For some people, COVID-19 ends in a week or two. For others, it doesn’t. Months – or even years – later, they may still be dealing with fatigue, brain fog, sleep problems, shortness of breath, digestive trouble, dizziness, changes in heart rate, pain, anxiety, weakness, or an inability to tolerate activity the way they once could.
Today we call this broad collection of persistent problems Long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC). And there’s something important to understand right at the beginning: Long COVID may not be one thing.
Even the CDC describes it as heterogeneous, with possible underlying processes including organ damage, ongoing inflammation, microvascular dysfunction, autoimmunity, inadequate antibody response, and continuing viral activity associated with reservoirs inside the body.
That immediately raises an interesting possibility. Maybe looking for one thing that fixes Long COVID is asking the wrong question.
And maybe some of the unusual recovery stories being reported around chlorine dioxide deserve to be examined from that perspective. Not as proof. Not as a cure. But as clues.
Something Doesn’t Quite Fit the “One Problem, One Solution” Model
Among chlorine dioxide users, reports occasionally surface from people who say persistent problems following COVID improved after chlorine dioxide became part of what they were doing. Those stories are anecdotal. They don’t establish that chlorine dioxide treats Long COVID, and they certainly don’t tell us why somebody improved.
But something about the reports is interesting. Frequently, chlorine dioxide isn’t described as the entire answer.
People experiment with nutrition, enzymes, supplements, lifestyle changes, anti-inflammatory approaches, microbiome support, and other interventions. Sometimes something helps. Sometimes several things appear to help. Sometimes nothing does.
That messiness might actually make sense if Long COVID itself represents several overlapping disturbances.
A 2025 review of viral persistence in Long COVID describes possible connections among persistent SARS-CoV-2 material, immune dysregulation, vascular and coagulation problems, microbiome dysbiosis, brainstem/vagus signaling, and latent-virus reactivation.
That’s a lot of moving parts. And it suggests an entirely different way of investigating the chlorine-dioxide reports.
Instead of asking: “Does chlorine dioxide cure Long COVID?” perhaps we should ask: “If some of these reports represent genuine effects, where in this complicated pathway could chlorine dioxide possibly be doing something?”
First Suspect: Persistent Viral Material
One increasingly studied Long-COVID hypothesis involves SARS-CoV-2 – or pieces of it – remaining in the body after the acute infection has passed.
Researchers have reported viral nucleic acids, proteins, or other evidence of persistent viral material in tissues, blood, and feces in some people following infection. This has led researchers to investigate whether continuing viral reservoirs could keep stimulating the immune system and contribute to persistent symptoms.
This doesn’t mean everybody with Long COVID has a hidden active infection. And it certainly doesn’t mean every symptom is caused by spike protein. But persistent viral material is no longer a fringe idea. It’s a legitimate research target. And one location keeps appearing in this story.
Something Interesting Is Happening in the Gut
SARS-CoV-2 isn’t exclusively a respiratory story. The gastrointestinal tract can be involved during infection, and researchers have become increasingly interested in the gut as one potential location for viral persistence after the acute illness.
A 2024 review specifically examined gut-related viral persistence in Long COVID, proposing that continuing gastrointestinal disruption associated with viral persistence could contribute to symptoms throughout the body.
At the same time, researchers have repeatedly found differences in the intestinal microbiomes of people with Long COVID.
A 2025 review reported patterns including reduced microbial diversity, decreases in some beneficial short-chain-fatty-acid-producing organisms, and increases in several pro-inflammatory bacterial groups. Proposed downstream effects include altered intestinal barriers, systemic inflammation, immune signaling and changes along the gut-brain and gut-lung axes.
Suddenly, the gut isn’t merely where food gets digested. It becomes a possible intersection between:
-
- persistent viral material,
- microbial ecology,
- immune activity,
- inflammation,
- metabolism,
- and signaling to other parts of the body.
And that’s where our investigation took an unexpected turn.
What Happens If We Change the Gut?
There’s a wonderful way to test whether something is merely associated with a problem or might actually participate in it.
Change it.
That’s where fecal microbiota transplantation – FMT – becomes particularly interesting.
FMT essentially introduces a carefully screened donor microbial community into another person’s intestinal ecosystem. It is about as different from chlorine dioxide as an intervention could possibly be.
Yet it helps us ask exactly the question we’re interested in: Can deliberately changing the gut environment change symptoms of post-COVID illness?
