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Peptides for Lyme Disease (Research Overview)

Lyme disease does not always end when the antibiotics stop. An estimated 476,000 Americans are diagnosed and treated for Lyme disease each year, and according to Johns Hopkins research, [up to 34% of patients report persistent symptoms](https://www.hopkinslyme.

Lyme disease does not always end when the antibiotics stop. An estimated 476,000 Americans are diagnosed and treated for Lyme disease each year, and according to Johns Hopkins research, up to 34% of patients report persistent symptoms after completing standard antibiotic therapy. Fatigue that will not lift. Joint pain that migrates without warning. Brain fog thick enough to disrupt work and daily life. The CDC calls it post-treatment Lyme disease syndrome. Patients call it something else: unfinished.

The bacterium responsible -- Borrelia burgdorferi -- has evolved to survive. It changes shape, hides inside biofilms, and shifts into dormant cystic forms that standard antibiotics cannot reliably reach. These evasion strategies help explain why so many patients remain symptomatic long after treatment. And they have led researchers and clinicians to look beyond antibiotics for answers.

Peptide therapy is one of the areas attracting attention. Short chains of amino acids with specific biological effects, peptides are being studied for their ability to fight infection directly, modulate dysregulated immune responses, repair damaged tissue, and restore mitochondrial energy production -- all problems that define chronic Lyme disease. None of these peptides are FDA-approved for Lyme treatment, and most of the evidence comes from animal studies, in vitro experiments, and clinical observation rather than large-scale randomized trials. But the research is worth understanding.

This guide covers the peptides most relevant to Lyme disease, what the data actually shows, and where the science still has gaps.

Table of Contents

Why Lyme Disease Is So Hard to Treat

To understand why peptides are being explored, you need to understand why Borrelia burgdorferi is such a difficult pathogen.

Most bacteria sit still and wait for antibiotics to kill them. Borrelia does not. It has developed at least three survival strategies that make standard treatment unreliable for some patients:

Shape-shifting. Borrelia exists in three morphological forms: the active spirochete (its normal corkscrew shape), a round cystic form (sometimes called a round body), and biofilm-embedded aggregates. Doxycycline -- the first-line antibiotic for Lyme -- is effective against the spirochete form but has limited activity against cystic forms and biofilms [1].

Biofilm protection. Borrelia can form protective aggregates surrounded by extracellular polysaccharides, similar to biofilms produced by other chronic infection-causing bacteria. These biofilms contain channels for oxygen and nutrient exchange, allowing the bacteria to survive antibiotic exposure that would kill free-floating spirochetes [2].

Immune evasion. Borrelia expresses surface proteins like BBA57 that actively suppress your body's production of antimicrobial peptides, weakening the innate immune response at the site of infection. It also downregulates the expression of key immune defense molecules including bactericidal/permeability-increasing protein and secretory leukocyte proteinase inhibitor [3].

These strategies mean that even after successful antibiotic treatment, patients may be left with residual inflammation, tissue damage, immune dysregulation, and mitochondrial dysfunction -- the quartet of problems that defines post-treatment Lyme disease syndrome. The largest prospective study to date, published in The Journal of Infectious Diseases in 2024, found that 27.2% of all Lyme patients and 34.4% of those with disseminated disease met the criteria for persistent symptoms at follow-up [4].

How Peptides Fit Into Lyme Recovery

Peptides are not replacements for antibiotics. If you have active Lyme disease, standard antimicrobial treatment remains the foundation. But peptides offer something antibiotics cannot: targeted support for the downstream damage that Borrelia leaves behind.

The peptides being studied for Lyme disease fall into five functional categories:

CategoryWhat It AddressesKey Peptides
AntimicrobialDirect action against Borrelia and co-infectionsLL-37, novel cyclic AMPs
Immune modulationRebalancing dysregulated immune responsesThymosin Alpha-1, KPV
Tissue repairHealing damaged gut, joints, and connective tissueBPC-157, TB-500
Growth hormone supportSystemic recovery, sleep, body compositionCJC-1295, Ipamorelin
Mitochondrial supportRestoring cellular energy productionSS-31 (Elamipretide)

Each category targets a different aspect of chronic Lyme pathology. In clinical practice, practitioners often combine peptides from multiple categories -- an approach called stacking -- though the evidence for specific combinations remains largely anecdotal. See our Peptide Stacking Guide for general principles.

