The DOI matches its Crossref record; 251 of the 251 references it cites were found in a registry or an index; 103 of the 163 sources its claims cite were checked for support.
Type 1 diabetes
Open accessAbstract
Over the past decade, knowledge of the pathogenesis and natural history of type 1 diabetes has grown substantially, particularly with regard to disease prediction and heterogeneity, pancreatic pathology, and epidemiology. Technological improvements in insulin pumps and continuous glucose monitors help patients with type 1 diabetes manage the challenge of lifelong insulin administration. Agents that show promise for averting debilitating disease-associated complications have also been identified. However, despite broad organisational, intellectual, and fiscal investments, no means for preventing or curing type 1 diabetes exists, and, globally, the quality of diabetes management remains uneven. This Seminar discusses current progress in epidemiology, pathology, diagnosis, and treatment of type 1 diabetes, and prospects for an improved future for individuals with this disease.
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Claims the paper makes
47 Partly supported · 44 No basis given · 39 No full text of the sources · 26 Supported · 15 Own interpretation · 5 Couldn’t confirm · 4 Supported so far · 4 Not checked yet · 3 Not supported · 1 Mixed support · accuracy not yet measured
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“For example, a third to half of Hispanic and African American children seem to have a form of type 1 diabetes without islet autoantibodies, and with pancreatic histology showing a lack of islets and complete loss of β cells—ie, pseudoatrophic islets.42”
§ Type 1 diabetes > Diagnosis > Disease heterogeneity
What the sources say
- Disputedcites [42] Gianani, 2010, Dimorphic histopathology of long-standing childhood-onset diabetes, Diabetologia sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) reports approximately 15%, not one-third to one-half, of children presenting with new-onset diabetes as autoantibody-negative in association with Hispanic and African-American ancestry. More decisively, the Results and Discussion (pages unavailable) say the two African-American and one Hispanic donors with the distinct pattern retained beta cells in every islet; they did not have the insulin-deficient islets described in the claim. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Disputed
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“In Finland, Germany, and Norway, annual increases in incidence of 2·4%, 2·6%, and 3·3%, respectively, have been reported.16,19,20”
§ Type 1 diabetes > Epidemiology
What the sources say
- Disputedcites [16] Patterson, 2009, Incidence trends for childhood type 1 diabetes in Europe during 1989–2003 and predicted new cases 2005–20: a multicentre prospective registration study, Lancet sourceExperimental — accuracy not yet measured
The Results table reports a 2·7% annual increase for the two Finnish regions studied, not the claimed 2·4%. It also reports 3·7% and 4·7% for the two German centres and 1·3% for the Norwegian counties, rather than the other figures in the sentence. These are centre-level estimates, not whole-country estimates. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
- Not checked — no full text of the sourcecites [19] Thunander, 2008, Incidence of type 1 and type 2 diabetes in adults and children in Kronoberg, Sweden, Diabetes Res Clin Pract source
- Disputedcites [20] Ehehalt, 2012, Prediction model for the incidence and prevalence of type 1 diabetes in childhood and adolescence: evidence for a cohort-dependent increase within the next two decades in Germany, Pediatr Diabetes sourceExperimental — accuracy not yet measured
The citation appears to be offered for the German figure. The Results (p. 15) report an average annual increase of 4.4% in the Baden-Württemberg childhood type 1 diabetes registry during 1987–2006, not 2.6%. The Discussion (page unavailable) repeats 4.4%; the paper does not establish the claimed 2.6% German rate. (LLM, conf=0.85)
Checked by a reasoning model — may be wrong.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Disputed
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“For example, the fusion protein CTLA4-Ig (abatacept) preserved stimulated C-peptide concentration for only 9 months despite continuous intravenous administration for 2 years.138”
§ Type 1 diabetes > Prevention and cure > Reversal
What the sources say
- Disputedcites [138] Orban, 2011, Co-stimulation modulation with abatacept in patients with recent-onset type 1 diabetes: a randomised, double-blind, placebo-controlled trial, Lancet sourceExperimental — accuracy not yet measured
The Results report an estimated 9.6-month delay in C-peptide decline, not preservation lasting only nine months. The Discussion says the difference from placebo was maintained throughout the two years of abatacept administration, despite a subsequent parallel decline in both groups. The supplied passages do not give page numbers. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Disputed
Every source the paper cites for this claim was checked and supports it.
In the paper
“The lack of firm diagnostic criteria for LADA, including retrospective criteria and similarities between patients with type 1 diabetes and LADA, have stunted enthusiasm for adopting it as a novel category for diabetes.40”
§ Type 1 diabetes > Diagnosis
What the sources say
- Supportedcites [40] Gale, 2005, Latent autoimmune diabetes in adults: a guide for the perplexed, Diabetologia source
In “Does LADA exist?” (page unavailable), Gale says the grounds for treating LADA as a distinct entity are insubstantial and that it is defined by characteristics it shares with type 1 diabetes. “Positive thinking” describes retrospectively selected antibody cut-offs and says they cannot cleanly separate diabetes variants. Together, these passages support the citing sentence’s paraphrase. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“leading to proposed classifications of type 1A (autoimmune) diabetes,41 for the 70–90% of patients with type 1 disease that have immunological, self-reactive autoantibodies”
§ Type 1 diabetes > Diagnosis > Disease heterogeneity
What the sources say
- Partly supportedcites [41] Eisenbarth, 2007, Update in type 1 diabetes, J Clin Endocrinol Metab sourceExperimental — accuracy not yet measured
The classification section identifies type 1A as immune-mediated diabetes and anti-islet autoantibodies as its best distinguishing markers. It says approximately 90% of newly diagnosed patients with type 1A diabetes have one or more measured autoantibodies; it does not say that 70–90% of all patients with type 1 diabetes have autoantibodies or belong to the type 1A category. (LLM, conf=0.88)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Around 5–15% of adults diagnosed with type 2 diabetes might actually have type 1 disease with islet autoantibodies present;36”
§ Type 1 diabetes > Diagnosis
What the sources say
- Partly supportedcites [36] Tuomi, 2005, Type 1 and type 2 diabetes: what do they have in common?, Diabetes sourceExperimental — accuracy not yet measured
The ‘Latent Autoimmune Diabetes in Adults’ section (p. S42) reports GAD autoantibodies in some adults diagnosed with type 2 diabetes and a LADA prevalence of about 4.2–13.2% in specified Caucasian populations. It reports different rates by age and ancestry, however, and calls LADA a heterogeneous group rather than saying all antibody-positive patients actually have type 1 diabetes. (LLM, conf=0.85)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“and being born in the spring is associated with a higher chance of having type 1 diabetes.8”
§ Type 1 diabetes > Epidemiology
What the sources say
- Supportedcites [8] Kahn, 2009, Association of type 1 diabetes with month of birth among US youth: the SEARCH for Diabetes in Youth study, Diabetes Care source
The Abstract Conclusions state that spring births were associated with an increased likelihood of type 1 diabetes. The Abstract Results report excess births in April–July among youth with type 1 diabetes, while noting that the association was not observed in the more southern study regions. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“and correctly noting diabetic ketoacidosis at diagnosis of type 1 disease represents a key window for survival.37”
§ Type 1 diabetes > Diagnosis
What the sources say
- Partly supportedcites [37] Usher-Smith, 2011, Factors associated with the presence of diabetic ketoacidosis at diagnosis of diabetes in children and young adults: a systematic review, BMJ sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) says diabetic ketoacidosis at diagnosis can cause life-threatening complications and is the commonest cause of diabetes-related death in children. The Discussion urges clinicians to be alert for it, supporting the importance of recognition, but the review does not establish that correctly identifying it at diagnosis improves survival or extend that conclusion beyond children and young adults. (LLM, conf=0.78)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Globally, the incidence and prevalence of type 1 diabetes vary substantially (figure 1).10”
§ Type 1 diabetes > Epidemiology
What the sources say
- Supportedcites [10] Maahs, 2010, Epidemiology of type 1 diabetes, Endocrinol Metab Clin North Am source
The “Incidence and Prevalence of T1D” section (page not provided) explicitly reports global variation in both incidence and prevalence. It also describes a greater than 350-fold difference in incidence among populations worldwide. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The presence of a chronic inflammatory infiltrate that affects pancreatic islets at symptomatic onset of type 1 diabetes is the basis of this observation (figure 2).49”
§ Type 1 diabetes > Pathophysiology
What the sources say
- Supportedcites [49] In't Veld, 2011, Insulitis in human type 1 diabetes: the quest for an elusive lesion, Islets source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“If incidence rates continue to increase on their existing path, global incidence could double over the next decade.16”
§ Type 1 diabetes > Epidemiology
What the sources say
- Partly supportedcites [16] Patterson, 2009, Incidence trends for childhood type 1 diabetes in Europe during 1989–2003 and predicted new cases 2005–20: a multicentre prospective registration study, Lancet sourceExperimental — accuracy not yet measured
The Abstract predicts that, if trends continue, new type 1 diabetes cases among European children younger than 5 will double between 2005 and 2020. It does not predict a doubling of global incidence over the next decade: the population is European children under 5, the measure is numbers of new cases, and the interval is 15 years. (LLM, conf=0.90)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Finally, genetic predisposition seems to be less of a factor now than it was in the past as a prerequisite for developing type 1 diabetes.23,24”
§ Type 1 diabetes > Epidemiology
What the sources say
- Not checked — no full text of the sourcecites [23] Gillespie, 2004, The rising incidence of childhood type 1 diabetes and reduced contribution of high-risk HLA haplotypes, Lancet source
- Supportedcites [24] Steck, 2011, Stepwise or linear decrease in penetrance of type 1 diabetes with lower-risk HLA genotypes over the past 40 years, Diabetes source
The Results report that the highest-risk HLA genotype became less common among children newly diagnosed with type 1 diabetes from the 1960s to the 2000s. The Discussion interprets this as a change in genetic risk, supporting the citing sentence’s cautious paraphrase. (LLM, conf=0.88)
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Every source the paper cites for this claim was checked and supports it.
In the paper
“More than 90% of individuals with newly diagnosed type 1 diabetes have one or more of the following autoantibodies at disease onset:53 those reactive to insulin (IAA), glutamic acid decarboxylase (GADA), insulinoma-associated autoantigen 2 (IA2A), and zinc transporter 8 (ZnT8A).65”
§ Type 1 diabetes > Pathophysiology > Serological
What the sources say
- Supportedcites [53] Bingley, 2010, Clinical applications of diabetes antibody testing, J Clin Endocrinol Metab source
The passage labeled Abstract states that, at disease onset, almost all patients with type 1 diabetes have islet autoantibodies. It reports that only 2–4% are antibody-negative when GADA, IA-2A, IAA, and ZnT8A are measured, supporting the claim that more than 90% have at least one. (LLM, conf=0.93)
- Supportedcites [65] Ziegler, 2010, Prediction and pathogenesis in type 1 diabetes, Immunity source
Citation 65 follows the list of autoantibodies; citation 53 is attached to the preceding prevalence statement. The “Biomarkers of susceptibility: Tools for disease prediction” section identifies the same four antigen groups: insulin or proinsulin, GAD, IA-2, and ZnT8. No page number is available in our copy. (LLM, conf=0.91)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“and many pancreata have non-inflamed insulin-containing islets that seem to be normal.58,59”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
What the sources say
- Not checked — no full text of the sourcecites [58] Gepts, 1965, Pathologic anatomy of the pancreas in juvenile diabetes mellitus, Diabetes source
- Supportedcites [59] Foulis, 1986, The histopathology of the pancreas in type 1 (insulin-dependent) diabetes mellitus: a 25-year review of deaths in patients under 20 years of age in the United Kingdom, Diabetologia source
The Discussion describes unaffected, insulin-containing islets in most cases. The ‘Islet pathology in recent onset Type I diabetes’ section says insulin-containing islets free of insulitis usually appeared normal, although some showed abnormalities. (LLM, conf=0.93)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“The loss of β-cell mass probably affects the performance of remaining β cells and other islet cell types, as shown by functional (and structural) studies.”
