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Peptides for Mold Toxicity Recovery

You cannot outrun a building that is making you sick. About 50% of U.S. buildings have some form of water damage, and the EPA estimates that up to 85% of homes contain significant mold growth.

You cannot outrun a building that is making you sick. About 50% of U.S. buildings have some form of water damage, and the EPA estimates that up to 85% of homes contain significant mold growth. For most people, this is a non-issue -- their immune systems identify mycotoxins, tag them for removal, and move on. But roughly 24% of the population carries HLA-DR gene variants that prevent their immune systems from recognizing and clearing these biotoxins. For these people, mold exposure triggers a self-perpetuating inflammatory cycle that standard medicine frequently misdiagnoses as chronic fatigue syndrome, fibromyalgia, depression, or anxiety.

Dr. Ritchie Shoemaker identified this condition as Chronic Inflammatory Response Syndrome (CIRS), and the treatment protocol he developed over two decades has become the clinical standard. That protocol is sequential and deliberate -- remove the source, bind the toxins, clear co-infections, correct hormonal disruption, and finally restore immune regulation. Peptides play specific roles at different stages of this recovery process, with VIP (Vasoactive Intestinal Peptide) standing as the capstone treatment that has generated the most published clinical data.

This guide covers the peptides most relevant to mold illness recovery, where they fit in the treatment sequence, and what the research actually supports.

Table of Contents

Understanding Mold Illness: Why It Persists

Mold illness is not an allergy. It is a multi-system inflammatory condition triggered by exposure to biotoxins produced by mold species like Aspergillus, Stachybotrys (black mold), Penicillium, and Chaetomium. These organisms produce mycotoxins -- secondary metabolites that are toxic to human cells -- along with volatile organic compounds, mold fragments, and beta-glucans that collectively assault the immune system.

In someone with normal HLA-DR genetics, the process works like this: the innate immune system detects the biotoxin, antigen-presenting cells tag it, the adaptive immune system produces antibodies, and the toxin is cleared through the liver and kidneys. The person might feel temporarily unwell, but the response resolves.

In the 24% of the population with susceptible HLA-DR haplotypes, that handoff between innate and adaptive immunity fails. The immune system detects the threat but cannot tag it for removal. The biotoxins accumulate. Inflammatory cytokines -- C4a, TGF-beta-1, MMP-9 -- rise and stay elevated. The body mounts an increasingly aggressive innate immune response against a threat it cannot actually eliminate, creating chronic inflammation that does not self-resolve [1].

This inflammatory cascade produces a predictable pattern of damage:

  • Alpha-MSH suppression: Over 95% of CIRS patients have depleted alpha-melanocyte stimulating hormone, a master regulatory hormone that controls inflammation, sleep, mood, gut integrity, and pain perception [2]
  • MARCoNS colonization: Multiple Antibiotic Resistant Coagulase Negative Staphylococci colonize the nasal passages of roughly 80% of patients with low MSH, further suppressing MSH through hemolysin production [3]
  • VEGF deficiency: Vascular endothelial growth factor drops, starving cells of oxygen and nutrients and causing the fatigue, muscle cramps, and cognitive impairment characteristic of CIRS [4]
  • Neuroinflammation: Inflammatory molecules cross a compromised blood-brain barrier, activating microglia and disrupting neurotransmitter function. Brain MRI studies show measurable grey matter atrophy in CIRS patients [5]
  • Gut barrier breakdown: Reduced MSH and chronic inflammation degrade the intestinal lining, creating leaky gut that amplifies systemic inflammation [2]

Understanding this cascade is critical because it explains why peptide therapy is not a first step. The foundation of mold illness recovery is removing exposure -- you cannot heal while the assault continues.

The Shoemaker Protocol: Where Peptides Fit

The Shoemaker Protocol is a 12-step sequential treatment program. Each step addresses a specific piece of the inflammatory cascade, and later steps depend on earlier ones being completed. Peptides appear primarily in the later stages, though some practitioners introduce certain peptides earlier as supportive therapy.

