reference | supports | snippet | explanation |
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PMID:34599655 | REFUTE | Global numbers of incident and prevalent cases of type 1 diabetes were estimated to be 234,710 and 9,004,610, respectively, in 2017...Globally, type 1 diabetes represents about 2% of the estimated total cases of diabetes. | The prevalence of type 1 diabetes globally is estimated to be around 2%, not 0.1-0.2%. |
PMID:16085737 | NO_EVIDENCE | The global prevalence of diabetes for all age groups is estimated to be 2.8%. Type 2 diabetes accounts for at least 90% of diabetes worldwide. | This study provides global prevalence data for diabetes in general and specifically mentions Type 2 diabetes but does not give a percentage for the prevalence of Type 1 diabetes. |
PMID:27959859 | REFUTE | The incidence of childhood-onset type 1 diabetes has been increasing at a rate of 3%-5% per year globally...no means for a practical 'cure' exist. | The increasing incidence suggests a prevalence higher than 0.1-0.2%. |
reference | supports | snippet | explanation |
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PMID:33825933 | SUPPORT | The incidence of type 1 diabetes (T1D) has been rising steadily over the last 30 years, especially among children and adolescents, with the result that the number of cases in this age group doubles every 20 years. | This study discusses the rising incidence of type 1 diabetes in children and adolescents, which aligns with the progression of T1D during childhood and adolescence. |
PMID:30628751 | PARTIAL | Twenty-one percent of subjects developed T1D by age 6. Logistic regression modeling identified 5 significant predictors. | This study focuses on predictors of T1D progression in children with high-risk HLA genes followed in The TEDDY study, providing partial support since it includes childhood but doesn't explicitly cover adolescence. |
PMID:20723813 | NO_EVIDENCE | This reference only provides a foreword and does not include specific information about the progression phase or onset of Type 1 Diabetes. | |
PMID:26404926 | SUPPORT | Stage 3 as onset of symptomatic disease ... Adoption of this staging classification provides a standardized taxonomy for type 1 diabetes. | This reference discusses the presymptomatic stages of T1D leading to symptomatic onset, supporting the progression during childhood and adolescence. |
PMID:31280235 | PARTIAL | We aimed to evaluate children with type 1 diabetes (T1D) with early age at onset (EAO) for clinical, immune and metabolic features in order to identify age-related disease phenotypes. | This study focuses on early age at onset and disease phenotypes in children, but doesn't explicitly cover the entire range including adolescence. |
PMID:33274481 | NO_EVIDENCE | The reference title suggests outcomes over a 20-year period but doesn't provide specific data on the progression phase or onset of Type 1 Diabetes during childhood and adolescence in the provided abstract. | |
PMID:26816135 | SUPPORT | Type 1 diabetes accounted for 368/421 (87.4 %) patients with age of onset <18 y and 99/156 (63.5 %) of patients with onset between 19 and 25 y of age. | This study identifies the proportion of various types of diabetes in youth, including the onset of T1D in children and adolescents. |
reference | supports | snippet | explanation |
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PMID:11554771 | SUPPORT | The HLA-DQ genes are the primary susceptibility genes within this region, although other genes may also contribute. The IDDM2 locus maps to a variable number of tandem repeats in the insulin gene region on chromosome 11. | The provided literature confirms that HLA-DQ and INS genes contribute to the genetic susceptibility to Type 1 Diabetes. |
PMID:31331105 | SUPPORT | HLA DQA1*05 and DQB1*02 alleles encoding the DQ2.5 molecule and HLA DQA1*03 and DQB1*03 alleles encoding DQ8 molecules are strongly associated with celiac disease and type 1 diabetes. | The presence of HLA-DQ2 and HLA-DQ8 variants contributing to the genetic susceptibility of Type I Diabetes is supported. |
PMID:3309680 | SUPPORT | Over half of the inherited predisposition to insulin-dependent diabetes mellitus maps to the region of chromosome 6 that contains the highly polymorphic HLA class II genes which determine immune responsiveness. | HLA class II genes, including HLA-DQ, play significant roles in the predisposition to Type I Diabetes. |