§ Type 1 diabetes > Pathophysiology > Natural history
What the sources say
- Could not verifycites [83] Greenbaum, 2012, Fall in C-peptide during first 2 years from diagnosis: evidence of at least two distinct phases from composite type 1 diabetes TrialNet data, Diabetes sourceExperimental — accuracy not yet measured
The Discussion describes declining insulin secretion and β-cell destruction in type 1 diabetes, but does not say that loss of β-cell mass changes the function of surviving β cells or other islet cell types. Searches for β-cell mass, structural studies, and other islet cells found no passage addressing that proposed effect. (LLM, conf=0.72)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In patients with type 1 diabetes with surviving β cells, insulitic lesions are usually lobular, analogous to the lobular loss of melanocytes in vitiligo.60”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
What the sources say
- Partly supportedcites [60] Michels, 2011, Immune intervention in type 1 diabetes, Semin Immunol sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) describes lobular β-cell destruction in patients with residual β cells, with normal-appearing islets beside areas lacking β cells. It does not describe insulitic lesions as usually lobular; it says insulitis is minimal in the great majority of pancreases examined at or after onset. Our copy also does not make the comparison with melanocyte loss in vitiligo. (LLM, conf=0.86)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The Epidemiology of Diabetes Interventions and Complications (EDIC) study,109 which followed participants with type 1 diabetes for long-term complications, found intensive diabetes treatment reduced the risk of cardiovascular events by 42% compared with conventional treatment.”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access > Complications associated with type 1 diabetes
What the sources say
- Supportedcites [109] Nathan, 2005, Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes, N Engl J Med source
The Results passage states that intensive therapy reduced the risk of a cardiovascular event by 42% compared with conventional therapy. The Methods passage identifies EDIC as the long-term follow-up of participants with type 1 diabetes originally assigned to those treatments in the DCCT. Page numbers are not provided in our copy. (LLM, conf=0.95)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“and analysis of C-peptide concentration after disease onset shows that loss is more rapid in the fi rst year after diagnosis than in the second year.83”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
What the sources say
- Partly supportedcites [83] Greenbaum, 2012, Fall in C-peptide during first 2 years from diagnosis: evidence of at least two distinct phases from composite type 1 diabetes TrialNet data, Diabetes sourceExperimental — accuracy not yet measured
The Results report a significantly faster C-peptide decline in the first 12 months of observation than in the next 12 months. The Discussion clarifies that observation began a median of 55 days after diagnosis, so those intervals do not correspond exactly to the first and second years after diagnosis; the paper has no data on the rate of decline between diagnosis and study entry. (LLM, conf=0.86)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Through these and other studies, analyses of pancreata from individuals with recent-onset type 1 diabetes suggest that around 70% of islets display complete insulin absence;51,52”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
What the sources say
- Could not verifycites [51] Gregg, 2012, Formation of a human beta-cell population within pancreatic islets is set early in life, J Clin Endocrinol Metab sourceExperimental — accuracy not yet measured
The study description (labeled Abstract in our copy; page unavailable) says the paper examined pancreatic sections from normal cadavers across the lifespan. Searches for recent-onset type 1 diabetes, insulin-negative islets, and 70% found no passage reporting the claimed finding. (LLM, conf=0.76)
- Partly supportedcites [52] Keenan, 2010, Residual insulin production and pancreatic ß-cell turnover after 50 years of diabetes: Joslin Medalist Study, Diabetes sourceExperimental — accuracy not yet measured
The Results (Histology; page not available) report that most islets in seven long-duration Joslin Medalists were atrophic and showed no insulin staining. The paper examines people with at least 50 years of diabetes, not recent-onset cases, and does not report that around 70% of islets lacked insulin. (LLM, conf=0.87)
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Could not verify
Every source the paper cites for this claim was checked and supports it.
In the paper
“Another study found higher concentrations of odd-chain triglycerides and poly-unsaturated fatty acid-containing phospholipids, and lower concentrations of methionine, in those who developed type 1 diabetes-associated autoantibodies.71”
§ Type 1 diabetes > Pathophysiology > Serological
What the sources say
- Supportedcites [71] Pflueger, 2011, Age- and islet autoimmunity-associated differences in amino acid and lipid metabolites in children at risk for type 1 diabetes, Diabetes source
The Results section reports lower median methionine and higher levels of the relevant lipid clusters in autoantibody-positive children than in autoantibody-negative children. The Discussion identifies the elevated lipids as odd-chain triglycerides and polyunsaturated fatty acid–containing phospholipids. It also notes that the methionine reduction was associated particularly with early autoimmunity. (LLM, conf=0.91)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“After diagnosis, the ability to retain residual β-cell function (assessed by production of C-peptide) is heterogeneous, in terms of the time it takes to reach an undetectable stage and the number of patients who, despite decades with type 1 diabetes, retain the ability to produce C-peptide.84”
§ Type 1 diabetes > Pathophysiology > Natural history
What the sources say
- Partly supportedcites [84] Keenan, 2010, Residual insulin production and pancreatic ss-cell turnover after 50 years of diabetes: Joslin Medalist Study, Diabetes sourceExperimental — accuracy not yet measured
The Results report that 67.4% of the Medalist cohort had detectable C-peptide after at least 50 years of diabetes, while 33.0% had undetectable levels. The Discussion also describes a wide range of C-peptide levels. These findings support variation in long-term residual function, but the study does not establish how long individuals took after diagnosis to reach undetectable levels. (LLM, conf=0.85)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Physiological events, including immune-system development and normal turnover of β cells, might also contribute to these pathogenic processes.55”
§ Type 1 diabetes > Pathophysiology > Natural history
What the sources say
- Partly supportedcites [55] Atkinson, 2011, How does type 1 diabetes develop?: the notion of homicide or beta-cell suicide revisited, Diabetes sourceExperimental — accuracy not yet measured
Figure 2 in “Novel mechanisms of antigenic processing that lead to immune responsiveness” describes thymic T-cell selection, the balance of regulatory and effector T-cells, and presentation of peptides from dead β-cells as parts of the model of type 1 diabetes pathogenesis. It does not identify normal β-cell turnover as a contributor to that process. No page number is available in our copy. (LLM, conf=0.78)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Children who received the hydrolysed formula were less likely to develop two or more islet autoantibodies compared with those who received the conventional formula, with an unadjusted hazard ratio of 0·52.128”
§ Type 1 diabetes > Prevention and cure > Primary and secondary prevention
What the sources say
- Supportedcites [128] Knip, 2010, Dietary intervention in infancy and later signs of beta-cell autoimmunity, N Engl J Med source
The Abstract Results report an unadjusted hazard ratio of 0.52 for positivity for two or more autoantibodies in the casein hydrolysate group versus the control group. The Abstract Methods identify the control as receiving a conventional cow’s-milk–based formula. The confidence interval (0.21 to 1.17) includes 1, but the claim does not assert statistical significance. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The HLA region on chromosome 6 (ie, the IDDM1 locus) provides perhaps one-half of the genetic susceptibility that leads to risk of type 1 diabetes.73”
§ Type 1 diabetes > Pathophysiology > Genetics
What the sources say
- Partly supportedcites [73] Noble, 2010, HLA class I and genetic susceptibility to type 1 diabetes: results from the type 1 Diabetes Genetics Consortium, Diabetes sourceExperimental — accuracy not yet measured
The introductory passage (labeled Abstract > CONCLUSIONS; page unavailable) identifies HLA loci on chromosome 6p21 as the major genetic susceptibility determinants for type 1 diabetes. Our copy does not quantify their contribution as approximately one-half or identify the region as IDDM1; searches for those terms and for a 50% contribution found no supporting passage. (LLM, conf=0.88)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In a second study, continuous glucose monitoring lowered nocturnal hypoglycaemia in children (<18 years) with type 1 diabetes, compared with self-monitored blood glucose.92”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
What the sources say
- Partly supportedcites [92] 2010, Prolonged nocturnal hypoglycemia is common during 12 months of continuous glucose monitoring in children and adults with type 1 diabetes, Diabetes Care sourceExperimental — accuracy not yet measured
The Research Design and Methods section includes children with type 1 diabetes, but this analysis uses only participants assigned to the CGM group. The Results report nocturnal hypoglycemia during CGM use; they do not compare it with self-monitored blood glucose or show that CGM lowered it in children. No page numbers are available in our copy. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“However, whether CSII is better, overall, than multiple daily injection for management of type 1 diabetes is debated, since outcomes reported in studies have varied substantially.90”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
What the sources say
- Could not verifycites [90] Pickup, 2011, Glycaemic control in type 1 diabetes during real time continuous glucose monitoring compared with self monitoring of blood glucose: meta-analysis of randomised controlled trials using individual patient data, BMJ sourceExperimental — accuracy not yet measured
The Methods (page unavailable) say the analysis compared continuous glucose monitoring with self-monitoring and excluded trials in which insulin treatment differed between arms. The Results’ Study characteristics (page unavailable) list CSII and multiple daily injections as delivery methods, but do not assess whether CSII is better or report variability in outcomes from that comparison. I searched for a discussion of conflicting CSII-versus-injection results and found none in our copy. (LLM, conf=0.76)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Could not verify
Every source the paper cites for this claim was checked and supports it.
In the paper
“Genetic susceptibility might also influence responses to environmental stimuli or physiological pathways (eg, vitamin D and interferon induced helicase).29,76”
§ Type 1 diabetes > Pathophysiology > Genetics
What the sources say
- Supportedcites [29] Cooper, 2011, Inherited variation in vitamin D genes is associated with predisposition to autoimmune disease type 1 diabetes, Diabetes source
The Results report associations between variants in vitamin D metabolism genes and type 1 diabetes. The Discussion links genetic determinants of vitamin D levels and signaling in T-cells to diabetes risk, supporting the hedged claim for the vitamin D example. This paper is not being cited for the interferon-induced helicase example. (LLM, conf=0.88)
- Supportedcites [76] Winkler, 2011, An interferon-induced helicase (IFIH1) gene polymorphism associates with different rates of progression from autoimmunity to type 1 diabetes, Diabetes source
The Abstract conclusions state that IFIH1 polymorphisms are consistent with a modified response to environmental factors during progression to type 1 diabetes. The Discussion identifies IFIH1 as a helicase involved in the interferon response to viral RNA, supporting the interferon-induced helicase example; this paper does not address the separate vitamin D example. (LLM, conf=0.92)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Class I MHCs also seem to influence risk for type 1 diabetes, independent of class II molecules.73”
§ Type 1 diabetes > Pathophysiology > Genetics
What the sources say
- Supportedcites [73] Noble, 2010, HLA class I and genetic susceptibility to type 1 diabetes: results from the type 1 Diabetes Genetics Consortium, Diabetes source
The Abstract Conclusions state that HLA class I alleles are associated with type 1 diabetes independently of HLA class II alleles. The Discussion likewise describes associations across multiple DR-DQ haplotypes as suggesting independent disease-associated alleles. No page numbers are supplied in our copy. (LLM, conf=0.95)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Much of what we understand about the pathogenesis of type 1 diabetes derives from analysis of pancreatic specimens, serum, and peripheral-blood lymphocytes obtained from patients with the disorder.53,54”
§ Type 1 diabetes > Pathophysiology
What the sources say
- Partly supportedcites [53] Bingley, 2010, Clinical applications of diabetes antibody testing, J Clin Endocrinol Metab sourceExperimental — accuracy not yet measured
The introductory passage under Abstract (page not provided) describes how detecting islet antibodies before diabetes onset revealed a long disease prodrome, supporting the serum-antibody part of the claim. The paper does not say that much of our understanding of pathogenesis derives from analysis of patient pancreatic specimens or peripheral-blood lymphocytes. (LLM, conf=0.78)
- Not checked — no full text of the sourcecites [54] Roep, 2011, Diabetogenic T lymphocytes in human type 1 diabetes, Curr Opin Immunol source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In one trial, individuals with at least two islet autoantibodies (one being an antibody against insulin) who had a first degree relative with type 1 diabetes, received oral insulin.130”
§ Type 1 diabetes > Prevention and cure > Primary and secondary prevention
What the sources say
- Partly supportedcites [130] Skyler, 2008, Update on worldwide efforts to prevent type 1 diabetes, Ann NY Acad Sci sourceExperimental — accuracy not yet measured
The paper’s DPT-1 discussion (page unavailable) reports an oral-insulin trial in relatives of people with type 1 diabetes and describes participants with insulin autoantibodies. Its risk discussion mentions two or more diabetes-related autoantibodies, but does not establish that this was an enrollment requirement for the oral-insulin trial; it also does not specify that those participants were first-degree relatives. (LLM, conf=0.83)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“IAA concentration correlates with the rate of progression to overt type 1 diabetes in children followed from birth.67,68”
§ Type 1 diabetes > Pathophysiology > Serological
What the sources say
- Supportedcites [67] Steck, 2011, Age of islet autoantibody appearance and mean levels of insulin, but not GAD or IA-2 autoantibodies, predict age of diagnosis of type 1 diabetes: diabetes autoimmunity study in the young, Diabetes Care source
The Conclusions (page not provided) state that mean IAA levels over time strongly correlate with time to diabetes. The study-population section describes prospective follow-up of young children at increased risk of diabetes, with IAA measured beginning at 9 months of age. (LLM, conf=0.91)
- Supportedcites [68] Parikka, 2012, Early seroconversion and rapidly increasing autoantibody concentrations predict prepubertal manifestation of type 1 diabetes in children at genetic risk, Diabetologia source
The Study design and individuals section says the children were monitored prospectively from birth. The Predictive value of early autoantibody concentration section reports that IAA concentration predicted progression to diabetes, with the fastest progression among children in the highest IAA quartile. The cohort was restricted to children with HLA-conferred genetic susceptibility. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The integrated closed-loop systems tested so far have reported favourable results;97”
§ Type 1 diabetes > Management of type 1 diabetes > Future care
What the sources say
- Supportedcites [97] Breton, 2012, Fully integrated artificial pancreas in type 1 diabetes: modular closed-loop glucose control maintains near normoglycemia, Diabetes source
The paper’s introductory passage says that several research groups reported promising results for subcutaneous closed-loop systems, including more time in the target glucose range and less hypoglycemia. Its Discussion also reports improved safety and glucose control in the two integrated systems tested in this paper. (LLM, conf=0.92)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“nearly 20% of insulin-containing islets, as opposed to only 1% of insulin-deficient islets, are inflamed (ie, insulitis),”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
What the sources say
- Not checked — no full text of the sourcecites [58] Gepts, 1965, Pathologic anatomy of the pancreas in juvenile diabetes mellitus, Diabetes source
- Partly supportedcites [59] Foulis, 1986, The histopathology of the pancreas in type 1 (insulin-dependent) diabetes mellitus: a 25-year review of deaths in patients under 20 years of age in the United Kingdom, Diabetologia sourceExperimental — accuracy not yet measured
The 'Islet pathology in recent onset Type 1 diabetes' section reports insulitis in 23% of insulin-containing islets and 1% of insulin-deficient islets, but only among cases where insulitis was present. The claim captures the contrast but omits that condition and describes 23% as 'nearly 20%.' (LLM, conf=0.84)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Every source the paper cites for this claim was checked and supports it.
