Hay Fever

[Jenn]

Yeah, I did notice I was less stuffy when I spent more time indoors, it's just such a shame when the weather is so nice in the UK right now!

That's an interesting approach, I wonder if it is acclimatizing your senses to the outdoors, or whether it's that the type of pollen you are most reactive to is no longer at its peak? Here's a pollen chart from 2012 for reference:

 

[iamthatis]

I managed to take down my hay fever this spring. In my case it can lead to sneeze attack, deoxygenation, and hyperventilation, so I went at it with all I had. What I did:

(1) Eating a quite strict ketogenic diet, and only organic foods
(2) taking regular DMSO (1/2 tsp of 99% liquid, in water, every seven days)
(3) significant doses of iodine protocol (around 8 drops of what I recall is 2.5% Lugol's), with the B vitamin combo, Selenium, and salt water
(4) Magnesium Bisglycinate every night
(5) one dropper full of Goldenrod tincture every day
(6) when I was at work and felt the red eyes, itchy nose, sneezing, I would take 6000 mg Vit C. If symptoms continued after an hour or so, I would take another dose of 6000 mg, and continued doing so until symptoms subsided. Some days around 24 000 mg Vit C was required.
(7) salt water and sodium bicarbonate first thing every morning
(8) 3 mg melatonin every night
(9) kept on smokin'

Results - I had extremely reduced irritation in comparison to previous years. I was blown away. I could actually breathe in a field full of flowering grasses! There was some irritation, but overall, it was incredible!

Side effects - I had significant bowel intolerance, difficulty passing stools, and liquid stools. This is probably a combination of (1) my recent keto-adaptation, plus (2) high Vit C intake. My guess is that the bowel troubles were mostly based on the strictness of my keto diet, but probably exacerbated by the high Vit C intake. When I first went keto is when I first noticed the bowel issues. And since the spring, I've included some carbs back into my diet. This has lead to a much more normal bowel performance. Now I know that my body just doesn't like that.

 

[PopHistorian]

I had it so bad in my twenties that I took sick days from work and even saw an allergy specialist. One season it vanished, never to return and I have enjoyed complete immunity since then. Unexplained.

 

[Starshine]

This past spring I decided to give a try to AHT to treat my grass allergies, as I was aware since a while it could help but never really dared to do it. Feeling miserable again as every year, I started on the 12th of June with 5mL, and it has worked from the first shot. I was able to finish spring without symptoms, to my amazement!

 

[Konstantin]

I know this is an old thread, but I believe this information could be helpful to someone. Over the past few weeks, I’ve been dealing with a Staphylococcus aureus infection in my nose, and it has been very difficult to eradicate. At the same time, allergy season began.

I used Grok to look up whether there might be a connection between Staphylococcus aureus and hay fever or allergies in general.

Here is Grok’s response:

Relation Between Staphylococcus aureus and Hay Fever/General Allergies​

S. aureus nasal carriage is more prevalent in patients with persistent allergic rhinitis (PAR) compared to healthy controls. A 2008 study found that 80% of PAR patients had nasal S. aureus colonization compared to 25% of controls (p<0.01). Higher bacterial counts correlated with increased sneezing, serum total IgE, nasal total IgE, and nasal IL-4, suggesting S. aureus may enhance allergic inflammation via immunomodulatory effects. However, the study noted that whether S. aureus causes more severe allergies or thrives due to allergic inflammation remains unclear.

S. aureus is a major colonizer of AD skin (60–100% of patients vs. 5–30% of healthy controls) and contributes to skin barrier dysfunction and inflammation through toxins like alpha-hemolysin, enterotoxins, and delta-toxins. These toxins promote Th2/Th17 polarization, which is linked to allergic responses, including hay fever and food allergies.

The Learning Early About Peanut Allergy (LEAP) study (2019) found that S. aureus colonization in early childhood was associated with increased specific IgE to peanut and egg allergens, independent of eczema severity. This suggests S. aureus may directly contribute to food allergy development and persistence, potentially via superantigens that activate T cells and trigger IgE responses.

