Objectives We sought to determine whether unhealthy behaviors play a stress-buffering role in observed racial disparities in physical and mental health. Methods We conducted logistic regressions by race on data from the first 2 waves of the Americans’ Changing Lives Survey to determine whether unhealthy behaviors had buffering effects on the relationship between major stressors and chronic health conditions, and on the relationship between major stressors and meeting the criteria for major depression. Results Among Whites, unhealthy behaviors strengthened the relationship between stressors and meeting major-depression criteria. Among Blacks, however, the relationship between stressors and meeting major-depression criteria was stronger among those who had not engaged in unhealthy behaviors than among those who had. Among both race groups there was a positive association between stressors and chronic health conditions. Among Blacks there was an additional positive association between number of unhealthy behaviors and number of chronic conditions. Conclusions Those who live in chronically stressful environments often cope with stressors by engaging in unhealthy behaviors that may have protective mental-health effects. However, such unhealthy behaviors can combine with negative environmental conditions to eventually contribute to morbidity and mortality disparities among social groups.

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Crucial advances have been made in our knowledge of the social determinants of health and health behaviors. Existing research on health disparities, however, generally fails to address a known paradox in the literature: While blacks have higher risk of medical morbidity relative to non-Hispanic whites, blacks have lower rates of common stress-related forms of psychopathology such as major depression and anxiety disorders. In this article we propose a new theoretical approach, the Environmental Affordances Model, as an integrative framework for the origins of both physical and mental health disparities. We highlight early empirical support and a growing body of experimental animal and human research on self-regulatory health behaviors and stress coping that is consistent with the proposed framework. We conclude that transdisciplinary approaches, such as the Environmental Affordances Model, are needed to understand the origins of group-based disparities to implement effective solutions to racial and ethnic group inequalities in physical and mental health.

Prevalence of depression is associated inversely with some indicators of socioeconomic position, and the stress of social disadvantage is hypothesized to mediate this relation. Relative to whites, blacks have a higher burden of most physical health conditions but, unexpectedly, a lower burden of depression. This study evaluated an etiologic model that integrates mental and physical health to account for this counterintuitive patterning. The Baltimore Epidemiologic Catchment Area Study (Maryland, 1993-2004) was used to evaluate the interaction between stress and poor health behaviors (smoking, alcohol use, poor diet, and obesity) and risk of depression 12 years later for 341 blacks and 601 whites. At baseline, blacks engaged in more poor health behaviors and had a lower prevalence of depression compared with whites (5.9% vs. 9.2%). The interaction between health behaviors and stress was nonsignificant for whites (odds ratio (OR = 1.04, 95% confidence interval: 0.98, 1.11); for blacks, the interaction term was significant and negative (β: -0.18, P < 0.014). For blacks, the association between median stress and depression was stronger for those who engaged in zero (OR = 1.34) relative to 1 (OR = 1.12) and ≥2 (OR = 0.94) poor health behaviors. Findings are consistent with the proposed model of mental and physical health disparities.

This study evaluated the effectiveness of a theoretically based, culturally specific family intervention designed to prevent youth risky behaviors by influencing the parenting attitudes and behaviors of nonresident African American fathers and the parent-child interactions, intentions to avoid violence, and aggressive behaviors of their preadolescent sons. A sample of 158 intervention and 129 comparison group families participated. ANCOVA results indicated that the intervention was promising for enhancing parental monitoring, communication about sex, intentions to communicate, race-related socialization practices, and parenting skills satisfaction among fathers. The intervention was also beneficial for sons who reported more monitoring by their fathers, improved communication about sex, and increased intentions to avoid violence. The intervention was not effective in reducing aggressive behaviors among sons. Findings are discussed from a family support perspective, including the need to involve nonresident African American fathers in youth risky behavior prevention efforts.

Correlational studies have identified worksite coping resources such as social support and perceived control, and have suggested a positive role for such resources in employee stress processes. However, little experimental evidence has demonstrated the causal role of worksite coping resources in improving mental health, nor how worksite coping resources can be enhanced. This paper reports the results of a field experiment intended to provide such evidence. Human service workers participated in a theory‐driven training program designed to increase individual and group psychosocial coping resources and individuals' abilities to use those resources when coping with job demands. The inclusion of selection variables in models used to estimate the impact of the intervention controlled for selection biases and also allowed for the assessment of the impact of the training on those workers identified as most prone to turnover and on those most likely to participate in such an intervention. Results indicated that the program enhanced the work team climate and reduced depresssive symptoms and somatization in those most at risk for leaving their jobs. The program was also effective in increasing the amount of supervisor support received on the job and strengthening perceptions of coping abilities in those workers most likely to participate in the program.

Firing of action potentials in excitable cells accelerates ATP turnover. The voltage-gated potassium channel Kv2.1 regulates action potential frequency in central neurons, whereas the ubiquitous cellular energy sensor AMP-activated protein kinase (AMPK) is activated by ATP depletion and protects cells by switching off energy-consuming processes. We show that treatment of HEK293 cells expressing Kv2.1 with the AMPK activator A-769662 caused hyperpolarizing shifts in the current-voltage relationship for channel activation and inactivation. We identified two sites (S440 and S537) directly phosphorylated on Kv2.1 by AMPK and, using phosphospecific antibodies and quantitative mass spectrometry, show that phosphorylation of both sites increased in A-769662-treated cells. Effects of A-769662 were abolished in cells expressing Kv2.1 with S440A but not with S537A substitutions, suggesting that phosphorylation of S440 was responsible for these effects. Identical shifts in voltage gating were observed after introducing into cells, via the patch pipette, recombinant AMPK rendered active but phosphatase-resistant by thiophosphorylation. Ionomycin caused changes in Kv2.1 gating very similar to those caused by A-769662 but acted via a different mechanism involving Kv2.1 dephosphorylation. In cultured rat hippocampal neurons, A-769662 caused hyperpolarizing shifts in voltage gating similar to those in HEK293 cells, effects that were abolished by intracellular dialysis with Kv2.1 antibodies. When active thiophosphorylated AMPK was introduced into cultured neurons via the patch pipette, a progressive, time-dependent decrease in the frequency of evoked action potentials was observed. Our results suggest that activation of AMPK in neurons during conditions of metabolic stress exerts a protective role by reducing neuronal excitability and thus conserving energy.calcineurin | calcium signaling | energy homeostasis A MP-activated protein kinase (AMPK) is a ubiquitously expressed sensor of cellular energy status (1). It is activated in response to increases in cellular AMP:ATP and ADP:ATP ratios by a mechanism involving allosteric activation and increased net phosphorylation at a conserved threonine (Thr172) mediated by the tumor-suppressor kinase, LKB1 (2). Thr172 phosphorylation and activation also can be triggered by increases in cytoplasmic Ca 2+ via the calmodulin-dependent kinase calcium/calmodulin kinase kinase β (CaMKKβ) (1, 2). Although AMPK initially was thought to maintain cellular energy homeostasis primarily by regulating metabolism, emerging evidence suggests that it also modulates cell function by phosphorylating other targets, including ion channels. This function may be of particular significance in excitable cells such as central neurons. Remarkably, ATP turnover in rodent brain is comparable with that in human leg muscle during marathon running, and it has been estimated that action potentials account for 25-50% of this turnover, with synaptic transmission (triggered by action potentials) accounting for all but 15% o...