Why my 8 minutes can change your life blog post is relevant.
Why the podcast, though primitive in understanding physiology, was sent to my colleagues yesterday.
Because it represents two important legs or foundations of neuroimmune regulation.
Cardiac autonomic dysfunction (30-70% in chronic diabetes) has a 5x mortality rate with dysfunction rather than function!
Function requires feedback and positive and negative controls.
The controls are focused in brain stem,the locus ceruleus,where fast neurotransmitters/neuromodulators and slow neuropeptides (bdnf and gdnf) affect structure (imaging and pathology) and function (imaging and nerve function testing.)
Also hidden in the article is the word antidromic which means backwards nerve transmission. This implies that nerve communication, though directional, actually goes both ways.
What does this have to do with daily hormetic doses of high intensity rest (vagal biofeedback breathing) and Tabata (high intensity interval feedback?
It strengthens and increases these chemical reserves and their responsiveness!
Consider shoulder pain secondary to tendinopathy.
Therapy stimulates a hormetic response that includes rest with progressive doses of exercise; isometric and passive motion, eccentric and passive and active motion, concentric and active followed by return to normal activities. Brief hormetic doses to stimulate nerves and growth factors for healing.
It takes a minimum of six minutes to stimulate a healing response.
Therefore, promoting healing and recovery forces is medicine's mandate.
The ANS is the systemic driver of healing for shoulders, brains and other organs.
In fact, the wandering vagus nerve, is the internet for compassion and healing both within and without.
Why not follow sage advice and exercise rest and therapeutic acute (not chronic) stress systems for enduring health, recovery and resilience?
Autonomic nervous system and neuroimmune interactions
New insights and clinical implications
Normal organ function, homeostasis, and adaptation through change (allostasis) require close reciprocal interactions between the autonomic and the immune systems. The 3 subdivisions of the autonomic nervous system—sympathetic, parasympathetic, and enteric nervous system (ENS)—as well as primary sensory afferents, receive signals from immune cells and release neurochemical transmitters that regulate the functions of these cells. These neuroimmune interactions occur at multiple levels, including the gut, the CNS, and lymphoid organs. For example, enteric neurons and glial cells interact with enteroendocrine cells and local macrophages and can sense signals from the gut lumen, including those from the microbiota; these signals elicit local immune responses and reach the CNS via humoral and neural pathways. Interleukins (ILs) and other signals from immune cells can access the hypothalamus via the neurovascular unit or circumventricular organs; these signals can also activate receptors in nerve terminals, such as vagal afferents, and thereby reach the brainstem. In response to these signals, the CNS initiates immunomodulatory autonomic and endocrine responses. For example, sympathetic output to lymphoid organs, including the spleen, elicits potent anti-inflammatory responses via β2 adrenergic receptors (adrenoceptors) expressed in multiple cells of the innate and adaptive immune systems. Vagal efferents affect immune responses in the gut via the ENS, and both vagal and dorsal root ganglion afferents trigger immunomodulatory responses via antidromic release of neuropeptides and other signals at the target organs. Since the last review on autonomic control of immune function in this series,1 studies performed primarily on mice have provided new insight into the role of the microbiota, enteric neurons and glial cells, and autonomic immunomodulatory pathways in these neuroimmune interactions. These studies have elucidated some mechanisms by which these interactions may contribute to the pathophysiology of neurologic disorders including multiple sclerosis (MS) and spinal cord injury (SCI). These findings thus have potential therapeutic implications. There are several recent reviews on these topics.2–12
Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the author, if any, are provided at the end of the article.
Joseph Thomas (Tony) Liverman, Jr.
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