Diabetes Mellitus Is the Most Common Endocrine Disease - Essay Example

I. Introduction Diabetes mellitus, which is the most common endocrine disease, is a chronic disorder characterized by impaired metabolism of carbohydrates, protein, and fats. There are two major forms of the syndrome: Insulin-Dependent Diabetes Mellitus (type1 IDDM) and Non-Insulin-Dependent Diabetes Mellitus (type 2 NIDDM). Pre-diabetes, also known as impaired glucose tolerance or impaired fasting glucose, is a condition in which the blood glucose levels are higher than normal but not high enough to be diagnosed as diabetes. Many individuals with this condition develop type 2 diabetes within a 10-year period. Gestational diabetes occurs during pregnancy, which can potentially develop into type 2 diabetes later in life. Diabetes mellitus is characterized by long-term complications involving small and large blood vessels (micro and macroangiopathy) affecting the eyes, kidneys, and nerves. II. The Causes of Diabetes A. Known Causes of Diabetes Type 1 diabetes is usually diagnosed in childhood and accounts for 5-10% of diabetes. Type 1 diabetes mellitus is considered to be an autoimmune disease, where there is destruction of the beta cells of the pancreas, which produces insulin. This results in absolute insulin deficiency. Type 2 diabetes is more common than type 1 and accounts for 90%-95% or more of all cases of diabetes. It is characterized by insulin resistance and relative insulin deficiency. Although it usually occurs in adults over the age of 45, it is increasingly being seen in obese individuals of all age groups, including children and adolescents (New York State Department of Health, 2006). Other causes of diabetes include: due to chronic pancreatitis in alcoholics, hormonal abnormalities like pheochromocytoma, acromegaly, and Cushing’s syndrome, steroid hormone administration, endogenous release of glucagon and catecholamines following severe burns, acute myocardial infarction (“stress hyperglycemia”), diabetes caused by drugs or chemicals, diabetes caused by insulin receptor abnormalities, and diabetes associated with genetic syndromes like lipodystrophies, myotonic dystrophy and ataxia-telangiectasia (Foster,1998.) B. Causes of Diabetes Being Researched It has been suggested that modern food processing methods result in glycation end products, oxidized ascorbic acid and lipoic acid, all of which are potential causes of diabetes. High levels of glycation products are also found in infant formula, which also has added ascorbic acid. Adverse immune effects leading to diabetes can result from glycation of a casomorphin released from A1 beta-casein (Elliott, 2006). Since the 1960s, there has been accumulating evidence that carbohydrate intake has increased, especially refined carbohydrate and high-fructose corn syrup, with an association of increasing prevalence of obesity and diabetes (Bloomgarden, 2004). A study by Beales et al., (2002) aimed to determine whether A (1)-beta-casein was more diabetogenic than A (2)-beta-casein and to test the diabetogenicity of a milk-free diet in animals representing different forms of spontaneous type I IDDM diabetes mellitus. They found that though milk caseins may not be exclusive promoters of type I diabetes, although in some cases, they might enhance the outcome of diabetes. Other dietary components like wheat might be an important promoter of type I diabetes. The cow’s milk hypothesis has been a controversial topic for a decade. Cows milk based infant formulas given within the first 3 months of birth and cows milk consumption in childhood have been implicated in the development of type 1 diabetes mellitus. However, several epidemiological studies and first prospective trials do not support this concept. There is increasing evidence that the gut-associated immune system plays a major role in the pathogenesis of diabetes mellitus because of disturbed oral tolerance mechanisms, which in turn is influenced by growth factors and cytokines from breast milk, normal bacterial colonization, infections and diet. These factors are proposed as risk factors for type 1 diabetes mellitus (Wasmuth & Kolb, 2000.) Other than autoimmunity, the interaction of environmental agents with the beta cells of pancreas or both factors together have been implicated in the development of insulin-dependent diabetes mellitus in a genetically susceptible host. The chemicals include: alloxan, streptozotocin etc (Kraine & Tisch, 1999.) Fourteen different viruses have been associated with the development of type 1 diabetes in humans and animal models. The pathogenesis by which these viruses induce diabetes include at least two distinct mechanisms: induction of beta cell-specific