Become a Participant in Your Return to Health
Some conditions are better managed with conventional medicine, and others have a better success rate using a natural approach. Type II diabetes appears to have an affinity for the natural, with remarkable gains reported. However, natural methods have little chance of succeeding without patient participation. This means the patient must refuse inappropriate foodstuffs, make time for exercise, and maintain weight within healthy standards. Diabetics should never blame themselves for their illness, but when the condition becomes manageable, the patient can justifiably claim much of the credit.

Results of the Finnish Diabetes Prevention Study (presented at the American Diabetes Association's 60th Annual Scientific Session in June 2000) illustrate the patient principle, i.e., the patient accepting much of the responsibility for the outcome of the disease process. The study showed that lifestyle modification (a structured dietary and exercise program) reduced the incidence of Type II diabetes by 58% in people at high risk for the disease.

The trial participants (522 prediabetic adults, 172 men and 350 women; average age 55 years) were divided into two groups and tracked over a 5-year period (1993-1998). Frequent dietary advice along with an individualized exercise program that included at least three supervised exercise sessions a week was assigned to the intervention group. The remainder of the individuals (acting as a control group) received nutritional tutorage at a yearly meeting and encouragement to upgrade their exercise regime. The weight reduction was about 4.2 kg at 1 year in the intervention group compared to 0.8 kg in the control group. Some backsliding occurred by the end of the second year in the intervention group, resulting in a 3.5-kg overall net weight loss; the control group's weight loss remained constant at 0.8 kg the second year.

At 1 year, the intervention group showed significantly greater reductions in 2-hour glucose, fasting, and insulin levels, as well as blood pressure and serum triglyceride levels. Most of the beneficial changes in cardiovascular risk factors were sustained for 2 years. The researchers concluded that Type II diabetes is preventable in high risk patients by lifestyle modification (Uusitupa et al. 2000; Tuomilehto et al. 2001).

Self-improvement programs, when faithfully approached, are more rewarding than easy. However, behavioral modification has proved successful in helping more people lose weight than any other kind of weight-loss program. Successful attempts at lifestyle modification should include family members and friends. Recall the number of social gatherings planned around carbohydrates. Sugary treats are foods for celebrating, partying, and showing affection. Finding alternatives to sugar is as possible as it is profitable, and the health dividends far more gratifying.

TREATMENT OPTIONS FOR SYNDROME X AND TYPE II DIABETES

Syndrome X is the term used to describe a variety of metabolic disturbances often seen in persons diagnosed with Type II diabetes. It is important for the Type II diabetic to treat all Syndrome X imbalances by lowering elevated triglycerides and blood pressure, while attempting to increase HDL levels. However, it is imperative for the Type II diabetic to address the primary conditions of insulin resistance, hyperinsulinemia, and hyperglycemia.

The following section, the Therapeutic Section, highlights nutrients and herbs that have won favor as antidiabetic agents. For example, the Helicon Foundation announced in 2000 that it may be possible to address dysfunctions that conspire to maintain hyperglycemia in Type II diabetes by ingesting specific supplemental nutrients such as chromium (for skeletal muscle insulin resistance), conjugated linoleic acid (for adipocyte insulin resistance), biotin (for excessive hepatic glucose output), and coenzyme Q10 (for beta cell function) (McCarty 1999, 2000). These and many other antidiabetic agents (found in natural pharmacology) are fully discussed in this section.

Although the material presented in the Therapeutic Section is well substantiated, diabetes represents a gravely serious condition, requiring a physician to structure the program and monitor progress. However, the patient must be a major team player to expect success. It is extremely important to note (before embarking on any diabetic regime) that the first treatment for Type II diabetes is always diet. Regardless as to whether natural agents or pharmaceuticals are used, dietary restraints are essential to enact change.

Therapeutic Section

Nutritional Interventions for the Prevention and Treatment of Syndrome X and Type II Diabetes
Supplemental suggestions are arranged in alphabetical order for easy reference, not in order of importance. Although the nutrients profiled perform multiple functions, only the activities of the supplement relative to Type II diabetes have been included in this material.

It is important for the patient to understand that there are multiple pathological factors involved in common diabetic complications such as neuropathy, blindness, arteriosclerosis, renal failure, and so forth. It is therefore necessary to guard against as many of these underlying mechanisms as is practical to avoid experiencing debilitating and lethal diabetic consequences.

