diabetestalk.net

Which Diabetes Is An Autoimmune Disease?

An Autoimmune Condition

An Autoimmune Condition

There are many pointers to an immune-mediated basis for human type 1 diabetes. These include the association of type 1 diabetes with other autoimmune disorders and with the HLA system, which modulates immune responses; lymphocytic infiltration of the islets in post mortem human pancreas (insulitis); evidence of cell-mediated and humoral immunity directed against islet constituents; transfer experiments in animals, evidence of transmission of diabetes from marrow donors to recipients; recrudescence of autoimmunity in pancreatic grafts between identical twins; and preservation of beta cell mass and function by immune interventions. Evidence that type 1 diabetes is immune-mediated One of the earliest pointers to an autoimmune aetiology was the observation that other autoimmune conditions were over-represented in juvenile cases of diabetes and their relatives, but not in late-onset cases. Type 1 diabetes overlaps with autoimmune thyroid disease, coeliac disease, Addison’s disease and pernicious anaemia among other organ-specific autoimmune conditions (see Figure 1). Autoantibodies directed against islet constituents precede the onset of clinical disease by many years and can be used to predict it; they are present in 95% of newly presenting patients. Moreover, they are also more prevalent in first degree relatives of patients than in the general population (Figure 2). Several islet antigens have been characterised, and these include insulin itself, the enzyme glutamic acid decarboxylase (GAD), protein tyrosine phosphatase (IA-2) and the cation transporter ZnT8. Animal models of autoimmune diabetes such as the non-obese diabetic (NOD) mouse have been extensively studied. The observation that treatment with immunosuppressive agents such as ciclosporin prolongs beta cell sur Continue reading >>

Type 2 Diabetes: Is It An Autoimmune Disease?

Type 2 Diabetes: Is It An Autoimmune Disease?

For decades, doctors and researchers have believed type 2 diabetes is a metabolic disorder. This type of disorder occurs when your body’s natural chemical processes don’t work properly. New research suggests type 2 diabetes may actually be an autoimmune disease. If that’s the case, new treatments and preventive measures may be developed to treat this condition. Currently, there isn’t enough evidence to fully support this idea. For now, doctors will continue to prevent and treat type 2 diabetes with diet, lifestyle changes, medications, and injected insulin. Read on to learn more about the research that’s being done and the implications it may have on the treatment and prevention of type 2 diabetes. Type 2 diabetes has historically been viewed as a different type of disease from type 1 diabetes, despite their similar name. Type 2 diabetes occurs when your body becomes resistant to insulin or can’t produce enough insulin. Insulin is a hormone that moves glucose from your blood to your cells. Your cells convert glucose to energy. Without insulin, your cells can’t use glucose, and symptoms of diabetes can occur. These symptoms may include fatigue, increased hunger, increased thirst, and blurred vision. Type 1 diabetes, sometimes called juvenile diabetes because it’s often diagnosed in children and teens, is an autoimmune disease. In people with type 1 diabetes, the immune system mistakenly attacks the healthy tissues of the body and destroys the insulin-producing cells of the pancreas. The damage from these attacks prevents the pancreas from supplying insulin to the body. Without an adequate supply of insulin, cells can’t get the energy they need. Blood sugar levels rise, leading to symptoms such as frequent urination, increased thirst, and irritability. E Continue reading >>

Could Diabetic Retinopathy Be An Autoimmune Disease?

Could Diabetic Retinopathy Be An Autoimmune Disease?