PMID:27411431 | SUPPORT | The summary effect of haplotypes was generally seen in genotypes, while the expected synergistic effect of DR3-DQ2 and DR4-DQ8 combination was also clear in the T1D risk association analysis. | Combinations of HLA variants, including HLA-DQ2 and HLA-DQ8, have a synergistic effect in increasing the risk of Type I Diabetes. |
PMID:15342014 | SUPPORT | Accumulating evidence suggests that MHC susceptibility for T1D is recessive, with susceptibility alleles more common than protective alleles. | The literature indicates that HLA alleles, specifically susceptibility alleles, are significant in the context of Type I Diabetes. |
PMID:17130534 | SUPPORT | DQ8 and DQ2 are associated with susceptibility to and DQ6 with protection from type 1 diabetes mellitus (T1DM). | The association of HLA-DQ2 and HLA-DQ8 with susceptibility to Type I Diabetes is supported by this reference. |
PMID:17496359 | SUPPORT | Susceptibility to T1D is strongly linked to a major genetic locus that is the major histocompatibility complex (MHC) and several other minor loci including insulin, CTLA4 that contribute to diabetes risk in an epistatic way. | INS gene contribution to the susceptibility of Type I Diabetes is supported along with HLA genes. |
reference | supports | snippet | explanation |
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PMID:10522815 | SUPPORT | Various exogenous triggers, such as certain dietary factors and viruses, are thought to induce the autoimmune process leading in some individuals to extensive beta-cell destruction and ultimately to the clinical manifestation of type 1 diabetes. | This reference supports the statement by mentioning that dietary factors and viruses can trigger the autoimmune process in genetically susceptible individuals. |
PMID:21162649 | SUPPORT | The ability to induce strong cellular immune responses and to cause inflammation in the target organ makes viral infections prime candidates for the initiation of islet autoreactivity. | The reference supports the role of viral infections in triggering autoimmune responses leading to type 1 diabetes. |
PMID:18357774 | SUPPORT | The most often cited environmental agents implicated as initiators of T1D are the human enteroviruses, in particular the group B coxsackieviruses (CVB). | This reference supports the statement by identifying enteroviruses as environmental triggers for type 1 diabetes. |
PMID:9645989 | SUPPORT | Serologic case-control studies have suggested an association between coxsackie group B viruses and insulin-dependent diabetes mellitus (IDDM). | This reference supports the role of viral infections in the onset of type 1 diabetes. |
PMID:31593953 | SUPPORT | Viral infections and early exposure to gluten or cow''s milk in the infant diet have been implicated in disease pathogenesis. | The reference supports the statement by linking viral infections and early dietary factors to the pathogenesis of type 1 diabetes. |
PMID:32680364 | SUPPORT | Enteroviruses (EVs) are perhaps the most investigated environmental agents in relationship to the pathogenesis of T1D. | This supports the idea that viral infections contribute to the development of type 1 diabetes. |
reference | supports | snippet | explanation |
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PMID:12185667 | PARTIAL | Type 1 diabetes mellitus is a T-cell-mediated autoimmune disease that results in the destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans. | While T-cell mediated cytotoxicity is mentioned, there is no reference to autoantibody production. |
PMID:23774118 | PARTIAL | Phenotypes of infiltrating cells around and/or into islets were mainly dendritic cells, macrophages and CD8+ T cells. | Supports T cell-mediated cytotoxicity but does not discuss autoantibody production. |
PMID:27659143 | PARTIAL | The autoimmune destruction of the pancreatic islet beta cells is due to a targeted lymphocyte attack. | Supports T cell-mediated cytotoxicity but does not mention autoantibody production. |
PMID:27017348 | PARTIAL | Type 1 diabetes (T1D) is an autoimmune disorder characterized by the destruction of insulin-producing pancreatic beta cells. | Describes immune-mediated destruction of beta cells but does not specifically mention autoantibody production. |
