Age-related Macular Degeneration (AMD for short) may be one of the most common forms of vision loss, but it can have a very frustrating impact on daily life.
If you know much about the disease, you may be familiar with some of its troubling symptoms. These range from blurred images to dark spots in the centre of vision and straight lines becoming wavy. The way we treat you will depend on which form of the disease you have, either “wet” or “dry” AMD (see below). Certain kinds of specialist surgery are available for the wet form, whereas the treatment for dry AMD focuses on managing symptoms. We can help you do that with expert advice, personalised support and some very effective Low Vision Aids.
Age-related macular degeneration (AMD) is a disease that causes progressive damage to the central area of the retina. It is the most common cause of visual impairment in people over the age of 65.
As the name suggests, the disease affects the macula. This is the very central part of the retina, a tiny, dense area of receptor cells which enable us to see colour and detail. In AMD, the extent of the degeneration may be different in each eye and may not progress at the same rate.
The earliest sign of macular degeneration is often the appearance of small yellow deposits, known as “drusen”, under the retina.
The presence of drusen does not necessarily mean you will have visual problems. Drusen can be found in younger people who do not have macular degeneration.
Over time, however, the drusen may increase in number and become larger. The pigment layer of the eye can also be disturbed, leading to a “patchy” appearance (known as atrophy). We use the term macular degeneration when the drusen or atrophy are accompanied by a decrease in vision.
Some of the telltale signs of AMD are:
- blurred vision.
- distortion of straight lines.
- a dark spot in your central vision.
- objects appearing the wrong shape, size or colour.
- objects moving or disappearing.
- difficulty in bright sunlight and dim lighting.
The small yellow deposits, or drusen, are formed by the accumulation of waste products from the retina. As these spots get larger, they stop the flow of nutrients to the retina. Drusen also cause the layer of supporting cells beneath the retina to become very thin. When cells in this layer (the retinal pigment epithelium) die, the overlying macula degenerates and loses its visual function.
This type of degeneration is called dry macular degeneration, since there is no leaking of fluid or blood. Over time – sometimes many years – the disease process worsens and more of the macula become affected. This degeneration is called geographic atrophy; we tend to think of it as the end stage of the dry form of AMD.
Of the two types of AMD, dry is much more common, but it allows many people to maintain a useful degree of vision.
AMD nearly always starts with the dry form of the disease. Ten percent of sufferers, however, will go on to develop what we call “wet” AMD. Although wet AMD is much less common than dry, it tends to be more aggressive, causing greater and more rapid visual loss.
As the retina degenerates, the eye sometimes responds by producing new blood vessels from the choroid (the deeper vascular layer of the eye). These develop beneath the retina, like weeds growing up through the cracks in a pavement. The process is called neovascularisation.
Unfortunately, neovascularisation does not usually help the retina because the vessels are very fragile and leak or bleed easily. Eventually they result in the formation of a disc-shaped grey scar in the middle of the visual field. The scar may take some time to form but, once established, all retinal tissue in the area is destroyed, leaving a large, central blind spot. Once this has occurred, macular degeneration cannot be reversed.
There are two types of neovascularisation. We can use special tests such as fluorescein angiography to differentiate them. One is called “classic”, in which the new vessels develop in a clear and well-defined manner. The second form of wet AMD is called “occult”, where the new vessels are hidden in deeper layers and are poorly defined.
Although the cause of AMD is currently not fully understood, a number of risk factors have been identified. These include:
Age: As you age, your risk of developing the condition increases.
Nutrition: This is one of the most contentious areas, as discussed below.
Genetics: Although there is rarely a strong hereditary pattern, we know that people with a family history of macular degeneration have an increased chance of developing AMD.
Exercise: Being active and avoiding obesity is definitely beneficial.
Smoking: Smoking has been linked to the development of AMD in a number of studies. Stopping smoking has also been shown to reduce the risk of AMD.
High blood pressure: Studies have shown that high blood pressure is linked to the likelihood of developing AMD.
Sunlight: There is some evidence that excessive sunlight might be detrimental. The use of good quality sunglasses may protect the eyes from this risk.
Gender: Women are more susceptible to developing AMD than men.
Ethnicity: The disease is generally more common in Caucasians.
How might nutrition impact AMD?
There is good evidence that AMD is becoming more common at a rate greater than that attributable to simple ageing of our population. Of the many potential causes, nutrition appears a likely candidate. There is no consensus view, but the following points are generally agreed:
Processed vegetable seed oils have been implicated in the development of AMD. We do not yet know whether this effect is direct or related to the gradual change we have witnessed in replacing animal fats with vegetable products.
Sugar, or foods which rapidly release sugar into our bloodstream (known as high glycaemic foods) are linked to an increased risk of AMD.
Populations that consume fish, and in particular oily fish, have a lower rate of AMD.
