11 research outputs found

    Association of Magnesium Intake With Sleep Duration and Sleep Quality: Findings From the CARDIA Study

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    OBJECTIVES: As an antagonist of calcium (Ca), magnesium (Mg) has been hypothesized to improve individualsā€™ 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 18ā€“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 (1985ā€“86), year 7 (1992ā€“93), and year 20 (2005ā€“06). Sleep measures, including self-reported sleep quality and sleep duration, were collected at year 15 (2000ā€“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: 9Ā 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% CIĀ =Ā 1.00, 1.50, P for trendĀ =Ā 0.052]. Participants in Q4 were also less likely to have short sleep (<7 hours) compared to those in Q1 (ORĀ =Ā 0.64; 95% CIĀ =Ā 0.51, 0.81, P for trendĀ =Ā 0.012). The observed association with short sleep persisted among participants without depressive disorders (Q4 vs. Q1: ORĀ =Ā 0.64; 95% CIĀ =Ā 0.49, 0.82, P for trendĀ <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 Alzheimerā€™s Disease Risk: Role of Exposure to Ambient Fine Particles

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    Background Whether racial/ethnic disparities in Alzheimerā€™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 (Ā±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 (14.38Ā±2.21 Āµg/m 3) than in White (12.55Ā±2.76 Āµg/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

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    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

    Association of Magnesium Intake With Sleep Duration and Sleep Quality: Findings From the CARDIA Study

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    OBJECTIVES: As an antagonist of calcium (Ca), magnesium (Mg) has been hypothesized to improve individualsā€™ 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 18ā€“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 (1985ā€“86), year 7 (1992ā€“93), and year 20 (2005ā€“06). Sleep measures, including self-reported sleep quality and sleep duration, were collected at year 15 (2000ā€“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: 9Ā 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% CIĀ =Ā 1.00, 1.50, P for trendĀ =Ā 0.052]. Participants in Q4 were also less likely to have short sleep (<7 hours) compared to those in Q1 (ORĀ =Ā 0.64; 95% CIĀ =Ā 0.51, 0.81, P for trendĀ =Ā 0.012). The observed association with short sleep persisted among participants without depressive disorders (Q4 vs. Q1: ORĀ =Ā 0.64; 95% CIĀ =Ā 0.49, 0.82, P for trendĀ <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)

    Association of omega-3 and omega-6 fatty acid intake with leukocyte telomere length in US males

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    Background Omega-3 (nā€“3) and omega-6 (nā€“6) fatty acids may contribute to oxidative stress and inflammation, which are related to telomere shortening. Evidence supporting an association between intake of nā€“3 or nā€“6 fatty acids and leukocyte telomere length (LTL) in males has been limited. Objectives We conducted a cross-sectional study to examine the associations of total or individual nā€“3 or total nā€“6 fatty acid intake with LTL in US males. Methods We included 2,494 US males with LTL measurement from 4 nested caseā€“control studies within the Health Professionals Follow-Up Study. Individuals with previous histories of cancers, diabetes, and cardiovascular diseases at or before blood collection were excluded. Blood collection was performed between 1993 and 1995, and relevant information including nā€“3 and nā€“6 intake was collected in 1994 by questionnaire. The LTL was log-transformed and Z scores of the LTL were calculated for statistical analyses by standardizing the LTL in comparison with the mean within each selected nested caseā€“control study. Results We found that consumption of DHA (22:6nā€“3) was positively associated with LTL. In the multivariable-adjusted model, compared with individuals who had the lowest intake of DHA (i.e., first quartile group), the percentage differences (95% CIs) of LTL were āˆ’3.7 (āˆ’13.7, 7.5), 7.0 (āˆ’4.3, 19.7), and 8.2 (āˆ’3.5, 21.3) for individuals in the second, third, and fourth quartiles of consumption, respectively (P-trend = 0.0498). We did not find significant associations between total nā€“3 or total nā€“6 fatty acid intakes and LTL. In addition, we found that males who consumed canned tuna had longer LTL than those who did not; in the multivariable-adjusted model, the percentage difference of LTL was 10.5 (95% CI: 1.3, 20.4) (P = 0.02). Conclusions Our results suggest that higher intakes of DHA and canned tuna consumption are associated with longer LTL

    Association of magnesium intake with sleep duration and sleep quality: findings from the CARDIA study