Simplified protocol overview:

StepActionRelevant Peptides
1-2Remove from exposure; confirm with ERMI/HERTSMI testingNone
3Cholestyramine or Welchol bindingNone
4Eradicate MARCoNSLL-37 (as adjunct)
5-8Correct hormonal and immune markersKPV, Thymosin Alpha-1
9-10Address VEGF, autoimmune markersBPC-157
11Correct residual brain inflammationCerebrolysin
12VIP nasal spray (final restoration)VIP

This sequencing is not arbitrary. Dr. Shoemaker has compared using VIP before completing the prior steps to "putting a coat of paint on a burning house" -- the treatment cannot work while the underlying problems remain unaddressed [6].

VIP: The Cornerstone Peptide for CIRS

VIP (Vasoactive Intestinal Peptide) is a 28-amino-acid neuropeptide with the most published clinical evidence of any peptide used in mold illness treatment. It is naturally produced in the gut, lungs, brain (particularly the suprachiasmatic nucleus), and pancreas. In CIRS patients, VIP levels are depleted in over 95% of cases [7].

The Clinical Evidence

VIP has the strongest research backing of any peptide in the CIRS space, including published clinical trial data:

The Shoemaker 2013 Study: An IRB-approved clinical trial published in Health showed that VIP nasal spray (50 mcg/spray, administered 4 times daily) reduced mean symptom scores from 12.9 to 3.3 -- a 74% improvement. The study documented significant changes in over 700 genes related to metabolism, inflammation, and immune function. 100% of properly prepared patients experienced quality of life improvement [7].

Biomarker corrections: VIP treatment corrected multiple inflammatory markers including C4a, TGF-beta-1, MMP-9, and VEGF. It restored hormone levels (vitamin D, estradiol, testosterone), normalized pulmonary artery systolic pressure, and produced a significant increase in CD4+ CD25+ T regulatory cells -- from 8.9 to 22.5 units -- restoring the immune regulation that CIRS patients lack [7].

Brain structure restoration: Shoemaker, Katz, McMahon, and Ryan published findings showing that intranasal VIP safely restores atrophic grey matter nuclei in patients with CIRS -- meaning the brain volume loss caused by chronic neuroinflammation was partially reversed with VIP treatment [5].

Transcriptomic changes: A 2016 study by Ryan and Shoemaker demonstrated that VIP treatment in CIRS patients shifted metabolic state and innate immune function at the genetic level, showing changes that coincided with clinical healing [8].

Safety record: Since its first use as a nasal spray in 2008, VIP at a dose of 50 mcg per spray (usually 4-8 sprays daily) has been used in over 10,000 patients with no reported toxicity. Over 314 physicians have filled more than 7,000 VIP prescriptions [7].

Prerequisites for VIP Therapy

VIP will not work -- and can actually make things worse -- if the patient has not been properly prepared:

  • ERMI mold testing must be below 2 (or HERTSMI-2 at or below 10). Ongoing exposure negates VIP's effects
  • MARCoNS must be eradicated. Biofilm-protected nasal bacteria will suppress VIP's activity
  • Visual Contrast Sensitivity (VCS) test must be clear
  • Any rise in TGF-beta-1 of 5,000 or more after the first VIP dose typically indicates ongoing mold exposure that has not been identified

Regulatory Concerns

The FDA has announced plans to remove VIP from the list of drugs that may be compounded by licensed pharmacies in the United States, which would significantly impact patient access if finalized [9]. The synthetic form, aviptadil, has Orphan Drug designation for ARDS and pulmonary hypertension but is not FDA-approved as a standalone drug.

KPV: Restoring Alpha-MSH Function

KPV is a tripeptide (lysine-proline-valine) from the C-terminal end of alpha-melanocyte stimulating hormone (alpha-MSH). Its relevance to mold illness is direct and specific: the near-total depletion of alpha-MSH is one of the defining features of CIRS, and KPV is the functional fragment responsible for alpha-MSH's anti-inflammatory activity.

