Homeopathic Treatment for Diabetes

The Diabetes Loophole

Diabetes Loophole is a step- by-step manual, your complete guide to reverse diabetes naturally and without any side effects.It was created by Reed Wilson who is an alternative health researcher. And has led his team to find answers to the diabetes epidemic that's been silently ravaging the nation.The secrets in this program helped a 10-year-old's life to begin when his diabetes ended, they also helped an elderly woman reduce her blood sugar level from 450 to normal levels and so many people to reduce their diabetic symptoms.The secrets will help you to reduce your risk of cancer by an incredible 67%, reduce cholesterol by 25 to 30% (as much as statin drugs and without the risky side-effects), reduce high blood pressure by as much as half and reduce the risk of a fatal heart attack by 70%The book by reading the book you will learn things like foods that will help you overcome diabetes and exercizes that will improve your health.When you order for this manual you get other books for free like: Super foods, the antiinflammatory diet, the top 20 inflammatory food and others.Everything in this program is focused on giving you exactly what you need in order to get the kind of freedom you've been denied You'll get results like so many others have before you. All you have to do is order. Read more...

The Diabetes Loophole Summary

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Evolution In Diagnostic Criteria For Diabetes

The question of diagnostic criteria for type 1 diabetes does not usually give risk to much debate because of its clear acute-onset phenotype, and the logical link between aetiology (lack of insulin) and treatment modality. However, the recognition of a non-insulin-dependent form of diabetes, in which there was a much less clear distinction between normality and disease, created a need for diagnostic criteria. Classification with only the help of symptoms and clinical signs was soon regarded as unsatisfactory. Another major impetus for the development of diagnostic criteria was the recognition that the absence of standardisation was an obstacle to epidemiological and clinical research. In 1964, the World Health Organisation (WHO) convened an Expert Committee on Diabetes Mellitus which attempted to provide a universal classification of the diabetes syndrome. But it was not until 1980 that an international accepted classification was established. Two international work groups, the...

Longterm Diabetes Complications As Used For Defining Diabetes Thresholds

Diabetes mellitus is characterised by hyperglycaemia, which is associated with long-term damage, dysfunction and failure of various organs. Several studies30,31 have confirmed relationships between hyperglycaemia and the risk of developing such micro- and macrovascular complications as retinopathy, neuropathy, nephropathy and cardiovascular disease. However, many have compared the rates of each condition in subjects already classified according to the diagnostic criteria as having diabetes or not. Few studies consider whether the current diagnostic glucose levels represent the best level for predicting an increased risk of such complications, and no formal statistical threshold for any complication has been consistently demonstrated. The relationships of FPG and 2 h PG with the development of retinopathy were evaluated in a study undertaken in the Pima Indian population over a wide range of plasma glucose cutpoints23. Both variables were similarly associated with retinopathy,...

Assessment Of Diabetesrelated Symptoms

The clinical diagnosis of diabetes is often prompted by symptoms such as polyuria and polydipsia, recurrent infections, unexplained weight loss and, in severe cases, drowsiness and coma. In such cases a single blood glucose determination in excess of the diagnostic values indicated in Figure 2.2 (black zone) establishes the diagnosis. Figure 2.2 also defines levels of blood glucose below which a diagnosis of diabetes is unlikely in non-pregnant individuals. These criteria are unchanged from the 1985 WHO report7. For clinical purposes, an OGTT to establish diagnostic status need only be considered if casual blood glucose values lie in the uncertain range (i.e. between the levels that establish or exclude diabetes) and fasting blood glucose levels are below those which establish the diagnosis of diabetes. Diabetes mellitus likely Diabetes mellitus uncertain Diabetes mellitus likely Diabetes mellitus uncertain Diabetes mellitus unlikely Figure 2.2. Unstandardised (casual, random) blood...

Diabetes Classification Beyond Stamp Collecting

Humans appear to have a powerful instinct to classify. In part this may spring from a purely intellectual and aesthetic requirement to create some sort of order from the bewildering chaos of observable natural phenomena. This inbuilt taxonomic imperative is likely, however, to have more utilitarian roots. To be able to manipulate the natural world to improves one's comfort and or survival, one needs to understand its nature. The classification of natural phenomena into related groups is an essential first step towards this comprehension. Given the powerful threat represented by illness, it is not surprising that the classification and reclassification of disease has been a continued obsession of the healing professions since their earliest recorded history. In Chapter 2, Max de Courten provides a balanced and thorough account of how we have reached the currently accepted glycaemic criteria for the diagnosis of diabetes mellitus, and its classification into sub-types. In this short...

Studies In Newly Diagnosed Diabetes

Several interventions have been evaluated in individuals with newly diagnosed type 1 diabetes, in an attempt to interdict the disease process and preserve B-cell function. Interpretation of these has been complicated by a number of factors. Early studies often used 'remission' as an outcome, based on cessation of insulin therapy or very low doses of insulin. In fact, there was even a recommended definition of remission promulgated52. Yet, most recent investigations have focused more on preservation of C-peptide as a biochemical marker of B-cell function2. Moreover, it has come to be appreciated that more intensive insulin therapy and or better maintenance of glycaemic control results in better preservation of B-cell function53-56. Of these, probably the best data come from the Diabetes Control and Complications Trial (DCCT)56. Individuals who entered the DCCT with high residual B-cell function (stimulated C-peptide levels of 0.2-0.5 pmol ml) (n 303) and who were randomized to...

Rationale For The Prevention Of Type Diabetes

Several observations align to indicate the increasing need to prevent type 2 diabetes, rather than simply treat it, once established. Chapter 1 has mentioned the increasing prevalence and incidence, excess mortality and limited effectiveness of interventions. In addition to these, diabetes, and particularly type 2 diabetes, incurs high health care costs. Estimates of costs vary depending on the methods used17, but from 6018 to 100 billion19 in health care costs were spent on diabetes in the USA in 1995, which is variously estimated to be 6-17 of all health care costs. The majority of health care costs for diabetes are spent in developed countries, whereas estimates suggest that the majority of disability-adjusted life years (DALYs) are lost in developing countries, where limited health care budgets are available to deal with the problems of diabetes18. Recent studies from US health maintenance organizations (HMOs) have shown approximately two-fold increases in medical care expenses...

Definition Of Type Diabetes Mellitus

The studies reviewed here use a variety of criteria to define type 2 diabetes. This is inevitable, given the long time period included. It was not possible to identify consistent criteria for all studies. However, the 1985 WHO criteria24 were used as a reference when possible since the majority of modern studies used them. In prevention trials, the development of any clinical diagnosis of diabetes or measured hyperglycemia meeting defined criteria was usually the outcome of the trial. No studies published to date have tested for autoimmune markers that would identify subjects developing type 1 diabetes. Since over 90 of people developing diabetes over the age of 50 years will have type 2 diabetes30, this is a minor limitation. However, proper diagnosis of the etiological type of diabetes as an outcome will become increasingly important in trials in the future, since specific interventions aimed at defined metabolic and immunological pathways will increasingly be tested.

Natural History And Risk Factors For Type Diabetes

Primary prevention of diabetes requires a thorough knowledge of the natural history of the development of glucose intolerance and risk factors. Once these have been established from observational studies, it is at least theoretically possible that interventions aimed at any of the factors could reduce diabetes risk. A number of recent reviews of risk factors exist8,31-39, and are summarized in Table 6.2 for individual level risk factors, that is, those that operate on or within a person. This table does not include group-, societal-, or populationlevel risk factors such as Westernization, commercialization of the food supply, increased motorized transport, television and computer time replacing group and individual activity and interaction, and changes in social mores which alter individual factors over large numbers of people simultaneously. The information about possible genes related to or causing type 2 diabetes is not included here, since, in the short term, gene-based...

Prevention of Cardiovascular Disease in Patients who have Diabetes

This article examines the evidence in favor or against choosing treatment with insulin secretagogues or sensitizers as the preferred way to prevent cardiovascular events. It should be emphasized that most patients eventually will be treated with a combination of therapies therefore, much of the discussion may not be relevant. Conversely, combination of two sensitizers may have added effects. Also, retrospective data suggest that a combination of sulfonylurea and metformin may be associated with increased cardiovascular events. Nevertheless, it is important to recognize the relative value of these different agents as we choose complex therapeutic regimens.

Grafting in Diabetic Patients

Clinical outcomes in diabetic patients following coronary revascularization procedures with bypass surgery (CABG) or percutaneous coronary intervention (PCI) are worse than in nondiabetics. Current evidence suggests that CABG is preferable to PCI for revascularization in patients who have diabetes and multi-vessel coronary artery disease. Most trials have not used contemporary adjunctive therapies, such as GP Ilb IIIa inhibitors and prolonged dual antiplatelet therapy. It is conceivable that implementation of these evidence-based therapies may improve clinical outcomes significantly in diabetic patients who undergo PCI. In the future, emerging technologies, such as drug-eluting stents and soluble receptor for advanced glycation end products, may further improve outcomes after PCI and make it the preferred revascularization modality in diabetics.

Therapeutic Strategies in Diabetes and Cardiovascular Disease

Diabetes is now considered the equivalent of having 2 or 3 major risk factors for coronary atherosclerosis. Also, the presence of diabetes increases the risk of any procedure and is associated with a poorer prognosis compared with individuals without diabetes. Also, diabetes dictates certain clinical approaches to disease. Thus today's clinician needs a full understanding of this disease and its effect on management decisions. I was delighted that Dr. Prakash Deedwania, who has had a long and productive interest in diabetes and cardiovascular disease, was willing to organize and contribute to articles on this topic. This broad topic has been divided between two issues of the Cardiology Clinics. The first issue (November 2004) dealt with pathophysiology, clinical epidemiology, and the relationship between diabetes and other diseases such as heart failure and hypertension. The second issue deals with management strategies for preventing and treating the cardiovascular complications of...

Impaired insulin secretion and insulinstimulated glucose uptake

Glucose oxidation requires less oxygen than FFA oxidation to maintain ATP production. Thus, myocardial energy use is more efficient during the increased dependence on glucose oxidation with ischemia (approximately 11 more ATP is generated from glucose oxidation as compared with FFA oxidation). In the setting of relative insulinopenia (insulin resistance or frank DM) that is exacerbated by the stress of AMI, the ischemic myocardium is forced to use FFAs more than glucose for an energy source because myo-cardial glucose uptake is impaired acutely. Thus, despite acute hyperglycemia, a metabolic crisis may ensue as the hypoxic myocardium becomes less energy efficient in the setting of frank DM or insulin resistance. Insulin augments the translocation of GLUT-1 and GLUT-4 receptors to the sarcolemma and can diminish FFA release from myocytes and adipocytes 27 . Thus, the extent to which the myocardium expresses an intact response to insulin, therapeutic augmentation of oxidative glucose...

