Diabetes is a chronic metabolic disorder that adversely affects the body’s ability to manufacture and use insulin, a hormone necessary for the conversion of food into energy. The disease greatly increases the risk of blindness, heart disease, kidney failure, neurological disease and other conditions for the approximately 16 million Americans who are affected by it. Type I, or juvenile onset diabetes, is the more severe form of the illness.
Type I diabetes is what is known as a ‘complex trait’, which means that mutations in several genes likely contribute to the disease. For example, it is now known that the insulin-dependent diabetes mellitus (IDDM1) locus on chromosome 6 may harbor at least one susceptibility gene for Type I diabetes. Exactly how a mutation at this locus adds to patient risk is not clear, although a gene maps to the region of chromosome 6 that also has genes for antigens (the molecules that normally tell the immune system not to attack itself). In Type I diabetes, the body’s immune system mounts an immunological assault on its own insulin and the pancreatic cells that manufacture it. However, the mechanism of how this happens is not yet understood.
About 10 loci in the human genome have now been found that seem to confer susceptibility to Type I diabetes. Among these are (1) a gene at the locus IDDM2 on chromosome 11 and (2) the gene for glucokinase (GCK), an enzyme that is key to glucose metabolism which helps modulate insulin secretion, on chromosome 7.
Conscientious patient care and daily insulin dosages can keep patients comparatively healthy. But in order to prevent the immunoresponses that often cause diabetes, we will need to experiment further with mouse models of the disease, and advance our understanding of how genes on other chromosomes might add to a patient’s risk of diabetes.
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People with diabetes have a higher than usual need for vitamin E, which improves insulin activity and acts as an antioxidant and a blood oxygenator. Research has shown that people with low blood levels of vitamin E are more likely to develop Type 2 diabetes. Double-blind studies show that vitamin E improves glucose tolerance in people with Type 2 diabetes (NIDDM). Vitamin E was found to improve glucose tolerance in elderly non-diabetics.
People with Type 1 diabetes (IDDM) have low vitamin C levels. Vitamin C lowers sorbitol in diabetics. Sorbitol is a sugar that can accumulate and damage the eyes, nerves, and kidneys of diabetics. Vitamin C may improve glucose tolerance in Type 2 diabetes (NIDDM).
The transport of vitamin C into cells is facilitated by insulin. It has been postulated that, due to impaired transport or dietary insufficiency, a relative vitamin C deficiency exists in the diabetic and that this may be responsible for the increased capillary permeability and other vascular disturbances seen in diabetics.
If you are diabetic, supplement your diet with 1-3 grams per day of vitamin C.
Vitamin B6 (Pyridoxine)
Diabetics with neuropathy have been shown to be deficient in vitamin B6 and benefit from supplementation. Peripheral neuropathy is a known result of pyridoxine deficiency and is indistinguishable from diabetic neuropathy. Vitamin B6 supplements improve glucose tolerance in women with diabetes caused by pregnancy. Vitamin B6 is also effective for glucose intolerance induced by the birth control pill. 1,800 mg per day of a special form of vitamin B6-pyridoxine alpha-ketoglutarate-improves glucose tolerance dramatically.
Vitamin B12 supplementation has been used with some success in treating diabetic neuropathy. It is not clear if this is due to the correcting of a deficiency state or normalizing vitamin B12 metabolism.
Vitamin B12 is needed for normal functioning of nerve cells. Vitamin B12 taken orally, intravenously, or by injection reduces nerve damage caused by diabetes in most people.
Oral supplementation may be sufficient, but intramuscular vitamin B12 may be necessary in many cases. Take up to 500 mcg of Vitamin B12 three times per day.
Biotin is a B vitamin needed to process glucose. It has been shown to work synergistically with insulin and independently in increasing the activity of glucokinase. This enzyme is responsible for the first step in glucose utilization. Glucokinase is present only in the liver, where, in diabetics, its concentration is very low.
Supplementation with large quantities of biotin may significantly enhance glucokinase activity, thereby improving glucose metabolism in diabetics. When people with Type 1 diabetes (IDDM) were given 16 mg of biotin per day for just one week, their fasting glucose levels dropped by 50%. Similar results have been reported using 9 mg per day for two months in people with Type 2 diabetes (NIDDM). Biotin may also reduce pain from diabetic nerve damage.
Take 16 mg of biotin for a few weeks to see if blood sugar levels will fall.
High levels-several grams per day-of niacin, a form of vitamin B3, impair glucose tolerance . So, avoid it if you are diabetic. Smaller amounts (500-750 mg per day for one month followed by 250 mg per day) of niacin may help some people with Type 2 diabetes (NIDDM).
