Nutritional Supplements in Dry Eye Disease (Based on the TFOS DEWS III Report (2025))

Dry Eye Disease (DED) is a multifactorial, symptomatic disease linked to loss of tear film and/or ocular surface homeostasis.¹ No single treatment reliably addresses every patient's needs. While artificial tear supplements and prescription therapies remain cornerstones of treatment, an often-overlooked pillar of care lies in nutritional modification.

This blog explores the evidence for dietary supplementation, particularly omega-3 polyunsaturated fatty acids (PUFAs), vitamins, and other micronutrients, as a safe, accessible, and clinically relevant adjunct in the management of dry eye disease (DED).

Key takeaways

• Nutritional support can play a useful adjunctive role in dry eye disease.

• Omega-3s have the strongest evidence among nutritional interventions.

• Some vitamins and micronutrients may also help in selected patients.

• Supplements should support standard dry eye treatment, not replace it.

• Results usually take time and work best as part of a broader care plan.

Where nutrition fits in dry eye disease management

Released in 2025 and developed by 80 experts across 18 countries, the TFOS DEWS III report is the most comprehensive evidence-based review of DED to date.³

Its management toolkit spans tear replenishment, meibomian gland dysfunction (MGD) care, eyelid disease management, and nutritional and lifestyle strategies.

The report expanded DED subclassification beyond aqueous-deficient vs. evaporative DED to include lipid layer abnormalities, blinking disorders, and lid pathology, reinforcing why individualised, multimodal care is essential.

Omega-3 fatty acids: the evidence

Omega-3 PUFAs, particularly EPA and DHA, are the most evidence-supported nutritional intervention in DED. Their anti-inflammatory derivatives, resolvins D1/E1 and protectins, inhibit leukocyte infiltration, enhance macrophage activity, improve corneal epithelial integrity, and stimulate tear production.⁴

The ratio of omega-6 to omega-3 in the diet is clinically significant: omega-6 fatty acids generate pro-inflammatory mediators, while omega-3s generate anti-inflammatory resolvins and protectins. Western diets, typically high in omega-6, increase the risk of DED signs and symptoms.⁴

Key clinical evidence

1. Multicentre RCT: Omega-3 supplementation (2,400 mg/day) produced significant improvements in symptoms, Schirmer scores, TBUT, tear osmolarity, and goblet cell density vs placebo.⁵

2. Meta-analysis (19 RCTs): Significant improvement in DED symptoms and clinical signs with omega-3 supplementation.⁶

3. Epidemiology: Higher omega-3 intake reduced DED risk in women aged 45–84; high omega-6:omega-3 ratio increased risk. Regular tuna consumption significantly reduced DED risk.⁷

4. DREAM study caveat: 3,000 mg n-3 fatty acids did not significantly outperform olive oil placebo at 12 months⁸, though genetic variability (LTα genotype) may explain some inter-study differences.⁹

The TFOS DEWS III report concludes that overall evidence supports a beneficial effect of oral omega-3 supplementation, whilst acknowledging that optimal source, dosage, and omega-3:omega-6 ratio require further investigation.⁴

Vitamins and micronutrients

1. Vitamin A: Topical vitamin A (retinyl palmitate 0.05%) has shown improvements in TBUT, corneal staining, and goblet cell density comparable to cyclosporine A.¹⁰ Caution: isotretinoin (a vitamin A metabolite) is detrimental to meibomian gland health and may induce MGD.¹¹

2. Vitamin B12: Deficiency is linked to increased DED risk. Topical B12/hyaluronic acid formulations have improved tear film stability and symptoms in postmenopausal women and Sjögren's patients.¹²˒¹³

3. Vitamin D: Serum 25-hydroxyvitamin D is significantly lower in DED patients.¹⁴ Oral supplementation for 8 weeks improved Schirmer scores, TBUT, and osmolarity in deficient patients in an RCT of 100 participants.¹⁵

4. Selenium: Essential for selenoprotein P generation in the lacrimal glands; levels are significantly lower in DED patients, associated with oxidative ocular surface damage.¹⁶

Other nutritional approaches

1. Combined supplements: Two prospective RCTs of Blink™ NutriTears® (lutein, zeaxanthin, curcumin, vitamin D) demonstrated significant improvements in tear volume, stability, and MMP-9 inflammatory biomarkers.¹⁷

2. Lactoferrin: An iron-binding glycoprotein found in tears; oral lactoferrin maintains tear secretion in animal models, potentially via gut microbiota modulation. Tear lactoferrin levels correlate inversely with DED severity.¹⁸

3. Hydration: Plasma osmolality correlates directly with tear osmolarity. Adequate fluid intake is a practical, risk-free recommendation for all DED patients.¹⁹

4. Manuka honey (topical): A meta-analysis of 5 studies (n=323) showed significant improvements in OSDI, Schirmer scores, and corneal fluorescein staining.²⁰

Practical dietary advice

Encourage oily fish (salmon, mackerel, sardines, tuna) 2–3 times weekly, extra virgin olive oil, and flaxseed oil. Advise reduction of palm, corn, and soybean oils (high in omega-6) and avoidance of trans fats from hydrogenated vegetable oils, which are associated with systemic inflammation.⁴

Practical guidelines

1. Consider screening for deficiencies: Consider serum vitamin D in chronic DED. Vitamin B12 assessment may be warranted in postmenopausal women or those at nutritional risk.

