Eye Health & Macular Degeneration: The Functional Approach

The Window That Wears Out

Your retina is brain tissue that happens to sit behind a lens. It is the only part of the central nervous system you can examine directly — and it consumes more oxygen per gram than any other tissue in the body. The macula, a 5.5mm spot at the center of the retina, contains the highest concentration of mitochondria of any human tissue, has no direct blood supply (it depends on diffusion from the choroid beneath), and is responsible for your sharpest vision — reading, recognizing faces, driving, everything that requires central detail.

When this tissue degenerates, the world blurs from the center outward. Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in adults over 50 in the developed world. Approximately 196 million people worldwide are affected. And it is overwhelmingly a disease of oxidative stress, mitochondrial failure, inflammation, and metabolic dysfunction — exactly the terrain functional medicine is designed to address.

AMD: Dry vs. Wet

Dry AMD (atrophic): 85-90% of cases. Characterized by drusen — yellowish deposits of lipid and protein beneath the retinal pigment epithelium (RPE). Early drusen are common and often benign. As they accumulate and enlarge, they disrupt the RPE’s ability to support photoreceptors. Geographic atrophy represents advanced dry AMD — patches of dead RPE and photoreceptors, visible as sharply demarcated areas of vision loss. Progression is slow (years to decades) but currently has limited treatment options.

Wet AMD (neovascular): 10-15% of cases but responsible for 90% of severe vision loss. Abnormal blood vessels grow from the choroid through Bruch’s membrane into the subretinal space (choroidal neovascularization). These vessels leak fluid and blood, rapidly destroying macular tissue. Symptoms include sudden distortion of straight lines (metamorphopsia) and rapid central vision loss. Treated with anti-VEGF injections (bevacizumab, ranibizumab, aflibercept) — these are life-changing treatments that can halt progression and sometimes restore vision, but require ongoing monthly to bimonthly injections.

Dry can convert to wet at any time. Patients with dry AMD should have regular OCT (optical coherence tomography) monitoring and use an Amsler grid at home to detect distortion early.

AREDS2: The Foundation

The Age-Related Eye Disease Studies (AREDS and AREDS2) are among the largest and most well-designed nutritional intervention trials in medicine.

The AREDS2 formulation (2013):

Component	Dose	Role
Lutein	10 mg	Macular pigment, blue light filter
Zeaxanthin	2 mg	Macular pigment, antioxidant
Vitamin C	500 mg	Antioxidant
Vitamin E	400 IU	Antioxidant
Zinc	80 mg (or 25 mg in modified versions)	RPE metabolism, antioxidant
Copper	2 mg	Prevents zinc-induced copper deficiency

Key finding: 25% reduction in progression from intermediate to advanced AMD over 5 years. This is significant — one in four people who would have gone blind did not.

AREDS2 replaced the original AREDS formulation’s beta-carotene (which increased lung cancer risk in smokers) with lutein and zeaxanthin. The lower zinc dose (25mg) showed similar efficacy with fewer GI side effects.

Who should take AREDS2: anyone with intermediate AMD (large drusen, pigmentary changes) in one or both eyes, or advanced AMD in one eye. Not indicated for early AMD or prevention in those without disease — the risk-benefit shifts at the population level.

Beyond AREDS2: The Functional Stack

Astaxanthin (4-6mg)

The retina’s photoreceptors face a unique oxidative challenge — they are constantly exposed to focused light while maintaining the highest metabolic rate in the body. Astaxanthin, a keto-carotenoid from Haematococcus pluvialis, crosses the blood-retinal barrier and accumulates in the retina and choroid.

Saito (2012) demonstrated that 6mg of astaxanthin daily improved retinal capillary blood flow in a randomized study. Given that choroidal blood flow decline is a primary pathogenic factor in AMD, this is mechanistically relevant. Astaxanthin also reduces CRP and IL-6, addressing the inflammatory component.

Omega-3 DHA (1-2g)

DHA (docosahexaenoic acid) constitutes 50-60% of the fatty acids in photoreceptor outer segment membranes — the highest concentration of any tissue. The retina actively concentrates and retains DHA. SanGiovanni’s analysis from the AREDS data (2008) found that participants with the highest dietary omega-3 intake had 38% reduced risk of progressing to advanced AMD compared to those with the lowest intake.

