Established 2006

Macula degeneration is very common, and care and treatment is available.  Below is a long guide of information, updated by Dr Peter Davies in June 2026.   

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Key points to remember

If you remember nothing else from this guide, remember these.

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The basics

• The macula is the small, high‑resolution centre of the retina — it gives you your sharp, detailed central vision.

• Every person’s macula ages throughout life; for some, that ageing leads to progressive loss of central vision.

• Macular degeneration is painless — any eye pain is a sign of something else and should be checked promptly.

• You do not go completely “black‑blind” from macular degeneration: it takes the fine central detail, but your peripheral vision — enough to move about and stay independent — remains.

What everyone should do

• Have an optometrist check your eyes every year once you are over 50.

• Monitor your own vision every day, one eye at a time — use the Amsler grid.

• Maintain a healthy diet and lifestyle; what is good for your heart is good for your macula, so keep your blood pressure, cholesterol and blood sugar controlled.

• If you smoke, stopping is the single most powerful thing you can do for your eyes.

• Tell your close relatives — macular degeneration runs in families, so they should have their eyes checked too.

• Some people — not everyone — should take vitamins; we will tell you if you are one of them.

Understanding the disease

• Wet macular degeneration grows on top of dry: it is not “wet OR dry” but dry PLUS leaking, so the dry ageing continues even after successful injections.

• A sudden change — new distortion, fresh blur, or a dark patch — is urgent; contact us straight away, because the sooner we treat wet AMD, the more sight we save.

Treatment

• All types of wet macular degeneration respond very well to injections: they usually improve vision at first, then slow further deterioration over time.

• Each drug’s effect is limited, so the injections must be repeated — indefinitely — to keep working.

• After each injection you are given a maximum treatment time interval. Do not stretch beyond it, or you risk permanent, irreversible loss of your central vision.

• Some forms of advanced dry macular degeneration (geographic atrophy) can now be treated with the new drugs Syfovre and Izervay, which slow the loss of central vision.

• We can control wet macular degeneration, but we cannot cure it — which is why treatment continues long‑term.

• Do not avoid cataract surgery out of fear for the macula — a treatable cataract should be treated.

• In Australia we are fortunate: government funding gives access to the best drugs, meaning the best results for the fewest injections.

Living well

• Needing treatment is not bad news — it means we finally have a powerful way to protect your sight; and if your mood suffers, please tell us, because help is available.

• Social support, and help from charities and visual‑aid services, matter enormously.

• A close, continuing relationship with your optometrist is vital to your care.

• Treatment is advancing quickly, with a real prospect that many patients will need fewer injections — or none — within a few years.

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Part A — Understanding your eyes and AMD

1.  What is macular degeneration?

Macular degeneration is ageing and damage to the macula — the small central part of the retina that gives you your sharp, detailed vision. It is what you use to read a book, to drive, to thread a needle, and to recognise a face across a room. When the macula stops working well, the centre of your vision becomes blurred, distorted, or patchy.

One reassuring fact comes up again and again, so it is worth saying first: macular degeneration never makes you completely, “black‑blind.” The disease attacks the centre of your vision and leaves the edges — your peripheral vision — working. People with even quite advanced AMD can still move around a room, see a doorway, and live independently. The loss is in the fine detail at the very centre, which is precious, but it is not the whole of your sight.

Although there are several causes of macular damage, by far the most common is simply age, which is why we call it age‑related macular degeneration, or AMD. It can begin in people as young as 50.

It is very common. Around one in seven people over 50 have some early ageing change in the macula, though only a small number go on to lose significant vision. Over the age of 75, roughly one in three show early signs. Because we are all living longer, AMD has become one of the leading causes of vision loss in older Australians — and advanced disease accounts for a large share of legal blindness in countries like ours.

For many years AMD was one of the most disheartening conditions we treated, because so little could be done. That has changed, and is still changing quickly. We now have powerful treatment for the “wet” form, the first treatments for advanced “dry” disease, and an active field of research. This guide walks through all of it.

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2.  A quick tour of the eye

It helps to picture the eye as a small, living camera.

Light first passes through the cornea, the clear front window of the eye. The cornea, together with the thin film of tears over it, does most of the focusing — which is one reason a healthy, well‑lubricated tear film matters so much. If your eyes feel dry or gritty, using lubricating drops genuinely helps your vision as well as your comfort.

Behind the cornea is the pupil, the adjustable opening that controls how much light enters, and then the lens, which fine‑tunes the focus. The large space behind the lens is filled with a clear jelly called the vitreous.

At the very back, lining the inside of the eye, is the retina — the light‑sensitive “film” that captures the picture. The small, central bullseye of the retina is the macula, and the pinpoint centre of the macula is the fovea, where your finest, most detailed colour vision is made. Every time you look directly at something, you are turning your eye so the image lands on this tiny spot.

From the retina, the picture travels down the optic nerve to the back of your brain, where most of what you actually “see” is assembled. Vision is as much a brain process as an eye process — a point that becomes important later when we talk about hallucinations in Charles Bonnet syndrome.

There is a short animation showing how the eye works — along with videos for most of the topics in this guide — on our website, www.huntereyesurgeons.com.

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3.  The RPE: the macula’s caretaker cells

Just behind the light‑sensing photoreceptors sits a single, vital layer of housekeeping cells called the retinal pigment epithelium, or RPE. You can think of the RPE as the macula’s caretaker or cleaning crew.

These are among the most metabolically active cells in the entire body. Every single day, each RPE cell recycles the worn‑out tips of the photoreceptors above it — an enormous, lifelong workload. As long as the RPE keeps up, the photoreceptors stay healthy and your vision stays sharp.

