Addressing The Root Cause Of Eczema with Functional Medicine Dermatology
Recently, I discovered a fantastic training on eczema treatment from a functional medicine dermatology perspective. If you’ve followed my journey healing from severe eczema and psoriasis, you already know I don’t believe eczema is "just a skin problem" and I'm trying to heal from the inside out. This training provided a really solid foundation for understanding the root cause of eczema and how to treat it holistically. I was especially happy to see that they went into specifics about what tests to run and how to chart a course of action based on the results.
Over the last few years, I’ve gone deep into the gut–immune–skin connection. Recently, I studied a comprehensive functional dermatology training by Dr. Greenberg that lays out a full “root-cause” blueprint for eczema treatment.
Here is the training video from Dr. Greenberg from Root Cause Dermatology:
👉 https://www.youtube.com/watch?v=QU8nWOm-wB8
This article is my notes from this training.
Core Philosophy
Functional medicine dermatology does not suppress symptoms with pharmaceuticals. The goal is to:
- Identify and treat the root cause
- Restore function to the body
- Achieve lasting clearance, not managed suppression
Pathophysiology of Eczema
What Is Eczema?
- "Atopic dermatitis" — atopic = allergic; dermatitis = skin inflammation
- Fundamentally a disease of Skin Barrier Dysfunction + deep systemic inflammation
- Not just a surface issue — the inflammation is internal and systemic
Immune Pathways Involved
Eczema is not driven by a single immune pathway. Multiple T-helper cell pathways are involved:
| Pathway | Trigger | Key Cytokines |
|---|---|---|
| Th2 (primary) | Allergens, fungi, worms | IL-4, IL-5, IL-13 |
| Th1 | Intracellular bacteria, viruses, protozoa | — |
| Th17 | Extracellular bacteria/fungi at mucocutaneous sites (gut, respiratory) | — |
| Th22 | Elevated in ALL chronic inflammatory skin conditions | — |
Key insight: Eczema has multiple subtypes (similar to breast cancer subtypes). European, Asian, African, and pediatric patient groups show different Th1/Th17 involvement profiles. Psoriasis has NO Th2 component — this is the primary distinguishing factor.
Leaky Skin: The Allergy Driver
How Leaky Skin Creates Food Allergies
- Normal intact skin prevents allergen entry — dendritic cells stay quiet
- Damaged/eczematous skin has breached barriers — allergens (dust mites, food proteins) penetrate
- Dendritic cells activate → present novel proteins to immune system → drives Th2 allergic response
- This is how eczema causes food allergies, not just the reverse
Evidence
- Food sensitization is 6x more likely in children with eczema vs. without
- Neonatal skin barrier dysfunction at birth predicts food allergies by age 2
- Children with skin barrier defects are more likely to develop asthma
- Recreated experimentally in mice: skin injury + protein exposure → eczema lesions, IgE + IgG antibodies, even anaphylaxis
The Atopic Triad / Atopic March
Eczema → Food Allergy → Asthma (both life-threatening)
- ~1/3 of children with early-onset eczema progress through this march
- Clearing eczema early can stop the atopic march — this is potentially life-saving
Food Triggers
Top 5 Food Groups Responsible for ~75% of Food-Induced Flares
- Dairy (all mammal milk — cow, goat, sheep, camel — no exceptions)
- Eggs
- Wheat/Gluten
- Soy
- Peanuts
These can trigger via IgE (true allergy) OR IgG/IgA (food sensitivity/delayed reaction).
Practical Approach to Food
- Dairy elimination is universal — applied to 100% of eczema patients regardless of allergy test results. No eczema patient benefits from dairy.
- Elimination diet for the other 5 groups is case-by-case
- Most patients already know their triggers — don't over-engineer the food piece
- ~2/3 of eczema patients show NO sensitization to food or environmental allergens — food elimination alone won't clear them
Clinical warning: Don't get stuck on food. If dietary changes aren't getting full resolution, move on to gut investigation. Food is one lever, not the whole answer.
