Allostatic Mechanism of Mind-Body Medicine for Neuroinflammation

Abstract

Chronic inflammatory diseases are the most significant cause of death in the world and entail severe impairment to quality of life. The World Health Organization (WHO) ranks chronic inflammatory diseases as the greatest threat to human health and wellbeing. Inflammation is epicentral to many clinical conditions and symptoms, and it is anticipated that the health, economic, and mortality burdens associated with chronic inflammation will steadily increase in the United States over the next 30 years. An inflammatory model of disease premises that peripheral injury/trauma/toxins release signaling mediators that activate glial components of peripheral and central cellular circuitry which if prolonged causes toxification of the central nervous system, or neuroinflammation. This inflammatory process is associated with an array of systemic symptomatology affecting somatic, neurocognitive, and affective domains, that can often be misdiagnosed and/or ineffectively treated in the clinic. Centralized neuroinflammation determines a range of conditions and their clinical trajectories, from autoimmune diseases, cancers, cardiovascular diseases, chronic pain, to neurological and psychiatric disorders. It is coming to light that mind-body medicine, defined here as mindfulness- and yoga-based interventions, appear to modulate peripheral cell signaling involved with inflammatory response. Translational mechanism nor intervention specificity of this early data is currently clearly delineated, posing an exciting and highly beneficial frontier for further empirical exploration in the field of integrative mind-body medicine. Here we initiate an allostasis model of working mechanism that aims to inform methodological design and ensuing empirical perspectives.

Increased microglia activation in late non‐central nervous system cancer survivors links to chronic systemic symptomatology

“…One explanation might be that since survivors were so far out from cancer remission and cancer treatment completion (average ~ 4.6 years, range 1–16 years), peripheral inflammation resolved and/or was no longer detectable while centralized neuroimmune toxic response continued, causing chronic systemic symptomatology. This is salient because it would also support a peripheral‐to‐centralized neuroimmune framework, where levels of peripheral inflammatory cells and mediators (i.e., as a consequence of the cancer and/or its treatments) become unmanageable and progress to toxification of the entire CNS, or centralized neuroinflammation (Schoenberg & Gonzalez, 2023 ). When one component of the inflammatory chain becomes dysregulated, continued inflammatory response ensues in the absence of the original peripheral cause (cancer/its treatments) which is no longer observable, say through standardized follow‐up bloodwork.…”

“…For example, emerging evidence supports the significant cross‐correlation between the neuroimmune system and neuroplastic mechanisms in neuroimmune plasticity factors involved in central nervous system injury such as traumatic brain injury, spinal cord injury, and/or stroke (O'Reilly & Tom, 2020b ; Tian et al, 2012 ), immune macroenvironment plasticity in cancer models (Allen et al, 2020 ), responsiveness to chronic pain (Pratscher et al, 2021 ; Sibille et al, 2016 ), and neuronal adaptation in mood disorders (Pittenger & Duman, 2007 ), to name a few. Incorporating measures to rule out centralized neuroinflammation and provide interventions that target such mechanisms without causing further toxification to the CNS (Schoenberg & Gonzalez, 2022 , 2023 ), will have broad clinical impact for the non‐CNS survivor population.…”