According to the NHS, age-related macular degeneration (ARMD) affects 600,000 people in the UK and this figure is expected to rise to over 700,000 by the year 2020. ARMD is a visual impairment that is so significant it is second only to cataracts in people over 65.
In this article, we will look at the different causes, who is most susceptible and how we can protect our eyesight to reduce the risk of developing this condition.
What exactly is macular degeneration?
Underneath the retina and located towards the back of both of your eyes sits the macular. The macular is 5.5mm in diameter and contains the fovea and the smaller foveola where the highest concentration of photoreceptors are present.
Photoreceptors determine your visual acuity (ie the clarity/sharpness of your vision). Photoreceptors receive light signals and convert them to chemical and then electrical impulses that are sent to the brain; they are exposed to significant oxidative stress in the form of light and oxygen and thus have a high turnover rate – each night the outer 10% of segments of photoreceptors are shed and engulfed by the Retinal Pigment Epithelium (RPE) which digests them and their associated metabolic waste. Adequate nutritional support to the RPE is important both for enabling efficient turnover and nutrient flow to the photoreceptors.
If this process is not working efficiently then debris can accumulate in the RPE cell between the basement membrane and plasma membrane. This eventually leads to the formation of drusen – deposits that contain a variety of lipids, proteins and advanced glycation end products (AGEs) as well as inflammatory mediators.
In early ARMD the drusen are small but they gradually increase in size and number as the disease progresses and this causes damage to the RPE.
Progressive visual loss is the result of macular degeneration with patients also experiencing blurred vision, objects seeming bent or distorted and black spots appearing in the centre of their vision.
The following forms of ARMD are the most common:
- Atrophic (dry) ARMD – Between 80-95% of patients that suffer from ARMD experience the atrophic or dry form. This form is thought to begin in early life and progresses slowly to remove central vision often leaving peripheral vision intact. It would be considered very rare for a patient to become completely blind from this form of ARMD however there is no medical treatment to reverse the effects of atrophic ARMD at this time.
- Neovascular (wet) ARMD – 5-20% of patients will suffer from the neovascular or wet form. The growth of abnormal blood vessels affects the macular which can, given time, cause more classic forms of ARMD to occur. The neovascular or wet form can be treated by laser photocoagulation therapy if diagnosed early on.
Recently, Alzheimer’s-linked beta-amyloid proteins have also been described as accumulating in the retina and may be linked to the pathology.
Risk factors for ARMD
As the name implies, the chance of a diagnosis increases with age. This is primarily down to the natural process of oxidation that occurs in our cells constantly from birth but it is not the only cause of age-related macular degeneration which can be accelerated by other factors.
New information on ARMD is pointing towards genetics as increasing the risk of developing the disease. Having any family members suffering the disease, in particular first degree relatives, increases risk; several single nucleotide polymorphisms (ie genetic mutations) associated with ARMD risk in certain populations have been identified.
Obesity is a significant risk factor for ARMD and it has even been shown that a 3% reduction in waist-hip ratio reduces risk for ARMD by 29%.
Diet and Lifestyle
While still a new area of investigation, data indicates that consuming higher glycemic index foods is associated with a greater risk for ARMD or ARMD progression.
Lifestyle factors which research has linked to increased risk of developing age related macular degeneration include:
- Smoking – this is the strongest modifiable risk factor, increasing ARMD risk by up to 7x
- Pesticides from food
- Radiation from the sun
These factors can lead to increased production of free radicals – molecules with an uneven number of electrons. The unpaired electron will attach itself to structures in the cell causing damage; their production is increased by certain diet and lifestyle choices. They are highly reactive and can cause a chain reaction of damage to cells in the body. In the case of ARMD, the free radicals cause chain reactions in the cells within the macular damaging the photoreceptors which in turn decreases visual acuity. ARMD is more common in those with atherosclerosis – the same pathological processes contribute to both conditions.
What can I do to combat ARMD?