Notes on Gluten
- Anti-gliadin IgA elevated on stool testing = clear reason to remove gluten
- Wheat challenge study: 13/18 eczema kids flared with wheat, and all 13 had positive IgE to gliadin/gluten
Bonus: Chronic Ear Infections
- Strong clinical overlap between eczema and recurrent ear infections
- Embryologically, middle ear/eustachian tube shares origins with the digestive system
- IGG food testing in chronic ear infection patients (n=44): 70% reacted to milk, 43% to gluten, 27% egg, 7% soy — mirrors eczema triggers exactly
- Try eliminating top food allergens before considering tympanostomy tubes
The Gut-Skin Axis
Why the Gut Matters
- The gut is one of the body's largest mucocutaneous sites
- Gut dysbiosis drives systemic inflammation — the engine behind eczema
- Eczema patients consistently show altered microbiome profiles
Microbiome Findings in Eczema Patients
Lower levels of beneficial bacteria:
- Bifidobacteria
- Bacteroides
- Phyla Bacteroidetes
Higher levels of pathogenic bacteria:
- C. diff
- E. coli
- Staph aureus (also over-colonizes the skin AND nose in eczema patients)
Fungal overgrowth:
- Candida albicans — statistically significant correlation with IgE antibodies to candida in eczema patients; anti-fungal treatment improves skin
Leaky Gut in Eczema
- The majority of eczema patients have increased intestinal permeability (leaky gut)
- Positive association: more leaky gut = more severe eczema
- Mechanism: degraded mucosal barrier → gut cells exposed to bacteria/fungi/food proteins → tight junctions fail → LPS (endotoxin from gram-negative bacteria) enters bloodstream → dendritic cells activate → systemic inflammation → triggers Th1, Th17, Th2
Butyrate — Critical for Gut Integrity
Short-chain fatty acid (SCFA) produced by beneficial bacteria (Faecalibacterium prausnitzii, Clostridium butyricum, Roseburia):
- Primary fuel for enterocytes (intestinal cells)
- Calms the immune system, suppresses inflammatory cytokines
- Strengthens tight junctions
- Research: Severity of eczema inversely correlates with microbiome diversity and butyrate-producing bacteria
Key butyrate producers to assess: Faecalibacterium prausnitzii, Roseburia, Akkermansia muciniphila (mucosal barrier protector)
Two Primary "Eczema Gut Profiles"
Profile 1: Dysbiosis with Candida (Most Common)
- High Staph aureus and Streptococcus
- High Candida overgrowth
- Low/absent Akkermansia muciniphila
- Low/absent Faecalibacterium prausnitzii, Roseburia (butyrate producers)
- Low secretory IgA → leaky gut picture
Profile 2: H. pylori + Protozoa
- H. pylori present (gram-negative, LPS-producing, biofilm-forming)
- Protozoa present (Blastocystis hominis, Giardia, Endolimax nana, Dientamoeba fragilis, etc.)
- H. pylori neutralizes stomach acid via urease → impairs digestion, kills protective acidity → enables protozoa to colonize
- Creates sub-optimal digestion: pancreatic enzyme signaling disrupted, bile secretion impaired
- Triggers Th1 inflammatory pathway
- Connection to: acne, rosacea, psoriasis as well
Additional Finding: Morganella
- Morganella morganii = high histamine producer
- Elevated in gut → drives Th2 itchy response
- Treat the morganella to reduce histamine (preferred over low-histamine diets as a long-term fix)
Functional Medicine Testing Protocol
Universal Baseline Tests (Every Patient)
-
GI-MAP Stool Test (Diagnostic Solutions)
- Bacterial profiles: H. pylori, commensal, opportunistic, pathogenic
- Fungi/yeast (partial — supplemented by OAT)
- Parasites, protozoa, worms, viruses
- Fat in stool (digestive dysfunction marker)
- Pancreatic elastase (enzyme production)
- Short-chain fatty acids (butyrate)
- Inflammatory markers: Calprotectin, Lactoferrin, Secretory IgA
- Permeability markers: Zonulin
-
OAT — Organic Acids Test (Mosaic Diagnostics, urine test, ~74 metabolites)
- Primary purpose: Yeast and fungal markers (stool testing insufficient for fungi)
- Arabinose = marker for Candida overgrowth
- Oxalic acid = byproduct of Candida metabolism (almost always high with Candida)
- Additional metabolite insights across nutrient status, mitochondrial function, etc.
- Clinical rule: Without the OAT, you're looking at half the picture
Additional Tests (As Indicated)
- Dutch Hormone Test
- Mycotoxin Testing
- Environmental Toxin Panel
Treatment Framework
Treatment Prioritization (Clinical Note)
In the classroom: treat H. pylori first (it's upstream, affects stomach acid)
In clinical practice: don't start with H. pylori — dosing is demanding (empty stomach required). Start with dysbiosis/candida to reduce inflammation and show early improvement, then address H. pylori in a subsequent plan.
Patient follow-up cadence: every 2–3 months, with updated protocols each visit.
