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Concordance Rate Type 2 Diabetes

Relationship Between Obesity And Concordance Rate For Type 2 (non-insulin-dependent) Diabetes Mellitus Among Twins

Relationship Between Obesity And Concordance Rate For Type 2 (non-insulin-dependent) Diabetes Mellitus Among Twins

Volume 26, Issue 2 , 16 December 1994, Pages 137-143 Relationship between obesity and concordance rate for Type 2 (non-insulin-dependent) diabetes mellitus among twins Author links open overlay panel AyakoMatsuda Get rights and content In order to analyse the relationship of genetic factors and the role of obesity in the pathogenesis of Type 2 (non-insulin-dependent) diabetes mellitus, we compared body mass index (BMI) and other parameters in 71 monozygotic and 17 dizygotic twins (MZT and DZT) with Type 2 diabetes, and analysed the relationship of maximal BMI in the past (max BMI) with the concordance and discordance for diabetes. Data were collected by mail from the members of the Japan Diabetes Society. Concordance rate for diabetes was higher in MZT than in DZT (72% vs. 41%, P = 0.017). Concordance rate in MZT varied in relation to the max BMI of the index twins who developed diabetes earlier. It was higher in non-obese and slightly obese groups (82% and 80% for those with max BMI < 24 and 2427.9, respectively) than in obese group (36%, max BMI 28) (P = 0.003). In MZT, diabetic twins of discordant pairs were significantly more obese at the survey and in the past than index twins of concordant pairs (mean BMI: 23.9 vs. 21.7, P = 0.007; mean max BMI, 27.7 vs. 24.3, P = 0.001). A similar tendency of differences in BMI was also observed in DZT. Intrapair comparison in discordant MZT and DZT pairs showed that diabetic twins were more obese than non-diabetic cotwins (mean max BMI, 27.7 vs. 24.7, P = 0.004 for MZT; and 27.3 vs. 23.9, P = 0.002 for DZT). In concordant DZT pairs, index twins with earlier onset of diabetes had been less obese than cotwins (mean max BMI, 23.6 vs. 26.0, P = 0.004). In conclusion, the comparison of the max BMI in twins suggests that the degree o Continue reading >>

Relationship Between Obesity And Concordance Rate For Type 2 (non-insulin-dependent) Diabetes Mellitus Among Twins

Relationship Between Obesity And Concordance Rate For Type 2 (non-insulin-dependent) Diabetes Mellitus Among Twins

Volume 26, Issue 2 , 16 December 1994, Pages 137-143 Relationship between obesity and concordance rate for Type 2 (non-insulin-dependent) diabetes mellitus among twins Author links open overlay panel AyakoMatsuda Get rights and content In order to analyse the relationship of genetic factors and the role of obesity in the pathogenesis of Type 2 (non-insulin-dependent) diabetes mellitus, we compared body mass index (BMI) and other parameters in 71 monozygotic and 17 dizygotic twins (MZT and DZT) with Type 2 diabetes, and analysed the relationship of maximal BMI in the past (max BMI) with the concordance and discordance for diabetes. Data were collected by mail from the members of the Japan Diabetes Society. Concordance rate for diabetes was higher in MZT than in DZT (72% vs. 41%, P = 0.017). Concordance rate in MZT varied in relation to the max BMI of the index twins who developed diabetes earlier. It was higher in non-obese and slightly obese groups (82% and 80% for those with max BMI < 24 and 2427.9, respectively) than in obese group (36%, max BMI 28) (P = 0.003). In MZT, diabetic twins of discordant pairs were significantly more obese at the survey and in the past than index twins of concordant pairs (mean BMI: 23.9 vs. 21.7, P = 0.007; mean max BMI, 27.7 vs. 24.3, P = 0.001). A similar tendency of differences in BMI was also observed in DZT. Intrapair comparison in discordant MZT and DZT pairs showed that diabetic twins were more obese than non-diabetic cotwins (mean max BMI, 27.7 vs. 24.7, P = 0.004 for MZT; and 27.3 vs. 23.9, P = 0.002 for DZT). In concordant DZT pairs, index twins with earlier onset of diabetes had been less obese than cotwins (mean max BMI, 23.6 vs. 26.0, P = 0.004). In conclusion, the comparison of the max BMI in twins suggests that the degree o Continue reading >>

The Accelerator Hypothesis: A Unifying Explanation For Type-1 And Type-2 Diabetes

The Accelerator Hypothesis: A Unifying Explanation For Type-1 And Type-2 Diabetes

