Orders shipped same day
HSA/ FSA Accepted

What Are the Root Causes of Atopic Dermatitis? 5 Factors

What Are the Root Causes of Atopic Dermatitis? 5 Factors

By Michael Anderson, Clinical Research Project Manager •

When did your eczema really begin: at birth, or nine months before? Research shows that filaggrin gene mutations, carried by ~9% of people of European origin, are major predisposing factors for atopic dermatitis[1], while environmental factors play an important role in disease pathogenesis and the dramatic increase in AD prevalence[2]. Understanding these root causes offers real hope for breaking the cycle of inflammation.

You've likely tried many treatments: prescription steroids, moisturizers, antihistamines, even dietary changes. Each promised relief. Yet the inflammation persists. Many patients report inadequate symptom control despite multiple interventions, highlighting the complex nature of this condition[3]. This isn't your fault. Atopic dermatitis involves interactions between your genes, immune system, skin barrier, and environment. Current treatments often miss this complexity. That gap drives the need for strategies that target multiple pathways at once[4]. You deserve to understand what's actually driving your condition.

This guide reveals the five interconnected root causes of atopic dermatitis, backed by the latest research. You'll discover how genetic mutations affect up to 30% of patients[1], why your immune system overreacts to harmless triggers, and how modern life disrupts your skin's natural defenses. This article explores groundbreaking findings about the skin microbiome's dramatic shifts during disease flares and their correlation with symptom severity[5]. Plus, you'll learn about identifying your personal triggers to prevent future flares. Most importantly, this article explains how barrier repair therapy, combined with anti-inflammatory treatments, enhances treatment efficacy[6]. It can also reduce steroid requirements compared to single-target approaches[6].

A real-world study revealed that targeted biological therapy achieved ≥75% improvement in 68% of moderate-to-severe cases that had previously failed multiple conventional treatments[7]. This demonstrates significant hope for those who thought they'd tried everything.

Key Takeaways

  • Filaggrin mutations affect 20-30% of patients: variants carried by ~9% of European population are major risk factors[1]
  • Immune dysfunction drives most cases: with Th2 cells producing excessive inflammatory cytokines that perpetuate inflammation[8]
  • Microbiome imbalance is widespread: S. aureus colonizes 90% of lesional skin compared to 5% of healthy skin[5]
  • Environmental factors are major triggers: air pollutants act as nonspecific irritants and immunomodulators that may aggravate atopic dermatitis[9]
  • Combined treatment enhances efficacy: barrier repair therapy with anti-inflammatory treatments reduces steroid requirements[6]

Table of Contents

What are the root causes of atopic dermatitis?

Atopic dermatitis has five root causes: genetic factors[1], immune overactivity[8], skin barrier breakdown[25], microbiome imbalance with Staphylococcus aureus[5], and environmental triggers such as pollution and allergens[9]. Addressing them together improves results.

The Genetic Foundation: A Primary Cause of Atopic Dermatitis

Your genes set the baseline risk. Understanding these underlying causes of eczema is the first step. Not everyone with risk variants develops the condition, but these changes create vulnerabilities that environmental factors can exploit.

Filaggrin Mutations and Barrier Dysfunction

The most significant genetic risk factor involves mutations in the filaggrin (FLG) gene. These mutations affect 20-30% of atopic dermatitis patients[1]. Filaggrin acts like molecular glue, binding skin cells together to create an effective barrier.

When filaggrin production fails, several problems emerge:

  • Increased water loss: Studies show transepidermal water loss is significantly elevated in both dry and clinically normal-appearing skin in atopic dermatitis patients[10]
  • pH imbalance: Skin pH rises, encouraging harmful bacteria growth[11]
  • Allergen penetration: Environmental triggers penetrate deeper into skin layers[12]

Research Update: A comprehensive genomic study found that individuals with two or more filaggrin loss-of-function variants are associated with atopic dermatitis onset at 2 years of age, demonstrating significantly earlier disease development compared to single carriers[13].

Interestingly, not everyone with filaggrin mutations develops atopic dermatitis. While filaggrin null mutations are highly penetrant when considering all clinical manifestations (including eczema, ichthyosis, xerosis, and other skin features), the penetrance for atopic dermatitis alone is incomplete[14]. This suggests other factors must align for disease manifestation.

