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The Foundations of Atopic Dermatitis

By Dr. Kori Macarthur, ND7/14/2025
The Foundations of Atopic Dermatitis

What Is Atopic Dermatitis?

Atopic dermatitis (AD), aka Eczema is an immune-mediated skin disorder associated with a compromised skin barrier and dysregulation of the immune system. It is part of the "atopic triad," which also includes asthma and allergic rhinitis. The condition is marked by cycles of flares and remission and is often linked to a genetic predisposition.

Key symptoms include:

  • Dry, scaly skin
  • Intense itching (pruritus)
  • Red, inflamed patches (commonly on the hands, face, elbows, and knees)
  • Skin thickening from chronic scratching (lichenification)

Types of Atopic Dermatitis

While atopic dermatitis is the most common form, it’s important to recognize that “eczema” is an umbrella term for several skin conditions. Each type may have distinct triggers and also requires a slightly different approach to treatment:

  • Atopic Dermatitis: Chronic and relapsing, often linked to allergies and asthma. Most common on the inside of the elbows, behind the knees, on the neck and even face around the eyes. 
  • Contact Dermatitis: Triggered by allergens or irritants like nickel, fragrances, or detergents.
  • Dyshidrotic Eczema: Small, itchy blisters on the hands and feet.
  • Nummular Eczema: Round, coin-shaped lesions, often very itchy and crusty.
  • Seborrheic Dermatitis: Affects oily areas like the scalp and face; can overlap with fungal imbalances.
  • Stasis Dermatitis: Occurs in the lower legs due to poor circulation or venous insufficiency.


What Science Tells Us about Eczema 

Eczema is far more than just “dry, itchy skin.” It's a complex inflammatory skin disease that involves immune system dysregulation, skin barrier dysfunction, microbiome imbalances, and genetic predisposition. Understanding the mechanisms behind eczema can help clarify why certain triggers cause flares—and why a root-cause approach is often more effective than simply just applying topical creams. Treatment to AD often requires a multi-factorial approach, not one thing or another. 


Let’s break down the current science behind eczema’s underlying mechanisms: 


1. Skin Barrier Dysfunction

The outer layer of the skin, known as the stratum corneum, acts as a protective shield, keeping moisture in and irritants out. In people with atopic dermatitis, this barrier is often compromised. A filaggrin deficiency is one of the most studied genetic factors in eczema is a mutation in the FLG gene, which codes for filaggrin—a protein essential for maintaining the skin’s structure and hydration. A filaggrin deficiency leads to increased trans-epidermal water loss and allows allergens, irritants, and microbes to penetrate more easily. A 2011 study in The Journal of Allergy and Clinical Immunology found that FLG mutations are associated with early-onset and more severe atopic dermatitis, as well as increased risk of developing asthma and allergic rhinitis.


2. Immune System Dysregulation

Eczema involves an imbalance in the immune system, particularly between the Th1 and Th2 immune responses. Th2 Dominance: In acute eczema flares, the body shows an exaggerated Th2 immune response, which promotes the production of IgE antibodies and inflammation. This leads to increased susceptibility to allergens and microbes. In chronic eczema, there is also an increase in Th1 and Th17 activity, perpetuating a cycle of inflammation. A 2014 review in Nature Reviews Immunology described AD as a “polarized Th2 disorder” with overlapping Th22 and Th17 pathways in chronic cases, suggesting why immunomodulatory treatments like dupilumab (IL-4/IL-13 blocker) can be effective.


3. Microbiome Imbalance (Dysbiosis)

People with atopic dermatitis (AD) often experience imbalances in both their skin and gut microbiomes, a state known as dysbiosis. On the skin, this typically involves reduced microbial diversity and an overgrowth of Staphylococcus aureus (S. aureus). This opportunistic bacteria produces toxins that weaken the skin barrier and trigger immune reactions, further driving inflammation and flare-ups. A 2018 study in JAMA Dermatology found a strong correlation between increased S. aureus colonization and eczema severity. Encouragingly, other studies have shown that restoring skin microbiome diversity may help improve symptoms and reduce flare frequency.