In the paper
“efforts are being made in Belgium, Finland, and the USA (Network for Pancreatic Organ Donors with Diabetes [nPOD]57) to collect tissues from cadaveric donors with serological evidence of anti-islet autoimmunity (ie, type 1 diabetes-associated autoantibodies)—a subset of whom would presumably have developed type 1 diabetes if they had survived.”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
What the sources say
- Supportedcites [57] Campbell-Thompson, 2012, Network for Pancreatic Organ Donors with Diabetes (nPOD): developing a tissue biobank for type 1 diabetes, Diabetes Metab Res Rev source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Disappointingly, after promising phase 1–2 trials in patients with recent-onset type 1 diabetes and detectable endogenous insulin production, phase 3 trials of anti-CD3 antibodies (otelixizumab and teplizumab), and the Diamyd vaccine (GAD-alum immunotherapy) did not meet primary endpoints.135–141”
§ Type 1 diabetes > Prevention and cure > Reversal
What the sources say
- Partly supportedcites [135] Walter, 2009, No effect of the altered peptide ligand NBI-6024 on beta-cell residual function and insulin needs in new-onset type 1 diabetes, Diabetes Care sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [136] Pescovitz, 2009, Rituximab, B-lymphocyte depletion, and preservation of beta-cell function, N Engl J Med sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.
- Supportedcites [137] Sherry, 2011, Teplizumab for treatment of type 1 diabetes (Protege study): 1-year results from a randomised, placebo-controlled trial, Lancet source
The Discussion’s Interpretation states that this phase 3 teplizumab trial did not meet its primary outcome. The Introduction reports promising earlier anti-CD3 results and says a phase 3 otelixizumab trial also missed its primary efficacy outcome. This trial paper supports the anti-CD3 portion of the multi-cited sentence; it is not being used here as evidence for the Diamyd vaccine result. (LLM, conf=0.92)
- Partly supportedcites [138] Orban, 2011, Co-stimulation modulation with abatacept in patients with recent-onset type 1 diabetes: a randomised, double-blind, placebo-controlled trial, Lancet sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked — no full text of the sourcecites [139] Bach, 2011, Anti-CD3 antibodies for type 1 diabetes: beyond expectations, Lancet source
- Not checked — no full text of the sourcecites [140] Ludvigsson, 2012, GAD65 antigen therapy in recently diagnosed type 1 diabetes mellitus, N Engl J Med source
- Partly supportedcites [141] Wherrett, 2011, Antigen-based therapy with glutamic acid decarboxylase (GAD) vaccine in patients with recent-onset type 1 diabetes: a randomised double-blind trial, Lancet sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Fortunately, well organised trial networks (eg, NIH TrialNet and Immune Tolerance Network) and registries (eg, T1D Exchange) can test agents capable of providing therapeutic benefit, improve patient recruitment, and increase the precision of disease prediction.155”
§ Type 1 diabetes > Unanswered questions > Lessons learned
What the sources say
- Could not verifycites [155] Sosenko, 2012, The application of the diabetes prevention trial-type 1 risk score for identifying a preclinical state of type 1 diabetes, Diabetes Care sourceExperimental — accuracy not yet measured
The Research Design and Methods section describes the DPT-1 and TrialNet cohorts, and the Conclusions propose using risk-score thresholds as prevention-trial entry criteria. Neither passage addresses whether well-organised trial networks or registries improve patient recruitment. Searches for recruitment and trial enrollment found no passage making that point. (LLM, conf=0.73)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, the effects of this invasive treat ment waned over time, with loss of insulin independence in most patients after 5 years.145”
§ Type 1 diabetes > Prevention and cure > Reversal
What the sources say
- Partly supportedcites [145] Couri, 2009, C-peptide levels and insulin independence following autologous nonmyeloablative hematopoietic stem cell transplantation in newly diagnosed type 1 diabetes mellitus, JAMA sourceExperimental — accuracy not yet measured
The Results (page not provided) report that 8 of 20 patients who became insulin-free later resumed insulin, supporting some waning of the effect. But 12 remained insulin-free during follow-up, which lasted at most 58 months; this paper does not establish that most patients lost insulin independence after five years. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Type 1 diabetes has proven to be much more resistant than initially expected to therapeutic interventions with conventional or experimental agents, whether the goal is disease prevention or reversal.152”
§ Type 1 diabetes > Unanswered questions > Lessons learned
What the sources say
- Partly supportedcites [152] Staeva, 2013, Recent lessons learned from prevention and recent-onset type 1 diabetes immunotherapy trials, Diabetes sourceExperimental — accuracy not yet measured
The paper’s opening section says that immunotherapies pursued for prevention or reversal showed promising phase II results, but phase III trials failed to demonstrate efficacy. Its discussion of recent-onset treatment also describes benefits that were temporary or limited by toxicity. Our copy does not establish the same degree of resistance for prevention interventions or for conventional and experimental agents generally. (LLM, conf=0.84)
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Large investments in terms of time, finances (foundation, government, and industry-based), and patient resources have been directed to several promising areas—ie, islet-cell transplantation, stem cells, genetics, primary and secondary disease prevention, and reversal of type 1 diabetes—with results that are often deemed to have limited benefit.134”
§ Type 1 diabetes > Unanswered questions > Lessons learned
What the sources say
- Partly supportedcites [134] Greenbaum, 2011, Persistence is the twin sister of excellence: an important lesson for attempts to prevent and reverse type 1 diabetes, Diabetes sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Fortunately, well organised trial networks (eg, NIH TrialNet and Immune Tolerance Network) and registries (eg, T1D Exchange) can test agents capable of providing therapeutic benefit, improve patient recruitment, and increase the precision of disease prediction.155”
§ Type 1 diabetes > Unanswered questions > Lessons learned
What the sources say
- Partly supportedcites [155] Sosenko, 2012, The application of the diabetes prevention trial-type 1 risk score for identifying a preclinical state of type 1 diabetes, Diabetes Care sourceExperimental — accuracy not yet measured
The Conclusions discuss using the risk score to select people for prevention trials, and the References list TrialNet studies of therapeutic agents. This supports the trial-network aspect, but the paper does not address registries testing agents or establish the broader claim about therapeutic benefit. No page numbers are available in our copy. (LLM, conf=0.82)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Overall, administration of oral insulin did not delay progression to overt diabetes,”
§ Type 1 diabetes > Prevention and cure > Primary and secondary prevention
What the sources say
- Supportedcites [130] Skyler, 2008, Update on worldwide efforts to prevent type 1 diabetes, Ann NY Acad Sci source
In the oral insulin study discussion (page not provided), the paper states that oral insulin did not prevent or delay development of type 1 diabetes overall. It separately reports an apparent delay in a subgroup, which does not change the overall finding attributed here. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Administration of DiaPep277, a synthetic immunomodulator, at 3-month intervals resulted in less of a decline in stimulated C-peptide concentrations at 1 year in adults with type 1 diabetes than in the cohort that received placebo.142,143”
§ Type 1 diabetes > Prevention and cure > Reversal
What the sources say
- Partly supportedcites [142] Buzzetti, 2011, C-peptide response and HLA genotypes in subjects with recent-onset type 1 diabetes after immunotherapy with DiaPep277: an exploratory study, Diabetes sourceExperimental — accuracy not yet measured
The Results report less decline in stimulated C-peptide at 12 months with DiaPep277 than with placebo in adults with moderate-risk HLA genotypes; adults with low-risk genotypes had an increase. The claim omits that genotype qualification. Research Design and Methods also lists dosing at baseline and at 1, 6, and 12 months, not at 3-month intervals. Page numbers are unavailable in our copy. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites [143] Schloot, 2007, Effect of heat shock protein peptide DiaPep277 on beta-cell function in paediatric and adult patients with recent-onset diabetes mellitus type 1: two prospective, randomized, double-blind phase II trials, Diabetes Metab Res Rev source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Fortunately, well organised trial networks (eg, NIH TrialNet and Immune Tolerance Network) and registries (eg, T1D Exchange) can test agents capable of providing therapeutic benefit, improve patient recruitment, and increase the precision of disease prediction.155”
§ Type 1 diabetes > Unanswered questions > Lessons learned
What the sources say
- Partly supportedcites [155] Sosenko, 2012, The application of the diabetes prevention trial-type 1 risk score for identifying a preclinical state of type 1 diabetes, Diabetes Care sourceExperimental — accuracy not yet measured
The Abstract (Research Design and Methods and Conclusions; page unavailable) says the risk score was developed from DPT-1 data, validated in a TrialNet cohort, and had strong prediction accuracy. This supports the role of trial-network data in predicting type 1 diabetes, but the paper does not establish that well-organised networks or registries increase prediction precision generally. (LLM, conf=0.78)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
In the paper
“More cases are diagnosed in autumn and winter,7”
§ Type 1 diabetes > Epidemiology
What the sources say
- Not checked — no full text of the sourcecites [7] Moltchanova, 2009, Seasonal variation of diagnosis of type 1 diabetes mellitus in children worldwide, Diabet Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“A subset of individuals within this latter group have monogenic forms of diabetes, such as maturity onset diabetes of the young (MODY).43”
§ Type 1 diabetes > Diagnosis > Disease heterogeneity
What the sources say
- Not checked — no full text of the sourcecites [43] Hattersley, 2009, The diagnosis and management of monogenic diabetes in children and adolescents, Pediatr Diabetes source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Peaks in presentation occur between 5–7 years of age and at or near puberty.5”
§ Type 1 diabetes > Epidemiology
What the sources say
- Not checked — no full text of the sourcecites [5] Harjutsalo, 2008, Time trends in the incidence of type 1 diabetes in Finnish children: a cohort study, Lancet source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“however, no specific agents with an unequivocal influence on pathogenesis have been identified.”
§ Type 1 diabetes > Epidemiology
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The incidence of type 1 diabetes has been increasing worldwide for several decades.18”
§ Type 1 diabetes > Epidemiology
What the sources say
- Not checked — no full text of the sourcecites [18] Dabelea, 2009, The accelerating epidemic of childhood diabetes, Lancet source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The global incidence of type 1 diabetes represents an epidemiological conundrum; wide variations in disease incidence are noted between neighbouring areas in Europe and in North America.”
§ Type 1 diabetes > Epidemiology
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“however, overall, type 1 diabetes seems to represent a heterogeneous disease whose pathogenic processes, genetics, and phenotypic characteristics show marked variation.”
