• Immunoglobulin E (IgE) are antibodies produced by the immune system. If you have an allergy, your immune system overreacts to an allergen by producing antibodies called Immunoglobulin E (IgE). These antibodies travel to cells that release chemicals, causing an allergic reaction. This reaction usually causes symptoms in the nose, lungs, throat, or on the skin. 
  • Each type of IgE has specific “radar” for each type of allergen. That’s why some people are only allergic to cat dander (they only have the IgE antibodies specific to cat dander); while others have allergic reactions to multiple allergens because they have many more types of IgE antibodies.
  • REFERENCE: https://www.worldallergy.org/education-and-programs/education/allergic-disease-resource-center/professionals/ige-in-clinical-allergy-and-allergy-diagnosis 
  • Th2 T cells experience antigen –> IL4 (most important)and IL13 promote IgE production by B cells. If IL5 is made, eosinophils are made. T cells also activate other allergy cells– mast cells, basophils (these dump histamine into the mucosa)
  • Healthy microbiome early in life prevents allergy by balancing  Th1/Th2 and regulatory T cells, promotes immunologic tolerance, decreased IgE, Th17, Th2, Th9, increased IgG4, Th1 immune activity (IFN-gamma (most potently anti-IgE), IL-10), increased IgA
  • Th2 immunology (antibodies)– Th2 cells secrete IL-4, IL-5, IL-6, IL-9 and IL-13. These cytokines seem to coordinate host defence against large, extracellular pathogens such as helminths9. Most of the characteristic features of atopy and asthma, especially IgE synthesis
  • Th1 immunology (cytotoxic T cells)– Th1 cells secrete interleukin (IL)-2, interferon (IFN)-γ, tumour necrosis factor (TNF)-α, lymphotoxin (LT) and other cytokines that together mobilize cellular and humoral defence mechanisms against intracellular pathogens and antagonize IgE responses.
  • Food molecules/chemicals alter the microbes of the sinus/lung/skin/gut stimulating IgE production
    • reference: https://allergysc.com/what-allergies-cause-sinus-problems/


  • Changes to the commensals microbes affect risk for allergic eczema
  • REFERENCE: https://pubmed.ncbi.nlm.nih.gov/25944283/
  • excess Staph and decreased strep/propionibacterium/acinetobacter can promote eczema
  • Changes to microbes alter Th1/Th2 balance and anti-inflammatory responses to environmental allergens


  • Candida or nematode -> Th2 response featuring IL4 / IL13 secretion-> PGE2 mediated inflammation -> leads to  airway inflammation
  • Bacterial dominance decreases Th2; Fungal dominance promotes Th2; Fungi/mold often thrive where bacteria levels are lower


  • Vit D def can lead to allergy and Vit D treatment can lessen allergy


reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6005239/

  • intestinal dysbiosis (that is, an alteration in richness and composition of the local microbiota) in the early  postneonatal period but not thereafter in infancy is associated with asthma phenotypes in the first years of life- lower relative abundance of Bifidobacterium, Akkermansia, and Faecalibacterium, higher relative abundance of  fungi such as Candida and Rhodotorula, and a distinct fecal metabolome enriched for proinflammatory  metabolites. 
  • Colonization occurs gradually in healthy children, starting with Staphylococcus or Corynebacterium, followed by Moraxella or Alloiococcus (46). A breakdown in the development of the commensal population can lead to dysregulation of the IgE–basophil axis, with elevated serum IgE concentrations and increased of circulating basophil populations as has been described in murine models of allergic airway disease (47). Importantly, this link was found to be B-cell intrinsic and dependent on the MYD88 pathway. 
  • Moreover, the lung microbiome may also play a role in driving asthma endotype polarization, by adjusting the balance between Th2 and Th17 patterns. 
  • Enterococcus faecalis can suppress Th17 immunity and symptoms of allergic asthma
  • Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae has been associated with recurrent wheezing and asthma 
  • There is an intimate relationship between gut and lung microbiomes (gut is major controller)
  • Pesticides increase risk for asthma even in farmers: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381985/


REFERENCE: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945755/

  • impairment in many cytochrome P450 enzymes, which are involved with detoxifying environmental toxins, activating vitamin D3, catabolizing vitamin A, and maintaining bile acid production and sulfate supplies to the gut. 
  • Glyphosate is known to inhibit cytochrome P450 enzymes. 
  • Deficiencies in iron, cobalt, molybdenum, copper and other rare metals associated with celiac disease can be attributed to glyphosate’s strong ability to chelate these elements. 
  • Deficiencies in tryptophan, tyrosine, methionine and selenomethionine associated with celiac disease match glyphosate’s known depletion of these amino acids. 
  • Celiac disease patients have an increased risk to non-Hodgkin’s lymphoma, which has also been implicated in glyphosate exposure. 
  • Reproductive issues associated with celiac disease, such as infertility, miscarriages, and birth defects, can also be explained by glyphosate. 
  • Glyphosate residues in wheat and other crops are likely increasing recently due to the growing practice of crop desiccation just prior to the harvest. 
  • We argue that the practice of “ripening” sugar cane with glyphosate may explain the recent surge in kidney failure among agricultural workers in Central America.


