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Skin, Hair & Nails

Eczema

Comprehensive integrative medicine approach for lasting healing and complete recovery

15,000+ Patients
DHA Licensed
Root Cause Focus
95% Success Rate

Understanding Eczema

Eczema, also known as atopic dermatitis, is a chronic inflammatory skin condition that causes intense itching, dry skin, and recurring rashes. It results from a defective skin barrier that allows moisture to escape and irritants to enter, combined with an overactive immune response. This condition often begins in early childhood and can persist into adulthood, frequently co-occurring with asthma and allergic rhinitis.

Key Symptoms

Recognizing Eczema

Common symptoms and warning signs to look for

Intense itching (pruritus) - especially at night, often before the rash appears

Dry, scaly skin - rough texture that cracks and flakes

Red, inflamed patches - typically on flexural surfaces (elbows, knees, neck)

Thickened, leathery skin - from chronic scratching (lichenification)

Weeping or oozing blisters - when scratched, leading to crust formation

What a Healthy System Looks Like

In a healthy individual, the skin barrier functions as the body's primary defense: The stratum corneum (outermost layer) maintains optimal hydration through properly organized corneocytes and intercellular lipids that prevent transepidermal water loss (TEWL). The epidermal tight junctions prevent allergen and pathogen penetration. The skin microbiome maintains a diverse community of beneficial bacteria (Staphylococcus epidermidis, Cutibacterium acnes) that outcompete pathogenic organisms. Resident immune cells (Langerhans cells, dermal dendrocytes) mount appropriate defensive responses without triggering excessive inflammation. The skin's natural moisturizing factor (NMF) - derived from filaggrin degradation - maintains optimal skin pH (5.5) and hydration. keratinocyte turnover is balanced, and the skin heals rapidly without scarring when damaged.

Mechanism

How the Condition Develops

Understanding the biological mechanisms

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Atopic dermatitis involves multi-system dysfunction: (1) Filaggrin deficiency - FLG gene mutations reduce filaggrin production, leading to impaired barrier function, increased TEWL, and decreased NMF; (2) Stratum corneum dysfunction - Abnormal lipid composition (reduced ceramides, cholesterol, free fatty acids) compromises the 'mortar and brick' structure, allowing water loss and allergen penetration; (3) Th2-mediated inflammation - Allergen exposure triggers IL-4, IL-5, IL-13, and IL-31 release from Th2 cells, driving eosinophilic infiltration and intense pruritus; (4) IgE elevation - Class-switching to IgE antibodies creates sensitization to environmental allergens, with mast cell and basophil degranulation releasing histamine, tryptase, and cytokines; (5) Epidermal barrier disruption - Tight junction dysfunction (claudin-1 deficiency) allows paracellular allergen passage; (6) Microbiome imbalance - Reduced microbial diversity, particularly Staphylococcus aureus colonization (80% of AD patients), triggers inflammation through superantigens and exotoxins; (7) Itch-scratch cycle - IL-31 (the 'itch cytokine') activates sensory nerves, triggering scratch that further damages the barrier; (8) Neuroimmune dysregulation - Increased nerve density and altered neuropeptide release amplify itch perception.

Lab Values

Key Laboratory Markers

Important values for diagnosis and monitoring

TestNormal RangeOptimalSignificance
Total Serum IgE<100 IU/mL<30 IU/mLElevated in 80% of AD patients; correlates with disease severity and atopic comorbidities; values >1000 IU/mL suggest severe atopy
Blood Eosinophils<500 cells/mcL<150 cells/mcLEosinophilia common in AD; elevated counts indicate Th2-driven inflammation and predict disease severity
IL-4 (Interleukin-4)<10 pg/mL<5 pg/mLKey Th2 cytokine elevated in AD; drives IgE class-switching and eosinophil recruitment
IL-13 (Interleukin-13)<10 pg/mL<5 pg/mLCentral cytokine in AD pathogenesis; promotes瘙痒, barrier dysfunction, and Th2 inflammation
IL-31 (Interleukin-31)<50 pg/mL<20 pg/mLPrimary itch cytokine; elevated levels correlate with pruritus severity and disease activity
25-Hydroxy Vitamin D30-100 ng/mL50-80 ng/mLVitamin D modulates immune function and skin barrier; deficiency associated with increased AD severity
Serum Zinc60-120 mcg/dL80-120 mcg/dLZinc essential for wound healing and immune function; deficiency impairs barrier repair
Transepidermal Water Loss (TEWL)<10 g/m²/h<8 g/m²/hDirect measure of barrier function; elevated TEWL indicates compromised stratum corneum
Root Causes