autoimmunity, with or without infection of the beta cells, and by cytolytic infection and destruction of the beta cells. The viruses, which have been implicated include: retrovirus, reovirus, KRV, bovine viral diarrhoea-mucosal disease virus, mumps virus, rubella virus, cytomegalovirus, Epstein-Barr virus (EBV), encephalomyocarditis virus, mengovirus, and coxsackie B virus (Jun et al., 2003.) III. Study on the rise of Diabetes in Children A. Epidemiology of Diabetes Among New York Children Presently in New York, at least 13,000 children are reported to be affected with type 1 diabetes, and this is the second leading childhood chronic disease. Although the majority of children have type 1 diabetes, the incidence of type 2 diabetes is also reported to be on the rise. Type 2 diabetes, typically, has an adult onset (over 45 years of age) but this is seen more frequently now in children and adolescents. At present, there are no estimates of the prevalence of type 2 diabetes among children in New York State, but according to pediatric endocrinologists, one of every three new cases in adolescents is type 2 diabetes. These low estimates could be due to the large number of undiagnosed or misdiagnosed cases. B. Causes of Diabetes in the Youth Some of the reasons attributed to the rise of type 2 diabetes are a lack of physical activity and the excess consumption of fast foods rich in calories and fat. In particular, children of ethnic minority groups including Native American, African American and Hispanic origins have an increased risk. The prevalence of diabetes also has been found to be high in those with less than a high school education (New York State Department of Health, 2006). When compared with non-Hispanic whites, Hispanics have higher rates (3.8 % in the age group 20-44) of type 2 diabetes (Escarce, Morales & Rumbaut, 2006). Non-Hispanic black and Hispanic youth with IDDM also have elevated short-term mortality. This may be due to inadequate access to comprehensive diabetes care (Lipton et al., 1999). Another reason for the higher prevalence in colored people could be due to the interaction of genetic risk factors and environmental factors (Hosey, Gordon & Levine, 1998). Other studies have supported this (Rosenbloom, House & Winter, 1998.) Studies have found a higher prevalence of NIDDM in Native American and African-American youth, with a higher preponderance in females. This is related to increasing rates of obesity and to a higher requirement for insulin at adolescence. The heterogeneity seen in the ethnic minority youth includes: typical NIDDM, atypical diabetes mellitus (ADM), and a range of defects in the pathway of insulin action (seen in a small proportion). The primary defect in NIDDM has been shown by clinical and experimental evidence to be insulin resistance or insulin deficiency. There is also evidence that fetal undernutrition may be a contributing factor (Rosenbloom, House & Winter, 1998.) Auslander et al (1997) aimed to describe the sociodemographic, family, and community factors that contribute to the glycemic control of African-American and Caucasian youths with diabetes. The results of the study revealed that African-American youths with diabetes have a poor metabolic control when compared to their Caucasian counterparts (1.5% difference in HbA1c levels). Other factors accounting for the poorer glycemic control includes: single-parent household status and lower levels of adherence to diet and glucose testing than Caucasian youths. The conclusions that can be drawn from this study is that African-American youths with diabetes may be at a higher risk for poor glycemic control due to the higher prevalence of single parenting and lower levels of adherence. IV. Treatment for those with Diabetes today A. Diet Control In NIDDM, the main treatment approach would be diet control, since most of the patients with insulin resistance are overweight and have an increase in VLDL and LDL, associated with decreased HDL, and presence of cholesterol and hypertension. The goals of diet therapy are: to maintain glucose at near normal levels, attain optimal serum lipid levels and calories to maintain a reasonable body weight. If the patient is obese or is a hypertensive, even a small weight loss can lead to an improvement in metabolic control and hypertension with a better life expectancy. In general, 50-60% of the total caloric amount should be from carbohydrates, 35% from lipids (less than 10% of these 10-15% from monounsaturated fats with less than 300 mg/day of cholesterol) and 10% from protein. One study has found that a low carbohydrate, calorie-restricted diet has beneficial short-term effects in type 2 diabetics who had no benefit with diet or sulfonylurea therapy