With age, the RPE gradually tires and falls behind. Waste material that should have been cleared starts to build up beneath the retina as tiny yellow deposits called drusen. Drusen are one of the earliest visible signs that AMD is beginning. If the RPE cells eventually fail and die, the photoreceptors they were supporting die too — and that is what produces the advanced “dry” disease we call geographic atrophy.

In one sentence

AMD is, at its heart, a disease of the macula’s caretaker cells — when the RPE tires and fails, the photoreceptors it looks after are lost, and central vision fades.

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4.  How the macula ages — a spectrum

AMD is not an on‑or‑off condition. It is better understood as a spectrum, running from a perfectly normal macula, through gentle ageing changes, to advanced disease. Knowing where you sit on this spectrum is what guides our advice and your monitoring.

Normal ageing

Some change in the macula with age is almost universal and causes no trouble at all. A few small drusen, on their own, are common and often harmless.

Early AMD — changes with no symptoms

Here we see more, or larger, drusen and subtle changes in the RPE pigment, but the vision is still normal and the person usually notices nothing. This stage matters enormously, because it is silent. It is found by examination and imaging, not by symptoms — which is exactly why everyone over 50, and certainly over 60, should have a regular check with their optometrist. Catching AMD early gives us the most options.

Intermediate AMD

Larger drusen and more definite pigment changes appear. Vision is often still good, but the risk of progressing to the advanced stages is now higher. This is the group in which vitamins (discussed later) can have a modest benefit, and the group that needs careful monitoring.

Advanced dry AMD — nascent and then geographic atrophy

As the disease advances on the dry pathway, the retina begins to thin and collapse in places. On detailed scans we can sometimes see the very earliest signs of impending atrophy, a stage called nascent geographic atrophy. This then develops into geographic atrophy (GA) — patches where the RPE and photoreceptors have actually died, leaving islands of non‑working retina. As these patches enlarge and approach the centre, reading and detailed vision are progressively lost.

Importantly, GA often spares the very centre (the fovea) until late. This is why some people with a surprising amount of atrophy can still read the eye chart reasonably well — for now. Protecting that central island for as long as possible is the whole goal of the new dry‑AMD injections.

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5.  The types of AMD — dry, new vessels, and wet

People often hear that there are simply two types of AMD, “dry” and “wet.” It helps to add one more in between, because modern imaging now shows the picture in far greater detail than the old two‑way split allowed.

Dry AMD (and its advanced form, geographic atrophy)

Dry AMD develops slowly, usually over many years. Cells in the macula fade and, in patches, die off — a little like a slow “dry rot” of the macula. Four out of five people with macular degeneration have the dry‑only type. For most, it progresses gently over years or even decades. Its advanced form is geographic atrophy, and for the first time we now have injections that can slow that down (Section 11).

New blood vessels that are not yet leaking (non‑exudative MNV)

Sometimes new, abnormal blood vessels begin to grow under the macula but have not yet started to leak. Doctors call these new vessels macular neovascularisation (MNV); when they are present but not leaking, the form is described as non‑exudative. We can now detect these silent vessels on a special scan called OCT angiography (OCTA) — a form of optical coherence tomography (OCT) that maps blood flow without any dye. By itself, a non‑leaking vessel may not need treatment — but it is a warning sign, and it means we watch that eye more closely, because it can convert to the leaking, “wet” form.

Wet AMD — leaking new vessels (exudative MNV)

In wet AMD, those new vessels leak fluid, fat and blood. This damages vision in two ways: the macula becomes water‑logged and stops working, and, if a vessel ruptures, a haemorrhage can cause sudden, severe loss. Left untreated, scar tissue eventually forms and central vision is destroyed. Wet AMD is the form we treat most powerfully — with injections (today most often Vabysmo or Eylea) — and treated early, the results can be dramatic.

If you have WET, you also have DRY.

This is one of the most important — and most confusing — ideas in the whole subject, so it is worth being very clear. It is not a case of wet or dry. It is wet and dry. Everyone with wet AMD also has the dry, ageing change underneath; the wet, leaking vessels are simply added on top of it.

The injections take away the wet component — the leaking blood vessels — and that is powerful. But they cannot touch the dry part: the slow “dry rot” of ageing in the macula continues underneath. So even after the injections have dried the macula beautifully, the underlying dry AMD remains and still needs watching.

Why this makes monitoring so important

Because wet AMD almost always develops from within existing dry AMD — and can appear quite suddenly — the single most valuable thing you and your optometrist can do is watch closely for the first sign of it. Catching the change from dry to wet within days, rather than weeks, is often the difference between keeping your central vision and losing it. This is why daily self‑checking matters so much.

Check each eye, every day

Use the Amsler grid (there is one at the back of this guide) one eye at a time, every day, and keep your regular optometrist appointments. A new patch of distortion, blur or a dark spot can mean dry AMD has turned wet — and the sooner we see it, the more sight we can save.

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6.  What you might notice — symptoms

In the early stages there are usually no symptoms at all, which is why regular checks matter so much. As AMD affects the working centre of vision, people may notice:

• Blurred or fuzzy central vision, or a general drop in sharpness.

• Distortion — straight lines (a door frame, a window, lines of text) appearing wavy or bent.

• A dark, grey or empty patch in the very centre of vision (a “scotoma”).

• Difficulty reading, recognising faces, or judging steps and kerbs.

• Needing more light than you used to, and struggling in dim or rainy conditions.

One very characteristic sign is that people start to look slightly to the side of what they want to see, using the healthier retina around the damaged centre. You may have noticed this in others — the actor Dame Judi Dench, who has AMD, describes having to look just past a person rather than straight at them. It is a normal and clever adaptation, not rudeness or confusion.

