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Type 2 diabetes (T2D) is a common disease caused by a complex interplay between many genetic and environmental factors. Both a population-based approach and a targeted high-risk approach are recommended as strategies for prevention of T2D. Genetic susceptibility testing for T2D is currently offered by several commercial companies that use genome-wide scans to deliver information about risk for many common complex diseases (see Table 1 ). Direct-to-consumer risk companies sell risk profiles that differ in the number of genetic markers included and in the exact SNPs used.
T2D is a metabolic disorder characterized by hyperglycemia, insulin resistance and relative insulin deficiency.
Preventive interventions for T2D, including medication, weight loss and increased physical activity, can slow or even reverse the disease process.
A European multidisciplinary consortium developed an evidence-based guideline for the prevention of T2D. Analytic Validity : Test accuracy and reliability in identifying multiple SNPs (analytic sensitivity and specificity). Navigenics reports an analytic accuracy of 99%, [15] deCODEme does not provide a measure of accuracy but describes the methods used to ensure good analytic validity, [16] 23andMe does not disclose the methods used, [17] and the same applies to Pathway Genomics. Direct-to-consumer genetic testing services are not clearly regulated by governmental agencies. Clinical Validity : Clinical validity refers to test accuracy and reliability in predicting risk of T2D (discrimination and calibration). Discrimination shows how well the model can distinguish between individuals with and without disease. In most empirical studies, the genetic risk scores had lower discriminative accuracy than the clinical risk factors. Search strategy: We performed a search in PubMed and HuGE Navigator to identify relevant studies, scanned the reference lists from the retrieved articles to identify additional studies, and further used Web of Science to identify studies that cited the selected articles.
Another important aspect when testing the performance of a prediction model is the model calibration.
We assessed clinical utility as the added benefit of the test beyond traditional clinical predictors in improving health outcomes, and as the impact of genetic testing on attitudes, beliefs and health related behavior in individuals who receive genetic risk information.
First, clinical utility is reflected in the impact of a risk prediction model on the classification of individuals in risk groups for which the preventive interventions differ. Second, when the impact on outcome prediction is not available, clinical utility is reflected in the public interest and health care provider interest in genetic testing, the uptake of the tests and the effect of testing on outcomes such as adherence to lifestyle changes or to medication for prevention and treatment of disease. A survey conducted among primary care physicians and endocrinologists (n = 304) and patients (152 non-diabetic and 89 with T2D) assessed beliefs regarding the clinical use of genetic testing for T2D. This study was supported by the Centre for Medical Systems Biology (CMSB) in the framework of the Netherlands Genomics Initiative (NGI).
Gene Mutations parallel Biological Alterations: The New War against Five Stages of type 2 Diabetes Mellitus. Millions of people around the world are affected by Diabetes, and almost most of them have the Type 2 diabetes, since it is the most common form of diabetes known to have affected 90% to 95% of diabetic people. Diabetes Type 2 is the most common type of diabetes, unlike Type 1; type 2 diabetes affected people can produce insulin in their body.
There is a reason diabetes is called ‘Silent Killer’, many patients suffering from severe diabetic conditions often do not know that they have diabetes because there are no distinct symptoms and often they vary from person to person. Diabetes type 2 is not the kind of disease which can be cured by just taking medicines, the determination of the patient to get better plays an important role when it comes to Type 2 diabetes.
Healthy eating – there is no specific diet that is specifically for type 2 diabetes patients, just eating lots of high fiber and low fat food stuffs will do wonders. Exercising – Aerobic exercises are good physical activity, however consult your doctor before starting any strict regime. Monitoring blood sugar and insulin intake–check your blood sugar levels based on your treatment plans and regularly if you are taking insulin. First of all, there is no true answer to the question of which type of diabetes is genetic. Some examples to support this evidence is, that families who have type 2 diabetes usually share the same lifestyle such as eating habits, exercise habits, as well as being overweight, which has been known to be one of the leading causes of type 2 diabetes. So to answer the question of which type of diabetes is genetic, the short answer is there is a high probability that type 2 diabetes will have a stronger predisposition to get it, compared to type 1 diabetes.
In other words, there is a predisposition of getting both type 1 and type 2 diabetes, but the type 2 diabetes has a bigger chance to run in the same family.
While we are not sure which type of diabetes is genetic for sure, or what triggers type 1 or type 2 diabetes to occur if you have a family member who suffers from it, the most important thing is to know that prevention is key especially in type 2 diabetes since studies have shown that diet and regular exercise can prevent it from happening, or in some cases reverse the symptoms. Recent Commentspatrice thompson on Free Diabetic Supplies – How to Get Them?munnaamalai on Type 1 vs Type 2 Diabetes ChartJessica I.