The AREDS2 trial itself did not show a statistically significant benefit of supplemental omega-3, but this was likely confounded by: (1) participants already had moderate omega-3 intake, (2) the dose (350mg DHA + 650mg EPA) may have been insufficient, and (3) the EPA:DHA ratio was not optimized for retinal tissue.

Recommendation: 1-2g DHA daily from triglyceride-form fish oil or algal DHA for AMD patients. This exceeds the AREDS2 dose and aligns with the epidemiological evidence.

Saffron (20mg)

Perhaps the most exciting nutraceutical development in AMD. Falsini (2010) conducted a randomized crossover trial: 20mg saffron daily for 3 months significantly improved macular function as measured by focal electroretinogram (fERG). Subsequent longer-term studies (Lashay 2016) confirmed sustained benefit. The active compounds — crocin and crocetin — have potent antioxidant, anti-inflammatory, and neuroprotective properties, and appear to protect RPE cells from oxidative damage.

Dose: 20mg standardized saffron extract daily. One of the few supplements with direct clinical evidence in macular function improvement.

Additional Retinal Support

• Bilberry (Vaccinium myrtillus): Rich in anthocyanins that support night vision and retinal microcirculation. 160-320mg standardized extract (25% anthocyanins). Historical use by WWII RAF pilots for night vision — the evidence base is modest but the safety profile is excellent
• Ginkgo biloba 120-240mg: Improves ocular blood flow. Quaranta (2003) showed benefit in glaucoma (improved visual field); rational for AMD given shared vascular pathology
• Alpha-lipoic acid 300-600mg: Mitochondrial antioxidant, crosses blood-retinal barrier, regenerates vitamins C and E
• Meso-zeaxanthin: The third macular pigment carotenoid (along with lutein and zeaxanthin). Found at the center of the fovea. Not readily obtained from diet. 10mg supplementation increases macular pigment optical density

Blue Light: The Modern Threat

The macula’s yellow pigment (lutein + zeaxanthin + meso-zeaxanthin) is a natural blue light filter — it absorbs blue-violet light (400-460nm) before it reaches the photoreceptors. This is why it is yellow — it absorbs blue. Individuals with low macular pigment density have higher AMD risk.

Blue light sources of concern:

• LED screens (phones, tablets, computers, TVs) emit disproportionate blue light
• LED lighting (especially cool white/daylight bulbs)
• Sunlight (the original and most intense source)

Practical strategies:

• Build macular pigment with supplemental lutein (10-20mg) + zeaxanthin (2-4mg) + meso-zeaxanthin (10mg) daily — takes 6-12 months to maximally increase macular pigment density
• Blue-blocking glasses for prolonged screen use (amber or orange tint lenses)
• Night mode / blue light filtering software (f.lux, Night Shift, built-in OS features) after sunset
• Warm-toned LED bulbs (2700K or lower) in home lighting
• The 20-20-20 rule: every 20 minutes, look at something 20 feet away for 20 seconds

Glaucoma: Functional Support

Glaucoma — progressive optic nerve damage, usually but not always associated with elevated intraocular pressure (IOP) — is the second leading cause of blindness worldwide. The functional approach supports conventional IOP-lowering treatment rather than replacing it.

• Magnesium: Vasodilator effect improves optic nerve head blood flow. Gaspar (1995) demonstrated improved visual field and ocular blood flow with magnesium supplementation. 400-600mg daily
• Ginkgo biloba 120-240mg: Quaranta (2003) — improved visual field in normal-tension glaucoma, likely through improved ocular blood flow and neuroprotection
• CoQ10: Neuroprotective for retinal ganglion cells. 100-200mg daily. Topical CoQ10 eye drops (where available) deliver directly
• Vitamin B3 (nicotinamide): Williams (2017) — NAD decline in aging retinal ganglion cells contributes to vulnerability. Nicotinamide 3g/day showed neuroprotective effects in a clinical trial. High dose requires monitoring
• Dark green leafy vegetables: Dietary nitrates convert to nitric oxide, which improves blood flow and may reduce IOP. Kang (2016) — higher green vegetable intake associated with 20-30% reduced glaucoma risk
• Exercise: Regular moderate aerobic exercise lowers IOP acutely and chronically (3-5 mmHg reduction). Weight training with Valsalva maneuver temporarily increases IOP — use caution, breathe continuously during resistance exercise
• Citicoline 500-1000mg: Neuroprotective, enhances retinal ganglion cell function, multiple studies show improved visual field and pattern electroretinogram in glaucoma

