How does the vagus nerve affect the stomach

I have a client with EDS and she has many of the same conditions. Since digestion is the biggest issue, you can speak to her doctor about using a prescription prokinetic to help with motility and ask if a gastroparesis diet is appropriate for her. It may help with vagal nerve function. It may be something to look into. I hope she gets some relief soon! Hi Dece, You might want to consider having your daughter checked for gastroptosis, Enteroptosis and maybe even nephroptosis.

Organs dropping more than they should when a person stands up. Some people with EDS can also suffer from one or more of those conditions. If any of her abdominal pain symptoms are worse when she sits up or stands up that could be an important clue to ptosis problems.

It takes radiology studies that are done when a person is standing to diagnose these conditions. You can google EDS with the ptosis conditions listed above. I would google each ptosis condition separately along with EDS. Also, Nutcracker Syndrome can lead to pelvic congestion syndrome and reproductive problems at reproductive age. Chiari CAN cause over different symptoms depending on the severity of the Malformation and if there is a Syringomyelia caused by the Chiari.

I hope the above information helps you in your research. Hi Sarah, Thank you for the information. I have a diagnosis of IBS-C which flares up a lot during periods of stress.

I have had to cut so many foods out of my life that never bothered me before and makes it very difficult to eat with friends or out. Even when I do and eat everything correct, my motility and bloating is still sometimes a huge issue.

A limited diet ends up doing more harm than good. For chronic constipation clients, finding the right stress management technique can be helpful which helps improve the tone of the vagus nerve but some clients may need pelvic floor physical therapy. Some clients have benefited from a motility study to see if they are a good candidate for prescription prokinetic.

There are lots of tools in the toolbox. Addressing the root cause of your constipation is the key to resolving it. One month into the treatment , I felt much better wrt anxiety but started having chronic digestive problems which was diagnosed later as IBS-D.

I would really appreciate your inputs on the same , thanks in advance! Please check Medline Plus for a list of potential side effects associated with antidepressant use. There are numerous digestive-related side effects that may be contributing to your symptoms. Hello Sara I go night over night not able to sleep because of severe cramps in my stomach which cause me to have to move continually.

I eat fish and vegetables and stay away from all allopathic drugs. I have ginger, garlic etc. I do eat wheat sometimes because it is in everything and it does affect me. I drink lots of water. In the morning normally I go to the loo and I am fine. Just recently I have been taking activated charcoal for gas but this has made me constipated.

At night I do exercises, deep breathing, stretching, praying… you name it. Any suggestions? Best wishes Ginny. Hi Ginny, sorry you have been struggling with stomach cramps. The first step is to get the right diagnosis from your gastroenterologist. Stomach cramping is associated with so many conditions. Hi Sara, 2 weeks post gastric bypass I developed an ulcer diag. By a scope. Any type of food is basically out of the question, except perhaps a tiny amount of mashed banana.

Even ice chips will cause nausea. Is there a particular area to stimulate the vagal nerve to help? Hi Sara, I am currently going through extreme stress. I have changed jobs after 15 years. Topped with the unpredictable belly and topped with anxiety as too whether I need to pass wind or will I follow through. Means I end up going to the loo just in case. Which is resulting in me not eating. Will this help? Anything that helps your body better respond to stress will help. I am find this article in one of the darkest points in my life.

Eight months ago, I was snowboarding when I slammed my chest into the ground at about 30 miles per hour. Ever since then I have been dealing with bouts of nausea and poor sleep every day without end.

I went to the ER directly after the injury and was told there is nothing they could do, I then went to the chiropractor six months later and he found that my ribs had knocked one of the vertebrae that hold the Vagus nerve. He has tried to get it in position but still every time I lay down, stand up, sit, or eat I nearly fall to the floor with nausea.

Do you know of anyways I could possibly heal this pain? I hope this finds you well.. Hi Noi, I am sorry to hear about your accident. Nerve damage and concussions can affect the vagus nerve. You may want to see a neurologist, since you seem to have a complex case. Often I have to take Ambien in order to fall asleep. Hi Laura — We have many clients who have digestive symptoms and find it hard to sleep.

