Please be advised that effective August 3, 2010, our new address will be:

B1-90 Garry Street

Winnipeg, MB R3C 4J9

by A. 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 foods, which were superior sources of nutrients, such as vitamins, minerals, antioxidants, phytochemicals, protein, essential fatty acids, and also fibre. As grains became an increasing part of our diets, consumption of fish, lean wild meats and animal organs also decreased.

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. Cereal grains also contain phosphorus compounds called phytates which, in their raw state, bind with minerals such as zinc, iron, copper, and calcium and prevent their absorption during digestion. (Long soaking or fermentation of grains is necessary to inactivate phytates.)

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.

Our Western diet is heavily weighted towards modern and refined grain-based carbohydrates. When we consume these foods, referred to as having a high glycemic load, the effect is a rapid spike in blood glucose and a rapid rise in blood insulin levels. The release of insulin into the blood-stream, which functions to deliver glucose to various cells for energy, is followed by a rapid drop in blood-sugar levels. This rapid drop in blood-glucose causes sugar levels to fall below normal (hypoglycemia), initiating hunger pangs and the craving for more sugar. This up and down roller-coaster of glucose-insulin responses lead eventually to insulin resistance, which is a decrease in the cellular response to the actions of insulin. This results in unstable and chronically high blood-glucose (hyperglycemia) and insulin levels (hyperinsulinemia.) Insulin evolved as a hormone to store excess carbohydrate calories in the form of saturated fat for times of food scarcity. If cells do not need the sugars, they are stored as saturated fat. Insulin resistance is the underlying basis of obesity.

When blood sugar levels are stable, glucose is not harmful. However, high blood-glucose levels 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 23^rd, 2010 in Toronto/Markham, Ontario. For more information visit www.visioninstitute.optometry.net“

This article was adapted from Nutrition and Gene Expression: Implications for Retinal Disease, Chris AP, Can J Optom, November 2007: 231-228     

CAWC is delighted to launch its monthly email foot care tip for people with diabetes, available in both English and French!  If you would like to be added to the email list, please  go to www.cawc.net/diabetesandhealthyfeet, scroll down to the sign up section, and just fill in your information. 

The purpose of the conference and an Aboriginal Vision Health Project that we are also actively engaged in is:

1) to raise the awareness of Canadian optometrists (who provide over 80% of the comprehensive eye examinations in Canada) about the vision health issues facing Aboriginal people;
2) to raise the awareness of Aboriginal leaders and health-care workers about the potential epidemic of preventable vision loss due to diabetic retinopathy that is facing the Aboriginal community due to the high rates of diabetes and the lack of vision care services available to them;
3) to raise the awareness of government and Aboriginal policy-makers about the need for an action plan to address the vision and eye health issues facing native people; and
4) to develop and implement out-reach programs to those native communities in need of  vision care services.

If you are interested to participate, please download AVHC brochure 2010 (189)

We believe it is important that the report include stories of Aboriginal People with diabetes. If you would like to share your experience of the struggles and obstacles you face in managing diabetes, please contact Jane Tsai of the CDA by May 31, 2010 at Jane.Tsai@diabetes.ca or at 1-800-BANTING (1-800-222-8464).

On April 30, 1999, Assembly of First Nations Grand Chief Phil Fontaine proclaimed the first Friday in May as “National Aboriginal Diabetes Awareness Day”. Since then, thousands of children, adults and Elders have participated in community walks, gatherings and events to promote the prevention and management of Type 2 diabetes.

NADA encourages your participation to make National Aboriginal Diabetes Awareness Day a successful one in your community by focusing on activities or hosting events that promote a healthy lifestyle. To mark this special occasion, we were pleased to provide materials and educational resources to Aboriginal schools, tribal councils, health centres and friendship centres  as examples of what you can do in your community to raise awareness, encourage physical activity and make healthy food choices.

Together, we can make National Aboriginal Diabetes Awareness Day on May 7^th, 2010 a fun, educational and inspirational event so that the devastating effects of diabetes among Aboriginal People will be a part of our history and not our future.

We look forward to hearing how National Aboriginal Diabetes Awareness Day has been promoted in your community. Please share your stories with us for our NADA Newsletter and website.

For further information please contact the NADA office, (204) 927-1220 or visit our website at www.nada.ca.