DIABETES Why Suffer With  Diabetes? Defining Diabetes Diabetes is one of the country's fastest growing and most dangerous diseases. Approximately 16 million people in  the U.S. (6% of the population) suffer from this disease and an  additional one million are diagnosed each year with an estimated 12% of the population being undiagnosed. That is a 40% increase over the past decade and has increased by 70% among people in their  30's and 10% among people under 30. It's at epidemic proportions  and it's an epidemic that leads to other chronic and life-threatening diseases, such as blindness, kidney failure, arteriosclerosis, and  is responsible for 90,000 amputations each year. A patient with diabetes can have up to four times the risk of developing heart  disease and stroke. A patient with diabetes is four times more likely  to die from their first myocardial infarction than a non-diabetic  patient and a significant number of initial myocardial infarctions are from undiagnosed diabetics. Type I Diabetes The onset  of type I diabetes is considered to be due to exposure of genetically  predisposed individuals to as yet to be identified environmental  triggers with subsequent beta-cell injury. Thus, type I diabetics  require insulin as beta-cell loss becomes substantial. Type I diabetes has a strong familial tendency…not necessarily genetic as thought  by most researchers and healthcare providers, but due to metabolic weaknesses or tension resulting from the children eating basically the same diet as their parents. Understanding Type I Diabetes: the inflammatory response Research is coming out demonstrating that inflammation (Pattern 5) and free-radical stress are the mediators of beta-cell destruction prior to the autoimmune response seen with the onset of IDDM, as inflammation most often  precedes more severe conditions such as autoimmune diseases, multiple sclerosis, cancer, etc. A number of studies have shown that antioxidant  therapy in an environment of tight glycemic control, decreased insulin  need and HbA-1c levels and led to prevention of beta-cell loss with new-onset type I diabetes. In another study, Arany and colleagues  found that supplementing the mother's diet with taurine decreased insulitis and the onset of type I diabetes. Taurine being a principle  component of taurocholic acid, which makes up 30% of the bile acids of the gall bladder. However, the primary insult on the gall bladder and taurine is excessive or starchy carbohydrates. Comments: Prolonged inflammation and inadequate anti-inflammatory  responses are the result of excess carbohydrate load placing aberrant  stress on lipid metabolism, (Pattern V): pushing lipid metabolism toward long-chain saturated fatty  acid synthesis resulting in compromised gall bladder and liver function,  and an exaggerated need for nutrients such as anti-oxidants and taurine. Therefore, "tight glycemic control" is paramount to the body's ability to address the anti-inflammatory response as well as oxidative stress. In fact, a number of studies have shown that  young patients on a low carbohydrate diet decreased insulin need and HbA-1c levels and led to prevention of beta-cell loss with new-onset  type I diabetes, indicating that there is no autoimmune response without prior inflammation of the pancreatic beta-cells. Additionally, studies have shown that adding short and medium-chain  saturated fatty acids help stabilize blood sugar, as they do not require carnitine for transport into the citric acid cycle like ALL OF THE OTHER FATTY ACIDS. Understanding Type II Diabetes: insulin demand Type II can be either insulin dependent (IDDM) or  insulin resistance (NIDDM, non-insulin dependent diabetes mellitus).  In NIDDM, there is usually adequate insulin secretion under normal physiologic requirements. However, if there is a situation that requires increased insulin secretion, such as obesity, severe stress,  pregnancy, or excessive glucocorticoids, then insulin requirements  are not met. Although there is controversy over whether the primary  abnormality is one of resistance to insulin or deficiency of insulin secretion in relation to insulin demand, it has been established  that hyperglycemia cannot occur without relative or absolute insulin deficiency being present. Initially in Type II diabetes, one may  have only postprandial hyperglycemia, but as the disease progresses fasting hyperglycemia develops. Type II diabetes is basically the result of too much carbohydrate in relation to insulin  demand or an insulin response out-of-time with demand. In the instance of the "out-of-time" response, there is a delay of insulin secretion immediately  following a meal and a delay in reducing insulin secretion as the blood  sugar drops. This results in exaggerated hyperglycemia after meals and  hypoglycemia between meals. Obesity is one of the most common physiologic  responses to NIDDM. Conventional treatment of obese NIDDM patients is often  unsatisfactory. Capstick, F. and colleagues showed that caloric restriction  is extremely effective at rapidly improving glycemic control as insulin therapy was significantly reduced in 50% of the patients and discontinued in the other 50%. However, replacing carbohydrates with a high protein  diet is not a better option. Schneider, et al. showed that a high protein diet (55% protein) promoted the onset of diabetes in non-obese mice indicating that a high protein, low carbohydrate diet is not a preventative measure  against diabetes. Although, protein initiates an insulin response that  is slightly less than that of carbohydrate, protein and carbohydrate combined  causes a two-fold increase in insulin secretion. Comments: A rise in blood glucose and protein triggers an  insulin release. Once released, insulin causes most cells to become  more permeable to glucose, amino acids, lipids, electrolytes, and other nutrients. Unfortunately, continued and excessive insulin  requirements can lead to a number of blood sugar related conditions as the body is not designed to rely primarily on insulin, but enzymes  (e.g., cellulases) and polysaccharides for nutrient delivery. Metabolic Therapies Approach to Type I and Type  II Diabetes Metabolic Therapies views the primary cause of disease as an out of balanced or strained relationship between two physiologic  processes resulting from a metabolic push which is driven by poor  quality or excessive intake of macronutrients, i.e., proteins, fats,  and carbohydrates. In type I diabetes, the ineffectual relationship is between carbohydrates  and fats, as seen in Pattern V. We use carbohydrates for the first ninety minutes after mealtime.  