§ Type 1 diabetes > Diagnosis > Disease heterogeneity
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These concepts support a theoretical role for an environ mental agent initiating or driving the pathogenic processes in type 1 diabetes.”
§ Type 1 diabetes > Epidemiology
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Particularly among adults, diagnosis of type 1 versus type 2 diabetes can be challenging.”
§ Type 1 diabetes > Diagnosis
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Development of type 1 diabetes-associated autoimmunity (ie, formation of islet autoantibodies) in the months or years before onset of symptomatic type 1 diabetes also shows some seasonal synchronisation.9”
§ Type 1 diabetes > Epidemiology
What the sources say
- Not checked — no full text of the sourcecites [9] Kukko, 2005, Dynamics of diabetes-associated autoantibodies in young children with human leukocyte antigen-conferred risk of type 1 diabetes recruited from the general population, J Clin Endocrinol Metab source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Attempts to distinguish adult cases of type 1 diabetes from those with type 2 disease have resulted in the proposal of new disease classifications, including latent autoimmune disease of adults (LADA) and ketosis-prone diabetes.38,39”
§ Type 1 diabetes > Diagnosis
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Finally, although controversial, therapeutic interventions have clearly benefited from studies in animal models of type 1 diabetes, particularly the NOD mouse.127”
§ Type 1 diabetes > Prevention and cure
What the sources say
- Not checked — no full text of the sourcecites [127] Atkinson, 2011, Evaluating preclinical efficacy, Sci Transl Med source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Over the past decade, use of continuous sub cutaneous insulin infusions (CSII; insulin pumps) has increased substantially.87”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
What the sources say
- Not checked — no full text of the sourcecites [87] Pickup, 2012, Insulin-pump therapy for type 1 diabetes mellitus, N Engl J Med source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“A key distinguishing feature between type 1 and type 2 diabetes is the presence of autoantibodies against β-cell autoantigens.”
§ Type 1 diabetes > Pathophysiology > Serological
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Studies of secondary prevention, to delay onset of type 1 diabetes, are done in individuals with multiple islet autoantibodies but without overt hyperglycaemia.”
§ Type 1 diabetes > Prevention and cure > Primary and secondary prevention
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Most studies of pancreatic pathology of type 1 diabetes involve retrospective, sample-based analysis of pancreata obtained at autopsy from individuals who died at or near the time of diagnosis, revealing a range of islet cell and whole organ features (figure 2).”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Among individuals who have had type 1 diabetes for more than 5 years, most of the remaining islets are insulin deficient, containing a normal complement of other hormone secreting cells (ie, α cells that secrete glucagon, δ cells that secrete somatostatin, and PP cells that secrete pancreatic polypeptide).62”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
What the sources say
- Not checked — no full text of the sourcecites [62] Willcox, 2009, Analysis of islet inflammation in human type 1 diabetes, Clin Exp Immunol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“This finding, combined with an extensive series of independent investigations in humans and in rodent models of type 1 diabetes, support the growing notion that proinsulin is a key autoantigen in the disease;69”
§ Type 1 diabetes > Pathophysiology > Serological
What the sources say
- Not checked — no full text of the sourcecites [69] Kent, 2005, Expanded T cells from pancreatic lymph nodes of type 1 diabetic subjects recognize an insulin epitope, Nature source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“A key element for such efforts involves low-glucose suspend systems that monitor blood glucose with a continuous glucose monitor and suspend insulin delivery when glucose falls below a preset threshold for up to 2 h, to prevent hypoglycaemic episodes.95”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
What the sources say
- Not checked — no full text of the sourcecites [95] Hirsch, 2012, Low glucose suspend: ready for prime time?, Diabetes Technol Ther source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In addition to having diagnostic value in type 1 diabetes, autoantibodies can help identify people with an increased risk for developing the disease, through detection in first-degree relatives or in the general population.”
§ Type 1 diabetes > Pathophysiology > Serological
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Despite the progress made for treatment of type 1 diabetes, individuals in many parts of the world die because of lack of access to insulin.122”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access > Access to insulin
What the sources say
- Not checked — no full text of the sourcecites [122] Gale, 2006, Dying of diabetes, Lancet source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Furthermore, children and adolescents lose endogenous insulin production at a greater rate than do adults with type 1 diabetes.”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This feature, combined with the absence of insulitis, suggests that multiple mechanisms lead to the loss of β cells in the pathogenesis of type 1 diabetes.”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Inherent immune dysregulation, probably facilitated by genetic susceptibility, results in early serological evidence of β-cell destruction—ie, altered aminoacids and autoantibodies associated with type 1 diabetes.”
§ Type 1 diabetes > Pathophysiology > Natural history
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Most of the loci associated with risk of type 1 diabetes are thought to involve immune responses,72”
§ Type 1 diabetes > Pathophysiology > Genetics
What the sources say
- Not checked — no full text of the sourcecites [72] Concannon, 2009, Genetics of type 1A diabetes, N Engl J Med source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“After initial diagnosis and metabolic stabilisation, some patients with type 1 diabetes retain the ability to produce endogenous insulin.”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“however, exogenous insulin replacement does not always provide the metabolic regulation necessary to avoid one or more disease associated-complications (eg, retinopathy, neuropathy, cardio vascular disease, and hypoglycaemia).”
§ Type 1 diabetes > Management of type 1 diabetes
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“C-peptide is secreted from β cells at a one-to-one ratio with insulin,”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
In the paper
“As a result, diabetes management in modern countries often includes use of insulin analogues and mechanical technologies (eg, insulin pumps and continuous glucose monitors) for improved treatment of type 1 disease.85”
§ Type 1 diabetes > Management of type 1 diabetes
What the sources say
- Not checked — no full text of the sourcecites [85] Hirsch, 2009, Clinical review: realistic expectations and practical use of continuous glucose monitoring for the endocrinologist, J Clin Endocrinol Metab source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In this study, the degree of HbA1C reduction directly correlated with higher HbA1C concentrations before beginning continuous glucose monitoring.”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
What the sources say
- Not checked — no full text of the sourcecites [91] Tamborlane, 2008, Continuous glucose monitoring and intensive treatment of type 1 diabetes, N Engl J Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Primary prevention studies, in individuals with a genetic risk for type 1 diabetes but without islet autoantibodies, have largely focused on dietary modifications early in infancy.”
§ Type 1 diabetes > Prevention and cure > Primary and secondary prevention
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Studies of these constituents suggest that a series of functional defects in the bone marrow and thymus, immune system, and β cells collectively contribute to the pathophysiology of type 1 diabetes (figure 3).”
§ Type 1 diabetes > Pathophysiology
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In most individuals, changes in insulin secretion and glucose tolerance occur months to decades after multiple islet autoantibodies are detected.79”
§ Type 1 diabetes > Pathophysiology > Natural history
What the sources say
- Not checked — no full text of the sourcecites [79] Bonifacio, 2010, Advances in the prediction and natural history of type 1 diabetes, Endocrinol Metab Clin North Am source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Another trial removed bovine insulin from infant formula and reported less progression (compared with infants who received normal cow's milk formula) to the development of one islet autoantibody after 3 years of follow-up.129”
§ Type 1 diabetes > Prevention and cure > Primary and secondary prevention
What the sources say
- Not checked — no full text of the sourcecites [129] Vaarala, 2012, Removal of bovine insulin from cow's milk formula and early initiation of beta-cell autoimmunity in the FINDIA pilot study, Arch Pediatr Adolesc Med source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“For example, environmental influences might occur as early as in utero and probably continue during the first months to years of life, thereby affecting the onset and continuance of β-cell autoimmunity.”
§ Type 1 diabetes > Pathophysiology > Natural history
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
In the paper
“Patients with type 1 diabetes have less favourable outcomes than non-diabetic patients after an acute coronary event,110”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access > Complications associated with type 1 diabetes
What the sources say
- Not checked — no full text of the sourcecites [110] Eckel, 2012, Autoimmune diabetes inflames the heart, Sci Transl Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, type 1 diabetes involves a selective loss of β cells.”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Most approaches involve provision of self-antigen (eg, vaccination with specific islet-cell proteins, such as insulin or GAD) or immune suppression (table 2).”
§ Type 1 diabetes > Prevention and cure > Reversal
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Inability to overcome the autoimmune nature of this disease, perhaps the result of robust immunological memory combined with failure to attenuate deleterious immune responses that are not subject to normal regulation, is a hurdle that needs to be addressed with intense research.”
§ Type 1 diabetes > Unanswered questions > Lessons learned
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The polygenic nature of type 1 diabetes (more than 40 loci have been associated with disease susceptibility or resistance72) combined with environmental associations mean that disease pathogenesis can be unpredictable.”
§ Type 1 diabetes > Unanswered questions > Lessons learned
What the sources say
- Not checked — no full text of the sourcecites [72] Concannon, 2009, Genetics of type 1A diabetes, N Engl J Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In 2000, a breakthrough protocol was developed for islet transplantation without the use of glucocorticoids for immune suppression;149”
§ Type 1 diabetes > Prevention and cure > Islet-cell transplantation
What the sources say
- Not checked — no full text of the sourcecites [149] Shapiro, 2000, Islet transplantation in seven patients with type 1 diabetes mellitus using a glucocorticoid-free immunosuppressive regimen, N Engl J Med source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The polygenic nature of type 1 diabetes (more than 40 loci have been associated with disease susceptibility or resistance72) combined with environmental associations mean that disease pathogenesis can be unpredictable.”
§ Type 1 diabetes > Unanswered questions > Lessons learned
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Currently, there are no approved agents to stop the autoimmune destruction of β cells after diagnosis of type 1 diabetes.”
§ Type 1 diabetes > Prevention and cure > Reversal
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“A 2007 trial of autologous haematopoietic stem-cell transplantation combined with high-dose immunosuppression (ie, cytoxan and thymoglobulin) reported increased C-peptide production and insulin independence in most patients who received treatment at disease onset.144”
§ Type 1 diabetes > Prevention and cure > Reversal
What the sources say
- Not checked — no full text of the sourcecites [144] Voltarelli, 2007, Autologous nonmyeloablative hematopoietic stem cell transplantation in newly diagnosed type 1 diabetes mellitus, JAMA source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Difficulty understanding the genetic complexity of type 1 diabetes is compounded by a lack of knowledge regarding the immune response in this disorder.”
