When Bedwetting Isn’t Just Bedwetting: The Hidden Link Between Mold, ADH Imbalances, and CIRS

Bedwetting that continues past the expected developmental age is often dismissed as behavioral or simply a matter of time. Yet, emerging research suggests that in some children the underlying cause may not be developmental at all, but biological. Specifically, exposure to mold and microbial toxins in water-damaged buildings can create a chain reaction in the body that alters hormone regulation in ways that make bedwetting not just possible, but likely.

This framework comes from medical research on Chronic Inflammatory Response Syndrome (CIRS), a multi-symptom and multi-system illness first described by Shoemaker (1997) and Grattan and colleagues (1998), followed by Shoemaker and House (2006). This work indicates that biotoxins, once inhaled or ingested, can lock the innate immune system into a state of chronic activation and in turn disrupt the brain’s most critical centers for regulating hormonal activity.

Background: How Inflammation Disrupts the Hypothalamus and Pituitary

The hypothalamus and pituitary form the master regulatory axis of the body. These structures constantly monitor signals from the immune system, metabolic tissues, and endocrine glands, and then adjust hormone output to maintain balance. In healthy conditions, this axis is resilient. However, Shoemaker and colleagues demonstrated that chronic exposure to mold and other biotoxins can overwhelm functions associated with these brain regions. In CIRS, elevated inflammatory cytokines circulate persistently, and both the pituitary and hypothalamus—highly sensitive to these molecules—begin to falter.

When the hypothalamic-pituitary axis is inflamed, hormone production becomes unstable. Research in CIRS patients has shown lowered levels of alpha melanocyte-stimulating hormone (MSH), vasoactive intestinal peptide (VIP), adrenocorticotropic hormone (ACTH), and antidiuretic hormone (ADH; Shoemaker et al., 2005), all of which are either produced in or regulated by the hypothalamic-pituitary regions. The clinical consequences vary depending on which hormone is most affected. For instance, low MSH can contribute to innate immune overactivity, fatigue, intestinal permeability, and dysregulated circadian activity (sleep and appetite disturbances); low VIP is associated with reduced vascular control and exercise intolerance; low ACTH disrupts cortisol rhythms and stress tolerance. For children who struggle with bedwetting, the most relevant change is in ADH.

ADH, or vasopressin, normally signals the kidneys to conserve water and concentrate urine. At night, this allows the bladder to remain relatively empty, so children can sleep without interruption. But when ADH is suppressed due to hypothalamic-pituitary inflammation, the kidneys excrete dilute urine in higher volumes. The bladder fills too quickly, and bedwetting becomes far more likely. In this context, bedwetting is not simply a behavioral or developmental lag, but the visible tip of a deeper neuroendocrine imbalance rooted in chronic inflammation.

More Than Bedwetting: ADH, Osmolality, and POTS

It is important to recognize that ADH/osmolality imbalance does not affect only the bladder. In both adults and children, low ADH with corresponding shifts in serum osmolality creates systemic problems with fluid balance and circulation. This can sometimes manifest as excessive thirst despite regular water consumption, constant electric shocks, and/or leg cramps especially in the morning. One of the most striking manifestations is postural orthostatic tachycardia syndrome (POTS), a form of dysautonomia characterized by rapid heart rate, dizziness, lightheadedness, and fatigue upon standing.

Shoemaker and colleagues have noted that many CIRS patients present with POTS-like symptoms due to the same ADH-driven dysregulation that causes bedwetting in children. Without adequate ADH, plasma volume is poorly conserved, blood vessels struggle to maintain tone, and the autonomic nervous system overcompensates. While POTS is often thought of as an adolescent or adult condition, this physiology can be observed even in younger children when mold-related illness disrupts pituitary regulation. In this way, the same root imbalance—low ADH and abnormal osmolality—may present in children as enuresis, in teens as orthostatic intolerance, and in adults as full-blown POTS.

Because low ADH and abnormal osmolality produce excessive thirst and dilute urine, some patients are mistakenly labeled with diabetes insipidus (DI). While the symptoms can look similar, the mechanism in CIRS is different: rather than structural damage to the pituitary or kidneys, the imbalance in CIRS is driven by chronic inflammatory signaling that suppresses hypothalamic regulation. This distinction is crucial, since treatment aimed at classic DI may not address the underlying biotoxin-induced inflammation, and without correcting exposure, symptoms often persist or recur.