Summary Diabetic retinopathy is a common and progressive complication of diabetes mellitus. It is characterized by the loss of pericytes, hypertrophy of basement membrane, microaneurysms formation, increased vascular permeability, capillary occlusions, neovascularisation and fibrovascular proliferation. The pathogenesis of diabetic retinopathy is still insufficiently understood, although some reports have implicated the role of the immune system. We hypothesize that, according to some current data diabetic retinopathy could also be considered as an autoimmune disease. The finding of antipericyte and antiendothelial cell autoantibodies in the circulation of diabetic patients strongly suggests that some autoimmune activity has been involved in the early pathophysiology of diabetic retinopathy. There is even more evidence that implicates the presence of autoimmune mechanisms in the proliferative stage of this disease: elevated levels of tumor necrosis factor-α, interleukin-8 and soluble interleukin-2 receptor in the serum of diabetic patients, increased vitreous concentration of the interleukin-6 and interleukin-8 in patients with proliferative retinopathy. Furthermore, preretinal membranes in diabetic patients contain deposits of immunoglobulins, activated complement components, monocytes, T and B lymphocytes, fibroblastes and lymphokynes. In diabetic patients human leukocyte antigen DR and DQ expression on the retinal vascular endothelial cells as well as on pigment and nonpigment epithelial cells was found. These antigens are normally restricted to immunocompetent cells and play an important regulatory role in the immune response. Their aberrant expression has been found on nonlymphoid cells in various autoimmune diseases whilst abnormal expression of DR and DQ antigen Continue reading >>

Type I (insulin-dependent) Diabetes Is A Th1- And Th2-mediated Autoimmune Disease

Type I (insulin-dependent) Diabetes Is A Th1- And Th2-mediated Autoimmune Disease

Type I (insulin-dependent) diabetes (IDDM) is an autoimmune disease with an unknown etiology but with a definite outcome, resulting in the progressive misdirected immunologic destruction of insulin-secreting pancreatic β islet cells by autoreactive leukocytes and their mediators (3). Even though the precise cause of the disease remains unclear, a combination of genetic, immunologic, and nongenetic factors contributes to the onset and progression of IDDM (3, 52). Specific HLA antigens, in particular DR3 and DR4, have been associated with increased risk for IDDM development (52, 89), while DR2 alleles generally have been described as “protective” of IDDM (86). In addition to HLA predisposing factors, viral infection (8), psychological factors (73), and dietary factors (8), among others, have been described as predisposing factors. Other investigators failed to demonstrate a strong cause-and-effect link between these factors and IDDM, which highlighted the need for further investigation and identification of causative agents and mechanisms underlying the pathogenesis of IDDM (77). The frequent coexistence of IDDM with immune disorders is well established and results from an inherent dysregulation in humoral immunity and cell-mediated immunity (3, 8). This is exemplified by the presence of autoreactive antibodies targeting select β-cell constituents and other autoantigens (23,28), circulating autoreactive T cells (78, 80), heightened expression of adhesion molecules (37, 60), reduced levels of serum cytokine inhibitors (57), and sustained expression of cytokines and their high-affinity receptors (36, 82). The development of hyperglycemia, a hallmark of IDDM, appears at later stages of the disease, months or years after the initiation of targeted autoimmune destruction Continue reading >>

Autoimmune Diseases (ad) | Natural Remedies & Treatments

Autoimmune Diseases (ad) | Natural Remedies & Treatments

Autoimmune Diseases (AD) Symptoms of AD Why Diagnosing AD Difficult Risk Factors of AD Root Causes of AD The Vaccine Issue Inflammation Connection Autoimmunity Pathogenesis Systemic Lupus Pathogenesis Guillain-Barré Pathogenesis Sjögren's Syndrome Pathogenesis AD and Type 2 Diabetes AD Wellness Program: 10 Steps AIP & AD Nutritional Program AIP & AD Nutritional Strategies AIP & AD Super Meal Plate AIP & AD Supplementation AD Lifestyle Changes Do you feel tired all the time? Are you struggling with losing weight no matter what you try to do? Or, are you losing unwanted weight? Do you feel bloated or constipated a lot of the time? Do you have any digestive problems? Do you have skin rashes or dry skin? Do you have cold hands or feet? Are you struggling with your blood sugar even when you eat right? Is your hair or skin thinning out too quickly? Are you taking thyroid medication? Do your joints or muscles ache? Do you have brain fog or problems with concentrating? Do you have any numbness or tingling in your hands or feet? Do you have any allergies or frequent colds or flu? Do you have any problems sleeping or waking up feeling dead-tired? If you answered "yes" to 3 or more of the questions, you may want to consider getting a complete physical exam that includes a full hormone panel and antibody tests -- to make sure that you're not in the early stages of an autoimmune dysfunction. If you've already has a complete physical and your doctor can't come up with a clear diagnosis, then, you may still be in the early stages of an autoimmune dysfunction. I know that may sound a little far-fetched, but, autoimmune disorders are on the rise and have exploded over the past 7-10 years, affecting everyone from babies to children, teens, young adults, older adults, and especially wom Continue reading >>