One reassuring point: AMD itself is completely painless. The changes happen quietly, with no ache or discomfort at all. So if you ever develop eye pain, that is a sign of something else — not your macular degeneration — and you should have it checked straight away.

The single most important symptom rule

Any new blur, distortion or dark patch — especially if it comes on suddenly — should be treated as urgent. Phone us the same day. It may be nothing, but it may be new wet AMD, where every day counts.

 

Part B — Treatment

We will deal with treatments in the order they matter most in day‑to‑day practice: first the injections for wet AMD, which is what most people are referred to us for; then the honest question of whether and when to continue them; then what you can do yourself for dry AMD; and finally the newest injections, which are for advanced dry disease.

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7.  Injections for wet AMD — our most powerful treatment

If you have wet AMD, injections into the eye are our most powerful and most established treatment, and the reason most people come to see us. We have been giving them since 2006, and they have transformed what used to be a hopeless diagnosis.

How they work

The medicines are called anti‑VEGF drugs. VEGF — vascular endothelial growth factor — is the signal the eye uses to grow new blood vessels; blocking it switches off the abnormal, leaking vessels, lets the macula “dry out,” and protects vision. For most people the vision first improves as the fluid clears, and then is held steady. The drugs do not cure the disease — the underlying dry AMD remains — but they control the dangerous, sight‑threatening leaking.

The drugs we use

The story of these drugs is one of steady improvement. We began in 2006 with Avastin (bevacizumab). It was then largely replaced by Lucentis (ranibizumab); both of those were in turn replaced by Eylea(aflibercept) 2 mg; and more recently Vabysmo (faricimab) arrived as a longer‑acting option. Today the two leading drugs, Eylea 8 mg and Vabysmo, are being compared to work out which gives the best result in an individual patient. A drug called Beovu was released in 2021 but is now rarely used, because in a small number of people it caused inflammation inside the eye.

In Australia we are very fortunate. Through federal government funding, we have access to the very best of these drugs for almost everyone who needs them. In many other countries — including the United States, where access is largely controlled by private health funds — most patients cannot get the best drugs. Australian patients therefore tend to receive the best treatment, which means the best results for the fewest injections.

We can treat wet AMD with ongoing injections, but we cannot cure it.

The injections control the leaking and protect your sight for as long as we keep giving them — but the underlying disease does not go away, which is why treatment continues over the long term.

What the injection is actually like

The procedure itself takes about two minutes and is easier than most people fear. We put in anaesthetic drops, then clean the eyelids and eye surface thoroughly with antiseptic — this cleaning is the single most important step in preventing infection. We usually use chlorhexidine: a study organised by Dr Davies and colleagues, published in the journal Ophthalmology (Merani and colleagues, 2016), found it to be a safe, well‑tolerated alternative that patients prefer. We use Betadine (an iodine antiseptic) only occasionally, for the few people who are allergic to chlorhexidine. You will then be asked to look in a set direction and to keep your lips sealed and not talk, because that is where stray bacteria come from. A very fine needle (30‑gauge — about the thickness of an eyelash) is used, and the medicine is gently injected. Most people feel only mild pressure; some feel a brief dull ache or, occasionally, a quick sharp sting that is over in a moment.

Afterwards

The eye may feel gritty for a day or two and can look bloodshot where a tiny surface vessel was nudged — this is harmless and clears over a couple of weeks. You may see floaters or small bubbles, and your vision may briefly dim as the eye pressure settles. All of this is normal.

Risks — small, but real

Serious complications are rare. The one we guard against most carefully is infection inside the eye (endophthalmitis), which occurs in roughly 1 in 5,000 injections. Because it can threaten sight, we take the cleaning and technique extremely seriously, and we need you to tell us at once if there is a problem (see the box below). Our practice has now performed well over 120,000 injections.

The “inject‑and‑extend” plan

Most people start with three injections 28 days (4 weeks) apart — the “induction” phase — to get the macula dry. After that we use a plan called inject‑and‑extend: at each visit, if the macula is dry, we stretch the gap (the treatment time interval, or TTI) to the next injection a little longer; if there is any fluid, we shorten it again. Over time we find the longest interval that keeps your macula dry, which for many people settles somewhere between 1 and 5 months. The aim is the fewest injections that fully control the disease. This plan is explained in much more detail in the next section.

What is coming

The field is moving fast, and several quite different approaches are in trials. There are new injected drugs, such as the tyrosine kinase inhibitors (TKIs), which block the same blood‑vessel signals in a different way. There are refillable slow‑release reservoirs implanted in the eye — a tiny port (one such device is called Susvimo) that is topped up only once or twice a year instead of regular injections. And there are gene therapies, showing very promising results, that prompt the eye to make its own anti‑VEGF, potentially from a single treatment. Putting it all together, we expect that within about three to five years these advances will mean no more injections for many patients.

New symptoms are an emergency — phone us the same day.

If you suddenly notice new blur, a new dark patch, or new distortion — or if after an injection you have increasing pain or worsening vision — contact us immediately. Do not wait, and do not “sit at home” hoping it settles.

I have seen patients lose sight over a single weekend from an untreated bleed. The sooner we act, the more vision we save.

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8.  Are the injections worth it? And when do we stop?

These are some of the most common — and most important — questions we are asked, by patients and by the families who love them. “Am I too old for this?” “My vision is already poor; is it really worth it?” “Is all this bother actually doing any good?” They deserve honest, careful answers, because the decision is genuinely yours to make. What follows is how we think about it together.

“Am I too old?”

