Targeting Gut Dysbiosis and Short-Chain Fatty Acid Deficiency in Chronic Eczema: A Case Report

June 16, 2026 Dick Benson 2026 AIC 0

Stephanie Daboub, BA; Emma J. Norton, ND, IFMCP; Sabrina Brakke, BS, BA; Samantha Wessel, BS; Alexandra Currell, BS

 

Stephanie Daboub, BA, Fourth Year Naturopathic Medical Student; Emma J. Norton, ND, IFMCP, Associate Professor; Sabrina Brakke, BA, Fourth Year Naturopathic Medical Student; Samantha Wessel, BS, Fourth Year Naturopathic Medical Student; Alexandra Currell, BS, Fourth Year Naturopathic Medical Student; Bastyr University, San Diego, CA, USA.

 

Corresponding author: Stephanie Daboub, BA

E-mail: stephanie.daboub@bastyr.edu

 

Keywords: Atopic dermatitis, Gut-skin axis, Dysbiosis, Short-chain fatty acids, Functional medicine.

 

 

Introduction

Atopic dermatitis (eczema) is a chronic inflammatory skin disorder characterized by pruritic, relapsing lesions that significantly impair quality of life. Conventional therapies target cutaneous inflammation, providing incomplete relief to many patients. Emerging evidence supports the gut-skin axis as a contributor to chronic dermatologic disease, with alterations in gut microbiota composition, reduced short-chain fatty acid (SCFA) production, and gram-negative bacterial overgrowth, thus promoting systemic inflammation through impaired intestinal barrier function and endotoxin-mediated immune activation.1,2 SCFAs, particularly butyrate, play an essential role in epithelial integrity and immune regulation.3

 

Case Report

Main Concerns, Diagnoses, and Important Clinical Findings of Patient

This case report describes a 36-year-old female with biopsy-confirmed, treatment-refractory eczema of four years’ duration involving the face, neck, torso, and extremities. Verbal informed consent for publication was obtained from the patient. At baseline, she reported severe pruritus requiring moisturizer application every two hours and sleep limited to four to five hours nightly. Stool analysis revealed low total SCFAs at 18.0 µmol/g (reference range: ≥ 23.3 µmol/g), low n-butyrate at 3.2 µmol/g (reference range: ≥ 3.6 µmol/g), reduced butyrate-producing bacteria, and 4+ overgrowth of Klebsiella pneumoniae and Citrobacter species.

A phased, gut-directed protocol emphasizing dietary fiber, prebiotic foods, targeted antimicrobial botanicals, and gut barrier support was initiated. At four-week follow-up, the patient reported 80% improvement in eczema severity, flattening of lesions, >50% reduction in moisturizer use, and restoration of seven to eight hours of uninterrupted sleep.

Antecedents, triggers, and mediators were identified to contextualize the root causes of disease. Antecedents included early life stress, formula feeding, recurrent childhood respiratory infections, secondhand smoke exposure, and significant psychosocial trauma, suggesting immune vulnerability and stress-mediated dysregulation. Reported triggers included gluten intake, mold and rodent exposure in the home, recurrent antibiotic use, and emotional stress preceding eczema onset and flares. Mediators and perpetuating factors included gut dysbiosis with gram-negative bacterial overgrowth, low SCFA production, and sleep disruption secondary to pruritus.

 

Interventions and Outcomes

Following receipt of comprehensive stool analysis, anti-tissue transglutaminase (IgA), and total IgA laboratory results on week 9, a phased gastrointestinal protocol was initiated to address intestinal dysbiosis, impaired microbial fermentation, and systemic inflammation, which contribute to eczema.4 The protocol emphasized dietary, botanical, and nutraceutical strategies to restore enterocyte integrity and immune balance. Table 1 summarizes the therapeutic agents, dosing schedule, and safety considerations across 3 visits. The patient began a daily, structured antimicrobial phase using a broad-spectrum botanical antimicrobial blend (Table 1) to target gram-negative bacterial overgrowth, including Klebsiella pneumoniae and Citrobacter species.5-10 A gastrointestinal binder (Table 1) was initiated with timing separation to minimize adsorption interference and support clearance of microbial byproducts.11,12

