Dry Eye Supplements: What the Clinical Evidence Actually Shows in 2026
Dry eye supplements — particularly omega-3 fatty acids (DHA and EPA) and, in deficient individuals, vitamin D — have a meaningful clinical evidence base for reducing dry eye symptoms, though the picture is more nuanced than most product marketing conveys. As a Registered Dietitian Nutritionist, I want to be precise about what the evidence actually shows: the strongest trial data comes from specific nutrient interventions at specific doses, not from generic “eye health blends.” This guide works through the evidence hierarchy for dry eye supplementation, from the large-scale DREAM trial data on omega-3 down to the emerging research on lactoferrin and antioxidants, so you can make a reasoned decision about what is and is not worth trying.
Dry eye disease affects an estimated 16-49 million Americans depending on diagnostic criteria, making it one of the most common ocular conditions treated in primary care and ophthalmology. The condition’s heterogeneity — aqueous-deficient vs. evaporative subtypes, inflammatory vs. meibomian gland dysfunction mechanisms — means that no single supplement benefits every patient. Understanding which supplement targets which pathological pathway is the prerequisite for a rational supplement approach.
TL;DR
- Strongest evidence: Omega-3 fatty acids (EPA + DHA, 2,000-3,000 mg/day) — the DREAM trial (NEJM 2018) was a null result vs. olive oil placebo, but earlier meta-analyses were positive; fish oil remains a reasonable first-line adjunct given its safety profile.
- For deficient individuals: Vitamin D supplementation to sufficiency (40-60 ng/mL) is well-supported by observational data linking deficiency to dry eye severity.
- For meibomian gland dysfunction: GLA (gamma-linolenic acid, 300-500 mg/day from evening primrose or black currant seed oil) targets the lipid-layer evaporative subtype through anti-inflammatory prostaglandin E1 pathways.
- Lactoferrin: Small controlled trials support 300 mg/day for aqueous-deficient and Sjogren’s-associated dry eye; evidence base is smaller but biologically coherent.
- Vitamin A: A direct cause of corneal dryness when deficient — but deficiency is rare in Western populations eating varied diets; supplementation beyond adequacy does not benefit otherwise-sufficient individuals.
- Diet first: A Mediterranean-pattern diet high in fatty fish, dark leafy greens, and olive oil provides overlapping omega-3 and antioxidant exposure without supplement dose uncertainty.
What Is Dry Eye Disease? Understanding the Pathology Supplements Target
Dry eye disease is defined by the TFOS DEWS II (2017) global consensus report as “a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles.” This clinical definition matters for supplement selection because different supplements target different nodes of this pathological cascade.
The two primary subtypes:
- Aqueous-deficient dry eye (ADDE): Reduced tear volume from lacrimal gland dysfunction, most commonly in Sjogren’s syndrome, post-radiation, or aging-related gland atrophy. The tear film is insufficient in quantity. Lactoferrin and omega-3 research has addressed this subtype.
- Evaporative dry eye (EDE): Normal tear production but excessive evaporation due to meibomian gland dysfunction (MGD). The lipid layer — secreted by meibomian glands along the eyelid margin — is insufficient in quantity or quality, causing rapid tear film breakup. GLA and omega-3 research has specifically addressed this subtype given their roles in meibomian gland lipid secretion.
Most patients have a mixed presentation with elements of both subtypes. The inflammatory cascade — driven by hyperosmolarity stimulating pro-inflammatory cytokines (IL-1, TNF-alpha, MMP-9) on the ocular surface — is present in both subtypes and explains why anti-inflammatory nutrients have biological rationale across dry eye presentations.
Understanding which subtype predominates helps predict which dry eye supplements are most likely to provide individual benefit. An ophthalmologist can assess tear volume (Schirmer test), tear film breakup time, and meibomian gland imaging to guide this distinction.
Omega-3 Fatty Acids: The Largest Evidence Base for Dry Eye Supplements
Omega-3 fatty acids — specifically DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) — are the most extensively studied dry eye supplements. The rationale is mechanistically compelling: DHA is a major structural component of cell membranes in the meibomian glands and lacrimal epithelium, while EPA is the precursor to SPMs (specialized pro-resolving mediators) including resolvins and protectins that downregulate inflammatory signaling on the ocular surface.
