Understanding the Gut–Skin Axis
How your gut microbiome may influence eczema, and what diet has to do with it.
This article covers the following topics:
- What is the microbiome?
- How microbes influence immunity
- The impact of diet & modern living on eczema
- Can improving gut health help eczema?
Click to skip ahead to a specific section.
Looking Beyond the Skin
For years, eczema has been treated purely as a skin condition. Treatments have primarily focused on fighting what can be seen, namely suppressing the visible inflammation on the skin. But over the past two decades, advances in microbiome research have shifted that perspective dramatically.
Scientists now understand that the skin does not operate in isolation. It is part of a larger network of immune signalling, microbial communities, and barrier systems that extend throughout the body, especially into the gut. This interconnected relationship is known as the gut–skin axis, and it is changing how we think about eczema.
What Is the Microbiome?
The microbiome refers to the trillions of bacteria, viruses, and fungi that live in and on the human body. The largest and most metabolically active of these communities lives in the gastrointestinal tract.
Far from being harmful, many of these microbes are vital to human health. They help digest food, produce vitamins, regulate immune activity, and generate important metabolic compounds that our bodies cannot make alone.
The gut microbiome begins forming at birth. During delivery, a baby passes through the birth canal and is coated in microbes from the mother’s vaginal and intestinal microbiota. Babies born by caesarean section are not exposed to this same microbial transfer. Instead, their early colonisation tends to reflect microbes from the surrounding environment and human skin. Studies have shown that this can result in delayed colonisation by certain beneficial bacteria, including species of Bifidobacterium that are important for early immune education.
Feeding method further shapes this process. Breast milk not only contains nutrients, but also human milk oligosaccharides (specialised carbohydrates that feed beneficial gut bacteria) along with live microbes and immune factors that support microbial balance. Formula-fed infants can still develop healthy microbiomes, but the pattern of microbial growth often differs.
Antibiotics can also significantly disrupt the colonisation process. While antibiotics are often necessary and life-saving, they do not discriminate between harmful and beneficial bacteria. A single course, particularly in early life, can reduce microbial diversity, and repeated exposure may have longer-lasting effects. This is less of an issue for adults, whose microbiomes are usually resilient enough to recover over time. But for infants and young children, whose microbial communities are still developing, disruption can have a more pronounced effect.
Diet is the dominant force that shapes the microbiome over time. We eat to feed our microbes. Diets rich in fibre, plant diversity, and whole foods tend to support a diverse and stable microbial community, whilst diets high in ultra-processed foods and low in fibre tend to reduce diversity and favour different bacterial patterns that can provoke inflammation.
This matters a lot in the context of eczema. Our microbes produce a wide range of bioactive compounds that influence the immune system. Among the most important of these are short-chain fatty acids (SCFAs), which play a central role in maintaining gut barrier integrity and regulating inflammation throughout the body.
How Microbes Influence Immunity and the Skin
The gut and the skin are both barrier organs. They protect us from the outside world while hosting vast microbial communities and dense populations of immune cells. Communication between these organs occurs through immune signalling molecules, microbial metabolites, and circulating inflammatory mediators.
One of the most important microbial products in this system is short-chain fatty acids (SCFAs). SCFAs, including butyrate, acetate, and propionate, are produced when certain gut bacteria ferment dietary fibre. These compounds perform several critical functions:
- They provide energy for intestinal cells.
- They strengthen tight junctions between gut lining cells, maintaining barrier integrity.
- They reduce intestinal permeability (often referred to as “leaky gut”).
- They promote the development of regulatory T cells – immune cells that help keep inflammation under control.
In people with eczema, research has repeatedly shown reduced abundance of SCFA-producing bacteria such as Faecalibacterium prausnitzii, alongside altered immune signalling.
When SCFA production declines, the gut barrier becomes more permeable. Microbial fragments and inflammatory molecules can enter circulation more easily, interacting with immune cells throughout the body, including in the skin.
This kind of systemic immune activation can shift the body toward what is known as a type 2 immune response, the same inflammatory pattern commonly seen in eczema. The type 2 pathway evolved as a defence against parasites and environmental threats. It is driven by signalling molecules called cytokines, particularly interleukin-4 (IL-4) and interleukin-13 (IL-13). In eczema, however, this pathway becomes overactive in response to otherwise harmless environmental triggers.
When IL-4 and IL-13 levels rise, several things happen. These cytokines stimulate the production of IgE antibodies, recruit inflammatory cells into tissues, and increase the sensitivity of nerve fibres involved in itch. Crucially, they also suppress the production of filaggrin within skin cells. Filaggrin is essential for maintaining the strength and hydration of the outer skin barrier. When its production is reduced, the barrier becomes more permeable, allowing more water to escape and more environmental irritants to enter.
