Bioelectronic medicine
The wiki’s first translational thread that treats the interoceptive pathway as the target rather than interoceptive attention. Everything else in the applications folder — interoceptive-training-clinical, mindfulness-interoceptive-training, somatic-experiencing, and the interoceptive-exposure method — works by changing how a person attends to, appraises, or tolerates bodily sensation. This works by putting current into the nerve.
Introduced with the Bonaz et al. (2021) ingest. Bruno Bonaz is a vagus-nerve-stimulation researcher and the review’s translational close is largely his programme; read accordingly. See bruno-bonaz.
The definition and the scope
Per the review’s glossary, bioelectronic medicine “builds upon mechanistic insights into neural control of biological processes that underlie disease. It is based on the development of devices to modulate these specific neural circuits as a therapy using electromagnetic fields.” The techniques named:
| technique | invasiveness | applications cited |
|---|---|---|
| Vagus nerve stimulation (VNS) | implanted | epilepsy, depression, inflammation, obesity |
| Spinal cord stimulation | implanted | chronic pain |
| Deep brain stimulation | implanted | — |
| Transcranial magnetic stimulation | non-invasive | — |
| Transcranial direct current stimulation | non-invasive | — |
Reported benefits are antinociceptive, antidepressive and anti-inflammatory. In animal work, optogenetics and pharmacogenetics are named as further stimulation approaches offering cell-type-specific manipulation.
Why the vagus is the centre of it
The vagus is the pathway that makes the framing coherent, and it does three jobs in this review:
- Immune-to-brain afferent signalling. Activation of the immune system is signalled to the brain particularly via the vagus; this is the interoceptive channel of sickness-behaviors and the entry point for inflammation into mood.
- The cholinergic anti-inflammatory pathway. Bonaz’s own line (Bonaz et al. 2013, 2016): efferent vagal activity suppresses peripheral inflammation, so stimulating the nerve is an anti-inflammatory intervention rather than merely a neural one. This is what makes VNS a candidate for inflammatory disease and, by the inflammation-to-depression bridge, for psychiatric disease.
- The microbiota-gut-brain-axis interface. Vagal afferents carry microbial signals, directly (TLR4) and via enteroendocrine relay.
The review adds that growing understanding of interoceptive immune pathways, VNS included, has “already opened up therapeutic applications” for psychiatric disorders — naming anticytokine therapy, NSAIDs, and minocycline suppression of microglial activation for depression. Those are pharmacological rather than bioelectronic, but they share the logic: treat the interoceptive signal, not the interpretation of it.
The obesity case, and its evidential shape
Worth recording because it shows the reasoning at its weakest. The argument: vagal afferent biophysical properties are impaired in obesity; leptin resistance of vagal afferents accompanies hyperphagia; disturbed vagal signalling favours overconsumption and weight gain; therefore VNS may help manage obesity. The evidence offered: “circumstantial evidence from patients losing weight following VNS applied for the treatment of epilepsy or depression, yet findings from clinical trials for obesity are awaited.” Chronic VNS reduced weight gain, food consumption and sweet craving in adult obese minipigs.
A mechanistic story, an incidental clinical observation, and a pig. The review states this plainly enough that the wiki can record it without editorializing further.
The comparison the wiki should hold
Set against the attention-based applications, bioelectronic medicine makes a different bet about where interoceptive disorders live. The contemplative and exposure traditions locate the problem in the relationship to bodily signal — avoidance, catastrophic appraisal, hypervigilance, or in Farb et al.’s terms a failure of interoceptive regulation. Bioelectronic medicine locates it in the signal and its conduction.
Bonaz et al.’s own framing licenses both, and that is the point of their Figure 1: dysfunction can strike at any level of the neuraxis, so an intervention at any level might be the right one. What the review does not offer — and what nothing in the wiki offers — is any way to tell which level a given patient’s problem is on. That is the same stratification gap interoceptive-training-clinical runs into from the psychological side and interoceptive-exposure runs into with Van der Does et al.’s ambulatory-monitoring proposal.
Status
Recorded as a real and growing clinical field with a genuine mechanistic rationale, held here entirely through one review section by an interested party, with no trial evidence read first-hand. Bonaz cites Pavlov & Tracey’s Bioelectronic Medicine volume (Cold Spring Harbor, 2019) as the field’s reference work; nothing of it is in raw/. Flagged for first-hand reading if a primary source arrives.