There are lots of potential reasons for this. How can stress affect our digestion? How can we test this? What is vagus nerve stimulation? Book online Call to make an appointment. By Professor Owen Epstein. View Profile Overall assessment of their patients See opinions View Profile Overall assessment of their patients. More articles from this doctor. More videos from this doctor. Professor Owen Epstein. This website uses its own and third-party cookies to collect information in order to improve our services, to show you advertising related to your preferences, as well as to analyse your browsing habits..

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The gut is an important control center of the immune system and the vagus nerve has immunomodulatory properties 6. As a result, this nerve plays important roles in the relationship between the gut, the brain, and inflammation. There are new treatment options for modulating the brain—gut axis, for example, vagus nerve stimulation VNS and meditation techniques.

These treatments have been shown to be beneficial in mood and anxiety disorders 7 — 9 , but also in other conditions associated with increased inflammation In particular, gut-directed hypnotherapy was shown to be effective in both, irritable bowel syndrome and IBD 11 , Finally, the vagus nerve also represents an important link between nutrition and psychiatric, neurological and inflammatory diseases.

The vagus nerve carries an extensive range of signals from digestive system and organs to the brain and vice versa. It is the tenth cranial nerve, extending from its origin in the brainstem through the neck and the thorax down to the abdomen.

The vagus nerve exits from the medulla oblongata in the groove between the olive and the inferior cerebellar peduncle, leaving the skull through the middle compartment of the jugular foramen.

In the neck, the vagus nerve provides required innervation to most of the muscles of the pharynx and larynx, which are responsible for swallowing and vocalization. In the thorax, it provides the main parasympathetic supply to the heart and stimulates a reduction in the heart rate.

In the intestines, the vagus nerve regulates the contraction of smooth muscles and glandular secretion. Preganglionic neurons of vagal efferent fibers emerge from the dorsal motor nucleus of the vagus nerve located in the medulla, and innervate the muscular and mucosal layers of the gut both in the lamina propria and in the muscularis externa The celiac branch supplies the intestine from proximal duodenum to the distal part of the descending colon 15 , The abdominal vagal afferents, include mucosal mechanoreceptors, chemoreceptors, and tension receptors in the esophagus, stomach, and proximal small intestine, and sensory endings in the liver and pancreas.

The NTS projects, the vagal sensory information to several regions of the CNS, such as the locus coeruleus LC , the rostral ventrolateral medulla, the amygdala, and the thalamus The vagus nerve is responsible for the regulation of internal organ functions, such as digestion, heart rate, and respiratory rate, as well as vasomotor activity, and certain reflex actions, such as coughing, sneezing, swallowing, and vomiting Its activation leads to the release of acetylcholine ACh at the synaptic junction with secreting cells, intrinsic nervous fibers, and smooth muscles ACh binds to nicotinic and muscarinic receptors and stimulates muscle contractions in the parasympathetic nervous system.

Animal studies have demonstrated a remarkable regeneration capacity of the vagus nerve. For example, subdiaphragmatic vagotomy induced transient withdrawal and restoration of central vagal afferents as well as synaptic plasticity in the NTS Alongside the sympathetic nervous system and the enteric nervous system ENS , the parasympathetic nervous system represents one of the three branches of the autonomic nervous system. The definition of the sympathetic and parasympathetic nervous systems is primarily anatomical.

The vagus nerve is the main contributor of the parasympathetic nervous system. Other three parasympathetic cranial nerves are the nervus oculomotorius, the nervus facialis, and the nervus glossopharyngeus. The most important function of the vagus nerve is afferent, bringing information of the inner organs, such as gut, liver, heart, and lungs to the brain. This suggests that the inner organs are major sources of sensory information to the brain.

The gut as the largest surface toward the outer world and might, therefore, be a particularly important sensory organ. Historically, the vagus has been studied as an efferent nerve and as an antagonist of the sympathetic nervous system. Most organs receive parasympathetic efferents through the vagus nerve and sympathetic efferents through the splanchnic nerves. Together with the sympathetic nervous systems, the parasympathetic nervous system is responsible for the regulation of vegetative functions by acting in opposition to each other The parasympathetic innervation causes a dilatation of blood vessels and bronchioles and a stimulation of salivary glands.