§ Type 1 diabetes > Unanswered questions > Lessons learned
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“the initially promising results deteriorated so that at 5 years, only 10% of patients remained independent of exogenous insulin.150”
§ Type 1 diabetes > Prevention and cure > Islet-cell transplantation
What the sources say
- Not checked — no full text of the sourcecites [150] Ryan, 2005, Five-year follow-up after clinical islet transplantation, Diabetes source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 58
- Probably not a substantial claim. 61
- The quote only partly states this claim. 1
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“Recent data suggest that although most patients with longstanding type 1 diabetes have few β cells, if any, there is evidence for β-cell regeneration in infants and very young children (but not in adolescents or adults).51,52”
§ Type 1 diabetes > Pathophysiology
What the sources say
- Partly supportedcites [51] Gregg, 2012, Formation of a human beta-cell population within pancreatic islets is set early in life, J Clin Endocrinol Metab sourceExperimental — accuracy not yet measured
The paper reports a burst of β-cell proliferation in the first two years of normal life, with little growth thereafter (Abstract; page unavailable). It does not establish regeneration in patients with longstanding type 1 diabetes or address how many β cells those patients retain. It also reports rare β-cell neogenesis in adolescents and adults, so the claim’s categorical exclusion of those ages is not supported. (LLM, conf=0.88)
- Disputedcites [52] Keenan, 2010, Residual insulin production and pancreatic ß-cell turnover after 50 years of diabetes: Joslin Medalist Study, Diabetes sourceExperimental — accuracy not yet measured
The Discussion (page unavailable in our copy) says β-cells can be replenished despite prolonged autoimmune stress and reports evidence of β-cell proliferation in people with type 1 diabetes for over 50 years. That is contrary to the claim that regeneration does not occur in adults. The paper does not establish the claimed contrast with infants and very young children. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Although type 1 diabetes can be diagnosed at any age, it is one of the most common chronic diseases of childhood.4”
§ Type 1 diabetes > Epidemiology
What the sources say
- Could not verifycites [4] Gale, 2005, Type 1 diabetes in the young: the harvest of sorrow goes on, Diabetologia sourceExperimental — accuracy not yet measured
The paper’s main text (page unavailable) discusses childhood-onset type 1 diabetes and reports rising incidence in Europe. It does not say whether type 1 diabetes is among the most common chronic diseases of childhood; searches for that phrase and for childhood disease prevalence found no comparison with other diseases. (LLM, conf=0.72)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, not all patients with type 1 diabetes have these characteristics, leading to proposed classifications of type 1A (autoimmune) diabetes,41 for the 70–90% of patients with type 1 disease that have immunological, self-reactive autoantibodies, and type 1B (idiopathic) diabetes, representing the remainder whose specific pathogenesis remains unclear.42”
§ Type 1 diabetes > Diagnosis > Disease heterogeneity
What the sources say
- Supportedcites [41] Eisenbarth, 2007, Update in type 1 diabetes, J Clin Endocrinol Metab source
The opening section describes type 1A as immune-mediated and type 1B as a non-autoimmune, idiopathic form of type 1 diabetes. It also identifies anti-islet autoantibodies as markers distinguishing type 1A from other forms, supporting the distinction attributed to this source. (LLM, conf=0.92)
- Partly supportedcites [42] Gianani, 2010, Dimorphic histopathology of long-standing childhood-onset diabetes, Diabetologia sourceExperimental — accuracy not yet measured
The Introduction reports that about 15% of children presenting with new-onset diabetes produce no islet autoantibodies, and the Discussion says the causes of some other forms of childhood-onset diabetes need further study. The paper does not identify this entire remainder as type 1B (idiopathic) diabetes; it also discusses other possible forms, including type 2 and monogenic diabetes. No page numbers are available in our copy. (LLM, conf=0.83)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Historically, type 1 diabetes was largely considered a disorder in children and adolescents, but this opinion has changed over the past decade, so that age at symptomatic onset is no longer a restricting factor.3”
§ Type 1 diabetes > Introduction
What the sources say
- Supportedcites [3] Leslie, 2010, Predicting adult-onset autoimmune diabetes: clarity from complexity, Diabetes source
In “Predicting Adult-Onset Autoimmune Diabetes” (page not supplied), the paper says the historical characterization of severe diabetes as childhood-onset was supplanted by classifications based on other features. Its Fig. 1 states that autoimmune diabetes extends across all ages, supporting the claim that age at onset is not a restricting factor. (LLM, conf=0.92)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“A 2011 study of adult-onset type 1 diabetes suggested that autoimmune type 1 diabetes in children and adults differs by just a few age-dependent genetic effects;48”
§ Type 1 diabetes > Diagnosis > Disease heterogeneity
What the sources say
- Supportedcites [48] Howson, 2011, Genetic analysis of adult-onset autoimmune diabetes, Diabetes source
The Abstract’s Conclusions state that the results are consistent with the hypothesis that autoimmune diabetes in adults and children differs by only relatively few age-dependent genetic effects. The citing sentence preserves that tentative wording by saying the study “suggested” this conclusion. (LLM, conf=0.95)
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In 2009, the American Diabetes Association modified their guidelines for diabetes diagnosis to include glycated haemoglobin (HbA1C; a test that averages blood glucose concentrations over 3 months) of 6·5% or higher.35”
§ Type 1 diabetes > Diagnosis
What the sources say
- Partly supportedcites [35] 2009, International Expert Committee report on the role of the A1C assay in the diagnosis of diabetes, Diabetes Care sourceExperimental — accuracy not yet measured
The Recommendations and conclusions section recommends diagnosing diabetes at A1C ≥6.5%. But the opening section says the report represents the International Expert Committee’s views, not necessarily those of the American Diabetes Association, and invites professional organizations to consider its recommendations. It does not establish that the ADA modified its guidelines in 2009. (LLM, conf=0.89)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“if this is the case, perhaps as many as 50% of actual type 1 diabetes cases are misdiagnosed as type 2, meaning that the number of cases of type 1 disease is vastly underestimated.”
§ Type 1 diabetes > Diagnosis
What the sources say
- Partly supportedcites [36] Tuomi, 2005, Type 1 and type 2 diabetes: what do they have in common?, Diabetes sourceExperimental — accuracy not yet measured
The ‘Latent Autoimmune Diabetes in Adults’ section (pp. S40–S45) reports LADA in some adults diagnosed with type 2 diabetes, including prevalence estimates of 4.2–13.2% in specified Caucasian populations. It does not estimate that 50% of actual type 1 cases are diagnosed as type 2 or conclude that type 1 case counts are vastly underestimated. Its discussion also treats LADA as heterogeneous, rather than equating every LADA case with type 1 diabetes. (LLM, conf=0.84)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“For example, incidence in Estonia is less than one-third of the incidence in Finland, although the two countries are separated by less than 120 km.17”
§ Type 1 diabetes > Epidemiology
What the sources say
- Partly supportedcites [17] Podar, 2001, Increasing incidence of childhood-onset type I diabetes in 3 Baltic countries and Finland 1983–1998, Diabetologia sourceExperimental — accuracy not yet measured
The Results report mean childhood-onset type 1 diabetes incidence of 11.2 in Estonia and 37.7 in Finland during 1983–1998, making Estonia’s rate less than one-third of Finland’s. The passages found do not state that the countries are separated by less than 120 km. (LLM, conf=0.87)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Both of these concepts of pathogenesis of type 1 diabetes have been debated.50,51”
§ Type 1 diabetes > Pathophysiology
What the sources say
- Not checked — no full text of the sourcecites [50] Butler, 2007, The replication of beta cells in normal physiology, in disease and for therapy, Nat Clin Pract Endocrinol Metab source
- Partly supportedcites [51] Gregg, 2012, Formation of a human beta-cell population within pancreatic islets is set early in life, J Clin Endocrinol Metab sourceExperimental — accuracy not yet measured
The passage labeled Abstract (page unavailable) reports occasional β-cell neogenesis in adults, which bears on the idea that β cells cannot regenerate. But the study examined normal human pancreases, not remaining β cells in type 1 diabetes, and our copy does not address whether autoimmune destruction is debated. (LLM, conf=0.78)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Genetic changes or more children being born from mothers with type 1 diabetes cannot solely explain such rapid rates of increased incidence.22”
§ Type 1 diabetes > Epidemiology
What the sources say
- Partly supportedcites [22] Soltesz, 2007, Worldwide childhood type 1 diabetes incidence—what can we learn from epidemiology?, Pediatr Diabetes sourceExperimental — accuracy not yet measured
The 'Temporal trends in incidence' section reports rising childhood type 1 diabetes incidence, and 'Childhood type 1 diabetes' offers environmental and lifestyle factors as potential explanations. This supports the broader point that genetics alone need not explain the increase, but the paper does not address whether an increase in births to mothers with type 1 diabetes could explain it. Page numbers were unavailable in our copy. (LLM, conf=0.78)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In many countries, the rise in incidence of type 1 diabetes has fluctuated, although Sweden has recently seen incidence rates plateau.12”
§ Type 1 diabetes > Epidemiology
What the sources say
- Partly supportedcites [12] Berhan, 2011, Thirty years of prospective nationwide incidence of childhood type 1 diabetes: the accelerating increase by time tends to level off in Sweden, Diabetes sourceExperimental — accuracy not yet measured
The Results (Generalized additive models; page unavailable) report that Swedish childhood type 1 diabetes incidence leveled off during the last seven years studied. The paper also describes rising incidence in many countries and short-term variation, but it does not establish that the rise fluctuated in many countries. (LLM, conf=0.84)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Type 1 diabetes is generally thought to be precipitated by an immune-associated, if not directly immune-mediated, destruction of insulin-producing pancreatic β cells.1,2”
§ Type 1 diabetes > Introduction
What the sources say
- Supportedcites [1] Todd, 2010, Etiology of type 1 diabetes, Immunity source
In the section headed “HLA Molecules and Insulin Peptides” (page not provided), the review calls pediatric type 1 diabetes an autoimmune disease and describes autoreactive T cells directed at islet antigens. It also identifies cytotoxic T cells as central to type 1 diabetes etiology and cites evidence that they target insulin-producing beta cells for killing. This supports the citing sentence’s hedged account of immune-associated beta-cell destruction. (LLM, conf=0.89)
- Supportedcites [2] Bluestone, 2010, Genetics, pathogenesis and clinical interventions in type 1 diabetes, Nature source
The Abstract (page not provided) states that type 1 diabetes occurs as a consequence of immune destruction of insulin-producing pancreatic β-cells. The Pathophysiology section (page not provided) also describes evidence that autoreactive T cells play a dominant role in disease initiation and progression. (LLM, conf=0.94)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“and type 1B (idiopathic) diabetes, representing the remainder whose specific pathogenesis remains unclear.42”
§ Type 1 diabetes > Diagnosis > Disease heterogeneity
What the sources say
- Partly supportedcites [42] Gianani, 2010, Dimorphic histopathology of long-standing childhood-onset diabetes, Diabetologia sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) says most childhood-onset diabetes is immune-mediated type 1A and identifies other, less well-characterised forms. The Discussion (page unavailable) calls for further study of the causes of a distinct histological pattern. Neither passage identifies those cases as type 1B (idiopathic) or says they constitute the remainder of type 1 diabetes cases. (LLM, conf=0.79)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Increases in incidence have not occurred equally across all age groups; in Europe, the most substantial increases have been noted in children younger than 5 years of age.5,21”
§ Type 1 diabetes > Epidemiology
What the sources say
- Not checked — no full text of the sourcecites [5] Harjutsalo, 2008, Time trends in the incidence of type 1 diabetes in Finnish children: a cohort study, Lancet source
- Supportedcites [21] 2006, Incidence and trends of childhood type 1 diabetes worldwide 1990–1999, Diabet Med source
The Global trend section reports that the annual increase was greatest among children aged 0–4 (4.0%), compared with ages 5–9 (3.0%) and 10–14 (2.1%), and says this age pattern was seen mainly in European populations. The Discussion likewise describes a particularly rapid increase in the youngest European age groups. Page numbers are not supplied in our copy. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Type 1 diabetes is most common in Finland (>60 cases per 100 000 people each year) and Sardinia (around 40 cases per 100 000 people each year).16”
§ Type 1 diabetes > Epidemiology
What the sources say
- Partly supportedcites [16] Patterson, 2009, Incidence trends for childhood type 1 diabetes in Europe during 1989–2003 and predicted new cases 2005–20: a multicentre prospective registration study, Lancet sourceExperimental — accuracy not yet measured
The Results table (page not available in our copy) shows high childhood type 1 diabetes incidence in two Finnish regions, but its highest reported rate is 52.6 per 100,000, not over 60. The paper does not report a rate for Sardinia, and its rates concern children aged 0–14 rather than people of all ages. (LLM, conf=0.85)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“similarly, subtypes of type 2 diabetes in children are poorly characterised, particularly in minority populations in the USA.44”
§ Type 1 diabetes > Diagnosis > Disease heterogeneity
What the sources say
- Partly supportedcites [44] Dabelea, 2007, Incidence of diabetes in youth in the United States, JAMA sourceExperimental — accuracy not yet measured
The Comment section reports that some US youth clinically diagnosed with type 2 diabetes had positive autoantibodies and says their role among minority youth requires further exploration. This supports uncertainty about one aspect of type 2 diabetes in minority children, but does not establish the broader claim that its subtypes generally are poorly characterised. (LLM, conf=0.82)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Other factors that complicate diagnosis of type 1 diabetes include the growing problem of obesity (both childhood and adult), difficulties in health-care provider recognition of disease, and increasingly diverse genetic admixtures due to migration and social changes.45–47”
§ Type 1 diabetes > Diagnosis > Disease heterogeneity
What the sources say
- Not checked — no full text of the sourcecites [45] Wilkin, 2009, The accelerator hypothesis: a review of the evidence for insulin resistance as the basis for type I as well as type II diabetes, Int J Obes (Lond) source
- Not checked — no full text of the sourcecites [46] Soderstrom, 2012, Being born in Sweden increases the risk for type 1 diabetes—a study of migration of children to Sweden as a natural experiment, Acta Paediatr source
- Could not verifycites [47] Puett, 2012, Neighborhood context and incidence of type 1 diabetes: the SEARCH for Diabetes in Youth study, Health Place sourceExperimental — accuracy not yet measured
The Introduction discusses type 1 diabetes incidence, genetics and environmental factors, while the Study design describes how cases were identified and validated; neither addresses obstacles to diagnosis. Searches for obesity, provider recognition and genetic admixture due to migration found no passage linking them to diagnostic difficulty in our copy. (LLM, conf=0.75)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A plethora of environmental influences have been purported to affect the epidemiology of type 1 diabetes,25 with infant and adolescent diets,26 vitamin D and vitamin D pathway constituents,27–29 and viruses receiving the most focus.30,31”
§ Type 1 diabetes > Epidemiology
What the sources say
- Not checked — no full text of the sourcecites [25] Maclaren, 1992, Is insulin-dependent diabetes mellitus environmentally induced?, N Engl J Med source
- Not checked — no full text of the sourcecites [26] Knip, 2010, Infant feeding and the risk of type 1 diabetes, Am J Clin Nutr source
- Partly supportedcites [27] Svoren, 2009, Significant vitamin D deficiency in youth with type 1 diabetes mellitus, J Pediatr sourceExperimental — accuracy not yet measured
The Methods and Results (page unavailable) show that this study measured vitamin D status in youth who already had type 1 diabetes, supporting vitamin D as a topic of research in this population. It does not examine whether vitamin D or its pathway constituents influence the incidence or epidemiology of type 1 diabetes; the diet and virus portions have separate citations. (LLM, conf=0.82)
- Supportedcites [28] Blanton, 2011, Reduced serum vitamin D-binding protein levels are associated with type 1 diabetes, Diabetes source
The citation is attached to the vitamin D and vitamin D pathway constituents portion of the sentence, not to diets or viruses. The paper’s Objective and Discussion (page numbers not provided) describe associations between type 1 diabetes and vitamin D levels, vitamin D pathway gene variants, and vitamin D–binding protein; it does not claim these relationships are causal. (LLM, conf=0.91)
- Supportedcites [29] Cooper, 2011, Inherited variation in vitamin D genes is associated with predisposition to autoimmune disease type 1 diabetes, Diabetes source
This source is cited for the vitamin D and vitamin D pathway constituents portion of the sentence, not for diets or viruses. The Conclusions and Discussion (page numbers not supplied) examine vitamin D status and report associations between vitamin D metabolism genes and type 1 diabetes risk. (LLM, conf=0.93)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Thus, disease hetero geneity is an important asp of type 1 diabetes, and suggests a role for genetics, age at disease onset, and intensity of disease management on the ability to retain β-cell”
§ Type 1 diabetes > Pathophysiology > Natural history
What the sources say
- Partly supportedcites [84] Keenan, 2010, Residual insulin production and pancreatic ss-cell turnover after 50 years of diabetes: Joslin Medalist Study, Diabetes sourceExperimental — accuracy not yet measured
The Results and Discussion (page unavailable in our copy) show substantial variation in residual C-peptide and associate higher levels with HLA genotype, later age at onset, and better glycemic control. They do not assess the intensity of disease management or establish that management intensity affects retention of β-cell function; glycemic control is not the same measure. (LLM, conf=0.85)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“For example, in Mozambique, the life expectancy for a newly diagnosed child with type 1 diabetes is 7 months.123”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access > Access to insulin
What the sources say
- Partly supportedcites [123] Beran, 2005, Access to care for patients with insulin-requiring diabetes in developing countries: case studies of Mozambique and Zambia, Diabetes Care sourceExperimental — accuracy not yet measured
In “Estimates of prevalence and prognosis” (Table 2; page not specified), the paper estimates 0.6 years—about seven months—for a child aged 0–14 with insulin-requiring diabetes in rural Mozambique. The claim omits the rural restriction: the paper’s national estimate for that age group is 3.5 years. The table also does not specify newly diagnosed children with type 1 diabetes. (LLM, conf=0.90)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These autoantibodies can appear as early as 6 months of age, with a peak incidence before 2 years of age in genetically susceptible individuals;66 thus, they are present months to years before symptomatic onset.”
