If you or someone you love has been diagnosed with Postural Orthostatic Tachycardia Syndrome (POTS), you've likely been through a long and often frustrating journey to get that diagnosis — and an equally frustrating search for answers about what to do next.

POTS is not an entirely rare condition. It is estimated to affect between 1 and 3 million people in Australia alone, with a significant overrepresentation of young women. Yet it remains poorly understood in mainstream medicine, frequently misdiagnosed, and often inadequately managed.

One of the reasons POTS is so complex, and so challenging to treat, is that it is fundamentally a disorder of the autonomic nervous system. And at the centre of that autonomic dysfunction is the vagus nerve.

This post is an overview of what the current research tells us about the relationship between POTS and the vagus nerve, why this matters, and what it points toward in terms of management.

What is POTS?

Postural Orthostatic Tachycardia Syndrome is a form of dysautonomia (a dysfunction of the autonomic nervous system) characterised by an excessive increase in heart rate upon standing. Specifically, POTS is diagnosed when heart rate increases by 30 beats per minute or more (or rises above 120 bpm) within 10 minutes of standing, in the absence of orthostatic hypotension.

But POTS is far more than a fast heart rate when standing. The symptom profile is extensive and often debilitating:

Lightheadedness, dizziness, and pre-syncope (near fainting)
Profound fatigue — often described as unlike ordinary tiredness
Brain fog and cognitive difficulties
Heart palpitations
Shortness of breath
Nausea and gut dysfunction
Temperature dysregulation
Exercise intolerance
Chest discomfort
Anxiety and panic-like symptoms
Sleep disruption

What unifies these diverse symptoms is a common underlying mechanism.. The autonomic nervous system's failure to appropriately regulate cardiovascular and systemic function in response to positional change and other demands. And the vagus nerve is at the heart of that failure.

The autonomic imbalance at the core of POTS

To understand POTS, you need to understand the two-branch architecture of the autonomic nervous system:

The sympathetic nervous system — the "fight or flight" branch, which accelerates heart rate, constricts blood vessels, and mobilises the body for action
The parasympathetic nervous system — the "rest and digest" branch, primarily driven by the vagus nerve, which decelerates heart rate, dilates blood vessels, and promotes recovery and repair

In a healthy autonomic nervous system, these two branches work in dynamic balance. When you stand up, the sympathetic system appropriately increases heart rate and constricts peripheral blood vessels to maintain blood pressure and cerebral perfusion. The parasympathetic system then moderates this response, preventing excessive tachycardia.

In POTS, this balance is disrupted. Research has consistently documented that the core autonomic abnormality in POTS involves attenuated parasympathetic response and augmented sympathetic activity — particularly during postural change. Ie the accelerator is pushing hard but the he brake isn't working. The sympathetic system accelerates, but the vagal parasympathetic counterbalance is insufficient to moderate the response.

A 2024 paper published in the Journal of Autonomic Neuroscience examining autonomic function in POTS versus controls confirmed this pattern, finding characteristic autonomic abnormalities including reduced HRV and impaired parasympathetic cardiovagal function in POTS patients.

The vagus nerve's specific role in POTS

The vagus nerve is the primary driver of parasympathetic activity in cardiovascular regulation. It innervates the sinoatrial node — the heart's natural pacemaker — and is the main mechanism through which the brain slows the heart rate. When vagal tone is adequate, the heart rate rise upon standing is moderated and proportionate. When vagal tone is insufficient, the heart rate overshoots.

A published study in Autonomic Neuroscience examining taVNS for POTS noted that while much POTS research has focused on hyperadrenergic features (excessive sympathetic activity), there is clear evidence of parasympathetic cardiovagal impairment in POTS patients — including diminished vagal markers of heart rate variability and abnormalities in the cardiovagal component of autonomic testing scales.

This is a crucial distinction. POTS is not simply a problem of too much sympathetic activity; it is also a problem of insufficient vagal counterbalance. These are related but distinct, and addressing the vagal deficit is an important and often underprioritised component of management.

What the research says about vagus nerve stimulation for POTS

The most direct evidence for the vagus nerve's role in POTS comes from clinical research on vagus nerve stimulation (VNS), both invasive and non-invasive.

