Cardiovascular Stress Reactivity and Health: Recent Questions and Future Directions.

OBJECTIVE: High cardiovascular reactions to psychological stress are associated with the development of hypertension, systemic atherosclerosis, and cardiovascular disease. However, it has become apparent that low biological stress reactivity also may have serious consequences for health, although less is known about the mechanisms of this. The objectives of this narrative review and opinion article are to summarize and consider where we are now in terms of the usefulness of the reactivity hypothesis and reactivity research, given that both ends of the reactivity spectrum seem to be associated with poor health, and to address some of the key criticisms and future challenges for the research area. METHODS: This review is authored by the members of a panel discussion held at the American Psychosomatic Society meeting in 2019, which included questions such as the following: How do we measure high and low reactivity? Can high reactivity ever indicate better health? Does low or blunted reactivity simply reflect less effort on task challenges? Where does low reactivity originate from, and what is a low reactor? RESULTS: Cardiovascular (and cortisol) stress reactivity are used as a model to demonstrate an increased understanding of the different individual pathways from stress responses to health/disease and show the challenges of how to understand and best use the reconstruction of the long-standing reactivity hypothesis given recent data. CONCLUSIONS: This discussion elucidates the gaps in knowledge and key research issues that still remain to be addressed in this field, and that systematic reviews and meta-analyses continue to be required.

Cortisol stress reactivity in women, diurnal variations, and hormonal contraceptives: studies from the Family Health Patterns Project.

Women have smaller cortisol responses to psychological stress than men do, and women taking hormonal contraceptives (HC+) have smaller responses than HC- women. Cortisol secretion undergoes substantial diurnal variation, with elevated levels in the morning and lower levels in the afternoon, and these variations are accompanied by differences in response to acute stress. However, the impact of HC use on these diurnal relationships has not been examined. We tested saliva cortisol values in 744 healthy young adults, 351 men and 393 women, 254 HC- and 139 HC+, who were assigned to morning (9:00 am) or afternoon (1:00 pm) test sessions that were held both on a rest day and on a stress day that included public speaking and mental arithmetic challenges. Saliva cortisol responses to stress were largest in men and progressively smaller in HC- and in HC+ women (F = 23.26, p < .0001). In the morning test sessions, HC+ women had significantly elevated rest day cortisol levels (t = 5.99, p ≪ .0001, Cohen's d = 0.95) along with a complete absence of response on the stress day. In the afternoon sessions, both HC+ and HC- women had normal rest-day cortisol levels and normal responses to the stressors. Heart rates at rest and during stress did not vary by time of day or HC status. Cortisol stress responses in HC+ women are absent in the morning and normal in size by early afternoon. Studies of stress reactivity should account for time of day in evaluating cortisol responses in women using hormonal contraceptives.

Early-Life Adversity and Blunted Stress Reactivity as Predictors of Alcohol and Drug use in Persons With COMT (rs4680) Val158Met Genotypes.

BACKGROUND: Risk for alcoholism may be enhanced by exposure to early-life adversity (ELA) in persons with genetic vulnerabilities. We examined ELA in the presence of a common variant of the gene for the enzyme catechol-O-methyltransferase (COMT, Val158Met, rs4680) in relation to cortisol reactivity, the onset of early drinking, and experimentation with drugs. METHODS: Saliva cortisol reactivity to speech and mental arithmetic stress was measured in 480 healthy young adults (23.5 years of age, 50% females) who experienced either 0, 1, or ≥ 2 forms of ELA during childhood and adolescence, provided information on use of alcohol and recreational drugs, and were genotyped for the Val158Met polymorphism. RESULTS: ELA led to progressively smaller cortisol responses in the Met/Met and Val/Met allele groups but to progressively larger responses in Val homozygotes, F = 3.29, p = 0.011. ELA independently predicted earlier age at first drink, F = 14.2, p < 0.0001, with a larger effect in Met-allele carriers, F = 13.95, p < 0.00001, and a smaller effect in Val homozygotes, F = 4.14, p = 0.02. Similar effects were seen in recreational drug use. Cortisol reactivity was unrelated to drinking behavior or drug experimentation. CONCLUSIONS: ELA leads to blunted stress reactivity and, independently, contributes to potentially risky drinking and drug-use behaviors in persons carrying 1 or 2 copies of the COMT 158Met allele. The results reinforce the impact of early experience on the stress axis and on risky behaviors, and they point to the 158Met allele as conveying a vulnerability to the early environment.