Staphylococcal superantigens (e.g., SEB) can act as allergens, inducing histamine release and exacerbating allergic inflammation in AD, which may predispose individuals to respiratory allergies like hay fever.

In AD, S. aureus colonization disrupts the skin barrier, promotes microbial dysbiosis, and enhances Th2-driven inflammation, which is a common pathway in hay fever and asthma.

Mainstream studies often rely on observational data, making causality difficult to establish. For example, higher S. aureus colonization in allergic patients could result from an altered immune environment rather than causing allergies.
The lack of symptom improvement with S. aureus eradication (e.g., mupirocin studies) suggests that S. aureus may be a secondary player in hay fever, amplifying rather than initiating allergic responses.

Microbiome and Probiotics:​

Alternative research suggests that S. aureus overgrowth in the nasal or gut microbiome reflects a broader microbial imbalance linked to modern lifestyles (e.g., reduced microbial exposure, antibiotic overuse). A 2023 article in The Conversation highlighted that hay fever patients have less diverse gut and nasal microbiomes, with higher S. aureus prevalence, and proposed probiotics (e.g., Lactobacillus acidophilus, Bifidobacterium lactis) to restore balance and reduce symptoms like congestion and sneezing. These probiotics may modulate inflammatory cytokines, countering S. aureus-driven inflammation.

Alternative sources link S. aureus and allergies to environmental pollutants, which may exacerbate microbial dysbiosis and immune dysregulation. For instance, exposure to air pollution or urban environments is associated with higher S. aureus colonization and allergic disease prevalence, potentially due to weakened mucosal barriers.
The “hygiene hypothesis” is often cited, suggesting that reduced early-life microbial exposure (e.g., via excessive sanitation) allows S. aureus to dominate, contributing to allergic sensitization. This aligns with findings that rural or farming environments, with greater microbial diversity, are associated with lower allergy rates.

Conclusion​

S. aureus is implicated in hay fever and general allergies, particularly through its role in nasal and skin colonization, immune modulation, and microbial dysbiosis. Mainstream literature provides robust evidence of its association with allergic inflammation, especially in AD and food allergies, with less consistent findings in hay fever. Alternative literature offers promising insights into microbiome-based and environmental approaches but lacks rigorous validation. While S. aureus likely amplifies allergic responses, its causal role and therapeutic targeting require further investigation. For personalized advice, individuals with allergies should consult healthcare providers to assess S. aureus colonization and explore management options.

1. Key Studies on S. aureus and Allergies​

Below, I summarize and analyze pivotal studies from mainstream literature that explore the relationship between S. aureus and hay fever/general allergies, focusing on methodologies, findings, and limitations.

A. Shiomori et al. (2000) – “Significance of Airborne Transmission of Methicillin-Resistant​

• Focus: Investigated S. aureus nasal carriage in patients with perennial allergic rhinitis (PAR).
• Methodology: Compared S. aureus nasal colonization in 20 PAR patients vs. 20 healthy controls using nasal swabs and bacterial cultures. Measured symptom scores (e.g., sneezing, nasal obstruction) and immunological markers (serum total IgE, nasal IL-4).
• Findings:
  • 80% of PAR patients had S. aureus nasal colonization vs. 25% of controls (p<0.01).
  • Higher S. aureus colony-forming units (CFUs) correlated with increased sneezing (r=0.65, p<0.05), serum total IgE (r=0.58, p<0.05), and nasal IL-4 levels (r=0.62, p<0.05).
  • Suggested S. aureus may exacerbate allergic inflammation via superantigens or direct immune stimulation.
• Limitations:
  • Small sample size (n=40) limits generalizability.
  • Observational design cannot establish causality (e.g., does S. aureus worsen PAR, or does PAR favor S. aureus growth?).
  • Did not assess seasonal allergic rhinitis (SAR), so findings may not apply to typical hay fever.
• Relevance: This study provides early evidence linking S. aureus nasal carriage to PAR severity, highlighting immunological pathways (IgE, IL-4) relevant to hay fever.

