Causes of distress-induced emotional eating

Distress is associated with both increased and decreased food intake, with eating less being the typical and predominant response. Distress is normally associated with physiological reactions that are designed to prepare the individual for a fight or flight response, thereby suppressing feelings of hunger. However, so-called emotional eaters show the atypical response to distress of eating similar or larger amounts of food. The present chapter explores possible causes of distress-induced emotional eating in terms of mechanisms and etiology. Possible mechanisms that are discussed are stress-induced hunger, interoceptive awareness, alexithymia, and changes in the stress responses of the hypothalamic–pituitary–adrenal (HPA) axis (cortisol). Etiology, that is, the emergence of emotional eating in adolescence will be examined by presenting studies on increases in emotional eating in association with inadequate parenting and depressive feelings in interaction with genetic vulnerability (the dopamine D2 receptor gene (DRD2) or serotonin transporter gene (SCL6A4/5-HTT)). Finally, emotional eating as a mediator between depression and both body mass index and weight gain will be examined and suggestions for obesity interventions and future research will be given.

Understanding risk and resilience in maltreated children

Individuals with a history of child abuse are at high risk for a broad range of psychiatric and substance use disorders. This chapter reviews key findings from research on the genetics of child abuse-related psychiatric disorders, neuroimaging investigations with maltreated youth, and resiliency studies. Relevant empirical work in the field was reviewed, with an emphasis on prior reviews, meta-analytic studies, and recent publications. Genetic factors are not associated with distinct psychiatric disorders but rather diverse clinical phenotypes, and a history of abuse is frequently associated with alterations in structural and functional brain changes across multiple brain regions and circuits that mediate a wide variety of emotional and cognitive processes. Heterogeneity in clinical outcome and brain measures varies as a function of a wide range of factors, and emerging findings on genetic and neural plasticity offers significant promise in understanding risk and resilience in maltreated youth. Child maltreatment is a strong predictor of early onset of psychiatric illness, increased comorbidity, and poor treatment response; however, a history of abuse need not lead to the development of psychiatric problems. Risk is altered by genetic factors, and can be ameliorated by positive factors in the environment—including the availability of positive support, enrichment experiences, and the delivery of evidence-based psychotherapeutic clinical interventions. Future multidisciplinary and translational studies will help to further delineate the mechanisms by which experiences of maltreatment confers risk for psychopathology, as well as help to further delineate factors associated with resiliency.

Resilience

Resilience refers to the process of adaptive recovery following adversity or trauma. It is likely to include an intertwined series of dynamic interactions between neural, developmental, environmental, genetic, and epigenetic factors over time. Neuroscientific research suggests the potential role of the brain’s threat and reward systems, as well as executive control networks. Developmental research provides insight into how the environment may affect these neural systems across the lifespan towards greater risk or resilience to stress. Genetic work has revealed numerous targets that alter key neurochemical systems in the brain to influence mental health. Current challenges include ambiguities in the definition and measurement of resilience and a simplified focus on resilience as the absence of psychopathology, irrespective of levels of positive mental functioning. Greater emphasis on understanding the protective aspects of resilience and related well-being outcomes are important to delineate the unique neurobiological factors that underpin this process, so that effective interventions can be developed to assist vulnerable populations and resilience promotion.

Gene–environment interactions in animal models of depression and anxiety

Depression and anxiety disorders cause the greatest global disability in terms of impact on the individual, family, and society at large. The etiology of these disorders is multifactorial and includes complex interactions between genetic and environmental risk factors. This chapter reviews preclinical studies assessing the importance of gene–environment (G×E) interaction. Specifically, we focus on G×E studies assessing the roles of the hypothalamic–pituitary–adrenal (HPA) axis, serotonergic system, GABAergic system, and brain-derived neurotrophic factor (BDNF) system. Finally, novel candidate target genes for the treatment of depression and anxiety disorders are considered.

Epigenetics and twin studies

Throughout life, human traits are characterized by variability: they show variation between people and within persons over a time period. Such variation between and within persons can be related to genotype or environment and can be examined in studies of mono- and dizygotic twins. Increasingly, twins are also studied to examine variation at the molecular level, including variation in epigenetic mechanisms, such as DNA methylation. These mechanisms regulate how the DNA code is used in cells and are increasingly recognized as important contributors to phenotypic differences. In the brain, epigenetic mechanisms are crucial to development and synaptic plasticity, and are probably at the molecular basis of processes such as learning and memory. Epigenetic mechanisms represent a biological path through which environment and DNA-sequence variants may exert their effects on complex traits. When studying epigenetic mechanisms in human traits and understanding the sources of epigenetic variation twin-based research offers exceptional opportunities. This chapter describes epigenetic mechanisms and the value of twin research, with a focus on DNA methylation and traits related to cognitive and mental health.

