Melissa
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The Prediabetic EpidemicSyndrome X is a relatively new diagnosis, but it is a condition as old as the typical American diet. Jack Challem, Nutrition Science News, March 2001
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The person with a "fat tire" carries an unmistakable clue to his health right around the waist: He either has or is at serious risk of developing Syndrome X. The condition isn't a household word quite yet, but it's getting there. An estimated 60 to 70 million Americans-about one of every four people-have some degree of Syndrome X, which sets the stage for adult-onset diabetes and coronary artery disease. The good news is that, like many other health problems, Syndrome X can be prevented and reversed through a combination of diet, supplementation, and moderate physical activity. The term Syndrome X was coined in 1988 by a Stanford University endocrinologist, although the cluster of signs and symptoms that distinguish it had previously been referred to as metabolic syndrome or insulin-resistance syndrome. Originally, Syndrome X was defined by four characteristics: (1) abdominal obesity, (2) elevated levels of triglycerides and low levels of high-density lipoproteins (HDL, or the "good" cholesterol), (3) hypertension, and (4) insulin resistance. Insulin resistance, the hallmark of adult-onset diabetes, also lies at the core of Syndrome X. This hormone imbalance alters blood-fat ratios, raises blood pressure, and increases fat storage. In the past 13 years, several other signs and symptoms have been associated with Syndrome X: low-density lipoprotein (LDL) cholesterol oxidized by free radicals, low levels of antioxidant vitamins, elevated C-reactive protein (C-RP, a marker of inflammation),1 low dehydroepiandrosterone (DHEA) levels, high cortisol levels, and sometimes androgen-dependent baldness.2 The current definition of Syndrome X is used flexibly in that some experts refer to a combination of just two or more of the characteristics as Syndrome X. By itself, each characteristic of Syndrome X increases the risk of diabetes and coronary artery disease. A combination of characteristics, such as abdominal obesity and hypertension, further increases the risk of these conditions. Furthermore, diabetics carry an increased risk of cardiovascular disease.3 To assess your clients' risk of developing Syndrome X, pose the following key questions. Each yes answer suggests the possibility of glucose intolerance, insulin resistance, or diabetes. The more of them, the greater the risk.
The Glucose/Insulin
Seesaw Although researchers are investigating genetic predispositions to insulin resistance and Syndrome X, the major influence appears to be dietary. For example, Native Americans and Hawaiians have a relatively high risk of developing insulin resistance and diabetes. However, these conditions did not occur within those cultures until they started eating foods rich in refined sugars and carbohydrates. In contrast, people of European descent may often take longer to develop insulin resistance, Syndrome X, and diabetes, but they are by no means invulnerable. To wit: A recent study in Diabetes Care found that the incidence of diabetes in the United States grew by 33 percent during the 1990s, and the incidence of diabetes among people in their 30s grew by 70 percent.4 Such enormous increases in the rate of occurrence of any disease had been previously unheard of in medicine, making it epidemic in proportions. To understand the role of diet in the genesis of insulin resistance and Syndrome X, it is essential to understand the evolution of diet. Our genes evolved in tandem with our diet, with certain nutrients turning on or off our genes and providing the body's biochemical building blocks. From 55 million to 2.5 million years ago, most of our primate ancestors ate a high-plant diet with small amounts of meat. This diverse array of plant foods were uncultivated, and many resembled today's kale or rose hips. During the last major ice age, from 2.5 million to 10,000 years ago, meat and fat played a much more significant role in the diet. Therefore, humans' evolutionary heritage is based on people gathering and hunting their foods, a mix of vegetables and low-fat animal protein--game meat is lean, lower in saturated fat, and higher in omega3 fatty acids. About 10,000 years ago, humans began developing agriculture and, in particular, cultivating grains. However, human teeth are not designed to properly chew grains. To be consumed and digested, grains have to be crushed, a process that immediately refines them and makes large amounts of carbohydrates available for digestion. During the past 50 years, dietary changes have accelerated, pushing us even further from our evolutionary