To assess the association between dietary magnesium intake and hyperuricemia in United States (US) adults, we extracted 26,796 US adults aged 20–85 years from the National Health and Nutrition Examination Survey (NHANES) in 2001–2014. All dietary intake was measured through 24 h dietary recall method. Multivariable logistic regression analysis was performed to investigate the association between magnesium intake and hyperuricemia after adjusting for several important confounding variables. When compared to the lowest quintile (Q1), for male, adjusted odds ratios (ORs) of hyperuricemia in the second quintile (Q2) to the fifth quintile (Q5) of the magnesium intake were 0.83 (95% CI: 0.72–0.95), 0.74 (0.64–0.85), 0.78 (0.67–0.90), and 0.70 (0.58–0.84, p for trend = 0.0003), respectively. For female, OR was 0.75 (0.62–0.90) in the fourth quintile (Q4) (p for trend = 0.0242). As compared to Q4 of magnesium intake (contains recommended amount), the relative odds of hyperuricemia were increased by 1.29 times in Q1 (OR = 1.29, 1.11–1.50) in male. The ORs were 1.33 (1.11–1.61) in Q1, 1.27 (1.07–1.50) in Q2 in female. Our results indicated that increased magnesium intake was associated with decreased hyperuricemia risk. It also indicated the importance of recommended dietary allowance (RDA) of magnesium and the potential function of magnesium intake in the prevention of hyperuricemia.

We aim to explore the associations between dietary zinc intake and hyperuricemia (HU) in United States (US) adults. 24,975 US adults aged 20 years or older from the National Health and Nutrition Examination Survey (NHANES) from 2001 to 2014 were stratified into quintiles based on zinc intake. All dietary intake measured through 24-h dietary recalls. Multivariable logistic regression analysis was performed to examine the association between zinc intake and HU after adjustment for possible confounders. For males, compared with respondents consuming less than 7.33 mg zinc daily, the adjusted odds ratios (ORs) were 0.83 (95% CI, 0.71, 0.97) among those consuming 10.26–13.54 mg zinc daily, 0.78 (95% CI, 0.63–0.96) among those consuming 18.50 mg or greater, and p for the trend was 0.0134. For females, compared with respondents consuming less than 5.38 mg zinc daily, the OR was 0.78 (95% CI, 0.63, 0.97) among those consuming 9.64–12.93 mg zinc daily, and p for the trend was 0.3024. Our findings indicated that dietary zinc intake is inversely associated with HU in US men and women, independent of some major confounding factors.

To assess the association between intake of folate, vitamin B6, and vitamin B12 with hyperuricemia (HU) among adults from the United States (US), we extracted relevant data from 24,975 US adults aged 20–85 years from the National Health and Nutrition Examination Survey (NHANES) in 2001–2014. All dietary intake was evaluated by 24-h dietary recalls. Multivariable logistic regression analysis was performed to explore the associations after adjustment for confounders. Compared to the lowest quintile (Q1), for males, adjusted odds ratios (ORs) of HU in Q2 to Q5 of folate (dietary folate equivalent, DFE) intake were 0.84 (95% CI, 0.73–0.96), 0.84 (0.73–0.97), 0.72 (0.62–0.84), and 0.64 (0.53–0.77), respectively (p for trend <0.0001). In females, adjusted ORs in Q2 to Q4 of folate (DFE) intake were 0.84 (95% CI, 0.71–0.99), 0.81 (0.68–0.96), and 0.82 (0.68–0.99), with a p for trend of 0.1475. Our findings indicated the intakes of total folate, folic acid, food folate, folate (DFE), vitamin B12, but not vitamin B6, were inversely related to the risk of HU in males. A lower risk of HU with higher intakes of total folate, food folate, and folate (DFE) was found in females, but with no association between intakes of folic acid, vitamin B6, B12, and the risk of HU for females.

