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Abstract Objective Numerous observational studies have found a relationship between systemic lupus erythematosus (SLE) and epilepsy; however, their causal relationship remains unclear. This study aimed to investigate the causal role of SLE in epilepsy or any of its subtypes using a two‐sample Mendelian randomization (MR) analysis. Methods Single nucleotide polymorphisms (SNPs) linked to SLE were utilized as instrumental variables in MR analysis to assess their causal impact on epilepsy. The primary MR findings were derived using the inverse variance weighted (IVW) method, which was further supported by the weighted median and MR‐Egger regression techniques. Additionally, sensitivity analyses, including Cochran's Q test and pleiotropy tests, were conducted to evaluate the influence of these SNPs on epilepsy, particularly looking for signs of horizontal pleiotropy and heterogeneity. Results We selected 43 SNPs that reached genome‐wide significance from genome‐wide association studies (GWASs) on SLE to serve as instrumental variables in this study. The IVW method showed no evidence to support a causal association between SLE and epilepsy (all epilepsy: odds ratio (OR) = 1.006, 95% confidence interval (CI) = 0.994–1.018; focal epilepsy: OR = 1.006, 95% CI = 0.994–1.019; generalized epilepsy: OR = 1.015, 95% CI = 0.996–1.035). Other MR complementary methods revealed consistent results. Furthermore, there was no evidence indicating heterogeneity or horizontal pleiotropy. Significance The findings of MR analysis did not support a genetically predicted causal relationship between SLE and epilepsy, but emphasized the need for further research on shared pathophysiological mechanisms, particularly the role of immune system abnormalities and potential influences such as chronic inflammation and therapeutic interventions. Plain Language Summary The etiology of epilepsy is complex and diverse, including immune factors. Through a Mendelian randomization analysis, we did not find evidence of a genetic causal relationship between systemic lupus erythematosus and epilepsy. However, this does not invalidate epidemiological evidence, and further exploration is needed to investigate factors influencing the relationship between the two.

Abstract Background With the increasing aging population, dementia has become a significant socioeconomic burden. However, the effects of albumin on delayed recall (DR) impairment remain unclear, and there are limited reports on sex and race differences in this relationship. This study aimed to investigate the association between albumin levels and DR impairment in older adults. Methods A total of 1507 normal cognitive function and 553 DR impairment from the National Health and Nutrition Examination Survey (NHANES) 2011–2014 were included in this cross‐sectional analysis. Participants aged 60 years and above were assessed using the Consortium to Establish a Registry for Alzheimer's Disease DR (CERAD‐DR) test to evaluate cognitive function. Participants were categorized into DR impairment and normal cognitive function groups according to their CERAD‐DR scores. Logistic regression analyses, generalized additive models, and fitted smoothing curves were utilized for data analysis. Results After adjusting for potential confounders, a negative association was found between albumin levels and cognitive function (odds ratio [OR] = 0.60, 95% confidence interval [CI] 0.41–0.87). Subgroup analysis stratified by sex, race/ethnicity, and age revealed that the negative association remained significant in men (OR = 0.53, 95%CI 032–0.87), Blacks (OR = 0.35, 95%CI 0.17–0.74), and the age group of 60–70 years (OR = 0.48, 95%CI 0.28–0.81). However, no significant association was observed in women (OR = 0.72, 95%CI 0.41–1.28), whites (OR = 0.58, 95%CI 0.31–1.07), or Mexican Americans (OR = 1.11, 95%CI 0.35–3.46), as well as the age group of 71–80 years (OR = 0.62, 95%CI 0.37–1.03). Conclusions Our study suggests that elevated albumin levels are associated with a decreased incidence of cognitive function impairment, particularly in older men and Blacks. This finding indicates that maintaining high levels of albumin may be beneficial for cognitive function in older adults.

Abstract Background Previous epidemiological studies have indicated that high‐density lipoprotein cholesterol (HDL‐C) is inversely associated with the risk of cardiovascular disease. However, this issue has aroused controversy in recent years. Besides, the relationship between HDL‐C and the risk of total stroke in sex and race is less clear. Thus, we aimed to examine the association between different ranges of HDL‐C and the risk of total stroke in adults over 40 years old. Methods This cross‐sectional study was conducted on a sample of 8643 participants (4222 men and 4421 women) aged ≥40 years old from the National Health and Nutrition Examination Survey 2007–2016. HDL‐C was an independent variable and stroke was a dependent variable in this study, with the other variables as potential effect modifiers. To examine the associations between them, we used multivariate logistical regression models and smooth curve fittings, as well as subgroup analyses. Results HDL‐C was inversely associated with stroke when HDL‐C was less than 1.55 mmol/L (odds ratio [OR] = 0.36, 95% confidence interval [CI] :0.21–0.62, p .05). Stratified by race/ethnicity and sex, the subgroup analyses demonstrated that HDL‐C was inversely associated with stroke in men and Whites, but no significant differences among women, Mexicans, blacks, and other races. Conclusion We found a nonlinear relationship between HDL‐C and total stroke. Our study reveals a range of inverse associations between HDL‐C and stroke (HDL‐C