baseline diet. Refined carbohydrates-pastas, breads, cereals, and breakfast bars-now dominate the diet. Many foods are breaded and fried, merging refined grains with refined and often oxidized oils. People did not consume pressed oils until relatively recently. In addition, many foods also contain large amounts of varying forms of sugar, along with partially hydrogenated oils (vegetable oils processed to have some of the characteristics of saturated fats). These foods, even with fortification, contain relatively few micronutrients such as vitamins, minerals, carotenoids, and flavonoids. Such a diet wreaks havoc on glucose and insulin levels. For example, refined sugars and carbohydrates rapidly boost glucose levels. To reduce high glucose levels (and to prevent kidney damage), the pancreas then secretes large amounts of insulin, which helps transport glucose into cells where it is burned for energy (chiefly in muscle cells) or stored as glycogen (in the liver) or fat (in adipose cells). Over time, elevated insulin levels overwhelm a finite number of insulin cell receptors. As a consequence, these cells become "resistant" (or insensitive) to insulin, and blood levels of glucose and insulin increase-hyperinsulinemia-setting the stage for Syndrome X, diabetes, heart disease, and other disorders. High glucose levels also generate large numbers of cell-damaging free radicals, which appear to cause or exacerbate many of the complications of diabetes such as eye and nerve diseases, and also increase antioxidant requirements.5 A Modern
Stone-Age Diet
In practice, these anti-X dietary principles are easy to follow because of the simplicity of meal preparation. For example, breakfast might consist of scrambled eggs with spinach. Lunch at a restaurant might be a turkey burger minus the bun and broccoli substituted for fries. For dinner, have customers try baked chicken (pull back the skin and sprinkle on Italian seasoning) with steamed vegetables. A healthy beverage is sparkling mineral water with a slice of lemon or lime. Can such a diet be adapted to vegetarians? It is possible, though not easy. Legumes are relatively high in carbohydrates, and a recent study found that canned baked beans were almost as bad as jelly beans in triggering intense glucose and insulin responses, though this likely resulted from the large amount of sugar in canned baked beans.8 If a vegetarian develops Syndrome X, it is a sign that he, too, should adjust his diet. Any diet that makes a person sicker instead of healthier is the wrong diet. Supplements
to Regulate Glucose and Insulin Alpha-Lipoic Acid*, a sulfur-containing fatty acid found in spinach and animal protein, has been prescribed for years in Germany to treat diabetic nerve disease. Only recently have researchers understood its antioxidant actions quench free radicals responsible for many diabetic complications. It also lowers glucose levels-by 10 to 30 percent-and improves insulin function.9
Vitamin E has been used by physicians since the 1940s to help prevent and reverse heart disease. During the past five years, medical acceptance of vitamin E supplements has grown substantially. A British study of 2,000 subjects with carefully diagnosed heart disease found that people taking 400800 IU natural vitamin E daily for an average of 18 months had a 77 percent lower prevalence of heart attacks, compared with people taking placebos.11
Vitamin C and glucose are similar chemically, and researchers have long believed the two compounds compete with each other. Increasing vitamin C intake seems to edge out some of the glucose or improve its disposal, perhaps by encouraging cells to burn more of it. Some research has found that 2,000 mg/day vitamin C daily lowers both glucose and glycosylated hemoglobin levels, the latter a standard marker of diabetic control.13
Chromium picolinate plays a key role in enhancing insulin function, which leads to more efficient glucose metabolism. In a study of Chinese adult-onset diabetics, 200 mcg chromium picolinate daily led to improvements in fasting glucose and postprandial insulin levels after four months. However, subjects taking 1,000 mcg daily also had "spectacular" decreases in glucose and insulin levels to near-normal levels.15
Silymarin (milkthistle) is an antioxidant extract of the herb milk thistle (Silybum marianum). It has been shown to reduce all of the major indicators of diabetes, including blood sugar, insulin, glycosuria, and glycosylated hemoglobin.16 Researchers achieved these results with 800 mg daily of a standardized silymarin extract given for one year. The benefits appeared consistently after about 60 days, and all diabetic signs improved further over the course of a year. However, lower doses are probably sufficient in combination with other supplements.