Joint Impact of Early Life Adversity and COMT Val158Met (rs4680) Genotypes on the Adult Cortisol Response to Psychological Stress.

OBJECTIVE: Exposure to stress during critical periods of development can diminish stress reactivity by the hypothalamic-pituitary-adrenocortical axis. Genetic characteristics may further modify this effect of early adversity, leading to a gene by environment (G × E) interaction on stress reactivity in adulthood. Val-allele carriers of a common polymorphism of the COMT gene (Val158Met, rs4680) have rapid removal of catecholamines in the prefrontal cortex, limbic system, and reward centers. Carriers of the Val and Met alleles may therefore respond differently to the environment and differ in the long-term impact of exposure to early life adversity (ELA). METHODS: We measured saliva cortisol reactivity to public speaking and mental arithmetic stress in 252 healthy young adults exposed to low, medium, and high levels of ELA and who were genotyped for the Val158Met polymorphism. RESULTS: Cortisol responses showed a G × E interaction (F(4,243) = 2.78, p = .028); simple effects tests showed that Met/Met carriers had progressively smaller cortisol responses with greater levels of ELA. In comparison, Val/Val homozygotes had blunted responses that did not vary with ELA exposure. CONCLUSIONS: Met/Met homozygotes seem sensitive to stressful events in childhood and adolescence, leading to environmental programming of the stress axis. Glucocorticoid responsivity may represent a common pathway revealing targeted genetic vulnerabilities to the long-term effects of early life stress. The results suggest that further G × E studies of ELA are warranted in relation to health behaviors and health outcomes in adulthood.

Can exaggerated stress reactivity and prolonged recovery predict negative health outcomes? The case of cardiovascular disease.

Researchers and laypersons have long argued that stress is bad for health, particularly when responses are large, prolonged, and frequent. By extension, individuals who have the largest and the most prolonged responses are assumed to have worse outcomes than do less reactive persons. Research in animals has been supportive of the connection between stress and poor health, but evidence in humans has been slow to accumulate. The current issue of Psychosomatic Medicine presents a meta-analysis of 33 studies of delayed recovery from stress and its association with poor cardiovascular disease outcomes and all-cause mortality. The analysis supports the contention that slower recovery to baseline after exercise or psychological stress may predict earlier death due to all causes. This finding raises questions for psychosomatic theories of disease and points the direction for further study of how or whether to incorporate reactivity measures into standard risk profiles.

Combining diffusion tensor imaging and magnetic resonance spectroscopy to study reduced frontal white matter integrity in youths with family histories of substance use disorders.

Individuals with a family history of substance use disorder (FH+) show impaired frontal white matter as indicated by diffusion tensor imaging (DTI). This impairment may be due to impaired or delayed development of myelin in frontal regions, potentially contributing to this population's increased risk for developing substance use disorders. In this study, we examined high angular resolution DTI and proton magnetic resonance spectroscopy data from the anterior corona radiata were collected in 80 FH+ and 34 FH- youths (12.9 ± 1.0 years old). White matter integrity indices included fractional anisotropy (FA), N-acetylaspartate (NAA), and total choline (tCho). Lower FA suggests decreased myelination. Decreased NAA coupled with higher tCho suggests impaired build-up and maintenance of cerebral myelin and consequently greater breakdown of cellular membranes. We found FH+ youths had lower FA (P < 0.0001) and NAA (P = 0.017) and higher tCho (P = 0.04). FH density (number of parents and grandparents with substance use disorders) was negatively correlated with FA (P < 0.0001) and NAA (P = 0.011) and positively correlated with tCho (P = 0.001). FA was independently predicted by both FH density (P = 0.006) and NAA (P = 0.002), and NAA and tCho were both independent predictors of FH density (P < 0.001). Our finding of lower frontal FA in FH+ youths corresponding to lower NAA and increased tCho is consistent with delayed or impaired development of frontal white matter in FH+ youths. Longitudinal studies are needed to determine how these differences relate to substance use outcomes.