PMID:16280652 | PARTIAL | Type 1 diabetes results from the destruction of insulin-producing pancreatic beta cells by a beta cell-specific autoimmune process. | Supports T cell-mediated cytotoxicity but does not address autoantibody production. |
PMID:34691077 | PARTIAL | Type 1 diabetes (T1D) is an autoimmune disease characterized by autoreactive T cell-mediated destruction of insulin-producing pancreatic beta-cells. | Supports T cell-mediated cytotoxicity but lacks information on autoantibody production. |
PMID:33479911 | PARTIAL | Type 1 diabetes is an organ-specific autoimmune disease characterized by immune-mediated beta cell destruction in pancreatic islets. | Describes immune-mediated destruction but not autoantibody production. |
PMID:28625830 | PARTIAL | Type 1 diabetes is an autoimmune disease marked by the destruction of insulin-producing beta cells in the pancreatic islets. | Indicates immune destruction of beta cells but does not mention autoantibody production. |
reference | supports | snippet | explanation |
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PMID:35254878 | SUPPORT | Type 1 diabetes mellitus (T1DM) is an endocrine disorder in which pancreatic beta cells stop producing insulin, typically due to autoimmune destruction. | This confirms that the loss of beta cells leads to a deficiency of insulin in Type 1 diabetes, as stated in the provided statement. |
PMID:21281836 | SUPPORT | Insulin resistance and defective glucose sensing at the beta-cell are the central pathophysiologic determinants that together cause hyperglycemia. | Although it primarily discusses prediabetes and Type 2 diabetes, the excerpt supports the idea that beta-cell issues lead to hyperglycemia. |
PMID:2006409 | SUPPORT | Glucose uptake into pancreatic beta cells by means of the glucose transporter GLUT-2, which has a high Michaelis constant, is essential for the normal insulin secretory response to hyperglycemia. | This indicates the importance of beta cells in glucose regulation and the resulting hyperglycemia when their function is impaired. |
PMID:11822099 | SUPPORT | Peripheral insulin-resistance and impairment of the hepatocellular function are two major possible causes of diabetes mellitus in liver cirrhosis. | This reference is more about liver cirrhosis but supports the general mechanism where insulin deficiency, due to impaired beta-cell function, leads to diabetes. |
PMID:11508279 | SUPPORT | Loss of blood glucose control might result from failure of the beta cells to secrete insulin, resistance of the tissues to its action, or a combination of both. | This also supports the idea that loss of beta cells leads to insulin deficiency and subsequent glucose control issues, relevant to both Type 1 and Type 2 diabetes. |
reference | supports | snippet | explanation |
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PMID:33970586 | SUPPORT | Type 1 diabetes is defined as a state of hyperglycemia due to insulin deficiency caused by autoimmune pancreatic beta-cell destruction. | The abstract from PMID:33970586 confirms that type 1 diabetes is characterized by hyperglycemia due to insulin deficiency, which supports the statement regarding elevated blood glucose and related downstream effects. |
PMID:37921158 | PARTIAL | HbA1c offers a trustworthy indicator of chronic hyperglycemia and strongly correlates with the likelihood of long-term consequences from diabetes. | Although this reference supports the relationship between elevated HbA1c and hyperglycemia, it does not specifically address all the downstream effects such as Glucosuria, Polyuria, Polydipsia, and Diabetic Ketoacidosis (DKA). |
PMID:21281836 | NO_EVIDENCE | The phenotype of prediabetes includes dyslipidemia and higher arterial blood pressure. | This study does not specifically address the pathophysiology of type 1 diabetes or the particular assays and downstream effects mentioned in the statement. |
PMID:11921414 | NO_EVIDENCE | Lack of insulin production or abnormalities affecting insulin secretion are key to the development of almost all forms of diabetes. | While it mentions insulin deficiency, this reference does not go into detail about the specific assays and downstream effects listed in the statement. |
PMID:15137354 | NO_EVIDENCE | The article points out the signs and symptoms to be aware of when the person is in the acute state of diabetic ketoacidosis. | This article touches on diabetic ketoacidosis but does not fully cover all the listed downstream effects and assays associated with type 1 diabetes pathophysiology. |
