• Type 1 ("insulin-dependent" and previously called "juvenile diabetes"). Type 1 diabetes is associated with a malfunctioning pancreas which does not produce adequate amounts of insulin. It develops most often in children and young adults. Type 1 diabetes is traditionally treated with insulin.

• Type 2 ("noninsulin-dependent" or sometimes called "adult-onset diabetes"). Type 2 diabetes is associated with insulin resistant cells. It is much more common and usually develops in older adults. Type 2 diabetes is now being found at younger ages and is even being diagnosed among children and teens.

• Gestational (pregnancy-related). Some women develop diabetes during pregnancy usually toward the end of pregnancy. It effects approximately 3 to 5 percent of all pregnant women. Although it goes away after pregnancy, these women have a higher risk for developing type 2 diabetes later in life.

According to the Centers for Disease Control:

• Diabetes is an epidemic.
• 30.3 million Americans have diabetes . . .
  with 7.2 million completely unaware that they even have the disease.
• Diabetes is the 5th leading cause of death in the United States . . .
  with over 1.6 million deaths each year from diabetes-related complications.
• It is projected that 1 in 5 of Americans will have diabetes by 2025, and 1 in 3 by 2050

Type 1 Diabetes

Interspersed evenly throughout the pancreas, is a very specialized tissue, containing cells which make and secrete hormones. This tissue, called the "Islets of Langerhans" is named after the German pathologist Paul Langerhans, who discovered them in 1869. Through a microscope, Langerhans observed these cells cluster in groups, which he likened to little islands in the pancreas.

One such group of cells, the beta cells, produce insulin in response to blood glucose. These beta cells are tiny insulin factories that sense the level of glucose in the blood stream, and produce insulin in precise proportion to that level. Therefore, following a meal, blood sugar levels will rise significantly, and the beta cells will release a large amount of insulin. This insulin will cause body cells to take up the sugar, causing blood sugar to quickly return to its normal range. Once blood sugar is in the normal range, the beta cells will reduce the output of insulin to an idling state. In this way, the beta cells adjust their production of insulin on a minute-by-minute basis, always producing just enough insulin to deal with the amount of blood sugar presently in the blood stream.

In type 1 diabetes, the islets are destroyed by the person's own immune system, which mistakenly identifies these essential cells as foreign invaders. This self-destructive mechanism is the basis of many so-called autoimmune diseases. Once the islets are killed, the ability to produce insulin is lost, and the overt symptoms and consequences of diabetes begin.

Type 2 Diabetes

The most common causes of type 2 diabetes are poor diet and/or lack of exercise, both of which can result in insulin resistance . . . a condition where the cells in our bodies aren't sensitive enough to react to the insulin produced by our pancreas.

Recent research suggests that the root cause of insulin resistance is a breakdown in intercellular signaling. Insulin is a chemical messenger. It signals proteins called GLUT-4 transporters (residing within the cell) to rise up to the cell's membrane, where they can grab on to glucose and take it inside the cell. In patients with insulin resistance, the cells don't get the message. They simply can't hear insulin "knocking" on the door, which results in elevated blood levels of both insulin and glucose.

In the early stages of insulin resistance, the pancreas compensates by producing more and more insulin, and so the "knocking" becomes louder and louder. The message is eventually "heard", enabling glucose transportation into the cells, resulting in the eventual normalization of blood glucose levels. This is known as "compensated insulin resistance".

Over time, the stress of excessive insulin production wears out the pancreas and it cannot keep up this accelerated output. As a result, glucose levels remain elevated for prolonged periods. This is called "uncompensated insulin resistance" and is the essence of advanced type 2 diabetes.

Type 2 diabetes is characterized by a series of chain reactions:

• The ingestion of too many carbohydrates leads to a spike in blood sugar levels.
• This is followed by a corresponding rise in insulin.
• This in turn causes blood sugar to drop.
• Eventually, this drastic up-and-down activity begins to take its toll on the body's ability to use insulin and thus metabolize sugar.
• Over time, the pancreas "wears out" and can no longer pump out enough insulin to overcome this insulin resistance.
• This results in a decreased insulin production and/or increased insulin resistance which propagates the cycle and leads to the onset of diabetes.

It is not known if obesity causes insulin resistance; or if insulin resistance causes obesity; or if they develop independently. We do know that insulin resistance is correlated to obesity . . . particularly the type where your weight collects around your middle (like an apple). We also know that physical inactivity contributes to insulin resistance, as does eating too much dietary carbohydrate.