On the contrary, the sympathetic innervation leads to a constriction of blood vessels, a dilatation of bronchioles, an increase in heart rate, and a constriction of intestinal and urinary sphincters. In the gastrointestinal tract, the activation of the parasympathetic nervous system increases bowel motility and glandular secretion.

In contrast to it, the sympathetic activity leads to a reduction of intestinal activity and a reduction of blood flow to the gut, allowing a higher blood flow to the heart and the muscles, when the individual faces existential stress. The ENS arises from neural crest cells of the primarily vagal origin and consists of a nerve plexus embedded in the intestinal wall, extending across the whole gastrointestinal tract from the esophagus to the anus.

It is estimated that the human ENS contains about — million neurons. This is the largest accumulation of nerve cells in the human body 23 — It consists of two ganglionated plexuses—the submucosal plexus, which regulates gastrointestinal blood flow and controls the epithelial cell functions and secretion and the myenteric plexus, which mainly regulates the relaxation and contraction of the intestinal wall The ENS serves as intestinal barrier and regulates the major enteric processes, such as immune response, detecting nutrients, motility, microvascular circulation, and epithelial secretion of fluids, ions, and bioactive peptides On the other hand, the ENS in the small and large bowel also is able to function quite independent of vagal control as it contains full reflex circuits, including sensory neurons and motor neurons.

They regulate muscle activity and motility, fluid fluxes, mucosal blood flow, and also mucosal barrier function. ENS neurons are also in close contact to cells of the adaptive and innate immune system and regulate their functions and activities. Aging and cell loss in the ENS are associated with complaints, such as constipation, incontinence, and evacuation disorders.

The connection between the CNS and the ENS, also referred to as the brain—gut axis enables the bidirectional connection between the brain and the gastrointestinal tract.

It is responsible for monitoring the physiological homeostasis and connecting the emotional and cognitive areas of the brain with peripheral intestinal functions, such as immune activation, intestinal permeability, enteric reflex, and enteroendocrine signaling 1.

This brain—gut axis, includes the brain, the spinal cord, the autonomic nervous system sympathetic, parasympathetic, and ENS , and the hypothalamic—pituitary—adrenal HPA axis 1. Environmental stress, as well as elevated systemic proinflammatory cytokines, activates the HPA axis through secretion of the corticotropin-releasing factor CRF from the hypothalamus This stimulation, in turn, leads to cortisol release from the adrenal glands.

Cortisol is a major stress hormone that affects many human organs, including the brain, bones, muscles, and body fat. Both neural vagus and hormonal HPA axis lines of communication combine to allow brain to influence the activities of intestinal functional effector cells, such as immune cells, epithelial cells, enteric neurons, smooth muscle cells, interstitial cells of Cajal, and enterochromaffin cells These cells, on the other hand, are under the influence of the gut microbiota.

The gut microbiota has an important impact on the brain—gut axis interacting not only locally with intestinal cells and ENS, but also by directly influencing neuroendocrine and metabolic systems Emerging data support the role of microbiota in influencing anxiety and depressive-like behaviors Studies conducted on germ-free animals demonstrated that microbiota influence stress reactivity and anxiety-like behavior and regulate the set point for HPA activity.

Thus, these animals generally show a decreased anxiety 35 and an increased stress response with augmented levels of ACTH and cortisol In case of food intake, vagal afferents innervating the gastrointestinal tract provide a rapid and discrete account of digestible food as well as circulating and stored fuels, while vagal efferents together with the hormonal mechanisms codetermine the rate of nutrient absorption, storage, and mobilization Histological and electrophysiological evidence indicates that visceral afferent endings of the vagus nerve in the intestine express a diverse array of chemical and mechanosensitive receptors.

