BackgroundPhysician behaviors that undermine a culture of safety have gained increasing attention as health-care organizations strive to create a culture of safety and reduce medical errors. We developed, implemented, and assessed a course to teach physicians skills regarding effective coping and interpersonal communication skills and present our results regarding outcomes.MethodsWe examined a professional development program specifically designed to address unprofessional or distressed behaviors of physicians, and we evaluated the impact on burnout, quality of life, and emotional flooding scores of the physicians. Assessments of burnout, quality of life, and emotional flooding were assessed preintervention and postintervention.ResultsResults demonstrated statistically significant reductions over time in physicians' emotional flooding and emotional exhaustion (EE). Specifically, using a Wilcoxon Signed-Rank test, results revealed that flooding scores at follow-up were statistically significantly lower than at baseline, V = 590, p < 0.05, and EE and personal accomplishment distributions were found to significantly deviate from normal as indicated by Shapiro–Wilks tests (p < 0.05). A Wilcoxon signed-rank test indicated that EE scores were significantly higher at baseline compared to follow-up 1, V = 285, p < 0.05.ConclusionWe conclude that the physician participants who enrolled in the educational skills training program improved scores on emotional flooding and EE and that this may be indicative of improved skills related to their experiences and learning in the program. These improved skills in physicians may have a positive impact on the overall culture of safety in the health system setting.

Although several studies have shown small longitudinal associations between baseline loneliness and subsequent dementia risk, studies rarely test whether change in loneliness predicts dementia risk. Furthermore, as both increase with advancing age, genetic and environmental selection processes may confound the putative causal association between loneliness and dementia risk. We used a sample of 2,476 individual twins from three longitudinal twin studies of aging in the Swedish Twin Registry to test the hypothesis that greater positive change in loneliness predicts greater dementia risk. We then used a sample of 1,632 pairs of twins to evaluate the hypothesis that effects of change in loneliness on dementia risk would remain after adjusting for effects of genetic and environmental variance. Phenotypic model results suggest that mild levels of baseline loneliness predict greater dementia risk. Contrary to our hypothesis, change in loneliness did not correlate with dementia risk, regardless of whether genetic and environmental selection confounds were taken into account. Worsening loneliness with age may not confer greater dementia risk.

Epigenetic clocks provide powerful tools for estimating health and lifespan but their ability to predict brain degeneration and neuronal damage during the aging process is unknown. In this study, we use GrimAge, an epigenetic clock correlated to several blood plasma proteins, to longitudinally investigate brain cellular microstructure in axonal white matter from a cohort of healthy aging individuals. Given the blood plasma correlations used to develop GrimAge, a specific focus was made on white matter hyperintensities, a visible neurological manifestation of small vessel disease, and the axonal pathways throughout each individual’s brain affected by their unique white matter hyperintensity location and volume. 98 subjects over 55 years of age were scanned at baseline with 41 returning for a follow-up scan 2 years later. Using diffusion MRI lesionometry, we reconstructed subject-specific networks of affected axonal tracts and examined the diffusion cellular microstructure composition of these areas, both at baseline and longitudinally, for evidence of cellular degeneration. A chronological age-adjusted version of GrimAge was significantly correlated with baseline WMH volume and markers of neuronal decline, indicated by increased extracellular free water, increased intracellular signal, and decreased axonal signal within WMH. By isolating subject-specific axonal regions ‘lesioned’ by crossing through a WMH, age-adjusted GrimAge was also able to predict longitudinal development of similar patterns of neuronal decline throughout the brain. This study is the first to establish a relationship between accelerated epigenetic GrimAge and brain cellular microstructure in humans.