In this way, an imbalance of microbes in the gut can contribute to immune signals that weaken the skin’s structural defences. The weakened barrier then allows further environmental penetration, which reinforces the same inflammatory pathway. What begins as a shift in microbial balance ripples outward, influencing immune behaviour and barrier integrity in the skin.
Diet, Modern Living, and Adult-Onset Eczema
Modern dietary patterns have shifted dramatically over the past century. Ultra-processed foods, refined sugars, emulsifiers, and low-fibre meals have become the norm, whilst plant diversity and fibre intake has declined.
Fibre is the primary fuel source for SCFA-producing bacteria. When fibre intake drops, these microbes struggle to survive. Over time, this can reduce microbial diversity and alter the immune-regulating signals produced in the gut. This shift may help explain why eczema is common in industrialised nations and why some adults develop eczema despite having no childhood history or clear genetic predisposition.
Stress adds another layer. Chronic psychological stress influences intestinal movement and rhythm, alters microbial composition, and affects immune regulation. Sleep disruption and sedentary lifestyles also shape inflammatory tone. Together, these factors may push the immune system toward a more reactive state, creating the internal conditions in which eczema is more likely to develop.
This becomes particularly relevant when we remember that many people who develop eczema do not carry the filaggrin “loss-of-function” mutation most strongly associated with the condition. Filaggrin helps maintain the strength and hydration of the skin barrier, and reduced production can increase vulnerability, but it is not the sole explanation. The fact that eczema frequently occurs in individuals without this mutation suggests that environmental triggers and lifestyle pressures, including diet, stress, and microbial imbalance, may be sufficient to disrupt immune regulation and weaken barrier function, even in those without a clear genetic predisposition.
Can Improving Gut Health Help Eczema?
A growing body of research suggests that modifying the gut microbiome can influence eczema severity. Studies of probiotics containing Lactobacillus and Bifidobacterium strains have shown reductions in eczema severity scores in some children and adults. Other research suggests that increasing dietary fibre intake can enhance SCFA production and support regulatory immune pathways.
Foods known to promote beneficial bacteria include:
- A wide range of vegetables (especially leafy greens, carrots, beetroot)
- Legumes (lentils, chickpeas, beans)
- Whole grains (oats, barley)
- Nuts and seeds
- Fermented foods (yoghurt with live cultures, kefir, sauerkraut)
- Foods rich in prebiotic fibres (onions, garlic, leeks, asparagus)
Increasing plant diversity appears particularly important. Some research, including data from studies by ZOE, have found that people who consume around 30 different plant foods per week tend to have more diverse gut microbiomes – a marker generally associated with better metabolic and immune health.
Probiotic supplements may benefit some individuals, particularly when specific strains are selected and used consistently. However, their effects are often strain-specific and vary from person to person. Most importantly, probiotics appear to work best when combined with wider dietary improvements. Introducing beneficial bacteria without providing the fibre and plant diversity they rely on may limit their ability to take hold and produce meaningful changes.
Diet, by contrast, shapes the broader microbial ecosystem. By increasing plant variety and fibre intake, it supports entire communities of beneficial bacteria, including those that produce anti-inflammatory metabolites. This tends to create more stable and sustainable shifts in microbial balance.
However, dietary changes are not a replacement for conventional eczema treatments, especially during active or severe flares. But, over the longer term, both clinical research and patient experience suggest that improving gut health may help reduce eczema severity, decrease flare frequency, and support more stable remission when combined with appropriate medical care.
A Balanced Perspective
Eczema is a multifactorial condition. Genetic susceptibility, skin barrier integrity, immune regulation, environmental exposures, stress, and microbial balance all contribute in different ways. No single factor acts alone. Instead, eczema develops when several pressures converge – weakening the barrier, amplifying immune responses, and sustaining inflammation over time.
Gut health does not provide a complete explanation, nor does it replace the importance of dermatological care. But it does appear to sit at a central junction in this network. The gut microbiome helps regulate immune tone, influences systemic inflammation, and shapes how strongly the body reacts to environmental stimuli. When microbial balance is disrupted, immune responses may become more easily activated – and once activated, they can directly affect skin barrier proteins such as filaggrin.
The encouraging aspect of this model is that the microbiome is dynamic. Unlike our genes, it is not fixed. Our microbiomes respond to diet, movement, sleep, stress, medication use, and environment. Supporting microbial diversity through a fibre-rich, plant-diverse diet, regular physical activity, restorative sleep, and stress management may help lower the background level of immune activation that allows eczema to persist.
For some individuals, these changes may reduce flare frequency or symptom severity. For others, they may complement conventional treatment and improve overall resilience. The goal is not to replace medical therapy when it is needed, but to address one of the upstream factors that may be influencing inflammation in the first place.