Researchers have actually tried it.
The Long COVID FMT Experiment
A prospective study published in 2024 recruited 60 people with post-acute COVID syndrome and insomnia. Thirty received FMT at weeks 0, 2, 4 and 8. Thirty served as controls.
At 12 weeks, insomnia remission occurred in 37.9% of the FMT group compared with 10.0% of the control group.
Participants receiving FMT also showed improvements from baseline in measures of sleep quality, anxiety, and daytime sleepiness, along with a reduction in blood cortisol.
But here’s the detail that may be even more interesting.
The microbiomes of the people who responded to FMT became more similar to their donors.
That same pattern wasn’t seen in the nonresponders. No serious adverse events were reported in this small study.
Now, we need to keep our feet on the ground. This was a small, nonrandomized, open-label pilot study. It does not establish FMT as a cure for Long COVID. But it gives us something more interesting than another correlation.
Researchers deliberately changed the intestinal microbial ecosystem; some non-gastrointestinal symptoms changed, and successful responders showed measurable microbial changes.
That’s a clue.
And FMT Isn’t the Only Microbiome Approach Being Investigated
Recent reviews describe preliminary Long-COVID intervention studies involving probiotics, prebiotics, synbiotics, and FMT.
Reported improvements across these early studies have included symptoms involving fatigue, concentration, memory, gastrointestinal function, sleep and mood.
The evidence remains limited and heterogeneous, and causality hasn’t been settled. But microbiome-directed treatment has moved beyond being merely an interesting theory.
That gives us an important distinction: Science hasn’t established that changing the microbiome solves Long COVID. But researchers are already experimentally changing the microbiome to see whether Long-COVID symptoms move with it.
That’s an important step.

Now Let’s Bring Chlorine Dioxide Back Into the Room
This is where we need to be careful. There is currently no good human clinical evidence demonstrating: chlorine dioxide → favorable gut-microbiome change → Long-COVID recovery.
We shouldn’t draw that arrow. But we can certainly ask whether it exists.
Chlorine dioxide is antimicrobial. As we’ve explored elsewhere, microorganisms can show different susceptibility to it, and its effects depend heavily upon concentration, exposure, environment, and competing reactive material.
So perhaps the most interesting chlorine-dioxide hypothesis isn’t: “Chlorine dioxide travels around the body hunting spike protein.” It may be much farther upstream: Could chlorine dioxide exposure alter some part of the gastrointestinal microbial or chemical environment in a way that changes downstream immune, inflammatory or metabolic signaling?
We don’t know. But now there’s a reason to investigate the question. And FMT helped us find it.
Two Completely Different Approaches Pointing Toward the Same Door
There’s an almost amusing contrast here. FMT says: Change the microbiome by putting a different microbial community in.
The chlorine-dioxide hypothesis might say: Change the microbial or chemical environment already there.
Those approaches couldn’t look much more different. Yet both lead to the same fundamental question: Can changing the gut environment alter symptoms elsewhere in the body after COVID?
Preliminary human microbiome-intervention research suggests that question deserves serious attention. It does not establish chlorine dioxide as the appropriate way to make that change. That’s the experiment that hasn’t been performed.
What About Spike Protein?
This subject becomes confusing quickly because “spike protein” has become a catch-all explanation for almost everything following COVID. The reality is more complicated.
Persistent viral antigen is one serious research hypothesis, but Long COVID also involves investigations of autoimmunity, inflammation, vascular dysfunction, microbiome changes, nervous-system dysfunction, and residual organ injury.
So even if researchers eventually develop an effective way to reduce persistent viral antigen, that might not repair every downstream consequence that has already developed.
Again: There may be more than one domino falling.
Nattokinase: An Interesting Laboratory Clue
Another substance appearing frequently in post-COVID discussions is nattokinase.
This one has an intriguing piece of laboratory evidence behind it. Researchers exposed SARS-CoV-2 spike protein to nattokinase in laboratory cell preparations and found that the spike protein was degraded in a dose- and time-dependent manner.
That’s interesting. But notice exactly what it tells us. It demonstrates that nattokinase can degrade spike protein under those experimental conditions.
It does not establish that taking oral nattokinase removes persistent spike protein throughout a living human body or treats Long COVID.
That’s precisely the distinction we need throughout this investigation: Mechanism worth studying ≠ treatment already proven.
