Diabetes Protocol

Magnesium--lowers blood glucose levels, increases insulin sensitivity, and calms the sympathetic nervous system
Although the relationship between magnesium and diabetes has been studied for decades, it is still poorly understood. However, what is known about diabetes and magnesium embodies a persuasive list encouraging supplementation:

Low magnesium levels are common findings in noninsulin-dependent diabetic patients (Paolisso et al. 1989). In fact, diabetes is a frequent cause of secondary hypomagnesemia (lower blood levels of magnesium). Poorly controlled diabetics excrete more magnesium than do nondiabetics.
Magnesium assists in the maintenance of functional beta cells (insulin factories) (Kowluru et al. 2001). Scientists believe that a magnesium deficiency interrupts insulin secretion and its activity. Magnesium, by enhancing the action of insulin, improves insulin's ability to transport glucose into the cell.
Magnesium increases the number and sensitivity of insulin receptors (Waterfall 2000).
An increase in red blood cell magnesium significantly and positively correlated with an increase in both insulin secretion and action. Correction of low erythrocyte magnesium concentrations may allow for improved glucose handling, particularly in elderly diabetic patients (Paolisso et al. 1992, 1993a).
As magnesium levels plummet, the incidence of diabetic complications escalates. Of particular concern is the association between low magnesium levels and ischemic heart disease and retinopathy. It appears that magnesium may prevent and retard the development of vascular complications common to diabetic patients (Elamin et al. 1990).
Magnesium not only plays a role in insulin resistance and hypertension, but also plays a role in the correction of carbohydrate intolerance (Murray 1996).
Magnesium is the mineral of choice to reduce hyperresponsiveness occurring in the sympathetic nervous system (SNS). This is important to the diabetic because when the SNS is alerted, blood glucose levels tend to be higher. The SNS is also associated with fostering greater levels of stress and anxiety, earning its reputation as the "flight or fight" division. Since diabetes is considered to be a disease promulgated by stress, supplementation that favors an inner calm is of significant advantage.

Serum magnesium levels are relatively insensitive assessments of magnesium status. Magnesium deficiency is far better detected by measuring mononuclear blood cell magnesium, as opposed to serum levels. A suggested magnesium dosage is 500 mg of elemental magnesium daily along with a diet favoring magnesium-rich foods, for example, whole grain cereals, nuts, legumes, and green vegetables. Since vitamin B6 is intricately involved in magnesium absorption, at least 30-50 mg of vitamin B6 should accompany magnesium supplementation.

N-Acetyl-L-Cysteine--protects beta cells against free-radical destruction
Free radicals flourish when blood glucose levels are high, causing various forms of tissue destruction in patients. A study examined the involvement of free radicals in the progression of pancreatic cell dysfunction and evaluated the usefulness of N-acetyl-L-cysteine (NAC), a potent antioxidant, to counter the attack (Kaneto et al. 1999). The study was reported in the journal Diabetes and the conclusion was that NAC exerts beneficial effects by preserving beta cell function. This finding supports the implication that free radicals promote beta cell dysfunction and that antioxidant therapy is a useful adjunct in diabetes management.

During NAC therapy, the following observations were made:

Pancreatic beta cells appeared to be protected against glucose toxicity (Kaneto et al. 1999).
The insulin-producing beta cell mass was larger in diabetic mice treated with NAC compared to untreated mice (Kaneto et al. 1999).
Beta cell death was suppressed. The journal Diabetes reported that high levels of glucose appeared to directly upregulate the cell death receptor Fas on human pancreatic beta cells. This finding may explain the loss of beta cell mass observed in Type II diabetes (Donath et al. 2001).
Glucose-stimulated insulin secretion continued, followed by a modest decrease in blood glucose levels with NAC supplementation (Kaneto et al. 1999).
A suggested NAC dosage is 600 mg a day on an empty stomach for optimal absorption.

Note: When taking NAC, it is recommended that two to three times as much vitamin C be taken conjunctively because of the prolonged presence of the oxidized form of L-cysteine.