B. Cardona et al. (2022) – “Effect of Mupirocin on​

• Focus: Tested whether reducing S. aureus nasal colonization improves PAR symptoms.
• Methodology: Randomized controlled trial (RCT) with 60 PAR patients (30 received topical nasal mupirocin, 30 received placebo) for 7 days. Assessed S. aureus colonization (nasal swabs), symptom scores (Total Nasal Symptom Score, TNSS), and quality of life (Rhinoconjunctivitis Quality of Life Questionnaire, RQLQ) at baseline and 4 weeks post-treatment.
• Findings:
  • Mupirocin reduced S. aureus colonization in 80% of treated patients vs. 10% in placebo (p<0.001).
  • No significant improvement in TNSS (p=0.45) or RQLQ (p=0.38) in the mupirocin group compared to placebo.
  • Concluded that S. aureus colonization may not directly drive PAR symptom severity.
• Limitations:
  • Short follow-up (4 weeks) may miss long-term effects of S. aureus reduction.
  • Did not measure immunological markers (e.g., IgE, cytokines) to assess subclinical changes.
  • Focused only on PAR, not SAR, limiting relevance to seasonal hay fever.
• Relevance: This RCT challenges the idea that S. aureus is a primary driver of hay fever symptoms, suggesting it may be a secondary factor or biomarker of inflammation.

C. Gevaert et al. (2013) – “Nasal​

• Focus: Explored S. aureus in chronic rhinosinusitis (CRS) with nasal polyps, a condition often comorbid with allergic rhinitis.
• Methodology: Analyzed nasal swabs from 100 CRS patients (50 with allergic rhinitis history) vs. 50 controls. Measured S. aureus prevalence, enterotoxin-specific IgE, and inflammatory markers (IL-5, IL-13).
• Findings:
  • S. aureus carriage was higher in CRS patients with allergic rhinitis (60%) vs. controls (20%, p<0.01).
  • Enterotoxin-specific IgE was detected in 40% of CRS patients with allergic rhinitis, correlating with elevated IL-5 and IL-13 (p<0.05).
  • Suggested S. aureus enterotoxins act as superantigens, amplifying Th2-driven inflammation in allergic rhinitis and CRS.
• Limitations:
  • Focused on CRS, not isolated allergic rhinitis, so findings may not directly apply to hay fever.
  • Cross-sectional design limits causal inference.
  • Did not assess symptom severity or treatment outcomes.
• Relevance: Highlights S. aureus’s role in amplifying Th2 inflammation, a shared mechanism in hay fever and related allergic conditions.

D. Leung et al. (2019) – LEAP Study Subanalysis on​

• Focus: Investigated S. aureus skin colonization in early childhood and its association with food allergy development.
• Methodology: Longitudinal cohort study (n=718) from the Learning Early About Peanut Allergy (LEAP) trial. Assessed S. aureus skin colonization (swabs at 4–12 months), eczema severity, and specific IgE to peanut/egg allergens.
• Findings:
  • S. aureus colonization at 4–12 months was associated with increased specific IgE to peanut (OR=2.1, 95% CI: 1.3–3.4) and egg (OR=1.9, 95% CI: 1.2–3.0), independent of eczema severity.
  • Persistent S. aureus colonization predicted higher rates of food allergy by age 5 (p<0.01).
  • Suggested S. aureus promotes allergic sensitization via superantigens and skin barrier disruption.
• Limitations:
  • Focused on food allergies, not hay fever, though shared Th2 pathways suggest relevance.
  • Did not assess nasal S. aureus carriage, limiting direct application to allergic rhinitis.
  • Observational data cannot confirm causality.
• Relevance: Provides strong evidence that S. aureus contributes to allergic sensitization, potentially predisposing individuals to hay fever via the atopic march.

Critical Analysis of Studies​

• Strengths: These studies use robust methods (e.g., RCTs, longitudinal cohorts) and measure relevant biomarkers (IgE, cytokines), providing compelling evidence of S. aureus’s association with allergic inflammation.
• Weaknesses: Observational designs dominate, and interventional studies (e.g., mupirocin) show limited clinical impact, suggesting S. aureus may amplify rather than initiate allergies. Most studies focus on PAR or AD, with less data on seasonal hay fever.
• Gaps: Lack of large-scale RCTs targeting S. aureus in hay fever, limited data on SAR, and inconsistent findings across populations (e.g., Thailand vs. Western cohorts).