What About Nicotine?
Nicotine presents another developing hypothesis involving nicotinic acetylcholine receptors and the body’s cholinergic signaling system.
Research has investigated interactions between SARS-CoV-2 proteins and nicotinic receptors, and preliminary reports have explored transdermal nicotine in Long COVID.
But the popular Internet explanation that a 7 mg nicotine patch for seven days simply knocks spike protein off cells and cleans everything up goes considerably beyond the evidence currently available. Nicotine also has genuine physiological effects and isn’t appropriate for everyone.
So again we have: interesting biological hypothesis rather than established Long-COVID treatment.
Maybe the “Stack” Is Telling Us Something Else
This brings us back to those anecdotal reports.
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- Someone takes chlorine dioxide.
- Someone else adds nattokinase.
- Someone adds bromelain.
- Someone changes diet.
- Another works on the microbiome.
- Another addresses deficiencies.
- Someone improves.
Then everybody argues about which ingredient deserves the credit.
But what if that isn’t the most interesting lesson? What if improvement sometimes requires addressing different parts of the system?
Imagine Long COVID as a collection of interconnected pathways:
Persistent viral material
↓
continued immune stimulation
Gut dysbiosis
↓
altered microbial metabolites and signaling
Intestinal-barrier disturbance
↓
systemic immune effects
Inflammatory dysregulation
↓
persistent symptoms
Microvascular dysfunction
↓
circulation and oxygen-delivery problems
Autonomic dysfunction
↓
heart-rate, blood-pressure and neurological symptoms
Previous tissue injury
↓
problems that may remain even after the original trigger disappears
Suddenly, the observation that “one thing helped, but didn’t fix everything” isn’t particularly surprising.
Where Does Chlorine Dioxide Fit?
We don’t know yet. And that’s precisely why this subject deserves better research. Perhaps chlorine dioxide ultimately proves irrelevant to Long COVID. Perhaps it affects something upstream. Perhaps only a particular subgroup responds. Perhaps reported improvements result from something entirely different. Or perhaps chlorine dioxide affects the system for reasons its current advocates don’t yet understand.
Those are all legitimate possibilities. The mistake would be deciding which one is true before measuring it.
We Actually Have a Negative Chlorine-Dioxide Result
This deserves inclusion because good investigations don’t hide inconvenient results. A randomized clinical trial tested 0.01% aqueous chlorine dioxide mouthwash in people with mild COVID-19. Under the conditions studied, chlorine dioxide mouthwash did not significantly reduce salivary SARS-CoV-2 viral titers compared with placebo at 10, 30, or 60 minutes.
That’s useful information. But it answers a very narrow question. It doesn’t tell us whether chlorine dioxide affects the intestinal microbiome, a gastrointestinal viral reservoir, Long COVID, systemic inflammation, or any other proposed pathway discussed here.
We shouldn’t turn a negative mouthwash experiment into proof against all possible chlorine dioxide hypotheses. But neither should we ignore it.
That’s how investigation works.
Anecdotes Aren’t Proof – But They Can Tell Us Where to Look
There’s an unfortunate tendency to put anecdotal observations into one of two boxes.
Believe everything.
Or:
Throw everything away.
Neither approach is particularly useful. Anecdotes are terrible at establishing causation.
-
- People recover naturally.
- They change several things simultaneously.
- They remember selectively.
- Symptoms fluctuate.
- Expectations matter.
- Other treatments matter.
But repeated observations can still generate research questions. That’s how many investigations begin.
The responsible progression is:
Observation
↓
Hypothesis
↓
Measurable prediction
↓
Experiment
↓
Replication
↓
Conclusion
The mistake isn’t listening to anecdotes. The mistake is skipping everything between observation and conclusion.
So Let’s Design the Experiment
This is where things become fun. Suppose researchers recruited people with well-characterized Long COVID. Before any chlorine dioxide exposure, measure:
-
- intestinal microbiome composition,
- microbial diversity,
- viral antigen or RNA where appropriate,
- inflammatory markers,
- intestinal-barrier markers,
- immune markers,
- symptom severity,
- fatigue,
- cognitive performance,
- sleep,
- autonomic function,
- and quality of life.
Then randomize participants appropriately. Measure again during and after intervention.
Now we could ask:
-
- Did the microbiome change?
- Which organisms changed?
- Did inflammatory markers move?
- Did persistent viral markers change?