Why Alpha-MSH Matters in Mold Illness

When mycotoxins and MARCoNS destroy alpha-MSH function, the downstream effects are widespread [2]:

  • Chronic pain from reduced endorphin production
  • Sleep disorders from disrupted melatonin regulation
  • Gut permeability from lost intestinal barrier maintenance
  • Hormone dysregulation from lost cortisol regulation (affected in 50% of low-MSH patients)
  • Increased susceptibility to infection from impaired immune signaling
  • Mood instability from altered neurotransmitter regulation

KPV does not replace alpha-MSH entirely, but research has shown it produces similar or even more pronounced anti-inflammatory activity than the full-length hormone. It works through a distinct mechanism: where alpha-MSH binds to melanocortin receptors on cell surfaces, KPV enters cells directly and inhibits NF-kB activation from inside the cell. This intracellular activity makes it effective at reducing IL-6, TNF-alpha, and other inflammatory mediators at their source [2].

Mast Cell Stabilization

Mast cell activation syndrome (MCAS) is common in mold illness patients. KPV is one of the strongest peptide mast cell stabilizers available -- significantly more potent than BPC-157 for this specific function. For patients with MCAS, practitioners typically recommend starting with KPV and adding BPC-157 after one to two months if needed [10].

Practical Use

KPV is available as a supplement in oral spray and capsule forms, typically dosed at 500 mcg twice daily. Practitioners recommend at least three months to assess response. Because it selectively affects inflamed tissues with minimal impact on healthy tissue, KPV has a favorable safety profile with minimal reported side effects [2].

BPC-157: VEGF Restoration and Gut Repair

BPC-157 (Body Protection Compound-157) addresses two of the most consistent deficiencies in mold illness: depleted VEGF and compromised gut integrity.

VEGF Restoration

VEGF deficiency is nearly universal in CIRS patients. Without adequate VEGF, new blood vessel formation stalls, and existing capillary beds fail to deliver sufficient oxygen and nutrients to tissues. The result is the fatigue, muscle cramps, cognitive fog, and exercise intolerance that define the CIRS patient experience [4].

BPC-157's primary mechanism is increasing VEGF activity and stimulating angiogenesis -- the creation of new blood vessels. This makes it one of the most targeted peptides for correcting a specific CIRS biomarker abnormality [4].

Gut Healing

Mold illness patients commonly develop leaky gut due to reduced alpha-MSH and chronic inflammation degrading the intestinal barrier. BPC-157 was originally isolated from human gastric juice and has the most extensive research backing for gut repair of any peptide studied. Animal models demonstrate its ability to heal gastric ulcers, intestinal lesions, and fistulas while restoring tight junction integrity [11].

For a comprehensive look at peptides for gut repair, see our Best Peptides for Gut Health guide.

Neuroprotection

BPC-157 has shown neuroprotective properties in animal models, including the ability to reverse damage from traumatic brain injury. Since CIRS patients frequently show structural brain abnormalities from chronic neuroinflammation, this neuroprotective capacity adds another dimension to its utility in mold illness protocols. Some practitioners administer BPC-157 as a nasal spray alongside RG3 Synapsin to support brain inflammation clearance and neuronal regeneration [4].

Administration

BPC-157 is used orally (for gut-focused effects) or subcutaneously (for systemic tissue repair and VEGF restoration). It can also be compounded as a nasal spray for targeted neurological support. The weak antimicrobial properties of BPC-157 mean some patients experience Herxheimer reactions when starting -- lower initial doses with gradual increases are standard practice [12].

LL-37: Antimicrobial Defense Against MARCoNS

LL-37 is a 37-amino-acid human antimicrobial peptide with specific relevance to two aspects of mold illness: MARCoNS eradication and antifungal defense.

MARCoNS and Biofilm Disruption

MARCoNS -- the antibiotic-resistant staph bacteria colonizing the nasal passages of roughly 80% of CIRS patients -- protect themselves within biofilms that conventional antibiotics cannot penetrate effectively. Traditional treatment has relied on compounded nasal sprays (originally BEG spray, now typically EDTA with colloidal silver), but LL-37 offers an alternative mechanism [3].

