Prevalence and risk factors of depressive symptoms among 140,259 college students during the COVID-19 epidemic normalization in China: A cross-sectional survey.
Frontiers in public health
Objective:College students are one of the most vulnerable populations to the COVID-19 pandemic's mental health effects. During the coronavirus disease 2019 (COVID-19) outbreak, we wanted to see how common depressive symptoms were among college students and what factors contributed to that. Methods:Between 21 and 27 May 2021, 140,259 college students from three cities in Henan Province, China, were involved. The Patient Health Questionnaire-9 was used to determine depressive symptoms (PHQ-9). Multiple logistic regression analysis was used to calculate odds ratios (ORs) and 95% CIs for potential depressive symptom factors. Results:Mild depressive symptoms and above are present in 21.12% of college students. Women had a higher prevalence of mild depressive symptoms than men (61.38 vs. 59.75%), and depressive symptoms were most prevalent among rural students and least prevalent among city students (21.44 vs. 20.29%). Participants with depressive symptoms are also more likely to have a poor-behavioral status. From none-to-severe depressive symptoms, 78.88, 15.78, 2.80, 1.67, and 0.88% had them. Gender, residential location, and behavioral status were found to be associated with depressive symptoms after adjusting for potential confounders. Conclusion:This cross-sectional study identified the factors that influence the prevalence of depression in college students. It found that the government should pay more attention to mental health issues affecting college students in combating the COVID-19 epidemic normalization.
Daytime eating prevents mood vulnerability in night work.
Proceedings of the National Academy of Sciences of the United States of America
Shift workers have a 25 to 40% higher risk of depression and anxiety partly due to a misalignment between the central circadian clock and daily environmental/behavioral cycles that may negatively affect mood and emotional well-being. Hence, evidence-based circadian interventions are required to prevent mood vulnerability in shift work settings. We used a stringently controlled 14-d circadian paradigm to assess mood vulnerability during simulated night work with either daytime and nighttime or daytime-only eating as compared with simulated day work (baseline). Simulated night work with daytime and nighttime eating increased depression-like mood levels by 26.2% (-value adjusted using False Discovery Rates, FDR = 0.001; effect-size = 0.78) and anxiety-like mood levels by 16.1% (FDR = 0.001; effect-size = 0.47) compared to baseline, whereas this did not occur with simulated night work in the daytime-only eating group. Importantly, a larger degree of internal circadian misalignment was robustly associated with more depression-like ( = 0.77; = 0.001) and anxiety-like ( = 0.67; = 0.002) mood levels during simulated night work. These findings offer a proof-of-concept demonstration of an evidence-based meal timing intervention that may prevent mood vulnerability in shift work settings. Future studies are required to establish if changes in meal timing can prevent mood vulnerability in night workers.
A new path to mental disorders: Through gap junction channels and hemichannels.
Neuroscience and biobehavioral reviews
Behavioral disturbances related to emotional regulation, reward processing, cognition, sleep-wake regulation and activity/movement represent core symptoms of most common mental disorders. Increasing empirical and theoretical evidence suggests that normal functioning of these behavioral domains relies on fine graded coordination of neural and glial networks which are maintained and modulated by intercellular gap junction channels and unapposed pannexin or connexin hemichannels. Dysfunctions in these networks might contribute to the development and maintenance of psychopathological and neurobiological features associated with mental disorders. Here we review and discuss the evidence indicating a prominent role of gap junction channel and hemichannel dysfunction in core symptoms of mental disorders. We further discuss how the increasing knowledge on intercellular gap junction channels and unapposed pannexin or connexin hemichannels in the brain might lead to deeper mechanistic insight in common mental disorders and to the development of novel treatment approaches. We further attempt to exemplify what type of future research on this topic could be integrated into multidimensional approaches to understand and cure mental disorders.
KangPiLao decoction modulates cognitive and emotional disorders in rats with central fatigue through the GABA/Glu pathway.
Frontiers in pharmacology
Central fatigue (CF) is a subjective sense of tiredness associated with cognitive and memory disorders, accompanied by reduced physical endurance and negative emotions, such as anxiety and depression. Disease progression and prognosis with regards to CF have been unfavorable and possibly contribute to dementia, schizophrenia, and other diseases. Additionally, effective treatments for CF are lacking. KangPiLao decoction (KPLD) has been widely applied in clinical treatment and is composed of six Chinese herbal medicines, some of which have confirmed anti-fatigue effects. While glutamic acid (Glu) is the main excitatory transmitter in the central nervous system (CNS), gamma-aminobutyric acid (GABA) is the major inhibitory transmitter. Both are involved in emotional, cognitive, and memory functions. This research was designed to explore how KPLD regulates cognitive and emotional disorders in rats with CF and to identify the relationship between the regulatory effect and the GABA/Glu pathway. The compounds comprising KPLD were analyzed using high-performance liquid chromatography-mass spectrometry. Sixty Wistar rats were randomly divided into six groups. The modified multiple platform method was used to induce CF. Cognitive, emotional, and fatigue states were evaluated by performing behavioral tests (Morris water maze [MWM], open-field test [OFT], and grip strength test). Histomorphology, western blotting, immunohistochemistry, and RT-qPCR were performed to investigate protein and mRNA expression levels in the hippocampus and prefrontal cortexes involved in the GABA/Glu pathway. Rats with CF exhibited impaired spatial cognition and increased negative emotions in the MWM and OFT. KPLD enabled the improvement of these symptoms, especially in the high-concentration group. Western blotting and RT-qPCR demonstrated that the expression of GABAARα1, GABAARγ2, GABABR1, and GAD67 in rats with CF was higher, whereas GAT-1 and NMDAR2B were lower in the hippocampus and prefrontal cortex. KPLD decreased the expression of GABAARα1, GABABR1, GABAARγ2, and GAD67 in the hippocampus and prefrontal cortex and enhanced the expression of NR2B in the prefrontal cortex. KPLD significantly improved cognitive and emotional disorders in rats with CF by regulating the GABA/Glu pathway. Overall, KPLD may be a promising candidate for developing a drug for treating CF.