Potential beneficial effects of insulinsensitizing agents on cardiovascular risk factors

Several epidemiologic studies showed that hyperinsulinemia is an independent risk factor for cardiovascular disease 18 . Correction of insulin resistance clearly is important in the management of type 2 diabetes mellitus and may decrease the risk for cardiovascular disease. In the UKPDS, patients who had type 2 diabetes melli-tus and were treated with metformin, which decreases hyperinsulinemia and insulin resistance, had a 30 reduction in cardiovascular disease events and mortality compared with those who received conventional treatment 11 . The thiazo-lidinediones also improve insulin sensitivity and may exert numerous nonglycemic effects in patients who have type 2 diabetes mellitus 19,20 . Additional clinical trials are being conducted to evaluate whether treatment of diabetes mellitus with agents that reduce insulin resistance, such as the thiazolidinediones, is superior to treatment with agents that stimulate insulin secretion, such as the sulfonylureas.

Selection of antihypertensive drug in diabetes mellitus

ACE inhibitors, nondihydropyridine CCBs, TDs, and bBs reduced CV complications in patients who had diabetes and hypertension in several long-term, large, RCTs (Tables 3 and 4). Limited data is available with direct comparisons of various drugs in diabetic, hypertensive patients (Table 5). INSIGHT 70 ) that newer agents, such as ACE inhibitors and CCBs, are better than diuretics and bBs in reducing CV events in treating hypertension in the general population. Because diabetes is an important and independent risk factor for CV morbidity and mortality and because most diabetics die of CV complications 1 , subgroup analysis of diabetic, hypertensive patients in these trials revealed that most required multiple drugs for adequate control of their BP. In the CAPPP trial, diabetic patients who were on captopril had less cardiac mortality and all-cause mortality than did those who were on bBs or TDs 26 . The report did not further divide the impact of captopril over bBs or TDs. However, the...

Diabetes as a coronary heart disease riskequivalent

Based on the observations from several epidemiologic studies, diabetes is designated a coronary heart disease (CHD)-risk equivalent by the National Cholesterol Education Program's Adult Treatment Panel III (ATPIII) 1 . The 10-year risk of major CHD events in patients who have diabetes is greater than 20 this is comparable to the rates that are observed in nondiabetic patients who have established CHD. This inference has been borne out, particularly by data from a population study in Finland 2 and a multi-national study, the Organization to Assess Strategies for Ischemic Syndromes 3 , of patients who had type 2 diabetes who frequently had multiple, coexisting risk factors for cardiovascular disease (CVD). The increased risk for CHD may precede the clinical diagnosis of diabetes by many years. This was documented best in the long-term study of more than 117,000 women in the Nurses' Health Study nearly 6000 women developed diabetes during 20 years of follow-up. There was an approximately...

Lipoprotein abnormalities associated with diabetes

Diabetes is associated with multiple disturbances in lipoprotein metabolism that are triggered by insulin deficiency, insulin resistance, and hyperglycemia 6,7 . The diabetic dyslipidemia of type 2 diabetes and insulin resistance is characterized several interrelated abnormalities, including triglyceride-rich lipoproteins (very low density lipoprotein VLDL , intermediate density lipoprotein IDL , and remnant particles), low high-density lipoprotein (HDL) cholesterol, and small, dense low-density lipoprotein (LDL) particles. There is an increase in the lipid-rich, large VLDL upregulation of hepatic sterol regulatory element binding protein-1, which stimulates de novo lipid synthesis and increased availability of free fatty acids, all of which probably are linked with insulin resistance 7 . The activity of lipoprotein lipase is suppressed which leads to reduced catabolism of triglyceride-rich particles, whereas hepatic lipase activity is increased which facilitates the compositional...

Evidence from lipid lowering trials in diabetes

Given the heterogeneity of lipoprotein and the complexity of lipoprotein metabolism in patients who have diabetes, the optimal approach for lipid management remains to be determined. Over the past 10 years, a variety of randomized, controlled trials with hydroxymethylglutaryl-coenzyme A reductase inhibitors (statins) established the efficacy of these LDL-lowering agents in reducing cardiovascular outcomes. In four of these large trials (Scandinavian Simvastatin Survival Study 4S , Cholesterol and Recurrent Events CARE , Long-term Intervention with Pravastatin in Ischemic Disease LIPID , and Air Force Texas Coronary Atherosclerosis Prevention Study AF-CAPS TexCAPS ), subgroup analyses revealed similar coronary artery disease risk reductions in smaller numbers of diabetic patients compared with the general population. (Table 1) 15-21 . The most recent and largest trial (more than 20,000 subjects) was the Heart Protection Study (HPS) which randomized 5963 patients who had diabetes 22,23...

The Collaborative Atorvastatin Diabetes Study

A Primary Prevention Trial, Collaborative Atorvastatin Diabetes Study (CARDS), exclusively in patients with type 2 diabetes who had one additional risk factor was recently published 28 . A total of 2838 patients, age range 40-75 years, were randomized to 10 mg atorvastatin versus placebo and followed over a mean period of 3.9 years. In this trial, the mean LDL-cholesterol level was 118 mg dL, which was reduced by 40 in the drug treated group. The combined primary end-points of acute CHD events, coronary re-vascularization or stroke were reduced by 37 (P 0.001), whereas stroke events were reduced by 48 , and total mortality by 27 (P 0.059). The risk reductions were independent of baseline lipid levels and in post-hoc analyses 743 patients with baseline LDL < 100 mg dL had a 26 reduction in major cardiovascular events, which is consistent with the results in the HPS 25 . Fig. 1. Effects of simvastatin on first major vascular event in patients who do or do not have diabetes according...

Lipid goals in patients who have diabetes

Diabetes is a CHD-risk equivalent, as defined by the ATPIII recommendations. Based on the evidence from the LDL-lowering clinical trials that were summarized above, most patients who have diabetes should have an LDL goal of less than 100 mg dL (Table 3). If LDL is grater than 130 mg dL, treatment with LDL-lowering drugs should be initiated simultaneously with therapeutic lifestyle changes (TLC) to achieve the LDL goal 1 . The American Diabetes Association (ADA) has the same recommendations for LDL goal 42 . In addition, the ADA recommends a triglyceride goal of less than 150 mg dL and an HDL cholesterol goal of greater than 40 mg dL in men and greater than 50 mg dL in women (see Table 3). According to ATPIII, however, when triglyceride levels are elevated (200-499 mg dL) after achieving LDL goal, non-HDL cholesterol should be the secondary target of therapy. No HDL goal is specified in ATPIII because of the lack of sufficient evidence. It is recommended that if HDL remains low after...

Role of combination therapy in diabetes and dyslipidemia

Despite the known pharmacologic effects of fibrates and nicotinic acid in ameliorating the underlying defects of diabetic dyslipidemia (increased triglyceride-rich lipoproteins low HDL cholesterol small, dense LDL particles), the role of combining these agents with statins remains uncertain and further clinical trials are needed. Trials like the VA-HIT and DAIS are supportive of the potential of adding fibrates to statins because combined lipid disorders are common in patients who have insulin resistance and type 2 diabetes. In short-term studies, statins and fibrates were more effective in normalizing all lipid abnormalities than either agent alone without significant risk for adverse events, including myositis 51,52 . Caution should be exercised in patients who have potential drug interactions (eg, cyclo-sporin, antifungal agents, protease inhibitors, erythromycin) or renal disease. Long-term trials of combination therapy with statins and fenofi-brate are in progress (Table 5)....

The burden of diabetes

Type 2 diabetes is a complex chronic disease with increasing microvascular and macrovascular complications imposing a significant public health and economic burden 1 . Even though a number of efficacious treatments are available, suboptimal applications of these in clinical practice has led to gaps in diabetes prevention and management. Barriers for providers include time constraints, forgetfulness, a perception of patients as noncom-pliant, and inadequate knowledge of outcomes from clinical trials. Barriers for patients include inadequate comprehension of the gravity of the disease, little motivation toward prevention of diabetes and its complications, insufficient time, and lack of socioeconomic resources and support 2-4 . The prevalence of diabetes has increased by 61 from 1990 to 2001 with type 2 diabetes accounting for 95 of this increase 5 . The annual cost of the disease is estimated at 132 billion accounting for more than 10 of the United States healthcare expenditure....

Clinical studies on renin angiotensin aldosterone system inhibition and outcomes of new onset diabetes

ACE inhibitors and ARBs have been studied extensively in hypertension, congestive heart failure, coronary artery disease, and renal disease (Table 6). Both drugs consistently reduce risk of coronary events (particularly ACE inhibitors), stroke, and diabetic complications of microvascu-lar disease. In addition, secondary endpoints of some of these studies have suggested reduced incidence of new-onset diabetes. In the Heart Outcomes Prevention Evaluation (HOPE), the incidence of diabetes was 34 lower in the ramipril-treated group than in the group receiving placebo 29,96 . In the LIFE study comparing losartan with atenolol for treating hypertension with left ventricular hypertrophy, losartan was associated with a 25 reduction in new-onset diabetes compared with atenolol 33,98 . Even in the more recent Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial, the incidence of new-onset diabetes was significantly lower in the lisinopril arm than in the chlorthalidone...

Coronary revascularization in diabetics

Diabetic patients who have coronary artery disease have significantly worse long-term outcomes compared with nondiabetic patients. The reasons for this are complex but relate, in part, to more extensive atherosclerosis, an increased risk of thrombosis, overexpression of mitogenic cyto-kines, higher oxidative stress, glycated end products, larger and more activated platelets, and more rapid progression of disease. Patients who have diabetes experience higher perioperative mortality rates compared with nondiabetics who undergo bypass surgery (CABG) 1,2 or percutaneous coronary intervention (PCI) 3,4 . Although outcomes after revascularization in diabetics are worse after either modality, CABG seems to be preferable to PCI in most patients who have multi-vessel disease (Fig. 1).

