Vagus Nerve Stimulation
Athletica Physical Health is home to the transcutaneous auricular vagus nerve stimulation (taVNS) method designed by Emrys Goldsworthy. The breakthrough occurred when the researcher Borovikova demonstrated that VNS attenuated the inflammatory response invoked by the injection of lipopolysaccharides (endotoxin) in rats. This confirmed that VNS prevents and reduces inflammation.
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See the following conditions and the associated VNS effects:
- Depression: VNS increases brain derived neurotrophic factor, noradrenaline and serotonin = increased dorsolateral prefrontal cortex activity and decreased amygdala/anterior cingulate activity.
- Digestion: VNS increases gastrin and hydrochloric acid production in the stomach and increases oesophageal/gastric motility = improved digestion and enzyme release
- Migraine: VNS decreases systemic TNF-a (a pro-inflammatory cytokine), increases the activity of the Raphe nuclei/locus coeruleus = reduced activation of the trigeminocervical nuclei
- Allergy: VNS increases the activity and number of T regulatory cells
- Inflammatory bowel diseases: VNS decreases systemic TNF-a levels and decreases gut macrophage release of TNF-a = reduced colitis
Evidence for VNS in the treatment of depression and anxiety
Rong et al (2016) found that after four weeks of taVNS, MDD patients in the taVNS group showed greater improvement compared with patients in the sham taVNS group as indicated by Hamilton score changes as well as response and remission rates at week four. In addition, they also found that the clinical improvements continued until week 12 during taVNS.
Kraus et al (2013) found that stimulation of the anterior wall evoked significant limbic deactivation at the parahippocampal gyrus and the posterior cingulate cortex
Fang et al (2015) found that after four weeks of taVNS in patients with MDD, resting state functional connectivity (rsFC) between the default mode network (DMN) and anterior insula and parahippocampus decreased while the rsFC between the DMN and precuneus and orbital prefrontal cortex increased compared with sham taVNS. All these FC increases are also associated with HAM-D-24 score reduction.
Evidence for VNS in the treatment of gastrointestinal disorders
Zhou et al (2013) showed that VNS caused closure of intestinal tight junctions and facilitate a neurally mediated enterocyte recovery from injury.
Straube et al (2015) found that VNS caused a reduction in headache days from 19 to 12 on average after 1 month of treatment.
Ellrich et al (2011) demonstrated that taVNS inhibits muscle pain and pain sensitivity associated with chronic and acute migraine.
Lenaerts et al (2008) showed that in a small cohort, 80% of participants had a 50% reduction in migraine frequency.
Stakenborg (2017) demonstrated that vagal nerve stimulation attenuates postoperative ileus - Inability of the intestine (bowel) to contract normally and elminate waste from the body. (Stakenborg 2017)
Langness et al (2015) showed vagotomy (removal of vagus nerve) results in an inability to recruit enteric nervous stem cells and thus an inability to resolve intestinal permeability after intestinal injury.
Evidence for VNS in the treatment of cognitive disorders
Sun et al (2017) found the VNS improved working memory performances seen in reduced errors on a subtask that relied on working memory.
Evidence for VNS in the treatment of atrial fibrillation
Stavrakis et al (2015) showed that taVNS suppresses atrial fibrillation and decreases TNF-a and CRP in patients with paroxysmal AF.
Evidence for VNS in the treatment of migraine
Bonaz et al (2017) showed that the lower the vagal tone, the higher the levels of TNF-a (driver of inflammatory diseases such as Crohn's diease).
VNS increases vagal tone and decreases systemic TNF-a levels.