Age, by itself, is almost never the deciding factor. What matters is not the number of years, but whether your eye is still benefiting from treatment and whether coming in for injections is manageable for you. We treat people well into their nineties who value their reading and their independence, and for whom the injections are straightforward. The right question is not “Am I too old?” but “Is this treatment still helping me live the way I want to?”

“Is my vision too bad to bother?”

This is a fair question, and the answer is usually no — for a few reasons. First, even when an eye cannot be made sharp again, controlling the wet disease prevents it from getting dramatically worse, including the kind of large, sudden bleed that can be painful and distressing. A controlled eye is a more comfortable, more stable eye.

Second, we always think about both eyes together. Often it is your better eye that does most of the work, and protecting it is very high value. But even an eye that is not your best contributes to your overall field of view, your balance, and your sense of the world — and it is insurance, in case anything ever happens to the other eye.

Third, vision is more than the eye chart. Many people who do not read more letters still report that the room looks brighter, faces are easier, or distortion has settled. Those things matter to daily life even when the chart score does not change.

Why we usually keep going — the maintenance phase

Once your eye is dry and stable, treatment moves into a maintenance phase. For most people, wet AMD is a long‑term condition that needs ongoing care, in the same way that blood pressure or diabetes does. We continue injections — at the longest comfortable interval — for as long as you are able and willing to come, because the evidence is clear that stopping treatment usually allows the disease to become active again and the vision to decline. Only occasionally does an eye “burn out” and stay quiet without treatment.

A small scar is better than a big one.

This is the simple idea at the heart of staying the course. We cannot undo the damage already done, but by keeping the disease controlled we keep any scar small, rather than letting it grow large and take the whole centre of your vision. Steady, modest treatment protects what you have.

Inject‑and‑extend, explained properly

The whole point of inject‑and‑extend is to give you the fewest injections that still keep the disease fully controlled — to reduce the bother without losing the benefit. It works by gradually increasing the treatment interval:

• We begin with the loading doses to dry the macula completely.

• At each visit we check the macula, usually with a scan. If the macula is dry, we lengthen the gap — the treatment time interval, or TTI — before the next injection (for example, from 4 weeks to 6, then 8, then 10, then 12).

• If a little fluid has returned, we shorten the gap again to the last interval that worked.

• Over time this finds your personal interval — the longest stretch your macula can go while staying dry. Some people reach 3–5 months between injections; others need them more often. Once I have found that longest safe stretch for you, I assign it as your maximum treatment time interval (TTI) for that particular drug.

Crucially, you generally still receive an injection at each visit, even when the macula is dry — the injection is what is keeping it dry. We are extending the interval, not skipping treatment. Stopping injections altogether is a different decision, discussed next.

So when do we actually stop?

Stopping is always a shared decision, never something done to you. There are a few situations where it is reasonable to consider it:

• When the disease appears truly inactive. Rarely, an eye stays dry with longer and longer gaps and seems to have settled. We may then carefully trial a pause, with close monitoring, ready to restart at the first sign of activity.

• When further treatment can no longer help that eye. If an eye has a dense central scar with no salvageable central vision, and there is no useful purpose in continuing, we may agree to stop — provided the other eye does not depend on the same decision.

• When coming in is no longer manageable. Frailty, illness, or the sheer effort of travel can tip the balance. We will always try to find an easier path first — longer intervals, a longer‑acting drug, help with transport — before stopping.

• When it is your considered wish. You are always free to choose. Our job is to make sure that choice is fully informed — including what is likely to happen to the vision if we stop — and then to support whatever you decide.

If treatment does stop, that is not the end of your care. Your optometrist continues to look after you, we continue to care for the comfort and health of the eye, and the door is always open to come back and restart if circumstances change.

The bottom line

Injections are worth it for most people, for most of the time, because they protect vision that would otherwise be lost — and a small scar really is better than a big one. But “worth it” is partly a personal judgement about your life, your energy and your priorities, and you should never feel you cannot raise it.

Please ask. If you are wondering whether the bother is worth it, say so at your visit. We would much rather talk it through honestly than have you quietly struggling with the decision alone.

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9.  Where injections are given, and what they cost

Eye injections can be given in three kinds of place: a government (public) hospital, or a doctor’s private rooms, or a licensed private day hospital. All are safe and effective — what differs is the drug used, the cost, the infection rate and the convenience. Which path suits you is a decision we make together.

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Public hospitals

Public hospitals typically provide a limited course — often around three injections — using a biosimilaranti‑VEGF drug. Biosimilars are cheaper, near‑copies of the original, fully‑researched drugs. They are highly similar, but not identical, to the brand‑name drugs (such as Eylea and Vabysmo) described earlier. Once a patient reaches the public hospital’s limit, schemes are in place to transfer ongoing care to doctors’ private rooms in the community.

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Private rooms and licensed hospitals

In private rooms or a licensed private hospital, the full range of the best‑researched drugs is available, and your care can continue with one doctor for as long as it is needed. What you pay depends on where the injection is given. If you choose to have your injection in a licensed hospital and you hold private health insurance, you can usually claim the treatment through your health fund — in Australia, eye injections are classified as a Level B procedure.

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Your choice, with full information

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Australian medical consent law requires your doctor to explain your treatment options — including the drug, the location, the costs, and what each choice means over the whole course of treatment — so that the decision is yours, made with full information. Please ask us about any of this; we are always happy to talk it through.

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10.  What you can do for dry AMD — lifestyle, diet, vitamins and light

For the dry, non‑leaking forms of AMD — which is most people — there is a great deal you can do yourself to look after your macula. None of it is a cure, but the habits below are genuinely worthwhile, and most are good for your heart and brain as well as your eyes.