Root Causes We Address

The underlying factors contributing to your condition

{"cause":"Genetic Filaggrin Deficiency","contribution":"30-50% of moderate-severe AD - FLG gene mutations (R501X, 2282del4) cause filaggrin deficiency leading to impaired barrier function, increased TEWL, and reduced NMF; inherited in autosomal dominant pattern with incomplete penetrance","assessment":"Genetic testing for FLG mutations; family history of atopy; early-onset severe AD suggests genetic etiology"}

{"cause":"Skin Barrier Dysfunction","contribution":"Universal in AD - Abnormal epidermal lipid composition (reduced ceramides 1, 3, 6-II), impaired corneocyte desquamation, and tight junction defects allow allergen penetration and water loss","assessment":"TEWL measurement; skin pH testing; lipid panel analysis; clinical assessment of xerosis severity"}

{"cause":"Immune Dysregulation (Th2 Dominance)","contribution":"Core mechanism - IL-4, IL-5, IL-13, IL-31 drive eosinophilic inflammation, IgE class-switching, and pruritus; impaired Th1 response reduces antimicrobial defense","assessment":"Serum IgE levels; eosinophil count; cytokine panels (IL-4, IL-13, IL-31); patch testing"}

{"cause":"Environmental Allergens","contribution":"60-80% of cases - Dust mites (Dermatophagoides pteronyssinus, D. farinae), pollen, pet dander, mold spores, and cockroach allergens penetrate defective barrier and trigger IgE-mediated inflammation","assessment":"Skin prick testing; serum specific IgE panel; environmental assessment of home"}

{"cause":"Microbiome Imbalance","contribution":"80% of AD patients have S. aureus colonization - Superantigens (toxic shock syndrome toxin-1, staphylococcal enterotoxins) trigger massive inflammation; reduced microbial diversity loses competitive inhibition","assessment":"Skin swab cultures; microbiome sequencing; clinical assessment of infected eczema lesions"}

{"cause":"Nutritional Deficiencies","contribution":"30-40% of cases - Vitamin D deficiency impairs immune regulation and barrier repair; zinc deficiency delays wound healing; omega-3 deficiency reduces anti-inflammatory mediators","assessment":"Serum 25-OH vitamin D; zinc levels; omega-3 index; dietary history"}

{"cause":"Psychological Stress and Emotional Factors","contribution":"Significant contributor - Stress activates HPA axis and sympathetic nervous system, releasing CRH, cortisol, and neuropeptides (substance P) that trigger itch and worsen inflammation; stress-induced scratching intensifies itch-scratch cycle","assessment":"Stress history; Perceived Stress Scale; itch diary; identification of emotional triggers"}

{"cause":"Food Sensitivities and Allergies","contribution":"30-40% of cases, especially in children - IgE-mediated (immediate) and non-IgE-mediated (delayed) reactions to cow's milk, eggs, peanuts, soy, wheat, fish; food challenges confirm diagnosis","assessment":"Food-specific IgE testing; elimination diets; oral food challenges under medical supervision"}

{"cause":"Climate and Environmental Factors","contribution":"Environmental triggers - Low humidity (winter, air conditioning), extreme temperatures, hard water (high calcium) strip skin lipids; UV exposure has variable effects (some benefit, some worsen)","assessment":"Climate history; seasonal pattern analysis; water hardness testing"}

Warning

Risks of Inaction

What happens if left untreated

{"complication":"Secondary Skin Infections","timeline":"Ongoing risk","impact":"Compromised barrier allows bacterial (Staphylococcus aureus, Streptococcus pyogenes), viral (HSV eczema herpeticum), and fungal invasion; recurrent infections increase antibiotic resistance and healthcare costs; eczema herpeticum can be life-threatening"}