Different trajectories of loneliness in late adulthood may explain differences in the effects of aging on dementia risk. We tested whether greater or increasing loneliness across three time points demonstrated stronger associations between aging and dementia risk in a sample of 1,814 Health and Retirement Study participants. Dementia risk was quantified using modified Telephone Interview for Cognitive Status scores (TICSm), age was quantified using the epigenetic clock DNAm PhenoAge, and loneliness was measured with the UCLA Loneliness short-form scale. Growth mixture modeling was used to identify loneliness latent classes that best represented trajectories according to model fit statistics. Five groups were identified: low loneliness, high declining, low increasing, moderate and stable, and a moderate declining group. Multivariate analysis of variance was used to test whether class membership differentially predicted TICSm scores, PhenoAge, and the correlation between TICSm and PhenoAge.TICSm scores were statistically significantly lower (worse) for the high-declining compared to the low (-1.08 95% CI [-1.75, -0.42]) and low-increasing groups (-1.63 95% CI [-2.28, -0.98]), and the moderate group was lower than the low-increasing group (-1.11 95% CI [-1.66, -0.57] and the low group (-0.57 [-1.13, -0.002]) (p’s &lt; 0.05). No significant differences in PhenoAge or the correlation between PhenoAge and TICSm were found between groups. Analyses statistically adjusted for demographic characteristics, objective social isolation, depression, BMI, smoking, self-rated health, and polygenic risk score for cognition. Results suggest that epigenome-wide ages are unlikely to mediate the relationship between loneliness and dementia risk.

In 2015, over 1.1 billion people smoked tobacco worldwide [1]. The World Health Organization (WHO) has estimated that tobacco use (smoking and smokeless) is responsible for the death of about six million people across the world each year [1]. This total includes about 600,000 people who are also estimated to die from the effects of second-hand smoke [1]. In the United States, smoking costs more than $193 billion in health care costs and lost productivity per year [2]. Although over 70% of smokers want to quit, fewer than 5% achieve this goal annually [2]. Mainstay behavioral treatments for smoking have focused on teaching individuals to avoid cues, foster positive affective states, develop lifestyle changes that reduce stress, divert attention from cravings, substitute other activities for smoking, learn cognitive strategies that reduce negative mood, and develop social support mechanisms. These interventions and methods have shown modest success, with abstinence rates between only 20-30% holding steady over the past thirty years. This low rate of abstinence attainment and lack of improvement in outcomes is presumably due to the complex nature of the acquisition and maintenance of nicotine addiction, including associative learning mechanisms as well as positive and negative reinforcement.The complex learning mechanisms behind the acquisition of nicotine dependence is related to the fact that over time cues that are judged to be positive or negative can induce affective states, which can then trigger a craving to use [3,4]. Though the centrality of craving remains controversial, evidence suggests that craving is strongly associated with using, which, mainly through the physiological properties of nicotine, results in the maintenance or improvement of positive or reduction of negative affective states [4]. This sets up reinforcement loops by reinforcing memories between affect and smoking [3]. Thus, recent attention has been focused on additional strategies to help people tolerate negative affect and cravings rather than only avoiding cues or substituting activities.Recent research suggests that another psychological intervention called mindfulness training (MT) may decouple the association between craving and smoking, thus facilitating smoking cessation. Mindfulness means paying attention in the present moment, non-judgmentally, without commentary or decision-making. MT targets affective or craving states by teaching individuals to observe aversive body and mind states instead of responding to them with habitual reactions, thus allowing more adaptive, healthier responses [5]. MT has shown promise in reducing anxiety and depression and has recently been explored in the treatment of addictions. Davis et al. [6] conducted a pilot study to explore the effect of using Mindfulness Based Stress Reduction (MBSR) (with minor modifications) as a smoking intervention. MBSR was employed in its standard 8 weekly group session format. Subjects attempted smoking cessation during week seven without pharmacotherapy. The researche...

Social isolation is one of the strongest predictors of increased risk of mortality in older adulthood. The ability to form and maintain the social relationships that mitigate this risk is partially regulated by the oxytocinergic system and one's ability to attend to and process social information. We have previously shown that an epigenetic change to the DNA of the oxytocin receptor gene (OXTR methylation) affects the salience of social information in young adults. Little is known about how the oxytocinergic system ages and what effect this aging system has on social cognitive abilities throughout the lifespan. Here we explore age-related differences in the association between neural response during selective social attention and OXTR DNA methylation in young and older adults. We find that older adults activate diffuse areas of visual cortex and dorsolateral prefrontal cortex during selective social attention, consistent with the dedifferentiation and compensatory neural activation commonly reported in aging. We find a significant age-by-OXTR methylation interaction on neural response when attending to social stimuli in a complex display; young adults display a positive association between OXTR methylation and neural activation, replicating our prior finding that young adults with presumed diminished endogenous access to oxytocin recruit regions of the attentional cortex to a greater extent. This association does not hold for older adults. Instead, perceived social support interacts with OXTR methylation to influence neural response during selective social attention. These data suggest that environmental factors like social support moderate biological processes in aging and highlight the importance of a lifespan perspective for understanding associations between individual differences in the oxytocinergic system, neural function, and social behavior.