Don’t smoke — the single most important thing

Smoking is the strongest risk factor you can actually change. It roughly doubles the risk of AMD and speeds its progression. Any exposure to smoke is harmful. If you smoke, stopping is the most powerful single step you can take for your macula — and it is never too late to benefit. We are happy to help you find support to quit.

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Eat for your eyes

A Mediterranean‑style diet, rich in vegetables and fish and low in processed and “trans” fats, is consistently linked with a lower risk of AMD progression. Practical points:

• Dark green leafy vegetables and fresh fruit, several times a week. Greens such as spinach and kale are rich in lutein, the natural pigment that protects the macula. Cook them lightly or eat them raw.

• Fish, two to three times a week, for omega‑3 fatty acids — good for the eye, the heart and the circulation.

• A handful of nuts a week, and eggs, which are a useful source of lutein and zeaxanthin.

• Limit saturated (animal) fats and especially “trans” fats from commercially processed foods. Extra‑virgin olive oil is a healthier choice; heavily modified commercial oils are best avoided.

The newer thinking on sugar

There is growing interest in the role of sugar. Modern diets are very high in sugar — commercially processed foods especially — and, with the loss of any natural fasting between meals, the cells of the body are bombarded with sugar almost continuously. Modern grains, such as those used in commercial bread, have been heavily modified and tend to release their sugar much faster (a higher glycaemic index) than older grains; put simply, the sugar‑chain molecules break down more quickly in modern food. Expert opinion is increasingly shifting towards the amount and type of sugar in our diet as a major cause of harm to our overall health — very likely including the health of the macula. This thinking is still developing, but moderating sugar and processed carbohydrates is sensible for the whole body.

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Look after your whole‑body health

What is good for your heart and circulation is good for your macula, because the macula has a rich and delicate blood supply. Stay physically active, keep to a healthy weight, and ask your GP to keep your blood pressure, cholesterol and blood sugar well controlled. The very things that damage blood vessels elsewhere in the body — smoking, high blood pressure, high cholesterol and diabetes — also work against your eyes, so managing them is one of the most useful things you can do for your sight.

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Vitamins — for the right people

The large Age‑Related Eye Disease Studies (AREDS and AREDS2) showed that a specific combination of antioxidant vitamins and minerals can modestly reduce the chance of progressing to advanced AMD — but only for a particular group: people with intermediate AMD, or advanced disease in one eye. The benefit is real but small, and there is no proven benefit for people with no AMD or only mild changes. So vitamins are not for everyone, and we will tell you whether you are in the group likely to benefit.

If they are recommended for you, a commercial AREDS2‑based preparation (brands change, so check the label) taken daily is the usual approach. Aside from the cost of buying them, these supplements are very unlikely to do you any harm. Our own preference, wherever possible, is that you obtain the nutrients you need from a healthy diet and lifestyle rather than from a bottle.

A natural question is whether vitamins also slow geographic atrophy, the advanced dry form. Here the evidence is genuinely mixed and still being argued over. One large 2024 re‑analysis of the AREDS studies suggested the supplements might slow atrophy spreading toward the centre of vision in people whose atrophy had not yet reached it. However, more recent analyses — including ones that used the untreated (placebo) groups from the new geographic‑atrophy drug trials and other modern studies with sharper imaging — found no clear effect on atrophy growth. So we cannot promise that vitamins slow geographic atrophy, and the question remains open.

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Sunglasses and light

The short, blue‑violet wavelengths of light carry the most energy and can stress the retina, partly by activating a waste pigment called lipofuscin that releases damaging free radicals. Good sunglasses in bright conditions are a sensible, low‑cost protection, especially for people with lighter eyes, who have less natural pigment to shield the retina.

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The newer light story — red and infrared light (photobiomodulation)

This is one of the most interesting areas of current research, and it is worth setting out carefully — because the science is promising but still emerging, and it is easy to get ahead of the evidence.

The idea is that longer wavelengths of light — deep red and near‑infrared, roughly 650 to 900 nanometres — are absorbed by the mitochondria, the tiny power plants inside our cells, and may help them work better and reduce inflammation. This same light also helps set the body’s daily “circadian” clock. The physician and researcher Martin Moore‑Ede, sometimes called “The Light Doctor,” has written about how modern lighting has shifted heavily towards the blue end and stripped much of this natural red and infrared light from our days.

None of the following is a prescription — it is simply where the thinking is heading, and what some of us are choosing to do in our own lives while the research matures:

• Getting outside around sunrise and sunset, when natural light is rich in red and infrared.

• Enjoying the warm light of an open fire or campfire, as our ancestors did.

• Turning lights down in the evening rather than living under bright light until late, and shifting computer, iPad or phone screens towards warmer tones at night.

Light‑treatment devices — photobiomodulation

A series of randomised trials — the LIGHTSITE I, II and III studies — tested one particular machine (the Valeda system) that delivers carefully controlled wavelengths of light to the eye. For the first time in dry AMD, a treatment showed a measurable improvement in vision on the eye chart, and the device has since received marketing authorisation in the United States.

That is genuinely encouraging, and we are watching it closely. In fairness, though, there are real reasons for caution. The gains were small — only a few letters — and, tellingly, the sham (placebo) group improved too, by about three letters, with the treated group only a little better. Vision in intermediate AMD also fluctuates naturally from visit to visit by as much as, or more than, the gains seen. For all these reasons, experts disagree about how much of the benefit is a true treatment effect, and larger, longer studies (such as the EUROLIGHT trial now under way) are needed before we can be confident how much it helps, and for whom.