The DREAM Trial: Understanding the Null Result
The DREAM trial (Dry Eye Assessment and Management), published in NEJM (2018), was a rigorous, multi-center, double-masked RCT enrolling 535 participants with moderate-to-severe symptomatic dry eye disease. Participants received either 3,000 mg/day omega-3 (2,000 mg EPA + 1,000 mg DHA) or olive oil placebo over 12 months. The primary outcome — change in OSDI (Ocular Surface Disease Index) symptom score — showed no statistically significant difference between groups.
Three factors complicate a simple “omega-3 does not work” conclusion from DREAM:
- The control was not inert: Olive oil contains oleic acid and polyphenols with documented anti-inflammatory activity. A true inert placebo (e.g., corn oil or mineral oil) might have produced a different effect estimate. The DREAM trial may have compared two active treatments rather than treatment vs. placebo.
- Enrolled population: DREAM enrolled patients with already-moderate-to-severe disease, most of whom were on concurrent dry eye therapies. Patients with milder disease who are earlier in their treatment journey may respond differently.
- Earlier trials were positive: A 2014 meta-analysis by Liu et al. (PLoS ONE) pooling 17 RCTs found statistically significant improvements in Schirmer test scores (tear production) and OSDI scores with omega-3 supplementation. Sheppard et al. (Clinical Ophthalmology, 2013) found significant OSDI and tear quality improvements at 3 months in an RCT of EPA/DHA in contact lens wearers with dry eye.
Clinical position: Given omega-3’s excellent safety profile and the mechanistic plausibility, a 3-6 month trial at 2,000-3,000 mg/day (combined EPA + DHA) is a reasonable first step for most adults with symptomatic dry eye. The dose form matters: triglyceride-form fish oil has approximately 70% greater bioavailability than ethyl ester form in some pharmacokinetic comparisons. Algae-derived DHA/EPA is an equivalent plant-based alternative — algae is the primary producer of marine omega-3s before fish accumulate it through the food chain.
For a detailed review of omega-3’s role across multiple eye conditions, including its null result in AMD progression in the AREDS2 trial, see our best eye vitamins evidence guide.
Vitamin D and Dry Eye: From Observational Association to Clinical Rationale
Vitamin D’s connection to dry eye disease has emerged from observational epidemiology rather than large interventional trials, but the biological plausibility is strong enough to warrant attention — particularly in the roughly 35% of American adults estimated to have insufficient vitamin D levels.
A 2014 South Korean population study by Song et al. (British Journal of Ophthalmology) analyzed data from 17,542 participants and found a statistically significant, dose-dependent inverse association between serum 25-hydroxyvitamin D (25-OH-D) levels and dry eye disease prevalence and severity. This was not a simple deficiency-vs-normal comparison — lower vitamin D within the sufficient range was associated with incrementally higher dry eye rates.
The mechanistic basis: Vitamin D receptors (VDRs) are expressed in the lacrimal gland, corneal epithelium, and conjunctival goblet cells — the key structures involved in tear production and ocular surface defense. Vitamin D3 activates VDRs in these tissues, where it modulates inflammatory cytokine expression and supports epithelial cell differentiation. In animal models, vitamin D-deficient mice develop lacrimal gland dysfunction with reduced tear production. Reins et al. (Investigative Ophthalmology and Visual Science, 2018) demonstrated that vitamin D3 directly suppressed inflammatory signaling in corneal epithelial cells challenged with lipopolysaccharide, supporting the anti-inflammatory mechanism.
Clinical application: For individuals with confirmed vitamin D deficiency (serum 25-OH-D below 20 ng/mL), supplementation to sufficiency is appropriate for multiple health reasons and plausibly beneficial for dry eye based on the observational data. A typical repletion dose for deficient adults is 2,000-4,000 IU vitamin D3 daily; sufficiency is generally defined as 40-60 ng/mL. For individuals with normal vitamin D status, supplementation beyond adequacy has not been demonstrated in RCTs to improve dry eye. Testing serum 25-OH-D through a primary care provider is a low-cost way to determine whether this intervention is relevant to your situation.