Non-Invasive Transcutaneous VNS (tVNS/taVNS)

A review published in Frontiers in Cardiovascular Medicine specifically examining non-invasive vagus nerve stimulation for POTS concluded that tVNS is emerging as a novel therapeutic strategy for the condition, noting that it is known to restore sympathovagal balance — the precise imbalance that underlies POTS pathophysiology.

The review noted that research on tVNS in POTS has found that markers of autonomic imbalance - including reduced HRV and elevated sympathetic indicators - were attenuated by tVNS, suggesting attenuation of the sympathetic response and improvement of parasympathetic response and sympathovagal balance. This was associated with reductions in the functional burden of POTS symptoms.

tVNS was also noted to exert immunomodulatory and anti-inflammatory effects, which is highly relevant given the growing evidence for an inflammatory and, in some patients, autoimmune component to POTS.

An earlier study referenced in the literature by Dums and colleagues found that vagus nerve stimulation in POTS patients improved symptoms including lightheadedness and fatigue - two of the most disabling and quality-of-life-impairing features of the condition.

The right vagus nerve and cardiac regulation

Research has also highlighted the importance of lateralisation in vagal cardiac regulation — specifically, the right vagus nerve's predominant role in sinoatrial node regulation and heart rate control. Evidence cited in the tVNS for POTS literature supports right-sided stimulation as potentially more effective for cardiovascular outcomes in POTS, which has implications for the choice of stimulation site in non-invasive approaches.

(It is however, important to note, that most tVNS companies prefer the left hand side as the choice of stimulation, because it is thought to lower the risk of heart stimulation. So to try a right hand side stimulation, you may need to request a special ‘right side’ ear piece - depending on the brand).

POTS, inflammation, and the vagus nerve's anti-inflammatory role

One of the most important and emerging areas in POTS research is the role of inflammation and immune dysregulation and the vagus nerve's central role in modulating both.

The vagus nerve is the primary mediator of the "cholinergic anti-inflammatory reflex" — a pathway by which the brain directly inhibits peripheral inflammatory activity through vagal signalling to the spleen and other immune organs. When vagal tone is low, this anti-inflammatory reflex is impaired, and inflammatory activity increases systemically.

In POTS, elevated inflammatory markers have been documented in multiple studies. Some patients show evidence of autoimmune mechanisms — including autoantibodies targeting adrenergic and muscarinic receptors that directly affect autonomic function. The overlap between POTS and mast cell activation syndrome (MCAS - in which mast cells release excessive inflammatory mediators) is increasingly well documented, with some researchers proposing a triad of POTS, MCAS, and hypermobile Ehlers-Danlos Syndrome (hEDS) as a distinct and common disease cluster.

The vagus nerve sits at the intersection of all of these: as the primary driver of the anti-inflammatory reflex, as a regulator of mast cell activity, and as the major communicator between the gut (where a significant proportion of immune activity occurs) and the brain.

Supporting vagal tone in POTS patients is therefore not only relevant to cardiovascular regulation. It is relevant to the underlying inflammatory and immune mechanisms that may be driving or perpetuating the condition in many patients.

I certainly see a lot of clients in my practice with this triad of symptoms [and typically neurodivergence too], and often, the goal is NOT cure (as nice as that would be), but it’s management of these conditions and how they intertwine, and how optimally we can get the vagus nerve to activate.

POTS and Long COVID - A vagal dimension

The dramatic rise in POTS diagnoses following COVID-19 infection (with POTS being one of the most consistently reported complications of long COVID) has brought fresh urgency to understanding its mechanisms.

Research published in Frontiers in Cellular and Infection Microbiology examining long COVID pathogenesis identified a vagus nerve-hypothalamic-pituitary-adrenal-mitochondrial axis dysfunction as a key mechanism, noting that impaired vagal signalling from the gut to the brain may be a significant contributor to the multisystem dysfunction seen in long COVID, including POTS-type autonomic symptoms.

The ACE2 receptor (which SARS-CoV-2 uses to enter human cells) is expressed on vagal neurons, raising the possibility of direct viral damage to vagal function. The chronic neuroinflammation documented in long COVID may further impair vagal signalling, creating a self-reinforcing cycle of autonomic dysregulation.

For patients who developed POTS following COVID-19, this neurological dimension of their condition is often missed in conventional management. The vagus nerve is not an afterthought in post-COVID POTS — it may be the primary site of injury.

The upper cervical spine - A missing piece in POTS

From a chiropractic perspective, one of the most clinically relevant and most frequently overlooked aspects of POTS is the relationship between the upper cervical spine and autonomic function.