Marquez M, Huyvaert M, Perry JR, Pearson RD, Falchi M, Morris AP, Vivequin S, Lobbens S, Yengo L, Gaget S, Pattou F, Poulain-Godefroy O, Charpentier G, Carlsson LM, Jacobson P, Sjostrom L, Lantieri O, Heude B, Walley A, Balkau B, Marre M, Froguel P, Cauchi S; DIAGRAM Consortium. Cauchi S, Rung J, Albrechtsen A, Shen L, Rocheleau G, Cavalcanti-Proenca C, Bacot F, Balkau B, Belisle A, Borch-Johnsen K, Charpentier G, Dina C, Durand E, Elliott P, Hadjadj S, Jarvelin MR, Laitinen J, Lauritzen T, Marre M, Mazur A, Meyre D, Montpetit A, Pisinger C, Posner B, Poulsen P, Pouta A, Prentki M, Ribel-Madsen R, Ruokonen A, Sandbaek A, Serre D, Tichet J, Vaxillaire M, Wojtaszewski JF, Vaag A, Hansen T, Polychronakos C, Pedersen O, Froguel P, Sladek R. The next EGID International Symposium will be held on 29 and 30 November in Lille Grand Palais. A schematic representation of proposed integration of mechanisms by the protein products of type 1 diabetes (T1D) loci that are involved in adaptive immunity, and for which the direction of the functional effect of the T1D-associated variants is known or suspected. Candidate gene studies and recent collaborative genome-wide association efforts revealed at least 38 common single nucleotide polymorphisms (SNPs) associated with increased risk of T2D. Several recent guidelines advocate screening for individuals at risk to develop T2D followed by blood glucose measurements to detect individuals with impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). For example, deCODEme offers predictions for 50 complex diseases and non-disease phenotypes that vary from breast cancer, atrial fibrillation, T2D or psoriasis, to eye color and bitter taste perception. For example, deCODEme uses 21 SNPs from the genome-wide scan to calculate the risk of T2D for individuals with European descent, 9 SNPs for East Asians and 2 SNPsfor African Americans.
The companies take an average risk from some epidemiological study and multiply this with the odds ratios from published meta-analyses or large scale genome-wide association studies. Diabetes is a leading cause of blindness, renal failure and limb amputation, and a major risk factor for cardiovascular morbidity and mortality. The consortium advocates the use of clinical risk scores as primary screening tools to identify high-risk groups in whom T2D screening may be targeted more efficiently.
Their services may bypass healthcare providers who are typically responsible for appropriate ordering of lab tests and for discussing with patients the implications of test results.


A commonly used measure of discrimination is the area under the receiver operating characteristic curve (AUC). The first column lists all SNPs included in genetic tests for T2D, either used by DTC companies or available from published studies. Measures of calibration were presented in some of the T2D risk prediction studies and generally showed sufficient model fit.
Percentage of reclassification and the net reclassification improvement (NRI) are recently developed measures that assess this aspect of clinical utility. Subjects answered questions related to three domains: testing for risk prediction, testing to motivate behavior change and testing to guide medication prescription. To retrieve information about companies that offer DTC genetic testing for T2D risk prediction we performed a search in Google, followed the list of companies from a published review on DTC genomic companies 27 and collected additional information from discussions with other researchers. Furthermore, this project was sponsored by the VIDI grant of the Netherlands Organization for Scientific Research (NWO). However, either their pancreas cannot make enough insulin or such patients’ bodies do not use the little insulin produced.
Some of the symptoms can be mild and therefore need to be recognized early to get treatment as soon as possible. Of course other than family history, the disease is also related to environmental factors and living conditions. These include vegetables, fruits and whole grains etc.Low glycemic index foods are especially helpful, since the glycemic index shows how some foodstuffs affect your blood sugar. Some people achieve balanced glucose levels by just healthy eating and exercise, however some need extra help by the form of insulin injections. This is one of the most common questions asked by people who are diagnosed with diabetes, or with parents who have children with diabetes.
Researchers have found that although there is a predisposition for someone to have a diabetes, there are other factors other than genetics that may trigger the diabetes to occur. If one twin get a diabetes, the other one will likely to have it as well, although the possibility differs depending on which type of diabetes it is. This means that if you have a family member with type 2 diabetes, you have a bigger chance of getting it too if you do not take extra measures in preventing it from happening. What researchers have not found out is the triggers that might shed a clue to why some identical twins both get it, and some others do not, even though they have the exact same genes. The pathogenesis of T2D is characterized by two major features: peripheral insulin resistance and impaired insulin secretion from pancreatic beta-cells. Even if it is still necessary to identify the etiologic variants, additional genetic and epigenetic factors may help understandig the missing heritability. Molecules in green actively participate in T cell activation through T cell receptor (TCR) signalling or downstream events, whereas red indicates inhibitors of these processes. Genetic testing of multiple SNPs is considered a potentially useful tool for early detection of individuals at high diabetes risk leading to improved targeting of preventive interventions.