Most researchers are in basic agreement that the theory of oxidative stress is central to explaining the cause of diabetes. To understand the theory, one must first conceptualize that a "free radical" is any atom or molecule which has an "unpaired electron" in it's outer ring. Because it is lacking an electron, it is unstable and very much wants to find one electron to fill its need. This "free radical" will steal an electron from any other molecule it encounters that is more willing to give one up . . . and thus it becomes satisfied . . . but now the victim molecule has become a free radical itself and so it now will look for another victim molecule to steal it's much desired electron from . . . thus propagating this cycle over and over again. This cycle is called "the chain reaction of free radicals".

The chief danger of free radicals comes from the damage they can do when they react with important cellular components such as DNA, or the cell membrane. Cells may function poorly or die if this occurs.

To prevent free radical damage the body has a defense system of antioxidants. Antioxidants are molecules which can safely interact with free radicals and terminate the chain reaction before vital molecules are damaged. Although there are several enzyme systems within the body that scavenge free radicals, the principle antioxidants are: glutathione, SOD (superoxide dismutase), beta carotene, vitamin E, vitamin C, CoQ10, melatonin, and alpha lipoic acid.

According to the theory of oxidative stress, free radicals run rampant through the body reeking havoc. In the case of type 1 diabetes . . . damaging beta cells in the pancreas, negatively impacting their ability to produce insulin . . . in the case if type 2 diabetes . . . damaging cell membranes, leading to a breakdown in intercellular signaling.

And if that were not bad enough . . . free radicals deplete our body's reserve of antioxidants . . . further contributing to the problem.

This is why it is so important to lower the oxidative stress with better diet, more exercise, improved lifestyle; and to take all the antioxidant supplements known to neutralize the excess free radicals.

There is still a lot to learn about the causes of diabetes, but what is known, is that our bodies may begin to malfunction five to seven years before we are ever diagnosed with diabetes. That is why researchers believe that nearly 30-50% of the people who have diabetes don't even know it.

Our typical diet has become way out of balance. We eat way too many simple sugars, way too often. Most people consume candy, french fries, potato chips, ice cream, pasta etc on a regular basis. We eat twice the calories we need, twice the protein we need, and each year the average person consumes over 160 pounds of sugars and sweeteners we don't need at all.

When you consider that so many of us are overfed and so few of us get any regular exercise. . . and then add to that . . . the fact that many of us overuse alcohol and nicotine which increases oxidative stress. . . it's no wonder that millions of us already suffer from diabetes, or are at great risk of developing diabetes in the near future.

The ever increasing number of overweight, out of shape, oxidatively stressed people in today’s societies around the world, is directly proportional to the epidemic rise of diabetes.

The following is a list of risk factors for getting diabetes:

• Being more than 20% overweight
• Physical inactivity
• Having a first degree relative with diabetes (parents or siblings)
• Belonging to any of the following ethnic groups:
  African American, Native American, Latin American, Asian American, Pacific Islander
• Having an "Impaired Fasting Glucose" (IFG)
  or "Impaired Glucose Tolerance" (IGF) on previous blood tests.
• Having Triglycerides (blood fats) which are more than 250 mg/dl
• Having HDL cholesterol ("good" cholesterol ) which is less than 35 mg/dl
• Having a history of hypertension (high blood pressure)
• Having a history of gestational (pregnancy-related) diabetes
  or giving birth to a baby which weighed more than 9 pounds

Complications related to artery damage

Diabetes causes damage to both large and small arteries. This artery damage results in medical problems that are both common and serious:

• Cardiovascular disease. Diabetics have up to a 400% greater chance of heart attack or stroke. Heart disease and stroke cause about 65% of deaths among people with diabetes.These deaths could be reduced by 30% with improved care to control blood pressure and blood glucose and lipid levels.
• Amputations. About 82,000 people have diabetes-related leg and foot amputations each year. Over 60% of non-traumatic lower limb amputations are diabetes related. Foot care programs that include regular examinations and patient education could prevent up to 85% of these amputations.
• Kidney disease. About 38,000 people with diabetes develop kidney failure each year. Treatment to better control blood pressure and blood glucose levels could reduce diabetes-related kidney failure by about 50%.
• Eye disease and blindness. Each year, 12,000-24,000 people become blind because of diabetic eye disease, including diabetic retinopathy. Diabetes is the leading cause of new cases of blindness among adults 20-74 years old. Screening and care could prevent up to 90% of diabetes-related blindness.
• Sexual Dysfunction. Approximately 70% of all adult males with diabetes currently suffer or will experience sexual dysfunction or impotence.

