antonio Verdejo-Garcia School of Psychological Sciences and Turner Institute for Brain and Mental Health, Monash University, Melbourne, VIC, Australia

Abstract

Contemporary models define addiction as a “brain disorder” characterized by drug/gambling-related neuroadaptations that ultimately have an impact on psychological functioning and social interaction. Critics of this view argue that it mistakenly reproduces a physical disease model and lacks integration of social drivers. In this chapter, I argue that a focus on cognition—encompassing thinking, emotion, and related behaviors, as well as their neural underpinnings—can provide a more comprehensive understanding of the nature and the course of addiction. Cognition sits at the interface of biological, psychological, and social drivers of addictive disorders, hinging on the interplay between nature and nurture. To articulate this vision, I summarize cognitive neuroscience evidence showing that individual variations in core cognitive traits and skills can explain both addiction vulnerability and disordered states and chronicity. This view stands on evidence from (1) longitudinal studies, (2) endophenotype-based approaches, and (3) “neurotoxicity-controlled designs” comparing people with addiction versus “nonaddicted” recreational users and people with substance versus behavioral addictions. This evidence suggest that higher-order cognitive traits and processes such as conscientiousness and response inhibition, as well as social-cognitive and affective characteristics (negative affectivity, self-oriented evaluations), confer vulnerability to addictive disorders, whereas cognitive deficits in working memory, flexibility, and decision-making are associated with the consequences of substance and behavioral addictions. There is a meaningful overlap and continuity between premorbid cognitive traits and cognitive-disordered states, supporting the centrality of cognition in understanding both the nature and the course of addiction.

Keywords

Chronicity; Cognition; Endophenotypes; Executive functions; Response inhibition; Vulnerability

Introduction

A key question in the field of addiction is whether some people are hardwired to develop addictive disorders or if, conversely, drugs and “addictive products” or related contexts generate addictions. Historically, the answers to this question have fluctuated as a function of prevailing theories. Old moral views and personality models saw inherent weaknesses in the individual (Eysenck, 1997; Peele, 1987). Learning theories have focused on the ability of drugs and “addictive products” (e.g., electronic gaming machines) to generate aberrant learning, which is then resistant to extinction relatively uniformly across individuals (Robinson and Berridge, 2003, 2008). Social theories have treated addiction as a manifestation of a certain context and environment (e.g., the classic studies on Vietnam War veterans) (Moore, 1993; Zinberg, 1984). Nowadays, there is agreement that none of these models, in isolation, can satisfactorily explain the nature and the course of addiction, but at the same time, there is a lack of comprehensive frameworks. Contemporary models have embraced a biopsychosocial approach, but there is a bias toward the bio-, at least in discovery science and therapeutic development, especially after the advent of neuroimaging tools and genetic manipulation techniques within animal studies (Hall et al., 2015a). The current prevailing view is that addiction is a “brain disorder,” characterized by drug- or gambling-related neuroadaptations that ultimately have an impact on psychological functioning (changes in thinking, emotions, and behaviors) and social interaction (Volkow et al., 2011; Volkow et al., 2016). Critics of this view argue that it mistakenly reproduces a physical disease model (inadequate for mental disorders or social constructs), lacks integration of social and environmental drivers, and fosters feelings of hopelessness and externalization among people with addiction (e.g., “I have a disease, I can't do anything about it”) (Hall et al., 2015b). In this chapter, I will argue that a focus on cognition—encompassing thinking, emotion, and related behaviors, as well as their neural underpinnings—can provide a more comprehensive and integrative understanding of the nature and the course of addiction. Cognition sits at the interface of biological, psychological, and social drivers of addictive disorders, hinging on the interplay between nature and nurture. Genetic and early environmental influences shape the cognitive traits that make us vulnerable or resilient to drug use/gambling and related social contexts (e.g., product availability, peer pressure) (Belcher et al., 2014). At the same time, drugs and gambling modify learning and cognitive control processes and change the way we interact with others and the environment (Everitt and Robbins, 2016; Goldstein and Volkow, 2011; Moeller and Goldstein, 2014). By focusing on cognition, we can overcome the reductionism of the “disease model,” i.e., it's not in the brain, it's at the interface between the brain and the environment, and foster self-agency about recovery, i.e., it's not indelible, the same influences that originally shaped cognition in a certain way can help restore or compensate cognitive mechanisms to facilitate recovery (Garavan and Weierstall, 2012). To articulate this vision, I will first discuss the role of cognition in contemporary addiction theories and outline a cognition-centered integrative approach. Next, I will summarize cognitive neuroscience evidence showing that individual variations in core cognitive processes, particularly reward-related processes and higher-order cognitive skills, plus disorder-specific impacts on such processes, can explain both addiction vulnerability and disordered states and chronicity.

