Age-related macular degeneration (ARMD) is a progressive eye condition that affects the macula, the central portion of the retina, (see image below) where our sharpest central vision is enabled. The macula and central vision is needed for seeing fine detail and objects clearly. As the macular tissue is destroyed and central vision deteriorates, only the outermost, or peripheral vision remains.
ARMD is associated with aging and is the most common cause of vision loss in the United States in those 50 or older. ARMD affects more than 1.75 million individuals in the United States with 200,000 new cases of ARMD reported each year. Owing to the rapid aging of the US population, this number is projected to increase to almost 3 million by 2020. While some sight is retained in most cases of ARMD, it remains the leading cause of legal blindness in people over the age of 65.
Macular degeneration is diagnosed as either dry (non-neovascular) or wet (neovascular). The dry form comprises about 85-90 percent of ARMD. The latter is marked by gradual deterioration of the light sensitive cells (cones) in the macula and the tissue underlying it. The first visible changes associated with dry ARMD, are deposits beneath the retina made of fat and cellular debris referred to as “drusen”. The type an amount of drusen formation is associated with aging, the severity of ARMD, and the progression of dry ARMD to wet ARMD. The formation of drusen is not completely understood, albeit inflammation and oxidative stress processes are thought to be largely responsible. Drusen can also occur without impairment to vision.
The wet form is characterized by the abnormal formation of blood vessels underneath the retina and macula. These delicate blood vessels tend to leak and bleed resulting in the separation of the retina from the posterior eye wall and more rapid damage to the macula. The dry form of ARMD can progress to wet ARMD, and the wet form of ARMD is associated with more serious vision loss.
Several risk factors for ARMD have been identified including genetics, aging, gender, smoking, sunlight or UV exposure, obesity, high blood pressure, diabetes, and cardiovascular disease. (1) Underlying these risk factors are inflammation and oxidative stress, which in turn are increasingly recognized as primary processes in the development of ARMD.
Several genes have been identified that highlight the role of inflammatory processes in AMD. An example is the factor H gene, also referred to as complement factor H (HF1/CFH). HF1/Complement Factor H genes and their related encoded proteins*, are constituents of the Complement system (Alternative complement pathway)**, which are immune/inflammation pathways that are activated by pathogens (bacteria and viruses) and chronic disease processes. A variant of HF1/CFH, CFH Y402H, is now identified to be a strong risk factor for developing AMD. The HF1/CHF gene encodes for a protein-HF1, that binds to the retina and functions to suppress some of the inflammation that the retina is exposed to. However, the CFH Y402H variant encoded protein does not bind to receptors on the cells of the retina and the choroid (see illustration), and therefore does not inhibit inflammation driven by the Complement system pathway at the retinal tissue. Thus CPH Y402H carriers are at increased risk for developing AMD. Recent evidence identifies a CFH Y402H variant as a contributing risk factor in as many as half of ARMD patients. (2)
As enlightening as the understanding of the genetic and inflammation links to the development of ARMD is, it is just as important to grasp that inflammation driven in the disease process of ARMD is not restricted to the events occurring in the eye. ARMD begins by what happens outside the tissues of the eye. ARMD is the tip of the iceberg. Underneath lies chronic infection and metabolic disease processes that drive the pro-inflammatory insults to the vulnerable tissues of the eye. (3) The immune system activation, and the associated inflammation, represent a cascade of related biological systemic processes, with the retina being the downstream destination endpoint. If one could view an illustration, you would see it as a cause and effect biological flow chart.
Whenever there is such activation of immune/inflammatory cascades, there is a burden put on to the anti-oxidative resources of the body. As the innate buffering and protective antioxidant systems are challenged and depleted by chronic pro-inflammatory insults, oxidative stress and subsequent tissue damage occurs. The Solution…
While buffering inflammation and oxidative stress is a key strategy to the ARMD process, the enlightened approach to prevention and halting more severe degeneration, is to identify and arrest the “triggers” to such immune/inflammatory responses that eventually target vulnerable tissues like the macula/retina of the eye. The good news is that nutrition can delay or prevent the more advanced form of ARMD. A diet rich in antioxidant rich vegetables (carotenoids), as well supplementation with vitamins, Omega 3 fatty acids and antioxidants, can slow or prevent the progression of dry ARMD to wet ARMD.
Studies that include the Age-Related Eye Disease Study (AREDS), which included more than 3,600 people, and the Lutein Antioxidant Supplementation Trial (LAST), demonstrate the efficacy of nutritional supplementation in the prevention or amelioration of AMD. In the aforementioned research trials, vitamin A, C, E, Carotenoids (lutein, zeaxanthin), zinc, were effective in reducing the risk of advanced AMD. A comprehensive core formula that includes these key nutrients is the Designs for Health OcuForce formula. Ocuforce contains all the nutrients used in both AREDS and LAST, along with additional synergistic vitamins, minerals and antioxidants.
As with any degenerative disorder, dietary influences are large. Therapeutic supplementation with the nutrients used in the AREDS and LAST studies are proven interventions in ARMD and other eye disorders, but diet is the foundation for prevention. Dietary factors are vital to controlling chronic inflammation and moderating oxidative stress in the body. A diet low in fruits and vegetables, or one high in Omega 6 fatty acids and low in Omega 3 fatty acids, have been directly linked to ARMD. Studies have shown that diets high in omega-3s, derived largely from fish, protects against wet (neovascular) ARMD. (4) Higher blood levels of vitamin D from dietary sources, have demonstrated a promising benefit in preventing early AMD. (5) The beneficial effects of vitamin D and Omega 3s are thought to derive from their anti-inflammatory effect. Higher dietary lutein/zeaxanthin intake from diet, has shown to a lower incidence of wet ARMD and more extensive and larger drusen formation.