and may not need insulin (Gutierrez et al., 1998) In the past, there has been much debate about the advantages of a high protein diet. Two prospective randomized controlled trials have reported greater weight loss with a high protein diet compared to a balanced diet. A high protein diet leads to lower incidence of obesity, cardiovascular disease, diabetes, and lower blood cholesterol levels (Stanton & Philips, 2005.) If the primary problem is raised very low density lipoproteins level, then 10% of the total caloric intake should be from saturated fats, 10% from polyunsaturated, and 15-20% from monounsaturated fats with less than 200 mg/day of cholesterol and 40% of carbohydrates (Cavallo-Perin, Bodoni & Marena, 1997.) Strychar et al (2003) in a study found that a high-monounsaturated-fat diet had a favorable effect on fasting lipoproteins in those with type 1 diabetes. However, more research is required before a high-monounsaturated-fat diet can be recommended as an alternative diet therapy in type 1 diabetes. One study, found that in type 2 diabetes patients, an ad libitum low-fat diet caused greater weight loss than a high-monounsaturated fat diet without any alterations in plasma lipids or glycemic control (Gerhard et al., 2004) Artificial sweeteners like saccharine or aspartame may be used instead of sugar. For proper metabolic control, daily consumption of 20-35 gram of dietary fibers from food sources is recommended (Cavallo-Perin, Bodoni & Marena, 1997.) In one randomized, crossover study (Chandalia M et al., 2000) it was found that a high-fiber diet lowered blood glucose levels, plasma total cholesterol, triglyceride, and very-low-density lipoprotein cholesterol concentrations. The study concluded that a high intake of dietary fiber, particularly of the soluble type, above the level recommended by the American Diabetes Association (ADA) i.e., total 50 g; 25 g of soluble fiber and 25 g of insoluble fiber, decreases hyperinsulinemia, and lowers plasma lipid concentrations in patients with type 2 diabetes. In addition to beneficial effects on insulin sensitivity and adiposity, fiber intake may also benefit pancreatic function (Liese et al., 2005.) It would be best to avoid alcohol, since it can worsen metabolic control and diet compliance, in addition to causing other health problems. If at all alcohol is consumed, it should not exceed 30 g/day for men, and 20 g/day for women. Patients with hypertension should restrict dietary sodium intake. Regular monitoring of metabolic parameters like blood pressure, and body weight is important (Cavallo-Perin, Bodoni & Marena, 1997.) B. Exercise Exercise is a very important aspect in the management of diabetes. Many studies have demonstrated that regular exercise improves the cardiovascular system, decreases the risk factors causing cardiovascular disease, promotes fat loss, increases muscle mass, increases the glucose uptake by cells, improves insulin sensitivity, and enhances the psychological well being of the diabetic. In addition, regular exercise improves cardiovascular fitness and work capacity, decreases blood pressure and peripheral vascular resistance. Finally, exercise improves total cholesterol and high-density lipoprotein levels (Jimenez, 1997.) The development of insulin resistance is associated with an increase in abdominal fat and loss of muscle mass. Exercise training causes selective loss of fat from the central regions of the body, prevents muscle atrophy and stimulates muscle development, and therefore, contributes in the prevention of insulin resistance. Regular weight training significantly lowers the insulin response to a glucose challenge without affecting the glucose tolerance. A characteristic feature of insulin-resistant obese individuals and individuals with NIDDM is a reduced ability of insulin to stimulate muscle blood flow. Exercise training significantly improves the control of insulin over blood glucose. Following exercise training, there are important changes in muscle morphology. There is an increase in the conversion of fast twitch glycolytic IIb fibers to fast twitch oxidative IIa fibers, along with an increase in capillary density. In addition to having a greater capillary density, the IIa fibers are more insulin-sensitive and responsive than the IIb fibers (Ivy, 1997.) Before starting an exercise regimen, a complete physical examination is recommended. All individuals above 35 years of age of should undergo an exercise stress test prior to the exercise program. This will identify individuals with previously undiagnosed ischaemic heart disease and abnormal blood pressure. It is also important to diagnose conditions like proliferative retinopathy, microalbuminuria, and peripheral and/or