Assessment of whole brain white matter integrity in youths and young adults with a family history of substance-use disorders.

Individuals with a family history of substance use disorders (FH+) are at a greater risk of developing substance use disorders than their peers with no such family histories (FH-) and this vulnerability is proportional to the number of affected relatives (FH density). The risk for developing substance use disorders peaks during adolescence to early adulthood in the general population, and that is thought to be related to delayed maturation of frontocortical and frontostriatal functional circuits. We hypothesized that FH+ youth and young adults have impaired myelination of frontocortical and frontostriatal white matter tracts. We examined fractional anisotropy (FA) data in 80 FH+ and 34 FH- youths (12.9 ± 1.0 years) and in 25 FH+ and 30 FH- young adults (24.3 ± 3.4 years). FH+ youths had lower FA values in both frontocortical and frontostriatal tracts as well as parietocortical tracts including the anterior, superior and posterior corona radiata and the superior frontal-occipital fasciculus. Moreover, FA values in these tracts were negatively correlated with FH density. FH+ adults had lower FA values in two frontocortical tracts: the genu of the corpus callosum and anterior corona radiata and also significant negative correlations between FA and FH density in these same tracts. In both groups, lower FA values corresponded to higher radial diffusivity suggesting reduced axonal myelination. We interpreted our findings as evidence for impaired myelination of frontal white matter that was proportional to FH density. Our data suggest that deficits may partially resolve with age, paralleling an age-related decline in risk for developing substance use disorders.

Anomalous temporoparietal activity in individuals with a family history of alcoholism: studies from the Oklahoma Family Health Patterns Project.

BACKGROUND: Individuals with a family history of alcoholism (FH+) are at enhanced risk of developing alcohol or other substance use disorders relative to those with no family history (FH-). Alcoholics and FH+ subjects have greater interference scores on the Stroop color-word task, suggesting these impairments may be a component of the cognitive phenotype of at-risk individuals. METHODS: In this study, we examined whole-brain activations in 24 FH+ and 28 FH- young adults performing the counting Stroop task, a variant of the Stroop task adapted for neuroimaging studies. RESULTS: Across all subjects, incongruent versus congruent comparisons showed activations in regions including parietal lobe areas, frontal eye fields, premotor areas, the anterior cingulate cortex, dorsolateral prefrontal cortex, and bilateral insula, indicating typical regions of activation involved in conflict resolution tasks. Compared with FH- participants, FH+ participants had greater activations in the left superior parietal lobule and precuneus (BA 7 and 19), inferior parietal lobule (BA 40), and middle temporal gyrus (BA 39 and 19), indicating a predominance of greater left hemisphere activity among FH+ in temporoparietal regions. There were no regions showing greater activations in the FH- group compared with the FH+ group. CONCLUSIONS: These results are consistent with less efficient cognitive functioning potentially due to poorer communication over long pathways connecting temporoparietal regions to prefrontal brain regions that participate in a distributed network involved in cognitive processing and working memory necessary for conflict resolution.

Differential impact of serotonin transporter activity on temperament and behavior in persons with a family history of alcoholism in the Oklahoma Family Health Patterns Project.

