Alternative, Complementary Therapies For Diabetes

By John E. Hahn, DPM, ND

Type 2 diabetes is one of the fastest growing diseases in the United States, with 15.7 million Americans afflicted with the disease, according to the American Diabetes Association. Diabetes is one of the leading causes of death in the United States, and the primary cause of blindness in people (due to diabetic retinopathy) between the ages of 20 and 70.1
Many people have Type 2 diabetes and are completely unaware of it. Ninety percent of diabetics have non-insulin dependent diabetes. Type 2 diabetes usually begins in later years, but it is now becoming more common in young people. Risk factors for developing class="checkity">diabetes type 2 include increased body weight, race, age, lack of exercise and heredity. It is much more common among American Indians, African-Americans, Latinos and American Asians than in Caucasians.
Podiatrists can make some basic nutritional recommendations to their diabetic patients. According to the literature, these recommendations can help to improve blood glucose control and reduce glycosylation. Researchers found that glycosylation is responsible for long-term effects of diabetes. Specifically, excessive glycosylation has many adverse effects in activation of enzymes, inhibition of regulatory molecule binding, cross-linking of glycosylated proteins and disruption of many cell functions.2
Indeed, dietary and nutriceutical recommendations can help diabetes patients control their blood sugar and insulin level, as well as helping to prevent pedal vascular disease. Some dietary recommendations that have proven to be effective in modifying blood glucose levels are increasing complex carbohydrates in the diet to 60 to 70 percent of the caloric intake and decreasing fat in the diet to 20 percent.3
Another recommendation is decreasing the consumption of sucrose and other simple carbohydrates and increasing consumption of complex carbohydrates with low glycemic indexes, especially legumes. Research from the American Journal of Clinical Nutrition demonstrated that when the glycemic index of carbohydrates were lowered to between 38 and 54, the glycosylated hemoglobin dropped by 9 percent and the fructosamine levels decreased by 8 percent.4
Studies showed chromium polyniacinate taken in the dosage of 400 to 600 micrograms per day improved insulin efficiency, which lowers blood sugar levels.5 L-Carnitine, an amino acid, taken twice a day at a dosage of 500 mg on an empty stomach, has been shown in studies to decrease ketones and LDL cholesterol in the body and improve circulation.6
Vanadium, taken in a dosage of 100 to 150 mg per day, has shown a dramatic affect on blood sugar levels. It works like an oral insulin and makes the cells more receptive to insulin by activating the insulin receptor sites at the cell level.7
Gymna Sylvestre, taken in a dose of 1,500 mg a day, has been shown to modify the rise in blood sugars postprandially. This plant extract is a native to the tropical forests of India and has historically been used as a treatment for diabetes for decades.8
Bitter melon, at a dosage of 125 mg per day, contains several confirmed anti-diabetic agents. Studies show that charantin and Polypeptide-P have a blood glucose lowering action.9 Fenugreek seeds have been shown in studies to reduce potassium blood sugar levels and improve glucose tolerance.10
When you are treating a diabetic patient who has ulcers that tend to exhibit poor wound healing, you may recommend zinc supplements at 70 mg three times per day with meals. Zinc is also involved in the synthesis, secretion and utilization of insulin.
Vitamin C for vascular fragility should be augmented at 500 mg to 1 gram per day. Vitamin C also has been shown to reduce glycosylation.12 Also keep in mind that the combination of Thiamin B-1 (50 mg per day) and vitamin B-6 (50 mg per day) has been shown to reduce the effect of painful neuropathy.13
Can Alpha Lipoic Acid Make A Difference?
Another substance that has received much acclaim for its value in treating peripheral neuropathy is Alpha Lipoic Acid and/or Thioctic acid. Alpha Lipoic Acid (ALA), a vitamin-like substance found in foods and produced by the body in limited amounts, may be the most valuable antioxidant of all for treating peripheral neuropathy. In addition to neutralizing both oxygen- and nitrogen-free radicals, ALA has been studied for its ability to actually repair oxidative damage, regenerate other antioxidants and chelate excess metal.14
Unlike other antioxidants, ALA is both water-soluble and fat-soluble, enabling it to act both inside the cell and in the intracellular spaces. This universal solubility enables ALA to deactivate both hydroxyl and singlet-oxygen free radicals, two of the most dangerous types of free radicals. ALA can prevent free radical damage in every setting, regardless of whether it is in the brain, fluids, blood, stored fat, heart, pancreas, kidneys, liver, bone or cartilage.