- Did symptoms change?
- Did biological changes correlate with clinical improvement?
- Did anything worsen?
And perhaps most importantly:
-
- Did responders have something biologically different from nonresponders before treatment began?
That could tell us far more than another thousand testimonials ever could.
The FMT Clue Changes the Question
This may be the most important part of our investigation. FMT doesn’t prove chlorine dioxide works. It does something more useful. It gives us an independent way of testing whether the pathway we’re interested in matters.
We started with reports of people improving after chlorine dioxide. Instead of assuming chlorine dioxide must somehow travel directly to every affected organ, we looked upstream. That led us toward the gut.
Then we discovered that researchers had independently manipulated the gut microbiome in people with post-COVID illness – and observed both microbial changes and clinical changes in a small prospective study.
That’s not confirmation. It’s triangulation. And triangulation tells us where another experiment might be worth conducting.
What We Know, What We’re Investigating, and What People Report
This may be the simplest way to keep everything straight.
What we know: Long COVID is real, heterogeneous, and can involve multiple biological systems. Researchers are investigating persistent viral material, immune dysregulation, vascular dysfunction, and microbiome changes as potential mechanisms.
What we’re investigating: The gut may participate in Long COVID through viral persistence, microbial dysbiosis, immune signaling, and gut-brain/gut-lung pathways. Preliminary microbiome interventions, including FMT, have produced encouraging findings that require larger controlled trials.
What people report: Some chlorine-dioxide users describe improvement in persistent post-COVID symptoms. Those reports haven’t established efficacy or mechanism.
The research question lies between those three statements.

Curiosity Without Getting Married to the Answer
This is where Herb Roi Richards‘ approach to experimentation has something useful to contribute – not as a medical protocol, but as an attitude toward investigation.
-
- Pay attention.
- Keep records.
- Don’t assume more is better.
- Don’t become so committed to one explanation that contrary evidence becomes invisible.
- Don’t assume improvement proves your theory about why improvement occurred.
- And use the resources available to you.
For Long COVID especially, significant cardiac, respiratory, neurological, vascular, and autonomic problems can occur, so persistent or serious symptoms deserve competent medical evaluation rather than experimentation alone.
Caution and curiosity can occupy the same room.
Maybe We’re Looking for Pathways, Not Miracles
Perhaps one day researchers will discover a single central mechanism tying most Long COVID together. Perhaps they won’t.
Current evidence suggests there may instead be several interacting pathways – and different people may have different combinations of them.
That changes how we should think about unusual recovery reports.
The question doesn’t have to be: “What cured this person?”
It can be: “What changed?” Then: “Where did it change?”
And finally: “Can we make that change happen again under controlled conditions?”
That’s where chlorine dioxide currently belongs in this story. Not at the finish line with a flag reading CURE. At the beginning of an interesting experiment.
Chlorine dioxide may prove irrelevant, important, helpful only for a subgroup, or useful for reasons its advocates currently misunderstand. We won’t know until somebody asks the question carefully enough to measure it.
And thanks to what researchers are beginning to discover about the gut, we may finally have a much better idea where to start looking.
A Note About the Evidence: The references below intentionally include established Long-COVID research, emerging mechanistic research, preliminary microbiome interventions, and exploratory studies. None establishes chlorine dioxide as a treatment for Long COVID. They are included because they help identify biological pathways—particularly viral persistence, the gut microbiome, immune signaling and related mechanisms—that could be investigated when evaluating anecdotal reports involving chlorine dioxide.
References & Further Reading
- Centers for Disease Control and Prevention. “Clinical Overview of Long COVID.” Updated March 9, 2026.
A useful foundation for the article. CDC describes Long COVID as a heterogeneous condition potentially involving organ damage, dysregulated inflammation, microvascular dysfunction, ongoing viral activity associated with reservoirs, autoimmunity, and inadequate antibody responses.
CDC: Clinical Overview of Long COVID - Du, H., et al. “Mechanisms of Gut-Related Viral Persistence in Long COVID.” 2024.
A particularly relevant review examining the hypothesis that persistent SARS-CoV-2 or viral material in the gastrointestinal system may contribute to Long COVID, including possible connections between the gut, inflammation, immune responses and systemic symptoms.
Read the full review on PMC - Lau, R.I., et al. “Fecal Microbiota Transplantation for Sleep Disturbance in Post-acute COVID-19 Syndrome.” Clinical Gastroenterology and Hepatology. 2024;22(12):2487–2496.e6.
