Converging Evidence of Similar Symptomatology of ME/CFS and PASC Indicating Multisystemic Dyshomeostasis.

The purpose of this article is to review the evidence of similar symptomatology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and post-acute sequelae of SARS-CoV-2 infection (PASC). Reanalysis of data from a study by Jason comparing symptom reports from two groups of ME/CFS and PASC patients shows a notably similar symptomatology. Symptom scores of the PASC group and the ME/CFS group correlated 0.902 (p < 0.0001) across items. The hypothesis is presented that ME/CFS and PASC are caused by a chronic state of multisystemic disequilibrium including endocrinological, immunological, and/or metabolic changes. The hypothesis holds that a changed set point persistently pushes the organism towards a pathological dysfunctional state which fails to reset. To use an analogy of a thermostat, if the 'off switch' of a thermostat intermittently stops working, for periods the house would become warmer and warmer without limit. The hypothesis draws on recent investigations of the Central Homeostasis Network showing multiple interconnections between the autonomic system, central nervous system, and brain stem. The hypothesis helps to explain the shared symptomatology of ME/CFS and PASC and the unpredictable, intermittent, and fluctuating pattern of symptoms of ME/CFS and PASC. The current theoretical approach remains speculative and requires in-depth investigation before any definite conclusions can be drawn.

The Interactions among Hypertension, Cancer, and COVID-19: Perspective with Regard to Ca2+/cAMP Signalling.

BACKGROUND: The hypothesis that hypertension is clinically associated with an enhanced risk of developing cancer has been highlighted. However, the working principles involved in this link are still under intensive discussion. A correlation among inflammation, hypertension, and cancer could accurately describe the clinical link between these diseases. In addition, dyshomeostasis of Ca2+ has been considered to be involved in both cancer and hypertension, and inflammation. There is a strong link between Ca2+ signalling, e.g. enhanced Ca2+ signals, and inflammatory outcomes. cAMP also modulates pro- and anti-inflammatory outcomes; pharmaceuticals, which increase intracellular cAMP levels, can decrease the production of proinflammatory mediators and enhance the production of antiinflammatory outcomes. OBJECTIVE: This article highlights the participation of Ca2+/cAMP signalling in the clinical association among inflammation, hypertension, and an enhanced risk for the development of cancer. In addition, considering that research on coronavirus disease 2019 (COVID-19) is a rapidly evolving field, this article also reviews recent reports related to the role of Ca2+ channel blockers in restoring Ca2+ signalling disruption due to COVID-19, including the relationship among COVID-19, cancer, and hypertension. CONCLUSION: An understanding of the association among these diseases could expand current pharmacotherapy, involving Ca2+ channel blockers and pharmaceuticals that facilitate a rise in cAMP levels.

Communication challenges in social isolation, subjective cognitive decline, and mental health status in older adults: A scoping review (2019-2021).

PURPOSE: Through an evolutionary concept analysis, social isolation (SI) was defined as lack of social belonging and engagement with others, minimal number of social contacts, and insufficient quality relationships. This definition represents broader understanding of most contributing factors to SI and supports the concepts of reduced communication and socialization experienced during the COVID-19 pandemic. The COVID-19 pandemic served to heighten this problem, including communication challenges, and brought negative outcomes of SI to light. The overall research question examined the impact of communication challenges and SI on OAs with Alzheimer's disease, related dementias, and subjective cognitive changes (2020-2021). This scoping literature review was developed to compare the psychosocial and mental health of older adults between prepandemic and pandemic lockdown of 2020-2021. DESIGN AND METHODS: This review followed the procedures for scoping review reporting as stated by the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) extension for Scoping Reviews (PRISMA-ScR). In collaboration with an expert scientific information specialist assigned to the college of nursing, the literature was queried through MEDLINE(R) and Epub Ahead of Print, In-Process, In-Data-Review & Other Non-Indexed Citations and Daily 1946 to September 02, 2021; APA PsycInfo 1806 to August Week 5 2021; and Embase Classic+Embase 1947 to 2021 September 02. Search terms included social isolation; nursing home; home for the aged; long-term care; old age homes or convalescent home or nursing home; long-term care, or long-term care; aged or elders or seniors, dementia, Alzheimer's or dementia; osteoporosis; and fragility fracture. FINDINGS: Quantitative data informed outcomes through increased depression and anxiety, higher rates of depression during the pandemic than prepandemic, and increased symptomology in neuropsychiatric profiles. Further, COVID19-related restrictions, including impaired communication streams, seemed to be the origin of stress-related cognitive changes and symptomology. Communication challenges in residents with dementia may lead to feelings of social isolation. Qualitative evidence supports that dementia has a social, psychological, material, and socio-demographic impact. Further, the lockdown disrupted the existing flow of communication between all stakeholders and residents, resulting in heightened perceptions of SI and a profound sense of loss. PRACTICE IMPLICATIONS: The results include a diverse and complex characterization of negative outcomes. Further, strong evidence indicates that communication and human contact can ameliorate negative outcomes.

The extended autonomic system, dyshomeostasis, and COVID-19.

The pandemic viral illness COVID-19 is especially life-threatening in the elderly and in those with any of a variety of chronic medical conditions. This essay explores the possibility that the heightened risk may involve activation of the "extended autonomic system" (EAS). Traditionally, the autonomic nervous system has been viewed as consisting of the sympathetic nervous system, the parasympathetic nervous system, and the enteric nervous system. Over the past century, however, neuroendocrine and neuroimmune systems have come to the fore, justifying expansion of the meaning of "autonomic." Additional facets include the sympathetic adrenergic system, for which adrenaline is the key effector; the hypothalamic-pituitary-adrenocortical axis; arginine vasopressin (synonymous with anti-diuretic hormone); the renin-angiotensin-aldosterone system, with angiotensin II and aldosterone the main effectors; and cholinergic anti-inflammatory and sympathetic inflammasomal pathways. A hierarchical brain network-the "central autonomic network"-regulates these systems; embedded within it are components of the Chrousos/Gold "stress system." Acute, coordinated alterations in homeostatic settings (allostasis) can be crucial for surviving stressors such as traumatic hemorrhage, asphyxiation, and sepsis, which throughout human evolution have threatened homeostasis; however, intense or long-term EAS activation may cause harm. While required for appropriate responses in emergencies, EAS activation in the setting of chronically decreased homeostatic efficiencies (dyshomeostasis) may reduce thresholds for induction of destabilizing, lethal vicious cycles. Testable hypotheses derived from these concepts are that biomarkers of EAS activation correlate with clinical and pathophysiologic data and predict outcome in COVID-19 and that treatments targeting specific abnormalities identified in individual patients may be beneficial.