Silymarin--improves liver function and blood glucose control and reduces free-radical activity
The liver performs more than 500 functions, including the regulation of blood glucose. According to information released from the Diabetes Forum (Gopi Memorial Hospital), the liver is the first and most important tissue involved in insulin utilization. In fact, if the liver becomes damaged, secondary diabetes can result. An injured liver is unable to respond to insulin normally and essential blood glucose regulatory systems become less functional. If glycogenolysis (the breakdown of glycogen to supply glucose), gluconeogeneis (the hepatic synthesis of glucose from noncarbohydrate sources), or glycogenesis (the synthesis of glycogen from glucose) is depreciated, tight blood glucose control becomes impossible.

A group of 60 patients with type II diabetes and alcohol-induced liver damage were divided into two groups: for 12 months, 30 received 600 mg per day of silymarin (an antioxidant flavonoid derived from the herb milk thistle) while 30 received a placebo. All subjects were classed as very ill at the onset of the study (Velussi et al. 1997; Challem et al.2000).

Those receiving silymarin evidenced a significant reduction in fasting blood glucose levels (an improvement also mirrored in urine glucose). Initially, average glucosuria (glucose in urine) was 37 grams, dropping to 22 grams during therapy. Fasting glucose levels rose slightly during the first month of supplementation but declined thereafter from an average of 190 mg/dL to 174 mg/dL. As daily glucose levels dropped (from an average of 202 mg/dL to 172 mg/dL), HbA1c also substantially decreased. Throughout the course of treatment, fasting insulin levels declined by almost one-half and daily insulin requirements decreased by about 24%. Liver enzymes (SGOT and SGPT) modulated, reflecting improved liver function. A lack of hypoglycemic episodes suggests silymarin not only lowers blood glucose levels, but also stabilizes them as well. Glucosuria, fasting insulin, and glucose levels, as well as HbA1c, remained unchanged in the nonsupplemented group.

In an 8-day, cell-culture study, German researchers found that a specific silymarin flavonoid, silibinin, prevented the accumulation of fibronectin protein in kidney cells. (Fibronectin is one of the principal causes of kidney damage in diabetics.) Simone Wenzel, Ph.D., incubated human mesangial cells (a type of kidney cell) in high concentrations of glucose or in a combination of glucose and silibinin. An accumulation of fibronectin was prevented, with protection attributed to silibinin's antioxidant properties (Wenzel et al. 1996).

Silibinin is the most active constituent of silymarin and is sold as a drug in Germany to treat hepatic disorders. Standardized milk thistle extract usually consists of 35% silibinin, whereas the silymarin concentrate used in Europe contains a minimum of 80% silibinin. A suggested silymarin dosage for Syndrome X patients (those not yet diagnosed with diabetes) is a supplement that provides 250 mg a day of silibinin and 60 mg of silymarin. Diabetic patients often take 2-3 silibinin/silymarin capsules providing the same amounts.

Vitamin C--lowers blood glucose and CRP levels, inhibits glycation, prevents accumulation of sorbitol, and protects against free radicals
An exchange occurring between hormones and nutrients maintains health at the cellular level. For example, insulin (by facilitating the transport of vitamin C into cells) decreases capillary permeability and aids in wound healing. Diabetics are often deficient in intracellular vitamin C; this deficiency deprives a diabetic of the protection this important nutrient delivers (Sinclair 1994).