Prevention of Cardiovascular Outcomes in Type Diabetes Mellitus Trials on the Horizon

ADivisions of Endocrinology and General Medicine and Clinical Epidemiology, Diabetes Care Center, University of North Carolina School of Medicine, CB 7110, 5039 Old Clinic Building, Chapel Hill, NC 27599-7110, USA bDalla,s Diabetes and Endocrine Center, 7777 Forest Lane, C-618, Dallas, TX 75230, USA cUniversity of Texas Southwestern Medical School, Dallas, TX, USA Type 2 diabetes mellitus is a clinical syndrome characterized by hyperglycemia in which early cardiovascular (CV) death is the predominant clinical outcome. In the last 20 years several clinical trials have demonstrated unequivocally techniques that reduce the risk for CV events in patients who have diabetes mellitus these studies form the basis for current guidelines regarding management of patients who have diabetes mellitus, specifically in the areas of lipid modification, blood pressure reduction, modulation of the renin-angiotensin system, antiplatelet therapy, and invasive revascu-larization procedures. Despite the...

Insulin resistance syndrome metabolic perspective

Reaven's original description of the metabolic syndrome consisted of obesity, insulin resistance, hypertension, impaired glucose tolerance or diabetes, hyper-insulinemia, and dyslipidemia characterized by elevated triglyceride and low HDL concentrations.1 All these features serve as risk factors for atherosclerosis and thus metabolic syndrome constitutes a significant risk for coronary heart disease2-5 (Table 2.1). The features of obesity or overweight and insulin resistance also provide significant risks for developing type 2 diabetes.5,6 The risks for CHD and diabetes with metabolic syndrome are greater than those for simple obesity alone without insulin resistance and therefore the understanding of the pathogen-esis and, through it, a rational approach to its therapy are of prime importance.

Global And National Prevalence Of Type Diabetes

The prevalence of diabetes has now been described in many different countries and settings, enabling a good understanding of global disease patterns. Interestingly, most of these large population-based studies do not differentiate between type 1 and type 2 diabetes and simply report the prevalence of all cases of diabetes. However, on the assumption that type 2 diabetes accounts for approximately 90 of all cases of diabetes, these data can be accepted as providing reliable information on type 2 diabetes. The large numbers of published prevalence reports has allowed several estimates to be made of the global and country-specific burden of diabetes. Recent publications from the World Health Organization (1) and from the International Diabetes Federation (2) have provided data on the current numbers of people with diabetes, and projections for the year 2025 (Fig. 1 and Color Plate 1, following p. 34). Table 1 indicates that although the methods of the 2 estimates are somewhat different,...

Effects of FFAs on local and systemic inflammation and link to insulin resistance

Elevated FFAs cause ectopic lipid deposition in nonadipose tissue, and this lipotoxicity may induce a pro-inflammatory response, which in turn may negatively interfere with insulin signalling. Supporting this concept, the use of high dose salicylate has been proven to decrease plasma glucose in type 2 diabetic patients (236). The molecular basis of this observation relies on decreased activity of a serine kinase called IkB kinase p (IKKP) of the NFkB signalling pathway (237), and subsequent impaired phosphorylation of IRS-1 and PI3Kinase (238). The link between IKKp and FFAs in insulin resistance has been further supported by the report that, in rats, salicylate prevents the deleterious effects of lipid infusion on muscle glucose metabolism and insulin secretion (238). In a recent report Cai and colleagues showed that obesity- or high fat-induced hepatic lipid deposition is accompanied by increased NFkB activity in the liver (239). Studies of genetically modified mice with either...

Ethnic Groups and Type Diabetes

Various ethnic groups in the United States have different rates of diabetes, mainly due to cultural, societal, and environmental reasons. Genetics had also been thought to play a large role, but a recent study by Australian and U.S. researchers seems to have changed that belief. When it comes to diabetes, we're finding that genes are no more important for ethnic minorities than for anyone else, said Stephanie Fullerton, a population geneticist and bioethicist at the University of Washington and coauthor of the study. Factors such as poor diet, housing segregation, and poverty were stronger indicators of the disease than genetic inheritance. Native Americans have the highest rates of diabetes not only in this country but in the world. This means that the disease and its complications are major causes of death and health problems for them. Amputations, a complication of diabetes, are three to four times higher in Native Americans than in other ethnic groups. African Americans are 1.7...

Are Insulin Pumps Risky for Teens

Scientists from the Food and Drug Administration (FDA) have found that insulin pumps may pose risks for adolescents. Their review discovered thirteen deaths and more than fifteen hundred injuries related to the pumps over a decade. Sometimes the pump did not work correctly, but teens also took risks with their pumps or were careless, dropping their pumps or not taking proper care of them. Two teens may have tried to commit suicide by giving themselves too much insulin through their pumps. Teens like the pumps, which are worn on the body and send insulin into the body through a tube inserted under the skin, because they eliminate the need to inject insulin manually several times a day. However, teens using the pumps must still frequently monitor their blood sugar and adjust their insulin intake through the pump. Doctors are advised to carefully screen their diabetic teen patients to make sure they are able to use and care for their insulin pumps correctly. Because diabetic teens can be...

Exercising with Diabetes

In general, the best time to exercise is when glucose peaks, about sixty to ninety minutes after eating. This timing provides enough energy, allows calories to be burned, and avoids high blood sugar after eating. Also important is to learn how to determine the right insulin dosages before, during, and after exercise. Why Too much insulin before a workout can lead to too-low blood sugar, or hypoglycemia, while not enough insulin can cause too-high blood sugar, or hyperglycemia. Stress and heat can affect the blood glucose insulin balance, so these factors must also be taken into account. A good idea is to have some carbohydrates available during exercise in case blood sugar needs to be raised quickly. Eating carbohydrates helps to prevent hypoglycemia. And exercising with a partner who knows what to do in case of a diabetic emergency can add a safety factor as well as make exercise more fun.

Autoimmunity In Type Diabetes

The presence of circulating islet autoantibodies can be used to identify p-cell autoimmunity and therefore confirm the diagnosis of type 1 diabetes. Diabetes was originally hypothesized to be an autoimmune disease for a number of reasons, including familial clustering with other organ-specific Table 2(ii).1 Clinical features of type 1 compared with type 2 diabetes. Type 1 diabetes Type 2 diabetes Plasma insulin C-peptide diseases such as thyroid autoimmunity. Autopsy studies showed that lymphocytic infiltration was evident in the pancreatic islets of patients with type 1 diabetes.9 The concept of type 1 diabetes as an autoimmune disease emerged in the mid-1970s with the identification of islet cell antibodies (ICA) in 1974 by Botazzo et al10 and Nerup et al,11 establishing HLA associations for genetic susceptibility to the disease. Not all p-cell loss is due to demonstrable autoimmunity, a fact which has led to the subclassification of type 1 diabetes into type 1a, related to...

Latent autoimmune diabetes in adults

Screening patients clinically diagnosed with type 2 diabetes who are not treated with insulin has identified a significant subgroup with evidence of p-cell autoimmunity.45,46 They appear to have a slowly progressive form of type 1 diabetes that has been termed latent autoimmune diabetes in adults (LADA).47 A substudy of the UKPDS identified that LADA has a frequency of approximately 10 of all adult-onset diabetes,48 and 94 of patients aged < 45 years with ICA required insulin 6 years after diagnosis, compared with 14 of the antibody-negative patients. The diagnosis of LADA is based on a combination of clinical and immunological features. The key features are gradual onset diabetes in adult life and detectable islet autoantibodies, most commonly GADAb. The presence of GADAb has been associated with a slightly lower body-mass index (BMI) than typically seen in type 2 diabetes patients,48 although it is not possible to specify a cut-off point BMI for the diagnosis of LADA. In contrast...

Genetics Of Type Diabetes

The concordance of type 1 diabetes in monozygotic twins is 30-40 , compared with 5 in siblings. This indicates the importance of genetic factors in the development of the disease,50 (Table 2(ii).2) but at the some time this intermediate level of concordance shows that non-genetic or environmental factors must also be involved. Transmission of type 1 diabetes is considered to be polygenic, meaning that several genetic loci are associated with an increased risk of diabetes. Non-Mendelian or polygenic inheritance and the probable heterogeneity of type 1 diabetes have contributed to the complexity of type 1 diabetes genetics. Table 2(ii).2 Lifetime risks of type 1 diabetes in first-degree relatives (proband diagnosed before 20 years of

Definition Of Diabetic Nephropathy Dn

The structural features of DN were described originally by Kimmelstiel and Wilson in 1936 as a glomerulopathy with diffuse and or nodular intercapillary glomerulosclerosis.9 The nodular changes are still considered specific for diabetes, although the diffuse lesions are also seen in other renal diseases. It was recognized that these ultrastructural changes were accompanied by increases in proteinuria. However, progress in the field was slow until the development of sensitive immunoassays for urinary albumin10 and the demonstration that increases in albuminuria are detectable several years before changes occur in total proteinuria.11-13 Although DN may be defined by both functional and structural criteria, functional criteria alone are generally used in clinical practice. The major functional parameter of DN is albumin excretion rate (AER), which may increase more than 100-fold during the evolution of DN (for example from 10 to 1000 g min). Biphasic changes in glomerular filtration...

Familial Aggregation Of Diabetic Nephropathy

The strongest evidence for an inherited susceptibility to diabetic nephropathy comes from studies showing that some families in particular have an increased risk of renal disease. A family history of nephropathy (or premature cardiovascular disease as its surrogate) continues to be the most accurate and available marker for identifying patients most at risk, with familial aggregation now described for nephropathy in both type 17-8 and type 2 diabetes.9,10 The diabetic offspring of parents with diabetes and proteinuria have three to four times the prevalence of nephropathy compared to the siblings of diabetic parents without renal disease.7,8 The risk appears to be further increased if both parents have diabetic nephropathy, as opposed to only one parent with albuminuria (Figure 4.1).9 This has led to the suggestion that the predisposition to diabetic nephropathy may be inherited as a dominant trait.7,11 In addition to proteinuria, familial aggregation has also been demonstrated in the...

Lipids And Diabetic Nephropathy

Dyslipidaemia is also an important component of the development of diabetic complications such as nephropathy.45 Triglycerides, intermediate-density lipoproteins, remnant-like particles and postprandial lipaemia are all increased in patients with albuminuria.46 In addition, low-density lipoprotein size is decreased in diabetic nephropathy. These changes may be apparent before the development of albuminuria.47 Several studies have correlated the presence of an abnormal lipid profile with the onset and progression of diabetic nephropathy.4849 Research in atherosclerosis disease has long established the importance of the genetic influences on lipid metabolism. It is therefore plausible that some of these modifiers may also contribute to the development and progression of diabetic renal disease. An example of the risk associated with inherited dyslipidaemia may be demonstrated in experimental studies using mice in whom the gene for apolipopro tein E (Apo E) has been 'knocked out'. These...