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A careful word about devices and marketing

Here it is worth being frank, because new machines for AMD appear regularly and are often marketed enthusiastically. The important thing to understand is a difference in the rules: a new drug must pass an enormous amount of independent research to prove it is both safe and effective before it can be sold. A device or machine, by contrast, does not face the same benefit test — it can be registered on the basis of safety and manufacturing quality alone, which is not the same as proof that it actually works.

Two examples make the point. A laser called the 2RT was studied in a large trial (the LEAD study). Overall it did not slow progression, and in one subgroup of patients it appeared to make things worse — a sharp reminder of why we wait for evidence. A microcurrent device marketed as MacuMira has a single, industry‑funded trial behind it, with limitations in how it was designed; its regulatory registration reflects safety and manufacturing standards, not a regulator’s finding that it works, and some of the marketing claims run ahead of what the published research actually shows.

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Our promise on new treatments

We treat every patient as we would treat our own family. If the evidence for a treatment or a machine becomes genuinely clear, we will offer it without hesitation. Until then, we will be honest that the proof is not yet there — and we would rather tell you that than sell you something that only shows promise.

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11.  New injections for geographic atrophy (Syfovre and Izervay)

For many years we had no treatments for dry AMD and geographic atrophy (GA). There are now new drugs approved for these conditions — the newest treatments in this guide. They are a completely different category from the wet‑AMD injections, and it is vital to understand how.

What they are, and how they work

Geographic atrophy is driven partly by over‑activity of the complement system, a part of the immune system that, when dysregulated, causes inflammation and unnecessary loss of retinal cells. The two new medicines calm this system. Syfovre (pegcetacoplan) blocks a step called C3; Izervay (avacincaptad pegol) blocks a later step called C5. Both are given as injections into the eye, roughly every one to two months.

What they do — and, just as importantly, what they don’t

This is the key point. In the major trials — OAKS and DERBY for Syfovre, and GATHER1 and GATHER2for Izervay — both drugs slowed the growth of the atrophy patches on retinal scans, by roughly a fifth to a quarter, with the effect building over time. But across the trials as a whole, they did not improve vision, and did not clearly slow the loss of vision in the first couple of years.

It is also worth being clear that, so far, all of this evidence comes from trials funded by the drug companies themselves. Independent, long‑term data are still awaited.

This is the crucial difference from wet AMD. For wet AMD, the injections usually improve vision. For geographic atrophy, the injections slow the disease on the pictures — they make the scans progress more slowly — but they do not restore sight, and the disease still advances, only more gently. It is because of this distinction that most countries have so far chosen not to approve them.

Why the scans can improve while the vision still fades

There is a thoughtful, science‑based explanation for this puzzle, sometimes called the “zombie cell” hypothesis. The complement system that these drugs block has an important normal job: it helps the body clear away sick and dying cells (cells dying in the controlled way known as apoptosis). If we block that pathway, we may slow the clearing‑away of those cells — so the area of visible atrophy on the scan grows more slowly, and the pictures look better, even though the cells left behind are not truly healthy and the vision continues to deteriorate. In other words, the drug may be preserving the appearance of the retina more than its function. This is only a hypothesis, but it is a credible attempt to explain why the scans and the vision can tell different stories.

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Who is likely to benefit most

When the trial results are looked at more closely, the people who appear to gain the most are those treated early — before the atrophy has reached the very centre (the fovea), while their vision is still normal. The logic is preventive: by slowing the patches before they reach the centre, we may buy extra years of useful central vision. This is exactly the group the federal government, through the TGA, has approved the drugs for: patients with normal vision and an intact fovea, whose central vision is threatened by atrophy that has not yet reached it.

This is more than just a hope. A later analysis of the OAKS and DERBY patients who still had good vision — including detailed maps of macular function (microperimetry, the kind of test the MAIA performs) — found that treatment delayed the time to significant loss of central vision by roughly six to twelve months. Put another way, it can mean extra months, or even years, of useful central vision compared with no treatment. For someone with early geographic atrophy and good vision, this is the single most important reason to consider treatment — and this is precisely the group we are aiming to treat. The catch is that these are often the very people who notice no symptoms at all yet, which is exactly why careful monitoring matters so much.

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Measuring it precisely matters

Deciding who fits this group, and tracking whether treatment is helping, has been transformed by modern imaging. Autofluorescence — including blue and green autofluorescence — maps the atrophy and the ellipsoid zone (EZ), the layer that reflects surviving photoreceptors; and MAIA microperimetry measures macular function across the whole macula, not just at the central fovea. Together these let us judge function, not just appearance — which, as the section above explains, is the distinction that really counts.

One group these drugs are not yet proven for

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If you are already having injections for wet AMD, there is currently no evidence of benefit from adding Syfovre or Izervay. The studies simply have not been done, and the data to answer that question are not yet published. So while it is a reasonable question to ask, we cannot honestly recommend it on the strength of evidence that does not exist.

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Risks to weigh

• A higher chance of developing wet AMD. These drugs roughly double the risk of the eye developing the leaking, wet form — which would then need its own anti‑VEGF injections. Spacing the dose to every other month reduces this risk.

• Inflammation inside the eye, and a rise in eye pressure (reported a little more with Izervay).

• Rare but serious events, including a form of retinal blood‑vessel inflammation called occlusive vasculitis, seen very rarely with Syfovre — estimated at about 1 in 10,000 injections. Because this rare complication usually happens with the very first injection, the medical advice is to give a test injection to the poorer‑seeing eye first, so that if it does occur, it affects the less important eye. To date, the published Izervay trials have not reported these vasculitis events.

