Background Emerging research suggests that young adult sexual minorities (identifying as lesbian, gay, or bisexual or engaging in same-sex attractions or behaviors) experience poorer health than their majority counterparts, but many measures of health inequity remain unexamined in population-based research. Purpose To describe a wide range of health status and healthcare access characteristics of sexual minorities in comparison with those of the majority population in a national sample of U.S. young adults. Methods Binary and multinomial logistic regression analyses of Wave IV data (2008) from the National Longitudinal Study of Adolescent Health (participants aged 24–32 years, n=13,088) were conducted. Health measures were self-rated health; diagnosis of any of several physical or mental illnesses or sexually transmitted infections; measured body mass index; depression classified from self-reported symptoms; use of antidepressant and anxiolytic medication; uninsured; forgone care; and receipt of physical, dental, and psychological services. Analyses were conducted in 2012–2013. Results Sexual minority women had elevated odds of most adverse health conditions and lower odds of receiving a physical or dental examination. Sexual minority men had elevated odds of fewer adverse health conditions. Conclusions Young adult sexual minorities are at higher risk of poor physical and mental health. The results highlight the multidimensionality of sexual minority status and respond to calls for greater understanding of the health of this population.

Objectives To examine the impact of preconception acute and chronic stressors on offspring birth weight and racial/ethnic birth weight disparities. Methods We included birth weights for singleton live first (n=3512) and second (n=1901) births to White, Mexican- and other-origin Latina, and Black women reported at Wave IV of the National Longitudinal Study of Adolescent Health (2007-2008; ages 24-32). We generated factor scores for preconception acute and chronic stressors from Wave I (1994-1995; ages 11-19) or III (2001-2002; ages 18-26) for the same cohort of women. Results Linear regression models indicated that chronic stressors, but not acute stressors, were inversely associated with birth weight for both first and second births (b= -192; 95% confidence interval [CI]: -270, -113; and b= -180; 95% CI: -315, -45 respectively), and partially explained the disparities in birth weight between the minority racial/ethnic groups and Whites. Conclusions Preconception chronic stressors contribute to restricted birth weight and to racial/ethnic birth weight disparities.

Chronic metabolic acidosis induces net Ca efflux from bone; this osteoclastic bone resorption is mediated by increased osteoblastic prostaglandin synthesis. Cyclooxygenase, the rate-limiting enzyme in prostaglandin synthesis, is present in both constitutive (COX-1) and inducible (COX-2) forms. We report here that acidosis increases both osteoblastic RNA and protein levels for COX-2 and that genetic deficiency or pharmacologic inhibition of COX-2 significantly reduces acid-induced Ca efflux from bone.Introduction: Incubation of neonatal mouse calvariae in medium simulating physiologic metabolic acidosis induces an increase in osteoblastic prostaglandin E 2 (PGE 2 ) release and net calcium (Ca) efflux from bone. Increased PGE 2 is necessary for acid-induced bone resorption, because inhibition of cyclooxygenase activity with indomethacin significantly decreases not only PGE 2 production but also Ca release. Cyclooxygenase is present in both constitutive (COX-1) and inducible (COX-2) forms. Because COX-2 activity has been implicated in several forms of pathological bone resorption, we tested the hypothesis that COX-2 is critical for acid-induced, cell-mediated bone Ca efflux. Materials and Methods:To determine the effect of metabolic acidosis on COX-2 RNA and protein, primary cells isolated from neonatal CD-1 mouse calvariae were cultured in neutral (Ntl) or physiologically acidic medium (Met). RNA levels for COX-2 and COX-1 were measured by quantitative real-time PCR. Levels of COX-2 and COX-1 protein were measured by immunoblot analysis. To determine the effect of acidosis on bone Ca efflux in genetically deficient COX-2 mice, mice heterozygous for the COX-2 knockout (strain B6;129S7-Ptgs2

Objective Hypertensive disorders in pregnancy signal an increased risk of cardiovascular disease for women. However, future hypertension risk among pregnant women with moderately elevated blood pressure (BP) is unknown. We examined associations among moderately elevated BP or hypertensive disorders during pregnancy and later prehypertension or hypertension. Design Longitudinal cohort study. Setting Five communities in Michigan, USA. Sample Data are from pregnant women enrolled in the Pregnancy Outcomes and Community Health Study. We included 667 women with gestational BP measurements who participated in the POUCHmoms Study follow-up 7-15 years later. Methods Moderately elevated BP was defined as two measures of systolic BP ≥120 mmHg or diastolic BP ≥80 mmHg among women without a hypertensive disorder. Weighted multinomial logistic regression models estimated odds of prehypertension or hypertension at follow-up, adjusted for maternal confounders and time to follow-up. Main Outcome Measures Prehypertension or hypertension. Results Women meeting the moderately elevated BP criteria (64%) had significantly higher odds of hypertension at follow-up (adjusted odds ratio =2.6; 95% confidence interval: 1.2-5.5). These increased odds were observed for moderately elevated BP first identified before or after 20 weeks, and for elevated systolic BP alone or combined with elevated diastolic BP. Conclusions Moderately elevated BP in pregnancy may be a risk factor for future hypertension. Pregnancy offers an opportunity to identify women at risk for hypertension who may not have been identified otherwise.