autonomic neuropathy in patients with NIDDM before they participate in an exercise program. If any such complications are present, it is necessary to modify the exercise protocol accordingly (Wallberg-Henriksson, Rincon, & Zierath, 1998) Generally, the exercise program should consist of moderate intensity aerobic exercise. Resistance training and high intensity exercises are recommended only for individuals without proliferative retinopathy or hypertension. Adequate intake of fluid is important when exercising for prolonged periods or in warm and humid environments (Wallberg-Henriksson, Rincon, & Zierath, 1998) However, it should be noted that although exercise has numerous benefits, it is not without risks in patients with diabetes mellitus. Increased hepatic glucose production can lead to hyperglycemia, and insufficient insulin levels can result in ketoacidosis from excess concentrations of fatty acids (Chipkin, Klugh & Chasan-Taber, 2001.) Excess uptake of glucose due to increased insulin concentrations, enhanced insulin action or impaired carbohydrate absorption can lead to hypoglycemia. In order to decrease the risk of hypoglycemia, insulin doses should be reduced before exercise. Other potential risk factors, although not well studied, are worsening of nephropathy or retinopathy, or precipitation of musculoskeletal injuries. Autonomic neuropathy may predispose to arrhythmias or precipitate a cardiac event in those with underlying coronary artery disease (CAD). Awareness of these risks and taking proper actions to minimize their impact would make an exercise regimen more beneficial. Exercise programs for diabetic patients should emphasize self-monitoring of blood glucose (SMBG), foot care and cardiovascular functional assessment. SMBG is recommended for all patients before, during and after exercise and provides crucial information on the impact of exercise. In those patients with hypoglycemia unawareness or those performing high-intensity exercise, more frequent monitoring is recommended. Carrying glucose tablets or gel, a diabetic identification bracelet or card, or exercising along with an individual who is aware of the medical condition of the patient can prevent exercise-induced severe hypoglycemic episodes. Proper foot care is critical in diabetics who are pursuing an exercise regimen. Careful choice of proper shoes, type of exercise, regular inspection of the skin surfaces and appropriate evaluation and treatment of lesions like calluses can prevent diabetic foot ulcers. Diabetics affected with severe neuropathy should consider alternatives to weight-bearing exercises (Chipkin, Klugh & Chasan-Taber, 2001.) In order to prevent the precipitation of clinical CAD, the initial cardiac assessment should include a record of the maximal heart rate, blood pressure, as well as ischaemic changes. Exercise tolerance testing can identify anginal thresholds and asymptomatic ischemia. In those with asymptomatic ischemia, counseling should be given regarding target pulse rates to avoid inducing ischemia (Chipkin, Klugh & Chasan-Taber, 2001.) C. Undergoing Treatment NIDDM, which is not controlled by dietary management, requires the use of oral agents like sulfonylureas. These drugs act by stimulating the release of insulin from the beta cells of the pancreas. In case of IDDM, insulin therapy is required. The three standard insulin treatment regimes include: conventional, multiple subcutaneous injections (MSI) and continuous subcutaneous insulin infusion (CSII). Conventional insulin therapy involves administration of one or two injections of intermediate-acting insulin like lente insulin or isophane insulin with or without the addition of regular insulin. MSI involves the administration of intermediate or long-acting insulin in the evening as a single dose, together with regular insulin prior to each meal. CSII involves the use of a small battery-driven pump, which delivers insulin subcutaneously into the abdominal wall through a needle, throughout the day (Foster, 1998.) D. Prevention of Diabetes Schools are an ideal setting to provide a safe and health-conscious environment for children with and at-risk for diabetes. However, currently, many schools do not provide for adequate physical activity, proper nutrition, or education for both the prevention and management of chronic disease. There is a lack of knowledgeable and well-trained staff in schools to ensure the immediate safety of children with diabetes requiring emergency administration of glucagon for the treatment of hypoglycemia. In September 2000, the New York State Diabetes Task Force was formed by the New York State Department of Health Diabetes Prevention and Control Program. This Task Force comprised of