LL-37 disrupts bacterial biofilms through direct membrane interaction, potentially making embedded bacteria more accessible to other antimicrobial treatments. Importantly, LL-37 works through membrane disruption rather than metabolic interference, which means bacteria cannot easily develop resistance to it the way they do with conventional antibiotics [13].

Antifungal Activity

LL-37 has also been studied against two fungal species directly relevant to mold illness:

  • Aspergillus fumigatus: LL-37 inhibited infection through multiple pathways
  • Candida albicans: The primary action involved binding to the fungal cell wall

This dual antimicrobial and antifungal activity makes LL-37 relevant in the earlier stages of mold illness treatment, when the goal is clearing infections and biofilm before moving to immune restoration [4].

Limitations

LL-37 is not FDA-approved for mold illness treatment. It can trigger inflammatory reactions in sensitive patients, and its effectiveness is reduced in physiological salt concentrations. Practitioners experienced in mold illness typically use it as part of a broader antimicrobial protocol rather than as a standalone treatment.

Thymosin Alpha-1: Immune Recalibration

Thymosin Alpha-1 (Ta1) addresses the immune dysregulation that sits at the center of CIRS. In mold illness, the innate immune system is chronically overactivated while the adaptive immune system -- the precision-targeting arm that should clear specific threats -- is suppressed. Ta1 works to correct both sides of this imbalance [14].

Ta1 promotes T cell maturation, activates natural killer cells, and acts through Toll-like receptors on dendritic cells. Its bidirectional immunomodulatory effect -- stimulating underactive responses while dampening overactive ones -- is what makes it particularly suited to CIRS, where immune regulation itself is the core problem [14].

In mold illness protocols, Ta1 is used during the immune correction phase, typically after MARCoNS eradication and before VIP. Its role is to restore the adaptive immune function that HLA-DR susceptible patients lack -- essentially helping the immune system do the job that genetics made difficult.

The synthetic form (thymalfasin/Zadaxin) has FDA orphan drug designation for hepatitis B and melanoma. Its use in CIRS is off-label but supported by clinical observation. See our Best Peptides for Immune Support guide for a deeper look at Ta1's immunology.

TB-500: Tissue Repair Support

TB-500 (a synthetic fragment of Thymosin Beta-4) supports systemic tissue repair through upregulation of actin -- a cell-building protein involved in wound healing, cell migration, and new blood vessel growth. In mold illness patients, chronic inflammation causes ongoing tissue damage across multiple systems: joints, muscles, gut lining, and neural tissue.

TB-500 addresses this by promoting repair at the cellular level, supporting both immune regulation and the physical reconstruction of damaged tissues. It pairs well with BPC-157, with each peptide working through complementary repair pathways. For patients with significant musculoskeletal symptoms or slow wound healing, TB-500 provides broader tissue support than BPC-157 alone.

Like BPC-157 and KPV, TB-500 fragments have weak antimicrobial properties and can trigger Herxheimer reactions in some patients. Gradual dose escalation is recommended [12].

Cerebrolysin: Addressing Neuroinflammation

Brain fog, memory loss, difficulty concentrating, and mood disorders are among the most debilitating symptoms of mold illness. Brain MRI studies of CIRS patients consistently show grey matter atrophy in regions affected by chronic neuroinflammation [5]. The blood-brain barrier becomes more permeable, inflammatory cytokines enter the brain, microglia become overactivated, and neurotransmitter systems (serotonin, dopamine, GABA, glutamate) are disrupted [15].

Cerebrolysin is a mixture of neurotrophic peptides and amino acids derived from porcine brain tissue. It has been studied extensively for neurodegenerative conditions and is approved in over 44 countries (primarily in Europe and Asia) for conditions including Alzheimer's disease and cerebrovascular disorders. Its peptides are small enough (under 10,000 Daltons) to cross the blood-brain barrier [15].

How it works: Cerebrolysin promotes neurogenesis through multiple neurotrophic factors -- BDNF, GDNF, NGF, and CNTF -- while decreasing neuroinflammation. It supports neuroplasticity, neuroprotection, and the regeneration of damaged neural tissue [15].