{"complication":"Sleep Deprivation and Cognitive Impairment","timeline":"Chronic","impact":"Nocturnal pruritus causes average 2+ hours sleep loss per night; children lose 1+ hours of learning time daily; chronic sleep debt increases accident risk, impairs concentration, and worsens mood disorders"}

{"complication":"Psychological Morbidity","timeline":"Chronic, progressive","impact":"AD patients have 2-3x higher rates of anxiety and depression; visible lesions cause social stigma; 30% report significant quality of life impact; children experience bullying and social exclusion"}

{"complication":"Atopic March Progression","timeline":"Months to years","impact":"50% of children with moderate-severe AD develop asthma (3-4x increased risk); 40% develop allergic rhinitis; early intervention may interrupt this progression"}

{"complication":"Permanent Skin Changes and Scarring","timeline":"Years of chronic disease","impact":"Chronic scratching causes lichenification, skin thickening, permanent pigment changes (hypopigmentation or hyperpigmentation), and scarring; affects self-esteem long-term"}

{"complication":"Workplace and Social Impairment","timeline":"Ongoing","impact":"AD causes more lost workdays than any other skin condition; visible lesions limit career choices (customer-facing roles); social activities curtailed; relationship strain"}

{"complication":"Treatment Burden and Healthcare Costs","timeline":"Lifetime","impact":"Average AD patient spends $2000+ annually on treatments, prescriptions, and doctor visits; emergency visits for infected eczema; indirect costs from lost productivity"}

Diagnostics

How We Diagnose

Comprehensive assessment methods we use

{"test":"Comprehensive Atopic Panel","purpose":"Confirm atopic diathesis and identify triggers","whatItShows":"Total IgE, specific IgE to common allergens (dust mites, pollen, foods), eosinophil count; guides allergen avoidance and immunotherapy"}

{"test":"Cytokine Panel (IL-4, IL-13, IL-31)","purpose":"Assess Th2 inflammatory burden","whatItShows":"Elevated Th2 cytokines confirm immune-driven pathogenesis; IL-31 levels correlate with pruritus severity"}

{"test":"Skin Barrier Assessment (TEWL, pH, Hydration)","purpose":"Quantify barrier dysfunction","whatItShows":"Elevated TEWL (>15 g/m²/h) indicates impaired barrier; elevated pH (>6.0) disrupts antimicrobial function; low hydration correlates with xerosis"}

{"test":"Patch Testing","purpose":"Identify allergic contact dermatitis","whatItShows":"Identifies contact allergens (fragrances, preservatives, metals, topical antibiotics) complicating AD; essential for refractory cases"}

{"test":"Microbiome Analysis","purpose":"Assess skin bacterial diversity","whatItShows":"Reduced diversity, S. aureus dominance (>50%) indicates dysbiosis; guides probiotic and antimicrobial strategies"}

{"test":"Nutritional Assessment","purpose":"Identify deficiency-related contributors","whatItShows":"Vitamin D, zinc, omega-3 index; deficiencies impair barrier repair and immune function"}

{"test":"Genetic Testing (FLG mutations)","purpose":"Confirm genetic predisposition","whatItShows":"FLG mutations confirm hereditary barrier defect; predicts disease severity and atopic march risk"}

Treatment

Our Treatment Approach

How we help you overcome Eczema

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Healers Skin Barrier Restoration Protocol

Healers Skin Barrier Restoration Protocol

Lifestyle

Diet & Lifestyle

Recommendations for optimal recovery

Timeline

Recovery Timeline

What to expect on your healing journey

{"initialImprovement":"2-4 weeks - Reduced pruritus intensity, improved sleep quality, decreased redness and scaling, fewer scratch-induced lesions","significantChanges":"3-6 months - Marked improvement in skin barrier function (reduced TEWL), normalized skin hydration, decreased flare frequency, visible healing of chronic lesions, improved quality of life scores","maintenancePhase":"6-12 months - Sustained remission with minimal active lesions, stable barrier function, reduced treatment requirements, ability to identify and manage early warning signs of flares"}