By looking after the systems that regulate immune balance from within, we may be able to influence the conditions that allow eczema to develop, and hopefully find ways to reduce its persistence.
Understanding the Gut-Skin axis
Lorem ipsum dolor sit amet, consectetur adipiscing elit. Ut elit tellus, luctus nec ullamcorper mattis, pulvinar dapibus leo.
The effect of & Nutrition on Inflammation
Lorem ipsum dolor sit amet, consectetur adipiscing elit. Ut elit tellus, luctus nec ullamcorper mattis, pulvinar dapibus leo.
References
- Arrieta, M.-C., Stiemsma, L.T., Amenyogbe, N., Brown, E.M. and Finlay, B.B. (2014) ‘The intestinal microbiome in early life: health and disease’, Frontiers in Immunology, 5, p. 427.
- Bäckhed, F., Roswall, J., Peng, Y., Feng, Q., Jia, H., Kovatcheva-Datchary, P., Li, Y., Xia, Y., Xie, H., Zhong, H., Khan, M.T., Zhang, J., Li, J., Xiao, L., Al-Aama, J., Zhang, D., Lee, Y.S., Kotowska, D., Colding, C., Tremaroli, V., Yin, Y., Bergman, S., Xu, X., Madsen, L., Kristiansen, K., Dahlgren, J. and Wang, J. (2015) ‘Dynamics and stabilization of the human gut microbiome during the first year of life’, Cell Host & Microbe, 17(5), pp. 690–703.
- Dominguez-Bello, M.G., Costello, E.K., Contreras, M., Magris, M., Hidalgo, G., Fierer, N. and Knight, R. (2010) ‘Delivery mode shapes the acquisition and structure of the initial microbiota across multiple body habitats in newborns’, Proceedings of the National Academy of Sciences, 107(26), pp. 11971–11975.
- Penders, J., Thijs, C., van den Brandt, P.A., Kummeling, I., Snijders, B., Stelma, F., Adams, H., van Ree, R. and Stobberingh, E.E. (2007) ‘Gut microbiota composition and development of atopic manifestations in infancy: the KOALA Birth Cohort Study’, Gut, 56(5), pp. 661–667.
- Tamburini, S., Shen, N., Wu, H.C. and Clemente, J.C. (2016) ‘The microbiome in early life: implications for health outcomes’, Nature Medicine, 22(7), pp. 713–722.
- Cox, L.M. and Blaser, M.J. (2015) ‘Antibiotics in early life and obesity’, Nature Reviews Endocrinology, 11(3), pp. 182–190.
- Rinninella, E., Raoul, P., Cintoni, M., Franceschi, F., Miggiano, G.A.D., Gasbarrini, A. and Mele, M.C. (2019) ‘What is the healthy gut microbiota composition? A changing ecosystem across age, environment, diet, and diseases’, Microorganisms, 7(1), p. 14.
- Singh, R.K., Chang, H.-W., Yan, D., Lee, K.M., Ucmak, D., Wong, K., Abrouk, M., Farahnik, B., Nakamura, M., Zhu, T.H., Bhutani, T. and Liao, W. (2017) ‘Influence of diet on the gut microbiome and implications for human health’, Journal of Translational Medicine, 15(1), p. 73.
- Sonnenburg, E.D. and Sonnenburg, J.L. (2014) ‘Starving our microbial self: the deleterious consequences of a diet deficient in microbiota-accessible carbohydrates’, Cell Metabolism, 20(5), pp. 779–786.
- Koh, A., De Vadder, F., Kovatcheva-Datchary, P. and Bäckhed, F. (2016) ‘From dietary fiber to host physiology: short-chain fatty acids as key bacterial metabolites’, Cell, 165(6), pp. 1332–1345.
- Parada Venegas, D., De la Fuente, M.K., Landskron, G., González, M.J., Quera, R., Dijkstra, G., Harmsen, H.J.M., Faber, K.N. and Hermoso, M.A. (2019) ‘Short chain fatty acids (SCFAs)-mediated gut epithelial and immune regulation and its relevance for inflammatory bowel diseases’, Frontiers in Immunology, 10, p. 277.
- Smith, P.M., Howitt, M.R., Panikov, N., Michaud, M., Gallini, C.A., Bohlooly-Y, M., Glickman, J.N. and Garrett, W.S. (2013) ‘The microbial metabolites, short-chain fatty acids, regulate colonic Treg cell homeostasis’, Science, 341(6145), pp. 569–573.
