Chronic Complications in Diabetes

AGE Products [B]

The two basic mechanisms of secondary complications of diabetes are the polyol pathway and non-enzymatic protein glycosylation. In non-enzymatic protein glycosylation, high amounts of circulating sugars start to attach to proteins, forming a compound called Amadori. After weeks to years, the Amadori product undergoes an irreversible conversion to form a complex compound called Advanced Glycosylation End (AGE) products.
    AGE products are found throughout the body but in high levels in connective tissues, blood vessels, the matrix of the renal glomerulus, and the phospholipid component of low-density lipoproteins (LDL). High levels of AGE are associated with structural alterations within the body, including increased vascular permeability, loss of vascular elasticity, reduced clearance of lipoproteins, and altered enzyme function. This reduced clearance of lipoproteins is one of the main contributing factors to the high cardiovascular mortality found in diabetic patients.
    AGE products are atherogenic and one of the main contributors to accelerating atherosclerosis in diabetics. Treating hypertension in long-term uncontrolled diabetics can be a very difficult challenge. It is not uncommon for these patients to be on three antihypertensive drugs and still not have adequate control.

Naturopathic Medical Alternatives [SH]

Hypertension drugs can decrease insulin sensitivity, so whenever possible natural medicine should be used in place of prescription antihypertensives.63 Vitamin E and lipoic acid are two supplements that will help prevent protein glycosylation, thereby indirectly decreasing atherosclerotic hypertension. Many of these patients would benefit greatly from IV EDTA chelation therapy.

Diabetic Retinopathy [B]

Hyperglycemia will eventually cause the retinal cells to have an accumulation of sorbitol through the polyol pathway, which causes an increase in osmosis. The high levels of sorbitol are not easily able to diffuse out of the cell in which it is produced. This causes a high osmotic swelling, in which water will enter the cell. Due to the buildup of water pressure in the cell, valuable antioxidants, such as glutathione and myoinositol are pushed out and thereby free radical damage occurs within the eye. This causes diabetic retinopathy.
     The progression of diabetic retinopathy may actually begin without any overt symptoms. Eye exam will initially reveal visible lesions. Micro-aneurysms on the terminal capillaries of the retina form quite similarly to balloons. They inflate but burst very easily. The increased fragility and weakness of the capillaries start to leak proteinaceous fluid, thereby causing hard exudates. The leaking of red blood cells form hemorrhages. In itself this process does not cause visual impairment. New capillaries do not form and the condition is thus coined non-proliferative retinopathy.
     This differs from proliferative retinopathy, in that the retinal vessels further deteriorate to the point of ischemia. The resultant ischemia causes new vessels to compensate for the lack of blood flow to the retina. Unfortunately, these vessels are very weak and tend to burst easily, causing hemorrhage into the preretinal areas or vitreous, causing significant vision loss. Diabetic macular edema occurs when fluid from abnormal vessels leaks into the macula. Retinal detachment is a medical emergency and needs to be treated by eye surgeons as soon as possible.

Progression of Diabetic Retinopathy

         Name of condition                                         Eye Exam

• Nonproliferative diabetic retinopathy        Retinal micro-aneurysms
• Proliferative diabetic retinopathy              New vessels on the disc
• High risk proliferative retinopathy             New vessels with vitreous as hemorrhage
• Diabetic macular edema                             Hard exudates < 2 disc

Naturopathic Medical Alternatives [SH]

Conventional therapies for diabetic retinopathy are primarily control measures to stop the hemorrhage by laser therapy. However, chronic diabetic retinopathy is very well treated with natural medicine. It is done by inhibiting the sorbitol pathway and saturating the eyes with antioxidants. Retinal hemorrhage is harder to treat naturally but can have its impact and at times cured with the use of high doses of antioxidants.
     Naturopathic treatment of diabetic retinopathy involves the administration of high doses of antioxidants, including super oxide dismutase and glutathione IV, as well as herbs that decrease diabetic complications, such as jambul and milk thistle. Blue Light therapy has shown to be helpful in eliminating edema.
    Aldose reductase inhibitors, such as quercetin and milk thistle, are valuable tools in preventing sorbitol production. Diabetic rats that have been given aldose reductase inhibitors have higher concentrations of glutathione reductase than diabetic rats that do not have aldose reductase inhibitors. Botanicals, such as jambul and milk thistle, have been found to increase the production of antioxidants, such as glutathione reductase and superoxide dismutase.64

Case Study

Diabetic Retinopathy

While conventional medicine is typically used to treat diabetic hemorrhage in the eye, naturopathic treatments have proven to be effective. A man in his mid-fifties with diabetic hemorrhage in the right eye visited our office for treatment. The right eye was 20/50.
    We prescribed the following nutritional and botanical therapy:

• Ambrotose ¼ tsp t.i.d.
• Bioflavonoids 500 mg t.i.d.
• Vitamin C 500 mg t.i.d.
• Digestive Enzymes 1 per meal
• Dioscorea dose 500 mg t.i.d.
• Vitamin E dose 400 IU t.i.d.
• Bilberry 500 mg t.i.d.
• Glutathione 5 mg sublingually t.i.d.

Within two and a half months, there was no more hemorrhage, and the right eye was 20/20.