Targeted Interventions by Finding
H. pylori:
- Mastic gum
- DGL (deglycyrrhizinated licorice)
- Berberine + Saccharomyces boulardii
Bacterial overgrowth (Staph, Strep, dysbiosis):
- Coptis (berberine-rich herb)
- Oregano oil
- Olive leaf
- Garlic
- Antimicrobial herbal blends
Fungal/Candida overgrowth:
- Rosemary
- Pau d'Arco
- Uva ursi
- Antifungal herbal blends
Protozoa/Parasites:
- Artemisia (wormwood)
- Black walnut
- Anti-parasitic herbal protocols
Leaky gut / mucosal restoration:
- Akkermansia probiotic (Pendulum brand)
- Clostridium butyricum probiotic (Pendulum brand)
- Fiber — target: 35 grams/day in adults (build up gradually)
- Prebiotics (cranberry, pomegranate-based) to encourage Faecalibacterium prausnitzii, Roseburia regrowth
General support (all patients):
- Multivitamin
- 4 core probiotics (adults)
- Anti-inflammatory foods: omega-3s (fish oil if not fish-allergic), fiber, clams
Dietary Protocol
- Remove dairy universally (100% of eczema patients)
- Elimination of top 5 food groups if indicated — not permanent, test for 4–6 weeks
- Remove gluten if anti-gliadin IgA elevated on testing
- Increase fiber, omega-3s, anti-inflammatory foods
- Nightshades: ~50% of patients report worsening — individualize
Topical Approach
Address topically in parallel with gut work, but topical alone is insufficient:
- Treat skin microbiome (Staph aureus overgrowth is almost universal on eczematous skin)
- Treat nasal colonization of Staph aureus
- Support filaggrin protein production (key for dry/leaky skin phenotype — filaggrin gene mutations common in early-onset eczema)
- Wet/oozing eczema = likely Staph aureus superinfection; may need short-term topical mupirocin or oral antibiotics (Keflex, doxycycline)
Case Study: "Tina" — Severe Adult Eczema
Presentation: 34F, eczema since infancy, severe flare x6 months, failed 5 steroids (including clobetasol — 600x strength of hydrocortisone), on montelukast, unable to work
GI-MAP Findings:
- H. pylori positive
- Akkermansia muciniphila: absent (leaky gut indicator)
- Bacteroidetes/Firmicutes overgrowth (dysbiosis)
- Morganella at E7 (high histamine producer)
- Staph aureus + Streptococcus elevated
- Blastocystis hominis (protozoa — expected given H. pylori)
- Anti-gliadin IgA: elevated → gluten must go
OAT Findings:
- Arabinose: elevated → Candida overgrowth
- Oxalic acid: elevated → confirms Candida
Treatment Plan (across multiple 2-3 month plans):
- H. pylori protocol: mastic gum, DGL, berberine
- Bacterial overgrowth: antimicrobial herbs (coptis, oregano, olive leaf, garlic)
- Anti-fungal herbs (rosemary, Pau d'Arco, uva ursi)
- Anti-parasitic herbs: artemisia, black walnut
- Akkermansia probiotic
- 4 core probiotics + multivitamin
- Fiber increase → 35g/day target
- Gluten removal
- Topical protocol (concurrent)
Outcomes:
- 2 months: Massive improvement, sleeping through the night
- 5 months: Continued clearing
- 7 months: Near complete resolution including lichenified plaques (popliteal fossa, hands, abdomen)
- Post-inflammatory pigmentation resolved with time once scratching stopped
Clinical Pearls
- "Bucket" mental model: Disease emerges when total inflammatory/toxic load overflows the body's capacity to compensate. Many inputs fill the bucket; the goal is to drain it from below.
- Probiotics alone rarely clear eczema — 2019 systematic review of 44 studies: 50/50 results. Too many variables (strain, dose, duration). Probiotics are a tool, not a solution.
- Chronic antibiotic use creates either "desert wasteland" gut (nothing surviving) or opportunistic overgrowth (C. diff, Pseudomonas). Functional medicine approach breaks the antibiotic cycle.
- Treat all pathogens found on testing, even if asymptomatic — broad-spectrum herbal protocols clean them up as a byproduct of treatment.
- Low-histamine diets = symptom control, not root cause — better to identify and eliminate the histamine-producing bacteria (e.g., Morganella). Add Mast Cell stabilization herbs (quercetin, vitamin C) while investigating root cause.
- Vaginal birth + breastfeeding = optimal microbiome seeding for infants, but C-section/formula-fed children are not predetermined for eczema — use testing to determine actual gut status.
- The skin repairs itself once the underlying drivers are cleared — hyperpigmentation and hypopigmentation resolve over time.
Key Tests to Order
| Test | Lab | Purpose |
|---|---|---|
| GI-MAP | Diagnostic Solutions | Full gut microbiome, H. pylori, parasites, inflammation |
| OAT (Organic Acids Test) | Mosaic Diagnostics | Candida/yeast, metabolic overview |
| Dutch Hormone Test | Dutch/Precision Analytics | Hormonal contributors |
| Mycotoxin Panel | Great Plains / Mosaic | Mold exposure |
| IgE Food Allergy Panel | Standard lab | True food allergies (especially in infants/children) |
| IgG/IgA Food Sensitivity | Various | Delayed food reactions |
Conditions Treated With This Framework
This gut-first approach applies broadly beyond eczema:
- Psoriasis (all types: guttate, palmar, scalp)
- Acne (including cystic/nodulocystic)
- Rosacea
- Seborrheic dermatitis
- Alopecia areata / hair loss
- Keratosis pilaris
All are fundamentally chronic systemic inflammatory conditions rooted in gut dysbiosis and immune dysregulation.