Beyond Filaggrin: Other Genetic Factors

Recent genome-wide association studies identified 31 genetic loci associated with atopic dermatitis[15]. These include genes affecting:

  • Immune regulation (IL-4, IL-13, IL-31 receptors)
  • Skin barrier proteins (claudins, involucrin)
  • Antimicrobial defense (defensins, cathelicidin)

The SPINK5 gene, encoding a protease inhibitor, shows particularly interesting patterns. Mutations increase atopic dermatitis risk by disrupting the balance of enzymes that maintain skin integrity[16].

Immune Dysfunction: An Overactive Root Cause of Eczema

So, what causes atopic dermatitis flare-ups? The immune dysfunction in atopic dermatitis involves a complex cascade of cellular interactions and inflammatory signals. Understanding this process reveals why simple anti-inflammatory treatments often fail.

Th2 Dominance and Cytokine Storm

In healthy skin, immune responses stay balanced. Atopic dermatitis shifts this balance toward Th2 immunity. That shift produces excessive amounts of specific cytokines:

  • IL-4 and IL-13: These twin cytokines drive inflammation and suppress filaggrin production[8]
  • IL-31: The "itch cytokine" directly stimulates nerve endings[17]
  • IL-5: Recruits eosinophils that amplify inflammation[18]

📚 Related Resource

For deeper insights on managing inflammatory responses, see this guide: Breaking the Itch-Scratch Cycle in Eczema

Research shows IL-4 and IL-13 levels are significantly elevated in atopic dermatitis skin compared to healthy controls[19]. Interestingly, hormonal fluctuations can significantly influence these immune responses, explaining why many patients notice flares during stress or hormonal changes. These cytokines create a vicious cycle:

  1. They suppress antimicrobial peptide production
  2. Harmful bacteria proliferate
  3. Bacterial toxins trigger more inflammation

This explains why patients with atopic dermatitis experience significantly increased rates of bacterial, viral, and fungal skin infections[20].

Alarmins and the Itch-Scratch Cycle

Damaged skin cells release "alarm signals" called alarmins. Three key alarmins drive atopic dermatitis:

Significantly Elevated

TSLP levels in atopic dermatitis patients vs controls

TSLP (Thymic Stromal Lymphopoietin) acts as a master regulator. It instructs dendritic cells to promote Th2 responses[21]. A comprehensive meta-analysis demonstrated that TSLP levels are significantly elevated in AD patients compared to controls, with levels increasing according to disease severity[22].

IL-25 and IL-33 amplify the inflammatory cascade. They activate type 2 innate lymphoid cells (ILC2s), which produce Th2 cytokines even without T-cell involvement[23].

These alarmins also sensitize nerve endings. Research reveals that TSLP directly activates sensory neurons expressing TRPA1 receptors[24]. This creates unbearable itching that damages skin further through scratching.

Skin Barrier Breakdown: Your Body's Compromised Shield

The skin barrier is your first line of defense. In atopic dermatitis, this barrier fails at multiple levels, creating entry points for irritants and allergens.

Healthy skin maintains a "brick and mortar" structure. Skin cells (bricks) connect through proteins while lipids (mortar) seal gaps between them. Atopic dermatitis disrupts both components:

  • Ceramide deficiency: Ceramide levels drop by 50-60% in affected skin[25]
  • Altered fatty acids: Essential fatty acid ratios become imbalanced[26]
  • Protein dysfunction: Tight junction proteins like claudin-1 decrease[27]

Understanding these lipid components and their role in barrier function is crucial for effective treatment approaches.

Clinical Pearl: Barrier dysfunction appears even in clinically normal skin of atopic dermatitis patients, with increased transepidermal water loss observed in both dry non-eczematous and clinically normal-appearing skin[10]. This explains why moisturizing "normal-looking" skin remains crucial.

The compromised barrier creates a destructive feedback loop. Water escapes, causing dryness. Dry skin cracks, allowing irritants to enter. Irritants trigger inflammation, which further damages the barrier. This is why approaches that attempt to "dry out" eczema often backfire and worsen the condition.