BACKGROUND: Central serotonergic (5-HT) function is implicated in pathways to alcohol dependence, including dysphoria manifested by symptoms of anxiety and depression. However, little is known about genetic variation in central 5-HT function and its potential impact on temperament and behavior in persons with a family history of alcoholism (FH+). METHODS: We tested 314 healthy young adults (23.5 years of age, 57% female; 193 FH- and 121 FH+) enrolled in the Oklahoma Family Health Patterns project, a study of alcoholism risk in relation to temperament and behavioral dyscontrol. Dysphoria was assessed using the Eysenck neuroticism and Beck depression scales, and Cloninger's Tridimensional Personality Questionnaire. Risk taking was assessed with the Iowa Gambling Task (IGT) and Balloon Analogue Response Task (BART). All subjects were genotyped for a functional polymorphism (5-HTTLPR) in the promoter region of the serotonin transporter gene (SLC6A4). RESULTS: FH+ subjects with the gain-of-function 5-HTTLPR genotype scored higher in neuroticism, harm avoidance, and symptoms of depression (p-values ≤ 0.03). No effect of 5-HTTLPR genotype was seen in FH-. FH+ carriers of the gain-of-function 5-HTTLPR genotype played to minimize their frequency of losses in the IGT, whereas FH- carriers played a balanced strategy (p < 0.003). No 5-HTTLPR effects were seen in the BART. Results were unaffected by sex, education, drug use, and antisocial characteristics. CONCLUSIONS: The functional 5-HTTLPR polymorphism predicted significant variation in negative moods and poorer affect regulation in FH+ persons, with possible consequences for behavior, as seen in a simulated gambling task. This pattern may contribute to a drinking pattern that is compensatory for such affective tendencies.

Early life adversity contributes to impaired cognition and impulsive behavior: studies from the Oklahoma Family Health Patterns Project.

BACKGROUND: Stressful early life experience may have adverse consequences in adulthood and may contribute to behavioral characteristics that increase vulnerability to alcoholism. We examined early life adverse experience in relation to cognitive deficits and impulsive behaviors with a reference to risk factors for alcoholism. METHODS: We tested 386 healthy young adults (18 to 30 years of age; 224 women; 171 family history positive for alcoholism) using a composite measure of adverse life experience (low socioeconomic status plus personally experienced adverse events including physical and sexual abuse and separation from parents) as a predictor of performance on the Shipley Institute of Living scale, the Stroop color-word task, and a delay discounting task assessing preference for smaller immediate rewards in favor of larger delayed rewards. Body mass index (BMI) was examined as an early indicator of altered health behavior. RESULTS: Greater levels of adversity predicted higher Stroop interference scores (F = 3.07, p = 0.048), faster discounting of delayed rewards (F = 3.79, p = 0.024), lower Shipley mental age scores (F = 4.01, p = 0.019), and higher BMIs in those with a family history of alcoholism (F = 3.40, p = 0.035). These effects were not explained by age, sex, race, education, or depression. CONCLUSIONS: The results indicate a long-term impact of stressful life experience on cognitive function, impulsive behaviors, and early health indicators that may contribute to risk in persons with a family history of alcoholism.

The functional connectivity of the human caudate: an application of meta-analytic connectivity modeling with behavioral filtering.

Meta-analysis based techniques are emerging as powerful, robust tools for developing models of connectivity in functional neuroimaging. Here, we apply meta-analytic connectivity modeling to the human caudate to 1) develop a model of functional connectivity, 2) determine if meta-analytic methods are sufficiently sensitive to detect behavioral domain specificity within region-specific functional connectivity networks, and 3) compare meta-analytic driven segmentation to structural connectivity parcellation using diffusion tensor imaging. Results demonstrate strong coherence between meta-analytic and data-driven methods. Specifically, we found that behavioral filtering resulted in cognition and emotion related structures and networks primarily localized to the head of the caudate nucleus, while perceptual and action specific regions localized to the body of the caudate, consistent with early models of nonhuman primate histological studies and postmortem studies in humans. Diffusion tensor imaging (DTI) revealed support for meta-analytic connectivity modeling's (MACM) utility in identifying both direct and indirect connectivity. Our results provide further validation of meta-analytic connectivity modeling, while also highlighting an additional potential, namely the extraction of behavioral domain specific functional connectivity.