These receptors are targets of gut hormones and regulatory peptides that are released from enteroendocrine cells of the gastrointestinal system in response to nutrients, by distension of the stomach and by neuronal signals They influence the control of food intake and regulation of satiety, gastric emptying and energy balance 39 by transmitting signals arising from the upper gut to the nucleus of the solitary tract in the brain Most of these hormones, such as peptide cholecystokinin CCK , ghrelin, and leptin are sensitive to the nutrient content in the gut and are involved in regulating short-term feelings of hunger and satiety Cholecystokinin regulates gastrointestinal functions, including inhibition of gastric emptying and food intake through activation of CCK-1 receptors on vagal afferent fibers innervating the gut In addition, CCK is important for secretion of pancreatic fluid and producing gastric acid, contracting the gallbladder, decreasing gastric emptying, and facilitating digestion Saturated fat, long-chain fatty acids, amino acids, and small peptides that result from protein digestion stimulate the release of CCK from the small intestine There are various biologically active forms of CCK, classified according to the number of amino acids they contain, i.

In rats, both long- and short-chain fatty acids from food activate jejunal vagal afferent nerve fibers, but do so by distinct mechanisms Short-chain fatty acids, such as butyric acid have a direct effect on vagal afferent terminals while the long-chain fatty acids activate vagal afferents via a CCK-dependent mechanism. CCK is also present in enteric vagal afferent neurons, in cerebral cortex, in the thalamus, hypothalamus, basal ganglia, and dorsal hindbrain, and functions as a neurotransmitter It directly activates vagal afferent terminals in the NTS by increasing calcium release Further, there is evidence that CCK can activate neurons in the hindbrain and intestinal myenteric plexus a plexus which provides motor innervation to both layers of the muscular layer of the gut , in rats and that vagotomy or capsaicin treatment results in an attenuation of CCK-induced Fos expression a type of a proto-oncogene in the brain There is also substantial evidence that elevated levels of CCK induce feelings of anxiety Therefore, CCK is used as a challenge agent to model anxiety disorders in humans and animals Ghrelin is another hormone released into circulation from the stomach and plays a key role in stimulating food intake by inhibiting vagal afferent firing Circulating ghrelin levels are increased by fasting and fall after a meal Central or peripheral administration of acylated ghrelin to rats acutely stimulates food intake and growth hormone release, and chronic administration causes weight gain In humans, intravenous infusion or subcutaneous injection increases both feelings of hunger and food intake, since ghrelin suppresses insulin release Therefore, it is not surprising that secretion is disturbed in obesity and insulin resistance Leptin receptors have also been identified in the vagus nerve.

Studies in rodents clearly indicate that leptin and CCK interact synergistically to induce short-term inhibition of food intake and long-term reduction of body weight The epithelial cells that respond to both ghrelin and leptin are located near the vagal mucosal endings and modulate the activity of vagal afferents, acting in concert to regulate food intake 58 , After fasting and diet-induced obesity in mice, leptin loses its potentiating effect on vagal mucosal afferents The gastrointestinal tract is the key interface between food and the human body and can sense basic tastes in much the same way as the tongue, through the use of similar G-protein-coupled taste receptors Different taste qualities induce the release of different gastric peptides.

Bitter taste receptors can be considered as potential targets to reduce hunger by stimulating the release of CCK Further, activation of bitter taste receptors stimulates ghrelin secretion 62 and, therefore, affects the vagus nerve.

The gastrointestinal tract is constantly confronted with food antigens, possible pathogens, and symbiotic intestinal microbiota that present a risk factor for intestinal inflammation It is highly innervated by vagal fibers that connect the CNS with the intestinal immune system, making vagus a major component, the neuroendocrine-immune axis. This axis is involved in coordinated neural, behavioral, and endocrine responses, important for the first-line defense against inflammation Counter-regulatory mechanisms, such as immunologically competent cells and anti-inflammatory cytokines normally limit the acute inflammatory response and prevent the spread of inflammatory mediators into the bloodstream.

