Can Mold, Lyme or CIRS Cause Dysautonomia?

What Is POTS, and Why Isn't a Trigger the Whole Answer?

POTS is "a chronic and often disabling disorder characterized by orthostatic intolerance with excessive heart rate increase without hypotension during upright posture" (Vernino, 2021). In adults, that means a sustained heart rate rise of 30 or more beats per minute within 10 minutes of standing, or 40 or more at ages 12 to 19, with symptoms for at least 3 months and no drop in blood pressure.

Our team sees that heart rate rise as a compensation. When you stand, gravity pulls blood away from your head, and if the systems that should hold brain blood flow steady fall behind, the heart speeds up to make up the difference. POTS is that rescue succeeding, and orthostatic hypotension, where blood pressure falls on standing, is the rescue falling short.

That view changes the question a mold or Lyme diagnosis raises. The NIH expert consensus says the onset of POTS "may be precipitated by immunological stressors such as a viral infection" (Vernino, 2021), so a Lyme history is worth taking seriously. In our team's experience, a trigger can be real and still not explain why brain blood flow stays low months later. Dysautonomia also travels with many other conditions: a 2025 review calls it "one of the common and under-recognized comorbidities of a wide variety of systemic disease" (Blitshteyn, 2025), so a POTS diagnosis can sit alongside another condition without that condition being the whole explanation. Whatever started it, the first question is what's keeping your system from holding brain blood flow upright.

What Does the Research Say About Mold and Dampness?

The mold studies we found looked at fatigue, allergy and asthma. A 2025 systematic review of 6 studies, 5 cross-sectional studies with 40,933 participants and 1 case-control study, concluded that "fatigue is associated with exposure to indoor mold and dampness" (Dooley, 2025). Cross-sectional studies can show an association, and they can't show that the mold caused the fatigue. The 2024 CIRS review cited in this article shares its first author with this one.

One widely cited occupational medicine statement, from 2003, is narrower. A 2003 statement from the American College of Occupational and Environmental Medicine concluded that "for almost all allergic individuals, the reactions will be limited to rhinitis or asthma," and advised that mold found in a home, school or office "should be remediated after the source of the moisture that supports its growth is identified" (Hardin, 2003). On mycotoxins, the same abstract concludes that "current scientific evidence does not support the proposition that human health has been adversely affected by inhaled mycotoxins in home, school, or office environments." That statement has been challenged. A 2008 critique argued it "resembled a litigation 'defense report'" that omitted or underplayed research linking mold to building-related symptoms (Craner, 2008). Neither paper is about POTS, so they speak to mold and health in general.

A search of Europe PMC for studies of mold exposure and postural orthostatic tachycardia turned up none. A second search pairing mold or mycotoxin terms with dysautonomia or autonomic dysfunction turned up nothing that tested whether mold causes either; the closest results were general dysautonomia reviews and ME/CFS research. That's a gap in the research, and a gap doesn't prove mold can never contribute. If your home has visible mold or water damage, finding the moisture source and remediating it makes sense on its own merits, and it's a separate question from what's driving your POTS.

Is CIRS an Established Diagnosis?

The review's authors define chronic inflammatory response syndrome (CIRS) as "an acquired medical condition characterized by innate immune dysregulation following respiratory exposure to water-damaged buildings" (Dooley, 2024). That 2024 review looked for evidence that CIRS treatments work. It found 13 articles on CIRS treatment, and the Shoemaker Protocol, described in 11 of them, was "the only treatment with documented clinical efficacy." That phrase is the review's own wording. The abstract describes a literature review and doesn't describe a trial behind it. The same review calls ME/CFS "a common misdiagnosis for CIRS," which is the review authors' view.

In the medical literature we searched, we found no neutral consensus statement that defines or endorses CIRS as a diagnosis. Our team treats it as contested: the symptoms people describe are real, and the evidence that this label and its protocol explain them is thin.

Tests used to support a CIRS diagnosis have the same problem. Visual contrast sensitivity (VCS), a vision test used in biotoxin evaluations, was checked 4 ways in a 2026 study of 28 biotoxin-exposed people and 30 controls, and "the Shoemaker handheld chart did not distinguish between groups." The authors suggested digital VCS testing and symptom questionnaires as practical tools (Jimenez-Barbosa, 2026). That's their suggestion, and our team doesn't endorse any of these as a CIRS test. Measuring mycotoxins in people is also an unsettled field. A recent review of mycotoxin biomonitoring lists "a lack of data for several mycotoxins such as (a) health-based guidance values (b) long-term biomarkers" (Cramer, 2026). In our team's view, for several mycotoxins, a result with no agreed value to compare it against can't tell you much about your POTS.

What Does the Research Show About Lyme and POTS?

Lyme disease is a tick-borne bacterial infection, and in the studies we found, its links to autonomic symptoms have been measured more directly than mold's. A 2025 study at 1 center looked at post-treatment Lyme disease (PTLD), symptoms that continue after a treated Lyme infection. In 37 patients with PTLD, the COMPASS-31 autonomic symptom questionnaire showed higher total scores than in healthy controls and a "similar vasomotor, urinary, and pupillomotor symptom burden as patients with POTS." Then 210 patients with PTLD did a 10-minute active stand test, and "9 of the 210 (4.29%) patients with PTLD had orthostatic tachycardia," a rate that "was not significantly different from that of healthy controls" (Adler, 2025).