Data regarding the association of sarcopenia with chronic lung disease (CLD) has led to inconclusive results. The main goal of this research was to investigate the association between sarcopenia and CLD in middle-aged and elderly individuals in China. The study sample consisted of 11,077 individuals without CLD at baseline chosen from the China Health and Retirement Longitudinal Study (CHARLS) data from 2015, followed up until 2018. Sarcopenia was identified utilizing the criteria set by the Asian Working Group on Sarcopenia (AWGS 2019) in 2019. Individuals were categorized into no-sarcopenia, possible-sarcopenia, and sarcopenia groups. The outcome of the study was considered to be incident CLD, which included chronic bronchitis, emphysema, pulmonary heart disease, and asthma. The association between sarcopenia and the risk of CLD was also examined by employing weighted Cox proportional hazard regression models. A total of 356 (3.20 %) participants developed CLD during the 3.6-year follow-up period. The cumulative incidence of CLD in the no-sarcopenia, possible-sarcopenia, and sarcopenia groups was 2.80 % (230/8222), 4.37 % (55/1260), and 4.45 % (71/1595), respectively. Individuals with possible sarcopenia {hazard ratio [HR] [95 % confidence interval (CI)]: 1.48 [1.04-2.09]} and sarcopenia [HR (95 % CI): 1.68 (1.12-2.51)] demonstrated a considerably high risk of developing CLD compared to individuals in the no-sarcopenia group. Moreover, individuals diagnosed with sarcopenia, as per the criteria established by the European Working Group on Sarcopenia in Older People (EWGSOP) 2018, were at considerably high risk for developing CLD compared to those in the no-sarcopenia group. This research involving adult Chinese individuals demonstrated a significant association between, possible sarcopenia and sarcopenia with an elevated risk of incident CLD, thereby emphasizing the importance of monitoring respiratory health in this population. Question: Whether muscle mass and sarcopenia are associated with the development of chronic lung disease (CLD) in Asian middle-aged and elderly individuals. This longitudinal study encompassing 11,077 adults aged ≥45 years from the China Health and Retirement Longitudinal Study (CHARLS) data with 3.6 years of follow-up revealed a positive association between sarcopenia at baseline and incidence of CLD. Meaning: The findings suggest that possible sarcopenia and sarcopenia are linked to the development of CLD. Consequently, middle-aged and elderly individuals with possible sarcopenia and sarcopenia can be considered vulnerable regarding the primary prevention strategies for CLD.

The evidence on the association between cobalamin (Cbl) and aging or relevant outcomes is limited and controversial. We aimed to investigate the relationships between cobalamin intake- and function-related biomarkers and biological aging. The study encompassed 22,812 participants aged 20 years and older from the National Health and Nutrition Examination Survey. A panel of biomarkers or algorithms was used to assess biological aging, including Klemera-Doubal Age Acceleration (KDMAccel), Phenotypic age acceleration (PhenoAgeAccel), telomere length, α-Klotho, and PhenoAge advancement. Weighted generalized linear regression analysis was used to assess the associations between cobalamin-intake biomarkers (serum cobalamin, cobalamin intake from food, cobalamin supplement use, serum methylmalonic acid [MMA], and homocysteine [Hcy]) and function-related biomarkers (functional cobalamin deficiency and cobalamin insensitivity index). Among the 22,812 individuals, the weighted mean (SE) age was 48.3 (0.2) years and 48.0% were males. Unexpectedly, serum and dietary cobalamin as well as serum MMA and Hcy levels were positively associated with most indicators of biological aging. Cobalamin sensitivity was assessed by the combination of binary Cbl_low/high and MMA_low/high or Hcy_low/high (cutoff values: 400 pg/mL for cobalamin, 250 nmol/L for MMA, and 12.1 μmol/l for Hcy) and a newly constructed cobalamin insensitivity index (based on the multiplicative term of serum cobalamin and serum MMA or Hcy). The multivariable-adjusted β (95%CIs) of KDMAccel in the MMA_lowCbl_low, MMA_lowCbl_high, MMA_highCbl_low, and MMA_highCbl_high groups were reference, 0.27 (0.03 to 0.51), 0.85 (0.41 to 1.29), and 7.97 years (5.77 to 10.17) respectively, which were consistent for the combination of serum Hcy and cobalamin. Both cobalamin insensitivity indices were robustly associated with biological aging acceleration in a dose-response pattern (each p < 0.001). Decreased cobalamin sensitivity but not cobalamin insufficiency might be associated with biological aging acceleration. Further studies would improve understanding of the underlying mechanisms between decreased cobalamin sensitivity and biological aging acceleration.