The anti-inflammatory capacities of the vagus nerve are mediated through three different pathways The first pathway is the HPA axis, which has been described above. The second pathway is the splenic sympathetic anti-inflammatory pathway, where the vagus nerve stimulates the splenic sympathetic nerve. The last pathway, called the cholinergic anti-inflammatory pathway CAIP , is mediated through vagal efferent fibers that synapse onto enteric neurons, which in turn release ACh at the synaptic junction with macrophages Compared to the HPA axis, the CAIP has some unique properties, such as a high speed of neural conductance, which enables an immediate modulatory input to the affected region of inflammation Therefore, the CAIP plays a crucial role in the intestinal immune response and homeostasis, and presents a highly interesting target for the development of novel treatments for inflammatory diseases related to the gut immune system 6 , The inflammation-sensing and inflammation-suppressing functions outlined above provide the principal components of the inflammatory reflex The appearance of pathogenic organisms activates innate immune cells that release cytokines.

These in turn activate sensory fibers that ascend in the vagus nerve to synapse in the nucleus tractus solitarius. Increased efferent signals in the vagus nerve suppress peripheral cytokine release through macrophage nicotinic receptors and the CAIP.

Vagus nerve stimulation is a medical treatment that is routinely used in the treatment of epilepsy and other neurological conditions. VNS studies are not just clinically, but also scientifically informative regarding the role of the vagus nerve in health and disease. Vagus nerve stimulation works by applying electrical impulses to the vagus nerve. The stimulation of the vagus nerve can be performed in two different ways: a direct invasive stimulation, which is currently the most frequent application and an indirect transcutaneous non-invasive stimulation.

Invasive VNS iVNS requires the surgical implantation of a small pulse generator subcutaneously in the left thoracic region. Electrodes are attached to the left cervical vagus nerve and are connected to the pulse generator by a lead, which is tunneled under the skin. The generator delivers intermittent electrical impulses through the vagus nerve to the brain It is postulated that these electrical impulses exert antiepileptic 75 , antidepressive 76 , and anti-inflammatory effects by altering the excitability of nerve cells.

Here, the stimulator is usually attached to the auricular concha via ear clips and delivers electrical impulses at the subcutaneous course of the afferent auricular branch of the vagus nerve Five years later, the stimulation of the vagus nerve for the treatment of refractory depression was approved by the U. Since then, the safety and efficacy of VNS in depression has been demonstrated in numerous observational studies as can be seen below.

In contrast, there is no randomized, placebo-control clinical trial that reliably demonstrates antidepressant effects of VNS. The mechanism by which VNS may benefit patients nonresponsive to conventional antidepressants is unclear, with further research needed to clarify this Functional neuroimaging studies have confirmed that VNS alters the activity of many cortical and subcortical regions Through direct or indirect anatomic connections via the NTS, the vagus nerve has structural connections with several mood regulating limbic and cortical brain areas Thus, in chronic VNS for depression, PET scans showed a decline in resting brain activity in the ventromedial prefrontal cortex vmPFC , which projects to the amygdala and other brain regions modulating emotion VNS results in chemical changes in monoamine metabolism in these regions possibly resulting in antidepressant action 84 , The relationship between monoamine and antidepressant action has been shown by various types of evidence.

All drugs that increase monoamines—serotonin 5-HT , NE, or dopamine DA —in the synaptic cleft have antidepressant properties Accordingly, depletion of monoamines induces depressive symptoms in individuals who have an increased risk of depression In rats, it has been shown that VNS treatments induce large time-dependent increases in basal neuronal firing in the brainstem nuclei for serotonin in the dorsal raphe nucleus Thus, chronic VNS was associated with increased extracellular levels of serotonin in the dorsal raphe Several lines of evidence suggest that NE is a neurotransmitter of major importance in the pathophysiology and treatment of depressive disorders Thus, experimental depletion of NE in the brain led to a return of depressive symptoms after successful treatment with NE antidepressant drugs The LC contains the largest population of noradrenergic neurons in the brain and receives projections from NTS, which, in turn, receives afferent input from the vagus nerve Thus, VNS leads to an enhancement of the firing activity of NE neurons 93 , and consequently, an increase in the firing activity of serotonin neurons The pharmacologic destruction of noradrenergic neurons resulted in the loss of antidepressant VNS effects DA is a catecholamine that to a large extent is synthesized in the gut and plays a crucial role in the reward system in the brain Further, beneficial effects of VNS might be exerted through a monoamine-independent way.

