Background Psychological distress tolerance, the ability to persist in goal directed activity when experiencing psychological distress, is associated with poor substance use treatment outcomes including drug and alcohol treatment dropout and relapse. Objective The current study examines if a brief distress tolerance intervention that was specifically developed as an adjunctive treatment for patients in residential substance abuse treatment shows efficacy in improving the patients’ distress tolerance. Methods Seventy-six individuals who were receiving treatment at a residential substance use treatment facility and indexed low distress tolerance on laboratory distress tolerance measures were randomized into three conditions: Treatment-As-Usual (TAU), six sessions of Supportive Counseling (SC), or six sessions of the novel distress tolerance treatment, Skills for Improving Distress Intolerance (SIDI). Measures Patients were assessed at baseline for DSM-IV psychiatric diagnoses, DSM-IV substance use disorders, distress tolerance, and depressive symptoms. Patients were again assessed at posttreatment. Therapeutic alliance and treatment expectancies and credibility were also assessed at posttreatment. Results Patients who received SIDI (n = 28) evidenced significantly greater improvements than SC (n = 24) and TAU participants (n = 24) on the distress tolerance laboratory measures, even when controlling for changes in negative affect (in the form of depression). Additionally, a higher percentage of patients in SIDI reached clinically significant improvement compared to patients in SC and TAU. Conclusion This study supports the efficacy of SIDI in improving distress tolerance levels among individuals with drug and alcohol use disorders currently receiving residential substance use treatment. SIDI appears to be a brief and feasible intervention for use within inpatient substance use facilities.
Although distress tolerance is an emerging construct of empirical interest, we know little about its temporal change, developmental trajectory, and prospective relationships with maladaptive behaviors. The current study examined the developmental trajectory (mean- and individual-level change, and rank-order stability) of distress tolerance in an adolescent sample of boys and girls (N=277) followed over a four-year period. Next we examined if distress tolerance influenced change in Externalizing (EXT) and Internalizing (INT) symptoms, and if EXT and INT symptoms in turn influenced change in distress tolerance. Finally, we examined if any of these trends differed by gender. Results indicated that distress tolerance is temporally stable, with little mean- or individual-level change. Latent growth models reported that level of distress tolerance is cross-sectionally associated with both EXT and INT symptoms, yet longitudinally, only associated with EXT symptoms. These results suggest that distress tolerance should be a focus of research on etiology and intervention.
The authors suggest a theoretical model of pathways of HIV progression, with a focus on the contributions of depression-as well as secondary, behavioral and emotional variables. Literature was reviewed regarding (a) comorbid depression and the direct physiological effects on HIV progression and (b) intermediary factors between HIV and disease progression. Intermediary factors included (a) substance use, (b) social support, (c) hopelessness, (d) medication nonadherence, and (e) risky sexual behavior and the contraction of secondary infections. The authors suggest direct physiological pathways from depression to HIV progression and indirect pathways (e.g., behavioral, social, and psychological). In addition to depression, substance use, poor social support, hopelessness, medication nonadherence, and risky sexual behavior seem to be integral in HIV progression. Based on the individual relationships of these variables to depression and HIV progression, a comprehensive multipath model, incorporating all factors, serves to explain how severe emotional distress may lead to accelerated progression to AIDS.
Identifying the point at which individuals become at risk for academic failure (grade point average [GPA] < 2.0) involves an understanding of which and how many factors contribute to poor outcomes. School-related factors appear to be among the many factors that significantly impact academic success or failure. This study focused on 12 school-related factors. Using a thorough 5-step process, we identified which unique risk factors place one at risk for academic failure. Academic engagement, academic expectations, academic self-efficacy, homework completion, school relevance, school safety, teacher relationships (positive relationship), grade retention, school mobility, and school misbehaviors (negative relationship) were uniquely related to GPA even after controlling for all relevant covariates. Next, a receiver operating characteristic curve was used to determine a cutoff point for determining how many risk factors predict academic failure (GPA < 2.0). Results yielded a cutoff point of 2 risk factors for predicting academic failure, which provides a way for early identification of individuals who are at risk. Further implications of these findings are discussed.
Background: Previous work reports an association between familial risk factors stemming from parental characteristics and offspring disruptive behavior disorders (DBDs). This association may reflect a) the direct effects of familial environment, and b) a passive gene-environment correlation, wherein the parents provide both the genes and the environment. The current study examined the contributions of direct environmental influences and passive gene-environment correlations by comparing the effects of familial risk factors on child DBDs in genetically related (biological) and non-related (adoptive) families. Method: Participants were 402 adoptive and 204 biological families. Familial environment was defined as maternal and paternal maladaptive parenting and antisociality, marital conflict, and divorce; offspring DBDs included attention deficit/hyperactivity disorder, conduct disorder, and oppositional defiant disorder. Mixed-level regressions estimated the main effects of familial environment, adoption status, and the familial environment by adoption status interaction term, which tested for a presence of passive gene-environment correlations. Results: There was a main effect of maternal and paternal maladaptive parenting and marital discord on child DBDs, indicating a direct environmental effect. There was no direct environmental effect of maternal or paternal antisociality, but maternal and paternal antisociality had stronger associations with child DBDs in biological families than adoptive families, indicating the presence of a passive gene-environment correlation. Conclusions: Many familial risk factors affected children equally across genetically-related and non-related families, providing evidence for direct environmental effects. The relationship of parental antisociality and offspring DBDs was best explained by a passive gene-environment correlation, where a general vulnerability toward externalizing psychopathology is passed down by the parents to the children.
Loneliness is linked with all‐cause mortality and coronary heart disease. Altered neuroendocrine and inflammatory responses to stress constitute potential pathways linking loneliness and ill‐health. Stress responsivity is modified in people with Type 2 diabetes, but it is unclear whether loneliness influences biological stress responses in this population. We assessed interleukin‐6 (IL‐6), interleukin‐1 receptor antagonist (IL‐1RA), monocyte chemoattractant protein‐1 (MCP‐1), and cortisol responses to acute stress in 135 people with Type 2 diabetes. Loneliness was measured used the Revised UCLA Loneliness Scale. Loneliness was inversely associated with cortisol output poststress ( B = −4.429, p = 0.019) independent of age, sex, education, marital status, body mass index, and smoking. Lonelier individuals had raised MCP‐1 concentrations 75 min poststress independent of covariates ( B = 0.713, p = 0.022). No associations between loneliness and IL‐6 or IL‐1RA concentrations were detected. These results suggest that loneliness is associated with disturbances in stress responsivity in people with diabetes, and the impact of loneliness on health in people with diabetes may be mediated in part through dysregulation of inflammatory and neuroendocrine systems. Future research is required to understand if such changes increase the risk of poorer outcomes in this population.
Children with conduct problems benefit less from empirically supported interventions for disruptive behaviors when callous-unemotional (CU) traits (i.e., lack of empathy/guilt) are also present. Traditional "gold-standard" interventions for disruptive behavior disorders that focus primarily on improving parenting skills fail to address the core deficits in emotional processing and empathic responding unique to children with co-occurring conduct problems and CU traits (CP + CU). This case study presents a follow-up of the treatment of a young boy with severe disruptive behavior and pronounced CU traits using a novel, brief adjunctive treatment called Coaching and Rewarding Emotional Skills (CARES). Findings (a) indicate short-term improvements in empathic responding and emotion recognition with CARES and (b) provide preliminary support for supplementing parent training with a brief adjunctive intervention to improve socioemotional behavior and CU traits. Novel targeted interventions for children with CP + CU are critically needed given their poor prognosis and long-term impairment.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.