- Furusawa, Y., Obata, Y., Fukuda, S., Endo, T.A., Nakato, G., Takahashi, D., Nakanishi, Y., Uetake, C., Kato, K., Kato, T., Takahashi, M., Fukuda, N.N., Murakami, S., Miyauchi, E., Hino, S., Atarashi, K., Onawa, S., Fujimura, Y., Lockett, T., Clarke, J.M., Topping, D.L., Tomita, M., Hori, S., Ohara, O., Morita, T., Koseki, H., Kikuchi, J., Honda, K., Hase, K. and Ohno, H. (2013) ‘Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells’, Nature, 504(7480), pp. 446–450.
- Brandt, E.B. and Sivaprasad, U. (2011) ‘Th2 cytokines and atopic dermatitis’, Journal of Clinical & Cellular Immunology, 2(3), p. 110.
- Guttman-Yassky, E., Nograles, K.E. and Krueger, J.G. (2011) ‘Contrasting pathogenesis of atopic dermatitis and psoriasis—Part I: clinical and pathologic concepts’, Journal of Allergy and Clinical Immunology, 127(5), pp. 1110–1118.
- Howell, M.D., Kim, B.E., Gao, P., Grant, A.V., Boguniewicz, M., Debenedetto, A., Schneider, L., Beck, L.A., Barnes, K.C. and Leung, D.Y.M. (2009) ‘Cytokine modulation of atopic dermatitis filaggrin skin expression’, Journal of Allergy and Clinical Immunology, 124(3), pp. R7–R12.
- Kim, B.E., Leung, D.Y.M., Boguniewicz, M. and Howell, M.D. (2008) ‘Lor icrin and involucrin expression is down-regulated by Th2 cytokines through STAT-6’, Journal of Investigative Dermatology, 128(6), pp. 1411–1417.
- Penders, J., Gerhold, K., Stobberingh, E.E., Thijs, C., Zimmermann, K., Lau, S., Hamelmann, E. and Kramer, U. (2013) ‘Establishment of the intestinal microbiota and its role for atopic dermatitis in early childhood’, Journal of Allergy and Clinical Immunology, 132(3), pp. 601–607.
- Song, H., Yoo, Y., Hwang, J., Na, Y.-C. and Kim, H.S. (2016) ‘Faecalibacterium prausnitzii subspecies-level dysbiosis in the human gut microbiome underlying atopic dermatitis’, Journal of Allergy and Clinical Immunology, 137(3), pp. 852–860.
- Lee, S.Y., Lee, E., Park, Y.M. and Hong, S.J. (2018) ‘Microbiome in the gut-skin axis in atopic dermatitis’, Allergy, Asthma & Immunology Research, 10(4), pp. 354–362.
- Huang, R., Ning, H., Shen, M., Li, J., Zhang, J. and Chen, X. (2017) ‘Probiotics for the treatment of atopic dermatitis in children: a systematic review and meta-analysis of randomized controlled trials’, Frontiers in Cellular and Infection Microbiology, 7, p. 392.
- Kim, S.O., Ah, Y.M., Yu, Y.M., Choi, K.H., Shin, W.G. and Lee, J.Y. (2014) ‘Effects of probiotics for the treatment of atopic dermatitis: a meta-analysis of randomized controlled trials’, Annals of Allergy, Asthma & Immunology, 113(2), pp. 217–226.
- Panduru, M., Panduru, N.M., Sălăvăstru, C.M. and Tiplica, G.S. (2015) ‘Probiotics and primary prevention of atopic dermatitis: a meta-analysis of randomized controlled studies’, Journal of the European Academy of Dermatology and Venereology, 29(2), pp. 232–242.
- Asnicar, F., Berry, S.E., Valdes, A.M., Nguyen, L.H., Piccinno, G., Drew, D.A., Leeming, E., Gibson, R., Le Roy, C., Al Khatib, H., Francis, L., Mazidi, M., Mompeó, O., Valles-Colomer, M., Tett, A., Beghini, F., Dubois, L., Huyghe, J.R., Collado, M.C., Spector, T.D., Frost, G., Segata, N. and Berry, S.E. (2021) ‘Microbiome connections with host metabolism and habitual diet from 1,098 deeply phenotyped individuals’, Nature Medicine, 27(2), pp. 321–332.
- Chrousos, G.P. (2009) ‘Stress and disorders of the stress system’, Nature Reviews Endocrinology, 5(7), pp. 374–381.
- Moloney, R.D., Desbonnet, L., Clarke, G., Dinan, T.G. and Cryan, J.F. (2014) ‘The microbiome: stress, health and disease’, Mammalian Genome, 25(1–2), pp. 49–74.
Disclaimer
The information provided on this website is for educational purposes only and is not intended as medical advice. Always consult a qualified healthcare professional before making changes to your diet, supplements, or treatment plan.
Important Links
Contact
About
Privacy Policy
Terms & Conditions