§ Type 1 diabetes > Pathophysiology > Serological
What the sources say
- Partly supportedcites [66] Ziegler, 2012, Age-related islet autoantibody incidence in offspring of patients with type 1 diabetes, Diabetologia sourceExperimental — accuracy not yet measured
The Results and Discussion report peak autoantibody incidence from 9 months to 2 years in genetically at-risk children. The claim that autoantibodies can appear as early as 6 months is not established by this study: the Discussion reports no seroconversion at 3 or 6 months in the BABYDIET cohort, while cautioning that its size cannot rule out occurrence then. The citation precedes the sentence’s concluding inference about symptomatic onset, so that inference is not part of the attributed claim. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A trial comparing a sensor-augmented pump with multiple daily injection therapy showed significant improvement in HbA1C reduction with less hypoglycaemia in the sensor-augmented pump cohort.88,94”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
What the sources say
- Partly supportedcites [88] Bergenstal, 2010, Effectiveness of sensor-augmented insulin-pump therapy in type 1 diabetes, N Engl J Med sourceExperimental — accuracy not yet measured
The Results report a significantly greater HbA1c reduction with sensor-augmented pump therapy. But the Adverse Events section says hypoglycemia measures were similar between groups, and the Results report no significant difference in severe hypoglycemia rates; the claim of less hypoglycaemia is not supported. Page numbers were unavailable in our copy. (LLM, conf=0.90)
- Partly supportedcites [94] 2011, Sensor-augmented pump therapy for A1C reduction (STAR 3) study: results from the 6-month continuation phase, Diabetes Care sourceExperimental — accuracy not yet measured
The Abstract Conclusions report greater A1C reductions with sensor-augmented pump therapy than with multiple daily injections. The Results do not support the claim of less hypoglycaemia: in the continuation phase, severe hypoglycaemia rates were not significantly different between the continuing-pump and crossover groups. Our copy does not establish a lower hypoglycaemia rate for the pump cohort versus the injection cohort. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“A study in Finland128 identified 230 infants with a first-degree relative with type 1 diabetes, and randomly assigned infants to receive a hydrolysed infant formula or conventional formula whenever breast milk was not available during the first 6–8 months of life.”
§ Type 1 diabetes > Prevention and cure > Primary and secondary prevention
What the sources say
- Supportedcites [128] Knip, 2010, Dietary intervention in infancy and later signs of beta-cell autoimmunity, N Engl J Med source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plainn = 230- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“when comparing the safety and efficacy of overnight closed-loop delivery of insulin with conventional insulin-pump therapy in adults with type 1 diabetes, closed-loop delivery improved overnight control of glycaemia and reduced the risk of nocturnal hypoglycaemia.98,99”
§ Type 1 diabetes > Management of type 1 diabetes > Future care
What the sources say
- Not checked — no full text of the sourcecites [98] Garg, 2012, Reduction in duration of hypoglycemia by automatic suspension of insulin delivery: the in-clinic ASPIRE study, Diabetes Technol Ther source
- Partly supportedcites [99] Buckingham, 2010, Prevention of nocturnal hypoglycemia using predictive alarm algorithms and insulin pump suspension, Diabetes Care sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Lipid and metabolite profiles can also serve as markers for impending type 1 diabetes; these markers include decreased phosphatidylcholine at birth, and reduced triglycerides and antioxidant ether phospholipids followed by increased proinflammatory lysophosphatidylcholine several months before seroconversion to auto antibody positivity.70”
§ Type 1 diabetes > Pathophysiology > Serological
What the sources say
- Supportedcites [70] Oresic, 2008, Dysregulation of lipid and amino acid metabolism precedes islet autoimmunity in children who later progress to type 1 diabetes, J Exp Med source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“A randomised controlled trial in adults with type 1 diabetes reported lower HbA1C concentrations with sensor-augmented pump therapy than with injection therapy, and a greater proportion of patients reaching the targeted levels of HbA1C.88”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
What the sources say
- Supportedcites [88] Bergenstal, 2010, Effectiveness of sensor-augmented insulin-pump therapy in type 1 diabetes, N Engl J Med source
The Methods describe a randomized controlled trial that included adults with type 1 diabetes. The Discussion reports that adults receiving sensor-augmented pump therapy had a greater reduction in glycated hemoglobin than those receiving injections, and that more pump-therapy patients reached the prespecified target. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Metabolic changes in the natural history of type 1 diabetes are marked by decreased early C-peptide response at least 2 years before onset,80 increased glucose fluctuations as an individual approaches onset,81 and an overall linear rise, with a last-minute surge, in plasma glucose in”
§ Type 1 diabetes > Pathophysiology > Natural history
What the sources say
- Partly supportedcites [80] Sosenko, 2010, Trends of earlier and later responses of C-peptide to oral glucose challenges with progression to type 1 diabetes in diabetes prevention trial-type 1 participants, Diabetes Care sourceExperimental — accuracy not yet measured
Split into 3 atoms — 1 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Supportedcites [81] Sosenko, 2010, Glucose excursions between states of glycemia with progression to type 1 diabetes in the diabetes prevention trial-type 1 (DPT-1), Diabetes source
Citation 81 is attached to the claim about glucose fluctuations, not the neighboring claims about C-peptide or a last-minute glucose surge. The Discussion says glucose levels can fluctuate widely within an individual and that this pattern extends into higher glycemic ranges as type 1 diabetes onset approaches. (LLM, conf=0.92)
- Partly supportedcites [82] Ferrannini, 2010, Progression to diabetes in relatives of type 1 diabetic patients: mechanisms and mode of onset, Diabetes sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Of the many HLA types, HLA class II show the strongest association with type 1 diabetes, where haplotypes DRB1*0401-DQB1*0302 and DRB1*0301-DQB1*0201 confer the greatest susceptibility, and DRB1*1501 and DQA1*0102-DQB1*0602 provide disease resistance.74”
§ Type 1 diabetes > Pathophysiology > Genetics
What the sources say
- Partly supportedcites [74] Erlich, 2008, HLA DR-DQ haplotypes and genotypes and type 1 diabetes risk: analysis of the type 1 diabetes genetics consortium families, Diabetes sourceExperimental — accuracy not yet measured
The Results (page not provided) place both named susceptibility haplotypes among the most susceptible and identify DRB1*1501-DQA1*0102-DQB1*0602 as highly protective. But DRB1*0405-DQA1*0301-DQB1*0302 has a higher reported odds ratio than either named susceptibility haplotype, so the claim that those two confer the greatest susceptibility overstates the risk ranking. The passages also do not compare the strength of class II associations with other HLA classes. (LLM, conf=0.86)
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Leptin, the adipocyte hormone, might also benefit type 1 diabetes therapy via its ability to reverse a catabolic state through suppression of hypergluca-gonaemia.103”
§ Type 1 diabetes > Management of type 1 diabetes > Future care
What the sources say
- Supportedcites [103] Oral, 2012, Leptin for type 1 diabetes: coming onto stage to be (or not?), Pediatr Diabetes source
In “Leptin can suppress glucagon levels and hyperglucagonemia is a hallmark feature of type 1 diabetes” (page unavailable), the paper reports that leptin reversed the diabetic state in insulin-deficient rodent models and that this effect was suggested to result from reduced plasma glucagon. Its discussion of relative leptin deficiency describes the energy-deficit and increased-lipolysis state in type 1 diabetes. The citing sentence’s “might” appropriately presents this as a potential therapeutic benefit, not an established clinical effect. (LLM, conf=0.85)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“GLP-1 might also prove beneficial, with studies noting that this incretin decreased peak postprandial glucose by 45% regardless of residual β-cell function.101”
§ Type 1 diabetes > Management of type 1 diabetes > Future care
What the sources say
- Supportedcites [101] Kielgast, 2011, Antidiabetic actions of endogenous and exogenous GLP-1 in type 1 diabetic patients with and without residual beta-cell function, Diabetes source
The Abstract Conclusions state that exogenous GLP-1 decreased peak postprandial glucose by 45% in patients with type 1 diabetes regardless of residual β-cell function. The Discussion Conclusions repeat the finding and recommend investigating longer-term GLP-1 therapy, consistent with the cautious suggestion that it might prove beneficial. (LLM, conf=0.95)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Not all individuals with anti-β-cell autoimmunity progress to overt disease (less than 5% who express a single type 1 diabetes-associated autoantibody progress41), for reasons unknown.”