In addition to deactivating the high levels of free radicals found in the blood and tissues of diabetic patients, ALA improves glucose transport from blood into the cells. In a study of adult diabetic patients, ALA increased cellular update and burning of glucose by approximately 50 percent.3
In two double-blind, placebo-controlled trials, ALA significantly reduced symptoms in diabetic peripheral neuropathy, including the pain, burning, paresthesias and numbness in the feet and improved cardiac autonomic dysfunction in non-insulin dependent diabetics.4 In both lean and obese diabetic patients, ALA also prevents hyperglycemia-induced increments of serum lactate and perutide levels, and increases insulin sensitivity and glucose effectiveness.
Is lipoic acid safe? Yes. In over three decades of use in Europe, no study has shown any serious adverse effects of taking lipoic acid supplements. Naturally, people who have serious illnesses (like diabetes, heart disease, liver disease, kidney disease or cancer) and pregnant women should consult with their physicians before beginning any significant nutrient supplement program, including the use of lipoic acid. The recommended dose for healthy adults is 100 to 400 mg a day. The toxic dose for humans amounts to 30 to 40 grams per day for the average male, which is hundreds of times higher than the effective recommended dose.15
A Few Notes Of Caution
You must take certain cautions into account when considering supplements for diabetic patients. For example, fish oil capsules or supplements containing large amounts of paraaminobenzoic acid (PABA) may elevate blood sugar.
Also be aware that dietary supplements containing the amino acid L-Cysteine can break down the bonds of the hormone insulin and interfere with the absorption of insulin into the cells. Extremely large doses of vitamin B-1 (thiamin) and vitamin C may then inactivate insulin. These vitamins may be taken in normal dose forms without adverse effects on insulin.
Patients must take caution when using niacin. Many patients utilize niacin to help reduce blood cholesterol and triglycerides. However, in one study, large amounts of niacin raised blood sugar levels in people with non-insulin dependent diabetes by as much as 16 percent. Over time, this could cause dependence on insulin or oral hypoglycemic medication for maintaining proper blood sugar levels. Niacin can also cause the level of uric acid in the blood to rise and increase the risk of gout. However, niacinamide and inositol hexaniacinate (a flush-free form of niacin) slow down the destruction of both cells and the regeneration of insulin-producing beta cells in the pancreas. Therefore, these may be helpful for treating those who have Type 1 diabetes.16
What About The Benefits Of Intravenous Chelation Therapy?
Using intravenous chelation therapy to help treat peripheral vascular disease associated with diabetes and peripheral neuropathy has been well documented in the scientific literature over a number of years. Podiatrists who have been in postgraduate residency programs have more than likely been involved with administering preoperative IV solutions, and possibly postoperatively as well.
Since the mid-‘50s, physicians in the United States have been using solutions containing magnesium edetate (EDTA) as a chelation agent for treating heavy metal poisoning and vascular disease.
In the diabetic patient, there is a complex pathophysiologic cascade for the development of peripheral vascular arteriosclerosis, with its major stages of lipid oxidation initiating vascular wall damage, ensuing coagulation and underlying cell death with calcification. This process poses a therapeutic challenge to both the podiatrist and the diabetologist who treat the ramifications of this vascular change. These individual processes occurring within the vascular system exist simultaneously at various sites and limits the applicability of therapeutic agents targeted to one or another component of the disease progression.
In this respect, EDTA chelation therapy has an implicit advantage in that it favorably influences all facets of the disease development. Therefore, it can also provide an alternative to the combination of drugs administered to maintain multiple therapeutic effects for the diabetic patient.