I've Been Diagnosed With Lada — Latent Autoimmune Diabetes In Adults. What's The Difference Between It And Other Forms Of Diabetes?

I've Been Diagnosed With Lada — Latent Autoimmune Diabetes In Adults. What's The Difference Between It And Other Forms Of Diabetes?

Latent autoimmune diabetes in adults (LADA) is a slow progressing form of autoimmune diabetes. Like the autoimmune disease type 1 diabetes, LADA occurs because your pancreas stops producing adequate insulin, most likely from some "insult" that slowly damages the insulin-producing cells in the pancreas. But unlike type 1 diabetes, with LADA, you often won't need insulin for several months up to years after you've been diagnosed. Many researchers believe LADA, sometimes called type 1.5 diabetes, is a subtype of type 1 diabetes. Other researchers believe diabetes occurs on a continuum, with LADA falling between type 1 and type 2 diabetes. People who have LADA are usually over age 30. Because they're older when symptoms develop than is typical for someone with type 1 diabetes and because initially their pancreases still produce some insulin, people with LADA are often misdiagnosed with type 2 diabetes. If you've been diagnosed with type 2 diabetes and you're lean and physically active or you've recently lost weight without effort, talk with your doctor about whether your current treatment is still the best one for you. At first, LADA can be managed by controlling your blood sugar with diet, weight reduction if appropriate, exercise and, possibly, oral medications. But as your body gradually loses its ability to produce insulin, insulin shots will eventually be needed. More research is needed before the best way to treat LADA is established. Talk with your doctor about the best LADA treatment options for you. As with any type of diabetes, you'll need close follow-up to minimize progression of your diabetes and potential complications. Continue reading >>

Autoimmune Type 1 Diabetes: Resolved And Unresolved Issues

Autoimmune Type 1 Diabetes: Resolved And Unresolved Issues

It is estimated that nearly a million people in the US are afflicted with this disease (1). The majority of the patients are diagnosed and classified with type 1 diabetes within the first two decades of life, but an increasing number of cases are being recognized in older individuals. The geographic incidence varies widely from 1.7/100,000 per year in Japan to more than 35/100,000 in Finland. In the US the lifetime prevalence approaches 0.4%, but in high-incidence countries, such as Finland and Sweden, it may be as high as 1%. Type 1 diabetes is due to a deficiency of insulin as a result of destruction of the pancreatic β cells. At the time of clinical symptoms, 60–80% of the β cells are destroyed. Cells secreting glucagon, somatostatin, and pancreatic polypeptide are generally preserved but may be redistributed within the islets. Insulitis, an inflammatory infiltrate (Figure 1) containing large numbers of mononuclear cells and CD8 T cells, typically occurs around or within individual islets. Figure 1 Inflammatory infiltrate of mononuclear cells in an islet from a 2-year-old patient with type 1 diabetes of short duration. Mononuclear cells in and around islets are shown by yellow arrows. This patient was reported by Willy Gepts in his original contribution on insulitis in 1965 (45). The photomicrograph comes from the collection of W. Gepts and was kindly provided by Danny Pipeleers. The cause of β cell destruction remained an enigma for years, but two discoveries in the 1970s provided the basis for our current thinking about the disease. The first was a strong linkage of type 1 diabetes to the highly polymorphic HLA class II immune recognition molecules — DR and, later, DQ — located on chromosome 6 (2, 3). Over the years, extensive studies have revealed a large Continue reading >>

