Syndrome X: A metabolic Typing Perspective

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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. Our work with Metabolic Typing - which uses a modified form of the glucose tolerance test to help determine the foods and supplements most appropriate for any given individual - puts us in a unique position to both observe and address this phenomenon.

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 glucagons, cortisol and adrenaline), 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 (such as Richard Bernstein, MD and Ron Rosedale, MD) 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. Eventually the cell receptors become saturated and may even start to shut down, so both glucose and insulin start to accumulate in the bloodstream. This can lead to elevated trigiycerides, lowered HDL cholesterol 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. Furthermore, there may be an accumulation of advanced glycation end products (AGEs), mutant glucose/protein hybrids that are implicated in multiple degenerative disease processes. Just as hypoglycemia is often a precursor to diabetes so too is insulin resistance frequently a precursor to CVD and accelerated aging.

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 to be impaired fasting glucose; if the glucose levels rise to between 140 and 200 after two hours, this is considered to be 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). Trigiycerides 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 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 the 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 try to make up the energy deficit. Unfortunately, this has the effect of stimulating the liver to make even more trigiycerides, 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 US has Syndrome X, and this goes a long way to explaining the epidemic levels of Type II diabetes and CVD found in this country. (Several other factors also contribute to high CVD rates, notable among them being high levels of the intermediary amine 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 disagreement and 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.

Metabolic Typing takes a different approach. Our protocol is centered around a mini-glucose challenge test. We check the fasting blood glucose level, administer 40 grams of glucose (plus a small amount of cream of tartar), 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 can clearly observe the phenomenon of Syndrome X. After successfully performing thousands of such tests over the years we can categorically state that there is no one diet that is right for everyone. In most cases, balancing the body chemistry metabolically with foods and supplements appropriate to the individual's metabolic type will correct glucose dysfunction and lipid abnormalities. In more extreme cases, however, it may be necessary to initiate a special diabetic protocol (emphasizing proteins, good quality fats and non-starchy carbohydrates) to stabilize blood sugar and triglyceride levels.

The following case history indicates the type of success we are experiencing with this approach. AZ is a 57-year-old attorney with a long history of lipid irregularities. He had been using the cholesterol lowering drug Lipiter[Trademark] for several years, with slow but pronounced effects. After less than three months on our program he wrote us the following letter indicating a greatly accelerated improvement in his condition: "I am faxing you a copy of the Lab Report from my recent physical. In 1995, before Lipitor and any attempt to lower cholesterol, my cholesterol was 292 and my triglycerides were 429. Last year, with Lipitor, my total serum cholesterol was 220, my triglycerides were 279, my HDL was 52, my LDL was 112 and my cholesterol/HDL ratio was 4.2. This year, with my new diet (and Lipitor), my total serum cholesterol is 168, my triglycerides are 147, my HDL is 45, my LDL is 94 and the cholesterol/HDL ratio is 3.7. Needless to say, I am very pleased. Thank you!"

The accelerated response that this client experienced results from first determining his metabolic type and then directing him to the diet and supplement regime most suited to that type. Thus we were first and foremost addressing him at the metabolic level, rather than attempting to "fix" a specific problem. Metabolic Typing hinges on the clinical observation that not all people respond the same way to the same foods and nutrients; or, stated differently, the pH effects &foods in the body are not fixed, or absolute, but, rather, depend on the metabolic type of the person consuming them. Any given food or nutrient will have different pH effects in people of different metabolic types. By addressing the individual at the metabolic level, we can maximize the digestion, absorption and utilization of all foods and nutrients and, by extension, the optimal production and processing of energy.

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. We feel that our work with Metabolic Typing has much to offer in addressing the detrimental effects of this insidious condition.

Dr Harold J. Kristal offers regular Personalized Metabolic Nutrition Seminars for interested health professionals on the theory and practice of Metabolic Typing. For more information call 415-924-2571, or fax to 415-927-4664, or e-mail hkristal@bloodph.com.

Bibliography

Bernstein. Richard K., M.D, Dr Bernstein's Diabetes Solution. Little Brown, 1997

Kristal, Harold J., D.D.S. & Bill Wolcott. Allopathic Nutrition vs. Metabolic Nutrition. Townsend letter #186, January 1999

Luzaker. Dan, N.D. Syndrome X. HealthComm International, 1998

Reaven, Gerald M., M.D. Pathophsiology of Insulin Resistance in Human Disease. Physiological Reviews 75(3):473-485, 1995

Rosedale. Ron, M.D. The Fountain of Truth. Tanner, 1999

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By Harold J. Kristal and James M. Haig

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