GLA and Meibomian Gland Dysfunction: Targeting the Lipid Layer
Gamma-linolenic acid (GLA) is an omega-6 fatty acid that takes a different metabolic route than the predominant dietary omega-6, arachidonic acid. Where arachidonic acid generates prostaglandin E2 (pro-inflammatory), GLA is elongated to DGLA (dihomo-gamma-linolenic acid), which primarily produces prostaglandin E1 — an anti-inflammatory mediator that relaxes smooth muscle and reduces inflammatory cell recruitment.
In meibomian gland dysfunction, the quality and quantity of the lipid secretion (meibum) that forms the tear film’s outermost layer is impaired. This lipid layer retards evaporation; when it is deficient, tear breakup time shortens dramatically and symptoms of grittiness, burning, and light sensitivity follow. GLA’s anti-inflammatory effects on meibomian gland epithelium may improve meibum quality and outflow.
Wojtowicz et al. (Cornea, 2011) conducted a 6-month, randomized, controlled trial of linolenic acid (ALA, 400 mg) combined with GLA (400 mg) vs. oleic acid placebo in 38 patients with moderate-to-severe meibomian gland dysfunction-related dry eye. The ALA + GLA group showed significant improvements in meibomian gland secretion quality, meibomian gland plugging scores, and OSDI symptom scores vs. placebo at 6 months. GLA has also been studied in two controlled trials in contact lens wearers with evaporative dry eye, with both reporting improved lens comfort and reduced dry eye symptoms.
Sources and dosing: GLA is found in evening primrose oil (8-10% GLA), borage oil (20-24% GLA), and black currant seed oil (15-20% GLA, plus ALA). Evening primrose oil is the most common supplement form; borage oil provides GLA more efficiently per gram of total oil. Clinical trials have typically used 300-500 mg GLA/day. GLA is often combined with omega-3 fatty acids in clinical approaches to evaporative dry eye, since the two nutrients target complementary anti-inflammatory pathways.
Vitamin A: The Classic Ocular Nutrient — With Important Limits
Vitamin A (retinol) is the vitamin most directly essential to corneal surface integrity. The conjunctival goblet cells — which produce mucin, the innermost layer of the tear film responsible for spreading tears evenly across the corneal surface — are critically dependent on vitamin A for differentiation and maintenance. Without adequate vitamin A, goblet cell density falls, mucin production declines, and corneal epithelial cells keratinize, producing a dry, irregular ocular surface.
In populations with vitamin A deficiency — primarily in sub-Saharan Africa and South and Southeast Asia — this produces xerophthalmia: a clinical syndrome ranging from night blindness through corneal desiccation to corneal ulceration and irreversible blindness. The WHO estimates vitamin A deficiency affects 250 million preschool-aged children globally and is a leading cause of preventable childhood blindness.
In Western populations eating varied diets containing liver, dairy, eggs, and orange-yellow vegetables (beta-carotene), true vitamin A deficiency severe enough to cause ocular symptoms is uncommon. It can occur in individuals with fat malabsorption syndromes (Crohn’s disease, celiac disease, cystic fibrosis, short bowel syndrome), those who have undergone bariatric surgery, heavy alcohol consumers, or those on severely restricted diets. In such individuals, vitamin A status assessment and supplementation can be cornea-preserving.
Critical caveat — toxicity and smoking risk: Preformed vitamin A (retinol) is teratogenic above 3,000 mcg/day and hepatotoxic with chronic high-dose use. Beta-carotene supplementation is contraindicated in current and former heavy smokers based on the CARET trial (which found increased lung cancer incidence and overall mortality in smokers supplementing beta-carotene combined with vitamin A). These risks apply to supplements, not to beta-carotene from food. In well-nourished individuals, supplementing vitamin A beyond dietary adequacy has not been shown to improve dry eye, tear production, or goblet cell density. The best eye vitamins evidence guide provides a full risk analysis of vitamin A and beta-carotene supplementation across all eye conditions.
Lactoferrin: Targeting Tear Protein Deficiency Directly
Lactoferrin is a multifunctional glycoprotein secreted naturally into tears by lacrimal gland acinar cells. It constitutes approximately 20-25% of total tear protein in healthy eyes, serving as an antimicrobial agent (it chelates iron, depriving pathogenic bacteria of a critical growth factor), an anti-inflammatory mediator (suppressing NF-kB signaling), and a surface lubrication contributor.