Abbreviations: CBASP, cognitive behavioral analysis system of psychotherapy; HAM-D, hamilton rating scale for depression; CIWA, clinical institute withdrawal assessment for alcohol; SA, situational analysis; SDU, standard drinking units; CBT, cognitive behavioral therapy; MI, motivational interviewing; CSQ, coping survey questionnaire; IMI-C, impact message inventory circumplex IntroductionAlcohol use disorder is frequently comorbid with other psychiatric disorders such as major depression, and professionals working with these patients are facing a unique challenge. 1 The estimated cost of excessive drinking in 2010 was $249.0 billion, which equates to $2.05 per drink or $807 per person. 2 The prevalence rate for major depression rose from 13.8 million to 15.4 million adults between 2005 and 2010, and this increased the cost by 21.5 % from $173.2 billion to $210.5 billion in 2010. 3 As a result of the deleterious psychological impact on the individual and the economic burden on society, there is a growing need to develop and evaluate effective treatments for these significant and prevalent disorders.There are currently multiple empirically supported behavioral treatments for depression and alcoholism as individual disorders. However, there have been few well-specified, empirically supported behavioral therapies with an integrated approach to treating symptoms of both disorders. [4][5][6] The most commonly evaluated types of behavioral therapies for co-occurring disorders include motivational interviewing (MI), cognitive behavioral therapy (CBT) and contingency management (CM); 4 research supports that an integrated therapy possessing components of MI, CBT, and CM would be most ideal to target co occurring depression and alcoholism. [4][5][6] The lack of successful treatment options for chronically depressed alcohol dependent individuals may be due in part to the complex characteristics these individuals possess that make their treatment more challenging. [7][8][9][10] Comorbid depression is associated with poorer prognosis during and after alcoholism treatment and depressed mood may be an important trigger of alcoholic relapse. 7,11 Interpersonal avoidance behaviors are salient variables in individuals diagnosed with both alcoholism and depression. These patients typically report a high rate of adverse early home environments, a lifelong history of intrapersonal and interpersonal failure, an earlier onset of depression and alcohol use disorders, more comorbidity, a more severe course of illness, and they demonstrate interpersonal avoidance and detachment. 8,12,13 Early abuse/trauma history impairs development of adequate interpersonal coping skills, resulting in depression, social isolation, or withdrawal. 14 In addition, real-world and prolonged environmental stressors usually accompany these individuals' presenting complaints. They are often skeptical or ambivalent about change, and the processes of change are often slow, irregular, and inconsistent. In fact, a pattern of success followed by a setback is commo...

Background: Over the last 10 years, numerous studies have been published reporting a small but significant correlation between loneliness and dementia risk. To date, few studies have tested mechanisms that mediate the longitudinal association between loneliness and dementia. DNA methylation may be one variable that explains this association, as when combined with other biomarkers, quantifies whether people's biological age is more (or less) advanced than their chronological age. The purpose of this study is to test whether epigenetic age moderates the longitudinal trajectory of loneliness on dementia risk. Method: The sample was drawn from the three waves of the Health and Retirement Study (n = 268, mean age = 69) collected four years apart from 2008-2016. Loneliness scores were composed using with 11 items of the UCLA Loneliness Questionnaire. Dementia risk was quantified according to Langa-Weir's approach that uses the modified Telephone Interview for Cognitive Status. Epigenetic age is quantified by DNAm PhenoAge (Levine et al., 2015.). Ordinary least squares regression was used to test the interaction effect of DNAm PhenoAge and loneliness on dementia risk.Result: A significant interaction effect between DNAmPhenoAge and longitudinal loneliness on dementia risk was found (F(7,268) = 6.98 , p < 0.001; adjusted R2 =.13).Effects of DNAm PhenoAge were greater in those with higher levels of loneliness over time, suggesting that effects of loneliness on dementia risk depend on epigenetic age. Conclusion:Study results suggest that the longitudinal association between loneliness and dementia risk depends on epigenetic age. One implication of the current results is that the epigenome may be a promising area of study for understanding the processes through which loneliness increases dementia risk.