The Role of Anxiety and Depression in the Relationship Among Emotional Eating, Sleep Quality, and Impulsivity.

ABSTRACT: The aim of this study was to investigate the relationship among sleep quality, impulsivity, anxiety, and depression in individuals with emotional eating behavior. The study was designed as a cross-sectional study. The study included 92 individuals (age 31.29 ± 9.17; female, 67.4% [n = 62]; male, 32.6% [n = 30]) with symptoms of emotional eating but no previous psychiatric diagnosis or treatment. Participants were administered a Structured Clinical Interview for DSM-5 Disorders interview form, a sociodemographic data form, the Emotional Eating Scale, the Beck Depression Scale, the Barratt Impulsivity Scale, the Beck Anxiety Scale, and the Pittsburgh Sleep Quality Index Scale. Emotional eating is positively correlated with anxiety (r = 0.377, p = 0.001), depression (r = 0.375, p = 0.001), impulsivity (r = 0.250, p = 0.016), and poor sleep quality (r = 0.478, p = 0.001). Obese individuals (defined as having a body mass index of 30 or higher) showed higher emotional eating (z = -2.552, p = 0.016) and poorer sleep quality (z = -2.089, p = 0.044) than nonobese individuals, and women showed higher emotional eating (t = 2116, p = 0.037) and poorer sleep quality (z = -2537, p = 0.010) than men. Poor sleep quality was associated with emotional eating. In this relationship, poor sleep quality influenced emotional eating through all mediators, including anxiety and depression (B = 3.491; standardized effect, 0.485; p = 0.001). Poor sleep quality directly influenced emotional eating (B = 2.806; standardized effect, 0.390; p = 0.001). The findings of the study suggest that emotional eating is associated with higher levels of anxiety, depression, impulsivity, and sleep problems, especially in women. It suggests that the interrelationships of psychological factors associated with emotional eating should be investigated.

The effect of Vortioxetine on the NLRP3 pathway and microglial activity in the prefrontal cortex in an experimental model of depression.

BACKGROUND: Increasing evidence suggests that early life stress (ELS) and neuroinflammation are associated with the pathophysiology of depression. The purpose of this study was to determine the effects of Vortioxetine (VOR), a novel antidepressant, on ELS-induced behavioral changes and neuroinflammation. METHOD: Wistar Albino 4-week-old male rats were divided into four groups: control; chronic unpredictable stress (CUMS), VOR, CUMS + VOR. Neurobehavioral assessment was performed on the first, 21st, and 42nd days. RT-PCR was used to detect the expression of P2X7, NLRP3, IL1ß, IL18 in the prefrontal cortex. To assess the microglial activities of the prefrontal cortex, immunohistochemically stained CD68, and leukocyte common antigen (LCA) preparations were scanned with Manual WSI software, Basler camera, and scored. RESULT AND DISCUSSION: Exposure to CUMS was associated with depression and anxiety-like behaviors, and administration of VOR led to improvement in these behaviors. NLRP3, IL-1ß, and IL-18 were shown to be upregulated in the prefrontal cortex of CUMS rats, while their high expression was inhibited by VOR treatment. CD68 and LCA expressions were significantly higher in the CUMS group compared to the other groups. CONCLUSION: According to these results, it may be considered that NLRP3 inflammasome-associated neuroinflammatory response and microglial activation may play a role in the etiopathogenesis of ELS.

Maternal prenatal stress and depression-like behavior associated with hippocampal and cortical neuroinflammation in the offspring: An experimental study.

Prenatal stress can negatively impact neonatal health, growth, and bonding with the mother. However, molecular basis of these modifications is not completely understood. The aim of this experimental study was to test the hypothesis that intrauterine stress exposure may contribute to subsequent depression-like comorbidities associated with neuroinflammation. Wistar Albino nulliparous female rats were divided into two groups (each, n = 6): controls and pregnancy stress (Days 1 through 21). Two live rat pups (one female and one male) from each term delivery were randomly selected, and depression-like behavior tests were performed on Postpartum Days 30-34, followed by euthanasia on Day 35. NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) pathway gene expressions in the hippocampus and immunohistochemical caspase 3 (cas-3), mammalian target of rapamycin (mTOR), and transient receptor potential melastatin (TRPM) staining in the temporal and prefrontal cortices were evaluated. Compared with controls, exposure to prenatal stress was associated with increased depression and anxiety-like behavior, hippocampal NLRP3 inflammasome activation (p = 0.022 and p = 0.035 for female and male pups, respectively), neuronal degeneration and increased cas-3, mTOR, and TRPM immunostaining in the prefrontal and temporal cortices of both female and male offspring (p < 0.05 for all comparisons except p < 0.01 for cas-3 in the male cortex and female temporal cortex). Exposure to antenatal stress can lead to depression-like behavior in the infant, mainly driven by hippocampal NLRP3 inflammasome activation, cortical neuroinflammation, and neurodegeneration. Future perspectives include NLRP3-targeted therapies with anti-inflammatory and anti-apoptotic effects against adverse prenatal effects of maternal stress.