Complications related to nerve damage

60 to 70% of people with diabetes have mild to severe forms of nervous system damage. This diabetic neuropathy may result in numbness, tingling, and paresthesias in the extremities and, less often, debilitating, severe, deep-seated pain and hyperesthesias. The following are examples of diabetic neuropathy

• Peripheral neuropathy The feet and legs can develop tingling, pain, or a loss of feeling. This problem makes foot ulcers and foot infections more common, adding to the possibility that an amputation may be needed.
• Stomach and bowel problems The nerves that trigger normal movements of the stomach and intestines can become less active or less predictable. This can result in nausea, constipation or diarrhea. A stomach that is slow to empty has a diabetes condition called gastroparesis.
• Dizziness when standing Your circulation has to make some adjustments to move blood from your toes to your torso when you are standing up, since it is pumping against gravity. When your body is working correctly, this adjustment includes tightening of blood vessels to prevent pooling of blood in your lower body. The circulation relies on nerve signals to know when to make this adjustment. These signals can fail in diabetes, leaving you with low blood pressure and lightheadedness when you are standing.
• Sexual-function problems Impotence is especially common in people with nerve damage from diabetes. Artery damage also contributes to impotence.
• Localized nerve failures A nerve that controls a single muscle can lose its function. Examples of problems that might result are eye movement problems with double vision, or drooping of the cheek on one side of the head (commonly known as Bell's palsy).

Other Complications

• Flu and pneumonia-related deaths. Each year, 10,000-30,000 people with diabetes die of complications from flu or pneumonia. They are roughly three times more likely to die of these complications than people without diabetes.
• Pregnancy complications. About 18,000 women with preexisting diabetes deliver babies each year, and an estimated 135,000 expectant mothers are diagnosed with gestational diabetes. These women and their babies have an increased risk for serious complications.

Many of these potential complications can significantly shorten the life of a person with diabetes, and all of them can diminish the quality of life.

Diabetes complications are primarily caused by 2 factors:
Excessive Glycosylation and Sorbitol Accumulation

Excessive Glycosylation

• Glycosylation is the process by which the sugar molecule binds irreversibly to a protein molecule. This process takes place in all humans, but because diabetics have higher levels of glucose in their blood and for longer durations than non diabetics, they have a much higher degree of glycosylation occurring.
• Excessive glycosylation results in abnormal protein structures which lead to a host of cellular dysfunctions such as: inactivation of enzymes, inhibition of regulatory molecule binding, decreased susceptibility to proteolysis, abnormalities of nucleic acid function, altered macromolecular recognitions and increased immunogenicity.
• In diabetics, glucose binds to proteins in the blood, nerves and the eyes. This pathological process causes much of the damage in the complications of diabetes.

Sorbitol Accumulation

• Sorbitol is the byproduct of glucose metabolism and is produced through the action of the enzyme aldose reductase.
• In non-diabetics, sorbitol is converted to fructose and is easily excreted from the cell, but inside the cells of diabetics, when glucose levels become elevated (even after glucose levels outside of the cell return to normal), sorbitol is produced faster than it can be broken down. Since it cannot cross the cell membrane, it builds up to a toxic level inside the cells, creating an imbalance and causing a loss of electrolytes and other minerals. This accumulated sorbitol draws water in to the cell, by the process known as osmosis, and ultimately leads to the collapse of its architecture and loss of its function.
• Sorbitol-induced osmotic swelling is believed to be one of the main causes of tissue damage in diabetics. This condition seems to target organs and tissues that are not dependent on insulin for their absorption of glucose. Elevations of sorbitol levels are a major problem in peripheral nerves, blood vessels, the cells of the retinal blood vessels, the lens of the eye, the pancreas, kidneys and other organs due to their lack of insulin dependence.

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There are various forms of chromium suitable for human ingestion. The picolinate form of chromium called "chromium picolinate" is the most absorbable. It is a unique molecule that combines chromium with picolinic acid, a compound found in breast milk, which helps the body better absorb and process minerals.

In June of 2002, Chromax® (the "Nutrition 21" patented brand of chromium picolinate) was affirmed by the FDA as "Generally Recognized as Safe" (GRAS) for use in food products, one of only a handful of ingredients to have secured this status at clinically effective doses for use in foods marketed for weight loss and glucose control. In addition, Chromax®; has demonstrated that it is significantly more bioactive than other forms of chromium.

Vandium (vanadyl sulfate) is a trace element that is thought to exhibit a variety of insulin-mimetic properties . . . such as being involved in transporting sugar to the cells.

Clinical trials indicate that "in vitro", vanadium salts have most of the same major effects of insulin on insulin-sensitive tissues.