by Paul Chris, OD
Vision Institute of Canada
The role of nutrition in diabetic retinopathy is of great importance but not often discussed. Diabetic retinopathy is a serious complication of diabetes that can result in blindness. It is caused by abnormal growth and damage to the blood vessels of the retina, the light-sensitive inner lining at the back of the eye. It can occur in anyone with type 1 or type 2 diabetes. Diabetic retinopathy will occur in 65% of people with type 2 diabetes within about ten years of onset of the disease.
In the early stages of diabetic retinopathy, symptoms are rare, and it is possible to have diabetic retinopathy and not know it. But as the disease progresses, symptoms include:
1) floaters, which are spots or worm-like lines seen floating in your vision;
2) blurred or fluctuating vision;
3) areas in your field of vision that seem dark or empty;
4) reduced night vision;
5) changes in colour vision; and
6) loss of central vision.
Diabetic retinopathy is the leading cause of blindness in individuals between 20 to 74 years old in Canada and the United States. People living with diabetes also have an increased risk of developing cataracts and glaucoma. Controlling blood sugar and having regular yearly eye exams with an optometrist or ophthalmologist are vital in protecting vision and eye health.
To understand the role of nutrition in diabetic retinopathy, it is necessary to look at the changes in global dietary patterns that began with the introduction of cereal grains into our food supply 10,000 years ago. This global change in dietary patterns, which represented the advent of agriculture and a shift away from hunter-gatherer lifestyles, raised the amount of carbohydrates in our diet to a point at odds with our hunter-gatherer genes. The increased consumption of carbohydrates from grains led to the decrease in the consumption of fruits, vegetables and wild plant and animal foods, which were superior sources of nutrients, such as vitamins, minerals, antioxidants, phytochemicals, protein, essential fatty acids, and also fibre.
Grains, however, have no vitamin B12 and are a poor source of folate. Vitamin B6 is not well absorbed from grains and they also disrupt vitamin D metabolism. Vitamin D deficiency is now recognized as an epidemic in the United States and Canada. Vitamin D, which acts more like a hormone than a vitamin, plays a major role in adult bone health and the prevention of many chronic diseases. Vitamin D deficiency is also a risk factor for diabetes and insulin resistance.
As hunter-gatherers, we evolved on a diet that contained nearly equal amounts of the essential polyunsaturated fatty acids known as omega-6 and omega-3 from fish, lean wild meats, and wild plants, nuts and seeds. It has been well established that omega-6 fatty acids promote inflammation and that omega-3 fatty acids reduce inflammation. A proper balance of these essential fats in the diet keeps the inflammatory process under control. Apart from their high carbohydrate content, grains also contain an enormous amount of omega-6 fatty acids in comparison to omega-3s. For example, oats contain sixteen times more omega-6s than omega-3s. Whole wheat contains seventeen times more omega-6s than omega-3s and corn (a grain, not a vegetable) contains forty-eight times more omega-6s than omega-3s. The use of grains, such as corn, to feed cattle and poultry has increased the amount of omega-6 fatty acids in our modern meat supply. These factors combined with our reliance on high omega-6 vegetable oils such as corn, safflower, soy and sunflower, have caused the shift from the one-to-one dietary balance of the essential fatty acids to a modern pro-inflammatory ratio of omega-6s to omega-3s estimated to be almost 17 to 1.
When blood sugar levels are stable, glucose is not harmful. However, high blood-glucose levels typical of diabetes lead to a process called glycation, in which sugars react with protein molecules. Through a further series of reactions in the body, these glycated molecules lead to the formation of what are called advanced glycation end products (AGEs.) These sugar-derived substances slow the normally free movement of the protein molecules causing them to accumulate in cell membranes. This accumulation leads to cellular membrane stiffness and cell function is impaired. They are found in the retinal vessels of people with diabetes and blood levels of AGEs correspond to the severity of diabetic retinopathy. A great deal of evidence implicates AGEs as agents in almost all diabetic complications. Blood serum AGEs are also significantly elevated in cigarette smokers due to the combustion and inhalation of pre-AGE substances in tobacco. People with diabetes who smoke show more AGE deposits in their arteries and the lens inside the eye, contributing to atherosclerosis and cataract formation. The formation and accumulation of AGEs are increased in environments of oxidative stress and are also implicated in the development and progression of macular degeneration.
Our Western diet is also a significant source of these oxidative and pro-inflammatory AGEs that are created by cooking and food processing. The generation of numerous advanced glycation end products, by heating foods that contain sugars and proteins, enhance the taste, aroma, colour, and texture of foods, hence the human preference for cooked foods over raw foods. In a study done at the Diabetes Research Institute in Germany, it was found that cooking egg whites in fructose increased advanced glycation end product immunoreactivity by 200 times over cooking egg whites without sugar. Sugar is added to many of our manufactured food products which increases the amounts of AGEs during processing. Many modern foods also contain synthetic AGEs that have been added by the food industry to boost the flavour of natural foods. As a result, the amount of glycotoxins in our Western diet has increased enormously since the 1950s. (It is interesting to note that before 1950, type 2 diabetes was rare in Aboriginal populations.)
Animal studies have demonstrated that AGEs act as mediators in the gene expression of a protein called vascular endothelial growth factor (VEGF.) VEGF stimulates vascular endothelial cell growth resulting in new blood vessels (neovascularization.) Since VEGF also stimulates vascular permeability, these new vessels are leaky and inflamed. VEGF levels are high in people with diabetes and there is now considerable evidence that AGEs play a significant role in the development of diabetic retinopathy. Antioxidants have been shown to block the AGE-induced increases in VEGF found in the retina. Of the two most important omega-3 fatty acids, EPA and DHA, EPA has been shown to inhibit the effects of VEGF which promotes the retinal vascular instability associated with diabetic retinopathy. (VEGF is a major factor in the development of wet macular degeneration.)
Thus, the importance of a healthy balanced gene-friendly diet that is high in antioxidant vitamins and minerals and low in oxidizing compounds (i.e.: glycotoxins, tobacco, food additives such as monosodium glutamate, etc.) cannot be overstated in its protective effect against diabetic retinopathy and the other ocular complications of diabetes.
“The Vision Institute of Canada is hosting an Aboriginal Vision Health Conference on October 22nd and 23rd, 2010 in Toronto/Markham, Ontario. For more information visit
www.visioninstitute.optometry.netThis article was adapted from Nutrition and Gene Expression: Implications for Retinal Disease, Chris AP, Can J Optom, November 2007: 231-228