Insulin And Nephropathy

Insulin sensitivity, while contributing to glycaemic control, is also a strong independent predictor of the development of diabetic nephropathy. This effect is not confined to patients with type 2 diabetes. There are now data describing the role of insulin sensitivity in the development of complications in type 1 diabetes.59 An association between insulin sensitivity and diabetic nephropathy may be inferred from the strong link between insulin sensitivity and cardiovascular mortality. In addition, markers of insulin resistance, such as triglyceride levels and waist to hip ratio, are also risk factors for albuminuria. Insulin sensitivity may also be genetically determined. Yip et al59 described familial clustering of insulin sensitivity in type 1 diabetes. Insulin resistance is also more common in the relatives of patients with nephropathy than in the relatives of patients with diabetes and normoalbuminuria. Similar findings have been reported in type 2 diabetes.60 In this context,...

The Reninangiotensin System Ras And Diabetic Nephropathy

The pivotal role of the RAS in the pathogenesis of diabetic nephropathy has long been recognized. This is perhaps best manifested by the unique protective effects conferred by inhibitors of the RAS in diabetic renal disease.68 In experimental models, upregulation of the RAS in the setting of diabetes is associated with accelerated nephropathy. In the transgenic (mRen-2)27 rat, a mouse Ren-2 gene is inserted into the genome of a Sprague-Dawley rat, resulting in the overexpression of renin at sites of normal physiological expression69 and activation of the intrarenal RAS.70 The induction of diabetes in this model results in progressive renal pathology with features similar to human diabetic nephropathy (Figure 4.4). Similarly, insertion of multiple copies of the human angiotensin-converting enzyme (ACE) gene into transgenic mice results in increased proteinuria in response to diabetes, correlating with plasma ACE activity.71 These studies suggest that genetic modifications in the RAS...

Growth hormone GH and insulinlike growth factors IGFs

Table 5.2 Growth hormones and cytokines that have been implicated in the pathogenesis of diabetic kidney desease list of different components of the growth hormone-insulin-like growth factor (GH-IGF) axis, transforming growth factor p (TGF-P) system, and vascular endothelial growth factor (VEGF) system and known or potential inhibitors of these systems.

Other Types Of Diabetes

There are less common forms of diabetes in which there is a specific cause for the beta cell failure or problems with insulin function. Some of these conditions are extremely rare, so I discuss only the more common ones in the following sections. Diabetes Due to Gene Mutations Maturity onset diabetes of the young (MODY) refers to diabetes that occurs in childhood or adolescence (before age twenty-five) and is inherited in an autosomal dominant fashion that is, if you have the condition, half of your children are also likely to have it. About one in one hundred people with diabetes have MODY. There are six known genetic defects for this kind of diabetes. One of the genetic defects (called MODY 2) is in the gene that enables the beta cells to sense the body's glucose level (the glucose kinase gene) and so regulate insulin release. MODY 2 is usually easily controlled with oral medications that stimulate insulin release. People with this type of diabetes are usually not obese. About one...

Certified Diabetes Educator

The certified diabetes educator (CDE) will educate you about the kind of diabetes you have and your medication options. She will educate you about the importance of controlling glucose, lipids, and blood pressure to prevent complications and about the effects of exercise and emotions on glucose control. She will also show you how to use glucose monitors, how to treat high and low glucose levels, and how to exercise safely. If you are on insulin, she will teach you how to inject insulin and how to use your insulin pens or pumps.

Diabetes Medicine Combinations

Many people with diabetes are on more than one medicine to control glucose levels, and pharmaceutical companies make combination pills that is, a pill containing two different diabetes medicines. Since many insurance companies make their customers pay a part of the cost of each prescription (a copayment), the combination pill has the benefit of eliminating one of the copayments. However, the disadvantage of these combinations is that you lose some of the flexibility of adjusting the individual doses of the medicines. Also, if you need to discontinue one of the two medications, you may have to go back to the doctor and get a prescription for the single medicine that you are continuing. The combination pill usually has a different name, and often patients (and physicians) forget that the pill contains two different medicines. If you are prescribed a combination pill, make sure that you are not taking both a combination pill and one of the components of the combination pill as a separate...

Fastacting Insulin Preparations

There are four fast-acting insulin preparations Regular insulin Insulin lispro Insulin aspart Insulin glulisine Table 6-9 Characteristics of the Currently Available Insulins Table 6-9 Characteristics of the Currently Available Insulins Insulin Preparations Insulins lispro, aspart, glulisine Insulin glargine Insulin detemir

The Technical Side of Regular Insulin

Regular insulin consists of aggregates of six molecules of insulin complexed to two zinc ions (a hexamer). After subcutaneous (under the skin) injection, the regular insulin hexam-ers become diluted by the tissue fluids and become monomers (single molecules), which then enter the circulation and have their effects. a shorter period of time about four hours (rather than six hours). These properties make these insulins more effective at controlling the glucose rise after meals. Clinical studies have shown that when these insulin analogs are used in an optimal manner, you can achieve improved glucose control with less risk of hypoglycemia. However, there are some cautionary notes first, because the peak level of the insulin with the analogs is higher after a meal, it is important for you to be more precise in counting the carbohydrates you are consuming. Regular insulin is more forgiving of errors in carbohydrate counting. Also, if you were to consume a very fatty meal, which delays...

Longacting Insulin Preparations

There are three long-acting insulin preparations NPH insulin Insulin glargine (brand name Lantus) Insulin detemir (brand name Levemir) Mixing regular insulin with a fish protein called protamine forms a crystal (neutral protamine Hagedorn, NPH), which dissolves slowly when injected subcutane-ously, so that the effect on average lasts for about eight hours (shorter duration for very small doses and longer duration for large doses). The crystals of NPH insulin appear white to the naked eye, and they tend to settle in the insulin vial. This is why you should mix the NPH insulin (by rolling the bottle between the palms of your hands) before drawing it up in the syringe. Insulin glargine is human insulin that is modified so that it is soluble in a more acidic solution. It looks clear in the bottle, and when injected it precipitates in the tissues and is then slowly released into the bloodstream. Since it is acidic, the manufacturer recommends it should be given as a separate injection and...

Using An Insulin Pump

An insulin pump is a device the size of a pager. It contains a syringe or reservoir filled with a fast-acting insulin, a battery-powered syringe plunger, and a small computer to control the insulin delivery. The syringe is attached to tubing, which in turn is attached to a small plastic tube (cannula) inserted under the skin (see Figure 6-1). The pump can be programmed to put tiny drops of insulin into the subcutane- Figure 6-1 Insulin Pump ous tissues every three to ten minutes day and night this is the basal insulin. When you eat, you can program the pump to give a bolus of insulin for the food. Thus, when you are on the pump, you use only a fast-acting insulin to provide both your basal and bolus needs. Often, people with type 1 diabetes will decide to go on an insulin pump for their diabetes control. The pump does not check glucose levels, nor does it decide how much insulin to give. It does allow you to tailor your basal insulin to your needs. With a pump, you are better able to...

Setting Up Your Insulin Pump

Show you how to fill a reservoir without getting bubbles and how to prime the tubing. An inch of bubble in your tubing is equivalent to half a unit of insulin. Thus, having bubbles in your tubing can reduce the amount of insulin you are getting and can lead to high glucose levels. Once the tubing is primed, you can insert the infusion set and attach the tubing. A 0.3- to 1.0-unit bolus may be needed to fill the dead space in the infusion set. The pump trainer should teach you how to use a pump using saline (salt water, as opposed to insulin). Ideally, you should do this for about a week before your planned initiation of insulin in the pump. During this time, you can practice changing sets, filling reservoirs, priming tubes, and adjusting basal and bolus doses.

The Cure for Type Diabetes

A pancreas transplant will cure type 1 diabetes. So why doesn't everyone with type 1 diabetes get a pancreas transplant There are two reasons. First, there are only a limited number of donor pancreata available a few thousand whereas there are about a million people with type 1 diabetes. Second, people who get an organ transplant have to be on medicines to prevent the body's immune system from attacking and rejecting the organ. These immunosuppressive medicines have serious side effects, such as making the individual more susceptible to infections and increasing the risk of developing a cancer in the future. You are likely to be offered a pancreas transplant if you have kidney failure and you are on a list for a donor kidney. Because getting two organs simultaneously has additional risks, some restrictions do apply. For example, if you have a history of heart attacks or strokes, you may not be a candidate for simultaneous pancreas-kidney transplant. A pancreas transplant alone that...

Nutrition in Type Diabetes

Most people with type 1 diabetes are of normal body weight, and they usually do not need to be on a calorie-restricted diet. They also do not tend to have the cholesterol abnormalities that are commonly seen in patients with type 2 diabetes. The American Diabetes Association recommends that an adult should obtain These recommendations also apply to lean individuals without diabetes. In other words, this is a normal, healthy diet. You should have a good idea of how much carbohydrate you are going to eat at a meal, because it will affect how much insulin you should take before the meal. Estimating the carbohydrate content of a meal is called carbohydrate counting or carbohydrate exchange. You need two pieces of information to count carbohydrates

Your Diet for Type Diabetes

People with type 2 diabetes are frequently overweight, so advice about nutrition is directed not only at controlling carbohydrate intake, but also at limiting calories. (I discuss caloric restriction and weight loss in Chapter 10.) If you have type 2 diabetes, there are several reasons why you still need to estimate the carbohydrate content of your food Abnormalities in insulin secretion mean that eating a high-carbohydrate meal results in high glucose levels immediately after the meal. You want to avoid these high postmeal glucose levels because they can contribute to increases in HbA1c levels (see Chapter 5). If you are using insulin injections, you need to count carbohydrates in order to adjust your insulin doses (just like people with type 1 diabetes). According to the ADA, a normal, healthy diet for people with diabetes should consist of The glucose rise after eating is due to the carbohydrates in the meal, and therefore all people with diabetes should learn carbohydrate...