The most important therapeutic modality in the control of Type II diabetes is weight loss. Therefore, the reader is advised to consult the Obesity protocol, which provides innovative methods of reducing excess body fat, while suppressing elevated levels of serum insulin (hyperinsulinemia).

Alpha-Lipoic Acid--lowers blood glucose and insulin levels, reduces insulin resistance, and improves insulin sensitivity
Alpha-lipoic acid, a sulfur-containing compound, may prove to be the "kingpin" in the fight against Type II diabetes and its many complications. Lipoic acid comes with impressive credentials, including the ability to increase the burning of glucose (Challem et al. 2000; Hinderliter 2002). The mitochondria (the powerhouses of the cell) are one of the benefactors of enhanced glucose utilization. This occurs via the Krebs's cycle, a process that utilizes glucose, amino acids, and fatty acids to yield high energy. Lipoic acid intervenes at several points in the Krebs's cycle, warranting a continuous supply of energy to the cell. Free radicals are produced as a byproduct of the energy generated during the Krebs's cycle, but alpha-lipoic acid appears to quench abhorrent free radicals that are not contained during the reactions.

Greater efficiency in the Krebs's cycle results in increased amounts of glucose used for energy production. This is very important for the diabetic: if glucose is used purposely, lesser amounts appear in the bloodstream. Also, the more glucose that is burned, the less insulin your body will have to provide. Lipoic acid resulted in a 50% increase in insulin-stimulated glucose disposal and a significant improvement in insulin sensitivity compared to a nonsupplemented placebo group (Jacob 1995, 1996, 1997). Alpha-lipoic acid appears able to deliver glucose into cells in ways independent of insulin participation. Researchers found that when lipoic acid was injected into fasting nondiabetics or diabetic rats, a rapid reduction in blood glucose occurred without a corresponding effect upon circulating insulin levels (Khamaisi et al. 1999).

Interestingly, lipoic acid protects not only against the damage that causes diabetes, but also against the damage caused by the disease. For example, alpha-lipoic acid guards against blood glucose accumulating in the bloodstream and also protects against the proliferation of free radicals. Oxidative stress is characterized by the excessive generation of free radicals, which injures cells throughout the body. Alpha-lipoic acid helps prevent free radical-induced damage to tissues and organs.

Antioxidants have distinctive characteristics. For example, vitamin C protects only the watery portions of cells from free-radical attack; vitamin E protects fatty membranes. Alpha-lipoic acid possesses antioxidant feats considered extraordinary: the ability to neutralize free radicals occurring in both watery and fatty regions of cells.

Lipoic acid's reputation as the universal antioxidant is justly earned because it unselfishly extends itself to other antioxidants (vitamins C and E, as well as glutathione and CoQ10), regenerating them for continued service and greater efficiency. Acting through its antioxidant powers, lipoic acid appears helpful in reducing the risk of cataracts, as well as increasing blood flow to peripheral nerves (Packer 1994). It is, in fact, approved for the prevention and treatment of diabetic neuropathy in Germany.

Data indicate that lipoic acid is effective in the prevention of early diabetic glomerular injury, proving more effective than high doses of either vitamins A or C (Melhem et al. 2001). (Recall that the kidneys are at particular risk in diabetic patients.)

Glucose increases advanced glycated end products (AGEs). (AGEs are formed when glucose reacts with a protein, damaging the protein in cells, preventing normal function.) Alpha-lipoic acid reduces levels of glycosylated hemoglobin, a standard marker of glucose-damaged proteins (Jain et al. 1998). (To read more about glycation and glycation inhibitors, consult the areas in this section devoted to aminoguanidine, carnosine, chromium, and vitamin C.)

The body makes only small amounts of alpha-lipoic acid; in fact, just enough to avoid deficiency states. By and large, foods that contain mitochondria (such as red meats and organ meats) are regarded as good sources of lipoic acid. According to Lester Packer (head of Membrane Bioenergetics Group at the University of California-Berkeley), other sources are spinach, potatoes, brewer's yeast, and wheat germ. For most individuals, supplementation appears the most reliable approach to provide therapeutic levels of lipoic acid.

If taken with a full spectrum antioxidant, 250-500 mg a day appear adequate, but diabetics often require larger amounts. For the last 30 years, German practitioners have used 600-1800 mg per day to improve diabetic conditions. Side effects include rare reports of a skin rash, hypoglycemia, and, if chronically used, interference with the actions of biotin. (If the daily dose of alpha-lipoic acid exceeds 100 mg, co-supplement with biotin.) Individuals deficient in vitamins B1 (such as alcohol abusers) and vitamin B12 should emphasize the B vitamins when supplementing with lipoic acid. Because alpha-lipoic acid frequently changes insulin requirements, higher doses should be administered under the observation of a qualified physician.

