BackgroundAnimal studies have demonstrated the toxicology and pathology of mercury in relation to brain function. However, human studies provided mixed findings in relation to cognitive aging. This study aims to examine the association between serum mercury concentration and the incidence of mild cognitive impairment (MCI).MethodParticipants were from a random sub‐cohort (n = 2666) of the REasons for Geographic and Racial Differences in Stroke cohort study (2003–present). After excluding participants with baseline MCI and stroke, and those with missing baseline serum mercury concentration, the final sample size was 2136. Participants were classified into tertiles based on serum mercury concentration (<0.023, 0.023–0.049, and >0.049 µg/dL). MCI was determined primarily based on most recent performance on the enhanced cognitive battery (ECB) containing assessments of Word List Learning, Delayed Recall, Animal Fluency, and letter F Fluency. For those who did not have a score on ECB (n = 474), the Six Item Screener (SIS) was used to determine MCI instead. Therefore, the outcome included three levels: MCI based on the ECB, MCI based on the SIS, and control. Multinomial logistic regression was used to assess serum mercury concentration in relation to incident MCI. We also performed stratified analyses to assess whether gender and race modified the potential associations. All tests were two‐sided with α = 0.05.ResultThe number of participants with MCI on the ECB and SIS were 48 and 36, respectively. After adjustment for the demographic and clinical characteristics in model 2 (Table 1), the direction suggests a positive association between mercury and incident MCI, although this is not statistically significant presumably due to insufficient statistical power (Tertile 3 vs. tertile 1: odds ratio (OR), 1.68; 95% confidence interval (CI), 0.79–3.55; P for trend = 0.025). After further adjustment for fish oil intake, the association became significant (OR: 2.56; 95% CI: 1.003‐6.55; P for trend = 0.043). The observed association was not materially modified by sex or race. We did not observe an association between serum mercury and impairment on SIS.ConclusionThis prospective study suggests that serum mercury concentrations are associated with incident MCI assessed by ECB in US population.
Objectives To examine serum selenium concentrations in relation to the incidence of cognitive impairment in apparently healthy US adults. Methods A random sub-cohort (N = 2,666) was drawn from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study consisting of Blacks and Whites, aged 45 or older across the United States. After excluding those with baseline cognitive impairment and stroke, and missing information on serum selenium, a total of 2,136 participants (mean age at baseline = 63 years) remained in the analyses. Serum selenium was assessed at baseline and was categorized into quartiles. The Six-item screener (SIS) was used to characterize global cognitive function, and the Enhanced Cognitive Battery (ECB), consisting of 4 assessments: Word List Learning, Delayed Recall, Animal Fluency, and letter F Fluency, was used to examine participants’ domains of cognitive function. Multivariable-adjusted odds ratio (ORs) and the corresponding 95% confidence intervals (CIs) were estimated using logistic regression models. Because 474 participants did not have the ECB score, we performed multiple imputation to account for the missingness. Restricted cubic spline analysis was performed to assess the potential non-linear associations. Results After adjusting for potential confounders, serum selenium was not associated with cognitive impairment. The multivariable-adjusted ORs (95% CI) from quintile 2 (Q2) to quintile 4 (Q4), with quintile 1 (Q1) as the referent were 1.07 (0.67, 1.71), 1.10 (0.68, 1.77), and 0.79 (0.49, 1.29); Plinear = 0.44 for SIS and 0.91 (0.38, 2.15), 0.53 (0.19, 1.47), and 1.16 (0.50, 2.68); Plinear = 0.67 for ECB. In the sensitivity analysis, which was conducted using an imputed dataset, a similar pattern of ORs was observed for ECB (Q2 vs. Q1 to Q4 vs. Q1): 0.98 (0.44, 2.18), 0.75 (0.27, 2.10), and 1.35 (0.58, 3.15); Plinear = 0.49]. Additionally, results from the spline analysis indicated that selenium was not associated with either outcome in a non-linear fashion. Conclusions Findings from this study do not support serum selenium as a predictor of incident cognitive impairment among US adults. Funding Sources National Institutes of Health.
BackgroundStudies have indicated neurotoxicity of cadmium (Cd) exposure. However, little is known about Cd exposure in relation to cognitive impairment.MethodA total of 2,172 participants (mean age: 64.1±9.0 years old; female: 54.8%; Black: 38.7%), without cognitive impairment or stroke at baseline (2003‐2007), from a random sub‐cohort (n = 2,666) of the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, were included in this study. Urinary creatinine‐corrected Cd concentrations were measured at baseline. The Enhanced Cognitive Battery (ECB) and Six Item Screener (SIS) were performed every two years (ECB) or annually (SIS) during an average of 10 years of follow‐up. The ECB consisted of 4 tests: Word list learning (WLL), Delayed Recall (WLD), Animal Fluency, and Letter F Fluency, and its composite score was used to determine our first outcome: cognitive impairment by ECB. Because of missing data on ECB scores (n = 482), we also defined a second outcome for cognitive impairment by assigning them a cognitive impairment status based on SIS. Therefore, in the secondary analysis, the outcomes consisted of three levels: ECB, SIS, and control. Odds ratios (OR) and corresponding 95% confidence intervals (CI) were examined using multivariable‐adjusted logistic regression for the ECB‐defined cognitive impairment or using multinomial logistic regression for the second outcome.ResultDuring the follow‐up, 53 participants developed cognitive impairment as assessed by the ECB and 36 cases were determined by the SIS. After adjustment for potential confounders, no significant association was observed between the urinary Cd concentration and incident cognitive impairment. Comparing the highest tertile of Cd concentration to the lowest, the OR (95% CI) of incident cognitive impairment was 1.07 (95% CI: 0.43, 2.67; P for trend = 0.87) for the cases measured by ECB (Table 1). In the analysis of multinomial logistic regression, the OR (95% CI) was 1.15 (95% CI: 0.47, 2.81; P for trend = 0.97) for ECB and 1.04 (95% CI: 0.34, 3.22; P for trend = 0.32) for SIS (tertile 3 vs. tertile 1) (Table 2).ConclusionFindings from this US cohort do not support the hypothesis that Cd exposure is associated with the risk of cognitive impairment.
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