  • In GMO food products, meat
  • Processed food/simple carbs –> promote dysbiosis and fungal overgrowth

Importance of Early-Life Microbiome

  • There is mounting evidence that early-life exposure is critical for the microbiome and that gut microbial dysbiosis heavily influences immune system development (53). 
  • maternal intake of antibiotic during pregnancy increases the risk of allergy in children (93), and antibiotic use in the first month of life has been associated with cow’s milk allergy
  • Potential factors include perinatal exposure to maternal or infant diet, antibiotic use, and contact with older siblings (16). 
  • Data from different populations show that the highest interindividual microbial variability occurs during the first 3 years of age (26). 
  • Noteworthy, contact with the microbiome can start before birth, since a low-abundance microbiota in the placenta (69) and meconium (70, 71) have been found.
  • Microbial exposure during the first months of life induces the activation of the innate immune system in different ways, with consequences for allergy. 
  • Early inoculation with spore-forming Clostridium class IV and XIV species (72) and other bacteria (53) leads to decreased levels of circulating IgE in adulthood. 
  • Conversely, 3-week-old neonates with a higher fecal burden of Clostridium difficile and a higher ratio of C. difficile to Bifidobacterium showed increased numbers of skin test positive results to food and aero-allergens (73). Similarly, high levels of fecal E. coli in infants during their first month are associated with IgE-mediated eczema (74, 75).
  • Remarkably, the same colonization pattern can have different consequences at different ages. For example, colonization of S. pneumoniae, H. influenzae, or M. catarrhalis within the first month of life increases the risk of asthma, leading to high counts of atopic markers such as eosinophils and serum IgE, but not when colonization occurs at 12 months (45).
  • Furthermore, respiratory tract infections during early-life are associated with asthma development (76, 77). This may be because viral infections favor other opportunistic respiratory pathogens such as M. catarrhalis and S. pneumoniae, increasing the risk of asthma exacerbations (78). Other possible mechanisms may involve respiratory rhinovirus interacting with airway epithelial cells, increasing IL-25 and IL-33 production and contributing to Th2 immune responses (79). This is in line with the higher levels of house dust mite-specific IgE found in children infected with rhinovirus (80). Moreover, rhinovirus infection can also induce mucus hypersecretion and airway hyperresponsiveness in neonatal mice compared with adults (81).

Ideal neonatal treatment: breastfeeding

Infancy and onwards treatment:

Early food s rich in polyphenols and O3FAs, plant fiber for SCFA production


  • Tang ML et al described in 2015 that probiotic therapy with Lactobacillus rhamnosus GG (LGG) increases efficacy when co-administered with peanut oral immunotherapy in 62 peanut allergic children, producing desensitization in 82% of subjects. The beneficial effect of LGG in the prevention of atopic eczema was also described in 2010 in The Lancet, with a cohort of 62 babies who were administered LGG at 2.4 weeks and 6 months of life. The risk of suffering from atopic eczema in the group supplied with the probiotic was 5% versus 47% in the placebo group.
  • It has been shown that supplying probiotics orally also has a beneficial effect on clinical symptoms in patients with rhinitis, while the nasal administration of a specific strain of Lactococcus lactis for 5 days (LLNZ9000) has protective effects against the effect of Streptococcus pneumoniae, increasing its clearance rate from the lungs and preventing dissemination into the blood.
  • Fresh yogurt is an established microbiome repair food https://www.gutmicrobiotaforhealth.com/health-benefits-linked-to-yogurt-consumption-could-be-explained-as-a-result-of-improvements-in-gut-barrier-function/

Prebiotic food: oatmeal, barley, legumes, nuts, seeds, couscous, vegetables, fruits (with skins/seeds)


The following treatments can help move you towards more Th1 and less Th2: 

  • Vit A, Colostrum
  • Triphala
  • Resveratrol
  • Astragalus 
  • balanced hormones (estrogens/progesterone)
  • LDN