Thus, VNS treatments might result in dynamic changes of monoamine metabolites in the hippocampus 93 and several studies reported the influence of VNS on hippocampal neurogenesis 99 , This process has been regarded as a key biological process indispensable for maintaining the normal mood Serotonin is also an important neurotransmitter in the gut that can stimulate peristalsis and induce nausea and vomiting by activating the vagus nerve.

In addition, it is essential for the regulation of vital functions, such as appetite and sleep, and contributes to feelings of well-being.

Serotonin is released from enterochromaffin cells in response to mechanical or chemical stimulation of the gastrointestinal tract which leads to activation of 5-HT3 receptors on the terminals of vagal afferents The central terminals of vagal afferents also exhibit 5-HT3 receptors that function to increase glutamatergic synaptic transmission to second order neurons of the nucleus tractus solitarius within the brainstem.

As a result, interactions between the vagus nerve and serotonin systems in the gut and in the brain appear to play an important role in the treatment of psychiatric conditions. Major depressive disorder ranks among the leading mental health causes of the global burden of disease With a lifetime prevalence of 1. The pathophysiology of depression is complex and includes social environmental stress factors; genetic and biological processes, such as the overdrive of the HPA axis, inflammation 31 , and disturbances in monamine neurotransmission as described above For example, a lack of the amino acid tryptophan, which is a precursor to serotonin, can induce depressive symptoms, such as depressed mood, sadness, and hopelessness The overdrive of the HPA axis is most consistently seen in subjects with more severe i.

It has been shown that chronic exposure to elevated inflammatory cytokines can lead to depression This might be explained by the fact that cytokine overexpression leads to a reduction of serotonin levels In line with that, treatment with anti-inflammatory agents has the potential to reduce depressive symptoms In line, IBD are important risk factor for mood and anxiety disorders , and these psychiatric conditions increase the risk of exacerbation of IBD A European multicenter study demonstrated a positive effect of VNS on depressive symptoms, in patients with treatment-resistant depression Several other studies also demonstrated an increasing long-term benefit of VNS in recurrent treatment-resistant depression 84 , 85 , Further, a 5-year prospective observational study which compared the effects of treatment as usual and VNS as adjunctive treatment with treatment as usual only in treatment-resistant depression, showed a better clinical outcome and a higher remission rate in the VNS group This was even the case in patients with comorbid depression and anxiety who are frequent non-responders in trials on antidepressant drugs.

It is important to note that all these studies were open-label and did not use a randomized, placebo-controlled study design. Patients with depression have elevated plasma and cerebrospinal fluid concentrations of proinflammatory cytokines. The benefit of VNS in depression might be due to the inhibitory action on the production of proinflammatory cytokines and marked peripheral increases in anti-inflammatory circulating cytokines Altered CRH production and secretion might result from a direct stimulatory effect, transmitted from the vagus nerve through the NTS to the paraventricular nucleus of the hypothalamus.

The gut microbiota is the potential key modulator of the immune and the nervous systems Targeting it could lead to a greater improvement in the emotional symptoms of patients suffering from depression or anxiety. There is growing evidence that nutritional components, such as probiotics , , gluten , as well as drugs, such as anti-oxidative agents and antibiotics , have a high impact on vagus nerve activity through the interaction with the gut microbiota and that this effect varies greatly between individuals.

Indeed, animal studies have provided evidence that microbiota communication with the brain involves the vagus nerve and this interaction can lead to mediating effects on the brain and subsequently, behavior For example, Lactobacillus -species have received tremendous attention due to their use as probiotics and their health-promoting properties Bravo et al.

It has been shown that chronic treatment with L. In addition, L. Importantly, L. This is not surprising, since alterations in central GABA receptor expression are implicated in the pathogenesis of anxiety and depression , The antidepressive and anxiolytic effects of L.