Adjust the Insulin Dose

Before exercise, adjust the bolus or basal insulin, or both, in anticipation of the exercise. A bolus of a fast-acting insulin analog lasts for about four hours, and the peak is at about one to one and a half hours. If you exercise within two hours, you will need to cut back on the premeal bolus (to 50 to 75 percent of your usual dose). Making an adjustment in basal insulin dosing is easier if you are on an insulin pump. If you are planning for exercise of long duration (longer than ninety minutes), you may want to cut back the amount of your basal insulin for up to two hours before the exercise. If you are participating in competitive sports, you may find that the adrenaline rush means that you may have to increase your basal insulin temporarily for up to two hours before the exercise. Adjusting the basal dosage of the long-acting insulins like glargine or detemir is trickier you can try cutting back to 50 to 80 percent of the dose on the days you exercise. Any high glucose levels...

Exercise and Type Diabetes

If you have type 2 diabetes and you are on insulin, you will face issues similar to those of a person with type 1 diabetes (see the tips and advice in the preceding section), except that generally, your glucose levels will be more stable. This is principally because most patients with type 2 diabetes still have functioning beta cells in their pancreas, with a significant contribution of their own insulin. If you take oral diabetes medications, you cannot assume that your health will be fine when you exercise if you take sulfonylureas, nateglinide, or repaglinide, you can get low glucose levels with exercise. Prepare for this by taking your meter and some glucose tablets or juice with you. If hypoglycemia occurs when you exercise, talk to your doctor about reducing the dose of your sulfonylurea medication.

Managing Diabetes Supplies

Take adequate supplies for your diabetes management when you travel. In fact, take twice the amount of diabetes medication and supplies that you will normally need. If you are on an insulin pump (see Chapter 6), take some basal insulin such as insulin glargine and syringes in case you have a pump failure. Keep the insulin cool by packing it in an insulated bag with refrigerated gel packs, or use Frio packs (see friouk.com index.php). You should also carry a travel letter from your doctor explaining that you have type 1 or 2 diabetes and the medications you are using to treat it. This note should also include the medicines you are taking for other conditions as well as any food and drug allergies you have. Also obtain a spare prescription for all your medications in case you lose your supplies or your stay is prolonged. Wear your MedicAlert bracelet at all times, and carry a card or letter explaining that you have diabetes written in the languages of the places you are visiting. Keep a...

Diabetes Management on the Airplane

If food will not be served on your flight, take food and fast-acting carbohydrate with you. If it is a long flight with a meal (and keep in mind that in-flight meals are rare these days), it is not necessary to order a special meal on the plane, but it is a good idea to have some food with you (two to three snacks) in case the meal is delayed. Inject your insulin dose after your meal arrives. Since the pressure in an airplane is different than the pressure on the ground, do not inject air into the vial before drawing up your insulin into the syringe. Check your blood glucose frequently during the flight. You may need a little more insulin because you are inactive. If you are traveling alone and are concerned that you might experience hypoglycemia, tell the flight attendants that you have diabetes so they can keep an eye on you.

What to Do if You Get Sick and Are on Insulin

Do not stop your insulin depending on the severity of the illness you may need the same or more insulin. If you have type 1 diabetes and you stop the insulin, you will go into DKA (see Chapter 3). If you are on a basal-bolus insulin regimen, take the same amount of the long-acting insulin as you normally do. If you are on a pump, keep the basal rates the same. Cover your carbohydrates with insulin in the usual way. If you have vomiting and you are not sure if you will keep the food down, you can give the insulin for the carbohydrates afterward. Correct any high glucose levels with fast-acting insulin analogs. If you have type 2 diabetes and are on premixed insulins twice a day, you may take the same amount of insulin if you know that you can keep some food down. If you are not sure that you will be able to eat, check with your doctor you may need to cut back on your premixed insulin to 50 to 75 percent of the dose. Contact your medical team (see Chapter 4) or go to the emergency room...

Diabetes and Pregnancy

Diabetes complicates about 8 percent of pregnancies each year. About 75 percent of these diabetic pregnancies are gestational diabetes that is, the woman is diagnosed as having diabetes during the pregnancy. Of the remaining, 23 percent involve preexisting type 2 diabetes and about 1 to 2 percent involves preexisting type 1 diabetes. The issues surrounding preexisting diabetes are slightly different from those faced by women who first develop diabetes during pregnancy. Women who have diabetes before they become pregnant have to deal with glucose control at conception and early in pregnancy. If there are any diabetes-related complications, these may also have an impact on the pregnancy. Women who have gestational diabetes are faced with learning all about diabetes, including watching their diet and taking insulin, while pregnant. This chapter gives you details on both situations.

The Risk of Your Child Developing Diabetes

Prospective parents may be fearful of transmitting diabetes to their children. The risk of transmitting type 1 diabetes is quite low (6 percent if the father has type 1 diabetes and 3 percent if the mother has type 1 diabetes). The risk of transmitting the genetic risk is higher in type 2 diabetes if the mother has type 2 diabetes, the risk is about 18 percent, increasing to 50 percent if both parents have type 2 diabetes. The environment, however, plays a bigger role in the development of type 2 diabetes, regardless of the genetic risk.

Complications of Diabetes

Two aspects of diabetes complications need to be considered when a woman is contemplating pregnancy. First, there is the impact of the pregnancy on diabetic corn- Diabetic retinopathy New diabetic retinopathy can suddenly appear during pregnancy, and retinopathy that is already present can get worse. There are two possible reasons for the deterioration First, if your diabetes control has been poor and you suddenly tighten it over a short period Diabetic kidney disease If you have kidney disease secondary to your diabetes, pregnancy can make the kidney disease worse. Often the kidney disease will recover after delivery, but it may not if the prepregnancy kidney failure is more severe. Women with diabetic kidney disease who are contemplating pregnancy should therefore consider getting an opinion from a nephrologist (kidney doctor). Preeclampsia Preeclampsia is a serious condition where there is severe elevation in blood pressure, fluid retention, and protein loss. It occurs more often...

Treatment of Diabetes During Pregnancy

Although there is evidence that oral glyburide is safe in pregnancy, the current practice is to have women control their diabetes with insulin when they are pregnant. If you have type 2 diabetes and you are using oral agents for your diabetes, you will be switched over to insulin before you start trying to get pregnant. Not all insulins, however, are approved for use during pregnancy. The fast-acting insulin analogs insulin lispro and insulin aspart are safe. Currently, the only long-acting insulin used during pregnancy is NPH. Recently, a small study of insulin glargine used in thirty-two pregnancies did not show any problems. There is no information about using insulin detemir during pregnancy. least three months to achieve this. You may need to visit your diabetes team every two to three weeks during this time. Once you have stable glucose levels in the target range, with a normal HbA1c, then you can try to get pregnant. Once you are pregnant, your care will be transi-tioned to a...

Gestational Diabetes

During pregnancy, women are screened for diabetes at twenty-four to twenty-eight weeks, or at the very first visit if they are at very high risk of diabetes as indicated by the following risk factors There are family members with diabetes. Her ethnic background is a group that is particularly susceptible to diabetes. She had diabetes with a previous pregnancy or delivered a baby weighing more than nine pounds. There are two tests that can determine whether a woman has gestational diabetes. The first test is performed on all non-high-risk women at the twenty-four to twenty-eight week visit. If this test is normal, no further testing is necessary. If this first test is positive, however, a second test is performed about a week later. First test One-hour 50-gram glucose challenge screening test. In this test you take a drink that contains 50 grams of glucose (there is no need to fast beforehand). The blood glucose level is checked after one hour. If your glucose level is greater than 130...

Public Schools and Diabetes Training

In the United States, the schools or day care centers that receive public funds are legally required to provide training to school staff on treating diabetes. The ADA has literature for teachers and child-care providers. Your health-care team can also help ensure that the staff members at your child's school are adequately trained. The degree of supervision by the staff of the school will vary with your child's age and abilities. may limit insulin use in order to lose weight. This leads to poor diabetes control and is harmful. Late adolescence ages fifteen to nineteen At this age your child will manage his or her diabetes fairly independently. You can help by guiding your teen to improve his or her coping skills and transition to full independence for college or work. Diabetes can impact the adolescent issues of smoking, alcohol, risky behaviors, and sexual activity. Smoking increases the risk for diabetes complications. Let your teenager know how alcohol causes hypoglycemia and what...

Adjusting Insulin Doses

Insulin dosages are based on weight of your child in kilograms (1 kg is equal to 2.2 pounds). The doses vary based on whether the child is in the honeymoon phase or not and whether he or she is going through puberty. During the honeymoon phase, your child will need very little insulin, and a simple insulin regimen with two or three injections a day may suffice. The basal insulin needs may be as low as 0.125 units per kilogram. The ratio for carbohydrate might be 1 unit of insulin for 60 to 75 grams carbohydrate, and your child may not need any insulin for corrections. Once the honeymoon phase is over, your child's basal insulin needs may go up to 0.25 units per kilogram, and the insulin to carbohydrate ratio may go up to 1 unit for 15 to 60 grams carbohydrate. He or she may also need insulin for correction, for example, 1 unit for every 50 to 200 mg dl blood glucose over her target. When your child goes through puberty, the insulin needs go up substantially this is principally because...

Type Diabetes in Children

The number of children that have type 2 diabetes is on the rise. Accurate numbers about how many children have this condition are hard to obtain, because the disease may have been present for a while before it is diagnosed. Anywhere between 8 to 46 percent of children with diabetes referred to pediatric centers have type 2 diabetes. The increase in childhood obesity is likely to be the main factor driving this increased incidence of type 2 diabetes. Your child might be diagnosed with diabetes during routine screening or because she may be unwell. The American Diabetes Association recommends screening any overweight child (more than 120 percent ideal body weight, body mass index greater than 85 percent) who has two of the following features Strong family history of type 2 diabetes (parents, siblings, uncles, aunts, grandparents, nephew, niece, half sibling) Evidence for insulin resistance or presence of conditions associated with insulin resistance, such as darkening of the skin under...

Treatment For Type Diabetes In Children

The treatment options for children with type 2 diabetes are the same as those available for adults with type 2 diabetes. They include diet, exercise, and oral and inject- able medications including insulin. The problem with medications is that there is limited information about their long-term use in children.

