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Metabolic Syndrome Expained by its Discoverer


Metabolic Syndrome ExplainedMetabolic Syndrome was discovered by Stanford University Professor and researcher Gerald Reaven, MD. In 1988, he first presented the results of twenty years of study that showed that the effect of an array of changes stemming from a then-little known medical disorder called Insulin Resistance led to Cardiovascular Disease.

In his book Metabolic Syndrome, Dr Reaven describes the condition as follows:

This deadly heart ailment begins in the bloodstream, shortly after we eat. That's not a startling idea, for we know that eating fatty or cholesterol-laden foods can be bad for our hearts. However, the Metabolic Syndrome culprit isn't red meat or butter, it's carbohydrates. Yet these carbohydrates are reluctant, inadvertent offenders.

Before entering the body proper, our food is broken down into various constituent parts in the intestine. One of these is glucose (blood sugar) from carbohydrates. Upon entering our cells, some of the glucose is put right to work providing the energy that cells need to perform their various tasks. The rest is stored in certain cells for later use. But the glucose doesn't simply flow into the storage cells. Instead, it must be guided in by insulin, a protein secreted by the pancreas.

Insulin acts like a shepherd, herding its precious flock into the cellular "corrals". Unfortunately, in many of us, glucose behaves like a group of errant sheep, stubbornly refusing to go where the shepherd directs. When that happens, the pancreas pumps out more and more insulin. That's the biochemical equivalent of sending out more and more "shepherds" to get the "sheep" into the "corrals". Imagine hundreds of shepherds chasing thousands of sheep across a pristine field covered with thick, beautiful green grass. Those hundreds of feet and thousands of hoofs will quickly tear up the field, ripping out or flattening down clumps of grass. Soon, the field that once looked so green and lush will be trampled and scarred, brown and dirty.

Something similar happens inside your body when glucose refuses to move into the storage cells at the insulin's command. The interior linings of your arteries, like the grassy field, are "ripped" and "trampled" as the body attempts to overcome this problem.

Eventually, the insulin "shepherds" corral the glucose, and order is restored in the body. But all is not well, for the "field" (the lining of your coronary arteries) has been damaged, and there's other damage, as well. This damage sets the stage for heart disease.


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"Researchers agree that insulin resistance is central to the metabolic syndrome. When target cells are unresponsive to insulin, the pancreas responds by pouring even more insulin into the bloodstream, leading to high levels of the hormone in the blood, a condition called compensatory hyperinsulinemia. The high level of insulin in the blood forces glucose into cells but also starts the events leading to arterial damage and eventually a heart attack. Under these conditions, a person may not manifest either diabetes or heart disease but could well be on the way to either or both."
A. MAUREEN ROUHI, Chemical and Engineering News. November 22, 2004.Vol. 82, No.47  
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"A non-pharmacologic treatment for these patients is needed, since drugs prescribed to lower blood pressure have been shown to actually worsen carbohydrate and lipid metabolism in Syndrome X patients, negating the beneficial effects of those drugs."
Duke University Study, results published in the Archives of Internal Medicine, September 2003.
Article by Dr. Sheri Colberg, Phd, FACSM
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"...approximately 90% of overweight Hispanic children with a family history for type 2 diabetes have at least one feature of the metabolic syndrome and 30% possess the metabolic syndrome.

Our results support the view that improving insulin resistance may be crucial in the prevention of both type 2 diabetes and premature cardiovascular disease in this at-risk subpopulation of Hispanic youth."
Cruz ML, Weigensberg MJ, Huang TT, Ball G, Shaibi GQ, Goran MI.,J Clin Endocrinol Metab. 2004 Jan;89(1):108-13.
"To gain the most benefit from modifying multiple metabolic risk factors, the underlying insulin-resistant state must become a target of therapy."
Bogdanovic, Streten and Langlans, Beata, "Metabolic Syndrome: New Opportunities in Diagnostics and Therapeutics", DMD Publications, 2004.  
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