Introduction: There has long been an interest in the effects of diet on mental health, and the interaction of the two with stress; however, the nature of these relationships is not well understood. Although associations between diet, obesity and the related metabolic syndrome (MetS), stress, and mental disorders exist, causal pathways have not been established. Methods: We reviewed the literature on the relationship between diet, stress, obesity and psychiatric disorders related to stress. Results: Diet and obesity can affect mood through direct effects, or stress-related mental disorders could lead to changes in diet habits that affect weight. Alternatively, common factors such as stress or predisposition could lead to both obesity and stress-related mental disorders, such as depression and posttraumatic stress disorder (PTSD). Specific aspects of diet can lead to acute changes in mood as well as stimulate inflammation, which has led to efforts to assess polyunsaturated fats (PUFA) as a treatment for depression. Bidirectional relationships between these different factors are also likely. Finally, there has been increased attention recently on the relationship between the gut and the brain, with the realization that the gut microbiome has an influence on brain function and probably also mood and behavior, introducing another way diet can influence mental health and disorders. Brain areas and neurotransmitters and neuropeptides that are involved in both mood and appetite likely play a role in mediating this relationship. Conclusions: Understanding the relationship between diet, stress and mood and behavior could have important implications for the treatment of both stress-related mental disorders and obesity.

Despite variability among studies, DEH impairs cognitive performance, particularly for tasks involving attention, executive function, and motor coordination when water deficits exceed 2% BML.

Background: Stress is associated with activation of the sympathetic nervous system, and can lead to lasting alterations in autonomic function and in extreme cases symptoms of posttraumatic stress disorder (PTSD). Vagal nerve stimulation (VNS) is a potentially useful tool as a modulator of autonomic nervous system function, however currently available implantable devices are limited by cost and inconvenience. Objective: The purpose of this study was to assess the effects of transcutaneous cervical VNS (tcVNS) on autonomic responses to stress. Methods: Using a double-blind approach, we investigated the effects of active or sham tcVNS on peripheral cardiovascular and autonomic responses to stress using wearable sensing devices in 24 healthy human participants with a history of exposure to psychological trauma. Participants were exposed to acute stressors over a three-day period, including personalized scripts of traumatic events, public speech, and mental arithmetic tasks. Results: tcVNS relative to sham applied immediately after traumatic stress resulted in a decrease in sympathetic function and modulated parasympathetic/sympathetic autonomic tone as measured by increased pre-ejection period (PEP) of the heart (a marker of cardiac sympathetic function) of 4.2 ms (95% CI 1.6e6.8 ms, p < 0.01), decreased peripheral sympathetic function as measured by increased photoplethysmogram (PPG) amplitude (decreased vasoconstriction) by 47.9% (1.4e94.5%, p < 0.05), a 9% decrease in respiratory rate (À14.3 to À3.7%, p < 0.01). Similar effects were seen when tcVNS was applied after other stressors and in the absence of a stressor. Conclusion: Wearable sensing modalities are feasible to use in experiments in human participants, and tcVNS modulates cardiovascular and peripheral autonomic responses to stress.

Effects of exercise‐heat stress with and without water replacement on brain structure and visuomotor performance were examined. Thirteen healthy adults (23.6 ± 4.2 years) completed counterbalanced 150 min trials of exercise‐heat stress (45°C, 15% RH) with water replacement (EHS) or without (~3% body mass loss; EHS‐DEH) compared to seated rest (CON). Anatomical scans and fMRI Blood‐Oxygen‐Level‐Dependent responses during a visuomotor pacing task were evaluated. Accuracy decreased (P < 0.05) despite water replacement during EHS (−8.2 ± 6.8% vs. CON) but further degraded with EHS‐DEH (−8.3 ± 6.4% vs. EHS and −16.5 ± 10.2% vs. CON). Relative to CON, EHS elicited opposing volumetric changes (P < 0.05) in brain ventricles (−5.3 ± 1.7%) and periventricular structures (cerebellum: 1.5 ± 0.8%) compared to EHS‐DEH (ventricles: 6.8 ± 3.4, cerebellum: −0.7 ± 0.7; thalamus: −2.7 ± 1.3%). Changes in plasma osmolality (EHS: −3.0 ± 2.1; EHS‐DEH: 9.3 ± 2.1 mOsm/kg) were related (P < 0.05) to thalamus (r = −0.45) and cerebellum volume (r = −0.61) which, in turn, were related (P < 0.05) to lateral (r = −0.41) and fourth ventricle volume (r = −0.67) changes, respectively; but, there were no associations (P > 0.50) between structural changes and visuomotor accuracy. EHS‐DEH increased neural activation (P < 0.05) within motor and visual areas versus EHS and CON. Brain structural changes are related to bidirectional plasma osmolality perturbations resulting from exercise‐heat stress (with and without water replacement), but do not explain visuomotor impairments. Negative impacts of exercise‐heat stress on visuomotor tasks are further exacerbated by dehydration.