diabetes experts from across the state. In order to make schools safe for children with diabetes, the Task Force has recommended the following strategies: a. Spread consensus guidelines for type 1 and type 2 diabetes. b. Educate primary health care providers on diabetes. c. Provide pre-service and in-service training for school personnel. d. Enhance primary prevention for type 2 diabetes through school food service and physical activity initiatives. e. Ensure that school personnel are aware of all policies related to diabetic children. f. Encourage the development of individual medical management plans for diabetic students. Another goal of the Task Force is to estimate the prevalence and incidence of diabetes and diabetes risk in children in New York State. They aim to do this by creating a public health diabetes registry for children, address the need for a population-based surveillance system, and support efforts to obtain aggregated height/weight measures on children. (New York State Department of Health, 2006.) Yamaoka & Tango (2005) conducted a meta-analysis of randomized controlled trials to determine the effect of lifestyle education for preventing type 2 diabetes in adults with high risk. This was determined by incidence and a reduced level of plasma glucose 2 hours after a 75-g oral glucose load (2-h plasma glucose). When compared with the control group, the study group showed reduced 2-hour plasma glucose by 0.84 mmol/l after the lifestyle education intervention. They thus concluded that lifestyle education intervention is effective for reducing both the 2-hour plasma glucose and the relative risk in high-risk individuals, and is thus, useful in preventing diabetes. The Diabetes Prevention Program (DPP) is a 4-year study, which analyzed more than 3200 overweight or obese persons with impaired glucose tolerance. This study found that a lifestyle intervention, which caused a 7% reduction in initial weight and increased physical activity to 150 min/week, reduced the risk of developing type 2 diabetes by 58% when compared with placebo (Wadden, Butryn & Byrne, 2004). E. Living with diabetes Diabetes mellitus is a chronic disease that requires psychological, social and physical adaptations. From the time diabetes is diagnosed, children are faced with the problem of coping with a restricted diet, insulin therapy and life style changes. This can result in feelings like fear, insecurity, and revolt, which later changes to acceptance and adaptation (Moreira & Dupas, 2006). Parents of recently diagnosed diabetic children are often inadequately prepared to deal with the situation due to the unexpectedness and speed of the diagnosis. They feel insecure and uncertain about the future. Most parents later on successfully adjust and adapt. (Lowes, Gregory & Lyne, 2005). In most adult patients with diabetes, the awareness that they are vulnerable to complications of diabetes with a possible shortening of their life-span, can lead to emotional distress, refusal to cooperate, or excessive preoccupation with their condition. The physician can play an important role in making the patient acknowledge their disease and make them realise that the goal is to live with diabetes, and not for it (Foster,1998.) V. Recent Advances and the Future A. Pancreas and Islet Cell Transplantation The pancreas contains islet cells, which are small clusters of endocrine cells that include insulin-producing beta cells. In type 1 diabetes, there is an autoimmune destruction of the beta cells, resulting in the loss of insulin production. Pancreas transplant alone (PTA) has been used in some type 1 diabetes patients with a history of frequent and severe metabolic complications, severe and clinical and emotional problems with receiving insulin injections, or consistent failure of insulin-based management to prevent acute complications. Alternatively, Islet cell transplantation has been tried instead of whole-organ pancreas transplantation, but early attempts failed. In 1999, the Edmonton transplant protocol was developed at the University of Alberta in Canada, and following this, major islet transplant centers have developed and refined new procedures. Islet transplantation has mainly been used in patients who are candidates for PTA. Islet transplantation using the Edmonton and other more recent protocols has demonstrated superior success, according to available evidence. The one-year follow-up of patients following Islet transplantation has shown that most patients are independent of the need for insulin and are free of severe hypoglycemic episodes. Currently, more than 100 patients have been followed for a period of 1 year post-transplantation, and the Edmonton group reported on 15 patients followed