One such example is the Finnish risk test (FINDRISC) that provides ten-year risks to develop T2D.
Not all companies explicitly report the analytic and clinical performance characteristics of their test systems. Like companies, all studies used multiplicative models or additive genetic effects, [24][25][26] but whether this is correct has not been demonstrated. Reclassification is the percentage of individuals that change from one risk category based on the original prediction model to a different risk category based on the updated model. Research shows us that people with diabetic type 2 and obesity family history, often have same eating and exercising habits which lead them to contract disease, one due to genetics, and two due to their lifestyle and environment.
The treatment plan for Type 2 diabetic starts with healthy eating habits, exercising daily, possibly intake of insulin injections and keep monitoring the glucose in blood. As you probably already know, there are two type of diabetes, type 1 diabetes and type 2 diabetes.
The reason is because even though type 1 diabetes and type 2 diabetes has different causes, but there is a bigger chance for both types of diabetes to happen if some family members also have it. Westernization may largely explain the progressive increase in the prevalence of type 2 diabetes in the early part of the 20th century, particularly in developing countries. Arrows in grey boxes show the functional effect (whether an increase or a decrease) on the protein by the T1D risk allele in the genes that encode these proteins. When available, some companies use sex, ethnicity and age matched population risks to depart from. This number is expected to increase by more than 50% in the next 20 years if no preventive strategies are implemented.
The FINDRISC score contains eight items: age, BMI, waist circumference, antihypertensive medication, history of elevated blood glucose, daily physical activity and daily intake of fruits or vegetables. Following a recent Government Accountability Office investigation of companies providing direct-to-consumer genetic tests, the US Food and Drug Administration is considering premarket review of some laboratory-derived tests that pose higher clinical risks, assuring that the tests are evaluatedfor analytical and clinical validity. AUC indicates the probability that, on average, an individual with the disease will be assigned a higher predicted risk than an individual without the disease. However, patients were more likely than physicians to request genetic testing for risk prediction and treatment guidance.
Therefore, it is necessary to find out if the disease is due to lifestyle habits or because of your genetic makeup.
On the other hand, type 2 diabetes twin will have a bigger chance of 75%, if the other twin has it. However, if your family member suffers from type 1 diabetes, your probability of getting it is slightly lower compared to type 2 diabetes. In the case of human leukocyte antigens (HLAs) of the major histocompatibility complex (MHC), reduced function by risk alleles is not proven but is widely suspected. In the context of targeted screening, the guideline includes the followingrecommendation about genetic testing : “despite the encouraging progress in our understanding of the genetic basis of T2DM, it is too early to use genetic information as a tool for targeting preventive efforts”. Calibration indicates how close the risks predicted by the model are to the actual observed risks.
Disagreement between results for identical DNA samples sent to 4 different companies reflects the use of different sets of markers to predict risk of disease and the use of different average risks to depart from.
Cases are correctly classified when they move to a higher risk category and wrongly classified when they move to a lower category. Patients, and to a lesser extent physicians, expressed expectations that knowledge of genetic risk would motivate adoption of preventive lifestyle recommendations and increase adherence to treatment.


Secondly, according to WHO competent Authorities, there were in 2010 250 milion of diabetics, and they will be 366 milion in 2030, indicating that type 2 DM is today’s growing epidemics (1-15).
The risk of a child getting diabetes type 2 diseases is more if he or she has a diabetic mother.
Reduced beta-cell compensation to the insulin resistance associated with sedentary lifestyle and central obesity can gradually lead to T2D.
As TCR activation is involved in both tolerance and immune attack, the prevailing effect of signalling alterations on autoimmunity risk is not immediately obvious. The Hosmer-Lemeshow (H-L) chi-square test is a commonly used summary measure of calibration.
However, this is not a true evidence that this is purely genetic, because it is very common in families to share the same lifestyle which is probably causing someone to have type 2 diabetes. However, the risk to develop the disease is very different between individuals of the same ethnic group living in the same environment. Where known, T1D-associated alleles impair T cell activation through a loss-of-function of activators or a gain-of-function of inhibitors. The H-L test compares the observed and predicted number of patients within specified risk groups, usually deciles of risk. Table 4 shows the SNPs included in genetic risk scores in the studies summarized in Table 1 and the SNPs used by three commercial companies to predict T2D risk. NRI is the sum of the net correct moves: the proportion of cases moving up minus the proportion of cases moving down, plus the proportion of non-cases moving down minus the proportion of non-cases moving up. The other companies do not specify on their websites which SNPs they use for T2D risk prediction.