§ Type 1 diabetes > Pathophysiology > Natural history
What the sources say
- Partly supportedcites [41] Eisenbarth, 2007, Update in type 1 diabetes, J Clin Endocrinol Metab sourceExperimental — accuracy not yet measured
The Prediction section (page unavailable) says that having at least two islet autoantibodies is highly predictive of progression, supporting the distinction between autoantibody expression and overt diabetes. It does not give a progression rate for people with a single autoantibody, so the claimed figure of less than 5% is unsupported. (LLM, conf=0.82)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“However, two studies have provided cost estimates specifically for type 1 diabetes, proposing an annual figure of $14·4–14·9 billion in the USA.104,105”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access
What the sources say
- Not checked — no full text of the sourcecites [104] Dall, 2009, Distinguishing the economic costs associated with type 1 and type 2 diabetes, Popul Health Manag source
- Supportedcites [105] Tao, 2010, Estimating the cost of type 1 diabetes in the US: a propensity score matching method, PLoS One source
The Abstract (Methodology/Principal Findings) estimates annual U.S. type 1 diabetes costs at $14.4 billion, and Table 11 in Discussion > Medical Costs gives the same total. This supports the $14.4 billion end of the range; the sentence cites two studies for the combined range, so it does not attribute the $14.9 billion figure to this paper alone. (LLM, conf=0.93)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“a finding that might be explained by a recent report that, after myocardial infarction, patients with type 1 diabetes express antibodies to cardiac proteins, whereas patients with type 2 diabetes do not.111”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access > Complications associated with type 1 diabetes
What the sources say
- Partly supportedcites [111] Gottumukkala, 2012, Myocardial infarction triggers chronic cardiac autoimmunity in type 1 diabetes, Sci Transl Med sourceExperimental — accuracy not yet measured
The Results section ('Discovery of a PIA syndrome in human T1D patients'; page not provided) reports cardiac autoantibodies in 15/18 post-MI patients with type 1 diabetes, supporting that part of the claim. It also reports them in 3/20 post-MI patients with type 2 diabetes, so the assertion that those patients do not express such antibodies is too absolute. (LLM, conf=0.92)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Although it is often stated that symptoms occur when 90–95% of β cells are lost, diagnosis of type 1 diabetes can occur when roughly two-thirds of the islets are devoid of insulin-producing cells.61,62”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
What the sources say
- Partly supportedcites [61] Foulis, 1984, The pancreas in recent-onset type 1 (insulin-dependent) diabetes mellitus: insulin content of islets, insulitis and associated changes in the exocrine acinar tissue, Diabetologia sourceExperimental — accuracy not yet measured
The Patients section says nine children died within 24 hours of diagnosis, and the Results and Discussion report many insulin-deficient islets in their pancreases. But the available Table 1 text does not provide usable counts, and no passage establishes that roughly two-thirds of islets lacked insulin-producing cells at diagnosis. The Discussion’s separate “two-thirds” figure describes the A-cell composition of insulin-deficient islets, not the proportion of islets affected. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [62] Willcox, 2009, Analysis of islet inflammation in human type 1 diabetes, Clin Exp Immunol source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The hormone pramlintide has been shown to reduce postprandial hyperglycaemia, bodyweight, insulin dosage, and HbA1C concentrations, and to reduce postprandial glucagon and glucose excursions and slow gastric emptying.102”
§ Type 1 diabetes > Management of type 1 diabetes > Future care
What the sources say
- Supportedcites [102] Ryan, 2009, Review of pramlintide as adjunctive therapy in treatment of type 1 and type 2 diabetes, Drug Des Devel Ther source
The Chemistry and preclinical pharmacology section reports reduced postprandial glucagon release and glucose, along with slower gastric emptying. The Discussion reports lower A1C and modest weight loss, while the Phase II and Phase III type 1 diabetes sections report reduced insulin doses. The review notes that weight loss may be transient. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Although this endogenous secretion is typically low, maintenance is important since it is associated with less retinopathy and less severe hypoglycaemia at later stages of the disease.86”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
What the sources say
- Partly supportedcites [86] Steffes, 2003, Beta-cell function and the development of diabetes-related complications in the diabetes control and complications trial, Diabetes Care sourceExperimental — accuracy not yet measured
The paper reports that sustained C-peptide (and thus insulin) secretion was associated with less retinopathy and fewer episodes of severe hypoglycemia in DCCT participants with type 1 diabetes (p. 1). It does not establish those associations specifically at later stages of disease; its discussion notes that most patients eventually lose β-cell function (p. 4). (LLM, conf=0.80)
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- Partly supported
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In the paper
“Individuals with type 1 diabetes have a ten-times higher risk for cardiovascular events (eg, myocardial infarction, stroke, angina, and the need for coronary-artery revascularisation) than age-matched non-diabetic populations.107”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access > Complications associated with type 1 diabetes
What the sources say
- Partly supportedcites [107] Orchard, 2006, Type 1 diabetes and coronary artery disease, Diabetes Care sourceExperimental — accuracy not yet measured
In “The Magnitude of the Problem” (page not available), the review reports a tenfold or greater increase in coronary heart disease mortality compared with U.S. national data. It also reports elevated coronary-event rates in people with type 1 diabetes, but does not establish a tenfold risk for the broader set of cardiovascular events listed in the citing sentence compared with age-matched people without diabetes. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This mechanism might help explain the differing rates of progression to type 1 diabetes in adults versus children, where only minor variations in genetic susceptibility have been noted.48”
§ Type 1 diabetes > Pathophysiology > Genetics
What the sources say
- Supportedcites [48] Howson, 2011, Genetic analysis of adult-onset autoimmune diabetes, Diabetes source
The Conclusions state that adult and childhood autoimmune diabetes differ by relatively few age-dependent genetic effects. They also propose that adults’ slower progression toward autoimmune insulin deficiency is probably due to a lower overall genetic load and subtle differences in HLA associations and autoreactivity. The Discussion likewise describes largely shared genetic architecture. (LLM, conf=0.91)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Similarly, islet-cell transplantation depends on overcoming recurrent autoimmunity and averting alloimmunity.153”
§ Type 1 diabetes > Unanswered questions > Lessons learned
What the sources say
- Partly supportedcites [153] Vendrame, 2010, Recurrence of type 1 diabetes after simultaneous pancreas-kidney transplantation, despite immunosuppression, is associated with autoantibodies and pathogenic autoreactive CD4 T-cells, Diabetes sourceExperimental — accuracy not yet measured
The Conclusions and Discussion describe recurrent autoimmunity as a cause of graft loss despite immunosuppression. The Results also document rejection of a second pancreas graft, supporting the need to avert alloimmune rejection. However, the patients received pancreas-kidney transplants, not islet-cell transplants, so the claim extends the clinical finding to a different transplant setting. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Therefore, islet transplantation remains an experimental procedure, with ongoing research focusing on new methods using biomaterials (eg, encapsulation), immune modulation, site of delivery, improved vascularisation, and more.151”
§ Type 1 diabetes > Prevention and cure > Islet-cell transplantation
What the sources say
- Supportedcites [151] Gibly, 2011, Advancing islet transplantation: from engraftment to the immune response, Diabetologia source
The Introduction describes islet transplantation as a therapy still being developed, with preliminary long-term results and a need to improve its effectiveness and availability. The Abstract and Engraftment section discuss the cited research directions: biomaterials, encapsulation, immunomodulation, alternative transplant sites, and revascularisation. (LLM, conf=0.86)
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Despite decades of investigation, the mechanisms by which β cells are eliminated or selectively destroyed (apart from antigen-specific immune responses) remain unclear.55”
§ Type 1 diabetes > Unanswered questions > Lessons learned
What the sources say
- Partly supportedcites [55] Atkinson, 2011, How does type 1 diabetes develop?: the notion of homicide or beta-cell suicide revisited, Diabetes sourceExperimental — accuracy not yet measured
The section on β-cell ‘suicide’ describes several possible contributors to selective destruction, including cytokine sensitivity and ER stress, while the section on immune-mediated destruction says multiple elimination pathways may operate together. The paper supports the idea that the process is not fully resolved, but it does not say that mechanisms apart from antigen-specific immune responses are simply unknown. (LLM, conf=0.78)
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In the past 5 years, interest in reversal of type 1 diabetes has grown.134”
§ Type 1 diabetes > Prevention and cure > Reversal
What the sources say
- Partly supportedcites [134] Greenbaum, 2011, Persistence is the twin sister of excellence: an important lesson for attempts to prevent and reverse type 1 diabetes, Diabetes sourceExperimental — accuracy not yet measured
The main text (page unavailable) describes expanding therapeutic approaches and pharmaceutical involvement, and Table 1 lists large trials seeking to reverse type 1 diabetes. This supports growing interest, but the paper describes developments over roughly a decade rather than establishing the claimed five-year period. (LLM, conf=0.82)
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“To achieve progress with islet-cell transplantation, investigators are focusing on xenotransplantation, encapsulation, novel sites for cell delivery (eg, eye), and development of surrogate insulin-producing cells.151”
§ Type 1 diabetes > Unanswered questions > Lessons learned
What the sources say
- Supportedcites [151] Gibly, 2011, Advancing islet transplantation: from engraftment to the immune response, Diabetologia source
The Biomaterial scaffolds section discusses encapsulation and alternative delivery sites, including the anterior chamber of the eye. The Introduction and A multi-pronged approach for long-term success discuss xenogeneic islets and other insulin-producing cells as alternative cell sources. Page numbers are not provided in our copy. (LLM, conf=0.91)
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Supported
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Despite knowledge gains that could allow for adopting this new set of terminologies for subgrouping cases of type 1 diabetes, the terms type 1A and type 1B diabetes are not commonly used;”
§ Type 1 diabetes > Diagnosis > Disease heterogeneity
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Diagnosis of diabetes has historically included fasting blood glucose higher than 7 mmol/L (126 mg/dL), any blood glucose of 11·1 mmol/L (200 mg/dL) or higher with symptoms of hyperglycaemia, or an abnormal 2 horal glucose-tolerance test.34”
§ Type 1 diabetes > Diagnosis
What the sources say
- Not checked yetcites [34] 2012, Diagnosis and classification of diabetes mellitus, Diabetes Care
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Over the past decade, knowledge of the pathogenesis and natural history of type 1 diabetes has grown substantially, particularly with regard to disease prediction and heterogeneity, pancreatic pathology, and epidemiology.”
§ Type 1 diabetes > Abstract
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Despite efforts to standardise diagnosis of type 1 diagnosis, the causes and typology remain unclear.”
§ Type 1 diabetes > Diagnosis
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Another dogma is that in patients with longstanding disease, the pancreas is devoid of insulin-producing cells and the remaining β cells are incapable of regeneration.”
§ Type 1 diabetes > Pathophysiology
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and, globally, the quality of diabetes management remains uneven.”
§ Type 1 diabetes > Abstract
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Technological improvements in insulin pumps and continuous glucose monitors help patients with type 1 diabetes manage the challenge of lifelong insulin administration.”
§ Type 1 diabetes > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“An immediate need for exogenous insulin replacement is also a hallmark of type 1 diabetes, for which lifetime treatment is needed.”
§ Type 1 diabetes > Introduction
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The incidence of type 1 diabetes varies with seasonal changes and birth month.”
§ Type 1 diabetes > Epidemiology
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“By contrast, the disorder is uncommon in China, India, and Venezuela (around 0·1 cases per 100 000 people each year).”
§ Type 1 diabetes > Epidemiology
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Polydipsia, polyphagia, and polyuria (the classic trio of symptoms associated with disease onset) along with overt hyperglycaemia remain diagnostic hallmarks in children and adolescents, and to a lesser extent in adults.”
§ Type 1 diabetes > Introduction
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, despite broad organisational, intellectual, and fiscal investments, no means for preventing or curing type 1 diabetes exists”
§ Type 1 diabetes > Abstract
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Most cases of type 1 diabetes represent an immune, if not autoimmune-mediated disorder, meaning patients often show features of an immunological contribution to disease pathogenesis (eg, autoantibodies or genetic associations with genes controlling immune responses).”
§ Type 1 diabetes > Diagnosis > Disease heterogeneity
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Whereas most autoimmune disorders disproportionately affect women, type 1 diabetes is slightly more common in boys and men.6”
§ Type 1 diabetes > Epidemiology
What the sources say
- Not checked — no full text of the sourcecites [6] Ostman, 2008, Gender differences and temporal variation in the incidence of type 1 diabetes: results of 8012 cases in the nationwide Diabetes Incidence Study in Sweden 1983–2002, J Intern Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Although type 1 diabetes can be diagnosed at any age, it is one of the most common chronic diseases of childhood.4”
§ Type 1 diabetes > Epidemiology
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Agents that show promise for averting debilitating disease-associated complications have also been identified.”