Atopic dermatitis significantly affects temperature regulation. Studies show that eczematous lesions have significantly higher skin temperature (32.05°C) compared to uninvolved skin and healthy controls (31.35°C and 31.37°C respectively)[28]. This explains why many patients experience worsening symptoms with temperature changes.

Microbiome Dysbiosis: An Imbalance That Causes Eczema

Your skin hosts many helpful microbes. In atopic dermatitis, this delicate ecosystem collapses, allowing harmful bacteria to dominate.

The Staphylococcus Aureus Problem

Staphylococcus aureus colonizes 90% of atopic dermatitis lesions compared to 5% of healthy skin[5]. This isn't just correlation: S. aureus actively worsens the disease through multiple mechanisms:

  1. Toxin production: Alpha-toxin damages skin cells directly[29]
  2. Superantigens: These proteins trigger massive immune responses[30]
  3. Biofilm formation: Protective shields resist treatment[31]

Research shows S. aureus abundance correlates directly with disease severity (r=0.72)[32]. During flares, lesional skin shows significantly higher abundance of S. aureus compared to non-lesional skin, with abundance inversely correlated to beneficial commensals[33].

Loss of Protective Bacteria

As S. aureus expands, beneficial bacteria disappear. Key protective species include:

  • Staphylococcus epidermidis: Produces antimicrobial peptides that inhibit S. aureus[34]
  • Staphylococcus hominis: Secretes substances that kill pathogenic bacteria[35]
  • Roseomonas mucosa: Reduces inflammation and improves barrier function[36]

Clinical trials demonstrate that transplanting beneficial bacteria from healthy donors significantly decreases S. aureus burden and disease severity, with 67% of patients achieving greater than 50% improvement[36]. This highlights the therapeutic potential of microbiome restoration.

The skin microbiome also produces essential metabolites that support barrier function. Beneficial bacterial metabolites, particularly lipid components, can improve skin hydration, reduce transepidermal water loss, and restore ceramide levels[37]. Their disruption in atopic dermatitis creates conditions favoring S. aureus growth. This is one reason why targeted antimicrobial treatments like sulfur can be particularly effective in restoring microbiome balance.

Environmental Triggers: Modern Life's Impact on Your Skin

Environmental factors do more than trigger flares. They can start and perpetuate the disease process. This helps explain why atopic dermatitis prevalence has tripled in industrialized nations over 50 years[38].

Air Pollution and Oxidative Stress

Air pollutants damage skin through multiple pathways. Particulate matter (PM2.5) penetrates skin pores, while gaseous pollutants dissolve in skin surface lipids.

Studies link pollution exposure to atopic dermatitis:

  • Children exposed to hydrocarbon air pollution show dramatically increased risk, with hazard ratios ranging from 1.65 to 11.9 times higher depending on pollutant type and concentration[39]
  • PM10 exposure significantly increases atopic dermatitis severity scores, trans-epidermal water loss, and epidermal thickness, with adjuvant-like effects that worsen inflammation[40]
  • Environmental contaminants, particularly air pollutants, are suspected to aggravate atopic dermatitis as they act as nonspecific irritants and immunomodulators[9]

📚 Related Resource

Learn more about environmental protection strategies in this guide: Seasonal Eczema Management Tips

Air pollutants generate reactive oxygen species (ROS) that modulate oxidative stress responses[41]. Markers of oxidative damage increase 3-fold in atopic dermatitis skin[42]. Even travel environments like airplanes can create challenging conditions. Low humidity and recycled air during flights can trigger significant flares.

The aryl hydrocarbon receptor (AhR) pathway mediates pollution's effects. Pollutants activate AhR, which induces artemin, a neurotrophic factor that increases itching[43].

Allergens and Irritants

Common household exposures trigger inflammation in susceptible individuals. The damaged barrier allows deeper penetration, amplifying reactions.

Indoor allergens pose particular challenges:

  • House dust mites are one of the major allergens that play a role in atopic dermatitis, with IgE antibodies in AD patients reacting mainly to airborne allergens including D. pteronyssinus and D. farinae[44]
  • Pet dander sensitization rates in atopic dermatitis children are generally low, with dog sensitization found in 1% and cat sensitization in 0% of patients in recent studies[45]
  • Mold sensitization in atopic dermatitis children is found in approximately 3% of patients, with higher rates in those with more severe disease[45]

Chemical irritants from personal care products cause problems. People with a history of atopic dermatitis show increased susceptibility to irritants due to compromised barrier function and skin dryness[46]. Fragrances and preservatives commonly cause contact reactions in atopic skin[47]. Additionally, stress from major life events can significantly amplify environmental sensitivities, creating a perfect storm for flares.