Types Of Diabetes

Types Of Diabetes

Pre-diabetes People with pre-diabetes have blood glucose levels that are higher than normal but not high enough for a diagnosis of diabetes. This condition raises the risk of developing type 2 diabetes, heart disease, and stroke. Pre-diabetes is also called impaired fasting glucose (IFG) or impaired glucose tolerance (IGT), depending on the test used to diagnose it. Some people have both IFG and IGT IFG is a condition in which the blood glucose level is high—100 to 125 mg/dL—after an overnight fast, but is not high enough to be classified as diabetes. The former definition of IFG was 110 mg/dL to 125 mg/dL IGT is a condition in which the blood glucose level is high—140 to 199 mg/dL—after a 2-hour OGTT, but is not high enough to be classified as diabetes. Pre-diabetes is becoming more common in the United States. The U.S. Department of Health and Human Services estimates that at least 57 million U.S. adults ages 20 or older had pre-diabetes in 2007. Those with pre-diabetes are likely to develop type 2 diabetes within 10 years, unless they take steps to prevent or delay diabetes. The good news is that people with pre-diabetes can do a lot to prevent or delay diabetes. Studies have clearly shown that people can lower their risk of developing diabetes by losing 5 to 7 percent of their body weight through diet and increased physical activity. A major study of more than 3,000 people with IGT found that diet and exercise resulting in a 5 to 7 percent weight loss—about 10 to 14 pounds in a person who weighs 200 pounds—lowered the incidence of type 2 diabetes by nearly 60 percent. Study participants lost weight by cutting fat and calories in their diet and by exercising—most chose walking—at least 30 minutes a day, 5 days a week. Type 1 Diabetes Type 1 diabetes i Continue reading >>

Type 2 Diabetes, Like Type 1, May Be An Autoimmune Disease, Researchers Say

Type 2 Diabetes, Like Type 1, May Be An Autoimmune Disease, Researchers Say

Type 2 diabetes, like Type 1, may be an autoimmune disease, but the immune system's target cells are different, Stanford researchers said Sunday. The discovery sheds new light on how obesity contributes to the onset of Type 2 diabetes and could lead to new types of treatment for the disorder, the researchers reported in the journal Nature Medicine. Diabetes is a growing problem in the United States, triggered in large part by the obesity epidemic. An estimated 27 million Americans are now thought to have diabetes, with the vast majority of them -- all but about a million -- afflicted with Type 2 diabetes. That disorder strikes in adulthood and is marked by a growing inability of cells to respond to insulin in the bloodstream, which necessitates using drugs to increase the output of the hormone by the pancreas. Intriguingly, not everyone who becomes obese develops diabetes, however, and researchers have never been sure why. Dr. Daniel Winer, an endocrine pathologist now at the University of Toronto, and his twin, Dr. Shawn Winer of the University of Toronto's Hospital for Sick Children, reasoned that the death of excess fat cells might trigger an autoimmune reaction. In an earlier study with senior author Dr. Edgar Engleman of the Stanford University School of Medicine, they demonstrated in mice that, as fat accumulates in the tissues surrounding organs, it outstrips its blood supply, leading to the death of cells on the periphery of the fat deposits. When that occurs, the body mobilizes its immune system to break down and carry off the dead cells. But that produces antibodies against the cells and many of the proteins normally found only inside the cells. Continue reading >>

Type 2 Diabetes Mellitus - An Autoimmune Disease?

Type 2 Diabetes Mellitus - An Autoimmune Disease?