Dry Eye: Beyond Artificial Tears

Dry eye disease affects 5-50% of the population depending on diagnostic criteria and geography. It is an inflammatory condition of the ocular surface — not simply insufficient tears.

• Omega-3: Anti-inflammatory effect on meibomian glands and tear film. 2-3g combined EPA/DHA daily. The DREAM study (2018) showed omega-3 did not outperform placebo in a specific population, but overall evidence across multiple trials remains positive, and clinical experience supports benefit
• Vitamin A: Maintains goblet cells that produce the mucin layer of the tear film. Deficiency is a classic cause of dry eye (xerophthalmia). 5000-10,000 IU retinol daily
• Warm compresses + lid hygiene: Meibomian gland dysfunction (MGD) is the leading cause of evaporative dry eye. Warm compresses (40-45 C for 10 minutes) melt inspissated meibum. Follow with gentle lid massage and lid scrubs (dilute tea tree oil or hypochlorous acid spray)
• Punctal plugs: Tiny silicone plugs inserted into tear drainage ducts to retain tears on the ocular surface. Simple in-office procedure, often dramatically effective
• Environmental: Humidifier (especially in heated/air-conditioned rooms), blink consciously during screen use (blink rate drops from 15/minute to 3-4/minute while reading screens), position screen below eye level (reduces exposed ocular surface area)
• Screen breaks: The 20-20-20 rule specifically helps dry eye by prompting complete blinks and distance refocusing

Diabetic Retinopathy

The primary intervention is glycemic control — every 1% reduction in HbA1c reduces microvascular complications (including retinopathy) by approximately 37% (DCCT/UKPDS data). Functional support:

• Alpha-lipoic acid 600mg: Improves insulin sensitivity and provides retinal antioxidant protection
• Pycnogenol 100-150mg: French maritime pine bark extract. Steigerwalt (2009) demonstrated improved retinal edema and visual acuity in early diabetic retinopathy
• Vitamin D: Deficiency correlates with diabetic retinopathy severity. Optimize to 50-70 ng/mL
• Curcumin 500-1000mg (bioavailable form): Anti-inflammatory, may protect retinal pericytes from hyperglycemia-induced damage

Cataracts: Prevention

The lens accumulates oxidative damage over a lifetime — cataracts are the result. Unlike the retina, the lens has no blood supply and limited antioxidant regeneration capacity once damaged.

• Vitamin C: Rautiainen (2010) — Swedish Mammography Cohort study of 24,593 women: those taking vitamin C supplements had 45% lower risk of cataracts. The aqueous humor concentrates vitamin C to 20-50x plasma levels, forming the lens’s primary antioxidant defense
• Lutein and zeaxanthin: Present in the lens as well as the retina, filtering blue light and quenching singlet oxygen
• NAC (N-acetylcarnosine) eye drops: Controversial. Some studies suggest benefit for early cataracts (Babizhayev 2009), but evidence quality is mixed. Not harmful — reasonable to try for early cataracts in patients wanting to delay surgery
• UV protection: Quality sunglasses (UV400 or 100% UV blocking) from childhood onward. UV-B is the primary cataractogenic wavelength
• Blood sugar control: Diabetes significantly accelerates cataract formation (sorbitol pathway)

The Integrated Vision Protocol

Vision loss is not an inevitable consequence of aging. It is a consequence of cumulative oxidative damage, chronic inflammation, metabolic dysfunction, and inadequate nutritional support to the most metabolically demanding tissue in the body. Every intervention that supports mitochondrial function, reduces inflammation, improves blood flow, and provides targeted antioxidant protection to the retina reduces risk.

The eyes see the world. But the body feeds the eyes. What are you feeding them?