Actionable Steps for Parents

The good news is that these disruptions are reversible once the underlying cause is addressed. Shoemaker’s clinical protocol, validated in multiple studies, shows that when exposure to water-damaged environments is removed and treatment steps are followed, hormone levels—including ADH—can recover. For parents, the first step is environmental: testing the home and school for mold and bacterial contamination using validated DNA-based methods such as ERMI, HERTSMI-2, actinobacteria, and endotoxin dust testing. If any of these tests are significantly elevated, remediation or relocation may be necessary to stop ongoing exposure and allow treatment to work.

Medical evaluation should then include targeted laboratory testing. Bloodwork measuring ADH and serum osmolality provides direct insight into fluid regulation. Markers such as MSH, VIP, and ACTH can give a fuller picture of hypothalamic-pituitary involvement, and innate immune markers such as MMP-9, TGF-B1, and VEGF, can help determine whether there is elevated cytokine activity. Functional screening with Visual Contrast Sensitivity (VCS) can further document the functional impact of biotoxins on the brain and nervous system (McMahon et al., 2017). VCS testing has been validated for pediatrics use including 7-8 year olds (McMahon, 2017). Together, these steps allow families to move beyond trial-and-error parenting strategies toward a medically informed understanding of the problem.

Treatment, once the diagnosis is established, follows a structured sequence. Removal from exposure comes first, followed by therapies to reduce toxin load that include the use of bile acid sequestrant medications such as Cholestyramine and Welchol/Colesevelam. These binder medications have been shown to normalize VCS performance and significantly improve symptoms associated with CIRS (Shoemaker & House, 2006). In children, these two steps alone can often resolve CIRS symptoms and normalize biomarkers. In cases of profound ADH suppression (usually in adults), medical providers may prescribe desmopressin (DDAVP) to help restore nighttime urine concentration until the hypothalamic-pituitary axis stabilizes. Families often report that as their child’s labs normalize and inflammation subsides, both bedwetting and orthostatic symptoms decrease.

For parents, the most hopeful message is that persistent bedwetting or dizziness upon standing is not a life sentence. These symptoms reflect a reversible imbalance in the brain’s regulatory centers, triggered by an environmental exposure that can be identified and corrected. With environmental testing, targeted labs, and treatment guided by established protocols, children and adults alike can move from confusion to clarity—and from chronic symptoms to recovery.

References

Dooley, M. (2025). Biomarkers over Time: From Visual Contrast Sensitivity to Transcriptomics in Differentiating Chronic Inflammatory Response Syndrome and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. International Journal of Molecular Sciences, 26(15), 7284.

Grattan, L. M., Oldach, D., Perl, T. M., Lowitt, M. H., Matuszak, D. L., Dickson, C., ... & Morris, J. G. (1998). Learning and memory difficulties after environmental exposure to waterways containing toxin-producing Pfiesteria or Pfiesteria-like dinoflagellates. The Lancet, 352(9127), 532-539.

Shoemaker, R. C. (1997). Diagnosis of Pfiesteria-human illness syndrome. MMJ, 46(10), 521523.

Shoemaker, R. C., Rash, J. M., & Simon, E. W. (2005). Sick building syndrome in water-damaged buildings: generalization of the chronic, biotoxin associated illness paradigm to indoor toxigenic fungi. Bioaerosols, Fungi, Bacteria, Mycotoxins and Human Health. Albany, NY: Eastern New York Occupational & Environmental Health Center, 66-77.

Shoemaker, R. C., & House, D. E. (2006). Sick building syndrome (SBS) and exposure to water-damaged buildings: time series study, clinical trial and mechanisms. Neurotoxicology and teratology, 28(5), 573-588.

McMahon, S. W., Kundomal, K. A., & Yangalasetty, S. (2017). Pediatrics Norms for Visual Contrast Sensitivity Using an APT VCS Tester. Medical Research Archives, 5(5).

McMahon, S., Shoemaker, R. C., & Ryan, J. C. (2017). Visual contrast sensitivity testing in biotoxin illness: reliability and predictive validity. Toxins, 9(9), 300.