Aminoguanidine (Pimagedine) and Other Inhibitors of Glycation: Aspirin, ALT-711, and ALT-946
Aminoguanidine appears to forestall the aging process by inhibiting the crosslinking of proteins. An apple slice, untreated and exposed to the environment, typifies the effects of crosslinking: the white fruit under the skin turns brown and loses texture. Diabetes is seen as a form of accelerated aging, with the effects of crosslinking often cited as a cog in its development.

Advanced glycated end products (AGEs) are an offshoot of a reaction occurring between a sugar and a free amino acid. (Free form amino acids are those that have not chained together to form peptides or proteins; they are singular entities.) Glucose is found in every cell of the body and is relatively stable, but it can join with proteins to form a glucose-protein combination. It is this combination that will eventually cause active crosslinks and hasten the aging process.

High glucose levels, even transiently elevated, supply the fuel for the glycation process. The levels of crosslinking products in diabetic patients appear to be 2-3 times higher than among nondiabetics. Compounding the problem, it is speculated that AGEs stay in the body for months, even years, crosslinking with other proteins.

There is emerging evidence that AGEs are potential uremic toxins that play a role in the pathogenesis of renal complications (nephropathy) associated with diabetes (Raj et al. 2000). A number of studies have shown that treatment with aminoguanidine also improves neuropathy (inflammation or degeneration of peripheral nerves) and delays the onset of retinopathy (a noninflammatory eye disorder resulting from changes occurring in retinal blood vessels.)

The good news is that crosslinking is preventable by using glycation inhibitors. For example, aminoguanidine is able to join with substances that cause crosslinks, disrupting the cycle that results in cellular damage. Because aminoguanidine is able to combat many of the complications associated with diabetes, the quality and length of life could be favorably impacted with glycation inhibitors (Friedman et al. 1997).

The importance of inhibiting AGEs was highlighted when Alteon Inc. (January 22, 2001) announced a novel AGE inhibitor, ALT-946. The objective of ALT-946 (now in human clinical development) is to inhibit glycation at the onset. ALT-711, another Alteon compound, targets existing glucose-protein crosslinks, breaking them up after they have formed. A company spokesperson stated that though the rationale is still hypothetical, the intent is to provide a comprehensive approach to control glycation, such as ALT-946 inhibiting new crosslinks and ALT-711 getting rid of old ones.

Researchers found ALT-946 to be more potent than aminoguanidine in preventing AGE's crosslinks in vivo and in vitro. This finding is significant, because heretofore, human clinical trials have shown a meaningful protective effect in diabetic complications, including kidney disease, retinopathy, and dyslipidemia when using aminoguanidine (Imanaga et al. 2000; Forbes et al. 2001; Du et al. 2002).

Since ALT-711 and ALT-946 are not yet available, the value of alternative glycation inhibitors (alpha-lipoic acid, aspirin, carnosine, chromium, and vitamin C) becomes even more relevant. Alteon Inc. does not project a time frame regarding the availability of their antiglycation products, but in the interim, the company is exploring further clinical development activities for aminoguanidine and proceeding with a preclinical development program for ALT-946 as their second generation AGE formation inhibitor.

Bilberry (Vaccinium myrtillus)--reduces blood glucose levels
According to Linda White, M.D., the fruit of the bilberry bush is a rich source of the bluish pigments called anthocyanidins and proanthocyanidins, two of the many types of flavonoids beneficial in the treatment of diabetes. In The Healing Power of Herbs, Dr. Michael Murray states that oral administration of bilberry reduced blood glucose levels in normal and depancreatized dogs, even when glucose was simultaneously injected (Murray 1995). Italian researchers reported that bilberry consistently decreased blood glucose levels by 26% and triglycerides by 39% in animal models (Cignarella et al. 1996).

Myrtillin appears the most active antidiabetic component in bilberry. An injection of myrtillin, although somewhat weaker than insulin, can be used without threat of toxicity, even at 50 times the recommended dose. The literature indicates bilberry sustains its antidiabetic advantage; that is, postinjection blood glucose levels remained stable for a longer period of time compared to many other hypoglycemic agents (Murray et al. 1991). A suggested oral dosage of bilberry is 100-200 mg, standardized to contain 25% anthocyanidins, 3 times a day.

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These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease