Investigating differential effects of socio-emotional and mindfulness-based online interventions on mental health, resilience and social capacities during the COVID-19 pandemic: The study protocol.

BACKGROUND: The SARS-CoV-2 pandemic has led to a mental health crisis on a global scale. Epidemiological studies have reported a drastic increase in mental health problems, such as depression and anxiety, increased loneliness and feelings of disconnectedness from others, while resilience levels have been negatively affected, indicating an urgent need for intervention. The current study is embedded within the larger CovSocial project which sought to evaluate longitudinal changes in vulnerability, resilience and social cohesion during the pandemic. The current second phase will investigate the efficacy of brief online mental training interventions in reducing mental health problems, and enhancing psychological resilience and social capacities. It further provides a unique opportunity for the prediction of intervention effects by individual biopsychosocial characteristics and preceding longitudinal change patterns during the pandemic in 2020/21. METHODS: We will examine the differential effects of a socio-emotional (including 'Affect Dyad') and a mindfulness-based (including 'Breathing Meditation') intervention, delivered through a web- and cellphone application. Participants will undergo 10 weeks of intervention, and will be compared to a retest control group. The effectiveness of the interventions will be evaluated in a community sample (N = 300), which is recruited from the original longitudinal CovSocial sample. The pre- to post-intervention changes, potential underlying mechanisms, and prediction thereof, will be assessed on a wide range of outcomes: levels of stress, loneliness, depression and anxiety, resilience, prosocial behavior, empathy, compassion, and the impact on neuroendocrine, immunological and epigenetic markers. The multi-method nature of the study will incorporate self-report questionnaires, behavioral tasks, ecological momentary assessment (EMA) approaches, and biological, hormonal and epigenetic markers assessed in saliva. DISCUSSION: Results will reveal the differential effectiveness of two brief online interventions in improving mental health outcomes, as well as enhancing social capacities and resilience. The present study will serve as a first step for future application of scalable, low-cost interventions at a broader level to reduce stress and loneliness, improve mental health and build resilience and social capacities in the face of global stressors. TRIAL REGISTRATION: This trial has been registered on May 17, 2020 with the ClinicalTrials.gov NCT04889508 registration number (clinicaltrials.gov/ct2/show/NCT04889508).

Mental stress as consequence and cause of vision loss: the dawn of psychosomatic ophthalmology for preventive and personalized medicine.

The loss of vision after damage to the retina, optic nerve, or brain has often grave consequences in everyday life such as problems with recognizing faces, reading, or mobility. Because vision loss is considered to be irreversible and often progressive, patients experience continuous mental stress due to worries, anxiety, or fear with secondary consequences such as depression and social isolation. While prolonged mental stress is clearly a consequence of vision loss, it may also aggravate the situation. In fact, continuous stress and elevated cortisol levels negatively impact the eye and brain due to autonomous nervous system (sympathetic) imbalance and vascular dysregulation; hence stress may also be one of the major causes of visual system diseases such as glaucoma and optic neuropathy. Although stress is a known risk factor, its causal role in the development or progression of certain visual system disorders is not widely appreciated. This review of the literature discusses the relationship of stress and ophthalmological diseases. We conclude that stress is both consequence and cause of vision loss. This creates a vicious cycle of a downward spiral, in which initial vision loss creates stress which further accelerates vision loss, creating even more stress and so forth. This new psychosomatic perspective has several implications for clinical practice. Firstly, stress reduction and relaxation techniques (e.g., meditation, autogenic training, stress management training, and psychotherapy to learn to cope) should be recommended not only as complementary to traditional treatments of vision loss but possibly as preventive means to reduce progression of vision loss. Secondly, doctors should try their best to inculcate positivity and optimism in their patients while giving them the information the patients are entitled to, especially regarding the important value of stress reduction. In this way, the vicious cycle could be interrupted. More clinical studies are now needed to confirm the causal role of stress in different low vision diseases to evaluate the efficacy of different anti-stress therapies for preventing progression and improving vision recovery and restoration in randomized trials as a foundation of psychosomatic ophthalmology.

A short review on the psychoneuroimmunology of posttraumatic stress disorder: from risk factors to medical comorbidities.

Posttraumatic stress disorder (PTSD) is a serious and debilitating condition with a prevalence rate of approximately 8% in the United States. Given the number of veterans returning from conflicts around the globe with PTSD, and the substantial number of civilians experiencing traumas, new perspectives on the biology of PTSD are needed. Based on the concept that PTSD is a disorder of stress response systems, numerous studies have suggested changes in hypothalamic-pituitary-adrenal (HPA) axis and sympathetic-adrenal-medullary (SAM) system function in patients with PTSD. Given that both glucocorticoids and catecholamines exert powerful effects on the immune system, it is surprising that relatively few studies have examined immune changes in patients with PTSD. Moreover, patients with PTSD are known to have increased rates of comorbidity with somatic disorders that involve immune and inflammatory processes. Patients with PTSD have been found to exhibit a number of immune changes including increased circulating inflammatory markers, increased reactivity to antigen skin tests, lower natural killer cell activity, and lower total T lymphocyte counts. Studies with humans and rodents suggest that certain proinflammatory cytokines are able to induce neurochemical and behavioral changes that resemble some key features of PTSD. This short article reviews immune alterations in PTSD, and considers possible mechanisms by which such changes may be related to neuroendocrine alterations and medical comorbidities of PTSD.

The low-dose dexamethasone suppression test in fibromyalgia.

OBJECTIVE: Fibromyalgia syndrome (FMS) has been associated with decreased cortisol secretion. Patients with posttraumatic stress disorder (PTSD) exhibit similar hypocortisolism in the context of increased negative feedback sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis. Because trauma and PTSD have been associated with fibromyalgia, we evaluated whether patients with fibromyalgia demonstrate increased HPA feedback sensitivity. METHOD: Baseline blood samples were obtained at 0800 h, and 0.5 mg of dexamethasone was administered to 15 female patients with FMS and 20 normal controls at 2300 h. Adrenocorticotropin (ACTH), cortisol, and dexamethasone levels were measured at 0800 h after dexamethasone intake. RESULTS: There were no group differences in mean ACTH or cortisol levels or in ACTH/cortisol ratio at baseline. After dexamethasone intake, patients with FMS exhibited more pronounced suppression of cortisol but not of ACTH, as well as increased ACTH/cortisol ratios compared with controls. Percent cortisol suppression was associated with pain and fatigue, while ACTH/cortisol ratio and dexamethasone availability were associated with stress and anxiety measures. CONCLUSION: Our results suggest increased sensitivity to glucocorticoid feedback, manifested at the adrenal level, in FMS.