Antimicrobial Peptides: Targeting Borrelia Directly

LL-37: The Body's Own Antibiotic

LL-37 is a 37-amino-acid peptide derived from cathelicidin, a protein your immune cells naturally produce in response to infection. It has broad-spectrum antimicrobial activity and is one of the most studied human antimicrobial peptides, with documented effects against bacteria, fungi, and biofilms [5].

What the Lyme-specific research shows:

The relationship between LL-37 and Borrelia is more complicated than you might expect. A 2016 in vitro study tested LL-37 in combination with common Lyme antibiotics (doxycycline, erythromycin, and tinidazole) against B. burgdorferi. The results showed synergy between LL-37 and tinidazole -- the combination reduced cystic form growth more than either agent alone (P=0.015). LL-37 also showed independent activity against the cyst form, which is notable because many antibiotics fail against this morphology [6].

However, Borrelia has evolved significant resistance to cathelicidin-derived peptides. Research published in Infection and Immunity found that B. burgdorferi is resistant to high concentrations (>200 ug/mL) of cathelicidin, likely because the spirochete lacks lipopolysaccharide -- the negatively charged membrane component that cationic peptides like LL-37 typically bind to [7].

LL-37's biofilm-disrupting properties remain relevant. The peptide can penetrate and break apart bacterial biofilms, potentially making embedded bacteria more susceptible to antibiotic therapy [5]. For Lyme patients, this combination approach -- using LL-37 to strip away biofilm protection while antibiotics target the exposed bacteria -- is the rationale most practitioners cite.

Limitations: LL-37 is susceptible to degradation by proteases, has reduced activity in physiological salt concentrations, and can be toxic to human cells at higher concentrations. It is not FDA-approved for Lyme treatment.

Novel Cyclic Antimicrobial Peptides (2025 Research)

A February 2025 study published in Nature Scientific Reports represents one of the most promising developments in peptide research for Lyme disease. Researchers developed cyclic antimicrobial peptides from a phage display library that target phosphatidylcholine in the Borrelia cell membrane [1].

The results stood out for several reasons:

  • All four peptides breached the borrelial cell membrane within one hour, causing depolarization and cell death
  • They killed multiple forms of Borrelia -- spirochetes, cystic forms, and biofilm aggregates -- whereas doxycycline failed against the cystic form
  • They crossed a blood-brain barrier model in vitro, a property that matters because Borrelia can invade the central nervous system (neuroborreliosis)
  • They did not harm human cells -- no inhibition of eukaryotic cell metabolism or proliferation, and no erythrocyte lysis
  • They remained stable in serum, unlike many linear antimicrobial peptides that degrade quickly

These are early-stage findings from laboratory research, not clinical trials. But the combination of multi-form killing, BBB penetration, and human cell safety addresses three of the biggest limitations of current Lyme treatment. The researchers recommended further investigation of cyclic AMPs fused with CNS-homing moieties for neuroborreliosis therapy.

Immune-Modulating Peptides

Chronic Lyme disease is not just about the bacteria. In many patients, the immune system itself becomes the problem -- either failing to mount an adequate response to clear remaining infection, or overreacting with persistent inflammation that causes symptoms independent of bacterial load.

Thymosin Alpha-1: Restoring Immune Surveillance

Thymosin Alpha-1 (Ta1) is a 28-amino-acid peptide originally isolated from thymic tissue. The thymus gland trains T cells -- the adaptive immune cells responsible for identifying and eliminating specific threats. As you age, the thymus shrinks, and T cell function declines. In chronic infections, circulating Ta1 levels drop further, compounding the immune deficit [8].

How it works in Lyme disease:

Ta1 acts through Toll-like receptors on dendritic cells, activating both innate and adaptive immune pathways. It promotes the maturation of T cells into CD4+ and CD8+ subtypes, activates natural killer cells, and modulates cytokine production. What makes it particularly relevant to Lyme disease is its bidirectional activity: it can stimulate a sluggish immune response while dampening excessive inflammation [8].

In patients with chronic Lyme, Ta1 is reported to help the immune system identify and clear Borrelia bacteria and infected cells, reduce chronic inflammatory cytokine levels, and decrease oxidative damage. The synthetic form, thymalfasin (brand name Zadaxin), is FDA-approved as an orphan drug for hepatitis B and melanoma, though its use in Lyme disease remains off-label [9].

