ABSTRACT
Seasonal affective disorder (SAD) is a type of depression in which symptoms occur during a particular season. While physical activity has been shown to improve symptoms for depression in general populations, the relationships between physical activity and experiences of seasonality and SAD remain underexplored. We conducted a survey with adult members of a recreational gym in Fairbanks, Alaska. The survey collected self-report data on sociodemographics, health behaviours, and elements of the Seasonal Pattern Assessment Questionnaire (SPAQ). Results indicate that 18.68% of our study participants meet the criteria for winter-pattern SAD and 43.96% meet the criteria for subsyndromal SAD ("winter blues"). We conducted two regressions to understand experiences of SAD and predictors of seasonality more generally. Gender was a significant predictor of SAD, with women more likely than men to experience SAD (p = .04). Being social at the gym, whether going to the gym with others or participating in activities with others, was associated with higher seasonality than being independent at the gym (p = .03). Younger age was also associated with higher seasonality (p < .001). This study contributes new insights about the relationship between engagement in physical activities and experiences of seasonality among adults in a northern latitude.
Subject(s)
Seasonal Affective Disorder , Adult , Alaska/epidemiology , Exercise , Female , Humans , Male , Seasonal Affective Disorder/diagnosis , Seasonal Affective Disorder/epidemiology , Seasons , Surveys and QuestionnairesABSTRACT
Activation of inflammation in white adipose tissue (WAT), includes infiltration/expansion of WAT macrophages, contributes pathogenesis of obesity, insulin resistance, and metabolic syndrome. The inflammasome comprises an intracellular sensor (NLR), caspase-1 and the adaptor ASC. Inflammasome activation leads to maturation of caspase-1 and processing of IL1ß, contributing to many metabolic disorders and directing adipocytes to a more insulin-resistant phenotype. Ablation of PDE3B in WAT prevents inflammasome activation by reducing expression of NLRP3, caspase-1, ASC, AIM2, TNFα, IL1ß and proinflammatory genes. Following IP injection of lipopolysaccharide (LPS), serum levels of IL1ß and TNFα were reduced in PDE3B(-/-)mice compared to WT. Activation of signaling cascades, which mediate inflammasome responses, were modulated in PDE3B(-/-)mice WAT, including smad, NFAT, NFkB, and MAP kinases. Moreover, expression of chemokine CCL2, MCP-1 and its receptor CCR2, which play an important role in macrophage chemotaxis, were reduced in WAT of PDE3B(-/-)mice. In addition, atherosclerotic plaque formation was significantly reduced in the aorta of apoE(-/-)/PDE3B(-/-)and LDL-R(-/-)/PDE3B(-/-)mice compared to apoE(-/-)and LDL-R(-/-)mice, respectively. Obesity-induced changes in serum-cholesterol were blocked in PDE3B(-/-)mice. Collectively, these data establish a role for PDE3B in modulating inflammatory response, which may contribute to a reduced inflammatory state in adipose tissue.