The vagus nerve exits the skull through the jugular foramen, immediately adjacent to the atlas (C1). The brainstem, which houses the autonomic control centres, including the nucleus tractus solitarius (the primary receiving station for vagal afferent signals) and the dorsal motor nucleus of the vagus, sits directly above the atlas.

Trauma to the upper cervical spine — including birth trauma, whiplash, concussion, and cumulative postural stress — can disrupt the biomechanics of this critical region, affecting both the structural support of the brainstem and the quality of vagal signalling through the adjacent tissues.

Throw in some hypermobility and you’ve got the added stress of too much ‘stretch’ being placed over the area - including the vagus nerve.

There is a notable clinical pattern of POTS arising or worsening following head and neck trauma, including sporting injuries and motor vehicle accidents. The hypothesis that upper cervical dysfunction may contribute to autonomic dysregulation in POTS is gaining traction in the literature, and is consistent with the anatomical and neurophysiological relationships described above.

Upper cervical chiropractic assessment is not a mainstream component of POTS management — but given the anatomy and the clinical patterns observed, it is a rational and low-risk area to investigate, particularly for patients whose POTS onset followed a head or neck injury, or who have concurrent cervical symptoms.

Practical implications in supporting vagal tone in POTS

The research landscape for vagal support in POTS is still developing, but the neurophysiological rationale is strong and the risk profile of most vagal support approaches is low. The following are evidence-informed approaches worth discussing with your treating practitioners:

Breathwork Slow, diaphragmatic breathing with an extended exhale is one of the most powerful and accessible tools for increasing vagal tone. For POTS patients, this needs to be adapted for energy levels — even short sessions of paced breathing (4 counts in, 6-8 counts out) can be beneficial without triggering post-exertional worsening.

Non-invasive vagus nerve stimulation devices Transcutaneous auricular VNS (taVNS) devices — which stimulate the vagus nerve through the ear — are increasingly accessible and are the subject of growing clinical research in POTS and dysautonomia. They offer a way to directly target vagal tone without the exercise demands or energy expenditure that can be problematic for POTS patients.

Humming and vocal exercises Humming directly activates the vagal branches innervating the throat musculature, providing a gentle and accessible form of vagal stimulation that most POTS patients can manage even on low-capacity days.

Upper cervical chiropractic assessment (well, a full body chiropractic assessment) Given the anatomical proximity of the upper cervical spine to the vagal pathway and brainstem autonomic centres, assessment of this region - particularly in patients with a history of head or neck trauma - is a rational component of a comprehensive approach. Trying to find a chiropractor who understands the autonomic nervous system will be beneficial here.

Paced, graduated movement Exercise is both one of the most evidence-based treatments for POTS and one of the most challenging to implement. Starting with recumbent exercise (swimming, rowing, cycling) that avoids the orthostatic challenge of upright exercise, and progressing gradually, is the established approach. The vagal benefits of aerobic activity are well documented and are an important reason why exercise remains central to POTS management.

Gut health support Given the vagus nerve's central role in gut-brain communication and the high prevalence of gut dysfunction in POTS, supporting gut microbiome health and addressing intestinal permeability may have upstream effects on vagal tone and autonomic function.

Addressing inflammation and mast cell activation For patients with the POTS-MCAS overlap, addressing mast cell activation — through dietary strategies, mast cell stabilisers, and reducing the overall inflammatory burden — may indirectly support vagal function by reducing the inflammatory environment in which vagal neurons are operating.

A note on the complexity of POTS

POTS is a heterogeneous condition — there are different subtypes (neuropathic, hyperadrenergic, hypovolaemic), different underlying triggers, and significant individual variation in presentation and response to treatment. The vagal dimension discussed in this post is a critical and often underemphasised component, but it is not the whole picture.

What this post is intended to offer is a neurophysiological framework for understanding why the autonomic nervous system (and specifically the vagus nerve) is so central to POTS, and why supporting vagal tone is a rationally grounded component of comprehensive management. It is not a substitute for individualised medical care, and significant decisions about POTS management should always involve your treating practitioners.

What the research is increasingly clear about is that POTS is a disorder of autonomic balance, vagal function is impaired in the condition, and approaches that directly target vagal tone have demonstrated meaningful clinical benefits. That is a foundation worth building on.