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Our obligation to social justice In the wake of the brutal murders of Ahmaud Arbery, Sean Reed, Breonna Taylor, and George Floyd and amidst international outcries for social justice, many [...]

In the past year, the COVID-19 pandemic has inflicted untold human suffering, remade the global economy, and highlighted numerous weaknesses in political, health, and social systems. In the United States, [...]

It was early evening in the fall of 1994 as I began my long call. I met the daughter of the next patient I was admitting while she was waiting [...]

Background: Autonomic nervous system effects have been hypothesized as a mechanism of air pollutant health effects, though scant prior epidemiologic research has examined the association between air pollutants and catecholamines. Objectives: To examine the association of long-term air pollutants with three urinary catecholamines: dopamine (DA), epinephrine (EPI), and norepinephrine (NE). As a secondary aim, we also examined the association between short-term (or acute) exposure to fine particulate matter [particulate matter with aerodynamic diameter [less than or equal to] 2.5[micro]m ([PM.sub.2.5])] and those catecholamines. Methods: We used data from the Multi-Ethnic Study of Atherosclerosis (MESA) and two of its ancillary studies, the MESA Air Pollution Study and the MESA Stress Study, to provide exposure and outcome data. DA, EPI, and NE from urine samples were collected from 2004 to 2006 from 1,002 participants in the New York, New York, and Los Angeles, California, study sites. Spatiotemporal models incorporated cohort-specific monitoring and estimated annual average pollutant concentrations ([PM.sub.2.5], N[O.sub.2], N[O.sub.x] and black carbon) at participants' homes the year prior to urine collection. Secondarily, short-term [PM.sub.2.5] was evaluated (day of, day prior, and 2- to 5-d lags prior to urine collection). Several covariates were considered confounders (age, race, sex, site, socioeconomic status, cardiovascular disease risk factors, psychosocial stressors, and medication use) in linear regression models. Results: A 17 ppb higher annual N[O.sub.x] concentration was associated with 6.3% higher mean EPI level [95% confidence interval (CI): 0.3%, 12.6%]. A 2-[micro]g/[m.sup.3] higher annual ambient [PM.sub.2.5] concentration was associated with 9.1% higher mean EPI (95% CI: 3.2%, 15.3%) and 4.4% higher DA level (95% CI: 1%, 7.9%). N[O.sub.2], black carbon, and short-term [PM.sub.2.5] exposures were not significantly associated with any of the catecholamines. Conclusions: We found an association between EPI and long-term concentrations of [PM.sub.2.5] and N[O.sub.x] and an association between DA and long-term ambient [PM.sub.2.5]. These novel findings provide modest support for the hypothesis that air pollutant exposures are related to sympathetic nervous system activation., Introduction Catecholamines act as both neurotransmitters and hormones produced by the sympathetic branch of the autonomic nervous system (ANS). Among other things, catecholamines play an important role in regulating heart [...]

Background. It is uncertain whether depression and antidepressant use are associated with decreased bone mineral density (BMD) and whether these relationships differ for men and women. Methods. The study used a case-cohort design within the Baltimore Epidemiologic Catchment Area Study, a population-based sample of adults that recently completed its 23-year follow-up. Depression was measured at four time points during the follow-up period by the Diagnostic Interview Schedule. Lower spine BMD was measured at the fourth wave by dual-energy x-ray absorptiometry. The association of BMD with lifetime history of depression and antidepressant medication use was studied using linear regression with bootstrap standard errors. Results. A history of depression was associated with lower spine BMD after controlling for age, sex, race, calcium intake, alcohol use, smoking status, level of physical activity, percent body fat, and antidepressant medication use (-0.140 g/[cm.sup.2]; p < .002). After controlling for depression, antidepressant medication use was associated with decreased BMD in women but not in men (-0.218 g/[cm.sup.2]; p < .016). Conclusions. A history of depression predicted decreased lumbar spine BMD in men and women, and antidepressant use predicted decreased BMD in women even after controlling for depression. The magnitude of the effect of depression on BMD was approximately equivalent to 1 standard deviation in BMD and was therefore clinically significant. Providers should be aware of the physiologic consequences of depression as well as the possible risks to bone strength associated with antidepressant use in older patients. Key Words: Depression--Antidepressants Bone mineral density--Osteoporosis--Cohort study.

Objectives. We investigated the association between major depressive disorder and type 2 diabetes, whether that association is explained by health behaviors, and whether it is influenced by educational attainment. Methods. We used discrete-time Cox proportional hazards models to determine the risk of type 2 diabetes associated with depression in a 23-year population-based cohort study. Results. Major depressive disorder was associated with higher risk of type 2 diabetes (hazard ratio [HR] = 1.62) after we controlled for age, gender, race, education, smoking status, alcohol use, social network size, and antidepressant use. This association was more pronounced after we controlled for body mass index, family history, and health behaviors (HR=2.04; 95% confidence interval= 1.09, 3.81). In stratified analyses, the risk associated with major depressive disorder was elevated among those with 12 or fewer years of education compared with those with at least some education beyond high school. Conclusions. The risk of type 2 diabetes associated with major depressive disorder persists over the life course and is independent of the effects of health behaviors, body mass index, and family history. Education is an important moderator of this association.

A study was conducted to establish the association between depressive symptoms and type 2 diabetes. Results indicated that individuals with elevated depressive symptoms have a modest increased risk of developing type 2 diabetes during follow-up, economic and metabolic factors.