for 2 years or more (AHRQ Evidence reports and summaries, 2004.) In an attempt to reproduce the physiological insulin secretion in diabetic patients, ultra-short-acting insulin analogues and ultra-long-acting analogues are being used with better results, and lower prevalence of hypoglycemia. The most exciting development in non-invasive delivery of insulin is inhaled insulin (Gomez-Perez & Rull, 2005). B. Inhalable insulin In the most advanced concept of therapy with inhalable insulin, insulin is delivered as a dry-powder insulin formulation via a special aerosol device system. Recent phase II studies have shown that the inhalable insulin is absorbed in a dose-dependent and reproducible manner, and the therapeutic efficacy and safety is comparable to subcutaneous insulin. Phase III studies are also underway (Harsch, Hahn & Konturek, 2001.) DeFronzo et al., (2005) in their study aimed to determine if inhaled insulin can achieve target glycemic control in those patients where diet and exercise have failed. The results of the study led them to conclude that inhalable insulin is an effective therapy in type 2 diabetes, if used early in the course of the disease. The obvious and most important advantage of inhalable insulin is the comfort of delivery. However, in patients with pulmonary diseases, there is still no available clinical data concerning the efficacy of the inhaled insulin. Another factor is that inhalable insulin requires larger doses of insulin compared to subcutaneous insulin, which raises the cost of treatment. Further studies are required to address these issues (Harsch, Hahn & Konturek, 2001.) C. Gene Therapy A cure for type 1 IDDM is possible if surrogate insulin-producing cells can be generated to replace beta cells. One promising gene therapy approach is to express pancreatic endocrine developmental factors, such as PDX-1, NeuroD/BETA2 and Neurogenin 3, to promote differentiation of non-endocrine cells into beta cells or islet phenotype, which will enable these cells to synthesize and secrete insulin (Samson & Chan, 2006.) Tuch et al., (2003) have described an alternative approach, wherein, genetically altered neoplastic liver cells can be used to synthesize, store and secrete insulin. VI. Conclusion Diabetes mellitus is the most common endocrine disease and is a chronic disorder of metabolism. The two major forms of the syndrome include, Insulin-Dependent Diabetes Mellitus (type1 IDDM) and Non-Insulin-Dependent Diabetes Mellitus (type 2 NIDDM). Other types include pre-diabetes and gestational diabetes. The causes of diabetes mellitus are varied and include autoimmune destruction of beta cells of the pancreas, hormonal abnormalities, genetic causes, insulin receptor abnormalities etc. Some other proposed causes include, cow’s milk infant formulas, gut associated immunity, various chemicals and viruses. Many studies have reported an increase in type 2 diabetes in youth. The reasons attributed for this is a lack of physical activity and the excess consumption of fast foods. Children of ethnic minority groups are known to have an increased risk, possibly to genetic and environmental influences and other factors. The treatment of diabetes is multi-pronged, and involves regular exercise, diet control and appropriate treatment with oral drugs and insulin. It is also important to prevent childhood diabetes with interventions aimed at school children. Although diabetes mellitus is a chronic disease with no permanent cure, promising research in gene therapy, pancreas and islet cell transplantation, and more effective forms of delivery of insulin like inhalable insulin gives hope to millions of people affected with this condition. The day is not far when an effective and permanent cure would be found. **************************************************************************************************** References AHRQ Evidence reports and summaries (2004). Islet Transplantation in Patients with Type 1 Diabetes Mellitus. Retrieved from, < http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat1.section.126482> Bloomgarden, ZT (2004). Diet and Diabetes. Diabetes Care, 2004. 27:2755-2760. Auslander, WF, Thompson, S, Dreitzer, D, White, NH and Santiago, JV(1997). Disparity in glycemic control and adherence between African-American and Caucasian youths with diabetes. Family and community contexts. Diabetes Care 1997, Oct;20(10):1569-75. Beales, PE, Elliott, RB, Flohe, S, Hill, JP, Kolb, H, Pozzilli, P, Wang, GS, Wasmuth, H and Scott FW (2002). A multi-centre, blinded international trial of the effect of A(1) and A(2) beta-casein variants on diabetes incidence in two rodent models of spontaneous Type I diabetes. Diabetologia. 