It is the leading cause of blindness in industrialised countries.1AMD most frequently affects people over 50 years of age. In its early stages, AMD is characterised by the presence of waste deposits under the macula, known as drusen, and by pigmentary abnormalities such as light or dark spots in the macula.2
AMD can be diagnosed with a simple eye examination. Detecting changes early through regular check-ups with your optometrist or ophthalmologist can identify the disease before sight-threatening complications occur.3,4
AMD is a complex condition and is the result of a number of factors, including ageing, environmental factors and genetics.
In the healthy eye, the retina is supported by an underlying cell layer called the retinal pigment epithelium (RPE). The RPE provides nutrition and removes waste products from the retina. Located immediately under the RPE is Bruch’s membrane.
As we age, Bruch’s membrane can thicken, which reduces the ability of the RPE to provide nutrition and remove waste products. This leads to the build-up of fatty waste deposits under the RPE called drusen. This is known as early or intermediate AMD, depending on the number, size and appearance of the drusen.
In time, these drusen deposits affect the health of the RPE, ultimately leading to the atrophy and death of the central retinal cells (atrophic dry AMD).
In some people, the damage stimulates the production of a protein (vascular endothelial growth factor, VEGF) which promotes the growth of new blood vessels under, and sometimes into, the retina. This is called choroidal neovascularisation (CNV) or “wet” AMD. These vessels can suddenly leak fluid or blood, changing the shape of the retina, and forming scar tissue. This can lead to rapid, substantial and potentially permanent vision loss.
AMD affects 1 in 7 Australians over the age of 50 and the incidence increases with age. The first evidence of AMD can be detected in an eye exam from age 50, although obvious symptoms and vision loss are unusual before age 65. This highlights the importance of regular eye tests from age 50 onwards. If you wait for symptoms, damage may have already occurred. AMD can also be hereditary, with a fifty percent chance of developing AMD if a direct family history of the disease is present.
Research shows that smoking more than doubles the risk of developing AMD.
A healthy well-balanced diet can reduce the likelihood of developing AMD. It is recommended to limit your intake of fats, eat fish two to three times a week, eat dark green leafy vegetables and fresh fruit daily, and a handful of nuts a week. Eating low glycemic index (GI) carbohydrates in preference to high GI has also been shown to reduce risk. In some people, a specific dietary supplement may also be beneficial, in consultation with your optometrist or ophthalmologist.
The retina is the light-sensitive nerve tissue at the back of the eye that converts light images from the environment into electrical impulses that are processed and sent along the optic nerve to the brain.
The macula is the small, critical central area of the retina responsible for acute, detailed central vision. In cases of AMD, the macula and its function are compromised.
Bruch’s membrane separates the photoreceptor cells and the RPE from the rich blood vessels of the choroid. It helps to regulate the exchange of nutrients, oxygen, fluids and metabolic waste products between the retina and the general circulation.
The retinal pigment epithelium (RPE) acts as a barrier between the choroid and the retina. It is responsible for maintaining and nourishing the retina, passing oxygen and nutrients to the retina and removing waste products to the blood vessels underneath.
Drusen are white or yellow fatty deposits located between the RPE and Bruch’s membrane and are common after age 60. Large macular drusen are a hallmark of AMD.
Reticular pseudodrusen (RPD) are distinct from the more common form of drusen. RPD are characteristic of more advanced stage of disease and a sign of RPE cell dysfunction.
Once AMD has been diagnosed, regular monitoring is essential.
In its early stages, AMD can have little or no effect on your vision. As AMD progresses, detailed, central vision is affected and becomes worse. In late, end-stage AMD all detailed central vision may be permanently lost and can result in legal blindness.
Vision with AMD
1. World Health Organisation (WHO), Global Initiative for the Elimination of Avoidable Blindness: action plan 2006-2011. [http://www.who.int/blindness/V... ]
2. Ferris FL et al; Clinical Classification of Age-related Macular Degeneration. Ophthalmology 2013;120:844-851.
3. Wang JJ, Rochtchina E, Lee AJ, et al. Ten-year incidence and progression of age-related maculopathy: the Blue Mountains Eye Study. Ophthalmology 2007;114:92-8.
4. Seddon JM, Sharma S, Adelman RA. Evaluation of the clinical age-related maculopathy staging system. Ophthalmology 2006;113:260-6.
5. A Simplified Severity Scale for Age-Related Macular Degeneration. AREDS Report No. 18.Arch Ophthalmol. 2005;123(11):1570-1574. doi:10.1001/archopht.123.11.1570
6. A Randomized, Placebo-Controlled, Clinical Trial of High-Dose Supplementation With Vitamins C and E, Beta Carotene, and Zinc for Age-Related Macular Degeneration and Vision Loss: AREDS Report No. 8; Arch Ophthalmol. 2001;119(10):1417-1436.