Dysbiosis isn’t limited to the skin. There is growing recognition of the gut-skin axis, where a disrupted gut microbiome, increased intestinal permeability (“leaky gut”), and chronic systemic inflammation can negatively impact immune balance and skin barrier function. Emerging research shows that individuals with AD—especially infants—often have altered gut microbiota early in life. In adults, AD frequently coexists with gastrointestinal symptoms or conditions such as irritable bowel syndrome (IBS), further suggesting a link. A 2020 review in Frontiers in Immunology emphasized the pivotal role of the gut microbiome in shaping systemic immune responses and maintaining skin health. The authors did support the use of targeted probiotics and modified dietary interventions as adjunctive therapies in managing atopic dermatitis.


4. Genetics and Epigenetics

While not all cases of eczema are hereditary, many individuals with AD have a family history of allergic conditions (asthma, hay fever, or eczema). Beyond single-gene mutations, epigenetic factors—such as environmental exposures, diet, and stress—can influence gene expression related to inflammation and skin health. An interesting 2015 review study in the Clinical Reviews of Allergy & Immunology suggested that prenatal factors (e.g. maternal stress or antibiotic exposure) can epigenetically program the immune system toward Th2 dominance, increasing eczema risk in infants.


5. The Role of Environmental Factors 

Eczema flares can be triggered by a range of external factors, but these typically act on an already dysfunctional skin-immune system. Common culprits include:

  • Harsh soaps and detergents
  • Low humidity or cold weather
  • Dust mites, pollen, pet dander
  • Food allergens or sensitivities

These factors can directly affect the skin or indirectly influence immune responses and hormone balance (e.g. cortisol, melatonin), contributing to flare-ups. Harsh soaps, detergents, wool fabrics, and cold/dry weather can compromise the skin barrier. Air pollution and indoor allergens like dust mites or pet dander can act as environmental triggers. A low-toxic lifestyle and barrier-protecting emollients are crucial for reducing flare frequency and intensity.


6. The Gut-Skin Axis and Food Sensitivities

There’s growing evidence for the gut-skin connection in eczema:

  • Altered gut microbiota, increased intestinal permeability ("leaky gut"), and food antigens may stimulate systemic inflammation and worsen skin conditions.
  • Food sensitivity tests (e.g. IgG testing) are controversial but may be helpful in identifying delayed hypersensitivity reactions that contribute to inflammation in susceptible individuals.

IgE-mediated allergies (e.g., peanuts, eggs, dairy, soy) are immediate hypersensitivity reactions and are more common in children with moderate-to-severe eczema. IgG food sensitivities are delayed immune responses that may not cause classic allergic reactions but can contribute to systemic inflammation and eczema flare-ups. Studies suggest that elimination diets and exploring food sensitivities — when guided by testing and professional supervision — may improve symptoms in select individuals.


7. Lifestyle Factors 

Sleep disruption is common in people with eczema, often driven by nighttime itching. However, poor sleep isn’t just a symptom—it can actively worsen inflammation, weaken the skin barrier, and delay healing. The research has shown a strong correlation between poor sleep quality and eczema severity, emphasizing the importance of supporting both sleep and skin simultaneously. Similarly, chronic stress contributes to eczema through activation of the hypothalamic-pituitary-adrenal (HPA) axis, which increases cortisol levels. Elevated cortisol can impair skin immunity and regeneration, while stress itself can worsen itching and perpetuate the itch-scratch-inflammation cycle. Evidence supports the use of mindfulness practices, cognitive behavioural therapy (CBT), and nervous system regulation techniques as effective tools to help reduce flare-ups and support long-term eczema management.


Final Thoughts

Atopic dermatitis is more than just a skin condition — it’s a complex, multifactorial disorder that reflects deeper immune, inflammatory, and barrier-related imbalances. It impacts not just the skin but also quality of life, sleep, mood, and long-term health. By understanding the different types, triggers, and systemic influences behind eczema, we can begin to move beyond symptom management and move toward healthier, well-managed skin.