Take the
Extra Step The major risk factor for Syndrome X-abdominal obesity-can be assessed visually. A blood-pressure cuff can identify hypertension, a second characteristic of Syndrome X. Another major clue is the medications a person takes, such as those that lower blood pressure, reduce cholesterol or lower blood sugar. Yet none of these medications actually addresses the underlying cause of Syndrome X. Only a revamped diet, supplements, and moderate physical activity can prevent and reverse Syndrome X. More on
Syndrome X Jack Challem, known as The Nutrition Reporter, is lead author of Syndrome X: The Complete Nutritional Program to Prevent and Reverse Insulin Resistance (John Wiley & Sons, 2000). References 1. Festa A, et al. Chronic subclinical inflammation as part of the insulin resistance syndrome. The Insulin Resistance Atheroscerlosis Study (IRAS). Circulation 2000;102:42-7. 2. Matilainen V, et al. Early androgenic alopecia as a marker of insulin resistance. Lancet 2000;356:1165-6. 3. Vidt DG. Good news for the older patient with diabetes: added cardiovascular risk reduction. Curr Hypertens Rep 1999 Oct;1(5):379-80. 4. Mokdad AH, et al. Diabetes trends in the U.S.: 1990-1998. Diabetes Care 2000;23:1278-83. 5. Mohanty P, et al. Glucose challenge stimulates reactive oxygen species (ROS) generated by leucocytes. J Clin Endocrinol Metab 2000;85:2970-3. 6. Ascherio A, Willet WC. Health effects of trans fatty acids. Am J Clin Nutr 1997;66(suppl):1006S-10S. 7. Oomen CM, et al. Fish consumption and coronary heart disease mortality in Finland, Italy, and the Netherlands. Am J Epidemiology 2000;151:999-1006. 8. Holt SH, et al. An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods. Am J Clin Nutr 1997;66:1264-76. 9. Jacob S, et al. The radical scavenger a-lipoic acid enhances insulin sensitivity in patients with NIDDM: a placebo-controlled trial. Presented at Oxidants and Antioxidants in Biology, Santa Barbara, Calif., 1997 Feb 26-Mar 1. 10. Rett K. Alpha-lipoic acid (thioctic acid) increases the insulin resistence in overweight patients with type II diabetes. Diabetes Metab 1996;5:59-62. 11. Stephens NG, et al. Randomized controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study (CHAOS). Lancet 1996;347:781-6. 12. Burton GW, et al. Human plasma and tissue a-tocopherol concentrations in response to supplementation with deuterated natural and synthetic vitamin E. Am J Clin Nutr 1998;67;669-84. 13. Eriksson J, Kohvakka A. Magnesium and ascorbic acid supplementation in diabetes mellitus. Ann Nutr Metab 1995;39:217-23. 14. Clementson CA. Ascorbic acid and diabetes mellitus. Med Hypothesis 1976 Sep-Oct;2(5):193-4. 15. Anderson RA, et al. Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. Diabetes 1997;46:1786-91. 16. Velussi M, et al. Long-term (12 months) treatment with an anti-oxidant drug (silymarin) is effective on hyperinsulinemia, exogenous insulin need and malondialdehyde levels in cirrhotic diabetic patients. J Hepatol 1997;26:871-9. Melissa Kaplan notes: Alpha lipoic acid (ALA) can transport mercury across the blood-brain barrier. If you have mercury toxicity, discuss the taking of this supplement first with your doctor. You may want to start out at a low dose, such as 30 mg, and work your way up, depending on your tolerance and side affects. According to my physician, some patients initially feel ill, with increased pain, fatigue, and cognitive dysfunction, until their body becomes used to it. You can then work up to the therapeutic dose as recommended in this article. On a personal note, I have moderate/severe mercury toxicity. I started out taking 100 mg ALA three times a day (after meals) and experienced no problems. YMMV. Related Reading Syndrome
X: The Complete Nutritional Program to Prevent and Reverse Insulin Resistance The
Good Carb Cookbook: Secrets of Eating Low on the Glycemic Index. National Institude of Diabetic & Digestive & Kidney Diseases |
www.anapsid.org/aboutmk/xenoest/prediabetes.html
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