How Diabetes Impacts Diseases of Aging

Elderly people with long-standing diabetes are more likely to have kidney disease, nerve damage, and circulation problems such as heart disease and stroke. They are less able to walk, do housework, prepare meals, and manage money when compared to age-matched individuals who do not have diabetes. Women with diabetes become disabled at approximately twice the rate of women without diabetes, and they have an increased risk of falls and hip fractures. Long-standing diabetes can affect bone quality, and diabetes increases the risk of fractures with falls. Neurological deterioration is greater in people with diabetes they are more likely to develop memory problems and have more rapid deterioration in memory with time. Part of the reason for the more severe deterioration in cognitive function may be the effect of diabetes on the blood vessels and increased risk of small strokes.

Institutional Aspects of Diabetes

Elderly people living in board and care and nursing facilities may have additional challenges regarding their diabetes management. They may have to rely on caregiv-ers to check their glucose levels and administer their diabetes medications. They may not have control over their meals. The staff may have limited understanding of diabetes management because type 2 diabetes is so much more common, people tend not to remember that older individuals can have type 1 diabetes. These type 1 patients may not get adequate insulin bolus for their meals. Due to limited supervision, sophisticated insulin basal-bolus regimens may not be realistic, and some level of control may have to be sacrificed for safety. In these situations, insulin injections once or twice a day may have to suffice. I would encourage family members to remain actively engaged in helping manage their elderly relative's diabetes care, and with their physician, carefully devise recommendations for the nursing staff in the...

Treatment of Diabetes Complications and Associated Disorders

Diabetes complications in elderly people are treated in the same ways as in younger individuals. Treating the lipid abnormalities (see Chapter 3) and blood pressure is equally beneficial in the elderly as in younger individuals. In fact, because the risk for heart attack and stroke is higher in the elderly, benefits may actually be greater than in the younger population. The blood pressure target is less than 140 80 if tolerated. ACE inhibitors and angiotensin receptor blockers (ARBs) can be used to lower blood pressure, but these medicines can raise the potassium and serum creati-nine levels. High potassium levels can be dangerous and affect the heart rhythm. Therefore, your doctor will ask you to get lab tests one week after you start taking these medicines to make sure that your potassium is in the safe range. Often, elderly people are on many different medications because they are being treated for other medical problems as well. In these situations, you need to watch out for drug...

Newly Diagnosed Type Diabetes

When you are first diagnosed with type 1 diabetes, you will meet your diabetes management team, which consists of your physician, the diabetes educator, and the nutritionist. The physician will answer your questions about diabetes and recommend an initial insulin regimen. The nutritionist will teach you about carbohydrate counting, give you a carbohydrate exchange book (the ADA publishes a good one), and explain The diabetes educator will teach you how to use a glucose monitor, how to keep a logbook, and how often you should monitor your glucose levels and will set your target glucose levels. She will also teach you how to draw up insulin in a syringe and give an injection. Even if you were prescribed insulin pens from the start, you should still know how to draw up insulin in a syringe just in case a pen is not available. The educator will go over the symptoms of low glucose reactions and how to treat them. She will also show you how glucagon works and instruct you and a family...

Established Type Diabetes

Currently, there is no way of preventing the decline in insulin secretion that occurs with time in those with type 1 diabetes. The honeymoon period can last only a few weeks, or it can last for more than a year or two. Generally speaking, children and young adults tend to have shorter honeymoons, whereas older individuals can maintain insulin secretion for several years. There are, however, many exceptions to this observation. As your insulin secretion declines, you will need more insulin to control the glucose. You may find that your glucose values drift upward overnight. This is a good time to add some long-acting basal insulin. Usually only a few units (2 to 3) of insu lin glargine or detemir might be necessary to start with, but then the doses go up with time. The ratios of insulin for carbohydrate and for correction also change, and more insulin is needed. The amount of insulin that you need will vary according to your age and weight a teenager going through puberty will need...

Optimizing Your Basal Insulin Dose

Ideally, if your basal insulin (insulin glargine, detemir, NPH, or pump basal) dose is correct, then even if you did not eat and had your normal activity, your glucose levels will stay in the normal range. This is usually not true in practice, and there is always some drift in your glucose levels. This is because of the day-to-day variability in the absorption of the injected insulin and the way the body responds to the insulin. Your goal is to minimize the upward and downward drift of your glucose levels. So, how do you determine if your basal insulin dose is correct You do this by looking at your glucose levels after eliminating the variables of food, exercise, and bolus insulin. Usually, overnight is the easiest time to assess your basal insulin needs Provided your glucose at bedtime is in the safe range say 100 to 150 mg dl, then you can set your alarm and check blood glucose levels at 2 a.m. and then again at 6 a.m. and 9 a.m. If your glucose levels drift up or down, you need...

Optimizing Your Bolus Insulin Dose

Once you are satisfied with your basal glucose control, you can look at the bolus insulin. Before you can do this, you have to know how to count carbohydrates (see Chapter 8). The way you assess your bolus ratio for carbohydrates is to eat your usual meal and give the calculated dose of insulin. Then check your blood glucose after the meal and find out how high it goes you are trying to keep it below 180 mg dl. Check three times, and if the glucose goes much higher than 180 consistently, you need to increase the ratio. For example, if you gave 1 unit for 15 grams carbohydrate at breakfast, try using 1 unit per 12 grams of carbohydrate, and check again. Sometimes, if you change the ratio, you find that your peak after the meal is below 180 mg dl, but then you go low later on. If this happens, you have a number of options Why do you have a correction insulin bolus The correction insulin is to correct the drift upward in your glucose levels because the basal insulin is not perfect. The...

Cohort Studies of People with Diabetes

The Framingham study, which has provided the foundation for so much of cardiovascular epidemiology over the past five decades, was one of the first to follow people with diabetes over time. From 1948 onwards over 5000 residents from the town of Framingham in Massachusetts were followed-up for mortality and morbidity. A cohort of people with diabetes was a subgroup of this population (Garcia etal., 1974 Kannel and McGee, 1979). About the same time a cohort of over 21 000 people with diabetes was also being followed-up from the Joslin Clinic in Boston (Kessler, 1971). Both of these cohort studies began within a decade or so of the introduction of insulin, and both studies reported a significant excess risk of death from CVD in patients with diabetes. Early studies rarely distinguished between patients with type 1 and type 2 diabetes. A recent meta-analysis (Kanters etal., 1999) was conducted to determine an estimate of mortality and the incidence of CVD events. Of the 27 studies that...

Cardiovascular Disease and Diabetes

Diabetes, both type 1 and type 2, is increasing in prevalence and it is estimated that three million individuals in the UK will have type 2 disease by 2010 (Gale, 2002 Fisher, 2003). Overall the numbers of people with type 2 far exceed those with type 1 and, in addition, they are usually middle aged or elderly and often present with concomitant CVD risk factors. However, comments such as 'Diabetes mellitus, and particularly non-insulin dependent diabetes mellitus increases the risk for all manifestations of vascular disease' (Laakso, 1998) and 'CVD complications occur more often in patients with NIDDM than in patients with IDDM' (Laakso and Lehto, 1997) can easily be misconstrued. Epidemiological studies measure outcome in a number of different ways. While absolute numbers can be counted, other measurements, adjusted for the size of the group, are more commonly used. For example, a rate (of an event) can be calculated as the number of such events per 100 000 people per year. Another...

Mortality from Cerebrovascular Disease Type diabetes

Clinical aspects of stroke disease in people with diabetes are described in Chapter 7. Mortality from cerebrovascular disease is barely mentioned in epidemiological studies of patients with type 1 disease and usually only gets a passing mention in studies of patients with type 2 diabetes (Barrett-Connor and Khaw, 1988 Manson etal., 1991 Moss etal., 1991 Lehto etal., 1996). Cerebrovascular disease is generally manifest in later years and most cohort studies of younger patients do not continue follow-up beyond their 40s. Further, cerebrovascular disease complications are not as frequent as heart disease and many studies will therefore be too small, with too few events, to draw any conclusions. This lack of data has led some to suggest that 'in the patient with insulin-dependent diabetes mellitus the frequency of stroke and death from stroke is less than in the patient with non-insulin dependent diabetes mellitus' (Bell, 1994). None the less it is a significant cause of mortality in...

Gender and cardiovascular risk in diabetes

One of the features of CVD complications in patients with diabetes that has been highlighted by epidemiological studies, and is of particular interest, is the relationship between CVD risk and gender. Mortality from cerebrovascular disease in the general population does not vary between the sexes. Although the rates are higher in the patients with type 1 diabetes these also do not differ between men and women except in the oldest age group where mortality from stroke appears to be a bit higher in women. Similar studies of patients with type 2 diabetes have also suggested that the stroke rate or the increased risk of stroke might be slightly higher for women at older ages. In contrast mortality from heart disease in the general population is higher in men than women at all ages, and premenopausal women have a degree of cardioprotection as CHD rates remain low at this age. This premenopausal protection appears to be completely lost in young women with type 1 diabetes and CHD mortality...

What is Insulin Resistance

The fundamental role of insulin is to facilitate cellular uptake of glucose in skeletal muscle and to limit hepatic gluconeogenesis, the other key determinant of steady-state plasma glucose levels. In the steady (or fasted) state the quantity of insulin required to maintain a plasma glucose level depends on muscle mass and hepatic glucose output. However, there is more than a twofold variation in the plasma insulin levels required to maintain identical plasma glucose levels in normal subjects (Hollenbeck and Reaven, 1987). This variation in insulin requirement for glucose disposal has been termed Figure 2.2 As insulin resistance worsens with age, the pancreas is often able to secrete increasing amounts of insulin over many years to maintain glucose homeostasis. In susceptible individuals, the pancreas eventually becomes 'exhausted' and subsequently glucose concentrations rise into the diabetic range. However, an array of other risk factor abnormalities such as elevations in...

Multiple roles of insulin

One way to better understand the link between many risk parameters and elevated risk for type 2 diabetes is to appreciate that insulin imparts its effects on many tissues, not just skeletal muscle and liver but also adipose, endothelium and immune cells (Ritchie etal., 2004 Bloomgarden, 2005 Reaven, 2005). Thus, insulin is relevant not simply to glucose uptake and metabolism, but it also helps maintain endothelial homeostasis, with a net vasodilatory effect in insulinsensitive subjects It can thus be seen that a partial failure of insulin action, or a resistance to its normal actions at each of these tissues, could lead to a spectrum of metabolic abnormalities that individually and collectively accelerate the atherogenic process. Each of these pathways is now discussed in greater detail. It is important to appreciate that insulin may also have some apparent 'deleterious' actions but that the balance of effects is always protective in insulin-sensitive subjects. This is discussed later...