Evidence level: Clinical observation and case reports rather than controlled trials specific to Lyme disease. The mechanistic rationale is strong -- Ta1's ability to restore T cell function, activate NK cells, and modulate inflammation addresses core features of chronic Lyme pathology. But large-scale human studies confirming efficacy in this population are lacking.

Important note: Ta1 requires adequate zinc status to function. Zinc is a critical cofactor for T cell and NK cell activation, and many chronically ill patients are zinc-deficient. Practitioners typically check zinc levels before starting Ta1 therapy.

KPV: Calming the Inflammatory Cascade

KPV is a tripeptide (lysine-proline-valine) derived from the C-terminal end of alpha-melanocyte stimulating hormone (alpha-MSH). It is one of the most potent anti-inflammatory peptides currently available, and it has particular relevance to Lyme patients because of its effect on mast cells.

Why mast cells matter in Lyme disease:

Many chronic Lyme patients develop mast cell activation syndrome (MCAS) -- a condition where mast cells release excessive amounts of histamine and other inflammatory mediators. The result is a constellation of symptoms including hives, food sensitivities, brain fog, headaches, bloating, anxiety, and fatigue. MCAS can develop secondary to the chronic immune activation caused by Borrelia and its co-infections.

KPV suppresses the NF-kB inflammatory pathway and stabilizes mast cells, reducing histamine release without suppressing overall immune function. Both BPC-157 and KPV stabilize mast cells, but KPV is significantly stronger at this specific function [10].

Clinical use in Lyme: Practitioners often use KPV early in treatment protocols for patients with high inflammatory burden or MCAS symptoms. The rationale is to calm immune reactivity before introducing peptides or treatments that could trigger Herxheimer reactions (temporary worsening of symptoms caused by bacterial die-off). KPV is typically dosed at 500 mcg twice daily as a spray or capsule, with practitioners recommending at least three months to assess response [10].

Evidence level: Preclinical studies demonstrate clear anti-inflammatory and mast cell-stabilizing effects. Clinical evidence specific to Lyme disease comes from practitioner reports rather than controlled trials.

Tissue Repair and Gut Healing Peptides

BPC-157: Gut Barrier and Tissue Recovery

BPC-157 (Body Protection Compound-157) is a 15-amino-acid peptide derived from a protein found in human gastric juice. It has been studied extensively in animal models for tissue repair, anti-inflammatory effects, and gut healing -- all directly relevant to chronic Lyme disease.

The gut-Lyme connection:

A damaged gut lining is common in Lyme patients. Chronic inflammation weakens the intestinal barrier, leading to increased permeability (leaky gut). This allows bacterial fragments, food particles, and toxins to enter the bloodstream, triggering additional immune activation and worsening systemic inflammation. The gut also houses roughly 70% of the immune system, making its integrity critical for recovery. See our Best Peptides for Gut Health guide for a deeper look at this topic.

How BPC-157 helps:

BPC-157 increases vascular endothelial growth factor (VEGF), promoting new blood vessel formation and improving oxygen delivery to damaged tissues. It accelerates collagen synthesis, repairs tendon and muscle damage, and restores gut barrier integrity. Animal studies show it heals gastric ulcers, intestinal lesions, and fistulas while reducing pro-inflammatory cytokines like TNF-alpha and IL-6 [11].

For Lyme patients, these properties address several specific problems:

  • Gut barrier repair from antibiotic-induced and inflammation-driven permeability
  • Joint and connective tissue healing from Borrelia-mediated arthritis and tissue damage
  • VEGF restoration -- patients with chronic inflammatory conditions frequently have low VEGF levels, and BPC-157 directly corrects this
  • Neuroprotection -- BPC-157 has shown the ability to reverse damage from traumatic brain injury in animal models, and structural brain abnormalities are well-documented in chronic Lyme [11]

Evidence level: Extensive animal research, limited human trial data. BPC-157 has not been tested in randomized controlled trials specific to Lyme disease. The mechanistic rationale is robust, particularly for gut healing and tissue repair.

TB-500: Systemic Tissue Repair

TB-500 (a synthetic fragment of Thymosin Beta-4) promotes tissue repair through a different mechanism than BPC-157. It upregulates actin, a cell-building protein involved in wound healing, cell migration, and blood vessel growth. TB-500 also modulates inflammatory pathways and supports immune regulation.

