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Syndrome X

Insulin & Diabetes

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Dr. Gerald Reaven, professor of medicine at Stanford University, noted in 1988 that many individuals were presenting with the phenomenon of insulin resistance, yet could not be classified as Type II diabetics. Furthermore, these same individuals were at greater risk for developing cardiovascular disease (CVD) than the general population.

What is insulin resistance? Essentially it involves the release by the pancreas of more insulin than the cell receptors can handle. Insulin is a hormone with many important metabolic functions, and it has a major impact on our overall endocrine balance. Insulin is essentially an energy delivery and storage hormone, with a mission to deliver glucose into the cells where it can be combusted for energy production, and to store any excess glucose as adipose (fat) tissue. Fat storage is an evolutionary device that allows us to store energy so that we can withstand the periods of food scarcity that were common for much of our history. There are several different hormones that can raise the blood sugar level (such as glucagon, cortisol and adrenalin), but insulin alone can lower it.

Professor Reaven believes that insulin resistance generally develops in response to excess body weight and/or lack of exercise, both of which are results of our increasingly sedentary lifestyles. Other researchers and clinicians point the finger at excess carbohydrate intake, especially in the form of sugar and starches (bread, pasta, bagels, chips, cookies, breakfast cereals, etc.). These food substances excessively raise blood glucose levels and, in response, the pancreas releases more and more insulin. After a while the cell receptors become saturated and may even start to shut down, so both glucose and insulin start to accumulate in the bloodstream. This tends to lead to elevated triglycerides, lowered HDL cholesterol levels and, frequently, high blood pressure, all risk factors for cardiovascular disease. The clotting factor plasminogen activator-1 may also be elevated, increasing the likelihood of excess clotting in the blood. Just as hypoglycemia is often a precursor to diabetes, so is insulin resistance frequently a precursor to CVD.

How does one test for insulin resistance? Measuring the amount of insulin in the blood is one method; however, it can be unreliable. The method of choice is the glucose tolerance test. If an individual’s fasting glucose registers between 110 and 126, this is considered impaired fasting glucose; if the glucose levels rise to between 140 and 200 after two hours, this is considered impaired glucose tolerance. These levels provide the two primary indicators for what Professor Reaven has termed syndrome X.

Syndrome X is generally accompanied by a fasting triglyceride level of 200, or greater (100 or less is the desirable level). Triglycerides are fats found in both the bloodstream and adipose tissue, and they serve as a fuel source for the heart and the muscles. Under normal circumstances triglycerides are released back into the bloodstream from the fat storage cells at times when glucose and insulin levels are low (such as first thing in the morning), as a substitute source of energy for the cells. Conversely, the release of insulin in response to ingested glucose will normally inhibit this release of triglycerides. In the case of insulin resistance, however, there may well be adequate glucose in the bloodstream to generate energy, but because the cells’ insulin receptors are overwhelmed, not enough glucose is getting into the cells to generate sufficient energy. Accordingly, triglycerides continue to be released into the bloodstream to make up the energy deficit. Unfortunately, this has the effect of stimulating the liver to make even more triglycerides, so that the bloodstream becomes overloaded with them - in addition to the excess glucose and insulin! This process accounts for the excess triglycerides found in people with syndrome X.

It is estimated that 25-30% of the adult population in the U.S. has syndrome X, and this goes a long way to explaining the epidemic levels of Type II diabetes and CVD found in this country. (Other factors also contribute to high CVD rates, notably high levels of the intermediary amino acid metabolite homocysteine, primarily due to inadequacies in the diet of the B-vitamins folic acid, B-12 and B-6).

Two of the most important strategies for both preventing and treating syndrome X are exercise and weight loss, both of which improve the cells’ ability to absorb insulin and, along with it, glucose. The other key area is diet, though confusion continues to abound as to what ratio of macronutrients is appropriate. Are Atkins, Sears or Ornish correct, each with their widely varying dietary recommendations? Professor Reaven does not think so, and he weighs in with his own plan: 45% of calories from carbohydrates; 40% from mostly unsaturated fats; and 15% from proteins. He recommends 1800 calories per day, supplemented with additional calcium. Once again we are looking at a "one-diet-fits-all" approach.

The Metabolic Typing protocol centers around a mini-glucose challenge test. We test the fasting blood glucose level, administer 40 grams of glucose (plus 2 grams of potassium), and then track how effectively the glucose is cleared from the blood over the next 95 minutes. Because insulin plays a central role in this process, we are in a perfect position to observe and address the phenomenon of syndrome X. After successfully performing thousands of such tests over the years we can categorically state that there is no diet that is right for everyone. In most cases, balancing the body chemistry metabolically with the diet and supplements appropriate to the individual’s metabolic type will correct glucose dysregulation and lipid abnormalities. In extreme cases, however, it is necessary to initiate the Diabetic Protocol (emphasizing proteins, good quality fats and non-starchy carbohydrates) to stabilize blood sugar and triglyceride levels.

We will be hearing a lot more about insulin resistance and syndrome X in the future, as it represents a major breakthrough in the understanding of the etiology of Type II diabetes and CVD. Our work with Metabolic Typing has much to offer in addressing the detrimental effects of this insidious condition.


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