Where things stand in Australia

Both drugs are now registered by the Therapeutic Goods Administration (TGA) — Syfovre in January 2025 and Izervay in October 2025 — for adults with geographic atrophy that spares the central fovea and where central vision is threatened. Registration, however, is not the same as government funding. Syfovre has received a positive recommendation from the committee that advises on the Pharmaceutical Benefits Scheme (PBS), an important step, but a listing has not yet been finalised. For now, the drugs are expensive — in the order of $20,000 per year. While the government decides whether to fund them, Syfovre is currently being made available at no charge to selected patients through a company access program. This is an active, fast‑moving area, and we will keep you informed as funding decisions are made.

An honest summary of the GA injections

These are a genuine milestone — the first treatments ever for advanced dry AMD — and for the right person, started early, they may preserve useful central vision for longer. But they slow the disease rather than reverse it, they carry real risks, and they are not yet funded. Whether they are right for you is very much an individual decision, weighed carefully together.

 

Part C — Measuring and monitoring

Looking after AMD well depends on measuring two different things: how your macula is functioning (what you can actually see), and how it looks anatomically (what the scans show). The two do not always agree — and the gap between them is one of the most important ideas in modern macular care.

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12.  How we measure your vision and visual function

The eye chart

The familiar letter chart remains the mainstay of measuring vision, and it is what the law uses for driving. But it has real limitations: it measures only the very best spot of remaining vision, in ideal lighting, and it can miss a great deal of what is happening across the rest of the macula.

Contrast sensitivity

This test measures your ability to tell apart subtle shades of grey, rather than sharp black letters. Real life is full of low‑contrast tasks — a step in dim light, a face in shadow — and contrast can be affected in AMD even when the letter chart looks reasonable.

Reading speed

How quickly and comfortably you can read a passage often reflects everyday function better than a single line of letters. Reading speed has been shown to be a useful measure of macular function, and a useful predictor of how the macula is likely to do over time, so we sometimes track it at successive visits.

MAIA microperimetry — measuring the macula point by point

This is a newer and very valuable test. The MAIA machine shines tiny spots of light at many different points across your macula and asks you to press a button each time you see one — a little like a visual field test, but focused on the macula itself. The result is a detailed map showing exactly which parts of your macula are working well and which are not. It is useful in two ways: it explains how a particular macula is actually functioning — not just the single best spot the eye chart measures — and, repeated over time, it measures change, so we can see whether an eye is stable or slipping. A healthy macula lights up green; weaker areas show as lower numbers or darker zones.

The eye‑chart paradox

We sometimes see a patient who can read well down the letter chart — close to normal — and yet whose MAIA map shows the macula is, in truth, working poorly across much of its area. The chart measures the best surviving spot; the MAIA measures the whole macula. This is why we increasingly rely on the macular map, not the chart alone, to understand how an eye is really doing and how it is changing over time.

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13.  How you monitor yourself, every day

Some of the most valuable monitoring is the kind you do at home. Two simple daily habits let you catch change early — and early change is exactly what we want to know about.

The one‑eye cover test, while you brush your teeth

Tie it to something you already do every day. While brushing your teeth, simply cover one eye, look at something detailed (a clock, a line of tiles, a face), then swap and check the other eye. You are asking a simple question of each eye on its own: is this as clear today as it was yesterday? Because we use both eyes together, a change in one eye is easily missed unless you check them separately.

The Amsler chart

The Amsler chart is a simple grid of straight lines with a dot in the middle. It is the single most useful tool for spotting change in the macula, and a copy is included at the back of this guide. Use it as follows:

• Wear your usual reading glasses.

• Hold the chart at comfortable reading distance in good light.

• Cover one eye, and look steadily at the central dot with the other.

• Note whether any of the lines look wavy, bent, broken or missing, or whether there is a blurred or grey patch. Then repeat with the other eye.

Put it where you’ll actually use it

The best place for the Amsler chart is not the fridge — it is the back of the toilet door, or beside the bathroom mirror, somewhere you will see it every single day. Check it daily, one eye at a time. If new waviness, distortion or a new dark patch appears, contact us promptly — it may be early wet AMD, where quick treatment makes all the difference.

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14.  How we measure the anatomy — imaging

Alongside your vision, we photograph and scan the structure of the macula. Modern imaging is painless, fast, and remarkably detailed.

• Colour photographs of the retina give the overall picture and track change over the years.

• Infrared imaging reveals features that are hard to see in ordinary colour.

• Autofluorescence (AF) is now the most important photograph for geographic atrophy. It maps the health of the RPE caretaker cells: dead areas appear black, while a bright ring around them shows cells that are sick and at risk. There are now different forms — blue‑light and green‑light autofluorescence, for example — which highlight slightly different details. Comparing the black centre and the bright ring over time tells us how fast the atrophy is advancing.

• OCT (optical coherence tomography) is a cross‑sectional scan — like a microscopic slice through the macula. We use it at almost every visit to detect fluid, the hallmark of active wet AMD, and to measure thinning.

• OCT angiography (OCTA) maps the macular blood vessels without any dye, and can reveal new vessels before they leak — the “silent” non‑exudative form mentioned earlier.

• Fluorescein and ICG (indocyanine green) angiography, which do use an injected dye, are reserved for when we need to see leakage in detail. There is a dedicated handout about this test at the back of the guide.

Computer and AI‑assisted mapping

The newest step is software that automatically measures and tracks features that are hard to judge by eye — for example, mapping the boundary of the healthy photoreceptor layer (the ellipsoid zone, or “EZ” line) in geographic atrophy, or precisely measuring the area of atrophy from one visit to the next. This kind of objective, repeatable measurement is becoming central to deciding who benefits from the new dry‑AMD injections, and to proving whether a treatment is working.