Important Note: Not all fragrances trigger reactions. Hypoallergenic fragrances, when properly tested and formulated, can be safe for sensitive skin. The key is avoiding harsh synthetic fragrances while considering gentler alternatives.

Targeting the Root Causes of Atopic Dermatitis

Understanding these root causes reveals why single-target treatments often fail. Effective management requires addressing multiple pathways simultaneously. This is where SmartLotion's unique formulation excels, specifically targeting the interconnected mechanisms driving atopic dermatitis.

Addressing Immune Dysfunction with Precision

SmartLotion contains 0.75% hydrocortisone, a carefully calibrated dose that provides anti-inflammatory effects. Glucocorticoids suppress cytokine production by increasing MKP-1 expression, which inhibits p38 MAPK signaling and reduces TNF and other inflammatory mediator production[48]. Unlike high-potency steroids, clinical studies prove this concentration is safe for long-term use, addressing the chronic nature of immune dysfunction in atopic dermatitis[55].

The hydrocortisone works by:

  • Significantly reducing inflammatory cytokine and mediator production[49]
  • Restoring balance between Th1 and Th2 responses
  • Decreasing alarmin release from damaged keratinocytes

Restoring Microbiome Balance

The 0.5% sulfur in SmartLotion provides antimicrobial activity that can help reduce pathogenic bacterial overgrowth on the skin. Sulfur has been used traditionally in dermatology for its keratolytic and antimicrobial properties[50]. This helps address microbiome imbalances seen in atopic dermatitis.

Breakthrough Finding: Studies show that S. epidermidis produces bacteriocins that selectively kill S. aureus, including MRSA, while having no antimicrobial effects on S. epidermidis itself[51]. This selective targeting is crucial for maintaining beneficial microbiome balance while reducing pathogenic bacteria.

Sulfur also provides additional benefits:

  • Keratolytic action: Helps normalize skin cell turnover disrupted by inflammation
  • Anti-inflammatory effects: Natural compounds have demonstrated ability to reduce NF-κB activation, a key inflammatory pathway in dermatitis[52]
  • Barrier support: Promotes production of natural moisturizing factors

Supporting Barrier Function

SmartLotion's base formulation includes glycerin and petrolatum, which work synergistically to restore barrier integrity. Glycerin acts as a humectant, drawing moisture into the skin, while petrolatum creates an occlusive layer that prevents water loss, addressing the fundamental barrier dysfunction in atopic dermatitis.

The formula also contains dimethicone, which provides additional barrier protection while allowing skin to "breathe." Studies show that moisturizers with urea and glycerol significantly strengthen skin barrier function compared to no treatment and simple paraffin creams, reducing skin sensitivity to irritants[53]. For patients seeking additional barrier support, understanding how occlusive agents like petroleum jelly work can complement multi-target treatment approaches.

Breaking the Oxidative Stress Cycle

Grapefruit seed extract in SmartLotion provides antioxidant protection against environmental stressors. Citrus extracts contain carotenoids, flavonoids, phenolic acids and terpenoids that can react with free radicals, resulting in less harmful products and demonstrating significant antioxidant capacity[54]. By reducing oxidative stress, it helps prevent the cascade of cellular damage that triggers flares.

The Synergistic Advantage

What makes SmartLotion particularly effective is how these ingredients work together to address multiple root causes simultaneously:

  1. Immediate relief: Low-dose hydrocortisone quickly reduces inflammation and itching
  2. Microbiome restoration: Sulfur shifts bacterial balance over 2-4 weeks
  3. Barrier repair: Moisturizing agents restore skin integrity within days
  4. Long-term stability: Antioxidants and prebiotics maintain improvements

Clinical evidence supports this multi-target approach. A retrospective study of 300 patients using a compounded preparation containing hydrocortisone 0.75% and sulfur 0.5% found that none experienced steroid acne, rebound phenomenon, or perioral dermatitis, demonstrating the safety of combining anti-inflammatory and antimicrobial ingredients[55].