reference | supports | snippet | explanation |
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PMID:12477252 | SUPPORT | Type 1 or insulin-dependent diabetes mellitus is caused by autoimmune attack and selective destruction of the pancreatic beta cells. | The lack of insulin in type 1 diabetes mellitus leads to impaired glucose utilization as described in the statement. |
PMID:15137354 | SUPPORT | The following article reviews the basic pathophysiology of both type 1 diabetes mellitus and type 2 diabetes mellitus as we understand it today. | This article explains that in diabetes, particularly type 1, the lack of insulin results in impaired glucose utilization, leading to characteristic symptoms like weight loss and fatigue. |
reference | supports | snippet | explanation |
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PMID:6409465 | SUPPORT | Insulin deficiency results in increased rates of lipolysis and provides increased substrate (free fatty acids) for ketogenesis. | The article explains that insulin deficiency leads to increased lipolysis, which eventually results in the production of ketone bodies. This supports the statement's claim about the pathophysiology involving lipolysis and ketone production in Type I Diabetes. |
PMID:15137354 | SUPPORT | The article points out the signs and symptoms to be aware of when the person is in the acute state of diabetic ketoacidosis. | The article suggests that DKA is a critical concern in Type I Diabetes due to insufficient insulin, which is aligned with the statement indicating the downstream effect of heightened lipolysis and ketone production. |
PMID:34922394 | PARTIAL | the involvement of B:9-23rPep-specific IFN-gamma-related immunoreactivity in the pathophysiology of some unprovoked A-beta+ KPD. | Although the study highlights immune responses related to ketosis-prone Type 2 Diabetes, it indirectly supports the notion that immune-mediated processes can contribute to ketosis and DKA. |
reference | supports | snippet | explanation |
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PMID:38272591 | SUPPORT | Chronic complications can be microvascular or macrovascular. Microvascular complications include retinopathy, nephropathy, and neuropathy. Patients with type 1 diabetes are also at increased risk of macrovascular complications including coronary artery disease and vascular disease. | This study supports the statement by indicating that persistent hyperglycemia can lead to chronic complications such as retinopathy, neuropathy, nephropathy, and cardiovascular disease. |
PMID:31346658 | SUPPORT | Hyperglycaemia, dyslipidaemia and hypertension combine with the duration and type of diabetes to define the distinct pathophysiology underlying diabetic kidney disease, diabetic retinopathy and diabetic neuropathy. | The literature indicates that hyperglycemia is a significant factor in the pathophysiology of diabetic complications including kidney disease (nephropathy), retinopathy, and neuropathy, thereby supporting the claim. |
PMID:34407376 | SUPPORT | Hyperglycemia is the common denominator for most of the chronic diabetic vascular complications, which represent the main cause of life reduction in T1D patients. | This reference indicates that hyperglycemia underlies various chronic vascular complications in type 1 diabetes, thus supporting the statement. |
PMID:3528691 | SUPPORT | The remaining 15 to 20% of patients have insulin-dependent diabetes mellitus, a disorder caused by the destruction of insulin-producing endocrine cells within the pancreas and currently considered to be the result of an autoimmune process. During the course of both types of diabetes mellitus, the so-called long-term complications of diabetes invariably occur to some extent in all patients. These complications include retinopathy, nephropathy, neuropathy, and premature atherosclerosis. | The study confirms that type 1 diabetes, which involves insulin-dependent diabetes mellitus, results in long-term complications such as retinopathy, nephropathy, neuropathy, and cardiovascular disease. |
PMID:35456511 | SUPPORT | The prevention of hyperglycemia is very important to avoid or at least postpone the development of micro- and macrovascular complications, also known as late complications. These include diabetic retinopathy, chronic renal failure, diabetic neuropathy, and cardiovascular diseases. | The literature points out that hyperglycemia leads to microvascular (retinopathy, nephropathy, neuropathy) and macrovascular (cardiovascular diseases) complications, supporting the statement. |