Early life adversity and increased antisocial and depressive tendencies in young adults with family histories of alcohol and other substance use disorders: Findings from the Family Health Patterns project.

Background: Individuals with a family history of alcohol and other substance use disorders (FH+) are several times more likely to develop alcohol problems compared to individuals with no such family histories (FH-). Here we sought to evaluate associations of early life adversity (ELA) with two key risk-related FH+ phenotypic characteristics: increased antisocial and depressive tendencies. Methods: We examined data from 1187 FH+ and FH- young adults (average age 23.6 years old) with and without personal histories of substance use disorders. Antisocial tendencies were evaluated with the Socialization scale of the California Personality Inventory (CPI-So), while depressive tendencies were evaluated with the Beck Depression Inventory II (BDI). Results: In general, being FH+, having a personal substance use disorder history, and experiencing greater levels of ELA were associated with lower CPI-So scores (indicating more antisocial tendencies) and higher BDI scores (indicating more depressive tendencies). Conclusions: These results suggest that ELA is linked to increased antisocial and depressive tendencies observed in FH+ persons. Given that FH+ individuals are disproportionately exposed to ELA, this increased exposure may be a major contributor to these and other risk-related characteristics commonly present in FH+ individuals. Additional studies are needed to evaluate the impact of ELA on risk-related phenotypic characteristics, including prospective studies in early childhood and mechanistic studies evaluating pathways by which ELA exerts its effects on FH phenotypic characteristics.

Greater discounting of delayed rewards in young adults with family histories of alcohol and drug use disorders: studies from the Oklahoma family health patterns project.

BACKGROUND: Increased discounting of delayed rewards may be a premorbid characteristic and possible risk factor for alcohol and other drug use disorders; however, previous studies have found no or minimal differences in delay discounting in individuals at risk for substance use disorders based on family history. It is possible that increased delay discounting may be more closely associated with antisocial traits, evident in a subset of individuals with positive family histories of alcohol and drug use disorders, and that previous studies were underpowered for detecting subtle to modest overall group differences. METHODS: In this study, we compared 143 young adults with family histories of alcohol and other drug use disorders (FH+) and 155 young adults with no such histories (FH-) on delay discounting and subsequently examined how delay discounting was related to antisocial traits and other selected psychological and demographic variables. RESULTS: The FH+ group discounted delayed rewards more than the FH- group. Subsequent analyses revealed that increased delay discounting was correlated with having more parents and grandparents with alcohol and drug use disorders, more antisocial traits, more depressive tendencies and lower IQs, and lower income. After controlling for all these relationships, more antisocial traits and lower IQ still predicted greater delay discounting, and subsequent analysis revealed that the greater delay discounting in the FH+ group was mediated by this group's greater number of individuals with antisocial traits. CONCLUSION: FH+ individuals who discount delayed rewards more may be at increased risk for developing alcohol and other drug use disorders; however, additional descriptive studies and longitudinal studies are needed.

Neurobiological mechanisms of early life adversity, blunted stress reactivity and risk for addiction.

Blunted stress reactivity resulting from early exposure to stress during childhood and adolescence may increase vulnerability to addiction. Early life adversity (ELA) affects brain structure and function and results in blunted stress axis reactivity. In this review, we focus on the underlying neurobiological mechanisms associated with a blunted response to stress, ELA, and risk for addictive disorders. ELA and blunted reactivity are accompanied by unstable mood regulation, impulsive behaviors, and reduced cognitive function. Neuroimaging studies reveal cortical and subcortical changes in persons exposed to ELA and those who have a genetic disposition for addiction. We propose a model in which blunted stress reactivity may be a marker of risk for addiction through an altered motivational and behavioral reactivity to stress that contribute to disinhibited behavioral reactivity and impulsivity leading in turn to increased vulnerability for substance use. Evidence supporting this hypothesis in the context of substance use initiation, maintenance, and risk for relapse is presented. The effects of ELA on persons at risk for addiction may lead to early experimentation with drugs of abuse. Early adoption of drug intake may alter neuroregulation in such vulnerable persons leading to a permanent dysregulation of motivational responses consistent with dependence. This article is part of the special issue on 'Vulnerabilities to Substance Abuse'.