2002 Sep;45(9):1240-6. Cavallo-Perin, P, Bodoni, P and Marena, S (1997) . Diet therapy in non-insulin dependent diabetes mellitus (NIDDM). Minerva Gastroenterol Dietol. 1997 Dec;43(4):175-81. Chandalia, M, Garg, A, Lutjohann, D, von Bergmann, K, Grundy, SM, and Brinkley, LJ (2000). Beneficial effects of high dietary fiber intake in patients with type 2 diabetes mellitus. N Engl J Med. 2000 May 11;342(19):1392-8. DeFronzo, RA, Bergenstal, RM, Cefalu, WT, Pullman, J, Lerman, S, Bode, BW, Phillips, LS (2005). Efficacy of Inhaled Insulin in Patients With Type 2 Diabetes not Controlled With Diet and Exercise. Diabetes Care. 2005. 28:1922-1928. Elliott, RB (2006). Diabetes - A man made disease. Med Hypotheses, 2006. Escarce, JJ, Morales, LS, and Rumbaut, RG (2006). The Health Status and Health Behaviors of Hispanics. Hispanics and the Future of America. The National Academies Press:368. Foster, DW (1998). Diabetes Mellitus. Harrison’s Principles of Internal Medicine, 1998, 14th edition, vol 2:2061. Gomez-Perez, FJ and Rull, JA (2005). Insulin therapy: current alternatives. Arch Med Res. 2005 May-Jun;36(3):258-72. Gerhard, GT, Ahmann, A, Meeuws, K, McMurry, MP, Duell, PB and Connor, WE (2004). Effects of a low-fat diet compared with those of a high-monounsaturated fat diet on body weight, plasma lipids and lipoproteins, and glycemic control in type 2 diabetes. American Journal of Clinical Nutrition 2004 September; 80(3): 668-673. Gutierrez, BS, Akhavan, M, Jovanovic, L and Peterson, CM (1998). Utility of a Short- Term 25% Carbohydrate Diet on Improving Glycemic Control in Type 2 Diabetes Mellitus. Journal of the American College of Nutrition, 1998; 17 (6): 595-600. Harsch, IA, Hahn, EG and Konturek, PC (2001). Syringe, pen, inhaler - the evolution of insulin therapy. Med Sci Monit. 2001 Jul-Aug;7(4):833-6. Hosey, G, Gordon, S and Levine, A (1998). Type 2 diabetes in people of color. Nurse Pract Forum 1998 Jun;9(2):108-14. Ivy, JL (1997). Role of exercise training in the prevention and treatment of insulin resistance and non-insulin-dependent diabetes mellitus. Sports Med. 1997 Nov;24(5):321-36. Jun, HS & Yoon, JW (2003). A new look at viruses in type 1 diabetes. Diabetes Metab Res Rev. 2003 Jan-Feb; 19(1): 8-31. Jimenez, CC (1997). Diabetes and Exercise: The Role of the Athletic Trainer. Journal of Athletic Training. 1997 Dec; 32(4) Kraine, MR & Tisch, RM (1999). The role of environmental factors in insulin-dependent diabetes mellitus: an unresolved issue. Environ Health Perspect. 1999. Lipton, R, Good, G, Mikhailov, T, Freels, S and Donoghue, E (1999). Ethnic differences in mortality from insulin-dependent diabetes mellitus among people less than 25 years of age. Pediatrics 1999 May;103(5 Pt 1):952-6. Liese, AD, Schulz, M, Fang, F, Woleverm, T, Agostino, RB, Sparks, KC, and Mayer- Davis, EJ (2005). Dietary Glycemic Index and Glycemic Load, Carbohydrate and Fiber Intake, and Measures of Insulin Sensitivity, Secretion, and Adiposity in the Insulin Resistance Atherosclerosis Study. Diabetes Care 2005, 28:2832-2838. Lowes, L, Gregory, JW, Lyne, P (2005). Newly diagnosed childhood diabetes: a psychosocial transition for parents? J Adv Nurs. 2005 May;50(3):253-61. Moreira, PL, Dupas, G (2006). Living with diabetes: the experience as it is told by children. Rev Lat Am Enfermagem. 2006 Feb;14(1):25-32. New York State Department of Health (2006). New York State Strategic Plan for the Prevention and Control of Diabetes. Retrieved from, Rosenbloom, AL, House, DV and Winter, WE (1998). Non-insulin dependent diabetes mellitus (NIDDM) in minority youth: research priorities and needs. Clin Pediatr (Phila) 1998 Feb;37(2):143-52. Strychar, I, Ishac, A, Rivard, M, Lussier-Cacan, S, Beauregard, H, Aris-Jilwan, N, Radwan, F and Yale, JF (2003). Impact of a high-monounsaturated-fat diet on lipid profile in subjects with type 1 diabetes. J Am Diet Assoc. 2003 Apr;103(4):467-74. Stanton, C & Philips, P (2005). Dietary dilemmas in diabetes. Australian Family Physician. 2005 June; 34 (6). Samson, SL & Chan, L (2006). Gene therapy for diabetes: reinventing the islet. Trends Endocrinol Metab. 2006. Tuch, BE, Szymanska, B, Yao, M, Tabiin, MT, Gross, DJ, Holman, S, Swan, MA, Humphrey, RK, Marshall, GM and Simpson, AM (2003). Function of a genetically modified human liver cell line that stores, processes and secretes insulin. Gene Ther. 2003 Mar;10(6):490-503. Wasmuth, HE, Kolb, H (2000). Cows milk and immune-mediated diabetes. Proc Nutr Soc. 2000 Nov;59(4):573-9. Wadden, TA, Butryn, ML & Byrne, KJ (2004). Efficacy of Lifestyle Modification for Long- Term Weight Control. Obesity Research. 2004. 12:151S-162S. Yamaoka, K & Tango, T (2005). Efficacy of Lifestyle Education to Prevent Type 2 Diabetes. Diabetes Care. 2005. 28:2780-2786. Read More