Fish oil supplements have not yet been shown to be effective. Some authorities believe that increasing our consumption of omega-3 polyunsaturated fats (present, for example, in fish oil) is ineffective when our diet is swamped by omega-6 polyunsaturated fats from vegetable seed oils.
The fragile cells of the macula are highly susceptible to damage from oxygen-charged molecules called free-radicals. It has been shown that people who have a low intake of antioxidants (nutrients that fight the damaging effects of free-radicals) may be at an increased risk of developing AMD. Excessive alcohol consumption may also deplete the levels of antioxidants in the body.
The Age-Related Eye Disease Study (AREDS) suggests that certain combinations of vitamins, pigments and zinc may slow the development of AMD in patients with early disease. Whilst this is undoubtedly true, the effect is not over-impressive: for every 13 people taking the supplements, only one will show significant benefit in avoiding disease progression.
When you come into the clinic for an appointment, we will analyse your eyes carefully to determine which form of AMD you may have. The main way to do this is with a test called an OCT scan. This is really just like having a photograph taken of the retina – it is quick and completely painless. Occasionally more information is required, for which you would be asked to attend a local hospital for a fluorescein angiogram. This involves injecting an orange dye into a blood vessel in your arm and then taking a series of photographs to watch the passage of the dye through retinal blood vessels.
We now have an OCT machine, which takes such detailed pictures that the actual blood vessel layer beneath the retina can be visualised. This is called OCT angiography (or OCT-A). This has dramatically decreased the need for the dye test.
Unfortunately, there are currently no treatments widely available for the dry form of AMD.
However, one avenue showing promise is that of Red Light Therapy.
Red Light Therapy for AMD (Photobiomodulation)
Experimental work and clinical studies have demonstrated the potential for red light to benefit retinal function in AMD, leading to both anatomical improvement and visual gain.
The treatment is thought to work through improvement in blood flow, decreased inflammation and increased mitochondrial function. Recent studies of patients with AMD have concentrated on dry disease, but earlier studies also show certain benefits for patients with wet AMD.
Suitable patients should have evidence of AMD sufficient to be considered for AREDS supplements. Visual acuity should be 6/36 or better in at least one eye. A therapy cycle consists of three treatments per week for three consecutive weeks.
A recent study suggested that further treatment cycles may be required after an interval of six months.
Although the wet form of AMD tends to be more aggressive than the dry form, it is susceptible to certain types of treatment. We can help you to decide which treatment might be most appropriate for you.
Anti-VEGF injection treatments for wet AMD
What are anti-VEGF injection treatments?
Anti-VEGF injections into the eye are the most recent and most successful treatment for wet age-related macular degeneration (AMD). Anti-VEGF injections work by blocking a protein called VEGF (vascular endothelial growth factor), which stimulates formation of new blood vessels. This means that the anti-VEGF injections inhibit the growth of abnormal new blood vessels in your eye.
Anti-VEGF injection treatments can help to slow the visual loss, and in some cases may even improve sight. The anti-VEGF injection treatments in current use are Lucentis, Avastin and Eylea.
How do Lucentis, Avastin and Eylea work?
Lucentis is an anti-VEGF injection treatment for the management of wet AMD. It acts as an antibody, both preventing the growth of abnormal blood vessels beneath the retina and stopping fluid from leaking. This can protect the central macular area of the retina from permanent damage. In formal clinical trials, Lucentis produced good results. It has now been approved for use by regulatory bodies in the United States, Europe and the United Kingdom.
Avastin is an alternative antibody treatment for wet age-related macular degeneration. It was actually developed to treat problems away from the eye and has never had formal ophthalmic evaluation. However, a number of studies have shown it to be equally effective with Lucentis, and in the United States this is now the commonest injection choice.
Eylea works in a slightly different way to Lucentis and Eylea, by trapping VEGF and protecting the macula from its damaging effects. There have been extensive trials of the drug; one potential advantage of Eylea is that it may require fewer injections.
Are anti-VEGF injections a proven treatment for wet AMD?
Extensive clinical testing on Lucentis and Eylea has established the effectiveness of anti-VEGF injections as an exciting and effective treatment for wet AMD.
Although there has been no clinical trial of Avastin in wet AMD, there are now many research reports and papers supporting its use. Avastin is closely related to Lucentis, which has produced spectacular results in formal clinical trials and has been approved by the National Institute for Health and Clinical Excellence (NICE) for routine use.
The initial trial required Lucentis to be given at monthly intervals for two years (totalling 24 injections), then potentially indefinitely. More recent studies have suggested that, following three injections at monthly intervals, it may be given on a “need-to-treat” basis. For the average patient, this is likely to mean around 14 injections over two years. Eylea has been shown to be similarly effective, but when used on a regular basis, a planned injection is only required every two months.