Abstract Inflammation-induced inhibition of the insulin signalling pathway can lead to insulin resistance and contribute to the development of type 2 diabetes mellitus (T2DM). Obesity and insulin resistance are associated with a chronic but subclinical inflammatory process that impairs insulin action in most tissues and could also hamper pancreatic β-cell function. The involvement of monocytic cells and the profiles of the chemokines and cytokines induced by this inflammation suggest an innate immune response. However, emerging data indicate that elements of the adaptive immune system could also be involved. As activation of an adaptive response requires antigen specificity, some researchers have hypothesized that T2DM evolves from an innate immune response to an autoimmune condition. In this Perspectives article, we present the arguments for and against this hypothesis and discuss which mechanisms could be involved in a putative switch from innate immunity to autoimmunity. Discover the world's research 14+ million members 100+ million publications 700k+ research projects Join for free a Continue reading >>

Type 1 Diabetes And Autoimmune Diseases

Type 1 Diabetes And Autoimmune Diseases

Type 1 diabetes is just one of multiple autoimmune diseases. We inherit risk of autoimmunity primarily in the HLA complex located on chromosome six. Due to the close linkage of genes coding particularly for type 1 diabetes, Hashimoto’s Thyroiditis, Juvenile Rheumatoid Arthritis, Graves, Celiac, and Addison’s disease, there is more than a random association of these diseases. A significant number of children have thyroid and celiac disease, which is the most common in association with Type 1 diabetes as demonstrated in evidence-based studies. Less commonly associated with type 1 diabetes are other autoimmune diseases such as Systemic Lupus Erythematosis and inflammatory bowel disease. Autoimmune thyroid disease in the form of hypothyroidism (Hashimoto’s Thyroiditis) and hyperthyroidism (Graves Disease) is most commonly associated with type 1 diabetes. Thus, at diagnosis, or shortly after, Thyroid stimulating hormone (TSH), thyroid antibodies (thyroid peroxidase, or antithyroglobulin antibodies) are obtained. If the TSH is elevated in association with a low thyroid hormone level (usually free T4), thyroid replacement medication begins (Synthroid). If the TSH is extremely low in association with higher free T4 levels, thyroid suppression medication (Methimazole, for example) is usually initiated. Celiac disease or gluten intolerance is the next most common autoimmune disease associated with type 1 diabetes. Symptoms of the disease may be vague so one must have a high suspicion to rule out the disease. Abdominal pain, growth failure, or menstrual irregularities are often associated with celiac disease; however, there may be no symptoms present. Therefore, laboratory screening is necessary requiring a serum tissue transglutaminase IgA, along with a total IgA (to ensure Continue reading >>

What Causes Autoimmune Diabetes?

What Causes Autoimmune Diabetes?

Autoimmune diabetes is influenced by genetics. What starts the autoimmune destruction is unknown, but it may be due to environmental factors. You may want to learn more about how type 1a diabetes develops. We know type 1a diabetes is caused by an autoimmune process in the body that mistakenly destroys the insulin-producing cells, or beta cells and occurs in genetically predisposed individuals. What starts the autoimmune destruction is unknown, but it may be due to environmental factors. In this section, you can learn more about: What is the Immune system? An overview of the different cells and organs in the immune system and how the immune system works Autoimmunity and diabetes: Current ideas about how the immune systems destroys insulin producing cells Continue reading >>

Are Obesity-related Insulin Resistance And Type 2 Diabetes Autoimmune Diseases?

Are Obesity-related Insulin Resistance And Type 2 Diabetes Autoimmune Diseases?

Obesity and associated insulin resistance predispose individuals to develop chronic metabolic diseases, such as type 2 diabetes and cardiovascular disease. Although these disorders affect a significant proportion of the global population, the underlying mechanisms of disease remain poorly understood. The discovery of elevated tumor necrosis factor-α in adipose tissue as an inducer of obesity-associated insulin resistance marked a new era of understanding that a subclinical inflammatory process underlies the insulin resistance and metabolic dysfunction that precedes type 2 diabetes. Advances in the field identified components of both the innate and adaptive immune response as key players in regulating such inflammatory processes. As antigen specificity is a hallmark of an adaptive immune response, its role in modulating the chronic inflammation that accompanies obesity and type 2 diabetes begs the question of whether insulin resistance and type 2 diabetes can have autoimmune components. In this Perspective, we summarize current data that pertain to the activation and perpetuation of adaptive immune responses during obesity and discuss key missing links and potential mechanisms for obesity-related insulin resistance and type 2 diabetes to be considered as potential autoimmune diseases. Traditional autoimmune diseases involve a wide spectrum of clinical pathology and include diseases such as systemic lupus erythematosus, multiple sclerosis, Sjögren’s syndrome, rheumatoid arthritis, and type 1 diabetes. A disease is considered autoimmune if its pathology is dictated by a self-antigen–specific adaptive immune response. Immunologists have adapted Koch’s postulates, originally conceived to establish a causative link between microbes and infectious diseases, to define k Continue reading >>