After that, most of the excess carbohydrates, whether from refined  or complex sources, are converted to long-chain saturated fats and  cholesterol via pyruvic acid. Thus, the metabolism is geared toward  making fats and cholesterol resulting in (1) a compromised ability  to use fats for energy; (2) an increase in bile concentration which  can eventually lead to liver and gall bladder dysfunction; and (3)  prolonged inflammatory responses and inflammatory diseases. Again,  inflammation of the pancreatic beta-cell is the initiator of the autoimmune response. In type II diabetes, the ineffectual relationship comes from excessive starch or carbohydrate intake and inadequate vegetable (cellulose  and cellulase) intake as seen in Pattern VI. The diet should play a primary role in controlling blood  sugar so as not to overtly-burden the pancreatic role of insulin  production. Shifting the diet from high carbohydrate to one of low carbohydrate with increased vegetable intake reduces the insulin need, thereby, reducing pancreatic stress. In fact, introducing  Metabolic Therapies' cellulase formulation will produce a fasting hypoglycemic response within minutes indicating that it is not fiber  alone (slowing carbohydrate absorption), nor is it increased insulin  secretion in response to cellulose that is responsible for cellulases'  beneficial effects on blood sugar control. There have been literally hundreds of studies proving the effectiveness  of aloe vera in controlling and many times "curing" diabetes. In a number of studies comparing whole leaf aloe vera to aloe vera  gel, the whole leaf is found to be more effective. 5000 patients  with atheromatous heart disease were given whole leaf aloe vera and followed for five years. A marked reduction in total serum cholesterol, triglycerides, fasting and postprandial blood sugar in diabetic patients, total lipids, and increased HDL were noted. Simultaneously,  drugs such verapamil, nifedipine, beta-blockers, and nitrates were tapered off. There were no side effects and all 5000 patients were surviving at the time the study was published, Agarwal, O.P. Angiology 1985 Aug;36(8):485-92 Unlike the "freeze-dried" aloe vera, which is actually pasturized before dried, the whole leaf aloe vera found in the Metabolic  Support is never subjected to more than 95°. This preserves  the most effective polysaccharides (i.e., 66,000 - 250,000 daltons). Ivan Danhof, Ph.D., M.D. of North Texas Research Laboratory, stated that this particular aloe vera maintained the very long polysaccharides  (100,000-250,000 daltons), which most processors cannot achieve, Additionally, it is only aloe vera source that we have found that  was not pasteurized at high temperatures before freeze-drying. The aloe in this product is at a concentration of 50:1. This equates  to one tablespoon of reconstituted aloe vera per one tablespoon of Metabolic Support formula. An enzymatic formula developed by Metabolic Therapies, not only  will create a fasting hypoglycemic response within minutes with  nondiabetics, but will also lower or eliminate the need for insulin in the IDDM patient many times within 24 to 48 hours. This does not mean that they are "cured" of diabetes, but with the proper  dietary recommendations of little or no starch, refined carbohydrates, and increased intake of green leafy vegetables, they will be well on their way to recovery. Optimally, this approach should be a lifestyle change and not a temporary treatment. Additional benefits of changing  the eating patterns in this way are greater clarity; less inflammatory conditions (not associated with diabetes); alleviates neurologic  conditions due to hyperglycemia such as migraines, tremors, epilepsy,  etc.; and prolonged life span (see Metabolic Papers on Caloric  Restriction and The Principles of Metabolic Therapies) are just a few. Metabolic Therapies' Treatment Protocol Metabolic Support: 1 to 1-1/2 Tablespoon (7-11 capsules) per day, which can be taken as one dose or divided into two or three  doses before meals. Metabolic Support: the high cellulase and polysaccharide content of whole  leaf aloe vera and slippery elm has been clinically proven to be extremely effective at increasing cell permeability  to carbohydrates, proteins, and essential nutrients. Diabetic Enzymatic Formula for increase cellulase and polysaccharide support: can be  added to the Metabolic Support powder or taken separately for difficult  cases. Decrease carbohydrates such as grain products, potatoes, and corn and increase green leafy vegetables (Pattern VI), increase primarily coconut (1 tablespoon/day) and olive  oil (2 tablespoons/day) (Pattern V), and add Aerobic Support for EPA and appetite control. Note: this protocol is so effective that the patient must monitor their blood glucose levels with the first dose of Metabolic Support. References Atkinson, et al., Diabetes. 1990(39):933-937 Pozzilli P, et al., 61 st Scientific Sessions of the ADA. June 22-26,  2001 Arany EJ, et al., 61 st Scientific Sessions of the ADA. June 22-26,  2001 Freeman DJ, et al. Circulation. 2001(103):357-362 Rabinovitch A, et al., J Lab Clin Med 1993 Apr;121(4):603-7 Agarwal OP, Angiology 1985 Aug;36(8)485-92 Ghannam, et al., Horm. Res. 1986;24(4):288-94 Ajabnoor, MA, J Ethnopharmacol 1990 Feb;28(2):215-220 Funda DP, et al., Diabetes Metab Res Rev 1999 Sep-Oct;15(5):323-7 Top of Page Back to Articles