Other recent studies revealed that individuals that consumed foods with the highest glycemic index, *** were at greater risk for AMD. (6,7) Conversely, a low glycemic index diet rich in vegetables that are high in carotenoids, lutein and zeaxanthin, that are found in raw spinach, kale, collard greens, broccoli and other vegetables and fruits, lowers the risk of ARMD. Egg yolks also provide a good source of lutein and zeaxanthin that are very well absorbed. Their total content of lutein and zeaxanthin is much lower in eggs than some vegetables and fruits, but the carotenoids are more bioavailable. Carotenoids like lutein are fat-soluble and thus are best absorbed in the presence of fat in a meal. Think spinach salad with eggs or avocado, or a vegetable dish drizzled with olive oil. Why are these foods and the lutein and zeaxanthin concentrated in them so beneficial for the eyes? Carotenoids are taken up readily in the tissues of the eye with lutein and zeaxanthin concentrated in the retina and macula respectively.
As with any chronic disorder, prevention is key, and diet is always the foundation to prevention. A lower glycemic index/load diet rich in nutrient dense vegetables and fruits, and full of natural occurring antioxidants, is not only associated with a reduced risk and incidence of ARMD, it is also associated with the reduced risk and occurrence of many other chronic degenerative diseases. The same is true for more favorable Omega 3 to Omega 6 ratio that accompanies regular consumption of fish.
Finally, if you have been diagnosed with ARMD, consider a nutritional and lifestyle evaluation with a qualified practitioner trained in nutritional therapies. I work with individuals throughout the country and am available by appointment. Please click here if you wish to contact me, or you can go to FunctionalHealthSolutions.com and go to the contact tab. As indicated above, supplementation with therapeutic levels of nutrients have shown some very strong benefits in the protection against advanced ARMD.
For a more thorough review of the nutritional factors and their mechanisms vital to the prevention and progression of ARMD, please review an excellent and comprehensive overview just below here, courtesy of Designs for Health.
Note: Click on the upper right hand icon on the AMD Eye Health overview for a full-page view.
If you are reading this article at another source other than FunctionalHealthSolutions.com, please visit the Articles & News section and click on the Eye Health category @ FunctionalHealthSolutions.com for more information about natural approaches to AMD, Glaucoma, Cataracts, and many other health disorders.
* Encode: Genes are components of DNA that contain the “code” for a specific protein that serves as a functional or structural entity. Therefore, a gene “encodes” for a protein.
Gene information, through a miraculous process, is transformed from one format to another. For a wonderful illustration of how that process works, I highly recommend you visit: http://learn.genetics.utah.edu/
** Complement system: Functions as part of the Innate Immune System (the immunity one is born with) that is best known for antibodies that are circulating and produced to fight off invaders and scavenge foreign substances. Antibodies identify a target, the Complement system destroys it. The Complement system is comprised of many proteins that assist antibodies-thus the “name Complement”.
*** Glycemic Index: The glycemic index (GI) is a measure of the effects of carbohydrates on blood glucose levels. Foods that are more processed (refined carbohydrates) have a higher glycemic index/load, and are more likely to increase blood sugar. Refined carbohydrates that break down rapidly during digestion results in glucose entering into the bloodstream more rapidly. However, glycemic load is a more accurate barometer for the effect of a food on blood glucose levels. The Glycemic Load takes into account the amount of fiber present in food, which is a significant factor in how that food impacts blood glucose.
1. Do age-related macular degeneration and cardiovascular disease share common antecedents? Snow K.K.; Seddon J.M. Ophthalmic Epidemiology, Volume 6, Number 2, June 1999 , pp. 125-143(19)A
2.Common Haplotype in the Complement Regulatory Gene, Factor H (HF1/CFH), Predisposes Individuals to Age-related Macular Degeneration. Hageman, G.S., et. al., Proc. Natl. Sci. Acad. USA, 2 May 2005; 102 (18).
3. Systemic Complement Activation in Age-Related Macular Degeneration Scholl HPN, Issa PC, Walier M, Janzer S, Pollok-Kopp B, et al. PLoS ONE. 2008; 3(7): e2593.
4. The Relationship of Dietary Lipid Intake and Age-Related Macular Degeneration in a Case-Control Study: AREDS Report No. 20 Authors: Age-Related Eye Disease Study Research Group Archives of Ophthalmology. May 125, Volume 125, Pages 671-679 5. Association Between Vitamin D and Age-Related Macular Degeneration in the Third National Health and Nutrition Examination Survey, 1988 Through 1994 N. Parekh, R.J. Chappell, A.E. Millen, D.M. Albert, J.A. Mares Archives of Ophthalmology. May 125, Volume 125, Pages 661-669
6. Dietary glycemic index and carbohydrate in relation to early age-related macular degeneration. C-J. Chiu, LD. Hubbard, J. Armstrong, et al., Am J Clin Nutr, 2006, vol. 83, pp. 880–886
7. Dietary glycemic index and the risk of age-related macular degeneration. Kaushik S, Wang JJ, Flood V, Tan JS, Barclay AW, Wong TY, Brand-Miller J, Mitchell P. Am J Clin Nutr. 2008 Oct;88(4):1104-10.