As a key constituent of the ‘glucose tolerance factor’, chromium is a critical nutrient in diabetes. Supplementation in the form of chromium chloride (200 micro g daily) or high-chromium-containing brewer’s yeast (9 g a day) has been demonstrated to decrease fasting glucose levels, improve glucose tolerance, lower insulin levels and decrease total cholesterol and triglyceride levels, while increasing HDL-cholesterol levels.
Double-blind research shows that chromium supplements improve glucose tolerance in people with both Type 1 and Type 2 diabetes, apparently by increasing sensitivity to insulin. Chromium improves the processing of glucose in people with pre-diabetic glucose intolerance and in women with diabetes associated with pregnancy.
Manganese is an important cofactor in the key enzymes of glucose metabolism. A deficiency of manganese was found to result in diabetes in guinea pigs. It also resulted in the frequent birth of offspring who develop pancreatic abnormalities or no pancreas at all. Diabetics have been shown to have only one-half the manganese of normal individuals.
Magnesium levels are significantly lowered in diabetics, and lowest in those with severe retinopathy. Studies suggest that a deficiency in magnesium may worsen the blood sugar control in Type 2 diabetes. Scientists believe that a deficiency of magnesium interrupts insulin secretion in the pancreas and increases insulin resistance in the body’s tissues. Studies suggest that a deficiency in magnesium may worsen the blood sugar control in Type 2 diabetes. Scientists believe that a deficiency of magnesium interrupts insulin secretion in the pancreas and increases insulin resistance in the body’s tissues.
Vanadium is a compound found in tiny amounts in plants and animals. Early studies showed that vanadium normalized blood glucose levels in animals with Type 1 and Type 2 diabetes. A recent study found that when people with diabetes were given vanadium, they developed a modest increase in insulin sensitivity and were able to decrease their insulin requirements.
Potassium supplementation yields improved insulin sensitivity, responsiveness and secretion in diabetics. Insulin administration often causes a potassium deficiency.
Zinc deficiency has been suggested to play a role in the development of diabetes in humans. Zinc is involved in virtually all aspects of insulin metabolism -synthesis, secretion and utilization. Zinc also has a protective effect against beta cell destruction, and has well-known anti-viral effects.
People with Type 1 diabetes (IDDM) tend to be zinc deficient, which may impair immune function. Zinc supplements have lowered blood sugar levels in people with IDDM. People with Type 2 diabetes (NIDDM) also have low zinc levels, caused by excess loss of zinc in their urine.
People with NIDDM are recommended to supplement their diet with moderate amounts of zinc (15-50 mg per day) as a way to correct for the deficit.
Note: Take zinc with food to prevent stomach upset. If you take over 30 milligrams of zinc on a daily basis for more than one or two months, you should also take 1 to 2 milligrams of copper each day to maintain a proper mineral balance.
People with diabetes cannot adequately process carbohydrates. Coenzyme Q10, or CoQ10, is needed for normal carbohydrate metabolism. Coenzyme Q10 is an antioxidant that fights free-radical damage and is a blood oxygenator.
Inositol is needed for normal nerve function. Diabetes can cause nerve damage, or diabetic neuropathy. Some of these abnormalities have been reversed by inositol supplementation (500 mg taken twice per day).
ALA and GLA
Alpha-lipoic acid (ALA) is a powerful natural antioxidant. It has been used to improve diabetic neuropathies (at an intake of 600 mg per day) and has reduced pain in several studies.
Gamma-linolenic acid (GLA), found in black currant seed oil, borage oil, and evening primrose oil, has been shown to be helpful for improving damaged nerve function, which is common in diabetes.
Supplementing with 4 grams of evening primrose oil per day for six months has been found to reverse the cause of diabetic nerve damage and improve this painful condition. In double-blind research, 6 grams per day helps reduce nerve damage in people with both Type 1 and Type 2 diabetes (IDDM and NIDDM).
Take 500 to 1,000 milligrams of any of these oils twice daily.
Carnitine is a substance needed for the body to properly use fat for energy. When diabetics are given carnitine (1 mg per 2.2 pounds of body weight), high blood levels of fats-both cholesterol and triglycerides-dropped 25-39% in just ten days. In addition, carnitine improves the breakdown of fatty acids, possibly playing a role in preventing diabetic ketoacidosis.
Taurine is an amino acid found in protein-rich food. People with Type 1 diabetes (IDDM) have low taurine levels, that leads to “thickened” blood-a condition which increases the risk of heart disease. Supplementing taurine (1.5 grams per day) restores taurine levels to normal and corrects the problem of blood viscosity within three months.