Free radical damage and poor oxygenation of the macular is linked to underlying pathophysiology. The unbalance in the body can be readdressed by reducing the risk of atherosclerosis and other risk factors e.g. wearing sunglasses to protect your eyes from light damage.
Omega-3 fatty acids, micronutrients and phytonutrients
Observational studies indicate that maintaining adequate levels of omega-3 fatty acids (i.e. with 2 servings/week of fish) and a low glycemic index diet may be particularly beneficial for early ARMD and that higher levels of carotenoids (eg lutein) may be protective, in particular, against neovascular ARMD.
There has been extensive research to determine if certain micronutrients can delay the progression of ARMD. Data from the Age-Related Eye Disease Study (AREDS) Research Group showed that provision of high-dose anti-oxidant vitamins and zinc to certain ARMD patients was clinically effective in slowing down the progression to wet ARMD by 35-30% over a 5 year period.
Vitamin C works as an antioxidant within the body in aqueous environments inside and outside our cells. When partnered with Vitamin E, a fat soluble antioxidant, they provide the primary protection against free radicals and are the foundations of the body’s antioxidant defense system. Vitamin C will also regenerate oxidized Vitamin E in the body boosting its potential health benefits as a result. The combination of Vitamin C and Vitamin E has been shown when supplemented together to prevent the oxidation of cholesterol and reduce the process of atherosclerosis 14% when supplementing 500mg. In short vitamin C acts as an antioxidant and strengthens the collagen structure of the arteries and thus may slow down the progression of atherosclerosis; as mentioned above, atherosclerosis is a risk factor for ARMD.
Other nutrients are being investigated for their potential role in protecting against ARMD. For example, curcumin which has been shown in vitro to protect RPE cells from oxidative stress; and B vitamins (folate, B12, B6) which are important for decreasing homocysteine which in turn reduces the risk of vascular diseases.
One phytonutrient that deserves special mention is lutein, a carotenoid. In plants carotenoids protect the plant cells from sun damage and lutein is also found at high levels in the macula area of the eye. Research has shown that increasing dietary or supplemental intake of lutein can increase macula pigments in the eye. In the Lutein Antioxidant Supplementation Trial (LAST), taking 10 mg of supplemental lutein per day for 12 months improved many aspects of vision including increasing ‘Snellen equivalent visual acuity’ (ie sharpness of vision and vision at distance), contrast sensitivity (ability to see details at low contrast levels eg at night) as well as macular pigment optical density (ie the thickness of the macular pigment), compared to placebo. Lutein is also found in foods such as eggs, leafy greens such as kale, broccoli and sprouts and gardens peas.
If you have any questions regarding the topics that have been raised, or any other health matters please do contact me (Clare) by phone or email at any time.
firstname.lastname@example.org, 01684 310099
The Cytoplan editorial team: Robin Gordon, Clare Daley and Joseph Forsyth.
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Chew EY et al (2013) – Long-term effects of vitamins C and E, ß-carotene, and zinc on age-related macular degeneration: AREDS report no 35. Ophthalmology. 2013;120:1604–11.e4.
Pizzorno Jr., J. and Murray, M. (2006). Textbook of Natural Medicine. 3rd ed. St. Louis: Elsevier Ltd, pp.1859-1861, 1514-1515.
Richer S et al (2004) – Double-masked, placebo-controlled, randomized trial of lutein and antioxidant supplementation in the intervention of atrophic age-related macular degeneration: The Veterans LAST study (Lutein Antioxidant Supplementation Trial) Optometry. 75:216–30.
Saxena N et al (2015) – Cost effectiveness of anti-oxidant vitamins plus zinc treatment to prevent the progression of intermediate age-related macular degeneration. A Singapore perspective. Indian J Ophthalmol, 63(6): 516–523.
Weikel K A & Taylor A (2012) – Nutritional modulation of age-related macular degeneration. Mol Aspects Med, 33, 4, 318-375
Last updated on 2nd June 2017 by cytoffice