All About EDTA
The chelating compound ethylene diamine tetraacetic acid (EDTA) was initially developed in the mid-‘30s, as a substitute for citric acid, to maintain the solubility of calcium magnesium in the alkaline solutions used in the textile and photographic industries.
Pharmaceutical applications of EDTA chelation followed a 1952 publication of the Chemistry of Metal Chelate Compounds.17 By 1989, EDTA production reached an international annual level of 40 tons.15 Initial use of the intravenous infusion of sodium Na EDTA for treating atherosclerotic disease has been superceded by its magnesium chelate, Na2 Mg EDTA, since the ‘60s. Although both compounds have the same spectrum of polyvalent level binding in vivo, infusion of the magnesium chelate is significantly less painful. When there is simultaneous release of magnesium and positive calcium chelation with hypocalcemia, the usual pharmacological consequences in intravenous magnesium administration are enhanced. These include blood pressure reduction and cutaneous vasodilation.
Since the 1960s, intravenous infusion of disodium magnesium EDTA to thousands of patients has essentially eliminated acute toxic responses.18 You can attain this by limiting the dose to a maximum of 3 grams for patients weighing 70 kilograms or more with infusion periods of 1.5 to three hours. However, recent studies done by Born and Geurkink have shown there is improved peripheral vascular function when you use 1.5 grams of IV ethyl diamine tetraacetic acid (EDTA) over a one-hour period. The actual
number of treatments is one to two per week for 15 to 20 weeks, followed by a rest period of four to six weeks between therapies. You may then repeat courses of therapy.
It is interesting to note the hypocalcemic response to EDTA administration stimulates the hormonal output of the parathyroid gland. One of these isomers has the unique property of increasing collateral blood flow.17,18 This pharmacological response complements the cutaneous vasodilation associated with intravenous magnesium released by magnesium edetate administration.
Since the ‘50s, EDTA has been added to foods and drugs as an oxidation inhibitor. In vivo, the formation of reactive free radicals by oxidative withdrawal of an electron from a saturated molecule is a common and essential step in the normal pathway of cell physiology. Since such free radicals are very reactive and potentially injurious, their metabolic occurrence and possible generation by low molecular weight iron complexes are usually controlled and restricted by a variety of endogenous systems. This antioxidant capability is enhanced by ascorbic acid in aqueous compartments, and vitamin E and carotene in lipid environments.
When there are inadequate protective mechanisms in cells, tissues and body fluids, the uncontrolled generation of free radicals leaves oxidized lipoproteins. Lipoprotein uptake by macrophages, the formation of foam cells, the generation of fatty streaks and calcification will occur within arterial walls. These processes are found more frequently in the diabetic patient, who also demonstrates higher levels of low-density lipoproteins (LDLs) and lipoprotein small A fraction. These oxidized LDLs are taken up by the macrophages, which form the foam cells characteristic of the fatty streaks on arterial linings. According to the literature, the oxidation of LDLs depends on the presence and concentration of ferric or cupric ions in plasma, which are completely inhibited by EDTA chelation.20, 21
What You Should Know About Vascular Disease And The Use Of EDTA
In a retrospective randomized study, Born and Geurkink reported improvement of peripheral vascular function, using a low-dose IV ethylene diamine tetraacetic acid over a one- to two-hour time period, instead of the traditional 3 gram EDTA dose.22 They utilized a 1.5 gram EDTA infusion mixed with magnesium chloride (1,200 mg), procaine hydrochloride 2% (20 mg), potassium chloride (5 Meq), ascorbic acid (5 grams), D-Panthenol (B5) (250 mg), pyridoxine hydrochloride (100 mg), and hydro cobalamine (B12) (1,000 mcg).