In line with that, in a model of chronic colitis associated to anxiety-like behavior, the anxiolytic effect obtained with a treatment with Bifidobacterium longum , was absent in mice that were vagotomized before the induction of colitis In humans, psychobiotics, a class of probiotics with anti-inflammatory effects might be useful to treat patients with psychiatric disorders due to their antidepressive and anxiolytic effects Differences in the composition of the gut microbiota in patients with depression compared with healthy individuals have been demonstrated Importantly, the fecal samples pooled from five patients with depression transferred into germ-free mice, resulted in depressive-like behavior.

It has been shown that self-generated positive emotions via loving-kindness meditation lead to an increase in positive emotions relative to the control group, an effect moderated by baseline vagal tone In turn, increased positive emotions produced increases in vagal tone, which is probably mediated by increased perceptions of social connections.

Individuals suffering from depression, anxiety, and chronic pain have benefited from regular mindfulness meditation training, demonstrating a remarkable improvement in symptom severity 9. Controlled studies have found yoga-based interventions to be effective in treating depression ranging from mild depressive symptoms to major depressive disorder MDD Some yoga practices can directly stimulate the vagus nerve, by increasing the vagal tone leading to an improvement of autonomic regulation, cognitive functions, and mood and stress coping The proposed neurophysiological mechanisms for the success of yoga-based therapies in alleviating depressive symptoms suggest that yoga breathing induces increased vagal tone Many studies demonstrate the effects of yogic breathing on brain function and physiologic parameters.

Thus, Sudarshan Kriya Yoga SKY , a breathing-based meditative technique, stimulates the vagus nerve and exerts numerous autonomic effects, including changes in heart rate, improved cognition, and improved bowel function During SKY, a sequence of breathing techniques of different frequencies, intensities, lengths, and with end-inspiratory and end-expiratory holds creates varied stimuli from multiple visceral afferents, sensory receptors, and baroreceptors.

These probably influence diverse vagal fibers, which in turn induce physiologic changes in organs, and influence the limbic system Iyengar yoga has been shown to decreased depressive symptoms in subjects with depression Iyengar yoga is associated with increased HRV, supporting the hypothesis that yoga breathing and postures work in part by increasing parasympathetic tone Posttraumatic stress disorder is an anxiety disorder that can develop after trauma and is characterized by experiencing intrusive memories, flashbacks, hypervigilance, nightmares, social avoidance, and social dysfunctions It has a lifetime prevalence of 8.

The symptoms of PTSD can be classified into four clusters: intrusion symptoms, avoidance behavior, cognitive and affective alterations, and changes in arousal and reactivity People who suffer from PTSD tend to live as though under a permanent threat.

They exhibit fight and flight behavior or a perpetual behavioral shutdown and dissociation, with no possibility of reaching a calm state and developing positive social interactions. Over time, these maladaptive autonomic responses lead to the development of an increased risk for psychiatric comorbidities, such as addiction and cardiovascular diseases Posttraumatic stress disorder symptoms are partly mediated by the vagus nerve.

There is evidence for diminished parasympathetic activity in PTSD, indicating an autonomic imbalance A study published in the Journal of Internal Medicine found that the vagus nerve is so closely entwined with the digestive system that stimulation of the nerve can improve irritable bowel syndrome. In recent decades, many researchers have found that this brain-gut axis has another counterpart — the bacteria that live inside the intestines. This microbiome communicates with the brain through the vagus nerve, affecting not just food intake but also mood and inflammation response, according to a review published in the journal Advances in Experimental Medicine and Biology.

Much of the existing research involves experiments with mice and rats rather than humans. Nonetheless, the results are striking and show that changes in the microbiome may cause changes in the brain. Stimulation of the vagus nerve has been effective in treating cases of epilepsy that do not respond to medication. Surgeons place an electrode around the right branch of the vagus nerve in the neck, with a battery implanted below the collarbone. The electrode provides regular stimulation to the nerve, which decreases, or in rare cases prevents, the excessive brain activity that causes seizures, according to the Epilepsy Foundation.

Europe has approved a vagus nerve stimulator that does not require surgical implantation, according to the Mayo Clinic.