For Lyme patients, TB-500 is primarily used for systemic tissue repair -- particularly for musculoskeletal damage, wound healing, and reducing chronic inflammation in joints and soft tissues. It pairs well with BPC-157 in clinical practice, with each peptide targeting repair through complementary pathways. See our Best Peptides for Inflammation guide for more on this combination.

Growth Hormone Peptides for Recovery Support

CJC-1295 and Ipamorelin

Chronic Lyme disease often disrupts sleep, body composition, energy levels, and overall metabolic function. CJC-1295 and Ipamorelin are growth hormone secretagogues -- peptides that stimulate your body's natural production of growth hormone (GH) -- which addresses several of these downstream effects.

How they support Lyme recovery:

CJC-1295 is a long-acting growth hormone releasing hormone (GHRH) analog. A single injection produces dose-dependent increases in growth hormone levels of 2- to 10-fold for six or more days, and IGF-1 elevations of 1.5- to 3-fold lasting 9 to 11 days [12]. Ipamorelin is a selective ghrelin receptor agonist that provides a quicker GH pulse. Used together, they create sustained GH elevation without the side effects of exogenous GH administration.

For chronic Lyme patients, the benefits include:

  • Immune modulation: IGF-1 has anti-inflammatory properties and modulates T cell and NK cell function
  • Tissue regeneration: GH stimulates fibroblast proliferation, collagen synthesis, and new blood vessel formation in damaged joints
  • Neuroprotection: GH and IGF-1 cross the blood-brain barrier and support neurogenesis, synaptic plasticity, and memory -- relevant for patients with Lyme-related cognitive symptoms
  • Metabolic support: Improved insulin sensitivity, fat metabolism, and appetite regulation for patients with Lyme-associated metabolic disruption
  • Sleep quality: GH secretagogues often improve deep sleep patterns, which is critical for immune function and recovery [12]

Evidence level: Well-established pharmacology for CJC-1295 and Ipamorelin individually. No controlled clinical trials for Lyme disease specifically. Anecdotal reports from patients and practitioners describe reduced joint pain, improved energy, and faster recovery after antibiotic treatment.

Mitochondrial Peptides: Restoring Cellular Energy

Fatigue is the most common and often most debilitating symptom of chronic Lyme disease. In many patients, this fatigue has a mitochondrial component. Borrelia infection triggers oxidative stress that damages mitochondrial membranes, reducing ATP production and leaving cells starved for energy.

SS-31 (elamipretide) is a mitochondria-targeting tetrapeptide that binds to cardiolipin in the inner mitochondrial membrane, stabilizing cristae structure and improving electron transport chain efficiency. It received FDA approval in 2025 for Barth syndrome, a rare mitochondrial disorder, based on clinical trial data showing improved exercise capacity [13].

For Lyme patients, SS-31's rationale is straightforward: if mitochondrial dysfunction drives fatigue, then a peptide that directly repairs mitochondrial membrane function should help restore energy production. Anecdotal reports from the Lyme community describe modest improvements in energy stability, though formal clinical evidence for this population does not yet exist [14].

MOTS-c is another mitochondrial peptide sometimes discussed in Lyme contexts, but it activates AMPK and exercise-mimetic pathways that can worsen post-exertional malaise -- a common feature of chronic Lyme. Patients and practitioners have reported that SS-31 is better tolerated for this reason [14].

Peptide Comparison Table

PeptidePrimary MechanismLyme-Specific RelevanceEvidence LevelRoute
LL-37Antimicrobial, biofilm disruptionSynergy with tinidazole against cystic forms; biofilm penetrationIn vitro studiesSubcutaneous, topical
Cyclic AMPsMembrane disruption across all Borrelia formsKills spirochetes, cysts, and biofilm forms; crosses BBBIn vitro (2025)Experimental
Thymosin Alpha-1T cell activation, NK cell stimulationRestores immune surveillance; reduces chronic inflammationApproved for other indications; Lyme use is off-labelSubcutaneous
KPVNF-kB suppression, mast cell stabilizationAddresses MCAS; calms immune reactivityPreclinical + clinical reportsOral spray, capsule
BPC-157VEGF upregulation, tissue repairGut healing, joint repair, VEGF restorationExtensive animal dataOral, subcutaneous
TB-500Actin upregulation, cell migrationMusculoskeletal repair, immune modulationAnimal studies + clinical useSubcutaneous
CJC-1295 + IpamorelinGH/IGF-1 stimulationSleep, tissue repair, immune support, neuroprotectionHuman pharmacology studies; Lyme use is anecdotalSubcutaneous
SS-31Mitochondrial membrane repairRestores ATP production; addresses fatigueFDA-approved for Barth syndrome; Lyme use is off-labelSubcutaneous

What About Peptide Stacking?