Why some practitioners prefer it for earlier use: Unlike VIP, which requires completion of the full Shoemaker Protocol before administration, Cerebrolysin can be used at earlier stages of treatment without the same prerequisite steps. Some clinicians argue that addressing neuroinflammation earlier -- rather than waiting for the final VIP stage -- provides faster cognitive improvement and quality of life gains for patients suffering from severe brain fog [15].

An oral alternative called CerebroPep (a porcine-derived peptide blend) has also entered the market for patients who prefer to avoid injections [15].

Evidence level: Extensive research for neurodegenerative conditions (Alzheimer's, stroke recovery, TBI). Use in CIRS specifically is based on clinical reasoning and practitioner observation rather than controlled trials for this indication.

Peptide Comparison Table

PeptidePrimary Role in Mold IllnessCIRS Biomarker TargetedProtocol StageEvidence Level
VIPImmune restoration, hormonal correction, brain repairC4a, TGF-beta-1, MMP-9, VEGF, T-regs, hormonesFinal (Step 12)Published clinical trials
KPVAlpha-MSH restoration, mast cell stabilizationalpha-MSH pathway, inflammatory cytokinesMid-protocolPreclinical + clinical use
BPC-157VEGF restoration, gut barrier repairVEGF, gut permeabilityMid-to-lateExtensive animal data
LL-37MARCoNS eradication, antifungal defenseMARCoNS statusEarly (Step 4)In vitro + clinical use
Thymosin Alpha-1Adaptive immune restorationT cell function, NK cellsMid-protocolApproved for other indications
TB-500Systemic tissue repairTissue damage markersMid-protocolAnimal studies + clinical use
CerebrolysinNeuroinflammation, cognitive restorationBrain volume, cognitive functionVariableApproved in 44+ countries for neuro conditions

Sequencing Matters: When to Use Which Peptide

The order in which you introduce peptides matters significantly in mold illness recovery. The general principle: remove the source, clear the infections, calm the inflammation, repair the damage, and restore regulation. Working backwards -- trying to restore immune regulation while still living in a water-damaged building, for example -- does not work.

Phase 1: Antimicrobial (after exposure removal and binding)

  • LL-37 to support MARCoNS eradication and biofilm disruption
  • Paired with standard antimicrobial nasal sprays

Phase 2: Inflammation reduction and immune calming

  • KPV to address alpha-MSH depletion and stabilize mast cells
  • Particularly important for patients with MCAS symptoms
  • Start before introducing peptides that might trigger Herxheimer reactions

Phase 3: Tissue repair and immune restoration

  • BPC-157 for VEGF correction and gut repair
  • TB-500 for systemic tissue support
  • Thymosin Alpha-1 for adaptive immune restoration
  • Cerebrolysin for brain fog and cognitive symptoms

Phase 4: Final restoration (Shoemaker Protocol Step 12)

  • VIP nasal spray -- only after prerequisites are met
  • Pre- and post-VIP lab panels to confirm biomarker response

For patients who cannot access VIP (due to regulatory restrictions or practitioner availability), the combination of KPV, BPC-157, and Thymosin Alpha-1 provides partial coverage of VIP's effects, though no single peptide or combination fully replicates VIP's documented multi-system restoration.

For broader guidance on combining peptides, see our Peptide Stacking Guide.

Important Limitations and Safety Notes

VIP is the only peptide with published clinical trial data specifically for CIRS/mold illness. Every other peptide discussed in this guide is used off-label based on mechanistic rationale, animal research, and clinical observation. The evidence base, while growing, is not equivalent.

The Shoemaker Protocol is sequential for a reason. Skipping steps or introducing peptides out of order can worsen symptoms or render treatment ineffective. VIP administered to a patient still living in a water-damaged environment will not produce the documented benefits.

Herxheimer reactions are common when starting peptide therapy in mold illness. Even repair-focused peptides like BPC-157 and KPV have weak antimicrobial properties. Patients prone to strong Herxheimer reactions should start at lower doses and increase gradually [12].

HLA-DR testing is important but not absolute. While approximately 24% of the population carries susceptible HLA-DR genes, about 10% of confirmed CIRS patients do not have an identified susceptible gene variant. HLA-DR testing informs but does not definitively rule out mold illness [1].