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    Study objectives: As an antagonist of calcium (Ca), magnesium (Mg) has been implicated in the regulation of sleep. We aimed to examine the longitudinal associations of Mg intake and Ca-to-Mg intake ratio (Ca:Mg) with sleep quality and duration. Methods: The study sample consisted of 3,964 participants from the Coronary Artery Risk Development in Young Adults (CARDIA) study. Dietary and supplementary intake of Mg were obtained using the CARDIA Dietary History at baseline (1985-1986), exam years 7 and 20. Self-reported sleep outcomes were measured at years 15 and 20. Sleep quality was rating from 1 (very good) to 5 (very bad). We categorized sleep duration to 9 h. Generalized estimating equation was used to examine the associations of interest as repeated measures at the two time points. Results: After adjustment for potential confounders, Mg intake was borderline associated with better sleep quality [highest quartile (Q4) vs. intake quartile (Q1): odds ratio (OR) = 1.23; 95% CI = 0.999, 1.50, ptrend = 0.051]. Participants in Q4 were also less likely to have short sleep (<7 h) compared to those in Q1 (OR = 0.64; 95% CI = 0.51, 0.81, ptrend = 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, ptrend < 0.001), but not among individuals with depressive disorder. Ca:Mg was not associated with either outcomes, regardless of depression status. Conclusions: Mg intake was associated with both sleep outcomes in this longitudinal analysis. Randomized controlled trials with objective measures of sleep are warranted to establish the potential causal inference

    Magnesium intake was inversely associated with hostility among American young adults

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    Hostility is a complex personality trait associated with many cardiovascular risk factor phenotypes. Although magnesium intake has been related to mood and cardio-metabolic disease, its relation with hostility remains unclear. We hypothesize that high total magnesium intake is associated with lower levels of hostility because of its putative antidepressant mechanisms. To test the hypothesis, we prospectively analyzed data in 4,716 young adults aged 18-30 years at baseline (1985-1986) from four U.S. cities over five years of follow-up using data from the Coronary Artery Risk Development in Young Adults (CARDIA) study. Magnesium intake was estimated from a dietary history questionnaire plus supplements at baseline. Levels of hostility were assessed using the Cook-Medley scale at baseline and year 5 (1990-1991). Generalized estimating equations were applied to estimate the association of magnesium intake with hostility as repeated measures at the two time-points (baseline and year 5). General linear model was used to determine the association between magnesium intake and change in hostility over 5 years. After adjustment for socio-demographic and major lifestyle factors, a significant inverse association was observed between magnesium intake and hostility level over 5 years of follow-up. Beta coefficients (95% CI) across higher quintiles of magnesium intake were 0 (reference), -1.28 (-1.92, -0.65), -1.45 (-2.09, -0.81), -1.41 (-2.08, -0.75) and -2.16 (-2.85, -1.47), respectively (Plinear-trend<.01). The inverse association was independent of socio-demographic and major lifestyle factors, supplement use, and depression status at year 5. This prospective study provides evidence that in young adults, high magnesium intake was inversely associated with hostility level independent of socio-demographic and major lifestyle factors

    Reply to "Recommendation on an updated standardization of serum magnesium reference ranges," Jeroen H.F. de Baaij et al

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    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]

    Recommendation on an updated standardization of serum magnesium reference ranges

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    Purpose Serum magnesium is the most frequently used laboratory test for evaluating clinical magnesium status. Hypomagnesemia (low magnesium status), which is associated with many chronic diseases, is diagnosed using the serum magnesium reference range. Currently, no international consensus for a magnesemia normal range exists. Two independent groups designated 0.85 mmol/L (2.07 mg/dL; 1.7 mEq/L) as the low cut-off point defining hypomagnesemia. MaGNet discussions revealed differences in serum magnesium reference ranges used by membersā€™ hospitals and laboratories, presenting an urgent need for standardization. Methods We gathered and compared serum magnesium reference range values from our institutions, hospitals, and colleagues worldwide. Results Serum magnesium levels designating ā€œhypomagnesemiaā€ differ widely. Of 43 collected values, only 2 met 0.85 mmol/L as the low cut-off point to define hypomagnesemia. The remainder had lower cut-off values, which may underestimate hypomagnesemia diagnosis in hospital, clinical, and research assessments. Current serum magnesium reference ranges stem from ā€œnormalā€ populations, which unknowingly include persons with chronic latent magnesium deficit (CLMD). Serum magnesium levels of patients with CLMD fall within widely used ā€œnormalā€ ranges, but their magnesium status is too low for long-term health. The lower serum magnesium reference (0.85 mmol/L) proposed specifically prevents the inclusion of patients with CLMD. Conclusions Widely varying serum magnesium reference ranges render our use of this important medical tool imprecise, minimizing impacts of low magnesium status or hypomagnesemia as a marker of disease risk. To appropriately diagnose, increase awareness of, and manage magnesium status, it is critical to standardize lower reference values for serum magnesium at 0.85 mmol/L (2.07 mg/dL; 1.7 mEq/L)
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