Practitioners working with chronic Lyme patients often combine peptides from different categories. Common stacking approaches include:

  • BPC-157 + KPV for patients with significant gut damage and mast cell activation. KPV calms the inflammatory environment while BPC-157 repairs the gut lining.
  • Thymosin Alpha-1 + LL-37 for immune restoration paired with antimicrobial support. Ta1 strengthens the adaptive immune response while LL-37 provides direct pathogen-fighting activity.
  • CJC-1295/Ipamorelin + BPC-157 for patients in recovery phase, combining growth hormone support with tissue repair.

A general principle in Lyme-focused peptide protocols is to start with immune calming (KPV) before introducing immune stimulation (Ta1) or antimicrobial peptides (LL-37), particularly in patients prone to Herxheimer reactions. BPC-157, KPV, and TB-500 fragments have weak antimicrobial properties, meaning even these "repair" peptides can trigger Herxheimer responses in some patients. Lower starting doses with gradual increases are standard practice.

For more on combining peptides safely, see our Peptide Stacking Guide.

Important Limitations

This section matters as much as everything above it.

No peptide is FDA-approved for Lyme disease treatment. The peptides discussed here are used off-label, and the evidence supporting their use in Lyme disease ranges from robust preclinical research (BPC-157, LL-37) to early laboratory findings (cyclic AMPs) to clinical anecdote (CJC-1295/Ipamorelin for Lyme specifically).

Most research is preclinical. The BPC-157 literature is extensive but almost entirely animal-based. The LL-37 data on Borrelia comes from in vitro experiments. The 2025 cyclic AMP study is laboratory research that has not been tested in humans. Thymosin Alpha-1 has the strongest regulatory track record (FDA orphan drug status for other conditions), but its use in Lyme disease specifically has not been validated in randomized controlled trials.

Lyme disease research is underfunded. Despite affecting nearly half a million Americans annually, Lyme disease receives less than 2% of the public funding allocated to West Nile virus and 0.2% of HIV/AIDS funding [15]. This funding gap directly limits the clinical trials needed to validate peptide therapies.

Peptides do not replace standard treatment. Anyone with suspected or confirmed Lyme disease should receive appropriate antibiotic therapy. Peptides are being explored as complementary support -- particularly for patients with persistent symptoms after completing antibiotic courses -- not as standalone treatments.

Work with a qualified practitioner. Peptide therapy requires proper assessment, monitoring, and dosing. Self-treatment carries risks including Herxheimer reactions, drug interactions, and potential complications in patients with specific contraindications.

Frequently Asked Questions

Can peptides cure Lyme disease? No. No peptide has been proven to cure Lyme disease. Antibiotics remain the standard treatment for active Borrelia infection. Peptides are being studied as supportive therapies that address specific aspects of chronic Lyme pathology -- inflammation, tissue damage, immune dysfunction, and energy depletion -- rather than as cures for the infection itself.

Which peptide should I start with for chronic Lyme symptoms? This depends entirely on your symptom profile, and the decision should be made with a qualified healthcare provider. For patients with significant inflammation or MCAS symptoms, practitioners often start with KPV to calm immune reactivity before introducing other peptides. For those with gut issues, BPC-157 is frequently the first choice. Immune support protocols often begin with Thymosin Alpha-1.

Are there Herxheimer risks with peptide therapy? Yes. Even peptides primarily used for repair (BPC-157, KPV, TB-500) have weak antimicrobial properties and can trigger Herxheimer reactions in some patients. Starting at lower doses and increasing gradually is standard practice, particularly for patients with high pathogen loads.

How long does peptide therapy take to show results in Lyme patients? Most practitioners recommend at least two to three months to evaluate whether a peptide regimen is working. If the regimen shows benefit, a minimum of six months is typical. For patients with chronic conditions, longer courses may be recommended.