Genes, brain and emotions: Introduction

Recent research has started to uncover genetic influences on emotion and intermediate neural phenotypes. This work has involved an extensive array of methods and developed at the intersection of psychology, genetics, and neuroscience. The aim of this volume is to offer a comprehensive account of current research on the genetics of emotion, including methods focused on multiple levels of analysis; cognitive and biological mechanisms involved in the pathways between genes and emotional experience; and clinical and translational research on the genetics of emotion dysregulation in neuropsychiatric disorders.

Genetics of obsessive–compulsive disorder and Tourette’s syndrome

Obsessive–compulsive disorder (OCD) and Tourette Syndrome (TS) are two common psychiatric disorders affecting approximately 1–3% of the population. Over the years, considerable progress has been made in conceptualizing these disorders, both clinically and genetically, from simple manifestations of psychological disturbances to highly polygenic, heritable disorders. Family and twin studies have shown that both disorders are familial, and partly influenced by genetic factors. Heritability estimates range between 0.26 and 0.60 for OCD, and 0.25 and 0.54 for TS, but despite this steady progress, results remain inconclusive regarding specific etiological genetic causes. Currently, a remarkable increase in international collaborative efforts within psychiatric genetics has opened new research possibilities, with larger datasets and multiple sources of genetic information available. This chapter provides a broad and updated overview of the genetics of OCD and TS and their genetic association. Historical evidence from past literature and recent results in light of current research are summarized.

Missing heritability in studies of trait anxiety and amygdala function

Ask any parent how early they could discern the temperament of their child, or when they noticed differences in temperament among their children, and the answer is likely to be: “almost immediately.” Anecdotally, personality traits are present from the first days of life and remain relatively stable throughout its course, suggesting a strong biological basis for these predispositions. Behavioral geneticists have quantified the heritability of personality traits, and molecular studies have eagerly sought to discover their associated genes. Curiously, the anticipated bonanza of gene discoveries has not materialized: heritability has gone missing. This chapter discusses the view on missing heritability and argues that current approaches have fallen short of expectations. Four ways in which missing heritability may be hiding in plain sight are presented. The chapter concludes by highlighting future directions for research that will hopefully find what has been missing thus far from our understanding of genes, brains, and behavioral traits.

Genetics of decision-making

Persistent maladaptive decision-making is central to several psychiatric conditions, particularly addiction. Decision-making measures may serve as promising intermediate phenotypes (i.e. intervening mechanisms that link genetic variation to clinical vulnerability) and thus elucidate biological mechanisms that increase risk for addiction and related psychiatric disorders. This chapter focuses on the heritability and specific genetic correlates of the three most widely studied experimental measures of decision-making: impulsivity, measured by delayed reward discounting; disadvantageous decision-making, measured by the Iowa Gambling Task; and risk sensitivity, measured by the Balloon Analogue Risk Task. Despite some evidence of heritability for all phenotypes, the candidate gene studies reveal inconsistent findings. The extant literature is limited by small sample sizes, and a focus on select candidate genes, primarily related to dopaminergic and serotonergic systems. To advance the science, research will need to aggregate studies, increase sample sizes, explore subpopulations, and utilize genome-wide association studies to expand the genomic scope.

Emotional memory

This chapter presents an overview of current conceptualizations of the emotional enhancement of explicit and implicit memory. It postulates that these processes depend largely on arousal-mediated noradrenergic influences on the amygdala, a key hub in a brain network, conveying information about the (emotional) salience of stimuli and events. Selected genetic polymorphisms known to cause individual differences in neurotransmitter systems mediating emotional memory enhancement are described, as well as how these may be used as tools to investigate effects of neuromodulators and hormones on emotional memory and learning. The conclusion drawn is that studies involving candidate gene approaches should be conducted alongside genome-wide association studies (GWAS) in order to improve understanding of how genetic variations and gene clusters affect emotional memory at a molecular level. Combining earlier findings with novel work obtained from genetic studies will help understand how heritability and life experience mediate and aid generate individual differences in brain and behavior function related to emotional memory.