The dry eye connection is direct: tear lactoferrin levels are measurably lower in patients with dry eye disease compared to age-matched controls, and the degree of lactoferrin reduction correlates with disease severity. Ohashi et al. (Cornea, 2006) documented this correlation across dry eye subtypes, with the lowest tear lactoferrin in patients with Sjogren’s syndrome-associated aqueous-deficient dry eye.
Does oral lactoferrin supplementation raise tear lactoferrin? A randomized, double-masked Japanese trial by Watanabe et al. (Ophthalmology, 2013) enrolled 60 patients with Sjogren’s syndrome-associated dry eye and found that 300 mg/day oral lactoferrin for 3 months significantly increased tear secretion volume, improved OSDI scores, and partially normalized tear lactoferrin levels compared to placebo. A smaller Italian controlled trial by Versura et al. (2013) confirmed improvements in tear film stability and symptom scores at 200 mg/day lactoferrin over 8 weeks.
The evidence base is smaller than for omega-3, but the mechanism is unusually direct — supplementation appears to restore a protein specifically depleted in dry eye disease. Dosages used in trials range from 200-600 mg/day; most commercially available lactoferrin supplements provide 200-300 mg per serving.
Antioxidants and Dry Eye: Vitamin C, E, and Carotenoids
The ocular surface — cornea, conjunctiva, and tear film — is continuously exposed to environmental oxidative stress: ultraviolet radiation, airborne pollutants, and the oxidative byproducts of cellular metabolism in metabolically active corneal epithelium. This makes antioxidant nutrient support conceptually appealing in dry eye disease.
Vitamin C is the dominant antioxidant in tears, present at levels 15-30 times greater than plasma. In dry eye disease, tear vitamin C concentrations are significantly reduced compared to healthy controls. Whether this reduction is a cause or consequence of dry eye pathology — or merely a marker of broader tear protein derangement — has not been definitively established. No large RCT has tested isolated vitamin C supplementation for dry eye endpoints; its role is currently best framed as supporting overall ocular surface antioxidant capacity as part of a diet-pattern approach.
Lutein and zeaxanthin are concentrated in the corneal epithelium and crystalline lens in addition to the macula, where they neutralize photo-oxidative stress. Several small studies have measured lutein levels in tears and found reductions in dry eye patients, suggesting that carotenoid depletion may contribute to oxidative stress on the ocular surface. This evidence is preliminary and observational rather than from RCTs testing lutein supplementation for dry eye endpoints. For the primary evidence base on lutein and zeaxanthin in eye health — including the AREDS2 dose data and macular degeneration evidence — see our lutein and zeaxanthin for vision guide.
Evaluating Dry Eye Supplement Products: What to Look For
The commercial dry eye supplement market ranges from evidence-aligned formulations to products built on vague “eye health” claims at sub-therapeutic doses. The principles for evaluation are the same regardless of brand:
Check the specific ingredient doses, not just the ingredient list. A supplement that “contains omega-3” but provides 300 mg total per serving (100 mg EPA + 200 mg DHA) is providing roughly one-tenth of the dose studied in positive omega-3 trials. The milligram quantity is everything.
Identify what subtype the product targets. Omega-3-centric formulas target the inflammatory cascade and meibomian gland membranes. GLA-forward formulas target meibomian gland secretion quality specifically. Products combining both may make sense for mixed presentation patients.
Assess ingredient transparency. Proprietary blends that conceal individual ingredient weights cannot be evaluated for clinical relevance against published trial doses. Manufacturers who specify milligrams of each ingredient are enabling informed comparison; those who do not are not.
Consider third-party testing. NSF International, USP, Informed Sport, and ConsumerLab certifications provide independent potency and purity verification — relevant for omega-3 products specifically given the oxidation stability challenges of polyunsaturated fatty acids.
iGenics is one of the more extensively positioned vision health supplements in this category — the full iGenics review examines its ingredient panel and whether its formulation matches evidence-based dose thresholds. VisiFlora takes an unusual angle based on the emerging gut-vision microbiome research; the VisiFlora review evaluates what the probiotic and prebiotic evidence actually supports for ocular surface health. TheYaVue and Vision 20 both use antioxidant-focused formulation approaches — their respective reviews assess whether the specific compounds and doses align with published clinical ranges.