Despite 30 years of research, the cause of type-1 diabetes remains unknown. Meanwhile, its incidence has risen three-fold, its clinical features have become increasingly difficult to distinguish from type-2 diabetes and the contribution of genes to its pathogenesis has changed. The accelerator hypothesis argues that type-1 and type-2 diabetes are the same disorder of insulin resistance set against different genetic backgrounds. It identifies three processes which variably accelerate Β cell loss: constitution, insulin resistance and the immune response to it. None of the accelerators leads to diabetes in the absence of weight gain, a trend which the hypothesis deems central to the rising incidence of all diabetes in the industrially developed and developing world. Weight gain causes an increase in insulin resistance, which results in the weakening of glucose control. The rising blood glucose accelerates Β cell apoptosis (glucotoxicity) and, by increasing Β cell immunogenicity, further accelerates apoptosis in a subset genetically predisposed to an intense immune response. Rather than overlap between the two types of diabetes, the accelerator hypothesis envisages overlay - one a subset of the other. Body mass is central to the development and rising incidence of all diabetes. Only tempo distinguishes type 1 from type 2. The control of weight gain, and with it insulin resistance, could be the means of preventing both by slowing their progression. Continue reading >>

Concordance Rate For Type Ii Diabetes Mellitus In Monozygotic Twins: Actuarial Analysis.

Concordance Rate For Type Ii Diabetes Mellitus In Monozygotic Twins: Actuarial Analysis.

Concordance rate for type II diabetes mellitus in monozygotic twins: actuarial analysis. Department of Diabetes and Metabolism, St. Bartholomew's Hospital, London, United Kingdom. To determine the concordance rate for Type II (non-insulin-dependent) diabetes mellitus in monozygotic twin pairs, initially ascertained discordant for diabetes, we carried out a prospective study on 44 non-diabetic subjects, each of whom had a sibling twin with diabetes (21 men, 23 women, median age 55 years, interquartile range 47-65). The subjects were referred as discordant for Type II diabetes. The twin pairs were part of the British Diabetic Twin Study and ascertained between May 1968 and January 1998. These subjects underwent an OGTT at time of referral and periodically thereafter. The mean follow-up was 8 years (range 0-18 years) and data were collected until January 1996. The percentage of twins who developed Type II diabetes was assessed by standard actuarial life-table methods and the pairwise concordance rate, that is the proportion of concordant pairs over the sum of concordant and discordant pairs, was calculated. The observed rates of concordance for Type II diabetes at 1, 5, 10, and 15 years follow-up were 17, 33, 57, and 76%, respectively. The concordance rate for any abnormality of glucose metabolism (either Type II diabetes or impaired glucose tolerance) at 15 years follow-up was 96%. The concordance rate for Type II diabetes in monozygotic twins is very high even in twins initially ascertained discordant for diabetes. Continue reading >>

Risk Of Developing Type 2 Diabetes If Family History Of Diabetes

Risk Of Developing Type 2 Diabetes If Family History Of Diabetes

There is evidence that Type 2 diabetes has a strong familial basis: at least 40% of siblings of subjects with type 2 diabetes can expect to also develop type 2 diabetes during their lifetime (1) risk is based on the assumption that survival will be to the age of 80 years (1) study evidence has revealed the relative risk of developing diabetes in a Pima Indian population (adjusted for age and obesity) was (2): 2.3 times in offspring with one affected parent 3.9 times greater in offspring with two affected parents evidence for the genetic nature of the disease of type 2 diabetes also comes from twin studies one study involving monozygotic twins revealed that the concordance rate for type 2 diabetes was increased at 58% (3). This compared with the expected prevalence of 10% (3) Reference: Kobberling JTH. Empirical risk figures for first degree relatives of noninsulin dependent diabetics. Academic Press London:201-09. Continue reading >>