Since 2007, genome-wide association studies have identified ~50 loci for the most part associated with beta-cell defect.
For most companies, algorithms or criteria for interpreting SNP results are not made clear to the consumer. Obviously that happens in individuals with defined Biophysical Semeiotics Constitutions, in our case, Diabetic “and” Dislipidaemic, according to Joslin(1-6, 12-15). In the presence of inflammation (for example, active insulitis, perhaps initiated by innate immune events) and increased antigen abundance (for example, ?-cell apoptosis from viral infection), the same partial loss-of-function could be overridden by the stronger signals in T cells that have previously escaped self-tolerance for the same antigen. Even when this information is made available, [24][25][26] it is sometimes difficult to know which effect sizes and genotype frequencies are used to calculate a composite risk. To realize on vast scale Diabetes both Pre-Primary, and Primary Prevention (PP),enrolling exclusively individuals at type 2 DM Inherited Real Risk, we need new clinical tools, aiming to lower the increasing number of patients, because the present, expensive screening has failed (14).
In addition, defective interleukin 2 (IL-2) signalling will compromise the function of regulatory T cells. As a result, no clinically defined risk categories exist that can be applied across different populations where the underlying risk of T2D varies and, therefore, the cut-off values chosen to define the risk groups differ among studies. For instance, in the normal Langheran’s islets microcirculatory bed, there are exclusively “normal” type II (= in arterioles, according to Hammersen), but not type I (= in small arterioles) endoarteriolar blocking devices, i.e.
This is an important aspect in the interpretation of reclassification measures, as the choice of cut-off has a high impact on the percentage of reclassification observed. In addition, the evaluation of Insulin Secretion Acute Pick Renal Test is significantly impaired, corroborating the clinical diagnosis (1-3) (See above cited- website, Practical Applications, and Glossary). Considering the frequent association between hypertension and diabetes, more important, in my opinion based on 53-year-long clinical experience, is bedside recognizing diabetic predisposition, now-a-days possible since birth, utilising a lot of methods, different in difficulty, but all reliable. For the first time, from the clinical view-point, I have recently illustrated an original manoeuvre, based on a singular activity of osteocalcin, and reliable in bedside detecting diabetes in one minute, with the aid of a stethoscope (10). In fact, osteocalcin, a product of osteoblasts, among other action mechanisms, stimulates both insulin secretion and insulin receptor sensitivity. Twelve type 2 diabetes susceptibility loci identified through large-scale association analysis. Pharmacological and lifestyle interventions to prevent or delay type 2 diabetes in people with impaired glucose tolerance: systematic review and meta-analysis.
Combining genetic markers and clinical risk factors improves the risk assessment of impaired glucose metabolism.
Improvement of risk prediction by genomic profiling: reclassification measures versus the area under the receiver operating characteristic curve. Combining information from common type 2 diabetes risk polymorphisms improves disease prediction.
Post genome-wide association studies of novel genes associated with type 2 diabetes show gene-gene interaction and high predictive value.
Predicting type 2 diabetes based on polymorphisms from genome-wide association studies: a population-based study.
Assessing the combined impact of 18 common genetic variants of modest effect sizes on type 2 diabetes risk. Risk prediction of prevalent diabetes in a Swiss population using a weighted genetic score--the CoLaus Study.
Combined analysis of 19 common validated type 2 diabetes susceptibility gene variants shows moderate discriminative value and no evidence of gene-gene interaction. Use of multiple metabolic and genetic markers to improve the prediction of type 2 diabetes: the EPIC-Potsdam Study. Utility of genetic and non-genetic risk factors in prediction of type 2 diabetes: Whitehall II prospective cohort study. Evaluating the discriminative power of multi-trait genetic risk scores for type 2 diabetes in a northern Swedish population. Identification of undiagnosed type 2 diabetic individuals by the finnish diabetes risk score and biochemical and genetic markers: a population-based study of 7232 Finnish men. Genetic risk reclassification for type 2 diabetes by age below or above 50 years using 40 type 2 diabetes risk single nucleotide polymorphisms.
Construction of a prediction model for type 2 diabetes mellitus in the Japanese population based on 11 genes with strong evidence of the association. Evaluating the added predictive ability of a new marker: from area under the ROC curve to reclassification and beyond. The clinical application of genetic testing in type 2 diabetes: a patient and physician survey.



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