Success

How We Measure Success

Outcomes that matter

Pruritus intensity reduced by >50% (validated itch scales)

SCORAD (Scoring Atopic Dermatitis) index improvement >50%

Transepidermal water loss reduced to <10 g/m²/h

Skin hydration restored to normal levels

Flare frequency reduced by >75%

Sleep quality restored (minimal nocturnal scratching)

No secondary infections during treatment period

Reduced topical steroid use (steroid-sparing achieved)

Improved quality of life (Eczema Area and Severity Index, DLQI)

Stable remission with maintenance therapy only

FAQ

Frequently Asked Questions

Common questions from patients

What is the best treatment for eczema?

The most effective eczema treatment combines barrier repair (regular moisturization with ceramide-rich emollients), anti-inflammatory therapy (topical corticosteroids or calcineurin inhibitors), and trigger avoidance. For moderate-severe cases, advanced treatments like dupilumab (an IL-4/IL-13 inhibitor) or JAK inhibitors may be prescribed. The key is a personalized approach addressing your specific triggers, barrier dysfunction, and inflammation. At Healers Clinic, we develop comprehensive protocols tailored to your unique pathophysiology.

Can eczema be cured permanently?

While there is no definitive cure for atopic dermatitis, it can be effectively controlled and many patients experience long periods of remission with proper treatment. Early intervention in childhood may prevent disease progression and reduce severity. Approximately 30-50% of children outgrow eczema by adolescence. With modern treatments targeting the underlying pathophysiology (barrier dysfunction, Th2 inflammation), many adults achieve near-complete control. The goal shifts from 'cure' to 'sustained remission with minimal treatment burden.'

What triggers eczema flare-ups?

Eczema flare-ups are triggered by a combination of factors: environmental allergens (dust mites, pollen, pet dander), dry skin and low humidity, hot showers/baths, sweating, stress, certain foods (in sensitive individuals), fragrances and skincare products, wool and rough fabrics, and infections. Keeping a symptom diary helps identify your personal triggers. At Healers Clinic, we use advanced testing to identify your specific triggers rather than relying on guesswork.

Is eczema related to diet?

Yes, diet can significantly impact eczema, though food triggers vary by individual. Common culprits include dairy, eggs, peanuts, soy, wheat, and fish in people with food allergies or sensitivities. Additionally, inflammatory foods (processed foods, refined sugars, excessive omega-6 oils) can worsen inflammation systemically. An elimination diet under medical supervision or food-specific IgE testing can identify your triggers. Conversely, anti-inflammatory foods (omega-3s, fruits, vegetables) and adequate vitamin D can help control inflammation.

Why does eczema itch more at night?

Nocturnal pruritus in eczema has several causes: circadian variation increases skin blood flow and temperature at night; reduced cortisol levels (which has anti-inflammatory effects) occur naturally at night; fewer distractions allow itch perception to increase; bedding warmth and sweat trigger itch; and sleep deprivation lowers itch threshold. Establishing a strict bedtime skincare routine, keeping bedroom cool, using cotton bedding, and applying moisturizer before sleep can help reduce nighttime itching.

Medical References

  1. 1.1. Boguniewicz M, Leung DY. Atopic dermatitis: a disease of altered skin barrier and immune dysregulation. Immunol Rev. 2011;242(1):233-246. doi:10.1111/j.1600-065X.2011.01027.x
  2. 2.2. Weidinger S, Beck LA, Bieber T, Kabashima K, Irvine AD. Atopic dermatitis. Nat Rev Dis Primers. 2024;10(1):52. doi:10.1038/s41572-024-00530-0
  3. 3.3. Simpson EL, Paller AS, Siegfried EC, et al. Efficacy and Safety of Dupilumab in Patients With Moderate-to-Severe Atopic Dermatitis: A Systematic Review and Meta-Analysis. JAMA Dermatol. 2020;156(10):1094-1104. doi:10.1001/jamadermatol.2020.2290

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Our integrative medicine experts are ready to help you overcome Eczema.

DHA Licensed
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15,000+ Patients