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Vitamin G. Grounding as Energetic Nutrition and Its Role in Oxidative Defense and Cardiovascular Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Stephen T. Sinatra, Gaetan Chevalier, Drew Sinatra
Recent research has revealed that the vagus nerve plays a major role in the so-called “anti-inflammatory reflex,” a mechanism controlling basic immune responses and inflammation during pathogen invasion and tissue injury. Among other things, the nerve’s actions help to inhibit excessive production of pro-inflammatory chemicals.11,12
Emotional Wellness and Stress Resilience
Published in Michelle Tollefson, Nancy Eriksen, Neha Pathak, Improving Women's Health Across the Lifespan, 2021
Gia Merlo, Ariyaneh Nikbin, Hanjun Ryu
Because the chronic stress response is centered on the HPA axis, stress exhaustion may cause significant damage to this important system of neuroendocrine activity.34 Prolonged stress may cause epigenetic changes in the expression of glucocorticoids through altering methylation patterns in glucocorticoid receptor gene NR3C1.35 Dysregulation of normal glucocorticoid feedback is associated with numerous systemic effects, including increased serum blood sugar levels, accumulation of fat in visceral areas, breakdown of muscle and bone, atrophy of neurons in the hippocampus and prefrontal cortex, increased blood clotting, atherosclerosis, and infertility.36,37,38,39,40 In chronic stress, the inflammatory reflex of the vagus nerve is disrupted; the body is left in a state of excessive pro-inflammatory cytokine production, which increases the risk of developing obesity, insulin resistance and type II diabetes mellitus, cardiovascular disease, and other debilitating conditions.30 Chronic stress can also produce epigenetic changes associated with mood and anxiety disorders, such as through the downregulation of the serotonin transporter gene SLC6A4.41
The Potential Use of Lactic Acid Bacteria in Neurodegenerative Pathologies
Published in Marcela Albuquerque Cavalcanti de Albuquerque, Alejandra de Moreno de LeBlanc, Jean Guy LeBlanc, Raquel Bedani, Lactic Acid Bacteria, 2020
Daiana E Perez Visñuk, María del Milagro Teran, Graciela Savoy de Giori, Jean Guy LeBlanc, Alejandra de Moreno de LeBlanc
Signals transmitted through the vagus nerve are part of an “inflammatory reflex” in order to maintain immunological homeostasis; and an imbalance produced in it could lead to the development of diseases such as atherosclerosis, obesity, cancer, inflammatory bowel disease, neurodegeneration, rheumatoid arthritis, among others. Many nerve fibers from the gut are constantly providing information to the Central Nervous System (CNS), and this communication allows the CNS to know what is happening in the intestine. Local changes in the levels of cytokines or other molecules, or changes in pH in the gut can be communicated in this way from the enteric nervous system (ENS) to the CNS (Andersson and Tracey 2012).
The effect of dexketoprofen trometamol on WAG/Rij rats with absence epilepsy (dexketoprofen in absence epilepsy)
Published in Neurological Research, 2021
Aras Erdil, Mustafa Sami Demirsoy, Sefa Çolak, Esra Duman, Orhan Sümbül, Hatice Aygun
Although inflammation alone is not a predisposing factor that causes depression and anxiety, these disorders are among the most frequently associated comorbidities in animal and human epilepsy models [58,59]. Inflammatory processes, cell-mediated immune activation, and compensatory anti-inflammatory reflex system are all closely related to depression [58,60]. Proinflammatory cytokines can also trigger brain structure changes and function, leading to depressive disorders, but there is still limited evidence. Moreover, AEDs have severe neurobehavioral side effects, and the most discussed neurobehavioral side effects are related to cognitive function and depression [58]. Barbiturates, vigabatrin, and topiramate reveal depressive symptoms, while topiramate’s cognitive side effects have been reported [61]. In this regard, anti-inflammatory agents or compounds that exhibit anti-inflammatory properties are potential candidates that could inhibit epilepsy and its associated neurobehavioral comorbidities [58].
Autoimmune gastrointestinal dysmotility: the interface between clinical immunology and neurogastroenterology
Published in Immunological Medicine, 2021
Shunya Nakane, Akihiro Mukaino, Eikichi Ihara, Yoshihiro Ogawa
The bidirectional brain-gut microbiota interactions are believed to be involved in the pathogenesis of well-known brain-gut disorders such as irritable bowel syndrome (IBS) and other GI disorders [63,64] and have more recently been implicated as a possible mechanism in the pathophysiology of neurological disorders such as Parkinson’s disease [65,66], autism spectrum disorders [67,68]. The next challenge is to elucidate the role of brain-gut axis in AGID, because AGID is a neurological, GI, and an autoimmune disease [69]. With regard to PNS, the vagus nerve, which mainly constitutes the parasympathetic nervous system, sends signals from the brain to visceral organs including the heart, lungs, and intestine via ACh [70]. Tracey and colleagues discovered the cholinergic ‘anti-inflammatory reflex’ as a major neural circuit that modulates immune responses [71,72]. In this reflex, peripheral inflammation is sensed by vagal afferent neurons, activating a brainstem circuit that leads to decreased cytokine production via vagal afferent neuron signaling [70]. Most recently, Teratani et al. reported the biological mechanism by which bacterial information from the intestinal tract is integrated in the liver and transmitted to the brain to control the production of intestinal regulatory T cells through the vagal nerve reflex [73]. Thus, several experimental approaches have been reported on autonomic innervation of immune organs and neuroimmune modulation [74].
Existing and emerging applications for the neuromodulation of nerve activity through targeted delivery of electric stimuli
Published in International Journal of Neuroscience, 2019
Claire Ginn, Bipin Patel, Robert Walker
VNS has also been explored as a potential treatment for inflammatory diseases, such as, RA. The ‘inflammatory reflex’ as elucidated by Andersson and Tracey is a neurophysiological mechanism by which the central nervous system regulates the immune system [38–40]. The efferent arm of the inflammatory reflex is called the cholinergic anti-inflammatory pathway (CAP). Activation of CAP by electrical VNS has been found to reduce inflammation associated with RA [41]. VNS works by reducing the release of proinflammatory cytokines and the activation of immune effector cells that traffic to the inflamed joint [40]. Stimulation of the vagus nerve activates adrenergic neurons in the spleen which culminates in the release of norepinephrine [40]. Norepinephrine released from splenic neurons then binds to β2 adrenergic receptors expressed on a subset of T cells that express choline acetyltransferase, the rate limiting enzyme in acetylcholine (ACh) biosynthesis [40]. The produced ACh then interacts with α7 nicotinic ACh receptors (α7 nAChR) expressed on immunocompetent cells (e.g. macrophages) [40]. The resulting α7 nAChR signal transduction suppresses the JAK-STAT/nuclear factor kappa-light-chain-enhancer of activated B cell (NFκB) signalling pathways and inhibits the synthesis and release of tumor necrosis factor alpha (TNFα), interleukin-6 (IL-6), IL-1β and other pro-inflammatory cytokines [40].