Diabetes Protocol

Approximately 8% of the population in the United States has diabetes. This computes to nearly 16 million people being diagnosed with the disease, based only on national statistics.

The American Diabetes Association announced that diabetes accounts for 178,000 deaths, 54,000 amputees, and 12,000-24,000 cases of blindness annually. Blindness is 25 times more common among diabetic patients compared to nondiabetics. It is proposed that by the year 2010, diabetes will exceed both heart disease and cancer as the leading cause of death through its many complications.

Considering these startling numbers, an insightful internist recently commented that physicians are losing more patients to diabetes than they are diagnosing. Additionally, it is estimated that 5.4 million people have the disease and are not aware of it. Minorities are at particular risk. Compared with Caucasians, blacks have a 60% higher risk of developing diabetes and Hispanics have a 90% increased risk.

Autoimmune (Type I) Diabetes

This type of diabetes has also been called Juvenile Onset Diabetes Mellitus, Insulin Dependent Diabetes, or Type I diabetes. For reasons we do not clearly understand, the body attacks its own insulin-producing tissue, the beta cells of the islets of Langerhans in the pancreas. When so many of these cells are destroyed that not enough are active to meet the body's need for insulin, the patient becomes diabetic and must take insulin injections.

At one time, we thought that this condition was only found in childhood, and so it was assumed that any young person who started showing signs of disturbed glucose metabolism was insulin deficient. Conversely, we concluded that patients who did not become diabetic until they were adults were not insulin deficient. Today, we know that young people can be metabolically diabetic and that adults can become autoimmune diabetic.

Autoimmune diabetes can be definitively diagnosed with blood testing.

Blood insulin and glucose levels, drawn together, will show a deficiency of insulin or an excess of glucose.
Anti-insulin antibodies/anti-islet cell antibodies are usually present in autoimmune diabetes (Type I).

Conventional treatment for this condition is not satisfactory. Replacement of insulin by injection can be used to keep blood sugar under control but will not prevent development of all of the dreaded complications of diabetes: loss of sexual function, diabetic retinopathy (blindness), peripheral neuropathy (approximately 10% of diabetics develop neuropathic symptoms, such as throbbing, aching, or numbness of the lower extremities), and peripheral vascular disease (diminished circulation, intermittent claudication, difficult wound healing, and the propensity for gangrenous body parts and eventual amputation). Typically, tight control of blood glucose levels prolongs the onset and progression of symptoms.

However, there is evidence that protecting cells against the adverse effects of unstable serum insulin and serum glucose can mitigate these complications. Therefore, while many of the supplements in this protocol have documented benefits in protecting against Type II diabetic complications, they can also prevent diseases commonly associated with Type I diabetes.

The Difference Between Type I and Type II Diabetes

Type I diabetes, sometimes referred to as insulin-dependent diabetes mellitus (IDDM), has both similar and dissimilar manifestations as compared to Type II diabetes mellitus. Although both Type I and Type II diabetes often result in similar disabilities, that is, neurological disorders, cardiovascular disease, and sometimes organ failure, the causal factors are quite different. For example, Type I diabetes reflects an inability to metabolize carbohydrates caused by an absolute insulin deficiency. This type of diabetes occurs most often in children and young adults as a result of inadequate insulin production in the beta cells of the pancreas.

The islets of Langerhans are microscopic structures within the pancreas that are composed of various cell types. The alpha cells secrete glucagon, which accelerates release of stored glucose in the liver (glycogenolysis). The beta cells are most abundant and secrete insulin. The delta cells secrete somatostatin, which regulates release of both glucagon and insulin, among others. (Anatomical Chart Company 2002®, Lippincott Williams & Wilkins)

Type II diabetes generally occurs because of a metabolic failure at the cellular level, a condition spurred by poor diet, obesity, environmental factors, and genetics. Body tissues, such as cell receptor sites, lose their sensitivity. As insulin attempts to deliver glucose into the cell, the "key no longer fits the lock." Blood glucose, barricaded from the cell, accumulates in the bloodstream. Unlike Type I diabetes, insulin therapy is usually not indicated in Type II diabetes because typically these individuals already have too much insulin in their bloodstream. However, after an extended period of excess insulin secretion, the pancreas may lose its ability to produce insulin and a Type II diabetic may then become insulin dependent.