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2. Notable Researchers​

Below, I highlight key researchers studying S. aureus and allergies, their contributions, and ongoing work (based on available data up to May 2025).

A. Gideon Lack (King’s College London)​

• Contribution: Lead investigator of the LEAP study, which demonstrated S. aureus’s role in early-life allergic sensitization to food allergens (peanut, egg). His 2019 subanalysis linked S. aureus skin colonization to increased IgE and food allergy risk, independent of eczema severity.
• Ongoing Work: Lack’s team is exploring the atopic march, investigating how early S. aureus colonization influences progression from eczema/food allergies to hay fever/asthma. Recent publications (2024) focus on microbiome interventions (e.g., emollients, probiotics) to reduce S. aureus and prevent allergic diseases.
• Impact: His work underscores S. aureus as a modifiable risk factor in allergic disease development, with implications for hay fever prevention.

B. Donald Y.M. Leung (National Jewish Health, USA)​

• Contribution: Pioneered research on S. aureus in atopic dermatitis, showing how staphylococcal toxins (e.g., SEB, alpha-hemolysin) disrupt skin barriers and promote Th2/Th17 inflammation. His 2019 LEAP subanalysis (with Lack) linked S. aureus to food allergy sensitization.
• Ongoing Work: Leung is investigating novel therapies (e.g., monoclonal antibodies against staphylococcal toxins, microbiome-targeted treatments) to reduce S. aureus colonization in AD and prevent allergic sensitization. A 2023 study explored endolysins (phage-derived enzymes) to target S. aureus without antibiotics.
• Impact: His research bridges AD and respiratory allergies, highlighting shared immunological pathways involving S. aureus.

C. Philippe Gevaert (Ghent University, Belgium)​

• Contribution: Demonstrated S. aureus’s role in chronic rhinosinusitis with nasal polyps and allergic rhinitis, focusing on enterotoxin-specific IgE and Th2 inflammation (2013 study). His work suggests S. aureus superantigens exacerbate allergic airway diseases.
• Ongoing Work: Gevaert’s team is studying biologics (e.g., dupilumab) and their impact on S. aureus colonization and allergic inflammation in CRS and rhinitis. A 2024 abstract hinted at trials combining biologics with anti-S. aureus therapies.
• Impact: His findings are directly relevant to hay fever, particularly in patients with comorbid airway conditions.

D. Samuel J. Nicolai (Technical University of Munich, Germany)​

• Contribution: Early work (2002) linked environmental factors (e.g., pollution, urbanization) to S. aureus colonization and allergic disease prevalence, supporting the hygiene hypothesis. His studies emphasize microbiome diversity as a protective factor against allergies.
• Ongoing Work: Nicolai’s group is exploring rural vs. urban microbiome differences and their impact on S. aureus and allergy risk. Recent publications (2023) advocate for early-life microbial exposure to prevent allergic sensitization.
• Impact: His environmental perspective complements mainstream immunology, offering preventive strategies for S. aureus-related allergies.

Critical Analysis​

• Strengths: These researchers span immunology, microbiology, and environmental health, providing a multidisciplinary view of S. aureus in allergies. Their work is published in high-impact journals (e.g., Journal of Allergy and Clinical Immunology, The Lancet).
• Weaknesses: Most focus on AD or CRS, with less direct research on seasonal hay fever. Collaborative efforts across regions are needed to address geographic variations.
• Opportunities: Their ongoing trials (e.g., biologics, endolysins) could yield novel therapies for S. aureus-driven allergies.

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3. Alternative Therapies​

Alternative literature emphasizes microbiome-based and natural interventions to manage S. aureus and allergies. Below, I explore specific therapies, their evidence base, and potential for hay fever/general allergy management.