reference | supports | snippet | explanation |
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PMID:38272591 | SUPPORT | Type 1 diabetes is associated with both acute and chronic complications. Acute complications include diabetic ketoacidosis and severe hypoglycemia. Chronic complications can be microvascular or macrovascular. Microvascular complications include retinopathy, nephropathy, and neuropathy. | This source supports the statement by associating Type I Diabetes with hyperglycemia and chronic complications such as retinopathy and neuropathy, as well as acute complications like diabetic ketoacidosis. |
PMID:28544185 | SUPPORT | Participation in prospective follow-up studies reduces the frequency of DKA in children at diagnosis of T1D, but genetic screening alone does not decrease DKA risk. | This source supports the statement by confirming that Diabetic Ketoacidosis (DKA) is a frequent acute complication in Type 1 Diabetes at the time of diagnosis. |
PMID:34362315 | SUPPORT | SH might be the first sign of insulinopenic status such as type 1 DM (T1DM). | This source supports the statement by describing stress hyperglycemia as a potential initial presentation of Type 1 Diabetes, thereby confirming hyperglycemia as a very frequent occurrence. |
reference | supports | snippet | explanation |
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PMID:23075321 | PARTIAL | Immune-mediated (auto-immune) Type 1 diabetes mellitus is not a homogenous entity, but nonetheless has distinctive characteristics. In children, it may present with classical insulin deficiency and ketoacidosis at disease onset, whereas autoimmune diabetes in adults may not always be insulin dependent. | The source does indicate that Type 1 diabetes has varied presentations, including insulin deficiency and potentially weight loss due to failure to utilize glucose. However, the excerpt does not specifically mention weight loss as a frequent phenotype. |
PMID:12949265 | NO_EVIDENCE | None | The provided literature does not directly discuss weight loss as a frequent systemic phenotype of Type 1 diabetes. |
PMID:11508279 | NO_EVIDENCE | None | This reference discusses the Accelerator Hypothesis and weight gain in diabetes but does not address weight loss in Type 1 diabetes. |
PMID:37065759 | PARTIAL | Almost (1/5) of cases involve people under the age of 20...The risk factors of weight gain included using exogenous insulin, intensifying insulin therapy, fear of hypoglycemia and related decrease in physical activity, and psychological factors, such as emotional eating and binge eating. | This reference addresses weight gain in relation to Type 1 Diabetes but does not state that weight loss is a frequent phenotype. |
PMID:19267337 | NO_EVIDENCE | None | The reference discusses the natural history of endogenous beta-cell function in Type 1 diabetes but does not mention weight loss being a frequent phenotype. |
name | presence | evidence | frequency |
---|---|---|---|
Blood Glucose | Elevated | TRUNCATED | VERY_FREQUENT |
Hemoglobin A1c (HbA1c) | Elevated | TRUNCATED | VERY_FREQUENT |
reference | supports | snippet | explanation |
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PMID:37560854 | SUPPORT | Individuals expressing HLA-DQ2 or DQ8, and DQ2/8 trans-dimers, have elevated risk for type 1 diabetes (T1D). | The reference explicitly states that individuals with HLA-DQ2 have an elevated risk for type 1 diabetes, supporting the statement of a genetic association between HLA-DQ2 and susceptibility to Type I Diabetes. |
reference | supports | snippet | explanation |
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PMID:22184118 | SUPPORT | HLA-DQ2 and HLA-DQ8 are strongly predisposing haplotypes for type 1 diabetes (T1D). | This statement specifically mentions HLA-DQ8 as a strong predisposing haplotype for type 1 diabetes, supporting the association with susceptibility. |
PMID:26492519 | SUPPORT | The DR3-DQ2/DR4-DQ8 genotype conferred the highest detected risk for T1D. | This study identifies the DR4-DQ8 genotype as highly associated with a risk for developing type 1 diabetes, thus supporting the genetic susceptibility. |