Endothelial function measures as predictors of diabetes or in prediabetes

There is a wealth of data suggesting a potential role for endothelial dysfunction in insulin resistance (Fonseca and Jawa, 2005). Although the direction of causality remains somewhat debated, circulating elevations in several endothelial-derived factors, cell adhesion molecules and t-PA, have been shown to predict risk for type 2 diabetes independently of other predictors (Meigs etal., 2006). Similar results have been seen with physiological tests of endothelial function. For example, Steinberg etal. (1996) showed that severely obese (mean body mass index 34kg m2) insulin-resistant individuals with normal glucose tolerance have the same degree of impairment in blood flow and vascular reactivity as those people with established type 2 diabetes. Similarly, when Caballero etal. examined endothelial function and vascular reactivity in two groups at risk for developing type 2 diabetes, subjects with impaired glucose tolerance and subjects with normal glucose tolerance but with a parental...

Elevated acutephase markers in subjects at risk of type diabetes

There are now robust data showing elevated inflammatory markers in obese men and women and in obese children. In addition, several other groups at risk of diabetes -including women with polycystic ovarian syndrome (PCOS), men and women of South Asian origin, Pima Indians, women with a family history of type 2 diabetes, and sedentary individuals - exhibit elevated inflammatory levels and do so independently of total body mass index (Ziegler, 2005 Sattar, 2006a). Markers of inflammation correlate with insulin resistance and predict type 2 diabetes, independently of other risk factors in several different populations (ARIC, WOSCOPS) (Schmidt etal., 1999 Freeman etal., 2002). Hence, it is clear that inflammatory perturbations predate diabetes by several years, and as such are potentially relevant to accelerated atherogenesis. The source for higher cytokine and acute-phase protein levels in pre-diabetes and diabetes remains unclear but will include adipocytes, endothelial cells and immune...

Haemostatic Changes in Type Diabetes

A full description of the haemostatic changes in diabetes is beyond the scope of this chapter and the reader is referred to some recent reviews on this topic (Juhan-Vague etal., 2002 Grant, 2003). In simple terms, however, it is clear that type 2 diabetes is a pro-coagulant state, increasing the chance of vessel thrombosis and therefore acute coronary syndrome. This pro-coagulant and pro-thrombotic state is manifest through many arms of the coagulation process, including abnormal platelet function, increased levels of coagulation factors and decreased levels of endogenous anticoagulants. Some of these changes are intimately linked to endothelial dysfunction. For example, endothelial dysfunction results in decreased release of prostacyclin and NO - factors that normally inhibit platelet aggregation within normal vessels. Endothelial dysfunction also increases platelet activation by the release of von Willebrand factor. Fibrinogen and Factor VII levels are also increased in diabetes...

Effects of Antidiabetic Drugs on Risk Factor Pathways

Of interest, there is now abundant evidence that insulin-sensitising therapies appear to offer benefits beyond just glucose lowering. Metformin, for example, has positive effects on FFAs, HDL-cholesterol, PAI-1 and vascular function, and may also lower markers of inflammation (Grant, 1995 Grant, 2003 Haffner etal., 2005). Glitazones also benefit each of the above parameters, although their actions on HDL-cholesterol and inflammatory parameters are more pronounced and in addition they tend to raise adiponectin and lower the proportion of small, dense LDL particles (Haffner etal., 2002). By contrast, sulphonylureas have far less and often negligible effects on such markers. Such observations emphasise once again the multiple linkages of insulin resistance on other risk factor pathways. They also concur with the greater benefits of metformin (and to a lesser extent glitazones) on CVD risk (Johnson etal., 2005 Evans etal., 2006). It is clear that by targeting glucose alone without...

Pharmacological Treatment of CHD in People with Diabetes

In the management of stable angina pectoris the first aim of treatment is to relieve symptoms (morbidity) by reducing myocardial oxygen demand, with a further aim of reducing mortality if possible. Nitrates, calcium channel blockers and the potassium channel opening agent nicorandil are all of symptomatic benefit. In the IONA study nicorandil reduced hospital admissions with angina (IONA Study Group, 2002). Eight per cent of the study subjects had diabetes, and there was similar benefit in the diabetes subgroup (IONA Study Group, 2004). As in non-diabetic subjects there are relatively few data that show prognostic benefit of pharmacological treatments for patients with stable angina, in contrast to patients following acute myocardial infarction (see Chapter 4). The most compelling evidence for prognostic benefit in diabetic subjects comes from subgroup analysis of multicentre studies for beta-blockers and ACE inhibitors, and from subgroup and meta-analysis of antiplatelet therapy.

Summary of findings comparing CABG with PTCA in diabetic patients

Recurrent ischaemia leading to angina, repeat revascularisation and cardiac mortality is more common after PTCA than with CABG, because PTCA more commonly results in incomplete revascularisation and an appreciable risk of ischaemia. Incomplete revascularisation is an independent predictor of adverse outcome (Cowley etal., 1993). Whilst several trials have found CABG to be superior to PTCA in diabetes (O'Keefe etal., 1998 Weintraub etal., 1998, 1999), whereas one other trial (Halon etal., 2000) and the Duke University registry (Barsness etal., 1997) did not. Overall, surgical revascularisation for multivessel CHD in diabetic patients, particularly in insulin-treated patients, is associated with a survival advantage compared with PTCA. However, studies with long-term follow-up beyond 10 years have indicated that the survival benefits of surgery may be attenuated. van Domburg etal. (2002) reported on 1041 surgically treated patients (8 diabetes) and 704 (11 ) medically treated patients...

Clinical trials of stents versus CABG involving diabetic patients

The Coronary Angioplasty versus Bypass Revascularisation Investigation (CABRI) was one of the largest trials of PTCA versus CABG and had follow-up over a 4-year period (Kurbaan etal., 2001). Complete revascularisation was mandatory, and in the percutaneous group new devices such as atherectomy or stents were allowable at the operator's discretion. A total of 1054 subjects, of whom 125 (12 ) had diabetes, were randomised to CABG or PTCA 37 of the CABG group received an IMA graft. Diabetic patients had a higher mortality rate than non-diabetic patients. Diabetic patients randomised to PTCA had a higher mortality rate than diabetic patients randomised to CABG (CABG vs. PTCA 8 63(12 ) vs. 14 62(23 )). Post-revascularisation angiographic evidence of residual CHD was consistently significantly greater in PTCA than in respective CABG subgroups. At 1 year, diabetic patients treated with stenting had the lowest event-free survival rate (63 ) because of a higher incidence of repeat...

Registry information for PCI with stenting in diabetic patients

Other data also suggest that outcomes after PCI can be similar to those after CABG in diabetic patients with multivessel CHD. In one registry of 9586 patients (n 1714 (18 ) diabetes), 970 patients had multivessel disease CABG was performed in 318 (33 ), PCI in 351 (36 ) and 301 (31 ) were treated medically (Kapur etal., 2003). In-hospital mortality was 3 in the CABG group and 2 in the PCI group, and 1-year mortality was 7 in the CABG group, 9 in the PCI group and 10 in the medical

Predictors of restenosis after stenting in diabetic patients

Intravascular ultrasound studies have shown that restenosis in both stented and non-stented lesions is due to intimal hyperplasia (Kornowski etal., 1997 Levine etal., 1997 Van Belle etal., 1997), which is a smooth-muscle-cell proliferative response. In one series of 241 patients (n 63 with diabetes) who had 251 native lesions stented, follow-up angiography with intravascular ultrasound demonstrated the late lumen loss was more pronounced in both stented and non-stented lesions of diabetic patients (Kornowski etal., 1997). Results from registries and clinical trials indicate that diabetic patients have an increased risk of restenosis, repeat revascularisation and death after PCI (Rozenman etal., 2000 Van Belle etal., 2001). A useful retrospective study of clinical trial participants was performed at the Cardialysis Core Laboratory in Rotterdam (West etal., 2004). Restenosis occurred in 550 of 2672 (21 ) non-diabetic and 130 of 418 (31 ) diabetic patients (P < 0.001). Reduced body...

Glycoprotein IlbIIIa inhibitor therapy and PCI in diabetic patients

The Evaluation of Platelet IIb IIIa Inhibition in Stenting (EPISTENT) trial was designed to assess the role of platelet GpIIb IIIa blockade for use in elective stenting (Marso etal., 1999). A total of 2399 patients with ischaemic heart disease and suitable coronary artery lesions were randomly assigned to stenting plus placebo (n 809 173 diabetes (21 )), stenting plus abciximab (n 794 162 diabetes (20 )), or balloon angioplasty plus abciximab (n 796 156 diabetes (20 )). The primary endpoint was a combination of death, MI or need for urgent revascularisation in the first 30 days, and this occurred in 87 (11 ) of patients in the stent plus placebo group, 42 (5 ) in the stent plus abciximab group and 55 (7 ) in the balloon plus abciximab group. In diabetic patients, the primary endpoint occurred in 12 of patients who received stent plus placebo compared with 6 in diabetics who received stent + GpIIb IIIa inhibitor therapy (P 0.04). These results indicated that platelet GpIIb IIIa...

Impact of antidiabetic therapies on coronary intervention

Thiazolidinediones improve insulin sensitivity, particularly in skeletal muscle, the liver and adipocytes (see Chapter 11). In a randomised study of troglitazone in consecutive diabetic patients undergoing elective PCI, 55 patients with 60 lesions were randomised to troglitazone (n 30 stents) or control (conventional therapy, n 26) (Takagi etal., 2002). Treatment with troglitazone reduced angiographic in-stent restenosis and target lesion revascularisation rates after coronary stent implementation, and serial intravascular ultrasound assessment demonstrated a reduction in neointimal tissue proliferation in the troglitazone group. A case-control study involving 83 patients with type 2 diabetes randomised patients to either rosiglitazone (8mg daily pre-PCI and 4mg daily thereafter) or placebo. Angiographic follow-up was performed at 6 months. The restenosis rates were 18 in the rosiglitazone group and 38 in the control group (P 0.002). The minimum lumen stent diameter was 2.49 (0.88)mm...