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Men outperform women in sports requiring muscular strength and/or endurance, but the relative influence of "nurture" versus "nature" remains difficult to quantify. Performance gaps between elite men and women are well documented using world records in second, centimeter, or kilogram sports. However, this approach is biased by global disparity in reward structures and opportunities for women. Despite policies enhancing female participation (Title IX legislation), US women only closed performance gaps by 2% and 5% in Olympic Trial swimming and running, respectively, from 1972 to 1980 (with no change thereafter through 2016). Performance gaps of 13% in elite middistance running and 8% in swimming (∼4-min duration) remain, the 5% differential between sports indicative of load carriage disadvantages of higher female body fatness in running. Conversely, sprint swimming exhibits a greater sex difference than sprint running, suggesting anthropometric/power advantages unique to swim-block starts. The ∼40-y plateau in the performance gap suggests a persistent dominance of biological influences (eg, longer limb levers, greater muscle mass, greater aerobic capacity, and lower fat mass) on performance. Current evidence suggests that women will not swim or run as fast as men in Olympic events, which speaks against eliminating sex segregation in these individual sports. Whether hormone reassignment sufficiently levels the playing field in Olympic sports for transgender females (born and socialized male) remains an issue to be tackled by sport-governing bodies.

Background: Psychological stress is a risk factor for major adverse cardiovascular events (MACE) in individuals with coronary artery disease (CAD). Certain brain regions that control both emotional states and cardiac physiology may be involved in this relationship. The rostromedial prefrontal cortex (rmPFC) is an important brain region that processes stress and regulates immune and autonomic functions. Changes in rmPFC activity with emotional stress (reactivity) may be informative of future risk for MACE. Methods: Participants with stable CAD underwent acute mental stress testing using a series of standardized speech/arithmetic stressors and simultaneous brain imaging with high resolution-positron emission tomography brain imaging. We defined high rmPFC activation as a difference between stress and control scans greater than the median value for the entire cohort. Interleukin-6 (IL-6) levels 90 minutes post-stress, and high-frequency heart rate variability (HF-HRV) during stress were also assessed. We defined MACE as a composite of cardiovascular death, myocardial infarction, unstable angina with revascularization and heart failure hospitalization. Results: We studied 148 subjects (69% male) with mean ± SD age of 62 ± 8 years. After adjustment for baseline demographics, risk factors, and baseline levels of IL-6 and HF-HRV, higher rmPFC stress reactivity was independently associated with higher IL-6 and lower HF-HRV with stress. During a median follow-up of 3 years, 34 subjects (21.3%) experienced a MACE. Each 1SD increase in rmPFC activation with mental stress was associated with a 21% increase risk of MACE (HR 1.21, 95% CI 1.08-1.37). Stress-induced IL-6 and HF-HRV explained 15.5% and 32.5% of the relationship between rmPFC reactivity and MACE, respectively. Addition of rmPFC reactivity to conventional risk factors improved risk reclassification for MACE prediction, and C-statistic improved from 0.71 to 0.76 (p=0.03). Conclusions: Greater rmPFC stress reactivity is associated with incident MACE. Immune and autonomic responses to mental stress may play a contributory role.

Background: Vagal Nerve Stimulation (VNS) has been shown to be efficacious for the treatment of depression, but to date, VNS devices have required surgical implantation, which has limited widespread implementation. Methods: New noninvasive VNS (nVNS) devices have been developed which allow external stimulation of the vagus nerve, and their effects on physiology in patients with stress-related psychiatric disorders can be measured with brain imaging, blood biomarkers, and wearable sensing devices. Advantages in terms of cost and convenience may lead to more widespread implementation in psychiatry, as well as facilitate research of the physiology of the vagus nerve in humans. nVNS has effects on autonomic tone, cardiovascular function, inflammatory responses, and central brain areas involved in modulation of emotion, all of which make it particularly applicable to patients with stress-related psychiatric disorders, including posttraumatic stress disorder (PTSD) and depression, since dysregulation of these circuits and systems underlies the symptomatology of these disorders. Results: This paper reviewed the physiology of the vagus nerve and its relevance to modulating the stress response in the context of application of nVNS to stress-related psychiatric disorders. Conclusions: nVNS has a favorable effect on stress physiology that is measurable using brain imaging, blood biomarkers of inflammation, and wearable sensing devices, and shows promise in the prevention and treatment of stress-related psychiatric disorders.