~Diabetes, Part 7 - Treatment Options for Syndrome X and Type II Diabetes

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
  • Alpha-Lipoic Acid
  • Aminoguanidine
  • Bilberry
  • Biotin
  • L-Carnitine
  • Carnosine and a Glycation Review
  • Chromium
  • Coenzyme Q10
  • Conjugated Linoleic Acid
  • DHEA
  • Essential Fatty Acids
  • Fiber
  • Magnesium
  • N-Acetyl-L-Cysteine
  • Silymarin
  • Vitamin C
  • Vitamin E
  • Vitamin K
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.

Biotin--aids in metabolism of macronutrients and glucose utilization and is beneficial in diabetic neuropathy

Biotin, a member of the vitamin B-complex family, assists in the metabolism of fats, proteins, and particularly carbohydrates. Enhanced metabolism is important to the diabetic, who often presents with allergies and food sensitivities, compounding absorption problems.

Biotin directly influences blood glucose levels by working synergistically with insulin to increase the activity of glucokinase, an enzyme responsible for the first step in glucose utilization (Murray 1996). Glucokinase is found concentrated in the liver, but the enzyme is usually very low in diabetic patients. If biotin supplementation is high enough (16,000 mcg/day), the activity of glucokinase is upgraded and a significant improvement in blood glucose control typically occurs (Coggeshall et al. 1985).

Although biotin supplementation plays a pivotal role in blood glucose control, a deficiency is rare. In fact, researchers have found that diabetics have higher levels of biotin (produced by bacteria in the intestines) than nondiabetics. Supplementing with high doses is apparently not correcting a deficiency but rather overcoming a defect in biotin metabolism.

Animal studies indicate that biotin reduces postprandial blood glucose levels and improves insulin's responsiveness (Zhang et al. 1997). Human studies reached similar conclusions, showing that 9 mg (9000 mcg) of biotin a day countered a glucose rise following meals (Maebashi et al. 1993). Diabetic neuropathy, a significant problem among diabetics, also responds well to high dose biotin supplementation (Koutsikos et al. 1990).

A suggested dosage is 8000-16,000 mcg/day for blood glucose management. Biotin is a water-soluble vitamin, meaning it does not accumulate in the body. Toxicity has not been reported, but pregnant and lactating women should avoid high doses.

Biotin food sources, enhancers, and antagonists. Cooked egg yolk, most fish (especially sardines), liver, poultry, dairy products, beans, and brewer's yeast are good sources of biotin. Enhancers are vitamins B12, folic acid, and B5, along with vitamin C, zinc, magnesium, and high-quality protein. Antagonists to biotin are raw egg whites, sulfa drugs, antibiotics, alcohol, coffee, and the antiseizure medications carbamazepine and primidone.

L-Carnitine--improves blood glucose and HbA1c levels, increases insulin sensitivity and glucose storage, and optimizes fat and carbohydrate metabolism; deficiencies appear allied to cardiomyopathy and diabetic neuropathy

Carnitine is a popular dietary supplement because it has been shown to produce many health benefits. The following list illustrates its multidirectional value in the treatment of diabetes:
  • Carnitine improves insulin sensitivity, increases glucose storage, and optimizes carbohydrate metabolism (Crayhon 1999). A significant effect on whole body insulin-mediated glucose uptake was also observed in normal subjects (Mingrone et al. 1999).
  • L-carnitine (200 mg daily), together with chromium (400-600 mcg daily) and moderate caloric restriction, typically results in impressive fat losses (Challem 2000).
  • Carnitine appears to protect against diabetic neuropathy. One of the mechanisms of neuropathy is the accumulation of polyols (alcohol) in nerve cells. In animal studies, acetyl-L-carnitine increased nerve carnitine levels and decreased the accumulation of sorbitol (a polyol) in nerves. This finding suggests a close relationship between increased polyol activity and a carnitine deficiency in the development of diabetic neuropathy (Nakamura 1998). Note: Diabetic neuropathy is a noninflammatory process characterized by sensory and/or motor disturbances in the peripheral nervous system. Symptoms (in those even mildly hyperglycemic) can include pain and loss of reflexes in the legs.
  • Carnitine deficiency is associated with cataract formation in diabetic patients. A significant loss of carnitine from the lens is observed in diabetic test animals, often foretelling the appearance of a cataract (Pessotto 1997). Because of the increased risk of cardiovascular disease and reduced kidney and liver function in diabetic patients, supplementation with L-carnitine appears warranted (Murray 1996).
  • A carnitine deficiency is linked to cardiomyopathy, a condition common among diabetics. In animal studies (6 months after developing diabetes), the myocardial ultrastructure often reveals abnormal-appearing mitochondria, consistent with a carnitine deficiency (Malone 1999). Note: Cardiomyopathy is the partial replacement of heart tissue with a nonfunctional fibrous material that lacks the ability to move blood efficiently.
Many animal and human studies have used acetyl-L-carnitine (the better absorbed and more active form of carnitine) in diabetic trials. Robert Crayhon, a carnitine expert, suggests avoiding carnitine supplements after 3 p.m. to preserve a restful night's sleep. Because increased energy production, a hallmark of carnitine, fosters a greater generation of free radicals, carnitine should always be used with an antioxidant program. A suggested acetyl-L-carnitine dosage is 500-1000 mg twice daily.