Who Benefits from Dry Eye Supplementation
Based on the current evidence, the following populations have the clearest rationale for specific dry eye supplement interventions:
Adults with symptomatic moderate dry eye and high omega-3 dietary gap: Western diets with low fatty fish consumption are typically low in EPA and DHA. Supplementation fills a genuine dietary shortfall while addressing the inflammatory component of dry eye. A 3-6 month trial of 2,000-3,000 mg/day EPA+DHA is evidence-consistent and low-risk.
Individuals with vitamin D deficiency confirmed by blood test: The observational data linking low vitamin D to dry eye severity, combined with the lacrimal gland VDR evidence, supports supplementation to normal range in deficient individuals. This is a “treat the deficiency” rationale, not a “take more than you need” rationale.
Patients with meibomian gland dysfunction-predominant dry eye: GLA at 300-500 mg/day has the most direct mechanistic support for this subtype. Combined omega-3 + GLA approaches may address both the lipid layer quality and the inflammatory signaling driving meibomian gland obstruction.
Individuals with Sjogren’s syndrome or other aqueous-deficient dry eye: Lactoferrin at 300 mg/day has RCT support specifically in Sjogren’s-associated dry eye. This is a niche application with a smaller evidence base, but biologically coherent given the tear lactoferrin depletion documented in this population.
Anyone with malabsorption or dietary restriction-based nutrient deficiency: If fat malabsorption is present (gastric bypass, inflammatory bowel disease, celiac), assessing and correcting fat-soluble vitamin status — particularly vitamin A and D — is clinically appropriate and addresses a potential driver of corneal surface dysfunction.
The broader context of supplement evidence for eye conditions — including AREDS2-formula nutrients for AMD — is covered in our macular degeneration supplements guide.
Who Probably Does Not Need Dry Eye Supplements
Adults with healthy eyes and no dry eye symptoms: No evidence supports preventive dry eye supplementation in asymptomatic individuals with healthy ocular surfaces. Dietary optimization (fatty fish 2+ times weekly, dark leafy greens daily) is the better primary prevention approach.
People with normal omega-3 status and primarily structural dry eye causes: Screen-heavy work patterns causing reduced blink rate, wind and dry air exposure, or LASIK-associated corneal nerve disruption produce dry eye through non-inflammatory mechanisms that supplements are unlikely to address. Addressing the environmental or structural root cause (blink exercises, humidifier, artificial tear selection) is more relevant in these presentations.
Contact lens wearers attributing discomfort solely to lens type: While omega-3 has some evidence in contact lens-associated dry eye (Sheppard et al., 2013), lens material, replacement schedule, and care solution compatibility should be evaluated before attributing lens discomfort to nutrient deficiency.
Individuals with normal vitamin D status expecting vision benefit from higher doses: Supplementing vitamin D beyond sufficiency (above 60 ng/mL) has not been shown to improve dry eye above what adequacy achieves, and at very high levels carries toxicity risk. More is not better once the biological requirement is met.
Frequently Asked Questions
What supplements actually help dry eyes?
The most clinically studied are omega-3 fatty acids (DHA + EPA, 2,000-3,000 mg/day), vitamin D (for deficient individuals), and GLA from evening primrose or black currant seed oil (300-500 mg/day). Lactoferrin at 300 mg/day has RCT support for Sjogren’s-associated dry eye. The evidence hierarchy places omega-3 and vitamin D at the top, with GLA and lactoferrin supported by smaller but coherent trial data. Vitamin A deficiency is a direct cause of corneal dryness but is uncommon in Western populations without malabsorption conditions.
Does fish oil help with dry eyes?
The evidence is mixed but overall supportive. The DREAM trial (NEJM, 2018) found no difference vs. olive oil placebo on the primary outcome, but the olive oil control may itself have had anti-inflammatory activity. Earlier meta-analyses (Liu et al., 2014) found significant improvements in tear production and symptoms. Given fish oil’s safety profile, a 3-6 month trial at 2,000-3,000 mg/day is a reasonable first step. Triglyceride-form fish oil has better bioavailability than ethyl ester form — worth checking on the label.
How long does it take for omega-3 to help dry eyes?
Plan for at least 12 weeks before assessing response. Tissue DHA incorporation into meibomian gland and lacrimal epithelium membranes takes 4-8 weeks; positive trial results have been reported at 3 months (Sheppard et al., 2013). Measuring change in OSDI score at baseline and 12 weeks provides an objective response assessment.