The patient was instructed to consume at least 25 g of soluble fermentable fiber daily to support SCFA production. Colonic microbiota ferment these fibers into butyrate, which supports mucosal energy metabolism, barrier integrity, and immune homeostasis (Table 1).13-15 Further, prebiotic-rich foods such as legumes, lentils, and quinoa were prescribed to selectively nourish SCFA-producing commensal bacteria and promote microbial fermentation, enhancing endogenous SCFA generation and gut eubiosis.13-15 Given the patient’s history of symptom provocation with gluten, dairy, and red meat, avoiding these was recommended to minimize potential immune-mediated inflammatory triggers. The patient was also encouraged to increase polyphenol-rich foods to support microbiome diversity and microbial metabolite production (including SCFAs), while reducing oxidative stress and proinflammatory signaling.16,17

A daily water intake target of 3 L was prescribed to support stool hydration, motility, and regular bowel elimination.18 Additional nutritional support was provided via an anti-inflammatory medical food with a complete vitamin-mineral profile to address increased macro- and micronutrient requirements in the setting of gastrointestinal inflammation and potential malabsorption, while supporting immune regulation and mucosal repair. (Table 1).19-22

For sleep disruption secondary to nocturnal pruritus, a targeted botanical sleep formula was initiated to support sleep onset and reduce inflammation associated with sleep deprivation. The formulation contains botanicals selected to promote GABAergic activity, circadian regulation, and stress reduction (Table 1).23-26 Additional sleep hygiene interventions were not emphasized initially due to the severity of pruritus-related sleep interruption, with priority placed on reducing inflammatory burden and nocturnal itching, the primary drivers of sleep disturbance.

 

Table 1. Therapeutic Agents, Doses, Safety, Risks

Visit Therapeutic agents/interventions (generic) Dose/schedule Safety/risks
Initial VisitDietary intervention: strict gluten elimination until next visitDiet: continuous gluten avoidanceGluten-free diet: ensure nutritional adequacy (fiber, micronutrients)
Week 9Nutrition/lifestyle program: 25 g fiber/d, increased prebiotic foods, avoid gluten/dairy/red meat, 3 L water/d, nutrient-dense smoothies, legume/quinoa + lean poultry meals

Botanical antimicrobial liquid (broad-spectrum) with titration: (Bilberry; grape seed; shiitake; goldenseal; noni; garlic; white willow; milk thistle; echinacea (purpurea, angustifolia); raspberry; black walnut (hull, leaf); lavender oil; oregano oil; galbanum oil; tea tree oil; fumitory; gentian 53 mg/drop)

GI binder/detox capsule taken away from food/medications: (Zeolite clay; activated charcoal; aloe vera leaf extract; apple pectin; bamboo shoot/leaf extract; humic powder 500 mg/capsule)

Anti-inflammatory medical food powder: (per 2 scoops/37 g: ALA 400 mg; curcumin blend 250 mg (curcuminoids 100 mg) + fenugreek galactomannans; hops extract blend 250 mg (xanthohumol standardized); quercetin 200 mg; rosemary 100 mg; ginger 100 mg)

Sleep-support capsules: (per 3 capsules): passionflower 450 mg; lemon balm 300 mg; hops 300 mg; valerian 225 mg; California poppy 225 mg; L-theanine 150 mg; lavender oil 60 mg; melatonin 0.75 mg

Fiber: 25 g/d. Water: 3 L/d

Antimicrobial liquid: Day 1 1 drop TID before meals; Day 2 2 drops TID; Day 3 3 drops TID; Day 4 4 drops TID; Day 5 5 drops TID; Day 6 6 drops TID; titrate to Day 8 8 drops TID Binder: 1 capsule AM on empty stomach; separate from food/supplements/medications ≥1 h Medical food: 2 scoops daily

Sleep support: 3 capsules before bed

Potential for herb–drug interactions (e.g., anticoagulants/antiplatelets); avoid in pregnancy/lactation; ethanol-containing liquid. Herxheimer reactions- headaches, bloating, change in bowel movements, abdominal discomfort, fatigue, rash High-fiber/prebiotic increase may cause gas/bloating; introduce gradually with hydration

Binder may reduce absorption of oral medications/supplements if not separated; constipation possible Sleep formula: additive sedation with alcohol/CNS depressants; next-day drowsiness

Week 14Continue: fiber goal, prebiotic foods, hydration, medical food powder, smoothies, diet pattern (legumes/quinoa + lean poultry), avoid gluten/dairy/red meat; sleep support as needed