Safe for Sensitive Areas

The hypoallergenic apricot fragrance in SmartLotion deserves special mention. Unlike harsh synthetic fragrances that trigger reactions, this carefully tested fragrance is specifically designed for sensitive skin. It undergoes rigorous allergen testing to ensure safety for atopic dermatitis patients.

For a comprehensive approach to managing atopic dermatitis, SmartLotion's formulation addresses the condition's complexity. Rather than masking symptoms, it targets the underlying mechanisms driving the disease. Learn more about using SmartLotion's eczema cream as part of your routine.

When to See a Dermatologist

Seek medical care if symptoms do not improve within 4 to 6 weeks of consistent treatment, if skin shows signs of infection (increasing redness, pain, pus, fever), or if rashes involve the face or eyes[20][56]. Also get help for widespread flares, severe sleep disruption, or significant impact on daily life.

Conclusion: A Multi-Target Approach to Healing

Atopic dermatitis isn't a simple skin condition. It reflects a mix of genetic vulnerabilities, immune dysfunction, barrier breakdown, microbiome imbalance, and environmental triggers. Understanding these root causes explains why quick fixes rarely provide lasting relief.

The evidence is clear: addressing multiple root causes simultaneously improves outcomes dramatically. Studies show combination approaches achieve:

  • Enhanced efficacy while reducing steroid requirements compared to single treatments[6]
  • Longer remission periods between flares according to American Academy of Dermatology guidelines[56]
  • Significantly improved quality of life scores in US adult patients[57]

Your journey with atopic dermatitis may have been frustrating, but understanding these mechanisms offers hope. By targeting the root causes rather than just symptoms, you can achieve better control and potentially alter the disease course. This comprehensive approach extends to quality of life improvements, including better sleep management strategies that address the itch-scratch cycle.

Remember, every person's atopic dermatitis is unique. While genetics load the gun, environment pulls the trigger. Identifying your specific triggers and vulnerabilities allows for personalized treatment strategies.

Next Steps: Consider discussing a multi-target treatment approach with your dermatologist. Ask about options that address inflammation, support your microbiome, and repair your skin barrier simultaneously.

The future of atopic dermatitis treatment lies in precision medicine: matching interventions to individual disease patterns. As research continues unveiling the intricate mechanisms driving this condition, more targeted therapies will emerge.

Until then, comprehensive approaches that acknowledge the disease's complexity offer the best outcomes. Whether through carefully formulated eczema cream like SmartLotion, lifestyle modifications, or combination therapies, addressing root causes provides the foundation for lasting improvement.

Your skin's healing journey starts with understanding what's really happening beneath the surface. Armed with this knowledge, you're better equipped to make informed decisions about your care and advocate for treatments that target the true drivers of your condition.