PMID:34946827 | SUPPORT | The combination of HLA-DQA1*03:01 and DQB1*03:02 alleles (summarized as 'HLA-DQ8') is reported to be among the two most prevalent HLA class II haplotypes in Caucasian type 1 diabetes patients. | This reference confirms that HLA-DQ8 is one of the most prevalent haplotypes among type 1 diabetes patients in the studied population, supporting its association with susceptibility. |
reference | supports | snippet | explanation |
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PMID:15529622 | SUPPORT | Our results indicate an exceptionally strong association of the class I INS-VNTR alleles with T1DM for the Romanian population. | The study presents evidence of a strong association between INS-VNTR alleles of the insulin gene and susceptibility to type 1 diabetes in the Romanian population. |
PMID:8934932 | SUPPORT | Genetic susceptibility predominantly results from specific alleles in the HLA complex and insulin gene region. | This paper states that genetic susceptibility to insulin-dependent diabetes mellitus predominantly results from specific alleles, including those in the insulin gene region. |
PMID:11845220 | SUPPORT | However, only within the past decade has it been possible to systematically attempt to identify the genes that increase susceptibility to this disorder using linkage and association analysis of genetic markers distributed across the genome. | This study discusses the identification of susceptibility genes for type 1 diabetes, including the insulin gene. |
PMID:11921414 | SUPPORT | Because insulin has such a central role in the pathogenesis of both forms of diabetes, the insulin gene (INS) has always been considered a candidate susceptibility gene. | The paper directly states that the insulin gene is considered a candidate susceptibility gene. |
PMID:11347740 | SUPPORT | The disease-associated INS genotype (Hph I) was identified in 87.5% of the concordant twins but only in 59.5% (P = 0.005) of the discordant twins. | The study demonstrates the presence of a disease-associated INS genotype in a high percentage of concordant twins for type 1 diabetes. |
PMID:33483996 | SUPPORT | Over half of the genetic risk has been attributed to the human leukocyte antigen (HLA) class II gene region and to the insulin (INS) gene locus. | This article attributes a significant portion of the genetic risk for type 1 diabetes to the insulin (INS) gene locus. |
reference | supports | snippet | explanation |
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PMID:23393684 | SUPPORT | One of the environmental risk factors identified by a series of independent studies is represented by viral infection, with strong evidence showing that viruses can indeed infect pancreatic beta cells with consequent effects ranging from functional damage to cell death. | This reference mentions that viral infections are a strong environmental risk factor for Type I Diabetes, affecting pancreatic beta cells which can lead to autoimmunity. |
PMID:22891485 | PARTIAL | Environmental factors must be involved such as viral infections, toxins from food, cow milk during childhood (instead of breast feeding) or vitamin D deficiency. | This reference suggests that viral infections are among several environmental factors associated with Type I Diabetes, but does not pinpoint them as the singularly most critical factor. |
PMID:34942009 | SUPPORT | Enteroviruses, especially CoxB and Echo, are most represented. | This reference supports the role of viral infections in Type I Diabetes, mentioning enteroviruses among others. |
PMID:18357774 | PARTIAL | The most often cited environmental agents implicated as initiators of T1D are the human enteroviruses, in particular the group B coxsackieviruses (CVB). | This reference supports the role of enteroviruses as environmental triggers for Type I Diabetes but notes that evidence is not firmly established. |
PMID:24003924 | PARTIAL | Enteroviruses are proposed candidate triggers due to temporal correlations between infection and T1D autoimmunity and to detection of viral proteins in diseased islets. | The reference suggests enteroviruses as potential triggers for Type I Diabetes but emphasizes the need for more robust evidence for a causative relationship. |
PMID:11334504 | SUPPORT | Congenital rubella is the only infection clearly associated with the development of type 1A diabetes. | This reference specifically mentions congenital rubella as an infection clearly associated with Type I Diabetes, supporting the statement. |