D/c botanical antimicrobial liquid and GI binder after bottles completed

Initiate berberine botanical complex (Barberry 400 mg; Oregon grape 400 mg; goldenseal 100 mg (standardized to 5% total alkaloids) incl berberine, hydrastine, canadine)

Add L-glutamine powder 3 g/serving

Algal omega-3: (per 2 softgels, total omega-3 715 mg; EPA 195 mg; DHA 390 mg)

Hyperpigmentation adjunct: red light therapy

Berberine complex: 2 capsules TID

L-glutamine: 3 g daily

Algal omega-3: 2 softgels TID

Red light therapy: parameters not specified

 

Berberine: avoid in pregnancy/lactation; review interactions (e.g., hypoglycemics, anticoagulants; CYP/P-gp substrates); monitor for GI intolerance Omega-3: caution with anticoagulants/bleeding risk L-glutamine: caution in advanced hepatic/renal disease contexts Photobiomodulation: screen photosensitizing medications/conditions; use eye protection

 

Abbreviations: ALA, alpha-linolenic acid; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; GI, gastrointestinal; TID, 3 times daily

 

At week 14, the patient transitioned to Phase 2 of the protocol, replacing the initial broad-spectrum botanical antimicrobial with a berberine-containing botanical extract (Table 1).5 L-glutamine was added to support intestinal barrier repair,27 and algal-derived omega-3 fatty acids were prescribed in divided doses to provide anti-inflammatory support (Table 1).28 Red light therapy was recommended for residual hyperpigmentation.29 A follow-up telephone call approximately 4.5 months after protocol initiation revealed complete resolution of eczema with no recurrence of symptoms. Repeat stool analysis was not performed since laboratory reassessment was not clinically indicated.

The patient reported 80% reduction in eczema severity within four weeks of a phased, functional medicine-based, gut-directed protocol.30 This highlights the clinical relevance of addressing dysbiosis in refractory atopic dermatitis.31 In this biopsy-confirmed case, baseline comprehensive stool analysis revealed low total SCFAs (18 mmol/kg) and low n-butyrate concentration (3.2 mmol/kg), reduced butyrate-producing bacteria, and 4+ overgrowth of Klebsiella pneumoniae and Citrobacter species. Given the central role of SCFAs in maintaining epithelial barrier integrity and immune regulation, and the capacity of gram-negative bacterial overgrowth to amplify inflammatory signaling through lipopolysaccharide-mediated tight junction disruption,32 interventions were selected to restore microbial fermentation, reduce pathogenic burden, and support gut repair.

Hence, this case demonstrates a clinically meaningful temporal association between correction of gut microbial imbalance and improvement in cutaneous and sleep outcomes, supporting the gut–skin axis as a potential therapeutic target.33

 

Conclusion

Refractory atopic dermatitis (eczema) is a chronic inflammatory skin disorder that significantly impairs the quality of life. The gut-skin axis contributes significantly to chronic dermatologic disease.

This case demonstrated the gut–skin axis as a potential therapeutic target and significantly reduced eczema severity within four weeks of a phased, functional medicine-based, gut-directed protocol. While causal conclusions cannot be drawn from a single case, and post-treatment stool testing was not performed, the observed clinical response supports further controlled investigation of microbiome-directed strategies in treatment-resistant atopic dermatitis.

 

Funding

This research received no external funding.