Defining The Genetic Contribution Of Type 2 Diabetes Mellitus

Defining The Genetic Contribution Of Type 2 Diabetes Mellitus

Diabetes mellitus (DM) affects over 150 million people world wide, with a prevalence that varies markedly from population to population.1 Estimates predict that almost 300 million people will suffer from DM by 2025 (fig 1) with the vast majority being cases of diabetes mellitus type 2. Many risk factors have been identified which influence the prevalence (total number of cases as a percentage of the total population) or incidence (total number of new cases per year as a percentage of the total population). Factors of particular importance are a family history of diabetes mellitus, age, overweight, increased abdominal fat, hypertension, lack of physical exercise, and ethnic background. Several biochemical markers have also been identified as risk factors, including fasting hyperinsulinaemia, increased fasting proinsulin, and decreased HDL cholesterol.2 Both diabetes mellitus types 1 and 2 show a familial predisposition, which is a strong indication for the involvement of genes in people's susceptibility to the disease. However, the aetiology underlying types 1 and 2 is different and different genes are likely to be involved in each type of diabetes mellitus. The following discussion focuses on a genetic dissection of type 2 diabetes mellitus. The two most common forms of diabetes mellitus, type 1 and type 2, are both characterised by raised plasma glucose levels. Normal glucose homeostasis depends on the balance between glucose production by the liver and kidneys and glucose uptake by the brain, kidneys, muscles, and adipose tissue. Insulin, the predominant anabolic hormone involved, increases the uptake of glucose from the blood, enhances its conversion to glycogen and triglyceride, and also increases glucose oxidation. Plasma glucose levels are normally kept within a s Continue reading >>

Genetics Of Type 2 Diabetes

Genetics Of Type 2 Diabetes

Until recently the genetic variation and genes involved in type 2 diabetes were very poorly characterised. Traditionally genetic studies focused on the collection and characterisation of multi-generation families but type 2 diabetes occurs in older age, making the collection of affected families difficult – the parents of most patients have died and most offspring have yet to develop the condition. Furthermore the increasing prevalence of type 2 diabetes over one or two generations proves that the changing environment has a strong role to play in type 2 diabetes risk – gene frequencies do not change appreciably in 1 or 2 generations, and certainly not those that influence a disease of largely post reproductive age. Two major developments mean that we now know of 65 regions of the human genome that influence type 2 diabetes risk. First, in 2007 genome wide association studies (GWAS) became possible. These studies provided scientists with the ability to analyse 100,000s of single nucleotide variants (the simplest and most abundant type of DNA marker) in a single experiment. Second, scientists realised that they would have to work together and combine case-control studies to achieve the very large sample sizes that provided adequate statistical power to identify the subtle effects of common genetic risk factors. These developments have resulted in the latest study of 35,000 European type 2 diabetes cases and 115,000 controls.[1] History and heritability of type 2 diabetes genetics. Before trying to identify genes, geneticists tend to perform twin or family studies in attempts to quantify the relative contributions of genes (heritability) and environment. Comparing disease concordance in identical twins to same sex non-identical twins is a powerful approach. However, th Continue reading >>

Preventing Chronic Disease: April 2005: 04_0131

Preventing Chronic Disease: April 2005: 04_0131

Family history of diabetes has been recognized as an important risk factor of thedisease. Family medical history represents valuable genomic information because itcharacterizes the combined interactions between environmental, behavioral, and geneticfactors. This study examined the strength and effect of having a family history ofdiabetes on the prevalence of self-reported, previously diagnosed diabetes among adultparticipants of the National Health and Nutrition Examination Survey 19992002. The study population included data from 10,283 participants aged 20 years and older.Gender, age, race/ethnicity, poverty income ratio, education level, body mass index, andfamily history of diabetes were examined in relation to diabetes status. Diabetesprevalence estimates and odds ratios of diabetes were calculated based on family historyand other factors. The prevalence of diabetes among individuals who have a first-degree relative withdiabetes (14.3%) was significantly higher than that of individuals without a familyhistory (3.2%), corresponding to a crude odds ratio of five. Both prevalence and oddsratio estimates significantly increased with the number of relatives affected withdiabetes. Family history was also associated with several demographic and riskfactors. Family history of diabetes was shown to be a significant predictor of diabetesprevalence in the adult U.S. population. We advocate the inclusion of family historyassessment in public health prevention and screening programs as an inexpensive andvaluable source of genomic information and measure of diabetes risk. Diabetes mellitus presents multiple challenges to public health. An estimated 18.2million individuals in the United States have diabetes (1). This disease contributes tosignificant morbidity, including cardiova Continue reading >>