PMID:31401790 | PARTIAL | The natural history of human type 1 diabetes (T1D) and the documented associations between virus infections (in particular the enteroviruses) and disease development. | This reference discusses associations between viral infections, particularly enteroviruses, and Type I Diabetes development, but indicates a need for further studies. |
PMID:17691946 | SUPPORT | evidence from various animal models suggests that viruses can indeed initiate or accelerate autoimmune diseases, such as type 1 diabetes... | This reference provides evidence from animal models that support the initiation or acceleration of Type I Diabetes by viruses. |
PMID:36950864 | SUPPORT | Convincing evidence indicates that viruses are associated with T1D development and progression. | This reference provides convincing evidence that viral infections, including SARS-CoV-2, may trigger or unmask Type I Diabetes. |
reference | supports | snippet | explanation |
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PMID:8741809 | PARTIAL | There is a relationship between early cow's milk exposure and the development of Type 1 diabetes in humans, and between early cow's milk exposure and the development of autoimmune diabetes in rodent models of Type 1 diabetes. | The reference supports early dietary factors such as cow's milk exposure but indicates that the data are insufficient to conclude a causal relationship. |
PMID:26605913 | NO_EVIDENCE | Recently, the results of two large randomized trials have shown that breastfeeding in general, breastfeeding during gluten introduction, and early or delayed gluten introduction do not influence the total risk of CD in genetically predisposed individuals. | The reference suggests that early or delayed introduction of gluten does not influence the risk of celiac disease, type 1 diabetes mellitus, and wheat allergy, providing no supporting evidence for early dietary factors as risk factors for Type 1 diabetes. |
PMID:20640941 | PARTIAL | Given that type 1 diabetes, and its preclinical autoimmunity, appear early in life, infant and childhood diet have been implicated as potential initiating exposures in the etiology of the disease. | The reference implicates early dietary factors in the risk of Type 1 diabetes but also highlights inconsistencies and the need for further research. |
PMID:21067389 | NO_EVIDENCE | There appears to be no evidence for a relationship between infant formula feeding and the risk for type 1 diabetes mellitus. | The reference indicates that there is no evidence supporting the risk of early dietary factors, specifically infant formula, in the development of Type 1 diabetes. |
PMID:17203405 | PARTIAL | Enteroviruses (especially Coxsackie B virus), breastfeeding, the early presence or lack of certain foods, birth weight, childhood over-nutrition, maternal islet autoimmunity, and negative stress events have been shown to be related to the prevalence of T1D. | The reference supports a link between early dietary factors and Type 1 diabetes but does not provide conclusive evidence. |
reference | supports | snippet | explanation |
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PMID:21584767 | SUPPORT | Insulin therapy is a vital hormone replacement therapy in type 1 diabetes mellitus. | None |
PMID:36476434 | SUPPORT | The current standard method for type 1 diabetes (T1D) management majorly focuses on controlling blood glucose levels with exogeneous insulin administration. | None |
PMID:32342453 | SUPPORT | T1DM is caused by absolute lack of insulin secretion, so the current treatment for T1DM patients is exogenous insulin replacement therapy. | None |
PMID:20723814 | NO_EVIDENCE | The reference lacks specific details pertaining to treatment. | |
PMID:31426099 | PARTIAL | Although a cure for T1D remains the ultimate goal, technology holds the promise of keeping youth with T1D in targeted control and minimize the burden of this chronic medical condition. | The reference acknowledges insulin therapy but focuses more on technological advancements rather than confirming insulin therapy as the essential treatment. |
PMID:28685788 | PARTIAL | Replacing C-peptide, a hormone normally co-secreted with insulin, has been shown to reduce diabetes-related complications. | This reference discusses auxiliary therapy but does not diminish the essential role of insulin therapy. |
