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What your doctor won’t tell you...
“Normal” blood glucose levels can kill you!

by Randy Drake

hat is “normal”? It depends on who you ask, and when. Until recently, medical guidelines stated that a fasting blood glucose (FBG) level over 109 on two consecutive occasions indicates a “prediabetic” state.  On October 24, 2003, the American Diabetes Association (ADA) released a new definition of “impaired glucose tolerance,” also known as the “prediabetic” state. They dropped the cutoff point for “normal” from 109 to 100 mg/dL.

If you look at what your body considers normal, you will get a far different answer. The pancreas is the organ responsible for regulating blood sugar levels. When the level is too high, it secretes insulin to transport glucose out of the bloodstream and into the cells. When the amount of glucose in the blood drops to a safe level, it stops secreting insulin. What is that “safe level”? In a healthy individual, the pancreas continues to secrete insulin to lower the blood glucose level until it drops below 83 mg/dL. The ADA may call 100 mg/dL “normal,” but a healthy pancreas calls any amount over 83 mg/dL “too high”!

New research suggests that the optimal FBG level should be between 70 and 85. This means that people with ADA-sanctioned “normal” levels of 86 to 100 have an increased risk of premature death. The medical establishment clearly understands the dangers of full-blown diabetes (FBG over 126), but they have yet to recognize that even “high normal” levels can pose a serious health threat.

Death by sugar.

Diabetes was listed as the sixth-leading cause of death on death certificates issued in 1999, and the percentage of the population with full-blown type II diabetes has been increasing. But this does not tell the whole story. Excess sugar in the blood causes a huge amount of damage to tissues and organs throughout the entire body. Heart disease, stroke, blindness, nerve damage, and kidney failure are well-known complications associated with persistently high blood sugar conditions. Lesser known complications include visceral obesity, abnormal blood coagulation, and loss of protein through the urine.

Persistently high blood sugar inflicts massive damage at the cellular level. Much cellular damage is caused by the cross-linking of glucose and protein molecules in a complex process called glycation (previously called glycosylation). Glycated proteins generate free radicals, which promote degenerative diseases. The hemoglobin A1c test gives a quantitative reading of the amount of damage sugar has done to circulating hemoglobin by measuring the percentage of glycated hemoglobin in the blood, which indirectly measures the amount of sugar in the blood over the previous three months. Fortunately, the body replaces old, damaged hemoglobin with new, pristine hemoglobin every three months. Unfortunately, damaged nerve cells and retinal cells are never replaced, so the damage accumulates.

What can be done?

Most doctors will do nothing until a patient’s FBG is consistently over 126 and a diagnosis of type II diabetes can be made. (Remember, doctors and drug companies make their money by treating disease, not by maintaining wellness.) But given a choice, most people would rather stay healthy than progress to the point that they need treatment for a disease. There are two strategies to achieve this goal: reduce blood glucose levels and/or reduce the damage caused by high blood glucose levels.

Several nutrients have been shown to reduce FBG levels: alpha lipoic acid, biotin, carnitine, chromium, magnesium, vanadium, and zinc. Oral antidiabetic prescription drugs, primarily metformin, also lower FBG levels without increasing insulin levels. (It may be difficult to find a doctor to prescribe metformin for FBG levels under 126, however.)

Some nutrients have been shown to prevent cellular damage due to high glucose levels. Carnosine (not carnitine) is the most effective natural inhibitor of glycation. It works by chelating (sequestering) copper and zinc, which are necessary catalysts in the glycation reaction. Endogenous carnosine levels decline with age, however, and should be supplemented. Carnosine is particularly effective in preventing the cross-linking of beta amyloid, which forms the senile plaques characteristic of Alzheimer disease, and has also been shown to improve the functioning of autistic children. Animal studies have shown that carnosine supplementation can extend life span by as much as 20%.

A new supplement currently in research is benfotiamine, a compound derived from thiamine (vitamin B1). Thiamine is a water-soluble vitamin; benfotiamine is its fat-soluble analogue. It has been used for more than a decade in Germany to treat diabetic neuropathy. New in vitro studies show that it can increase by 300% a key enzyme (transketolase) that blocks glucose absorption by the cells. High levels of this enzyme also blocked three of the four major pathways that lead to blood vessel damage, and blocked activation of the pro-inflammatory nuclear factor-kappa B (NF-kB). Benfotiamine supplementation has completely prevented retinal damage in live laboratory animals. Limited human studies have been conducted on diabetic patients in Europe, with very positive results and no reported side-effects. Benfotiamine has recently become available in the U.S. as a dietary supplement.

(Source: Life Extension Foundation)

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