This is probably our article’s most intriguing reference. Sixty people with post-acute COVID syndrome and insomnia participated in a prospective, nonrandomized study. Insomnia remission at 12 weeks was 37.9% in the FMT group versus 10% among controls. Responders’ gut microbiomes became more similar to their donors, providing a particularly interesting biological correlate to the clinical changes.
FMT and Post-COVID Insomnia — PubMed - Jiang, X., et al. “Fecal microbiota transplantation alleviates mild-moderate COVID-19 associated diarrhoea and depression symptoms: A prospective study of a randomized, double-blind clinical trial.” Journal of Medical Virology. 2024;96(8):e29812.
A separate randomized, double-blind investigation of FMT during mild-to-moderate COVID-19. This isn’t a Long-COVID treatment trial, so we shouldn’t present it as one, but it provides another experimental connection between manipulating the intestinal microbiome and COVID-associated symptoms.
FMT Randomized Trial — PubMed - “Long COVID and gut microbiome: insights into pathogenesis and therapeutics.”
This review pulls together observational and intervention research concerning the microbiome and post-acute COVID syndrome. Particularly useful for our purposes, it discusses probiotics, prebiotics and FMT and notes that some intervention studies reported improvements in fatigue, memory, concentration, gastrointestinal problems, sleep and mood—while other controlled microbiome interventions did not significantly improve post-COVID symptoms. That mixed evidence is important.
Long COVID and the Gut Microbiome — Full Review - “Microbiome and Long COVID-19: Current Evidence and Insights.” 2025.
Another useful recent review concluding that preliminary microbiome-directed interventions are encouraging but that evidence remains limited and heterogeneous. It is a good reference for our distinction between an exciting research pathway and an established treatment.
Microbiome and Long COVID Review - Taniguchi, Y., et al. “Degradative Effect of Nattokinase on Spike Protein of SARS-CoV-2.” Molecules. 2022.
The laboratory study behind many nattokinase/spike discussions. Nattokinase degraded SARS-CoV-2 spike protein in transfected cell lysates in a dose- and time-dependent manner and also degraded cell-surface spike under the experimental conditions. Importantly, this was laboratory evidence, not a clinical demonstration that oral nattokinase clears persistent spike from people.
Nattokinase and SARS-CoV-2 Spike — PubMed - “Long COVID — a critical disruption of cholinergic neurotransmission?” 2025.
An exploratory paper behind the nicotine/nicotinic-acetylcholine-receptor discussion. It includes a patient investigation and survey observations concerning low-dose transdermal nicotine. The results are provocative, but they don’t establish the popular claim that a particular nicotine-patch regimen simply “removes spike from cells.”
Long COVID and Cholinergic Neurotransmission — PubMed - Onozuka, D., et al. “A Multicenter, Randomized, Open-Label, Placebo-Controlled Clinical Trial of the Effect of Cetylpyridinium Chloride Mouthwash and On-Demand Aqueous Chlorine Dioxide Mouthwash on SARS-CoV-2 Viral Titer in Patients With Mild COVID-19.” Journal of Evidence-Based Dental Practice. 2024;24(4):102040.
Worth including precisely because it didn’t produce a positive chlorine-dioxide result. In this small randomized study, 0.01% aqueous chlorine-dioxide mouthwash did not significantly reduce salivary SARS-CoV-2 viral titers versus placebo at the measured time points. It tested a local mouthwash intervention in acute mild COVID—not oral chlorine dioxide, Long COVID, gut reservoirs or microbiome effects—so its negative result should be interpreted within that scope.
Chlorine Dioxide Mouthwash COVID Trial — PubMed
Informational Notice
This article explores emerging Long COVID research and hypotheses prompted partly by anecdotal reports involving chlorine dioxide. It does not establish chlorine dioxide, nicotine, nattokinase, FMT, or any combination of interventions as a treatment for Long COVID. Chlorine dioxide and sodium chlorite are reactive chemicals, nicotine has significant physiological effects, and FMT requires medical donor screening because infectious organisms can be transmitted. People experiencing persistent symptoms after COVID – particularly chest pain, breathing difficulty, fainting, neurological changes, abnormal heart rhythms, or other serious symptoms – should seek appropriate medical evaluation.




