PMID:33970586 | SUPPORT | The mainstay of management is a regimen of multiple daily injections of insulin or continuous subcutaneous insulin delivered via an insulin pump. | None |
PMID:15306833 | SUPPORT | Most national bodies have recommended glycaemic targets, with an HbA(1c) to achieve between 6.5 and 7.5%...However, there is, however, a limit to what can be achieved with existing exogenous insulin therapies due to their imperfect pharmacokinetic and pharmacodynamic profiles. | None |
PMID:6749365 | SUPPORT | Replacement treatment with insulin is potentially capable of normalizing the metabolic abnormalities; and normalization of the metabolic abnormalities can be expected to prevent or ameliorate the complications of the disease. | None |
PMID:20666700 | PARTIAL | Insulin is the primary medication in the treatment of type 1 diabetes. New therapeutic options and prevention strategies (cellular therapies, immunomodulation and vaccination) aim to preserve residual beta-cell function. | The focus on insulin as primary treatment supports the statement, despite mentioning new therapeutic options. |
reference | supports | snippet | explanation |
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PMID:30215903 | SUPPORT | There is considerable benefit of tight glucose control in patients with type 1 diabetes mellitus. ... Greater frequency of glucose monitoring and continuous glucose monitoring are both associated with lower A1C levels. | The abstract emphasizes the importance of glucose monitoring in managing type 1 diabetes, supporting the statement that regular monitoring is crucial for effective glucose level management. |
PMID:32256447 | SUPPORT | Regular self-monitoring of blood glucose levels, and ketones when indicated, is an essential component of type 1 diabetes (T1D) management. | The abstract reaffirms that regular monitoring of blood glucose is essential for managing type 1 diabetes, supporting the statement. |
PMID:38551884 | SUPPORT | Blood glucose monitoring has been an integral part of diabetes treatment for many years, whether for type 1 diabetic patients on multiple daily injections of insulin, insulin pumps or artificial pancreas, and now for patients with type 2 diabetes... | The abstract describes blood glucose monitoring as a cornerstone in diabetes treatment, which includes the management of type 1 diabetes, thus supporting the statement. |
PMID:11149158 | SUPPORT | Sick-day management requires increased monitoring of blood glucose and assessment for ketosis. | The abstract highlights that during illness, increased blood glucose monitoring is necessary for managing type 1 diabetes, further supporting the statement about regular monitoring. |
reference | supports | snippet | explanation |
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PMID:9314011 | SUPPORT | Nutrition therapy and physical activity can assist persons with diabetes to achieve metabolic goals. Several lifestyle strategies can be used. | The text supports the assertion that maintaining a balanced diet and regular physical activity can assist in managing diabetes through lifestyle modifications. |
PMID:16529680 | SUPPORT | The patient and physician must work together to optimize glucose control involving both insulin administration and caloric intake. Exercise has numerous benefits and the type 1 diabetic should take advantage of these benefits. | This supports the statement that lifestyle modifications, including diet and physical activity, are important in managing type 1 diabetes. |
PMID:24485215 | SUPPORT | Poor lifestyle habits (poor diet quality, sedentary behaviours and smoking) are known to be driving factors for increased CMR factors in the general population. | The text underlines the significance of maintaining a good lifestyle, including a balanced diet and physical activity, as part of diabetes management. |
PMID:32312302 | SUPPORT | Innovative, cost-effective interventions along with beneficial lifestyle modifications can improve home-based self-monitoring of blood glucose in T1D patients. | This reference highlights the role of lifestyle modifications in managing type 1 diabetes through controlling blood glucose levels. |
PMID:37820077 | SUPPORT | Weight loss treatments provide a wide-range of benefits in reducing both morbidity and mortality in those who are obese. | It mentions lifestyle interventions as a part of weight loss treatments that benefit T1D management, highlighting their efficacy and safety. |