References

  1. Pessôa R, Clissa PB, Sanabani SS. The interaction between the host genome, epigenome, and the gut-skin axis microbiome in atopic dermatitis. Int J Mol Sci. 2023;24(18):14322. doi:10.3390/ijms241814322
  2. Rios-Carlos M, Cervantes-García D, Córdova-Dávalos LE, Bermúdez-Humarán LG, Salinas E. Unraveling the gut-skin axis in atopic dermatitis: exploiting insights for therapeutic strategies. Gut Microbes. 2024;16(1):2430420. doi:10.1080/19490976.2024.2430420
  3. Singh V, Lee G, Son H, et al. Butyrate producers, “The Sentinel of Gut”: their intestinal significance with and beyond butyrate, and prospective use as microbial therapeutics. Front Microbiol. 2023;13:1103836. doi:10.3389/fmicb.2022.1103836
  4. Sanchez-Lopez MF, Barrero-Caicedo PA, Olmos-Carval HM, Torres-Medina AF, Alzate-Granados JP. Relationship between skin and gut microbiota dysbiosis and inflammatory skin diseases in adult patients: A systematic review. Microbe. 2025;7:100342. doi:10.1016/j.microb.2025.100342
  5. Zhou H, Wang W, Cai L, Yang T. Potentiation and mechanism of berberine as an antibiotic adjuvant against multidrug-resistant bacteria. Infect Drug Resist. 2023;16:7313-7326. doi:10.2147/IDR.S431256
  6. Kwiatkowski P, Sienkiewicz M, Pruss A, et al. Antibacterial and anti-biofilm activities of essential oil compounds against New Delhi metallo-β-lactamase-1-producing uropathogenicKlebsiella pneumoniae strains. Antibiotics (Basel). 2022;11(2):147. doi:10.3390/antibiotics11020147
  7. Fournomiti M, Kimbaris A, Mantzourani I, et al. Antimicrobial activity of essential oils of cultivated oregano (Origanum vulgare), sage (Salvia officinalis), and thyme (Thymus vulgaris) against clinical isolates of Escherichia coli, Klebsiella oxytoca, and Klebsiella pneumoniae.Microb Ecol Health Dis. 2015;26(0):23289. doi:10.3402/mehd.v26.23289
  8. Ankri S, Mirelman D. Antimicrobial properties of allicin from garlic. Microbes Infect. 1999;1(2):125-129. doi:10.1016/S1286-4579(99)80003-3
  9. Abidullah M, Jadhav P, Sujan SS, Shrimanikandan AG, Reddy CR, Wasan RK. Potential antibacterial efficacy of garlic extract on Staphylococcus aureus, Escherichia coli, and Klebsiella pneumoniae: an in vitro study. J Pharm Bioallied Sci. 2021;13(suppl 1):S590-S594. doi:10.4103/jpbs.JPBS_681_20
  10. Majdi C, Duvauchelle V, Meffre P, Benfodda Z. An overview on the antibacterial properties of juglone, naphthazarin, plumbagin and lawsone derivatives and their metal complexes. Biomed Pharmacother. 2023;162:114690. doi:10.1016/j.biopha.2023.114690
  11. Du XN, Niu Z, Zhou GZ, Li ZM. Effect of activated charcoal on endotoxin adsorption. Part I. An in vitro study. Biomater Artif Cells Artif Organs. 1987;15(1):229-235. doi:10.3109/10731198709118523
  12. Schaumberger S, Ladinig A, Reisinger N, Ritzmann M, Schatzmayr G. Evaluation of the endotoxin binding efficiency of clay minerals using the Limulus Amebocyte lysate test: an in vitro study. AMB Express. 2014;4(1):1. doi:10.1186/2191-0855-4-1
  13. Liu XF, Shao JH, Liao YT, et al. Regulation of short-chain fatty acids in the immune system. Front Immunol. 2023;14:1186892. doi:10.3389/fimmu.2023.1186892
  14. Tan JK, Macia L, Mackay CR. Dietary fiber and SCFAs in the regulation of mucosal immunity. J Allergy Clin Immunol. 2023;151(2):361-370. doi:10.1016/j.jaci.2022.11.007
  15. McLoughlin RF, Berthon BS, Jensen ME, Baines KJ, Wood LG. Short-chain fatty acids, prebiotics, synbiotics, and systemic inflammation: a systematic review and meta-analysis. Am J Clin Nutr. 2017;106(3):930-945. doi:10.3945/ajcn.117.156265
  16. Bolte LA, Vich Vila A, Imhann F, et al. Long-term dietary patterns are associated with pro-inflammatory and anti-inflammatory features of the gut microbiome. Gut. 2021;70(7):1287-1298. doi:10.1136/gutjnl-2020-322670
  17. Yap YA, Mariño E. An insight into the intestinal web of mucosal immunity, microbiota, and diet in inflammation. Front Immunol. 2018;9:2617. doi:10.3389/fimmu.2018.02617