Increased Risk Of Type 2 Diabetes In Elderly Twins

Increased Risk Of Type 2 Diabetes In Elderly Twins

Increased risk of type 2 diabetes in elderly twins Research output: Contribution to journal Journal article Increased risk of type 2 diabetes in elderly twins. / Poulsen, Pernille; Grunnet, Louise G; Pilgaard, Kasper; Storgaard, Heidi; Alibegovic, Amra; Sonne, Mette P; Carstensen, Bendix; Beck-Nielsen, Henning; Vaag, Allan. In: Diabetes, Vol. 58, No. 6, 2009, p. 1350-5. Research output: Contribution to journal Journal article Poulsen, P, Grunnet, LG, Pilgaard, K, Storgaard, H, Alibegovic, A, Sonne, MP, Carstensen, B, Beck-Nielsen, H & Vaag, A 2009, 'Increased risk of type 2 diabetes in elderly twins' Diabetes, vol 58, no. 6, pp. 1350-5. DOI: 10.2337/db08-1714 Poulsen, P., Grunnet, L. G., Pilgaard, K., Storgaard, H., Alibegovic, A., Sonne, M. P., ... Vaag, A. (2009). Increased risk of type 2 diabetes in elderly twins. Diabetes, 58(6), 1350-5. DOI: 10.2337/db08-1714 Poulsen P, Grunnet LG, Pilgaard K, Storgaard H, Alibegovic A, Sonne MP et al. Increased risk of type 2 diabetes in elderly twins. Diabetes. 2009;58(6):1350-5. Available from, DOI: 10.2337/db08-1714 Poulsen, Pernille ; Grunnet, Louise G ; Pilgaard, Kasper ; Storgaard, Heidi ; Alibegovic, Amra ; Sonne, Mette P ; Carstensen, Bendix ; Beck-Nielsen, Henning ; Vaag, Allan. / Increased risk of type 2 diabetes in elderly twins. In: Diabetes. 2009 ; Vol. 58, No. 6. pp. 1350-5 @article{59544720366011df8ed1000ea68e967b, title = "Increased risk of type 2 diabetes in elderly twins", abstract = "OBJECTIVE: Genetic susceptibility, low birth weight (LBW), and aging are key etiological factors in the development of type 2 diabetes. LBW is common among twins. It is unknown whether twin status per se is associated with risk of type 2 diabetes, and valid concordance rates of type 2 diabetes in twins on a lifetime perspective are Continue reading >>

Type 2 Diabetes Mellitus In Childhood: Obesity And Insulin Resistance

Type 2 Diabetes Mellitus In Childhood: Obesity And Insulin Resistance

As rates of childhood obesity climb, type 2 diabetes mellitus has increasingly been diagnosed in children and adolescents, with the highest incidence occurring among youth from racial and ethnic minority backgrounds. The serious complications associated with type 2 diabetes mellitus make it essential for physicians to be aware of risk factors and screening guidelines, allowing for earlier patient diagnosis and treatment. It is also important for physicians to be aware of the treatment options available, including weight control through diet and exercise as well as common pharmacotherapeutic options. According to the SEARCH for Diabetes in Youth Study Group,8 incidence rates among American Indians aged 15 to 19 years is 49.4%, compared to 5.6% in non-Hispanic whites of the same age group. Among youth in the United States, Pima Indian adolescents have the highest reported prevalence of type 2 diabetes mellitus. For Pima Indian children aged 5 to 9 years, the incidence rate is less than 0.5%; for children and adolescents aged 10 to 14 years, 1.5% to 3%; and for adolescents and young adults aged 15 to 19 years, 4% to 5%.7 Neel9 postulated that, when humans were hunter-gatherers and did not know when the next meal was expected, some individuals developed “thrifty genes.” These genes caused the body to become insulin resistant by interfering with mechanisms that allowed blood glucose to be transported into cells where it would be phosphorylated and used for energy. Consequently, the pancreas had to make more insulin. The excess insulin allowed cells to store fat for use during times of relative famine, leading to a much higher survival rate.9-11 These genes may include uncoupling proteins, PPAR-γ and PPAR-α, CALPAIN 10, and adrenergic receptor polymorphisms.12-14 Athero Continue reading >>

