Inflammation is the body’s response to insults. During inflammation, various inflammatory cells are activated to release cytokines and mediators and orchestrate progressing inflammation.

The evidence for stress contributing to the onset and course of autoimmune disease is circumstantial and the mechanisms by which stress affects autoimmune disease remain poorly understood.

Current therapeutic strategies in medicine emphasize the influence of “mind” over “body” in the maintenance of health and development, progression, and recovery from diseases.

Psychological stress is defined as a “state in which homeostasis is actually threatened or perceived to be so”, whereas homeostasis represents the complex and dynamic equilibrium between all systems functioning in a living organism [1, 2].

Adaptation is one of the core characteristics of living organisms, wherever it refers to proximate adjustments at individual level to inner or outer events, or to ultimate evolutionary processes at species-level.

The sympathetic nervous system (SNS) is an integrative interface between the central nervous system and viscera that contributes to the maintenance of homeostasis.

Some stress protocols show a pro-inflammatory response in the brain and other systems characterized by a complex release of several inflammatory mediators such as cytokines, transcription factors, prostanoids and free radicals.

Chronic stress can be an extremely detrimental phenomenon because it maintains an artificial state of excitation, whereas acute stress ends this process in a more timely manner.