 

Part D — Living well with AMD

15.  Driving, faces and everyday life

 

Driving

This is the question almost everyone wants to ask, and it is a delicate one. The legal standard for driving is based mainly on how far down the letter chart you can read, plus an adequate width of peripheral vision. Many people with macular disease meet that standard and are perfectly entitled to drive, and we can sign the licence accordingly.

But meeting the standard is not quite the same as being at your best behind the wheel. Because the chart measures only your best central spot, a person can pass it and still find real driving harder than it used to be — particularly the part we call fixation stability. A healthy macula holds steadily on a target, giving the brain time to read it. When the macula is damaged, the eyes wander a little and fixation is less steady, which makes fast, detailed tasks — reading the number on an approaching bus, judging a moving car at dusk — noticeably harder.

So our advice is balanced: if you meet the standard you may drive, but be honest with yourself about difficult conditions — night, rain, glare, unfamiliar roads — and be willing to limit your driving to the situations where you feel genuinely safe. It is about caution and self‑awareness, not blanket rules.

 

Faces, steps and moving objects

Day to day, AMD can make it harder to recognise faces (you may need to get a little closer, which is entirely normal), to judge steps and kerbs, and to track moving objects such as a ball or a grandchild running past. Good lighting, magnifiers, high‑contrast markings on steps, and the low‑vision aids available through the support services below can all make a real difference.

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16.  Cataract surgery when you also have AMD

Cataracts — a clouding of the eye’s natural lens — and AMD are both common with age, and a great many people have both at once. A frequent and understandable worry is whether having cataract surgery might make the macular degeneration worse. It is an important question, so it is worth answering clearly.

We do not let people lose vision to a cataract out of fear of the macula

A treatable cataract is a fixable cause of poor vision, and the evidence does not support withholding surgery because of AMD. We will not let you give up sight you could keep.

The reassurance is grounded in good evidence. In the large AREDS2 study, people with AMD who had cataract surgery showed no increased risk of their AMD progressing over many years of follow‑up. Some very long‑term studies hint at a possible small risk many years later, but the overall picture is reassuring, and the benefit of restoring vision is real and immediate.

What we do first is work out how much of your blurring comes from the cataract and how much from the macula, using examination and imaging. If the cataract is a genuine contributor, removing it can give a worthwhile improvement — and, as a bonus, it usually makes it easier for us to see and monitor your macula afterwards. If the macula is severely affected, the gain may be more modest, and we will always be honest with you about what to realistically expect. As with everything in this guide, the decision is made together.

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17.  Looking after your emotional wellbeing

Changes to your sight, or the prospect of a long course of treatment, can affect your mood as well as your vision — and that is completely understandable. Low mood and worry are common among people with AMD; feeling this way is not a weakness, and you are far from alone in it.

It also helps to turn one idea on its head. Needing treatment is not bad news. For wet AMD especially, the fact that we have a treatment — and such a powerful one — is the good news. Needing injections means we have a real and effective way to protect your sight, which only a generation ago we simply did not have. The treatment is a reason for hope, not for dismay.

A great deal can also be done to help you keep doing the things you love. Low‑vision rehabilitation provides practical tools — magnifiers, brighter and better‑placed lighting, large‑print and audio books, simple apps on a phone or tablet, and techniques such as “eccentric viewing,” where you learn to look just to the side of what you want to see, using the healthy retina around the worn centre. This kind of support does more than help you see: structured low‑vision rehabilitation has been shown to roughly halve the risk of becoming depressed after vision loss.

Because reduced central vision can affect balance and judging steps, it is also worth taking simple care against falls — good lighting, removing trip hazards, and marking the edges of steps all help. And if low mood, worry or a loss of interest lasts more than a week or two, please tell us or your GP. It is common, it is treatable, and support is available — the Macular Disease Foundation, Vision Australia and Guide Dogs all offer practical help and a friendly ear.

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18.  Charles Bonnet syndrome

This is important to know about, because it frightens people who have not been told about it. When vision is significantly reduced, the visual part of the brain can begin to “fill in the gaps” by inserting vivid, detailed images that are not really there — patterns, figures, animals, faces. These are called Charles Bonnet hallucinations.

The key reassurance is this: people who experience them are not losing their minds, and it is not a sign of dementia or mental illness. It is simply the higher visual brain reacting to reduced input — rather like phantom sensations after a limb is lost. It affects about 5% (1 in 20) of people with significant visual impairment, usually those with reduced vision in both eyes. Knowing what it is takes away most of the distress. If you ever experience this, please mention it; we can explain it properly and reassure you and your family.

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19.  Support, and a final word

You are not navigating this alone, and you should not try to. Several excellent organisations provide information, low‑vision aids, home visits and practical help:

• Macular Disease Foundation Australia — outstanding patient information, a help line, and advocacy. We recommend that every one of our macular patients join. They support all macular disease, not only AMD.

• Vision Australia and Guide Dogs — practical support, orientation and home assessments to keep you safe and independent.

Your optometrist is also a central part of the team. They are often the first to detect change, they keep you up to date as research moves, and they share your care with us. Looking after AMD is a long‑term partnership between you, your optometrist, your eye specialist and these support services.

A final word of hope

AMD is a serious condition, but this is the most hopeful time we have ever known in caring for it. We have powerful treatment for wet AMD, the first treatments for advanced dry disease, better ways to measure what is really happening, and a research pipeline full of promise — with dozens of new treatments in trials.

And remember the fact we began with: macular degeneration takes the centre, but it leaves the edges. With good care, monitoring, and the right treatment for you, the goal is always the same — to keep you seeing the people and the life you love, clearly, for as long as possible.

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