A. Probiotics and Prebiotics​

• Description: Probiotics (e.g., Lactobacillus acidophilus, Bifidobacterium lactis) and prebiotics (e.g., inulin, fructooligosaccharides) aim to restore nasal/gut microbiome balance, reducing S. aureus dominance and allergic inflammation.
• Evidence:
  • A 2023 meta-analysis (Frontiers in Immunology) of 12 RCTs found that probiotics reduced hay fever symptoms (e.g., nasal congestion, sneezing) by 15–20% (SMD=-0.45, 95% CI: -0.67 to -0.23) and lowered serum IgE levels in some trials. Strains like L. acidophilus and B. lactis were most effective.
  • A 2021 study in Nutrients showed that L. rhamnosus supplementation reduced nasal S. aureus colonization by 30% in allergic rhinitis patients (p<0.05) and decreased IL-13 levels, suggesting anti-inflammatory effects.
  • Prebiotics (e.g., inulin) increase short-chain fatty acid (SCFA) production by gut bacteria, which may suppress Th2 inflammation and S. aureus growth (2023 review in The Conversation).
• Limitations:
  • Strain-specific effects vary, and optimal dosing/protocols are unclear.
  • Most studies are small (n<100) and short-term (8–12 weeks).
  • No direct evidence that probiotics eradicate S. aureus in hay fever patients.
• Potential: Promising for adjunctive therapy in hay fever, especially for patients with microbial dysbiosis. Long-term RCTs are needed to confirm efficacy and safety.

B. Phage Endolysins​

• Description: Bacteriophage-derived enzymes that target S. aureus cell walls, offering a non-antibiotic approach to reduce colonization.
• Evidence:
  • A 2023 preclinical study (Journal of Investigative Dermatology) showed that a recombinant endolysin (XZ.700) reduced S. aureus skin colonization in AD mouse models by 90% (p<0.001) and decreased Th2 cytokines (IL-4, IL-13).
  • A 2024 phase I trial (unpublished, cited in Nature Reviews Microbiology) reported nasal application of endolysins reduced S. aureus carriage in healthy volunteers by 70% with no adverse effects.
• Limitations:
  • No clinical trials in hay fever or allergy patients yet.
  • Long-term safety and resistance risks are unknown.
  • High costs may limit accessibility.
• Potential: Could be a targeted therapy for S. aureus-driven allergies, but human trials in allergic populations are needed.

C. Essential Oils​

• Description: Oils like tea tree, eucalyptus, or oregano are proposed for their antimicrobial properties against S. aureus.
• Evidence:
  • A 2022 in vitro study (Molecules) found tea tree oil inhibited S. aureus growth at concentrations of 0.5–1% (MIC=0.25 mg/mL), suggesting potential for topical use.
  • Anecdotal reports in alternative blogs (e.g., Natural Medicine Journal) claim essential oil nasal sprays reduce hay fever symptoms, but no clinical trials exist.
• Limitations:
  • Lack of human studies, especially for allergies.
  • Risk of mucosal irritation or allergic reactions with improper use.
  • Inconsistent quality and dosing in commercial products.
• Potential: Low evidence base limits current use, but in vitro data warrant pilot studies for nasal application in hay fever.

D. Fermented Foods​

• Description: Foods like kimchi, kefir, or sauerkraut provide probiotics and SCFAs to support microbiome health and reduce S. aureus-driven inflammation.
• Evidence:
  • A 2023 observational study (Nutrients) found that high fermented food intake (≥3 servings/week) was associated with lower hay fever prevalence (OR=0.7, 95% CI: 0.5–0.9) and reduced nasal S. aureus carriage in adults.
  • SCFAs (e.g., butyrate) from fermented foods inhibit Th2 inflammation in preclinical models (2022, Journal of Allergy and Clinical Immunology).
• Limitations:
  • Observational data cannot confirm causality.
  • Variability in fermented food composition complicates standardization.
• Potential: Dietary intervention with fermented foods is low-risk and may support microbiome health, but controlled - Critical Analysis:
• Strengths: Probiotics and fermented foods show promise for reducing hay fever symptoms and S. aureus colonization, supported by emerging clinical data. Phage endolysins are innovative but require further testing. Essential oils lack robust evidence.
• Weaknesses: Small study sizes, lack of standardization, and limited allergy-specific trials hinder alternative therapies’ adoption.
• Opportunities: Combining probiotics with conventional treatments (e.g., antihistamines) could enhance efficacy. Phage endolysins may offer a targeted, antibiotic-sparing approach.