Carnosine and a Glycation Review

Glycation, a reaction occurring between proteins and glucose, is recognized as a major contributor to aging and perhaps cancer, as well as the complications arising from diabetes. Glucose provides the fuel for glycation, the insidious protein-glucose combination that (following several steps including the oxidation process) results in the formation of an advanced glycated end product or AGEs. Once AGEs are formed, they interact with neighboring proteins to produce pathological crosslinks that toughen tissues. It has been speculated that no other molecule has the potential toxic effects on proteins as AGEs.

Diabetic individuals form excessive amounts of AGEs earlier in life than nondiabetics, a process that disrupts the normality of organs that depend on flexibility for function. AGEs impair proteins, DNA, and lipids as well as triggering a cascade of destructive events as AGEs cling to cellular binding sites. One of the consequences of AGEs is a 50-fold increase in free-radical formation. Because diabetes (a condition of accelerated aging) spawns a harvest of AGEs, the kidneys are under specific attack.

By opposing glycation, glomerular damage and the resulting inflammation and renal degeneration are reduced. Diabetic rats that were not treated with glycation inhibitors showed a twofold increase in glomerular staining for AGEs compared with a similar group of diabetic rats receiving treatment (Forbes et al. 2001). In addition, glycation inhibitors (protecting against protein damage) are likely to inhibit cataract formation, a complication common to diabetics.

If ever approved by the FDA, glycation inhibitors such as aminoguanidine will enable humans to prevent many of the adversities that accompany aging. In the interim, carnosine (an amino acid peptide) has demonstrated in several studies to be a safe and effective antiglycating agent. Because carnosine structurally resembles the sites that glycating agents attack, it appears to sacrifice itself to spare the target (Hipkiss et al. 2000). Carnosine also bolsters proteolytic pathways, a function that enhances the disposal of damaged and potentially destructive proteins. A suggested carnosine dosage is 1000 mg/day.

Chromium--modulates blood glucose levels, fights insulin resistance, lowers HbA1c levels, aids weight loss, and inhibits glycation

Anecdotal but confirmed reports of brewer's yeast (a source of chromium) normalizing blood glucose levels hints of chromium's remarkable contribution to diabetic care. Researchers validated the anecdotal stories when the results of a study involving 78 Type II diabetics were published (Bahijiri et al. 2000). One-half of the enrollees received an inorganic chromium (200 mcg a day); the other half received brewer's yeast (supplying 23.3 mcg of chromium per day). Both groups realized a significant decrease in glucose in urine and fasting blood glucose levels as well as after a 2-hour, 75-gram glucose load. In fact, some trial participants were able to decrease antidiabetic drugs, and others no longer required insulin. Interestingly, a higher percentage responded positively to brewer's yeast, presumably because of better absorption; that is, the body retained more of the trace mineral.

The literature teems with similar reports regarding chromium's ability to modulate errant blood glucose levels. In fact, chromium is so important it is considered essential nearly every time you eat. Unfortunately, about 90% of adults are chromium deficient, according to the U.S. Department of Agriculture. (The highest tissue levels of chromium are found in newborns, with the tissue levels dwindling over a lifetime.) The conundrum surrounding chromium is that as chromium becomes deficient, more insulin is required, and as insulin production becomes excessive, a chromium deficiency occurs. In addition, chromium levels are seriously depleted when eating a diet high in refined sugar and white flour products.

It was known by the 1950s that chromium was required by animals to control blood sugar, but it was not until the 1970s that chromium's essential role in humans was clearly proven. The following chance finding established chromium's validity in reducing diabetic symptoms: patients receiving Total Parenteral Nutrition (TPN), a specially prepared feeding solution delivered through the patient's veins, developed high blood sugar in the absence of diabetes. Insulin therapy was begun but without satisfying results. It was determined that the TPN was deficient in amounts of chromium adequate to stave off diabetes-like symptoms. When 50 mcg of chromium were added to their IV feedings, the patients no longer required insulin and their blood glucose levels returned to normal (Mennen 1996).