Age-dependent Influences On The Origins Of Autoimmune Diabetes

Age-dependent Influences On The Origins Of Autoimmune Diabetes

Age-Dependent Influences on the Origins of Autoimmune Diabetes R. David G. Leslie; Michela Delli Castelli Type 1 diabetes is genetically determined as shown by family, twin, and genetic studies. The frequency of type 1 diabetes is higher in siblings of diabetic patients (e.g., 6% by age 30 years in the U.K.) than in the general population (0.4% by age 30 years).[ 6 ] Familial clustering could be caused by shared genetic or environmental factors, and to distinguish between them, twin studies have been used. Higher concordance rates for autoimmune diseases in identical compared with nonidentical twins is consistent with a genetic influence on these diseases.[ 7 ] Of genes implicated in the genetic susceptibility to type 1 diabetes, the most important are in the histocompatibility (HLA) region of chromosome 6.[ 6 , 8 ] Age-related genetic factors not only influence the risk of type 1 diabetes, but also the presence of diabetes-associated autoantibodies, the rate of progression to clinical diabetes, and the severity of reduced insulin secretory capacity. Not only is the age incidence of type 1 diabetes lower than in children, but the range of incidence across European countries is also reduced.[ 9 ] Furthermore, there is a male excess in disease incidence that becomes evident during puberty and is most striking in the age-group 25-29 years.[ 9 ] Survival analysis estimated that nondiabetic identical twins of probands diagnosed with type 1 diabetes <25 years of age had, in one study, a 38% probability of developing diabetes compared with 6% for twins of probands diagnosed later[ 10 , 11 , 12 ] ( Table 1 ). Such a remarkably low twin concordance rate for adult-onset type 1 diabetes, lower than that for influenza, implies that the genetic impact in adult-onset diabetes is lim Continue reading >>

Payperview: Genetics Of Type 2 Diabetes - Karger Publishers

Payperview: Genetics Of Type 2 Diabetes - Karger Publishers

Markku Laakso, MD, PhD, Academy Professor Institute of Clinical Medicine, Internal Medicine University of Eastern Finland and Kuopio University Hospital I have read the Karger Terms and Conditions and agree. Genetic and environmental factors as well as their interactions contribute to the pathogenesis of type 2 diabetes. Linkage analysis, candidate gene approaches, genome-wide association studies, and sequencing have been used in the identification of common, low-frequency and rare variants for type 2 diabetes. Genome-wide association studies have identified >80 common variants for type 2 diabetes, with small effect sizes (risk of type 2 diabetes increased by 5-40%). Almost all of these variants regulate insulin secretion, and only a few regulate insulin sensitivity. Common variants capture only 10% of the heritability of type 2 diabetes. Low-frequency and rare variants with large effects have also been identified, but their contribution to missing heritability' at the population level is limited. Gene-environment and gene-gene interactions and epigenetics are likely to contribute to the missing heritability of type 2 diabetes. Epigenetic factors (DNA methylations and histone modifications) are especially important because they might mediate the effects of environmental exposures on the risk of type 2 diabetes. Although understanding of the genetics of type 2 diabetes has exhibited great progress in the past few years, a substantial amount of additional work will be required to identify causal variants/genes and molecular mechanisms via which the association signals found confer diabetes risk. World Health Organization: Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications. Geneva: World Health Organization, 1999. International Diabetes Fe Continue reading >>

The Concordance And Heritability Of Type 2 Diabetes In 34,166 Twin Pairs From International Twin Registers: The Discordant Twin (discotwin) Consortium

The Concordance And Heritability Of Type 2 Diabetes In 34,166 Twin Pairs From International Twin Registers: The Discordant Twin (discotwin) Consortium

This article has been cited by the following publications. This list is generated based on data provided by CrossRef . Jensen, Rikke BeckThankamony, AjayHolst, Klaus KJanssen, Joseph A M J LJuul, AndersDunger, DavidPoulsen, PernilleandScheike, Thomas2018.Genetic influence on the associations between IGF-I and glucose metabolism in a cohort of elderly twins.European Journal of Endocrinology,Vol. 178,Issue. 2,p.155. Fuchsberger, ChristianFlannick, JasonTeslovich, Tanya M.Mahajan, AnubhaAgarwala, VineetaGaulton, Kyle J.Ma, ClementFontanillas, PierreMoutsianas, LoukasMcCarthy, Davis J.Rivas, Manuel A.Perry, John R. B.Sim, XuelingBlackwell, Thomas W.Robertson, Neil R.Rayner, N. WilliamCingolani, PabloLocke, Adam E.Tajes, Juan FernandezHighland, Heather M.Dupuis, JoseeChines, Peter S.Lindgren, Cecilia M.Hartl, ChristopherJackson, Anne U.Chen, HanHuyghe, Jeroen R.van de Bunt, MartijnPearson, Richard D.Kumar, AshishMller-Nurasyid, MartinaGrarup, NielsStringham, Heather M.Gamazon, Eric R.Lee, JaehoonChen, YuhuiScott, Robert A.Below, Jennifer E. Chen, PengHuang, JinyanGo, Min JinStitzel, Michael L.Pasko, DorotaParker, Stephen C. J.Varga, Tibor V.Green, ToddBeer, Nicola L.Day-Williams, Aaron G.Ferreira, TeresaFingerlin, TashaHorikoshi, MomokoHu, ChengHuh, IksooIkram, Mohammad KamranKim, Bong-JoKim, YongkangKim, Young JinKwon, Min-SeokLee, JuyoungLee, SelyeongLin, Keng-HanMaxwell, Taylor J.Nagai, YoshihikoWang, XuWelch, Ryan P.Yoon, JoonZhang, WeihuaBarzilai, NirVoight, Benjamin F.Han, Bok-GheeJenkinson, Christopher P.Kuulasmaa, TeemuKuusisto, JohannaManning, AlisaNg, Maggie C. Y.Palmer, Nicholette D.Balkau, BeverleyStankov, AlenaAbboud, Hanna E.Boeing, HeinerGiedraitis, VilmantasPrabhakaran, DorairajGottesman, OmriScott, JamesCarey, JasonKwan, PhoenixGrant, GeorgeSmith, Joshua D. Continue reading >>

