The phrase ‘we are what we eat’ may sound simplistic, but it seems to be increasingly relevant to dry eye disease (DED).
While treatment traditionally focuses on the ocular surface, emerging evidence suggests that systemic health, diet and the intestinal microbiome may influence ocular surface inflammation and tear film function1-4.
An interesting starting point is the review by Campagnoli and colleagues, which describes the ‘gut–eye axis’ as a biologically plausible link between gut microbiota, immune regulation and ocular surface disease, including DED1.
The authors emphasise that the gut microbiome influences systemic immunity, epithelial barrier integrity, inflammatory signalling and metabolite production, all of which could affect distant mucosal sites such as the ocular surface1.
In parallel, the TFOS DEWS III Digest states that although nutrition may play a role in DED, the evidence is not yet strong enough to support recommendation of an optimal diet for our dry eye patients5.
Why the gut might matter to the eye
The ocular surface is not an isolated structure. It is an interconnected microenvironment and ecosystem – encompassing the cornea, conjunctiva, eyelids, meibomian glands, and neural pathways – that can experience a primary loss of homeostasis alongside or independently of the tear film5,6.
Disturbance at one site can amplify inflammation elsewhere. The gut microbiome may interact with this system through several pathways: shaping T-cell responses, influencing regulatory immune mechanisms, producing short-chain fatty acids, affecting intestinal barrier integrity and altering systemic inflammatory tone1,3,4. This is particularly important because many dry eye phenotypes are inflammatory5,6. In Sjögren disease, graft-versus-host disease and other immune-mediated conditions, lacrimal gland and ocular surface inflammation are central1,5.
Current microbiome evidence appears strongest for immune-mediated dry eye phenotypes and remains more indirect for predominantly evaporative disease.1-4
Dietary risk factors: what is established?
The strongest dietary messages remain broad rather than prescriptive5. The TFOS DEWS III Digest states that poor nutrition driving systemic disease may be associated with DED risk factors, and that deficiencies of vitamin A, vitamin C and omega-3 fatty acids have evidence as DED risk factors5. Moderate evidence is also reported for vitamin B12 and vitamin D deficiencies5.
This aligns with ocular biology: vitamin A is essential for conjunctival epithelial differentiation and mucin production; vitamin C contributes antioxidant support; vitamin D has immune-modulating properties; and vitamin B12 is relevant to neurosensory function, which may matter in patients whose symptoms exceed signs5,6.
Omega-3 fatty acids remain a constant topic in practice, Omega 3 deficiency remains a risk factor for DED, there is moderate evidence for a beneficial effect on MGD especially when used in combination with other treatments5. However, clinical trial results have been varied, reflecting differences in dose, formulation, background diet, dry eye phenotype, outcome measures and study duration5. Consequently, recommending omega-3 as a universal dry eye treatment may overstate the evidence, but identifying low dietary intake, poor diet quality or deficiency states remains clinically sensible5.
The microbiome hypothesis
Campagnoli et al describe the gut microbiota as a potentially modifiable contributor to ocular disease through immune and metabolic signalling.1 Subsequent reviews similarly argue that dysbiosis may contribute to ocular inflammation by reducing beneficial metabolites, impairing mucosal tolerance and increasing systemic inflammatory activity2-4. Short-chain fatty acids, such as butyrate, are of particular interest because they support epithelial barrier function and regulatory immune responses1,3. If dysbiosis reduces these protective signals, the threshold for ocular surface inflammation may fall1,3,4.
Animal studies provide some of the most compelling mechanistic support1,3,4. Germ-free and antibiotic-treated models show that altering gut microbial communities can change immune responses and ocular surface inflammation1,3. Patient-derived microbiota transplantation experiments have also suggested that microbial communities from individuals with immune-mediated dry eye can transfer inflammatory tendencies in experimental settings1-4. These studies do not prove that ordinary dietary changes will treat dry eye in humans, but they strengthen the biological plausibility of a gut-ocular surface connection1-4.
What can be recommended in clinic?
As with most of our advice, the practical message should be balanced: diet is an important part of dry eye management, not a substitute for diagnosis or targeted therapy5,6. For most patients, we should encourage a varied, minimally processed diet rich in vegetables, fruit, legumes, whole grains, nuts, seeds and oily fish where appropriate. This type of diet supports micronutrient adequacy, provides fibre for microbial diversity and may reduce systemic inflammatory load1,3,5. This is consistent with general health advice and avoids implying that one particular diet has been proven to help with DED5.
Screening for nutritional risk is also reasonable5. Patients with restricted diets, malabsorption, bariatric surgery, inflammatory bowel disease, vegan diets without supplementation, frailty or unexplained neuropathic symptoms may warrant discussion with their GP or dietitian and, where appropriate, testing for vitamin D, B12, iron or other deficiencies5.
Probiotics, prebiotics and synbiotics are promising but not yet mature interventions for routine prescribing for DED2,3,4. Reviews of microbiome-based therapeutics highlight early evidence and plausible mechanisms, but also stress the need for better-controlled human studies, clearer phenotype selection and standardised outcomes2-4. It is plausible that future research will move away from generic ‘gut health’ claims towards precision approaches: identifying which dry eye phenotypes, microbial signatures and metabolites are most clinically relevant2-4.
Conclusion
The gut–eye axis is one of the most interesting developments in ocular surface research1-4. It offers a plausible explanation for why systemic inflammation, immune dysregulation and diet quality may influence dry eye symptoms and signs1,3,4,5. However, the evidence remains limited2,5. It is certainly worth noting deficiencies of vitamins A and C, omega-3 fatty acids, and possibly vitamins B12 and D and discussing the importance of a balanced diet with our DED patients.
For now, the best clinical message is cautious optimism: support whole-body health, identify nutritional risk, manage the ocular surface directly, and watch this field closely as the evidence develops2-6.
References
1. Campagnoli LIM, Varesi A, Barbieri A, Marchesi N, Pascale A. Targeting the gut-eye axis: an emerging strategy to face ocular diseases. Int. J. Mol. Sci. 2023;24(17):13338.
2. Berzack S, Galor A. Microbiome-based therapeutics for ocular diseases. Clin. Exp. Optom. 2024;108(2):115-122.
3. Nguyen Y, Manis JRZ, Ronczkowski NM, Bui T, Oxenrider A, Jadeja RN, Thounaojam MC. Unveiling the gut-eye axis: how microbial metabolites influence ocular health and disease. Front. Med. 2024;11:1377186.
4. Tîrziu AT, Susan M, Susan R et al. From gut to eye: exploring the role of microbiome imbalance in ocular diseases. J. Clin. Med. 2024;13(18):5611.
5. Perez VL, Chen W, Craig JP, Stapleton F, Wolffsohn JS, Sullivan DA et al. TFOS DEWS III: Executive summary. Am. J. Ophthalmol. 2026;282:135-145
6. Stapleton F, Argüeso P, Asbell P, Azar D et al. TFOS DEWS III: Digest. Am. J. Ophthalmol. 2025;279:451-553.
Keith Tempany FBDO CL FBCLA qualified in 1976 and worked in both independent and multiple practice before opening a fee-based contact lens only practice in 2002. He is a fellow and a past president of the British Contact Lens Association (BCLA) and oversaw the development and launch of its Myopia Management Certificate. Keith is the store director of Leightons & Tempany Opticians & Hearing Care in Poole, and works as an independent consultant. He is an experienced author, lecturer and facilitator of contact lens and dry eye education both nationally and internationally.