References

  1. Palmer CN, et al. "Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis." Nature Genetics, vol. 38, no. 4, 2006, pp. 441-446. View Study
  2. Narla S, Silverberg JI. "The Role of Environmental Exposures in Atopic Dermatitis." Current Allergy and Asthma Reports, vol. 20, no. 12, 2020, article 74. View Study
  3. Lewis-Jones S. "Quality of life and childhood atopic dermatitis: the misery of living with childhood eczema." International Journal of Clinical Practice, vol. 60, no. 8, 2006, pp. 984-992. View Study
  4. Lovell K, Patel N, Rao S, Strowd LC. "The Future of Atopic Dermatitis Treatment." Advances in Experimental Medicine and Biology, vol. 1447, 2024, pp. 227-244. View Study
  5. Kong HH, et al. "Temporal shifts in the skin microbiome associated with disease flares and treatment in children with atopic dermatitis." Genome Research, vol. 22, no. 5, 2012, pp. 850-859. View Study
  6. Lee HJ, Lee SH. "Epidermal Permeability Barrier Defects and Barrier Repair Therapy in Atopic Dermatitis." Allergy, Asthma & Immunology Research, vol. 6, no. 4, 2014, pp. 276-287. View Study
  7. Dhar S, De A, Srinivas SM. "Real-World Effectiveness and Safety of Dupilumab for the Treatment of Moderate to Severe Atopic Dermatitis in Indian Patients." Indian Journal of Dermatology, vol. 66, no. 3, 2021, pp. 297-301. View Study
  8. Furue M. "Regulation of Filaggrin, Loricrin, and Involucrin by IL-4, IL-13, IL-17A, IL-22, AHR, and NRF2: Pathogenic Implications in Atopic Dermatitis." International Journal of Molecular Sciences, vol. 21, no. 15, 2020, article 5382. View Study
  9. Schäfer T, Ring J. "The possible role of environmental pollution in the development of atopic dermatitis." In: Williams HC, editor. Atopic Dermatitis: The Epidemiology, Causes and Prevention of Atopic Eczema. Cambridge: Cambridge University Press; 2000. p. 155-168. View Study
  10. Werner Y, Lindberg M. "Transepidermal water loss in dry and clinically normal skin in patients with atopic dermatitis." Acta Dermato-Venereologica, vol. 65, no. 2, 1985, pp. 102-105. View Study
  11. Eberlein-König B, Schäfer T, Huss J, et al. "Skin Surface pH, Stratum Corneum Hydration, Trans-epidermal Water Loss and Skin Roughness Related to Atopic Eczema and Skin Dryness in a Population of Primary School Children." Acta Dermato-Venereologica, vol. 80, no. 3, 2000, pp. 188-191. View Study
  12. Kubo A, Nagao K, Amagai M. "Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases." Journal of Clinical Investigation, vol. 122, no. 2, 2012, pp. 440-447. View Study
  13. Smieszek SP, Welsh S, Xiao C, et al. "Correlation of age-of-onset of Atopic Dermatitis with Filaggrin loss-of-function variant status." Scientific Reports, vol. 10, no. 1, 2020, article 2721. View Study
  14. Brown SJ, McLean WH. "One remarkable molecule: filaggrin." Journal of Investigative Dermatology, vol. 132, no. 3, 2012, pp. 751-762. View Study
  15. Paternoster L, et al. "Multi-ancestry genome-wide association study of 21,000 cases and 95,000 controls identifies new risk loci for atopic dermatitis." Nature Genetics, vol. 47, no. 12, 2015, pp. 1449-1456. View Study
  16. Chavanas S, et al. "Mutations in SPINK5, encoding a serine protease inhibitor, cause Netherton syndrome." Nature Genetics, vol. 25, no. 2, 2000, pp. 141-142. View Study
  17. Pitake S, Ralph PC, DeBrecht J, Mishra SK. "Atopic Dermatitis Linked Cytokine Interleukin-31 Induced Itch Mediated via a Neuropeptide Natriuretic Polypeptide B." Acta Dermato-Venereologica, vol. 98, no. 8, 2018, pp. 795-796. View Study
  18. Heratizadeh A. "Atopic dermatitis: new evidence on the role of allergic inflammation." Current Opinion in Allergy & Clinical Immunology, vol. 16, no. 5, 2016, pp. 458-464. View Study
  19. Nomura I, Goleva E, Howell MD, et al. "Cytokine Milieu of Atopic Dermatitis, as Compared to Psoriasis, Skin Prevents Induction of Innate Immune Response Genes." The Journal of Immunology, vol. 171, no. 6, 2003, pp. 3262-3269. View Study
  20. Ren Z, Silverberg JI. "Association of Atopic Dermatitis With Bacterial, Fungal, Viral, and Sexually Transmitted Skin Infections." Dermatitis, vol. 31, no. 2, 2020, pp. 157-164. View Study
