1. Two diseases under one name
Age-related macular degeneration attacks the macula — the small central part of the retina that does reading, faces and detail. It is the reverse of glaucoma: it takes the middle and leaves the edges, so people keep their navigational vision and lose the vision they most notice using.
| Dry AMD | Wet AMD | |
|---|---|---|
| How common | The large majority | Less common |
| What happens | Drusen accumulate, then cells are lost. Advanced form is geographic atrophy | Abnormal leaky vessels grow under the retina and bleed or leak |
| Speed | Years, usually slow | Days to weeks |
| Treatment | Historically none; the newer drugs slow atrophy rather than restore sight | Anti-VEGF injections into the eye, and they work |
The practical instruction that matters most on this page. New distortion — straight lines looking bent or wavy, a doorframe kinking, letters missing from the middle of a word — is a same-week problem and possibly same-day. That is how wet AMD presents, it moves fast, and anti-VEGF treatment protects the sight you still have rather than returning what has gone. Delay is what costs people the central vision in their better eye.
Cover one eye and then the other occasionally. Wet AMD in one eye is easy to miss entirely because the other eye compensates, and people discover it when the second eye goes.
2. Risk, and the one factor that dominates
Smoking is by a distance the largest modifiable risk factor for AMD, and this is one of the places where the effect is large enough that it should change behaviour on its own. Age and genetics are the other big contributors and neither is modifiable.
Beyond that: blood pressure and cardiovascular health plausibly matter through retinal microcirculation, and a diet with plenty of dark leafy greens and coloured vegetables supplies the carotenoids the macula concentrates. That is the same dietary advice as the eating topic gives for other reasons, which is a point in its favour rather than a coincidence.
3. AREDS2, and the thing almost everyone gets wrong about it
The Age-Related Eye Disease Study 2 produced the only supplement formulation in this whole site with a genuine, large, randomised evidence base behind it. The daily formula:
| Component | Dose |
|---|---|
| Vitamin C | 500 mg |
| Vitamin E | 400 IU |
| Zinc | 80 mg — or 25 mg in lower-zinc versions |
| Copper | 2 mg — present only to prevent the anaemia that high-dose zinc causes |
| Lutein | 10 mg |
| Zeaxanthin | 2 mg |
AREDS2 was tested in people who already had intermediate AMD, or advanced AMD in one eye. It is sold to people who have neither.
What the trial showed is a reduced rate of progression to advanced disease in that population. It did not show that a healthy person taking it will avoid AMD, and it was never designed to. Anyone selling it as eye insurance for a person with normal maculae is selling a result that does not exist — and doing so at a dose of zinc far above any nutritional requirement.
The right route is the boring one: have an eye examination, find out whether you have drusen and how much, and take the formula if an optometrist or ophthalmologist says your stage is the stage it was tested in.
Why beta-carotene came out, which is the best safety lesson in ophthalmology. The original AREDS formula contained beta-carotene. It was removed in AREDS2 because beta-carotene increased lung cancer risk in smokers and former smokers — a finding first seen in earlier trials of beta-carotene supplementation and confirmed as a real hazard. Lutein and zeaxanthin replaced it and performed at least as well. If you are looking at an old formulation on a shelf, that is a reason to check the label rather than a historical footnote.
4. Geographic atrophy — where the newest drugs are, and where they are not
Advanced dry AMD had nothing at all until recently. Two complement inhibitors — pegcetacoplan and avacincaptad pegol — were approved in the United States on the basis that they slow the rate at which the atrophic patch expands.
Three things belong with that, and rarely travel with it.
- They slow a lesion; they do not improve vision. The trials measured how fast the area of atrophy grew. Whether that translates into vision a patient notices keeping has been the central criticism of the class.
- They are monthly or two-monthly injections into the eye, indefinitely, with a real if uncommon rate of inflammatory complications.
- And in the UK they were not merely unavailable — they were refused. Pegcetacoplan was refused a marketing authorisation by the MHRA, and refused by the EMA; NICE suspended its appraisal on that basis. The manufacturer of avacincaptad withdrew its European application, and its UK appraisal is listed as awaiting development. The regulators' stated reason is the objection in the bullet above: slower lesion growth was not matched by a measurable visual benefit. That is a substantive judgement about the evidence, not a delay in the queue, and it is worth knowing before reading American coverage that describes these as available treatments. Checked August 2026 — a moving position, and worth confirming rather than relying on this page.
For wet AMD the picture is entirely different and much better: anti-VEGF injections are well established NHS treatment, they work, and the limiting factor is how quickly someone is seen. Which returns the chapter to its first instruction.
5. What to actually do
- Do not smoke. Largest modifiable factor, not close.
- Have your eyes examined, and find out whether you have drusen — that is what decides whether AREDS2 applies to you.
- Check each eye separately, occasionally. One eye hides the other's problems.
- Treat new distortion as urgent, not as something to mention at the next appointment.
- Eat the greens because the dietary evidence is reasonable and the same pattern is well evidenced for other things — not because a capsule of it will do the same job.