Association between weekend catch-up sleep and depression of the United States population from 2017 to 2018: A cross-sectional study.

Insufficient sleep on weekdays has become a societal norm, and studies have shown that sleep deprivation increases the risk of depression. Although individuals often resort to weekend catch-up sleep (CUS) as a compensatory measure, the present evidence supporting its efficacy in mitigating the risk of depression is limited. This article attempts to explore the relationship between CUS and depression. In this study, a total of 5510 participants were included, characterized into two groups: nondepressed (n = 5051) and depressed (n = 459), with data extracted from the National Health and Nutrition Examination Survey (NHANES). Compared with people without CUS, those practicing CUS exhibited a significantly lower risk of depression (OR = 0.81, P = 0.048). In subgroup analysis, this reduction effect was only observed in males (OR = 0.70, 95 % CI 0.05 to 0.99, P = 0.04), middle-aged (>40, ≤60) (OR: 0.57, 95 % CI: 0.40 to 0.81, P = 0.002), married or living with parents (OR: 0.61, 95 % CI: 0.44 to 0.86, P = 0.004), groups with three or more family members (OR: 0.69, 95 % CI: 0.52 to 0.93, P = 0.01), and individuals without alcohol intake (OR: 0.24,95 % CI: 0.09 to 0.67, P = 0.006). Therefore, in the realm of depression treatment, doctors may consider advising patients to get adequate sleep on weekends as part of their overall treatment plan. At the same time, individuals can also choose weekend sleep as a proactive strategy for regulating their psychological status.

A clinical and experimental study on the protective effects of jiangzhi tongmai fang on endothelial injury.

31 cases of atherosclerosis (AS) were treated with Jiang Zhi Tong Mai Fang ([symbol: see text], formula of JZTMF), and its effect was compared with 30 cases treated with lovastatin in the control group. Clinically, the JZTMF formula showed an effect of regulating blood lipids, and therefore it was antiatherosclerotic. The mechanism is, probably, restoration of the function of endothelial cells (EC) by increasing the synthesis of 6-keto-PGF1 alpha and decreasing the release of endothelin (ET) as evidenced in the experimental study.