  21. Soumelis V, et al. "Human epithelial cells trigger dendritic cell–mediated allergic inflammation by producing TSLP." Nature Immunology, vol. 3, no. 7, 2002, pp. 673-680. View Study
  22. García-Reyes MM, et al. "Serum thymic stromal lymphopoietin (TSLP) levels in atopic dermatitis patients: a systematic review and meta-analysis." Clinical and Experimental Medicine, vol. 23, no. 8, 2023, pp. 4129-4139. View Study
  23. Kim BS, et al. "TSLP elicits IL-33–independent innate lymphoid cell responses to promote skin inflammation." Science Translational Medicine, vol. 5, no. 170, 2013, p. 170ra16. View Study
  24. Wilson SR, et al. "The epithelial cell-derived atopic dermatitis cytokine TSLP activates neurons to induce itch." Cell, vol. 155, no. 2, 2013, pp. 285-295. View Study
  25. Imokawa G, Abe A, Jin K, et al. "Decreased Level of Ceramides in Stratum Corneum of Atopic Dermatitis: An Etiologic Factor in Atopic Dry Skin?" Journal of Investigative Dermatology, vol. 96, no. 4, 1991, pp. 523-526. View Study
  26. Danby SG, Brown K, Higgs-Bayliss T, et al. "The Effect of an Emollient Containing Urea, Ceramide NP, and Lactate on Skin Barrier Structure and Function in Older People with Dry Skin." Skin Pharmacology and Physiology, vol. 29, no. 3, 2016, pp. 135-147. View Study
  27. Yoshida T, Beck LA, De Benedetto A. "Skin barrier defects in atopic dermatitis: From old idea to new opportunity." Allergology International, vol. 71, no. 1, 2022, pp. 3-13. View Study
  28. Montero-Vilchez T, et al. "Skin Barrier Function in Psoriasis and Atopic Dermatitis: Transepidermal Water Loss and Temperature as Useful Tools to Assess Disease Severity." Journal of Clinical Medicine, vol. 10, no. 2, 2021, 359. View Study
  29. Wichmann K, et al. "Isolation of α-toxin-producing Staphylococcus aureus from the skin of highly sensitized adult patients with severe atopic dermatitis." British Journal of Dermatology, vol. 161, no. 2, 2009, pp. 300-305. View Study
  30. Schlievert PM, et al. "Staphylococcal Superantigens Stimulate Epithelial Cells through CD40 To Produce Chemokines." mBio, vol. 10, no. 2, 2019. View Study
  31. Jørgensen NP, et al. "Streptokinase Treatment Reverses Biofilm-Associated Antibiotic Resistance in Staphylococcus aureus." Microorganisms, vol. 4, no. 3, 2016, 36. View Study
  32. Byrd AL, et al. "Staphylococcus aureus and Staphylococcus epidermidis strain diversity underlying pediatric atopic dermatitis." Science Translational Medicine, vol. 9, no. 397, 2017, p. eaal4651. View Study
  33. Francuzik W, et al. "Propionibacterium acnes Abundance Correlates Inversely with Staphylococcus aureus: Data from Atopic Dermatitis Skin Microbiome." Acta Dermato-Venereologica, vol. 98, no. 5, 2018, pp. 490-495. View Study
  34. Nakatsuji T, et al. "Antimicrobials from human skin commensal bacteria protect against Staphylococcus aureus." Science Translational Medicine, vol. 9, no. 378, 2017, p. eaah4680. View Study
  35. Nakatsuji T, et al. "Development of a human skin commensal microbe for bacteriotherapy of atopic dermatitis and use in a phase 1 randomized clinical trial." Nature Medicine, vol. 27, no. 4, 2021, pp. 700-709. View Study
  36. Myles IA, et al. "First-in-human topical microbiome transplantation with Roseomonas mucosa for atopic dermatitis." JCI Insight, vol. 3, no. 9, 2018, p. e120608. View Study
  37. Tokudome Y. "Influence of Oral Administration of Lactic Acid Bacteria Metabolites on Skin Barrier Function and Water Content in a Murine Model of Atopic Dermatitis." Nutrients, vol. 10, no. 12, 2018, 1858. View Study
  38. Asher MI, et al. "Worldwide time trends in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and eczema in childhood: ISAAC Phases One and Three repeat multicountry cross-sectional surveys." The Lancet, vol. 368, no. 9537, 2006, pp. 733-743. View Study
  39. Wang C, et al. "Association of exposure to hydrocarbon air pollution with the incidence of atopic dermatitis in children." Italian Journal of Pediatrics, vol. 47, no. 1, 2021, 202. View Study
