Pain, stress and relaxation: Involvement of basic biological principles and healthy autoregulation

Abstract

Trauma and stress often involve the expression of pain. In the course of traumatic and stressful events, an ‘orchestra’ of neurobiological mechanisms and signaling molecules get activated with the primary goal of ensuring survival and fighting against the perturbating event, i.e., stressor. Pain can be a major process in this phenomenon, directing attention to the initial trigger situation. It is now known that pain processes also involve local and/or systemic immune as well as cardiovascular and neuronal pathways, including proinflammtory endogenous opioid peptides (e.g., endorphins) and down-regulatory opiate alkaloids (e.g., morphine). Usually, relaxation is a result of the systemic down-regulation that occurs after stress response pathways get shut-down, following their initial induction. As pain occurs in the primary phase of this process, it gets an inhibitory push-back under the influence of endorphins and other analgetic endogenous signaling molecules in this still early, i.e., stress response-associated stage. The rationale of this phase would be that the ‘stressed’ organism chiefly fights against the stressor and then, subsequently, cares about the possible wounds and traumas acquired. These secondary processes include endogenous morphine signaling, allowing the pain to come back again, yet in an altered and more ‘distant’ way, enabling the organism to face it and decide upon necessary actions for recovery and learning. This secondary phase also reduces over-stimulation, e.g., of the immune system, involving anti-inflammation. Hence, down-regulation serves recovery, i.e., systemic back-up. Stress induction and subsequent termination follow each other automatically and naturally, i.e., ideally, therefore activating, among others, endogenous limbic reward and motivation circuitries. However, little is known about the interplay between pain perception and its relationship with catecholamine molecules other than dopamine serving as an endogenous morphine precursor. We believe that the perception of pain and the body's self-attempt to alleviate it, utilizing conventional homeostatic mechanisms, is mediated by key catecholamines, and that this effect is further modulated by nitric oxide. We further propose a paradigm which biologically links pain, autoregulation, endogenous morphine and the catecholamines together, demonstrating a complex symbiotic signalling system. Integrative, complementary and mind–body medicine would, by their nature, include this paradigm in their underlying concepts and therapeutic strategies.