Detoxification support is foundational. Peptides work better when the body's detox pathways are functioning. Practitioners commonly recommend glutathione (oral or liposomal), NAC, alpha-lipoic acid, and sauna therapy alongside peptide protocols. Some protocols include a three-day prep period with curcumin and glutathione before starting peptide therapy to reduce Herxheimer reactions [12].

Work with a practitioner experienced in CIRS. Mold illness is complex, multi-system, and individual. Lab markers, symptom patterns, exposure history, and genetic susceptibility all factor into peptide selection and dosing. Self-treatment carries real risks.

Frequently Asked Questions

Is VIP the most important peptide for mold illness? VIP has the most published clinical data of any peptide used in CIRS treatment, including an IRB-approved trial showing 74% symptom reduction and correction of multiple inflammatory biomarkers. It is considered the capstone treatment of the Shoemaker Protocol. However, it only works when the patient has been properly prepared through the earlier protocol steps. Other peptides (KPV, BPC-157, Thymosin Alpha-1) play important roles in those earlier phases.

Can I use peptides without doing the full Shoemaker Protocol? Peptides can provide symptomatic improvement without completing the full protocol, but the results will likely be partial and temporary if fundamental issues like ongoing exposure and MARCoNS colonization are not addressed. The protocol exists because each step resolves a specific problem that prevents the next step from working.

How do I know if I have mold illness? CIRS is diagnosed through a combination of symptom clusters, biomarker testing (C4a, TGF-beta-1, MMP-9, MSH, VIP, VEGF, and others), HLA-DR genetic testing, Visual Contrast Sensitivity (VCS) testing (which shows 92% accuracy for detecting biotoxin illness), and exposure history. A qualified practitioner can order and interpret these tests.

What is MARCoNS and why does it matter for peptide therapy? MARCoNS (Multiple Antibiotic Resistant Coagulase Negative Staphylococci) is an antibiotic-resistant staph bacteria found in the nasal passages of about 80% of CIRS patients. It produces hemolysins that destroy alpha-MSH, worsening the hormonal and immune dysregulation of mold illness. MARCoNS must be eradicated before VIP therapy can work, and its presence can reduce the effectiveness of other peptides as well.

Is there overlap between mold illness and Lyme disease peptide protocols? Significant overlap. About 20% of CIRS cases are caused by Lyme disease rather than mold exposure, and many patients have both. Peptides like KPV, BPC-157, Thymosin Alpha-1, and LL-37 appear in protocols for both conditions. See our guide on Peptides for Lyme Disease and Best Peptides for Autoimmune Conditions for related information.

How long does mold illness recovery take with peptide therapy? Recovery timelines vary widely based on duration of exposure, genetic susceptibility, co-infections, and compliance with the full protocol. Most practitioners recommend at least two to three months to evaluate any individual peptide, with total recovery timelines often spanning six months to two years or longer. VIP treatment specifically has shown results within the 28-day study period, but the prerequisite protocol steps may take months to complete.

Are these peptides FDA-approved for mold illness? No peptide is FDA-approved specifically for CIRS or mold illness. VIP (as aviptadil) has FDA Orphan Drug designation for ARDS and pulmonary hypertension. Thymosin Alpha-1 (as thymalfasin) has FDA orphan drug designation for hepatitis B and melanoma. All use in mold illness is off-label.

The Bottom Line

Mold illness is a condition where the immune system's response to biotoxins causes more damage than the toxins themselves. For the roughly one in four people with susceptible genetics, exposure to water-damaged buildings can trigger a self-sustaining inflammatory cycle that affects nearly every system in the body.

Peptide therapy offers targeted interventions at specific points in this cascade. VIP stands alone in having published clinical trial data for CIRS, with documented improvements in symptoms, biomarkers, gene expression, and brain structure. KPV addresses the alpha-MSH depletion that drives so many downstream symptoms. BPC-157 corrects VEGF deficiency and repairs the gut barrier. LL-37 fights the biofilm-protected infections that prevent recovery. And Thymosin Alpha-1 restores the adaptive immune function that susceptible genetics compromise.