Baseline associations between biomarkers, cognitive function, and self-regulation indices in the Cognitive and Self-regulatory Mechanisms of Obesity Study.

OBJECTIVE: Understanding how biological, cognitive, and self-regulatory factors are related to obesity, and weight regulation is clearly needed to optimize obesity prevention and treatment. The objective of this investigation was to understand how baseline biological, cognitive, and self-regulatory factors are related to adiposity at the initiation of a behavioral weight loss intervention among treatment-seeking adults with overweight/obesity. METHODS: Participants (N = 107) in the Cognitive and Self-regulatory Mechanisms of Obesity Study (Identifier-NCT02786238) completed a baseline assessment with anthropometric, cardiometabolic, inflammatory, cognitive function, and self-regulation measures as part of a larger on-going trial. Data were analyzed with linear regression. RESULTS: At baseline, body mass index, body fat percentage, and waist circumference (WC) were positively associated with fasting insulin and insulin resistance. Higher WC was related to higher fasting glucose and hemoglobin A1c (HbA1c). Higher glucose and insulin resistance levels were related to lower list sorting working memory. Higher glucose and HbA1c levels were negatively associated with reading scores. Cognitive function and self-regulation indices were unrelated. CONCLUSIONS: In adults with overweight/obesity entering a weight loss treatment study: (1) elevated WC and associated glycemic impairment were negatively associated with cognition, (2) poorer executive function and reading abilities were associated with poorer glycemic control, and (3) objectively measured cognitive functions were unrelated to self-reported/behavioral measures of self-regulation. Such findings increase understanding of the relationships between adiposity, biomarkers, cognition, and self-regulation at treatment initiation and may ultimately inform barriers to successful obesity treatment response.

Metaanalytic connectivity modeling: delineating the functional connectivity of the human amygdala.

Functional neuroimaging has evolved into an indispensable tool for noninvasively investigating brain function. A recent development of such methodology is the creation of connectivity models for brain regions and related networks, efforts that have been inhibited by notable limitations. We present a new method for ascertaining functional connectivity of specific brain structures using metaanalytic connectivity modeling (MACM), along with validation of our method using a nonhuman primate database. Drawing from decades of neuroimaging research and spanning multiple behavioral domains, the method overcomes many weaknesses of conventional connectivity analyses and provides a simple, automated alternative to developing accurate and robust models of anatomically-defined human functional connectivity. Applying MACM to the amygdala, a small structure of the brain with a complex network of connections, we found high coherence with anatomical studies in nonhuman primates as well as human-based theoretical models of emotive-cognitive integration, providing evidence for this novel method's utility.

Deficits in affective prosody comprehension: family history of alcoholism versus alcohol exposure.

BACKGROUND: Abstinent alcoholics have deficits in comprehending the affective intonation in speech. Prior work suggests that these deficits are due to alcohol exposure rather than preexisting risk factors for alcoholism. The present paper examines whether family history of alcoholism is a contributor to affective prosody deficits in alcoholics. METHODS: Fifty-eight healthy, nonabusing young adults with and without a family history of alcoholism or other substance abuse (29 FH+ and 29 FH-) were compared on affective prosody comprehension using the Aprosodia Battery. A secondary analysis was done comparing affective prosody comprehension in FH+ and FH- detoxified alcoholics from an earlier study (17 FH+ and 14 FH-). RESULTS: Performance on the Aprosodia Battery was not related to FH status in either the healthy, nonabusing sample or in the detoxified alcoholic group. CONCLUSIONS: The present study lends support to previous research suggesting that deficits in affective prosody comprehension observed in detoxified alcoholics are associated with a history of heavy drinking rather than with a family history of alcoholism.