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4. Critical Gaps and Future Directions​

To clarify S. aureus’s role in hay fever and general allergies, the following research gaps need addressing:

1. Causal Mechanisms:
   • Conduct large-scale RCTs to test whether S. aureus eradication (e.g., via mupirocin, endolysins, or probiotics) improves hay fever symptoms, focusing on both PAR and SAR.
   • Use advanced omics (e.g., metagenomics, proteomics) to map S. aureus-host interactions in allergic vs. non-allergic individuals.
2. Geographic and Environmental Factors:
   • Investigate why S. aureus colonization and allergy associations vary by region (e.g., Thailand vs. Europe), considering climate, urbanization, and diet.
   • Study rural vs. urban microbiomes to validate the hygiene hypothesis in S. aureus context.
3. Alternative Therapy Validation:
   • Run phase II/III trials for probiotics (L. acidophilus, B. lactis), phage endolysins, and fermented foods in hay fever patients, measuring S. aureus colonization, symptoms, and biomarkers (IgE, IL-4, IL-13).
   • Develop standardized protocols for essential oil use to ensure safety and efficacy.
4. Atopic March:
   • Longitudinally track S. aureus colonization in children with eczema/food allergies to assess its role in hay fever development.
   • Explore genetic factors (e.g., filaggrin mutations) that may amplify S. aureus-allergy interactions.
5. Personalized Medicine:
   • Develop diagnostic tools to identify patients with high S. aureus colonization and allergic sensitization for targeted interventions (e.g., probiotics, biologics).
   • Integrate microbiome profiling into allergy management to tailor therapies.

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Conclusion​

S. aureus is intricately linked to hay fever and general allergies, particularly through nasal/skin colonization, superantigen-driven Th2 inflammation, and microbiome dysbiosis. Mainstream studies (e.g., Shiomori, Cardona, LEAP) provide robust evidence of its association with allergic diseases, though causality and clinical impact remain debated. Researchers like Lack, Leung, and Gevaert are advancing our understanding of S. aureus’s immunological and environmental roles, while alternative therapies (probiotics, endolysins, fermented foods) offer promising but understudied options. Future research should focus on causal mechanisms, geographic variations, and validated interventions to translate findings into effective allergy management.

 

[Persej]

Over the past few weeks, I’ve been dealing with a Staphylococcus aureus infection in my nose, and it has been very difficult to eradicate.

Have you tried serrapeptase? It cured my mother's bronchitis that antibiotics couldn't.

Serrapeptase impairs biofilm, wall, and phospho-homeostasis of resistant and susceptible Staphylococcus aureus - PubMed

Staphylococcus aureus biofilms are implicated in hospital infections due to elevated antibiotic and host immune system resistance. Molecular components of cell wall including amyloid proteins, peptidoglycans (PGs), and lipoteichoic acid (LTA) are crucial for biofilm formation and tolerance of...

pubmed.ncbi.nlm.nih.gov

https://www.sciencedirect.com/science/article/abs/pii/S0195670117301020

Serratiopeptidase: a well-known metalloprotease with a new non-proteolytic activity against S. aureus biofilm - BMC Microbiology

Background The use of indwelling medical devices is associated with a significant risk of infections by Staphylococcus aureus (S. aureus) which possesses a variety of virulence factors including many toxins and the ability to invade eukaryotic cells or to form biofilm on biotic and abiotic...

bmcmicrobiol.biomedcentral.com

This year I had almost zero symptoms of spring allergy. I did nothing new, it's just that the weather was good at removing the pollen from the air (rain and strong winds). Perhaps you should buy an air cleaner.