Vitamin C, an antioxidant, protects against free-radical activity, which is notoriously aggressive in diabetic patients.
Vitamin C makes blood glucose management easier. Vitamin C deficiencies increase HbA1c (an average measurement of blood glucose levels over the last several weeks) (Sargeant 2000).
Vitamin C inhibits glycation, a destructive process that occurs when glucose reacts with a protein (Emekli 1996; Vincent 1999). The glycosylation of proteins in red blood cells, the lens of the eye, and nerve cells causes abnormal structure and function of cells and tissues. This untoward sequence contributes to many of the complications common to diabetes (Brownlee et al. 1984).
C-reactive protein (CRP) is higher in individuals with clinical evidence of insulin resistance. It appears some of the increase in winter cardiovascular mortality may be related not only to a rise in fibrinogen, but also to an increase in other inflammatory markers, such as CRP. This cycle may be spurred as winter infections increase and vitamin C intake decreases because of less availability of fruits and vegetables (Khaw et al. 1997).
Vitamin C might be able to influence cardiovascular and diabetic risks by modulating the inflammatory response to infection.
Vitamin C reduces sorbitol accumulating within the cell and the risk of diabetic complications, including cataracts (Murray 1996).
Administering vitamin C in amounts of 1000-3000 mg daily (in divided doses) has been shown to significantly improve a diabetic's prognosis.

Food sources of vitamin C, enhancers, and antagonists
Fresh vegetables and fruits (particularly citrus) are excellent sources of vitamin C. Bioflavonoids are vitamin C enhancers. Antibiotics, antihistamines, steroid drugs, birth control pills, tobacco, stress, and aspirin are vitamin C antagonists.

Vitamin E--reduces C-reactive protein (CRP) and oxidative stress, enhances insulin sensitivity and glucose transport, and prevents complications arising from inflammation
Vitamin E's antioxidant properties and its ability to enhance insulin's responsiveness are but a few of the reasons the nutrient should be included in a diabetic protocol. This was clearly evidenced in a 4-month study reported in the American Journal of Clinical Nutrition with subjects receiving (approximately) 900 mg of vitamin E a day. The researchers assessed how well 15 Type II diabetics and 10 healthy controls tolerated glucose before and after vitamin E supplementation. In healthy subjects, glucose removal from the blood increased 17%. In diabetics, total glucose removal increased 47% and nonoxidative glucose metabolism increased 63%. The study established that pharmacologic doses of vitamin E in Type II diabetes improve insulin's action and reduce free-radical activity (Paolisso 1993b).

Vascular endothelial dysfunction (an early marker of atherosclerosis) has been demonstrated in Type II diabetes mellitus. It appears hyperglycemia is particularly destructive to endothelial cells because it increases oxidative stress and impairs the activity of nitric oxide, the endothelial derived relaxing factor (Giugliano et al. 1995). Oxidative injury may be increased in diabetes mellitus because of a weakened defense due to reduced endogenous antioxidants (vitamin E and reduced glutathione). With compromised nitric oxide activity, diabetic-cardiovascular complications (smooth muscle proliferation, platelet activation/aggregation, and leukocyte adherence to the endothelium) are compounded.

Some of the strongest recent evidence of a vitamin E-diabetes benefit comes from researchers at the University of Texas Southwestern Medical Center in Dallas. Scientists found that vitamin E (1200 IU daily) reduced the risk of heart failure in 75 diabetics by curtailing vascular inflammation in the heart. Left unchecked, inflammation can cause cardiac vessels to swell, promoting cardiovascular disease. Dr. Sridevi Devaraj, assistant professor of pathology and lead researcher, termed the end results of the study very encouraging (Devaraj 2001).

Last, elevated levels of CRP, an inflammatory marker, have recently been found to predict the development of Type II diabetes. A newer finding relating to the functions of vitamin E is that high dose vitamin E lowers CRP. Administering 1200 IU of alpha-tocopherol (daily for 3 months) lowered CRP levels by 30%. CRP levels remained reduced 2 months postsupplementation. By preventing vascular inflammation, many of the complications arising from diabetes are overcome (Devaraj et al. 2000). A suggested vitamin E dosage is 400-1200 IU of vitamin E per day along with at least 200 mg of gamma tocopherol.

Vitamin K--may play a role in insulin's response to glucose
To evaluate the effects of vitamin K on pancreatic function, 25 healthy young male volunteers were evaluated as to plasma-glucose vitamin K levels at baseline and after an oral glucose load. Concurrently, a 1-week food diary estimated mean daily vitamin K intake.