But peptides are not shortcuts. They work best -- and in the case of VIP, only work -- when integrated into a systematic treatment approach that starts with removing the source of exposure and moves methodically through each stage of recovery. The science supporting their use ranges from published clinical trials (VIP) to extensive preclinical data (BPC-157) to clinical observation (most others). For patients navigating mold illness recovery, they represent some of the most biologically targeted tools available -- provided they are used in the right order, at the right time, and under qualified supervision.

References

  1. McMahon, S.W., et al. "Chronic inflammatory response syndrome: a review of the evidence of clinical efficacy of treatment." Journal of Inflammation Research 17: 8647-8673 (2024). https://pmc.ncbi.nlm.nih.gov/articles/PMC11623837/

  2. Alana, J. "Best Peptides For Mold Illness, Toxicity and Chronic Inflammatory Response Syndrome (CIRS)." JessicaLana.com. https://www.jessicalana.com/library/best-peptides-for-mold-illness-toxicity-and-chronic-inflammatory-response-syndrome-cirs

  3. MicrobiologyDX. "About MARCoNS." https://www.microbiologydx.com/marcons-testing

  4. Carnahan, J. "Vasoactive Intestinal Peptide (VIP): Therapeutic Uses." JillCarnahan.com (2021). https://www.jillcarnahan.com/2021/04/07/vasoactive-intestinal-peptide-therapeutic-uses-for-this-powerful-peptide/

  5. Shoemaker, R., Katz, D., McMahon, S., Ryan, J. "Intranasal VIP safely restores atrophic grey matter nuclei in patients with CIRS." Internal Medicine Review (2017). Referenced in https://www.survivingmold.com/save-vip/support-for-use-of-vip-in-seid

  6. Shoemaker, R. "12 Step Shoemaker Protocol for CIRS." SurvivingMold.com. https://www.survivingmold.com/docs/12_STEP_SHOEMAKER_PROTOCOL_FOR_CIRS.PDF

  7. Shoemaker, R., House, D., Ryan, J. "Vasoactive intestinal polypeptide (VIP) corrects chronic inflammatory response syndrome (CIRS) acquired following exposure to water-damaged buildings." Health 5(3): 396-401 (2013). https://www.survivingmold.com/docs/VIP_published_3_2013.pdf

  8. Ryan, J., Shoemaker, R. "RNA-Seq on patients with CIRS treated with VIP shows a shift in metabolic state and innate immune functions that coincide with healing." Medical Research Archives 4(7): 1-11 (2016).

  9. SurvivingMold.com. "Support for Use of VIP in SEID." https://www.survivingmold.com/save-vip/support-for-use-of-vip-in-seid

  10. Ross, M. "The Best Oral Peptide Guide for Lyme, Tick-borne Infections, & Mold Toxicity." TreatLyme.com. https://treatlyme.com/guide/best-oral-peptide-guide-for-lyme-tick-borne-infections-mold/

  11. Sikiric, P., et al. "Brain-gut axis and pentadecapeptide BPC 157: Theoretical and practical implications." Current Neuropharmacology 14(8): 857-865 (2016). https://pubmed.ncbi.nlm.nih.gov/27306034/

  12. Ross, M. "Mast Cell Activation Syndrome in Infections & Mold Toxicity." TreatLyme.com. https://treatlyme.com/guide/mast-cell-activation-syndrome-lyme/

  13. Ridyard, K.E. and Bhatt, A. "The Potential of Human Peptide LL-37 as an Antimicrobial and Anti-Biofilm Agent." Antibiotics 10(6): 650 (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8227053/

  14. Dominari, A., et al. "Thymosin alpha 1: A comprehensive review of the literature." World Journal of Virology 9(5): 67-78 (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7747025/

  15. Alana, J. "Is Cerebrolysin Better Than VIP for Mold Illness and CIRS?" JessicaLana.com. https://www.jessicalana.com/library/is-cerebrolysin-better-than-vip-for-mold-illness-and-cirs