Type 2 Diabetes Mellitus—an Autoimmune Disease?

Type 2 Diabetes Mellitus—an Autoimmune Disease?

Inflammation-induced inhibition of the insulin signalling pathway can lead to insulin resistance and contribute to the development of type 2 diabetes mellitus (T2DM). Obesity and insulin resistance are associated with a chronic but subclinical inflammatory process that impairs insulin action in most tissues and could also hamper pancreatic β-cell function. The involvement of monocytic cells and the profiles of the chemokines and cytokines induced by this inflammation suggest an innate immune response. However, emerging data indicate that elements of the adaptive immune system could also be involved. As activation of an adaptive response requires antigen specificity, some researchers have hypothesized that T2DM evolves from an innate immune response to an autoimmune condition. In this Perspectives article, we present the arguments for and against this hypothesis and discuss which mechanisms could be involved in a putative switch from innate immunity to autoimmunity. Danaei, G. et al. National, regional, and global trends in fasting plasma glucose and diabetes prevalence since 1980: systematic analysis of health examination surveys and epidemiological studies with 370 country-years and 2.7 million participants. Lancet 378, 31–40 (2011). Yang, H. et al. Obesity increases the production of proinflammatory mediators from adipose tissue T cells and compromises TCR repertoire diversity: implications for systemic inflammation and insulin resistance. J. Immunol. 185, 1836–1845 (2010). The authors' research is supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (Brazil), the Communauté Française de Belgique—Actions de Recherche Concertées, and the European Union projects Naimit and BetaBat, in the Framework Programme 7 of the European Community. The au Continue reading >>

Autoimmune Aspects Of Type 2 Diabetes Mellitus - A Mini-review

Autoimmune Aspects Of Type 2 Diabetes Mellitus - A Mini-review

Abstract Autoimmunity is a well-known pathogenic component in type 1 diabetes (T1DM). The assumption that the pathogenesis of type 2 diabetes (T2DM) also encompasses autoimmune aspects is recognized increasingly, based on the presence of circulating autoantibodies against β cells, self-reactive T cells, but also on the glucose-lowering efficacy of some immunomodulatory therapies in T2DM. The identification of these autoantibodies in elderly patients with slowly progressive manifestation of diabetes led to the introduction of a distinct clinical entity termed latent autoimmune diabetes of the adult (LADA), which combines features of both T1DM and T2DM. The autoantibody cluster differs in patients with LADA from patients with T1DM, but their presence indicates steady progression towards β-cell death and subsequent need for initiation of insulin treatment in a shorter period of time compared to autoantibody-negative T2DM patients. Autoimmune aspects in T2DM are not solely restricted to autoantibodies and thus LADA. They include the self-reactive T cells or defects in regulatory T cells (Tregs), which have been detected in autoantibody-negative T2DM patients as well. One contributor to the autoimmune activation in T2DM seems to be the chronic inflammatory state, characteristic of this disease. Upon inflammation-induced tissue destruction, cryptic ‘self' antigens can trigger an autoimmune response, which in turn accelerates β-cell death. Both innate and adaptive immune system components, specifically macrophages and self-reactive T cells, contribute to an increased secretion of inflammatory cytokines involved in inflammatory and autoimmune processes. However, the extent to which inflammation overlaps with autoimmunity is not known. Our review focuses on autoimmune invol Continue reading >>

More in diabetes