2. Dietary omega-3 first: Oily fish 2–3 times weekly, olive oil as primary cooking fat, flaxseed where appropriate, particularly relevant for high omega-6 Western diets.

3. Supplement pragmatically: Where dietary change is not practical, or eye drop compliance is poor, omega-3 supplements (1,000–3,000 mg EPA/DHA daily) are a reasonable and safe adjunct.

4. Set realistic expectations: Nutritional benefits typically take weeks to months to manifest. Combined with standard treatment, outcomes are likely better than either approach alone.

5. Revisit drop barriers: Reconsider why topical therapy is not being maintained and modify treatment options in favour of compliance.

Why this matters in practice

Many patients find topical eye drop therapy challenging. The landscape of artificial tear products is vast and confusing, and patients frequently report a trial-and-error approach to product selection, leading to significant wasted cost and frustration.¹

A Cochrane systematic review of 43 randomised controlled trials (RCTs) involving 3,497 people with DED found that while tear supplements may provide symptomatic relief, the relative lack of head-to-head studies makes it difficult to determine which products are most effective.² This uncertainty, combined with the tactile discomfort some patients experience instilling drops, creates a genuine barrier to consistent treatment adherence.

For these patients, and as part of a broader, multimodal approach for all patients, nutritional supplementation offers a compelling alternative or adjunct. It is taken orally, requires no technique, and works from the inside out to support ocular surface health.

Conclusion

The TFOS DEWS III report (2025) reinforces that dry eye disease (DED) is a multifactorial disease requiring a multimodal approach to management. Nutritional supplementation, particularly omega-3 PUFAs, vitamin D, and targeted antioxidant combinations, represents a clinically supported, patient-friendly adjunct to standard care.

For patients who are confused by the proliferation of eye drop products, or who struggle with topical instillation, dietary and supplemental strategies offer a valuable, accessible intervention. Whilst not a replacement for artificial tears, anti-inflammatory therapy, or MGD-targeted treatments, nutritional optimisation can meaningfully support ocular surface health when integrated into a holistic, personalised care plan.

As with all emerging evidence, optimal dosing, formulation, and patient selection criteria require further investigation, but the current evidence is sufficient to support informed, proactive guidance in clinical practice.

‘The overall evidence would suggest a beneficial effect of oral supplementation of omega-3 PUFAs; however, the optimal source, dosage, and ratio of omega-3 to omega-6 require further investigation.’
— TFOS DEWS III (2025

References

1. TFOS DEWS III (2025). Management of Dry Eye Disease. American Journal of Ophthalmology.

2. Cochrane review of nonprescription tear supplements: 43 RCTs, n=3,497. (TFOS DEWS III, ref 178.)

3. TFOS DEWS III overview. American Journal of Ophthalmology, 2025. 80 experts, 18 countries.

4. TFOS DEWS III (2025). Section 9.1: Macronutrients — Omega-3 PUFAs. (Refs 853–874.)

5. Multicenter RCT: omega-3 PUFAs 2,400 mg/day. (TFOS DEWS III, ref 865.)

6. Meta-analysis of 19 RCTs: omega-3 PUFA for DED. (TFOS DEWS III, ref 866.)

7. Cross-sectional study, women aged 45–84 and omega-3 intake. (TFOS DEWS III, ref 867.)

8. DREAM Study. (TFOS DEWS III, refs 862–863.)

9. LTα genotype and omega-3 inflammatory response. (TFOS DEWS III, ref 864.)

10. RCT: topical vitamin A vs cyclosporine A, 150 DED participants. (TFOS DEWS III, ref 164.)

11. Isotretinoin and meibomian gland health. (TFOS DEWS III, refs 165–167.)

12. Vitamin B12/HA drops in postmenopausal women. (TFOS DEWS III, ref 168.)

13. Vitamin B12/HA in Sjögren's disease. (TFOS DEWS III, ref 883.)

14. Meta-analysis of 14 observational studies: vitamin D and DED. (TFOS DEWS III, ref 172.)

15. RCT: oral vitamin D, 8 weeks, 100 deficient patients. (TFOS DEWS III, ref 885.)

16. Selenoprotein P in lacrimal glands and DED. (TFOS DEWS III, ref 887.)

17. Blink™ NutriTears® (lutein, zeaxanthin, curcumin, vitamin D): 2 prospective RCTs. (TFOS DEWS III, refs 175, 935.)

18. Oral lactoferrin and tear secretion. (TFOS DEWS III, ref 923.)

19. Plasma osmolality and tear film osmolarity. (TFOS DEWS III, refs 915–917.)

20. Meta-analysis of topical honey in DED (5 studies, n=323). (TFOS DEWS III, ref 929.)