Cognition to bridge the gap between neurobiological models and social accounts of addiction

Contemporary theories of addiction generally posit neurobiological alterations in three systems: the incentive salience (or reward) system, the stress system, and the executive control system, which map into the striatum, extended amygdala, and prefrontal cortex circuits, respectively (Koob and Volkow, 2010). Incentive salience alterations are responsible for reward sensitization (increased motivation toward drugs/gambling resulting from repeated administration—i.e., instead of the expected habituation) and reward prediction errors (i.e., expecting more reward than what is actually received). Heightened motivation toward drugs/gambling also occurs at the cost of reduced motivation toward natural reinforcers (Goldstein and Volkow, 2002, 2011). Alterations in the stress system account for persistently elevated negative affect, which can manifest as chronic stress and depression, as well as predominance of negative reinforcement mechanisms in the control of behavior. That is, negative affective states become the norm, behaviors are mostly energized to try to get rid of unpleasant feelings, and this behavior results in short-term relief but long-term augmentation of the stress response. Finally, executive alterations are responsible for the tendency to focus on immediate responses and short-term outcomes, neglecting goals and long-term consequences. Different theories emphasize two or more of these alterations and related brain systems. For example, “dual models” focus on the imbalance between incentive salience (ventral striatum) and executive control (dorsolateral prefrontal cortex [DLPFC] and anterior cingulate cortex) (McClure and Bickel, 2014). Stress models emphasize the link between negative affect (hypothalamic–pituitary–adrenal axis, amygdala, hippocampus) and poor control over stress-related responses (dorsal striatum, DLPFC), which has been ascribed to impulsivity (e.g., negative urgency—the tendency to act impulsively under negative affect) or compulsivity (e.g., repetitive behaviors that “fly under the radar” of top-down executive supervision) (Figee et al., 2016; Verdejo-García et al., 2007). Executive control and decision-making models highlight the misalignment between goal-related systems (ventromedial prefrontal cortex) and motivational, emotional, and contextual drivers (striatum, insula, amygdala/hippocampus) (Bechara, 2005; Redish et al., 2008; Verdejo-García and Bechara, 2009). Although the significance of these models dwells in the way they characterize the drivers of addictive behaviors, while acknowledging that these drivers are shaped by and operate in social contexts, they often come across as reductionist biological accounts of behavior.

Translating the key notions of these models into a cognitive framework can help to broaden their scope and impact. Essentially, contemporary neurobiological theories characterize the “backend” of addiction-related alterations. The “frontline” is the complex harmful behavior and the negative social consequences that policy makers and preventionists try to counteract and clinicians have to face (i.e., uncontrolled drug/gambling use, distress, deterioration of health and quality of life, lack of social support, personal and social burden). In between these two, there is a range of cognitive alterations involving reward valuation and learning, emotion processing and affect regulation, and executive control and decision-making affecting personal and social domains (e.g., valuation of individual rewards such as salary and career and social rewards such as friendships and relationships). And these alterations trace back to specific traits that interact with environmental and social factors before and during the emergence of addiction and can potentially cooperate with contextual factors in the path to addiction recovery (Celma-Merola et al., 2018). As addictions take time to develop, we can chronologically map the unfolding of cognitive drivers and their interaction with environmental and social factors. Cognitive-affective traits, such as reward sensitivity, negative affectivity, and impulsivity/self-control, influence child and adolescent learning and academic and social development. The interaction between these traits and environmental/social influences (socioeconomic disadvantage, trauma, poor parenting, academic failure, peer pressure or social isolation) predicts the onset of addictive behaviors. Once initiated, drug use and gambling contribute to exacerbate preexisting traits, for example, they sensitize reward learning and stress responses and deteriorate cognitive control, fostering impulsive decisions and compulsive behaviors. These changes contribute to worsen the contextual milieu (i.e., loss of productivity, income, social capital, and support) and foster a spiral of distress and impoverishment of quality of life. Although this scenario describes ...