  18. Popkin BM, D’Anci KE, Rosenberg IH. Water, hydration, and health. Nutr Rev. 2010;68(8):439-458. doi:10.1111/j.1753-4887.2010.00304.x
  19. Morvaridzadeh M, Fazelian S, Agah S, et al. Effect of ginger (Zingiber officinale) on inflammatory markers: A systematic review and meta-analysis of randomized controlled trials. Cytokine. 2020;135:155224. doi:10.1016/j.cyto.2020.155224
  20. Kasprzak-Drozd K, Niziński P, Hawrył A, et al. Potential of curcumin in the management of skin diseases. Int J Mol Sci. 2024;25(7):3617. doi:10.3390/ijms25073617
  21. Karuppagounder V, Arumugam S, Thandavarayan RA, Sreedhar R, Giridharan VV, Watanabe K. Molecular targets of quercetin with anti-inflammatory properties in atopic dermatitis. Drug Discov Today. 2016;21(4):632-639. doi:10.1016/j.drudis.2016.02.011
  22. la Torre RS, Ureña-Paniego C, Arias-Santiago S, Montero-Vílchez T. Impact of the Mediterranean diet and physical activity on the severity of atopic dermatitis. Dermatitis. 2025;17103568251376645:17103568251376645. doi:10.1177/17103568251376645
  23. Bent S, Padula A, Moore D, Patterson M, Mehling W. Valerian for sleep: a systematic review and meta-analysis. Am J Med. 2006;119(12):1005-1012. doi:10.1016/j.amjmed.2006.02.026
  24. Guadagna S, Barattini DF, Rosu S, Ferini-Strambi L. Plant extracts for sleep disturbances: A systematic review. Evid Based Complement Alternat Med. 2020;2020(1):3792390. doi:10.1155/2020/3792390
  25. Cruz-Sanabria F, Bruno S, Crippa A, et al. Optimizing the time and dose of melatonin as a sleep-promoting drug: A systematic review and dose-response meta-analysis. J Pineal Res. 2024;76(5):e12985. doi:10.1111/jpi.12985
  26. Bulman A, D’Cunha NM, Marx W, Turner M, McKune A, Naumovski N. The effects of L-theanine consumption on sleep outcomes: A systematic review and meta-analysis. Sleep Med Rev. 2025;81:102076. doi:10.1016/j.smrv.2025.102076
  27. Abbasi F, Haghighat Lari MM, Khosravi GR, Mansouri E, Payandeh N, Milajerdi A. A systematic review and meta-analysis of clinical trials on the effects of glutamine supplementation on gut permeability in adults. Amino Acids. 2024;56(1):60. doi:10.1007/s00726-024-03420-7
  28. Lin JY, Ma LJ, Yuan JP, Yu P, Bai BX. Causal effects of fatty acids on atopic dermatitis: A Mendelian randomization study. Front Nutr. 2023;10:1083455. doi:10.3389/fnut.2023.1083455
  29. Molla A. A comprehensive review of phototherapy in atopic dermatitis: Mechanisms, modalities, and clinical efficacy. Cureus. 2024;16(3):e56890. doi:10.7759/cureus.56890
  30. Beidelschies M, Alejandro-Rodriguez M, Ji X, Lapin B, Hanaway P, Rothberg MB. Association of the functional medicine model of care with patient-reported health-related quality-of-life outcomes. JAMA Netw Open. 2019;2(10):e1914017. doi:10.1001/jamanetworkopen.2019.14017
  31. Wrześniewska M, Wołoszczak J, Świrkosz G, Szyller H, Gomułka K. The role of the microbiota in the pathogenesis and treatment of atopic dermatitis—A literature review. Int J Mol Sci. 2024;25(12):6539. doi:10.3390/ijms25126539
  32. Guo S, Nighot M, Al-Sadi R, Alhmoud T, Nighot P, Ma TY. Lipopolysaccharide regulation of intestinal tight junction permeability is mediated by TLR-4 signal transduction pathway activation of FAK and MyD88. J Immunol. 2015;195(10):4999-5010. doi:10.4049/jimmunol.1402598
  33. Zhao Y, Zhang X, Wang Y, et al. The gut-skin axis: emerging insights in understanding and treating skin diseases through gut microbiome modulation [review]. Exp Ther Med. 2023;26(4):466. doi:10.3892/etm.2023.12163
  34. Zhao Y, Yu C, Zhang J, Yao Q, Zhu X, Zhou X. The gutskin axis: emerging insights in understanding and treating skin diseases through gut microbiome modulation (Review). [Review]. Int J Mol Med. 2025;56(6):210. doi:10.3892/ijmm.2025.5651
  35. Zhao Y, Yu C, Zhang J, Yao Q, Zhu X, Zhou X. The gutskin axis: emerging insights in understanding and treating skin diseases through gut microbiome modulation (Review). [Review]. Int J Mol Med. 2025;56(6):210. doi:10.3892/ijmm.2025.5651

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