Five or ten years after the onset of diabetes, many diabetics begin to notice that their vision is just a little fuzzy. They may think they need new glasses, but the changing lens does not help. In far too many cases the visual impairment is diabetic retinopathy, a condition caused by uncontrolled high blood sugars and high blood pressure that can lead to blindness if left untreated.
Diabetic retinopathy can strike both type 1 (insulin-dependent) and type 2 (initially non-insulin dependent) diabetics. There are two types of the disease.
The more common, less serious form of the disease is known as background, nonproliferative, or simple retinopathy. This kind of retina damage is due to increased “leakiness” in the microscopic capillaries providing blood supply to the eye. There can be tiny sites of hemorrhage, swelling, or “oozing,” tiny aneurysms in the retina. Where the blood vessels leak, the visual field is impaired.
The second, less common, and more serious form of the disease is known as proliferative or malignant retinopathy. (The term “malignant” here refers to the severity of the condition, not to any danger of cancer.) Proliferative retinopathy, new blood vessels start growing forward from the retina into the fluid filling the eyeball. There can be scarring, and the fibers supporting the new blood vessels obscure the fall of light onto the retina where images are received and processed to be sent to the brain.
Both kinds of diabetic retinopathy result from a process called glycoslylation. Most diabetics are familiar with glycosylation from the measurement of glycosylated hemoglobin, of HbA1C. When blood sugars stay high, red blood cells eventually become “caramel coated.” They stick to the linings of blood vessels, and the injury slows the flow of blood, which in turn triggers the growth of misplaced, competing, microscopic blood vessels.
One of the risk factors for retinopathy diabetics are seldom warned about is high homocysteine. It’s a special risk factor for any diabetic who has kidney damage. And the damage done by too much homocysteine is compounded by high LDL or low HDL.
And if there’s any dietary additive that can bump up the risk of retinopathy even more than sugar, it’s the sweetener sorbitol. In diabetics and non-diabetics alike, sorbitol is a byproduct of the breakdown of blucose. In non-diabetics, sorbitol can be turned into fructose and flow into circulation. In diabetics, sorbitol, whether a byproduct of burning glucose or absorbed from the bloodstream, stays in the cell. The cell takes in water to dilute the sorbitol and swells, interfering with normal circulation. Sorbitol causes problems all over the body, but especially in the eye.
A reader question:
Q. What's effect of kidney transplants on diabetic retinopathy?
A. Generally, it's positive, but the longer the period of dialysis before transplant, the greater the risk of eye complications after transplant, and the older the kidney, the greater the risk of retinopathy. Drug treatment makes a difference, too. Diabetic retinopathy is accelerated by the administration of recombinant erythropoietin to patients waiting for transplant. Getting off the erythropoietin may halt the progression of retinopathy.