Replay

The authors conclude that autonomic symptoms are common in PTLD, and that the stand test "identified a subgroup of patients with orthostatic tachycardia that associated with distinct clinical features of Lyme disease" (Adler, 2025). Lyme can leave people with autonomic symptoms that overlap with POTS, while only a small subgroup shows the heart rate rise seen in POTS when they stand. Orthostatic tachycardia on 1 stand is a heart rate finding, not a POTS diagnosis. Case reports describe POTS starting after treated Lyme, including a series of 5 women (Kanjwal, 2011), but they can't show how often it happens or that Lyme caused it. That's why our team puts more weight on a measured stand than on a symptom checklist.

Autonomic findings have also been studied in late-stage disease. In a 2026 cross-sectional study of 233 people with late-stage Lyme disease and 91 healthy controls, the abstract reports "significantly higher rates of both sympathetic and parasympathetic dysfunction compared with controls" (Milovanovic, 2026). That ties late Lyme to autonomic dysfunction, and a study at 1 point in time can't show that the infection caused it.

For symptoms that outlast treatment, French guidelines from 2025 describe post-treatment Lyme disease syndrome (PTLDS) as fatigue, diffuse pain and cognitive dysfunction lasting more than 6 months after a documented and adequately treated Lyme episode, which "is not attributable to persistent infection or other identifiable causes." For persistent symptoms, they call for "a systematic clinical reassessment" that checks the accuracy of the first diagnosis, the antibiotic treatment and other possible explanations (Arias, 2025). In the US, a 2020 guideline from the Infectious Diseases Society of America, the American Academy of Neurology and the American College of Rheumatology recommends "against additional antibiotic therapy" for people with "persistent or recurring nonspecific symptoms such as fatigue, pain, or cognitive impairment following recommended treatment for Lyme disease, but who lack objective evidence of reinfection or treatment failure" (Lantos, 2021). In a 2026 prospective study using xenodiagnosis, where larval ticks feed on a patient and are then tested for the Lyme bacterium, the ticks "showed no evidence of B. burgdorferi in most patients after treatment, irrespective of symptoms." The authors note this "may be due to the absence of bacteria or to the low sensitivity of the technique in humans," and the study was stopped early for futility (Marques, 2026).

Lyme blood tests have limits of their own. In a 2026 evaluation of early Lyme samples from 107 cases and 144 controls in areas where Lyme is common, standard and modified 2-tier testing algorithms had a sensitivity of 22% to 36% at the first blood draw, with specificity of 98% to 100% (Horn, 2026). That study covers early infection at the first blood draw, and testing convalescent samples didn't improve detection, so it says nothing about symptoms that last after treatment. A 2026 neurology review adds that headaches, lethargy and other non-specific symptoms of tick-borne infections "are generally not evidence of nervous system infection" (Halperin, 2026).

Diagnosing and treating Lyme belongs with your physician or an infectious disease specialist, and questions about antibiotics go to them.

How Should You Weigh a Mold, CIRS or Lyme Explanation?

When someone brings us a mold, CIRS or Lyme explanation for their POTS, we sort it on 4 questions: what the claim targets, how it fits a brain-first view, where acting on it may help and where it may hurt.

What the claim targets	The belief that mold, CIRS or Lyme is the cause of your POTS, and the tests and protocols based on that belief.
Our team's brain-first view	In our view, a trigger can start the process, and the useful question is what's keeping brain blood flow low now, so we test the stand, the vessels and brain blood flow before naming a cause.
Where it may help	A documented mold or water damage problem gets its moisture source found and remediated (Hardin, 2003). In our team's view, a Lyme history with symptoms on standing calls for a 10-minute stand and an autonomic review, the measures these studies used (Adler, 2025; Milovanovic, 2026).
Where it may hurt	Relying on urine mycotoxin panels or the handheld contrast chart as proof of a cause, when several mycotoxins lack health-based guidance values and the chart didn't separate exposed people from controls in testing (Cramer, 2026; Jimenez-Barbosa, 2026). Treating post-treatment symptoms as a persistent infection without objective evidence of one: the US guideline recommends against additional antibiotics in that case (Lantos, 2021), and a xenodiagnosis study found no bacteria in most treated patients, though its authors note the technique may miss infection (Marques, 2026).

The order we suggest

1. A slow or irregular pulse, fainting or chest pain after a tick bite or a Lyme diagnosis, and new weakness, numbness or trouble speaking at any time, need urgent medical care first.
2. Confirm the standing pattern with a 10-minute stand or a tilt table test.
3. Confirm any Lyme diagnosis and treatment history with your physician, and if symptoms continued after treatment, start with a reassessment of the diagnosis (Arias, 2025).
4. If mold or water damage is documented, find the moisture source and remediate it (Hardin, 2003).
5. Check brain blood flow and vascular function, the brain-first step in our team's approach.
6. Order a further test only when its result would change your care.

What Does Our Team Look For First?

Our team doesn't brush mold, Lyme or CIRS aside, and we also rule out other explanations before putting anyone in that bucket. In 1 case from our team's experience, a person was being evaluated for mold, Lyme, candida and chronic fatigue. The clinic found a compression problem lowering blood flow to the brain, and once it was addressed, the person's symptoms improved. That's 1 case, which can't show how common compression is. It's an example of why we check the brain's blood supply before settling on a label.

Our team's view is that neurological and vascular function, the infrastructure that supports the brain, shapes many of the downstream symptoms people attribute to a trigger. Depending on the person, the exam can include how heart rate, blood pressure and brain blood flow respond to standing, covered in autonomic testing for POTS; whether small nerve fibers are involved, covered in small fiber neuropathy and POTS; and whether brain fog follows posture, covered in POTS brain fog. If mast cell flares are part of your picture, see MCAS and dysautonomia. Why chasing a single lab panel so often stalls is the subject of why most dysautonomia treatments don't work.

Mold, Lyme, CIRS and POTS: FAQ