In Type II diabetes, the onset is usually after 40 years of age, but the onset can occur at any age. In fact, the incidence of Type II diabetes among 30-year-olds has gone up over 70% in the last decade. Physicians are increasingly reporting the diagnosis of Type II diabetes in teenagers, as well. The number of teenagers (an age group not normally targeted) being diagnosed with Type II diabetes indicates that a diet structured around high glycemic carbohydrates causes chronic states of hyperinsulinemia. A poorly selected diet, along with a lack of exercise, increases the risk of diabetes and premature cardiovascular disease.

Dr. Alan R. Sinaiko (University of Minnesota) in 2001 announced an association between insulin resistance and an elevation in blood pressure among teenage boys. The teenagers were tested when they were 13 years old and again when they were 15 years of age. By the second test, there was a definite association between the teenage boys' insulin resistance and their blood pressure (Smith 2001). (The reason this did not apply to the girls may be due to the fact that males have a higher overall early risk than females.)

Signs and Symptoms of Diabetes

The symptoms of Type II diabetes can be so subtle that they may be overlooked. But, extreme fatigue (particularly 2-4 hours after a meal), a change in weight, blurred vision, drowsiness, tingling or numbness in hands and feet, slow wound healing, unwarranted hunger (polyphagia), frequent urination (polyuria), and excessive thirst (polydipsia) can be warning signs of abnormal blood glucose levels. Note: Polydipsia and polyuria are homeostatic mechanisms that the body uses to extract sugar from the system.

Diagnostic standards for diabetes have been fasting plasma glucose levels greater than 140 mg/dL on two occasions and plasma glucose greater than 200 mg/dL following a 75-gram glucose load. More recently, the American Diabetes Association lowered the criteria for a diabetes diagnosis to fasting plasma glucose levels equal to or greater than 126 mg/dL. Fasting plasma levels outside the normal boundaries require additional testing, usually by repeating the fasting plasma glucose test and (if indicated) undergoing an oral glucose tolerance test.

Glucosuria (sugar in the urine) usually occurs when blood glucose levels reach 160-180 mg per 100 mL of blood. However, this does not confirm diabetes because a nondiabetic can have a normally low renal threshold (Krause et al. 1984).

Diabetic patients often have skin tags, that is, pouches of skin that tend to grow on the neck and in the armpit and groin regions (Kahana et al. 1987). Researchers studied 35 men and women with skin tags (average age of 52 years). The association between skin tags and diabetes appeared in 62.8% (22 patients) (Thappa 1995). A similar study concluded with like findings. After evaluating a small group of subjects in regard to the significance of skin tags, the researchers concluded that skin tags appear to be a useful clinical assessment in identifying individuals at high risk for coronary artery disease, hypertriglyceridemia, decreased HDL, impaired glucose tolerance, and Type II diabetes (Crook 2000). Note: The frequency with which skin tags coexist with diabetes mellitus, rather than the localization, size, color, or number, indicates that clinicians should note skin tags in physical examinations (Thappa 1995).

Secondary diabetes is a condition with a different pathogenesis (source or cause) than either Type I or Type II diabetes. In secondary diabetes, a primary condition, such as chronic or recurrent pancreatitis (an inflammatory condition of the pancreas), can result in diabetes. Also, adverse responses to medications can bring on secondary diabetes. For example, Skarfors et al. (1991) announced that certain drugs prescribed to treat hypertension (beta blocking agents, thiazides, or hydralazine) decreased insulin sensitivity. According to information released from Oregon Health Sciences University (Portland), antipsychotic medications (clozapine, olanzapine, or quetiapine) increased the occurrence of diabetes (Muench et al. 2001). Navajo women receiving Depo-Provera (medroxyprogesterone, an injectable contraceptive) also had a greater incidence of diabetes, compared to those receiving oral estrogen and progestin combinations (Kim et al. 2001).

About 2-5% of all pregnancies induce gestational diabetes, but it is usually a transient condition that terminates postpartum. However, the risk of developing diabetes in later years is greater for both mother and infant.

