5 research outputs found
Association of Magnesium Intake With Sleep Duration and Sleep Quality: Findings From the CARDIA Study
OBJECTIVES: As an antagonist of calcium (Ca), magnesium (Mg) has been hypothesized to improve individuals’ sleep disturbances, a common health problem, through regulating the glutamatergic and GABAergic systems. The objectives of this study were to examine the longitudinal associations of Mg intake and Ca-to-Mg intake ratio with sleep quality and duration. METHODS: A total of 5115 American young adults, aged 18–30 years, were enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA) study. Dietary information, including intakes of Mg and other nutrients, was obtained using the CARDIA dietary history at baseline (1985–86), year 7 (1992–93), and year 20 (2005–06). Sleep measures, including self-reported sleep quality and sleep duration, were collected at year 15 (2000–01) and year 20. Sleep quality was assessed on a scale of 1 (very good) to 5 (very bad), whereas sleep duration was grouped into three categories: 9 hours. Generalized estimating equation (GEE) was used to examine the associations of interest. RESULTS: After adjustment for potential demographical, behavioral, and nutritional confounders, Mg intake was associated with better sleep quality [highest intake quartile (Q4) vs. lowest intake quartile (Q1): odds ratio (OR) = 1.23; 95% CI = 1.00, 1.50, P for trend = 0.052]. Participants in Q4 were also less likely to have short sleep (<7 hours) compared to those in Q1 (OR = 0.64; 95% CI = 0.51, 0.81, P for trend = 0.012). The observed association with short sleep persisted among participants without depressive disorders (Q4 vs. Q1: OR = 0.64; 95% CI = 0.49, 0.82, P for trend <0.001), but not among individuals with depressive disorder. Ca-to-Mg intake ratio was not associated with either sleep quality or sleep duration regardless of depression status. CONCLUSIONS: Mg intake was associated with sleep quality and duration in this longitudinal analysis. Randomized controlled trials with objective measures of sleep are warranted to establish the potential causal inference. FUNDING SOURCES: National Institutes of Health (NIH)
Racial/Ethnic Disparities in Alzheimer’s Disease Risk: Role of Exposure to Ambient Fine Particles
Background
Whether racial/ethnic disparities in Alzheimer’s disease (AD) risk may be explained by ambient fine particles (PM2.5) has not been studied.
Methods
We conducted a prospective, population-based study on a cohort of Black (n=481) and White (n=6004) older women (aged 65-79) without dementia at enrollment (1995-98). Cox models accounting for competing risk were used to estimate the hazard ratio (HR) for racial/ethnic disparities in AD (1996-2010) defined by DSM-IV and the association with time-varying annual average PM2.5 (1999-2010) estimated by spatiotemporal model.
Results
Over an average follow-up of 8.3 (±3.5) years with 158 incident cases (21 in Black women), the racial disparities in AD risk (range of adjusted HRBlack women = 1.85-2.41) observed in various models could not be explained by geographic region, age, socioeconomic characteristics, lifestyle factors, cardiovascular risk factors, and hormone therapy assignment. Estimated PM2.5 exposure was higher in Black (14.38±2.21 µg/m 3) than in White (12.55±2.76 µg/m 3) women, and further adjustment for the association between PM2.5 and AD (adjusted HRPM2.5 = 1.18-1.28) slightly reduced the racial disparities by 2-6% (HRBlack women = 1.81-2.26). The observed association between PM2.5 and AD risk was ~2 times greater in Black (HRPM2.5 = 2.10-2.60) than in White (HRPM2.5 = 1.07-1.15) women (range of interaction Ps: Conclusions
PM2.5 may contribute to racial/ethnic disparities in AD risk and its associated increase in AD risk was stronger amongst Black women
Do B Vitamins Enhance the Effect of Omega-3 Polyunsaturated Fatty Acids on Cardiovascular Diseases? A Systematic Review of Clinical Trials
Studies have suggested that B vitamins or omega-3 polyunsaturated fatty acids (PUFAs) may deter the development of cardiovascular disease (CVD). This systematic review aims to examine whether the combined supplementation of both B vitamins and omega-3 PUFAs could provide additional beneficial effects to prevent CVD beyond the effect of each supplement based on clinical trials published up to December 2021. The overall findings are inconsistent and inconclusive, yet the combined supplementation of these two nutrients may be more effective at reducing plasma homocysteine, triglyceride, and low-density lipoprotein-cholesterol than the individual components. The underlying mechanisms mainly include alleviating endothelial dysfunction, inhibiting atherosclerosis and lesion initiation, reducing oxidative stress, suppressing activation of pro-inflammatory cytokines, regulating endothelial nitric oxide synthase, and interfering with methylation of genes that promote atherogenesis. Although biologically plausible, the existing literature is insufficient to draw any firm conclusion regarding whether B vitamins can further enhance the potential beneficial effects of omega-3 PUFA intake on either primary or secondary prevention of CVD. The inconsistent findings may be largely explained by the methodological challenges. Therefore, well-designed high-quality trials that will use the combined supplementation of B vitamins and omega-3 PUFAs or dietary patterns rich in these two types of nutrients are warranted
Reply to "Recommendation on an updated standardization of serum magnesium reference ranges," Jeroen H.F. de Baaij et al
We thank de Baaij et al. [1] for their provocative and
thoughtful letter regarding our paper on the need to
standardize serum magnesium reference ranges in clinical
medicine [2]. We are especially pleased that the authors
emphasize the essential role of magnesium in health and
disease and the importance of measuring serum magnesium
in the clinical setting. We also thank the authors for their
appraisal of cohort studies and randomized clinical trials
relative to magnesium reference ranges that may interest the
readership of the European Journal of Nutrition. However,
we would like to emphasize that any discussion related to
the measurement of serum magnesium needs to consider
that even the gold-standard methods have limitations [3, 4]