Can I use peptides alongside antibiotics? Some peptides may complement antibiotic therapy -- the LL-37/tinidazole synergy study suggests potential benefits of combining antimicrobial peptides with specific antibiotics. However, any combination therapy should be supervised by a healthcare provider familiar with both approaches.

Is there overlap between Lyme and mold illness peptide protocols? Significant overlap. Both conditions involve chronic inflammation, immune dysregulation, and often co-occur. VIP, KPV, BPC-157, and Thymosin Alpha-1 appear in protocols for both conditions. See our guide on Peptides for Mold Toxicity for specific information on mold-related protocols.

The Bottom Line

Peptide therapy for Lyme disease sits at the intersection of promising science and insufficient clinical evidence. The mechanistic rationale is strong: antimicrobial peptides that can target Borrelia in its protected forms, immune-modulating peptides that address the dysregulation driving chronic symptoms, tissue repair peptides that heal the damage infection leaves behind, and mitochondrial peptides that restore the energy production chronic inflammation disrupts.

The 2025 research on cyclic antimicrobial peptides -- killing all three forms of Borrelia, crossing the blood-brain barrier, and sparing human cells -- is genuinely exciting. But it remains laboratory science. The gap between a promising in vitro study and a validated treatment is wide, and that gap is made wider by the chronic underfunding of Lyme disease research.

For patients dealing with persistent Lyme symptoms, peptides offer a toolkit of targeted interventions worth discussing with a knowledgeable practitioner. They are not miracle cures, they are not replacements for antibiotics, and they are not without risks. But for the hundreds of thousands of Americans whose symptoms persist after standard treatment, they represent one of the more biologically rational areas of investigation available.

References

  1. Karvonen, K., et al. "Antimicrobial cyclic peptides effectively inhibit multiple forms of Borrelia and cross the blood-brain barrier model." Scientific Reports 15, 5632 (2025). https://www.nature.com/articles/s41598-025-90605-z

  2. Sapi, E., et al. "Characterization of biofilm formation by Borrelia burgdorferi in vitro." PLoS ONE 7(10): e48277 (2012). https://pubmed.ncbi.nlm.nih.gov/23110225/

  3. Booth, C.E., et al. "The Brilliance of Borrelia: Mechanisms of Host Immune Evasion by Lyme Disease-Causing Spirochetes." Frontiers in Immunology 12: 665397 (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8001052/

  4. Ursinus, J., et al. "Persistent Symptoms After Lyme Disease: Clinical Characteristics, Predictors, and Classification." The Journal of Infectious Diseases 230(Supplement_1): S62-S70 (2024). https://academic.oup.com/jid/article/230/Supplement_1/S62/7733438

  5. 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/

  6. Babb, K.R., et al. "In-Vitro Susceptibility of Different Morphological Forms of Borrelia Burgdorferi to Common Lyme Antibiotics in Combination with Antimicrobial Peptides." Journal of Microbiology & Experimentation 4(5): 00126 (2016). https://medcraveonline.com/JMEN/in-vitro-susceptibility-of-different-morphological-forms-of-borrelia-burgdorferi-to-common-lyme-antibiotics-in-combination-with-antimicrobial-peptides.html

  7. Sambri, V., et al. "Borrelia burgdorferi Resistance to a Major Skin Antimicrobial Peptide Is Independent of Outer Surface Lipoprotein Content." Infection and Immunity 77(12): 5604-5611 (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2764146/

  8. 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/

  9. Garaci, E. "Immune Modulation with Thymosin Alpha 1 Treatment." Vitam Horm 102: 151-178 (2016). https://pubmed.ncbi.nlm.nih.gov/27450734/

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

  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. Teichman, S.L., et al. "Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults." Journal of Clinical Endocrinology & Metabolism 91(3): 799-805 (2006). https://pubmed.ncbi.nlm.nih.gov/16352683/

  13. Johns Hopkins Medicine. "FDA approves drug for treatment of rare mitochondrial disorder." The Hub (2025). https://hub.jhu.edu/2025/09/25/fda-approves-barth-syndrome-treatment/

  14. Patient discussion thread. "SS-31 Peptide (Elamipretide) for Lyme and co-infections / fatigue." HealingWell.com. https://www.healingwell.com/community/default.aspx?f=30&m=4344395

  15. Bay Area Lyme Foundation. "Lyme Disease Facts and Statistics." https://www.bayarealyme.org/about-lyme/lyme-disease-facts-statistics/