The focus of this protocol is on Type II diabetes, the type that affects 90-95% of the diabetic population, defining contributing factors and detailing a comprehensive program to render the condition (if not reversible) highly manageable. If you are a Type I diabetic, many of the therapeutic recommendations contained in this protocol can reduce the incidence of common diabetic complications.

Note: Type II diabetes is sometimes referred to as noninsulin dependent diabetes or adult-onset diabetes. These terms are being discontinued because some Type II diabetics go untreated so long that they become dependent on insulin injections; in addition, there are very young people developing Type II diabetes primarily from poor diet and lack of exercise.

ARE SYNDROME X AND TYPE II DIABETES THE SAME CONDITION?

Dr. Gerald Reaven, M.D., an authority on insulin resistance and hyperinsulinemia, coined the term Syndrome X (in 1988) to identify clusters of symptoms that often accompany abnormal blood glucose levels: hyperlipidemia (too much cholesterol and triglycerides in the blood), hyperinsulinemia (too much insulin in the bloodstream), obesity, and hypertension. Syndrome X, like Type II diabetes, is a condition of insulin resistance, a disorder in which insulin does not produce the same glucose-lowering effects seen in otherwise normal, insulin-sensitive individuals. The failure occurs at the cellular level, robbing insulin of its primary role of glucose delivery.

Syndrome X and many cases of early stage Type II diabetes are conditions of insulin resistance and excesses of compensatory insulin. Hyperinsulinemia, in most cases is only a temporary reprieve in delaying the onset of full-blown diabetes. The pancreas will eventually become weary in its effort to supply the extra insulin needed to forestall the disease.

It is important to note that while almost all Type II diabetic patients are insulin resistant, not all individuals with hyperinsulinemia become diabetics. Although opinions are varied as to the numbers, some speculate that one in four hyperinsulinemic individuals will become diabetics (Lukaczer 1999). Should the individual escape diabetes, hyperinsulinemia is still a significant risk to long-term survival. Note: Several decades ago, investigators at the Bronx Veterans Administration Hospital showed that patients with Type II diabetes could have elevated blood glucose levels despite having higher insulin levels, a revelation that stunned the medical community.

Diagnosis of Syndrome X

There are clusters of symptoms that make up a syndrome, and the symptoms common to Syndrome X deserve close monitoring. For example, men with a previous history of recurrent calcium oxalate kidney stones may have elevated insulin levels (Schwille et al. 1997). Women with a history of hirsutism (excessive body hair), oligomenorrhea (scanty periods), infertility, or polycystic ovary disease often have an underlying hyperinsulinemic condition (Nestler et al. 1991, 1996, 2002).

Part of the Syndrome X profile includes an earlobe crease appearing at a 45-degree downward angle toward the shoulder and an elevated waist to hip circumference. Bouts with low blood sugar, carbohydrate intolerance, sugar cravings, sleepiness after meals, insomnia (relieved by snacking), adult acne, and central abdominal obesity are signs suggestive of insulin excess. The patient may present with elevated serum uric acid and ferritin levels, moderately elevated blood pressure, and an abnormal lipid profile. While these factors are commonly observed in the hyperinsulinemic adult, longitudinal studies suggest that elevated insulin levels may start in childhood, particularly in the overweight youngster displaying abnormal blood lipids (Bernard et al. 1992; Lukaczer 1999; Goran 2001).

Triglycerides and HDL cholesterol are significantly impacted by hyperinsulinemia (triglyceride levels are typically elevated and HDL levels are depressed). Insulin actually has very little effect quantitatively on total cholesterol or LDL cholesterol levels (Bland 2000). It is speculated that either the elevated triglycerides or the insulin resistance and the resulting excess of insulin may, however, cause the LDL cholesterol particles to assume a smaller, denser configuration, a hallmark of Syndrome X. Studies have shown an association between the highly atherogenic, smaller diameter LDL particles and insulin resistance (Reaven 2000).

The decrease in the "good" cholesterol (HDL) also impacts the ratio between LDL and HDL cholesterol (a high LDL-to HDL ratio is another risk factor associated with cardiovascular disease). Persons with Syndrome X often present with HDL levels less than one-fourth of the total cholesterol, a burdening handicap to cardiac health (Challem, 2000).

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