The patients had documented evidence of peripheral vascular disease (defined by a baseline Doppler ultrasound value of less than 55 mm of mercury) and clinical symptoms (including intermittent claudication, loss of palpable pedal pulses, cold extremities and paresthesias). Using a videoscope vascular analyzer (Model 2100 by Vascular Diagnostic Instruments), Born and Geurkink evaluated four of the peripheral arteries before and after using IV EDTA therapy. The 1.5-gram EDTA group experienced a greater overall improvement with a group mean improvement of 123.1 percent in vascular flow.22
In a large population, double-blind study on using sodium-magnesium EDTA to help treat peripheral vascular disease, Olszewer, et. al., demonstrated significant improvement in peripheral blood flow and reduction of intermittent claudication. Arteriographic studies have shown that using EDTA chelation therapy leads to significant improvement in peripheral blood flow.23
Comparing Chelation And Bypass Surgery
What about bypass surgery? A 10-year study, conducted by the National Institutes of Health (NIH), found many of the 200,000-plus bypasses and other invasive procedures performed each year in the U.S. for the relief of pain and other symptoms brought on by clogged or blocked arteries are unnecessary.
The study compared postoperative survival rates of “bypassed” patients with a matched group of equally diseased patients who were treated non-surgically. The study uncovered no additional benefits for the majority of patients who underwent an operation. (It is important to note the nonsurgical therapy reported in that study did not include either chelation therapy or the new calcium channel blocker drugs, and only half of the patients received beta blocker drugs.) When the results were statistically analyzed, bypass surgery did not improve the patients’ chances to live longer and healthier lives.
Most importantly, cardiovascular surgery does nothing to arrest or reverse the underlying disease which exists in varying degrees throughout the body. Studies have also shown that by 10 years after surgery, grafted vessels had closed in 40 percent of patients who had bypass surgery. In the remaining 60 percent of the patients, half developed further coronary narrowing. Once a bypass is done, the chances of having another bypass go up about 5 percent per year. After five years, the chances of undergoing a second bypass could be as high as 30 to 40 percent.
On the other hand, chelation patients are frequently able to return to work and resume their sports and other activities, without the need to undergo surgery.
Total costs for bypass surgery average about $45,000 and can be as high as $60,000. Chelation therapy is an office procedure that improves blood flow throughout the entire vascular system at a fraction of the cost. For example, if 20 to 40 chelation treatments were required for a given patient, it would cost an estimated $2,000 to $4,000.
Several respected physician organizations sponsor educational courses in the proper and safe use of intravenous EDTA chelation. The American College of Advancement in Medicine (ACAM) publishes a protocol for the safe and effective method of treatment with EDTA. This protocol is used in training courses and in a certification program. ACAM’s educational programs for physicians, followed by oral and written examinations, lead to credentials that certify demonstrated competence in the proper use of EDTA chelation therapy.25 The Great Lakes College of Medicine is another organization that provides quality training programs in this area.
Final Notes
Podiatrists need to take the initiative in the care of the diabetic foot, and employ all modalities, both traditional and alternative, to enhance the quality of life and longevity of their diabetic patients.

Dr. Hahn practices at Trinity Clinic, Inc. in Bend, Ore. He is board-certified by the American Board of Podiatric Surgery and is a member of the American Association of Naturopathic Physicians.