Individuals consuming a vitamin K-rich diet tended to have higher blood vitamin K status then those participants who had less vitamin K in their diet (conclusion reached by examining an average of five blood samples). Fasting plasma glucose levels were not markedly different between the groups, showing about 86 mg/dL among all subjects. However, 30 minutes after a glucose load, the group with the higher vitamin K status had a plasma glucose level of 145 mg/dL; the group with the lower vitamin K levels presented with a plasma glucose level of 160 mg/dL. According to researchers, the results suggest that vitamin K may play an important role on the acute insulin response to glucose tolerance (Nishiike et al. 1999).

Elevated levels of C-reactive protein (CRP) and interleukin-6 (IL-6) have recently been found to predict the development of Type II diabetes mellitus. Since Vitamin K reduces levels of IL-6, it appears equally probable that vitamin K may also be effective in attenuating elevations in CRP. A suggested vitamin K dosage is 10 mg per day.

Note: Persons on anticoagulant drugs such as Coumadin cannot take vitamin K.
Vitamin K-rich food sources and antagonists.
Although friendly bacteria in the intestines synthesize the majority of vitamin K, the total requirement cannot be met by bacterial synthesis alone. Vitamin K-rich foodstuffs are liver and green leafy vegetables (especially broccoli, turnip greens, lettuce, and cabbage). Antibiotics increase the need for vitamin K, and vitamin E (doses less than 600 IU) antagonizes vitamin K activity.

WHY CONVENTIONAL TREATMENT FOR DIABETES CAN BE WORRISOME

By now, the reader is keenly aware that insulin in excess is dangerous. Too often, Type II diabetes patients are treated with insulin as the treatment of choice to control blood glucose levels. Most Type II diabetics have copious levels of insulin, at least before the disease becomes chronic and the pancreas exhausted. Injecting insulin into an already expanded insulin pool is a difficult rationale to justify. Once the pancreas fails, insulin therapy becomes essential.

When Type II diabetes is diagnosed, patients are often treated with antidiabetic drugs that lower blood glucose by stimulating the pancreas to secrete more insulin. These insulin-stimulating agents are classified as sulfonylureas drugs. Conventional medicine also recommends dieting to control obesity (should it exist).

The problem with these conventional treatments is that the vast majority of diets fail to induce long-term weight control. While sulfonylureas drugs temporarily lower blood glucose, they saturate the blood with insulin and worsen the long-term prognosis. Examples of popular sulfonylureas medications and their mode of operation follow:

Glimepiride (Amaryl) lowers blood glucose by stimulating the pancreas to produce more insulin.
Glipizide (Glucatrol) controls diabetes by goading the pancreas into secreting more insulin.
Glyburide (Micronase) controls blood glucose by stimulating the pancreas to produce more insulin and by helping insulin work more efficiently.
Drugs that continuously "whip" the pancreas into producing more insulin appear to be a shortsighted approach to treating the problem. This mechanism weakens the beta cells of the pancreas much quicker, plus the body must deal with the toxic effects of the additional insulin load. Chronically elevated levels of insulin raise the risk of degenerative disease (such as cancer and heart attack) and exacerbate the effect of diabetes.

When profiling many of the sulfonylureas drugs, the Physician's Desk Reference includes a perceptive comment: "It is possible that some oral diabetic drugs may lead to more heart problems than diet treatment alone, or diet plus insulin." (Recall that heart disease is regarded as the major complication arising from diabetes.)

Relying upon a sulfonylurea drug to correct a condition, often amendable through discipline, is asking more of a drug than we are asking of ourselves. If attempts at lifestyle modification fail to ameliorate hyperglycemia, oral agents may become necessary but are by no means desirable.

Too often the antidiabetic diet endorsed by orthodox physicians allows far too many carbohydrates to be effective. Recall that Dr. Steven Whiting, Ph.D., believes that chronic adherence to a high carbohydrate diet ensures that the diabetic individual will be a patient for life.

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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