Several mechanisms render chromium valuable in blood glucose management:
  • Chromium is essential in glucose metabolism. Note: It is estimated only about 3% of ingested chromium is absorbed into body tissues. The mineral is stored primarily in the spleen, skin, kidneys, and testes (Whiting 1989).
  • Chromium assists in overcoming insulin resistance (McCarty 2000).
  • Chromium appears to be involved in the insulin-induced movement of glucose into cells, probably by encouraging the binding of insulin to the receptor site or participating in reactions that occur immediately after the binding process, called postreceptor events.
The results of a 4-month study, presented at the 57th Annual Scientific Session of the American Diabetes Association Meeting in 1997, demonstrated that daily supplementation with 1000 mcg of chromium (supplied as chromium picolinate) significantly enhanced the action of insulin. The trial participants (29 overweight individuals with a family history of diabetes) completed the randomized, double-blind, placebo-controlled clinical trial showing that chromium reduced insulin resistance by 40% over the placebo group. (The study was conducted by William Cefalu, M.D., director of the Diabetes Comprehensive Care and Research Program at the Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC.)

High blood glucose damages proteins, a process called glycation. When blood sugar is high, glucose becomes attached to various proteins, including hemoglobin (the oxygen-carrying protein in red blood cells). A protein with glucose attached is said to be glycosylated, and in the case of hemoglobin is measured as HbA1c. Glycation is responsible for many of the complications of diabetes, a process that chromium inhibits.

To assess the effects of chromium on glycosylated hemoglobin levels, 180 Type II diabetes patients were divided into three groups and supplemented daily with 200 mcg of chromium, 1000 mcg of chromium, or a placebo (Baker 1996). After 4 months, there was improvement in both chromium-treated groups. Glycosylated hemoglobin (a measurement of average blood glucose) over a 2- to 3-month period was (on an average) 6.6% in the high dose group, 7.5% in the low-dose group, and 8.5% in the placebo group. For a nondiabetic, HbA1c is normal at 4-6%; for a diabetic, the goal is to maintain HbA1c at less than 7%.

To fully understand the previous study, HbA1c (expressed in percentages) and the blood sugar equivalents (mg/dL) follow:
  • 4.0% = an average of 60 mg/dL of glucose
  • 5.0% = an average of 90 mg/dL of glucose
  • 6.0% = an average of 120 mg/dL of glucose
  • 6.6% = an average of 138 mg/dL of glucose
  • 7.0% = an average of 150 mg/dL of glucose
  • 7.5% = an average of 165 mg/dL of glucose
  • 8.5% = an average of 195 mg/dL of glucose
The data presented show how the HbA1c blood test measures average glucose levels over an extended period of time. When interpreting HbA1c, keep in mind that the results differ depending upon the test method used. Some laboratories measure hemoglobin A1, which is different from A1c. Also, the results may reflect the averaging of a period of high glucose with a period of low glucose as opposed to the consistent readings required for diabetes control.

Unfortunately, chromium supplementation is not as popular as it should be. One of the major problems hindering chromium usage is the fact that deficiencies are not easily gauged. Supplementation, followed by the laboratory assessment of blood glucose levels, appears the best appraisal of chromium's worth.

A chromium dosage of 50-100 mcg daily is high enough to correct a deficiency but not sufficient to improve blood sugar control. Dr. Richard Anderson (a biochemist and nutritionist with the Department of Agriculture) recommends that persons with diabetes and impaired glucose tolerance take 400-600 mcg of chromium daily. (Some practitioners report superior results in treating diabetes with the polynicotinate form of chromium, citing greater absorptive powers as the biological advantage.) Because significant changes in insulin requirements can occur with chromium therapy, physician monitoring is advisable.

Note: In the mid-1990s, chromium picolinate came under fire when it was linked with chromosome damage. Extensive toxicological testing proved that this indictment was invalid. Multiple trials have shown it is extremely difficult to harm laboratory animals with oral chromium supplementation. The public can be grateful for this because chromium is the chief nutritional barrier between healthy blood glucose levels and diabetes..

Chromium food sources, enhancers, and antagonists. Brewer's yeast, whole grains, liver, cheese, meat, and potatoes are good sources of chromium. Enhancers are essential amino acids, selenium, and vitamin E. Hemochromatosis (excesses of iron) antagonizes chromium absorption.

Continued . . .


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