References 1. Blach, J.E., et. al. Prescription for Nutritional Healing, 2000, pg. 321-322. 2. M. Brownlee, H. Valassava, and A. Cerami. Nonenzymatic Glycosylation and the Pathogenesis of Diabetic Complications, Ann Int. Med. 101 (1984): pg. 527-537. 3. Chait, A. Dietary Management of DM., Contemp. Nutr. (2), Feb, 1984. 4. Research from the American Journal of Clinical Nutrition, 9:1265-69, 1994. 5. Liu, V. Abernathy, R. Chromium and Insulin in Young Subjects with Normal Glucose Tolerance. Am. J. Clin. Nut., 25 (4): 661-67, 1982. R. Anderson, et. al. Beneficial Effect of Chromium for People with Type II Diabetes, Diabetes 45 Suppl 2 (1996): 124A/454. 6. Annon Role of Carnitine in Branched Chain Ketsacid Metabolis. Nutrition Reviews 39(11) 406-7, 1981. 7. Rossetti, L., et. al. In Vivo Metabolic Effects of Vanadium on Skeletal Muscle and Hepatic Glucose Metabolism. Canadian Journal of Phsysiol. And Pharm; 72:11, 1994. 8. Baskaran K. et. al. Anti-Diabetic Effect of a Leaf Extract of Gymnema Sylvestre in Non-Insulin Dependent Diabetes Mellitus, J. Ethnopharmcol, 30: 295-3056, 1990. 9. Welhinda, J., et. al. Effect of Momordica Charantia on the Glucose Tolerance in maturity Onset Diabetes: J. Ethnopharmacol. 17:277-28. 1986. 10. Maddar, A. et. al. Glucose Lowering Affect of Fenugreek in Non-Insulin Dependent Diabetes. Eur. J. Clinical Nutrition. 42:51-4, 1986. 11. Diabetes Care Volume 5, #5, May, 1994. 12. S. J. Davie, J.B. Gould, and J.S. Yudkin, Effect of Vitamin C on Glycosylation of Proteins, Diabetes 41 (1992) 167-73. 13. Davis, R., Calder, J. and Curnow, D., Serum Pyridoxal and Folate Concentrations in Diabetics. Pathology, April, 151-156, 1976. Jones, Charles, Gonzalez, Pyridoxine Deficiencies; A New Factor in Diabetic Neuropathy. J. of Am. Podiatry Assoc., Sept 645-653, 1978. 14. Pharmacology of Anti-Oxidant Alpha Lipoic Acid, General Pharmacology; 1997. 15. Jacob, S. et. al. Enhancement of Glucose Disposal in Patients with Type II Diabetes by Alpha Lipoic Acid, Arzn-Forsch, 1995; 45:872-4. Ziegler D., Gries, F., Alpha Lipoic Acid in the Treatment of Diabetic Peripheral and Cardiac Antonomic Neuropathy, Diabetes, 1997, Sept; 46 Suppl. 16. Cleary, J., Vitamin B-3 in the Treatment of DM; Case reports and literature review, J. of Nut. Med. 1:217-25, 1990. 17. Messerli, Franz H., Cardiovascular Drug Therapy – Second Edition, 1998. WB Saunders Co. 18. Martell A.E. Calvin Dem: Chemistry of Metal Chelate Compounds, New York. Prentice Hall, 1952. 19. Chappell, Terry L., Janson, Michael. J. Cardiovascular Nurs. 1996 10 (8) 73-86. 20. Pang PKT, Yang MCM, Keutmann, H.T., Kenny AD; Structure Activity Relationship of Parathyroid Hormones; Separation of Hypotensive and Hypercalcemic Properties. Endocrinology 112: 284, 1983. 21. Schwartz, C.J., Valente A.J., Sprague, E.A.; A Modern View of Atherogenesis. AMJ Cardiol 71:9B, 1993. 22. Owlin, J, II, Koppel, J.L., Reduction of Elevated Plasma Lipid Levels in Atherosclerosis Following EDTA Chelation Therapy. Proc. Soc. Exp. Biol. Med. 128: 1137, 1968. 23. Born, Grant R., Geurkink, Tammy L., Improved Peripheral Vascular Function with Low Doses Intravenous Ethylene Diamine Tetia Acetic Acid (EDTA), Townsend Letter for Doctors, #132, July, 1994, 722-726. 24. Olszewer, E. Sabbag, F.C. Carter, J.P, A Double Blind Study of Sodium-Magnesium EDTA in Peripheral Vascular Disease. J. Nat Med Assoc. 1990; 82:173-177. Sloth-Neilsen, J., Gunderger B., Mourition C., et al. Atherographic Findings in EDTA Chelation Therapy on Peripheral Arteriosclerosis. Am J. Sug. 1991: 162:122-125. 25. Cranton, Elmer M. ed. A Textbook on EDTA Chelation Therapy. J. Adv. Med. 1989, 2:1-416. 26. American College for Advancement in Medicine, 23121 Verdugo Drive, Suite 204, Laguna Hills, CA 92653. Telephone: (714) 583-7666.

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