Search

Objective·To explore the effects of hypertension and dyslipidemia on cognitive function in the elderly.Methods·A dynamic population cohort was established by using prospective cohort study methods. In 2019, a complete cohort was selected from residents aged 65 and above who voluntarily participated in a free physical examination program in a community in Shanghai, serving as the baseline cohort. In 2022, 512 community-dwelling elderly aged 67 to 93 were randomly selected from the same community as the follow-up cohort for the study. The collected date included residents′ health records, various physical examination measurements, and Mini-mental State Examination (MMSE) scale scores.Results·Of the 512 cases that were followed up, the valid sample size was reduced to 495 after data cleaning. According to the baseline and follow-up cognitive assessments and changes, the cases were categorized into three cognitive groups: the improvement group, the normal group, and the decline group. The prevalence of hypertension in the decline group was 43.14% higher than that in the improvement group and 24.39% higher than that in the normal group (66.67% in the decline group vs 23.53% in the improvement group, P=0.011; 66.67% in the decline group vs 42.28% in the normal group, P=0.040). Total cholesterol (TC) in the improvement group was lower than that in the normal group [improvement group (4.38±1.04) mmol/L vs normal group (5.11±1.12) mmol/L, P=0.009]. Additionally, TC in the decline group in 2022 was higher than that in 2019 [paired difference (0.46±0.87) mmol/L, 95% CI 0.08‒0.84, P=0.021]. LDL-Ch in the improvement group was lower than that in the normal group [improved group (2.51±0.92) mmol/L vs normal group (3.07±1.00) mmol/L, P=0.024], and their HDL-Ch in 2022 was higher than that in 2019 [paired difference (0.16±0.20) mmol/L, 95% CI 0.06‒0.26, P=0.005]. The results of multinomial Logistic regression showed: TC in the improved group was lower than that in the normal group [β=4.12, OR=61.64, 95% CI 1.52‒2494.07, P=0.029] and the decline group [β=5.88, OR=357.35, 95% CI 4.54‒28149.75, P=0.008]; the TAG [β=1.85, OR=6.34, 95% CI 1.05‒38.43, P=0.045], LDL-Ch [β=5.61, OR=274.06, 95% CI 3.65‒20567.57, P=0.011], and hypertension [β=1.90, OR=6.69, 95% CI 1.53‒29.16, P=0.011] in the decline group were higher than those in the improvement group; the age of the decline group was greater than that of the normal group [β=0.08, OR=1.08, 95% CI 1.00‒1.16, P=0.041], and the education level was lower than that of the normal group [β=1.22, OR=3.39, 95% CI 1.28‒8.94, P=0.014].Conclusion·Low TC and LDL-Ch and high HDL-Ch are beneficial to cognitive improvement. Conversely, hypertension, high TC, high TAG, high LDL-Ch, low education level, and advanced ages are risk factors for cognitive decline.

Background: Nirmatrelvir/Ritonavir is an orally administered anti-SARS-Cov-2 drug used in mild-to-moderate COVID-19 patients. Our retrospective cohort study aims to evaluate the efficacy and safety of Nirmatrelvir/Ritonavir in severe hospitalized patients with Omicron infection, as well as in patients at high risk for progression to critical illness in real-world settings. Methods: A total of 350 patients received Nirmatrelvir/Ritonavir while 350 matched controls did not. Patients with confirmed COVID-19 were administered Nirmatrelvir 300 mg and Ritonavir 100 mg orally twice a day for 5 days, with the medication initiated on the first day after admission. The primary endpoint of the study was a composite outcome of hospitalization or death from any cause within 28 days. Secondary endpoints included the occurrence of adverse events and the evaluation of serum levels of IL-6 and viral load. Results: We documented the mortality risk from any cause within 28 days, viral load, serum IL-6 levels, and adverse events. Nirmatrelvir/Ritonavir reduced the 28-day risk of all-cause mortality by 86% (P =.011, hazard ratio (HR) = 0.14, 95% confidence interval (CI) = 0.03, 0.64). At baseline, the serum level of IL-6 was significantly higher in the antiviral treatment group compared to the control group (P <.001), but no significant difference (P =.990) was found between the two groups at discharge. In CKD patients undergoing hemodialysis, no significant worsening of renal function was observed in the Nirmatrelvir/Ritonavir treatment group compared to the control group. Conclusion: Nirmatrelvir/Ritonavir may reduce the 28-day risk of all-cause mortality in critically ill patients with COVID-19 and in patients at high risk for critical disease progression. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Whether genetic susceptibility to disease and dietary cholesterol (DC) absorption contribute to inconsistent associations of DC consumption with diabetes and cardiovascular disease (CVD) remains unclear. RESEARCH DESIGN AND METHODS: DC consumption was assessed by repeated 24-h dietary recalls in the UK Biobank. A polygenetic risk score (PRS) for DC absorption was constructed using genetic variants in the Niemann-Pick C1-Like 1 and ATP Binding Cassettes G5 and G8 genes. PRSs for diabetes, coronary artery disease, and stroke were also created. The associations of DC consumption with incident diabetes (n = 96,826) and CVD (n = 94,536) in the overall sample and by PRS subgroups were evaluated using adjusted Cox models. RESULTS: Each additional 300 mg/day of DC consumption was associated with incident diabetes (hazard ratio [HR], 1.17 [95% CI, 1.07–1.27]) and CVD (HR, 1.09 [95% CI, 1.03–1.17]), but further adjusting for BMI nullified these associations (HR for diabetes, 0.99 [95% CI, 0.90–1.09]; HR for CVD, 1.04 [95% CI, 0.98–1.12]). Genetic susceptibility to the diseases did not modify these associations (P for interaction ≥0.06). The DC-CVD association appeared to be stronger in people with greater genetic susceptibility to cholesterol absorption assessed by the non-high-density lipoprotein cholesterol-related PRS (P for interaction = 0.04), but the stratum-level association estimates were not statistically significant. CONCLUSIONS: DC consumption was not associated with incident diabetes and CVD, after adjusting for BMI, in the overall sample and in subgroups stratified by genetic predisposition to cholesterol absorption and the diseases. Nevertheless, whether genetic predisposition to cholesterol absorption modifies the DC-CVD association requires further investigation. [ABSTRACT FROM AUTHOR]