Prevalence of CHF in populations with diabetes

Approximately 12 of patients with diabetes in general population studies have CHF (Figure 5.1) (Nichols etal., 2001 Thrainsdottir etal., 2005), and in diabetic No Diabetes Diabetes Figure 5.1 The prevalence of CHF in men and women in the Rekjavik population study. Reproduced from Thrainsdottir IS, Aspelund T, Thorgeirsson G, Gudnason V, Hardarson T, Malmberg K et al. (2005). The association between glucose abnormalities and heart failure in the population-based Reykjavik study. Diabetes Care 28 612-16. All large-scale clinical trials on glycaemia in patients with diabetes have either excluded patients with CHF by design (UK Prospective Diabetes Study (UKPDS) Group, 1998 The Diabetes Control and Complications Trial Epidemiology of Diabetes Interventions and Complications (DCCT EDIC) Study Research Group, 2005) or not reported CHF as a co-morbidity.

Prevalence of diabetes in populations with CHF

The prevalence of diabetes in populations with left ventricular systolic dysfunction (LVSD) varies from 6 to 25 (Table 5.1) (McDonagh etal., 1997 Morgan etal., 1999 Davies etal., 2001 Hedberg etal., 2001 Raymond etal., 2003 Redfield etal., 2003 Kistorp etal., 2005). In population studies of CHF, the prevalence of diabetes in patients with CHF was between 12 and 30 (Table 5.2) (Amato etal., 1997 Mosterd etal., 2001 Thrainsdottir etal., 2005). The absolute numbers of patients with diabetes who also suffer from CHF in these epidemiological studies are small, making further groupings by age and gender inaccurate. In populations of patients hospitalised with CHF, the prevalence of diabetes is greater than that found in general population studies (Table 5.3). The prevalence of diabetes Table 5.1 The prevalence of diabetes in populations with and without left ventricular systolic dysfunction (LVSD). Table 5.1 The prevalence of diabetes in populations with and without left ventricular...

Incidence of CHF in patients with diabetes

Chronic heart failure is more common in patients with diabetes than in those without diabetes. In the NHANES and Framingham studies, the incidence of CHF in patients with diabetes was two- and fourfold higher than in patients without diabetes (Kannel etal., 1974 He etal., 2001). A UK case-control study also found that both male and female patients with diabetes have a twofold greater risk of developing CHF than those without diabetes (Johansson etal., 2001). In the USA, a retrospective study of 9951 patients with diabetes, matched with patients without diabetes, found an incidence of CHF in patients with diabetes 2.5 times that of those without diabetes (30.9 vs. 12.4 cases per 1000 person-years) (Nichols etal., 2004). In a UK population of patients with diabetes, the incidence of CHF was 21 cases per 1000 person-years (Maru etal., 2005). Over 4 years, 39 of elderly nursing home residents with diabetes developed CHF compared to 23 of those without (Aronow and Ahn, 1999). This high...

Incidence of diabetes in patients with CHF

There is only one study of the incidence of diabetes in a population with CHF outwith clinical trials. In a group of elderly Italians with CHF, the 3-year incidence of new-onset diabetes was 28.8 compared to 18.3 in matched controls without CHF (Amato etal., 1997). Of the patients with CHF in the placebo arm of the CHARM study, 7.4 (n 202) developed diabetes over a median follow-up of 3.1 years (Yusuf etal., 2005). A single-centre substudy of the SOLVD trial found an incidence of diabetes in the treatment arm of 5.9 (n 9) over a mean of 2.9 years (Vermes etal., 2003).

Risks of Developing CHF and Diabetes Which patients with diabetes develop CHF

Diabetes is an independent risk factor for the development of CHF (Kannel etal., 1974 He etal., 2001 Thrainsdottir etal., 2005). In the Framingham study, for those between the ages of 45 and 74 years the presence of diabetes increased the risk of CHF in men by twofold and in women by fivefold (Kannel etal., 1974). This effect was even more apparent in the younger age group. Under the age of 65 years, diabetes increased the risk of developing CHF by four- and eightfold for men and women, respectively. In the NHANES study, diabetes was an independent risk factor for CHF with a hazard ratio of 1.85 (1.51-2.28, P< 0.001) (He etal., 2001). In Iceland, the age-adjusted odds ratio for development of CHF in those with diabetes compared to those without diabetes was 2.8 (2.2-3.6) (Thrainsdottir etal., 2005), and several other studies have identified diabetes as an independent risk factor for CHF (Aronow and Ahn, 1999 Chen etal., 1999 Iribarren etal., 2001). In populations with diabetes there...

Risk of developing diabetes in patients with CHF

Patients with advanced CHF (i.e. those in New York Heart Association (NYHA) classes III and IV) appear to have a greater risk of developing diabetes than those with milder symptoms (i.e. those in NYHA class II). In a subgroup analysis of 630 patients with CHF secondary to CHD in the Bezafibrate Infarction Prevention (BIP) study, NYHA class III was an independent risk factor for diabetes while NYHA class II was not (Tenenbaum etal., 2003). In an Italian longitudinal study of 1339 elderly patients, CHF was an independent predictor of diabetes (Amato etal., 1997). The association of CHF with diabetes was greater in patients in NYHA III and IV than those in NYHA I and II.

Chronic Heart Failure and Abnormalities of Insulin and Glucose Metabolism

The prevalence of diabetes in populations with CHF has already been discussed. Insulin resistance, impaired fasting glucose and hyperinsulinaemia in the absence of diabetes are also common in CHF (Paolisso etal., 1991, 1999 Swan etal., 1994, Suskin etal., 2000). Hyperinsulinaemia, impaired glucose tolerance and insulin resistance are risk factors for CHF, independent of diabetes and other established risk factors (Ingelsson etal., 2005 Nielson and Lange, 2005). A substudy of RESOLVD measured fasting glucose and insulin concentrations in 663 patients with NYHA class II-IV CHF (Suskin etal., 2000). Of these patients 27 had diabetes. Of the 'non-diabetics' 11 met diagnostic criteria for diabetes, 12 had impaired fasting glucose concentrations and 34 had elevated plasma insulin concentration and insulin resistance (Figure 5.2). The presence of insulin resistance, hyperinsulinaemia or impaired fasting glucose was associated with lower functional capacity and more severe CHF symptoms....

The sympathetic nervous system SNS and insulin resistance

Patients with CHF have persistent activation of their sympathetic nervous system (SNS) (Reaven etal., 1996 Scherrer and Sartori, 1997), and excessive activation of the SNS might lead to insulin resistance. In normal individuals, adrenaline infusion leads to acute insulin resistance (Scherrer and Sartori, 1997). Insulin increases skeletal muscle uptake of glucose. In healthy subjects, acute SNS activation decreases glucose uptake by skeletal muscles. Unloading of cardiopulmonary receptors, a manoeuvre that leads to selective reflex sympathetic activation in skeletal muscle, reduces insulin-induced stimulation of muscle glucose uptake by up to 25 (Scherrer and Sartori, 1997). Stimulation of -receptors in humans increases lipolysis, resulting in raised plasma free fatty acid (FFA) levels (Schiffelers etal., 2001). In normal subjects infusion of norepinephrine results in increased plasma levels of FFAs (Marangou etal., 1988). In patients with CHF, norepinephrine concentrations have been...

Effects of diabetes on the myocardium

Both systolic and diastolic abnormalities have been demonstrated in patients with diabetes without symptomatic evidence of cardiovascular disease. These abnormalities correlate with duration of diabetes and evidence of retinopathy neuropathy (Annonu etal., 2001). A full review of the molecular processes occurring in the heart of patients with diabetes is outwith the scope of this chapter and has been reviewed elsewhere (Taegtmeyer etal., 2002 Young etal., 2002). There are many putative metabolic mechanisms of the effect of diabetes on the myocardium, but most have been demonstrated in animals rather than in patients with CHF Hyperinsulinaemia - In rats, insulin stimulates an increase in myocardial mass (Holmang etal., 1996). Insulin may be a myocardial growth factor, increasing myocardial hypertrophy. in diabetes. For example, in the myocardium of dogs with diabetes, cross-linking of collagen and subsequent deposition in the myocardium leads to increased chamber stiffness (Jyothirmayi...

Treatment of CHF in Patients with Diabetes The diagnosis of diabetes in clinical trials of CHF

Various definitions of diabetes are used in clinical trials of CHF. For example, in ATLAS only those receiving medical therapy for diabetes were considered as having diabetes (Ryden etal., 2000) whereas in SOLVD the diagnosis was based on self-reporting by the patient or documentation in the patient's medical records (Shindler etal., 1996). The unrecognised prevalence of diabetes and impaired glucose tolerance in RESOLVD suggests that it is likely that many patients with unrecognised abnormalities of glucose metabolism are included in the major trials of CHF. The diagnostic criteria for diabetes in clinical practice are described in Chapter 11.

Role of reninangiotensin system in diabetes mellitus and vascular complications

Local formation of angiotensin II by tissue-based renin-angiotensin systems in cardiac, renal and vascular tissues represents an important pathophysiological mechanism that is upregulated in diabetes. Short-term moderate hyperglycaemia without glycosuria during the early stages of diabetes is linked with increased plasma renin activity, mean arterial pressure and renal vascular resistance (Miller etal., 1996) with activation of circulating and local renin-angiotensin systems. In animal models of diabetes, inhibition of the renin-angiotensin system with ACE inhibitor (Candido etal., 2002) or angiotensin receptor blocker (Candido etal., 2004) has been shown to prevent atherosclerosis independent of blood pressure reduction. Improvement in insulin sensitivity follows ACE inhibition (Pollare etal., 1989 Berne etal., 1991 Donnelly, 1992 Ferrannini etal., 1994), particularly in hypertensives with type 2 diabetes (Torlone etal., 1991, 1993). Many of the initial reports were based on...

Risk of Diabetes Mellitus with Antihypertensive Drugs

Individuals with hypertension, whether treated or untreated, are at increased risk of developing type 2 diabetes. In treated hypertensive subjects, compared with those who received no antihypertensive therapy, the risk of development of diabetes was not significantly altered with ACE inhibitors, calcium channel blockers or thiazide diuretics. Only those treated with beta-blockers were of increased risk of developing diabetes (Gress etal., 2000). Figure 6.5 Intensive strategies to control blood pressure, lipids and glucose. Kaplin-Maier estimates for the composite endpoint of nephropathy, retinopathy, neuropathy and death from cardiovascular causes. Reproduced from Gaede P, Vedel P, Larsen N etal. (2003). Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes. New England Journal of Medicine 348 383-93. Copyright Massachusetts Medical Society. All rights reserved. Epidemiological studies and clinical trials support the causal link between use of...

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