What vitamin deficiency causes dry eyes?
Vitamin A deficiency classically causes corneal dryness and goblet cell loss leading to xerophthalmia — but this is uncommon in Western populations without fat malabsorption disorders. Vitamin D deficiency is more commonly encountered in Western adults and is associated with dry eye severity in observational studies. Omega-3 dietary inadequacy (low fatty fish intake) is the most widespread nutritional factor connected to dry eye in populations with Western dietary patterns.
Is vitamin D good for dry eyes?
For deficient individuals (25-OH-D below 20 ng/mL), supplementing to sufficiency has a plausible benefit for dry eye based on observational evidence and lacrimal gland VDR expression data. For people with normal vitamin D levels, there is no RCT evidence that higher doses improve dry eye. Testing your 25-OH-D through a primary care provider before treating vitamin D as a dry eye intervention is the evidence-consistent starting point.
What is GLA and how does it help dry eye?
GLA (gamma-linolenic acid) is an omega-6 fatty acid from evening primrose, black currant seed, or borage oil that is metabolized to produce anti-inflammatory prostaglandin E1 rather than the pro-inflammatory prostaglandin E2 produced from arachidonic acid. In meibomian gland dysfunction — the most common dry eye subtype — GLA may improve meibum quality and reduce meibomian gland plugging. Wojtowicz et al. (Cornea, 2011) showed significant improvements in a 6-month RCT. Standard dose is 300-500 mg GLA/day, often combined with omega-3.
Are there dry eye supplements without fish oil?
Yes. Algae-derived DHA and EPA (from Schizochytrium or Nannochloropsis species) provides equivalent omega-3 bioavailability and is the plant-based alternative used in vegetarian and vegan formulations. Flaxseed oil provides ALA but converts inefficiently to DHA/EPA. GLA from evening primrose oil targets the meibomian gland lipid pathway through a complementary mechanism and does not require fish-derived ingredients.
Can lactoferrin supplements help dry eyes?
Small but well-designed RCTs support lactoferrin at 300 mg/day for Sjogren’s-associated and general aqueous-deficient dry eye. Tear lactoferrin is measurably depleted in dry eye patients, and oral supplementation appears to partially restore tear lactoferrin levels (Watanabe et al., 2013). The mechanism is direct and the trial results are positive, though the evidence base is smaller than for omega-3. It is a reasonable adjunct for aqueous-deficient presentations, particularly in Sjogren’s syndrome patients.
The Bottom Line
The supplement evidence for dry eye is more nuanced than most product marketing suggests. Omega-3 fatty acids are the most studied intervention with the largest evidence body, despite the DREAM trial null result introducing important caveats. Vitamin D deficiency correction is well-supported in deficient individuals. GLA has specific applicability to meibomian gland dysfunction and the evaporative dry eye subtype. Lactoferrin has biologically coherent small-trial evidence for aqueous-deficient presentations.
What none of these supplements is: a replacement for ophthalmologic evaluation, appropriate artificial tear selection, or addressing environmental and behavioral dry eye contributors (screen time, blink rate, humidity, contact lens practices). Supplements address nutrient-pathway components of dry eye pathology — they work alongside the broader management approach, not instead of it.
The practical starting point for most adults with dry eye symptoms and a Western diet: a 3-6 month trial of 2,000-3,000 mg/day EPA + DHA from triglyceride-form fish oil (or algae-based equivalent), with serum 25-OH-D testing to determine whether vitamin D correction is relevant. If meibomian gland dysfunction is the predominant presentation, adding GLA (300-500 mg/day from evening primrose or black currant seed oil) addresses the lipid-layer pathway through a complementary mechanism.
For the broader evidence landscape covering lutein, zeaxanthin, the AREDS2 formula, and the full spectrum of eye health nutrients, the best eye vitamins evidence guide provides the comprehensive clinical framework. Reviewer credentials and methodology are described on our About page. Disclosure practices are detailed on our disclosure page.
These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease. The information in this article is for educational purposes only and does not constitute medical advice. Consult a qualified healthcare professional — including a board-certified ophthalmologist for dry eye concerns — before starting any supplement program, especially if you have a diagnosed eye condition, are pregnant, nursing, or take prescription medications including anticoagulants.