Sleep, an intrinsic aspect of human life, is experienced by individuals differently which may be influenced by personality traits and characteristics. Exploring how these traits influence behaviors and sleep routines could be used to inform more personalized and effective interventions to promote better sleep. Our objective was to summarize the existing literature on the relationship between personality traits and sleep patterns through a systematic review. An abstract and keyword search was conducted in PsycINFO, Cochrane and PubMed, collecting relevant literature, published between January 1980 and June 2024. A total of 1713 records were found, of which 18 studies were analyzed in the descriptive synthesis. Relevant studies covered populations in 11 different countries, Australia, China, Estonia, Finland, Germany, Italy, Japan, Poland, Turkey, the United Kingdom, and the United States, comprising a total of 58,812 subjects. All studies reported an association between a sleep pattern with at least one of the Big Five personality traits (agreeableness, conscientiousness, extraversion, neuroticism, openness to experience). Ten studies found associations between personality and sleep quality, all of which reported a link between neuroticism and sleep quality (effect sizes 0.183-0.40). Five studies found an association between conscientiousness and morningness (effect sizes 0.16-0.35). Other sleep patterns linked to personality traits included sleep duration, nightmare frequency and distress, sleep deficiency, sleep continuity, insomnia severity and sleep problems, sleep hygiene, sleep latency and daytime sleepiness. This novel systematic review confirms that sleep and personality traits are related, suggesting that those traits should be considered when trying to understand or change one's sleep behavior.
Introduction: Sleep deprivation(SD) has numerous negative effects on mental health. A growing body of research has confirmed the implication of gut microbiota in mental disorders. However, the specific modifications in mammalian gut microbiota following SD exhibit variations across different studies.
Methods: Male specific-pathogen-free Wistar rats were given a modified multiple-platform exposure for 7 days of SD. Fecal samples were obtained from the control and SD groups both at baseline and after 7 days of SD. We utilized 16S rDNA gene sequencing to investigate the gut microbial composition and functional pathways in rats.
Results: Analysis of the microbiota composition revealed a significant change in gut microbial composition after chronic SD, especially at the phylum level. The relative abundances of p_Firmicutes, g_Romboutsia, and g_Enterococcus increased, whereas those of p_Bacteroidetes, p_Verrucomicrobia, p_Fusobacteria, g_Akkermansia, and g_Cetobacterium decreased in animals after chronic SD compared with controls or animals before SD. The ratio of Firmicutes to Bacteroidetes exhibited an increase following SD. The relative abundance of gut microbiota related to the functional pathways of GABAergic and glutamatergic synapses was observed to be diminished in rats following SD compared to pre-SD.
Conclusion: Collectively, these findings suggest that chronic SD causes significant alterations in both the structural composition and functional pathways of the gut microbiome. Further researches are necessary to investigate the chronological and causal connections among SD, the gut microbiota and mental disorders.
Objective: We aimed to evaluate the effect of light-dark cycle alteration and soft drink consumption on the acceleration of type 1 diabetes mellitus (T1DM) development among non-obese diabetic (NOD) mice model.
Methods: We exposed female NOD and C57BL/6 mice from the age of 5 weeks to either adlib soft drink consumption and/or T20 light-dark cycle alteration until the development of diabetes, or the mice reached the age of 30 weeks. Each group consisted of 7-15 mice. We monitored weight, length, blood glucose level, and insulin autoantibody (IAA) levels weekly.
Results: Out of 75 NOD and 22 C57BL/6 mice, 41 NOD mice developed diabetes, and 6 mice died between 7 and 8 weeks of age. The mean time to development of T1DM among NOD control mice was 20 weeks. The time to development of T1DM was accelerated by two weeks in the NOD mice exposed to light-dark cycle alteration, hazard ratio of 2.65,95th CI (0.70, 10.04) p = 0.15). The other groups developed T1DM, similar to the control group.
Conclusion: There was a trend toward earlier development of T1DM among NOD mice exposed to light-dark cycle alteration, but this difference was not statistically significant. Further studies are needed to confirm our findings using larger sample sizes and different animal species.