Diabetes Flashcards | Quizlet

Diabetes Flashcards | Quizlet

Islet destruction is mediated by ______________rather than ______________ Islet destruction is mediated by T lymphocytes rather than islet auto-antibodies Autoimmune process triggered by a putative infectious (________, rubella, and ___________) or environmental stimuli (milk bovine proteins, nitrosourea compounds) Autoimmune process triggered by a putative infectious (coxsackie, rubella, and enteroviruses) or environmental stimuli (milk bovine proteins, nitrosourea compounds) which type of diabetes has a higher concordance rate Greatest risk of type 2 diabetes with Transcription factor ____ like ____ (________) Time course of symptoms for type 1 diabetes -features become evident when 70-80% of pancreatic beta cells have been destroyed -rate of beta cell decline varies among individuals -secondary to obesity in children and young adults -incidence peak during mid-puberty when normal increase of growth hormone levels add to the obseity-associated burden of insulin resistance -Latent autoimmune diabetes of adulthood (LADA) Ketosis is common in what type of diabetes? >100 mg/dl fasting plasma glucose but under <126 mg/dl -diminished insulin/glucagon --> osmotic diuresis, dehydration, weakness, weight loss, shock -ketone body formation --> metabolic acidosis, impaired cardiovascular function -screen for undiagnosed T2DM at first prenatal visit -women with diabetes diagnosed in the first trimester classified as overt DM not GDM -Screen for GDM at 24-48 weeks of pregnancy -clinically heterogenous disorder resulting from mutations in genese involved in pancreatic B-cell development, function, and regulation -most common form of monogenic diabetes (2-5%) hypertrophied darker skin on the back of the neck, axilla, umbilicus, back of hand, and feet, due to chronic elevation in in Continue reading >>

Type 2 Diabetes Mellitus (t2d)

Type 2 Diabetes Mellitus (t2d)

Diabetes Type II is caused by a reduction of insulin sensitivity. Diabetes ranks in the top 5 for mortality in developed countries. Obesity and sedentary life-style are largely to blame for the diabetes epidemic. Adipocyte-secreted factors can induce insulin resistance in skeletal muscle. antibodies-online offers a large number of well established antibodies for research on PREVALENCE AND PATHOLOGY OF TYPE 2 DIABETES MELLITUS mellitus (T2D or T2DM) has already been described in the medical books of the ancient civilizations of Egypt, Greece, India, Rome and China. It has been claimed that the ancient Chinese have tested for diabetes by observing whether ants were attracted to a person?s urine or not. Medieval European doctors have tested for diabetes, by tasting the urine of diabetic patients, and named it ?sweet urine disease?. The urine contains saccharides because glucose can not be utilized by the organs due to reduced insulin sensitivity. mellitus occurs throughout the world, it is most common in more developed countries. 2006 246 Million or 6,0 % of the world population were known to be affected. In 2025 that number is expected to rise to 380 Million (7,3 %). Type 2 causes complex and multi-factorial metabolic changes which ultimately lead to damage and function impairment of many organs, most importantly the cardiovascular system, and hence increase the mortality and morbidity significantly. It has been suggested that in developed countries there are about five times as many deaths indirectly attributable to diabetes than directly attributable. This stems for example from the fact that mortality from diabetes is related to heart disease. This would mean that accounts for about one in twenty of all deaths. (Murray CJL, Lopex A (1996) The Global Burden of Disease. Continue reading >>

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