Background Glucosamine and chondroitin are products commonly used by older adults in the US and Europe. There is limited evidence that they have anti-inflammatory properties, which could provide risk reduction of several diseases. However, data on their long-term health effects is lacking. Objective To evaluate whether use of glucosamine and chondroitin are associated with cause-specific and total mortality. Design Participants (n = 77 510) were members of a cohort study of Washington State (US) residents aged 50–76 y who entered the cohort in 2000–2002 by completing a baseline questionnaire that included questions on glucosamine and chondroitin use. Participants were followed for mortality through 2008 (n = 5362 deaths). Hazard ratios for death adjusted for multiple covariates were estimated using Cox models. Results Current (baseline) glucosamine and chondroitin use were associated with a decreased risk of total mortality compared to never use. The adjusted hazard ratio (HR) associated with current use of glucosamine (with or without chondroitin) was 0.82 (95% CI 0.75–0.90) and 0.86 (95% CI 0.78–0.96) for chondroitin (included in two-thirds of glucosamine supplements). Current use of glucosamine was associated with a significant decreased risk of death from cancer (HR 0.87 95% CI 0.76–0.98) and with a large risk reduction for death from respiratory diseases (HR 0.59 95% CI 0.41–0.83). Conclusions Use of glucosamine with or without chondroitin was associated with reduced total mortality and with reductions of several broad causes of death. Although bias cannot be ruled out, these results suggest that glucosamine may provide some mortality benefit.

To identify novel modifiable risk factors of gestational diabetes mellitus (GDM) by examining the association between prepregnancy habitual folate intake and GDM risk. RESEARCH DESIGN AND METHODS The study included 14,553 women in the Nurses' Health Study II who reported at least one singleton pregnancy between the 1991 and 2001 questionnaires. Prepregnancy intakes of total folate, supplemental folate, and food folate were assessed using a food frequency questionnaire administered every 4 years. Incident GDM was ascertained from a self-reported physician diagnosis. Relative risks (RRs) of GDM were estimated using log-binomial models, with adjustment for demographic, lifestyle, and dietary factors. RESULTS Over the study follow-up, 824 incident GDM cases were reported among 20,199 pregnancies. Women with adequate total folate intake (‡400 mg/day) had an RR of GDM of 0.83 (95% CI 0.72, 0,95, P = 0.007) compared with women with inadequate intake (<400 mg/day). This association was entirely driven by supplemental folate intake. The RRs of GDM for 1-399, 400-599, and ‡600 mg/day of supplemental folate intake were 0.83, 0.77, and 0.70, respectively, compared with no supplemental folate intake (P trend = 0.002). The association between supplemental folate intake and GDM risk largely persisted after additional adjustment for intake of multivitamins and other micronutrients, as well as among women who likely planned for the pregnancy. CONCLUSIONS Higher habitual intakes of supplemental folate before pregnancy were significantly associated with lower GDM risk. If confirmed, these findings indicate that prepregnancy folic acid supplementation could offer a novel and low-cost avenue to reduce GDM risk.

OBJECTIVE The relationship between air pollution and cardiovascular disease may be explained by changes in high-density lipoprotein (HDL). APPROACH AND RESULTS We examined the cross-sectional relationship between air pollution and both HDL cholesterol (HDL-C) and HDL particle number (HDL-P) in the Multi-Ethnic Study of Atherosclerosis Air Pollution study (MESA Air). Study participants were 6,654 white, African-American, Hispanic, and Chinese men and women, 45–84 years of age. We estimated individual residential ambient fine particulate pollution exposure (PM2.5) and black carbon (BC) concentrations using a fine-scale likelihood-based spatiotemporal model and cohort-specific monitoring. Exposure periods were averaged to 12 months, 3 months, and two weeks prior to exam. HDL-C and HDL-P were measured in the year 2000 using the cholesterol oxidase method and nuclear magnetic resonance spectroscopy, respectively. We used multivariable linear regression to examine the relationship between air pollution exposure and HDL measures. A 0.7 10−6m−1 higher exposure to black carbon (a marker of traffic-related pollution) averaged over a one year period was significantly associated with a lower HDL-C (−1.68 mg/dL (95% CI: −2.86, −0.50), and approached significance with HDL-P (−0.55 mg/dL (95% CI: −1.13, 0.03). In the three month averaging time period, a 5 μg/m3 higher PM2.5 was associated with lower HDL-P (−0.64 μmol/L (95% CI: −1.01, −0.26), but not HDL-C (−0.05 mg/dL (95% CI: −0.82, 0.71). CONCLUSIONS These data are consistent with the hypothesis that exposure to air pollution is adversely associated with measures of HDL.