The rebirth of neuroscience in psychosomatic medicine, Part I: historical context, methods, and relevant basic science.

Neuroscience was an integral part of psychosomatic medicine at its inception in the early 20th century. Since the mid-20th century, however, psychosomatic research has largely ignored the brain. The field of neuroscience has burgeoned in recent years largely because a variety of powerful new methods have become available. Many of these methods allow for the noninvasive study of the living human brain and thus are potentially available for integration into psychosomatic medicine research at this time. In this first paper we examine various methods available for human neuroscientific investigation and discuss their relative strengths and weaknesses. We next review some basic functional neuroanatomy involving structures that are increasingly being identified as relevant for psychosomatic processes. We then discuss, and provide examples of, how the brain influences end organs through "information transfer systems," including the autonomic, neuroendocrine, and immune systems. The evidence currently available suggests that neuroscience holds great promise for advancing the goal of understanding the mechanisms by which psychosocial variables influence physical disease outcomes. An increased focus on such mechanistic research in psychosomatic medicine is needed to further its acceptance into the field of medicine.

The rebirth of neuroscience in psychosomatic medicine, Part II: clinical applications and implications for research.

During the second half of the last century, biopsychosocial research in psychosomatic medicine largely ignored the brain. Neuroscience has started to make a comeback in psychosomatic medicine research and promises to advance the field in important ways. In this paper we briefly review select brain imaging research findings in psychosomatic medicine in four key areas: cardiovascular regulation, visceral pain in the context of functional gastrointestinal disorders, acute and chronic somatic pain and placebo. In each area, there is a growing literature that is beginning to define a network of brain areas that participate in the functions in question. Evidence to date suggests that cortical and subcortical areas that are involved in emotion and emotion regulation play an important role in each domain. Neuroscientific research is therefore validating findings from previous psychosomatic research and has the potential to extend knowledge by delineating the biological mechanisms that link mind and body more completely and with greater specificity. We conclude with a discussion of the implications of this work for how research in psychosomatic medicine is conducted, the ways in which neuroscientific advances can lead to new clinical applications in psychosomatic contexts, the implications of this work for the field of medicine more generally, and the priorities for research in the next 5 to 10 years.

Influence of antisocial and psychopathic traits on decision-making biases in alcoholics.

BACKGROUND: Although decision-making processes have become a principal target of study among addiction researchers, few studies have specifically examined decision-making among individuals with alcohol dependence (AD) and findings to date are mixed. The present study examined the relationship between AD and decision-making, and tested whether different facets of antisocial and psychopathic traits explain this association. METHODS: Participants were men with AD (n = 22), AD and comorbid antisocial personality disorder (AD + ASPD; n = 17), or a history of recreational alcohol use, but no current or lifetime symptoms of a substance use disorder, conduct disorder, or ASPD (n = 21). Decision-making was tested using the Iowa Gambling Task (IGT). RESULTS: Across groups, participants reported similar levels of awareness of the contingencies of the task, but the AD groups with and without ASPD had poorer IGT performance compared with controls (p < 0.05). A block-by-block analysis revealed that while AD had slow but steady improvement across the task, AD + ASPD exhibited initial improvement followed by a significant decrease in advantageous decision-making during the last 20 trials (p < 0.05). This was further confirmed via evidence that impulsive/antisocial personality traits but not psychopathic traits mediated poor IGT performance beyond ASPD diagnosis. CONCLUSIONS: Alcohol-dependent males favored risky choices regardless of whether they met criteria for ASPD. However, decision-making deficits were more pronounced among those with ASPD, and personality traits characterized by impulsive and antisocial tendencies mediated the relationship between AD and decision-making.