In upcoming blog posts, I’ll be sharing how, as a naturopathic doctor, I addresses adult onset eczema — from gut and immune support to topical therapies and stress modulation. You’ll also hear from a special guest Dr. Shantel Simpson, ND, who brings her clinical expertise in pediatric eczema, offering practical and effective strategies for managing eczema in children — from nutrition and microbiome support to reducing environmental triggers and rebuilding skin resilience.


Stay tuned as we dive deeper into the naturopathic approach to skin health — at every age.


Curious to learn more? 

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References


  • Deleuran, M., & Thyssen, J. P. (2024). Staphylococcus aureus: The bug behind the itch in atopic dermatitis. Journal of Investigative Dermatology.
  • Kun z, B., Oranje, A. P., Labrèze, L., Stalder, J. F., & Ring, J. (1997). Clinical validation and guidelines for the SCORAD index: Consensus report of the European Task Force on Atopic Dermatitis. Dermatology.
  • Royalty, C., et al. (2020). The role of probiotics in the treatment of adult atopic dermatitis: A meta‑analysis of randomized controlled trials. Journal of Health, Population, and Nutrition.
  • Williams, H., et al. (2019). Probiotics for treating eczema. The Cochrane Database of Systematic Reviews.
  • Zhang, Y., Li, M., & Zhou, Y. (2021). Nutritional factors in the prevention of atopic dermatitis in children. Frontiers in Pediatrics.
  • Gittler, J. K., Shemer, A., Suarez-Fariñas, M., Fuentes-Duculan, J., Gulewicz, K. J., Wang, C. Q. F., ... Krueger, J. G. (2014). Progressive activation of TH2/TH22 cytokines and selective epidermal proteins characterizes acute and chronic atopic dermatitis. Nature Reviews Immunology, 14(8), 435–446. https://doi.org/10.1038/nri3682
  • Canadian Dermatology Association. (n.d.). Eczema. Retrieved July 2025, from Canadian Dermatology Association website: estimated that up to 17% of Canadians will experience atopic dermatitis in their lifetime
  • Eczema Society of Canada. (2021). Itch in atopic dermatitis: Survey report. Retrieved July 2025, from Eczema Society of Canada: key data on itch, sleep disturbance (difficulty falling asleep 74%, staying asleep 67%, awakened by itch 76%) among children with moderate‑severe AD
  • van den Elsen, L. W. J., Garssen, J., & Burcelin, R. (2015). Early life programming of allergic disease: The role of epigenetic regulation and the microbiome. Clinical Reviews in Allergy & Immunology, 49(2), 103–114. https://doi.org/10.1007/s12016-015-8493-4
  • Palmer, C. N. A., Irvine, A. D., Terron-Kwiatkowski, A., Zhao, Y., Liao, H., Lee, S. P., ... McLean, W. H. I. (2006). Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis with associated allergic phenotypes. The Journal of Allergy and Clinical Immunology, 118(1), 214–225.
  • Pellegrini, C., Antonioli, L., Colucci, R., & Blandizzi, C. (2020). The gut microbiota in the pathogenesis of atopic dermatitis: A review. Frontiers in Immunology, 11, 610907. https://doi.org/10.3389/fimmu.2020.610907
  • Myles, I. A., Earland, N. J., Anderson, E. D., Huda, M., Belkaid, Y., & Williams, M. R. (2018). Staphylococcus aureus colonization is associated with atopic dermatitis severity and distinct cutaneous immune responses. JAMA Dermatology, 154(3), 293–301. https://doi.org/10.1001/jamadermatol.2017.4776
  • Odhiambo, J. A., Williams, H. C., Clayton, T. O., Robertson, C. F., & Asher, M. I. (2009). Global variations in prevalence of eczema symptoms in children from ISAAC Phase Three. Journal of Allergy and Clinical Immunology, 124(6), 1251–1258.e23. https://doi.org/10.1016/j.jaci.2009.09.038


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