Testing Nurosym VNS

Does Nurosym work for POTS and dysautonomia?

Five months of daily Nurosym taVNS for post-viral POTS and dysautonomia. HRV has doubled and resting heart rate is down 16 bpm — but an amitriptyline taper, ivabradine, and midodrine overlap the data, and symptoms haven't changed. Here's what the numbers can and can't say.

I’ve now been using the Nurosym daily for just over five months. I’ve tracked my heart rate, heart rate variability and my symptoms during that time. This post looks at that data, tries to isolate what (if anything) is attributable to the device, and explains why that turns out to be very difficult.

TLDR: my autonomic metrics have improved substantially, but the data can’t attribute this to Nurosym specifically. My symptoms haven’t dramatically changed.

Other interventions muddying the water

Since starting Nurosym in late March, I’ve also:

There is no period in the data where Nurosym was the only variable changing. I wish that weren’t the case and I could have had more of a research-fun approach to it. But my symptoms and pain have prioritised going for any pharmaceutical intervention with evidence behind it, and there are others that are much more of a priority than Nurosym alone.

What I’ve tried to do is separate out the impact as much as I reasonably can.

The numbers

Here are monthly averages at four points across the tracking period. HRV is overnight RMSSD from a Fitbit (see HRV as a tracking metric for why I use that number); fatigue and head pain are self-reported on a 0 to 10 scale, logged with the same approach as my symptom diary template.

PeriodAmitriptylineNurosymHRV (ms)RHR (bpm)FatigueHead pain
Nov 2025100mgNo158373
Feb 202650mgNo168173
Apr/May 202625mgYes217973
Aug 20260mgYes306784

Two things stand out immediately. HRV has roughly doubled and RHR has dropped by 16 bpm. But symptom scores are flat, and if anything have drifted slightly worse (more on that below).

HRV: real improvement, unclear cause

HRV has risen from a baseline of around 15 to 30 in August. That’s a substantial and sustained improvement. But the strongest predictor of HRV in this dataset looks to be amitriptyline dose, not Nurosym.

Amitriptyline is anticholinergic, which means it directly suppresses vagal tone. Removing it would be expected to raise HRV, and that’s what the data shows. The biggest single jump in HRV (from around 22 to 30) happened in late July when I stopped amitriptyline entirely.

The most suggestive signal for Nurosym is at the start. HRV had been flat at 15 to 17 from October through mid-March, and it began rising in the weeks after I started the device — the pattern I first reported in the week 3 update. In the two weeks before Nurosym, HRV averaged 17. In the two weeks after, it averaged 19. That’s a modest improvement, and might be because of Nurosym.

Because Nurosym’s mechanism (increased vagal tone via nerve stimulation) produces the same measurable outcome as removing an anticholinergic (increased vagal tone via less suppression), the two effects are particularly difficult to separate.

Resting heart rate

RHR has dropped from 83 to 67. But the steepest decline came in late July and August, coinciding with ivabradine (which directly slows the sinus node), amitriptyline cessation, and midodrine. Any contribution from Nurosym is buried under much larger pharmacological effects.

Symptoms haven’t changed

This is the most notable finding, and the one that diverges most clearly from the Stavrakis et al. (2024) trial, which reported symptomatic improvement alongside physiological changes in POTS patients over two months.

My fatigue and breathlessness scores have hovered at 7 to 8 throughout the entire tracking period, regardless of intervention. Head pain has stayed at 3 to 4. The only sustained dip (fatigue down to 5) was during annual leave at Christmas, suggesting that rest and reduced cognitive load were the relevant factors rather than any medication. Heatwaves have reliably pushed both scores up by 1 to 2 points, which is the most reproducible signal in the symptom data.

If Nurosym were producing a clinically meaningful effect for me, I’d expect at least a gradual drift in symptom scores over five months. That hasn’t happened.

How this compares to the evidence

The Stavrakis trial found improved HRV, reduced orthostatic tachycardia, lower inflammatory markers, and symptomatic improvement over two months in 26 POTS patients. My situation differs in several ways: I’m male, my dysautonomia is post-viral rather than idiopathic, I was on concurrent medications that the trial participants were not, and my tracking period is longer.

My HRV improvement is consistent with what the trial found, but it’s also consistent with the expected effect of tapering an anticholinergic medication. The absence of symptomatic improvement is harder to square with the trial results, though the differences in population and medication regimen make direct comparison unreliable.

Does Nurosym work for POTS and dysautonomia?

I don’t know. The data is compatible with Nurosym contributing to the HRV improvement, but it cannot demonstrate it. The amitriptyline taper is the dominant signal and it overlaps too heavily with the Nurosym period to separate the two. On symptoms, there’s no evidence of benefit so far.

The cleanest next step would be to pause Nurosym for three to four weeks while keeping everything else stable, and see whether HRV drifts downward or symptoms shift. Now that my medication regimen is more settled, that’s feasible. It would give me a within-person withdrawal design which, while still n=1, would at least control for the medication confounders that currently make the data unreadable on this specific question. I’ll consider doing that in the coming months and if so I will report the results either way.

Would I purchase one again, knowing what I know now? No.

Previous posts in this series: Starting Nurosym: why I’m trying vagal nerve stimulation · Week 3: early HRV gains · 3 months: metrics holding, symptoms flat

The Nurosym device was purchased at my own expense. I have no affiliation with the manufacturer.

Stavrakis S, Chakraborty P, Farhat K, et al. Noninvasive vagus nerve stimulation in postural tachycardia syndrome: a randomized clinical trial. JACC Clin Electrophysiol. 2024;10(2):346–355.

Further reading