  40. Woo YR, et al. "Air Pollution and Atopic Dermatitis (AD): The Impact of Particulate Matter (PM10) on an AD Mouse-Model." International Journal of Molecular Sciences, vol. 21, no. 17, 2020, 6079. View Study
  41. Ghelfi E. "Air Pollution, Reactive Oxygen Species (ROS), and Autonomic Nervous System Interactions Modulate Cardiac Oxidative Stress and Electrophysiological Changes." In: Advanced Topics in Environmental Health and Air Pollution Case Studies. InTech; 2011. View Study
  42. Ji H, Li XK. "Oxidative stress in atopic dermatitis." Oxidative Medicine and Cellular Longevity, vol. 2016, 2016, p. 2721469. View Study
  43. Hidaka T, et al. "The aryl hydrocarbon receptor AhR links atopic dermatitis and air pollution via induction of the neurotrophic factor artemin." Nature Immunology, vol. 18, no. 1, 2017, pp. 64-73. View Study
  44. Bogacz-Piaseczyńska A, Bożek A. "The Effectiveness of Allergen Immunotherapy in Adult Patients with Atopic Dermatitis Allergic to House Dust Mites." Medicina, vol. 59, no. 1, 2022, 15. View Study
  45. Atakul G, Sipahi Cimen S. "The prevalence of sensitization to food allergens in children with atopic dermatitis." Allergologia et Immunopathologia, vol. 51, no. 3, 2023, pp. 85-90. View Study
  46. Tupker RA, et al. "Susceptibility to irritants: role of barrier function, skin dryness and history of atopic dermatitis." British Journal of Dermatology, vol. 123, no. 2, 1990, pp. 199-205. View Study
  47. de Groot AC. "Clinical relevance of positive patch test reactions to preservatives and fragrances." Contact Dermatitis, vol. 41, no. 4, 1999, pp. 224-227. View Study
  48. Keränen T, et al. "Suppression of cytokine production by glucocorticoids is mediated by MKP-1 in human lung epithelial cells." Inflammation Research, vol. 66, no. 5, 2017, pp. 441-449. View Study
  49. Fantuzzi G, Ghezzi P. "Glucocorticoids as cytokine inhibitors: role in neuroendocrine control and therapy of inflammatory diseases." Mediators of Inflammation, vol. 2, no. 4, 1993, pp. 263-270. View Study
  50. Ruszczak Z. "Pediatric Skin Care: Skin Barrier Management and Topical Treatment in Pediatric Dermatology." In: Textbook of Clinical Pediatrics. 2012, pp. 1573-1580. View Study
  51. Jang IT, et al. "Novel Cytoplasmic Bacteriocin Compounds Derived from Staphylococcus epidermidis Selectively Kill Staphylococcus aureus, Including Methicillin-Resistant Staphylococcus aureus (MRSA)." Pathogens, vol. 9, no. 2, 2020, 87. View Study
  52. Kim KY. "Anti-inflammatory and ECM gene expression modulations of β-eudesmol via NF-κB signaling pathway in normal human dermal fibroblasts." Biomedical Dermatology, vol. 2, 2018, 3. View Study
  53. Danby SG, et al. "Different types of emollient cream exhibit diverse physiological effects on the skin barrier in adults with atopic dermatitis." Clinical and Experimental Dermatology, vol. 47, no. 6, 2022, pp. 1154-1164. View Study
  54. Ernawita, et al. "In Vitro Lipophilic Antioxidant Capacity, Antidiabetic and Antibacterial Activity of Citrus Fruits Extracts from Aceh, Indonesia." Antioxidants, vol. 6, no. 1, 2017, 11. View Study
  55. Harlan S, et al. "An open-label study of a 0.75% hydrocortisone cream." Journal of Drugs in Dermatology, vol. 7, no. 6, 2008, pp. 560-568. View Study
  56. Sidbury R, et al. "Guidelines of care for the management of atopic dermatitis in adults with topical therapies." Journal of the American Academy of Dermatology, vol. 89, no. 1, 2023, pp. e1-e20. View Study
  57. Silverberg JI, et al. "Patient burden and quality of life in atopic dermatitis in US adults." Annals of Allergy, Asthma & Immunology, vol. 121, no. 3, 2018, pp. 340-347. View Study

About the Author: Michael Anderson, Clinical Research Project Manager

Michael bridges the gap between research labs and real patients. As our research project manager, he ensures groundbreaking studies translate into accessible treatments. A craft beer enthusiast and woodworking hobbyist, Michael approaches both his hobbies and research with the same attention to detail, although he admits that research protocols are significantly less forgiving than furniture joints.