§ Type 1 diabetes > Abstract
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“In terms of potential pathogenic mechanisms, CD8+ T cells are the most predominant population within the insulitis lesion, followed by (in declining order) macrophages (CD68+), CD4+ T cells, B lymphocytes (CD20+), and plasma cells (CD138+).62”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
What the sources say
- Not checked — no full text of the sourcecites [62] Willcox, 2009, Analysis of islet inflammation in human type 1 diabetes, Clin Exp Immunol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Examples include insulin degludec (recently approved for use in the EU, although approval declined by the US Food and Drug Administration), an analogue that might improve basal insulin administration in patients with type 1 diabetes, since it provides effective glycaemic control and reduces the risk of nocturnal hypoglycaemia.100”
§ Type 1 diabetes > Management of type 1 diabetes > Future care
What the sources say
- Not checked — no full text of the sourcecites [100] Heller, 2012, Insulin degludec, an ultra-longacting basal insulin, versus insulin glargine in basal-bolus treatment with mealtime insulin aspart in type 1 diabetes (BEGIN Basal-Bolus Type 1): a phase 3, randomised, open-label, treat-to-target non-inferiority trial, Lancet source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A meta-analysis has also shown that insulin pumps lower HbA1C concentrations more than multiple daily injections in adults with type 1 diabetes, with similar rates of hypoglycaemia.89”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
What the sources say
- Not checked — no full text of the sourcecites [89] Yeh, 2012, Comparative effectiveness and safety of methods of insulin delivery and glucose monitoring for diabetes mellitus: a systematic review and meta-analysis, Ann Intern Med source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Surprisingly, FOXP3+ cells (ie, regulatory T cells; a population of intense research interest2) and natural killer cells are rare in this lesion.”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
What the sources say
- Not checked — no full text of the sourcecites [62] Willcox, 2009, Analysis of islet inflammation in human type 1 diabetes, Clin Exp Immunol source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Fortunately, organisations such as the International Diabetes Federation, Life for a Child, Insulin for Life, and others are developing means to alleviate this disparity.”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access > Access to insulin
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Low-glucose suspend systems are currently available for clinical use in Europe, but remain in clinic trial testing in the USA.”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The discovery of insulin in 1921–22 was clearly the most significant therapeutic event in the history of type 1 diabetes;”
§ Type 1 diabetes > Management of type 1 diabetes
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
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Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“Nearly three decades have passed since the first immune-based therapies, using ciclosporin, were attempted to reverse type 1 diabetes.125”
§ Type 1 diabetes > Prevention and cure
What the sources say
- Not checked — no full text of the sourcecites [125] Bach, 2011, A historical view from thirty eventful years of immunotherapy in autoimmune diabetes, Semin Immunol source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The physical, social, and economic costs of type 1 diabetes are difficult to calculate, and attempts to quantify these variables typically do not distinguish between type 1 and type 2 disease.”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Therefore, continuous glucose monitoring is most appropriate for highly motivated patients with type 1 diabetes who are willing to wear the monitoring device, and those with continuous poor control during intensive insulin therapy.93”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
What the sources say
- Not checked — no full text of the sourcecites [93] Ahmet, 2011, Prevalence of nocturnal hypoglycemia in pediatric type 1 diabetes: a pilot study using continuous glucose monitoring, J Pediatr source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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Probably not a substantial claim. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Since type 1 diabetes is now a predictable disease, several large trials are investigating methods to prevent or delay the onset of disease.”
§ Type 1 diabetes > Prevention and cure > Primary and secondary prevention
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Efforts are underway to combine insulin pumps and continuous glucose monitors with a computer algorithm—ie, an integrated closed-loop system, or artificial pancreas (figure 5).”
§ Type 1 diabetes > Management of type 1 diabetes > Future care
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Additionally, the nPOD effort attempts to extend investigations to the entire pancreas, rather than be limited by use of a biopsy sample.”
§ Type 1 diabetes > Pathophysiology > Pancreatic pathology
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Although current sensor-augmented pump therapy uses each device independently, integration of both systems is being investigated.”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Once a critical mass (not well defined) of β cells is destroyed, symptomatic onset occurs, and the need for exogenous insulin replacement begins.”
§ Type 1 diabetes > Pathophysiology > Natural history
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
In the paper
“Of the remaining loci, only those for the insulin VNTR, PTPN22, CTLA4, and IL2RA are associated with odds ratios greater than 1·1.75”
§ Type 1 diabetes > Pathophysiology > Genetics
What the sources say
- Not checked — no full text of the sourcecites [75] Polychronakos, 2011, Understanding type 1 diabetes through genetics: advances and prospects, Nat Rev Genet source
plaincorrelational- Asserted: unclear — It is unclear whether the authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
The quote only partly states this claim.
In the paper
“Cardiovascular disease is becoming a more common macrovasular complication as individuals with in type 1 diabetes live longer.106”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access > Complications associated with type 1 diabetes
What the sources say
- Not checked — no full text of the sourcecites [106] Melendez-Ramirez, 2010, Complications of type 1 diabetes, Endocrinol Metab Clin North Am source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Inequalities in the availability of technologies to reduce complications, improve quality of life, and improve diabetes manage ment (eg, HbA1C testing and blood-glucose monitoring) also raise ethical concerns.”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access > Access to insulin
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This classification seems appropriate in view of the ongoing disease processes and the near certainty that such individuals will eventually become symptomatic (insulin dependent).”
§ Type 1 diabetes > Pathophysiology > Natural history
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“A model originally posed in 1986,77 updated in our 2001 article,78 and modified subsequently, poses that individuals are born with various degrees of genetic susceptibility for type 1 diabetes.”
§ Type 1 diabetes > Pathophysiology > Natural history
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Although this model has stood the test of time, some modifications should be considered due to knowledge gains (figure 4).”
§ Type 1 diabetes > Pathophysiology > Natural history
plain- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Many practical and intellectual advances have been made since then, including improved metabolic testing, better understanding of disease pathogenesis, and availability of immune markers.126”
§ Type 1 diabetes > Prevention and cure
What the sources say
- Not checked — no full text of the sourcecites [126] van Belle, 2011, Type 1 diabetes: etiology, immunology, and therapeutic strategies, Physiol Rev source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The risk for microvascular complications, including retinopathy, nephropathy, and neuropathy, decreases with intensive insulin therapy.”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access > Complications associated with type 1 diabetes
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Over the past 5 years, several large clinical trials have advanced the prediction and prevention of microvascular complications (table 1).”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access > Complications associated with type 1 diabetes
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Therefore, preserving insulin secretion after disease onset is increasingly a therapeutic goal, and can involve intensive insulin therapy, mechanical technologies, or, as in several trials, immune intervention to disrupt β-cell destruction.”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“This symptomatic onset happens after a silent phase that lasts for months to many years, that could, in genetically susceptible individuals with multiple autoantibodies, be considered asymptomatic type 1 diabetes.”
§ Type 1 diabetes > Pathophysiology > Natural history
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Efforts to prevent or cure type 1 diabetes are now done via large collaborative networks (eg, NIH TrialNet, Immune Tolerance Network, and Islet Cell Transplantation Consortium), with rigorous mechanistic assays and uniform protocols.”
§ Type 1 diabetes > Prevention and cure
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Type 1 diabetes is clearly a polygenic disorder, with nearly 40 loci (so far) known to affect disease susceptibility.72”
§ Type 1 diabetes > Pathophysiology > Genetics
What the sources say
- Not checked — no full text of the sourcecites [72] Concannon, 2009, Genetics of type 1A diabetes, N Engl J Med source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Tamborlane and colleagues91 reported that a real-time continuous glucose monitoring system decreased the amount of time spent in hypoglycaemia (<4 mmol/L [70 mg/dL]) and lowered HbA1C when used by patients an average of 6 days a week.”
§ Type 1 diabetes > Management of type 1 diabetes > Present care
What the sources say
- Not checked — no full text of the sourcecites [91] Tamborlane, 2008, Continuous glucose monitoring and intensive treatment of type 1 diabetes, N Engl J Med source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The Pittsburgh Epidemiology of Diabetes Complications study108 of type 1 diabetes reported cardiovascular events in adult patients younger than 40 years of age to be 1% per year, and three times higher in individuals older than 55 years.”
§ Type 1 diabetes > Burden of type 1 diabetes: complications, excess mortality, and insulin access > Complications associated with type 1 diabetes
What the sources say
- Not checked — no full text of the sourcecites [108] Maser, 1991, Cardiovascular disease and arterial calcification in insulin-dependent diabetes mellitus: interrelations and risk factor profiles. Pittsburgh Epidemiology of Diabetes Complications Study-V, Arterioscler Thromb source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These results imply that single-agent immunosuppression alone might be insufficient to completely control the autoimmune destruction of β cells, or that more specific and targeted therapies are needed.”
§ Type 1 diabetes > Prevention and cure > Reversal
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In addition to preserving production of C-peptide, a key goal is to induce immune tolerance against β cells and thereby halt autoimmune destruction.”
§ Type 1 diabetes > Prevention and cure > Reversal
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Despite the advances in type 1 diabetes research and therapy, some researchers and clinicians are disappointed by a perceived lack of progress.”
§ Type 1 diabetes > Unanswered questions > Lessons learned
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Combination therapies that target several pathogenic pathways and improve β-cell viability might be needed to preserve endogenous insulin production in patients with type 1 diabetes.”
§ Type 1 diabetes > Prevention and cure > Reversal
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Other phase 2 studies of immune modulators showed evidence of therapeutic efficacy in settings of recent-onset type 1 diabetes; however, even with continued use, most did not show durable effects.”
§ Type 1 diabetes > Prevention and cure > Reversal
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Knowledge voids that have long existed for type 1 diabetes, unfortunately, remain today.”
§ Type 1 diabetes > Unanswered questions > Where do we go from here?
plain- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence.
In the paper
“Efforts are underway to assign specific phenotypes to genotypes, and to improve understanding of the genetic risk for type 1 diabetes by genotyping at multiple susceptibility loci.154”
§ Type 1 diabetes > Unanswered questions > Lessons learned
What the sources say
- Not checked — no full text of the sourcecites [154] Winkler, 2012, A strategy for combining minor genetic susceptibility genes to improve prediction of disease in type 1 diabetes, Genes Immun source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Rests on an assumption: Although many genotypic associations with type 1 diabetes exist, the specific phenotypes resulting from these genetic influences are largely unknown.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Other agents used for secondary prevention, nicotinamide and intranasal insulin, have not been shown to delay or prevent diabetes onset.132,133”
§ Type 1 diabetes > Prevention and cure > Primary and secondary prevention
What the sources say
- Not checked — no full text of the sourcecites [132] Gale, 2004, European Nicotinamide Diabetes Intervention Trial (ENDIT): a randomised controlled trial of intervention before the onset of type 1 diabetes, Lancet source
- Not checked — no full text of the sourcecites [133] Näntö-Salonen, 2008, Nasal insulin to prevent type 1 diabetes in children with HLA genotypes and autoantibodies conferring increased risk of disease: a double-blind, randomised controlled trial, Lancet source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Many of the limitations for islet transplantation hold true for another promising area, the use of stem cells as insulin-producing surrogates for β cells.”
§ Type 1 diabetes > Prevention and cure > Islet-cell transplantation
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“but a post-hoc analysis suggested that individuals with high titre insulin autoantibodies benefited from treatment—it was estimated that diabetes onset was delayed as much as 5 years.131”
§ Type 1 diabetes > Prevention and cure > Primary and secondary prevention
What the sources say
- Not checked — no full text of the sourcecites [131] Skyler, 2005, Effects of oral insulin in relatives of patients with type 1 diabetes: the Diabetes Prevention Trial—Type 1, Diabetes Care source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
A limited donor pool is a hurdle for islet-cell transplantation.
“Additional hurdles for islet-cell transplantation include a limited donor pool and the need for chronic immunosuppression (or a method to induce long-term immunological tolerance) to allow for functional engraftment.”
The paper relies on this without support.
The need for chronic immunosuppression (or a method to induce long-term immunological tolerance) is a hurdle for islet-cell transplantation to allow for functional engraftment.
“Additional hurdles for islet-cell transplantation include a limited donor pool and the need for chronic immunosuppression (or a method to induce long-term immunological tolerance) to allow for functional engraftment.”
The paper relies on this without support.
Although many genotypic associations with type 1 diabetes exist, the specific phenotypes resulting from these genetic influences are largely unknown.
“An additional complication arises from the fact that although many genotypic associations with the disease exist, the specific phenotypes resulting from these genetic influences are largely unknown.”
The paper relies on this without support.
Earlier interventions in animal models of type 1 diabetes seem to be more efficacious.
“This concept is based on studies in animal models of type 1 diabetes, where earlier interventions seem to be more efficacious, and the belief that intervention before a critical threshold of remnant β-cell mass is lost would avoid several sequelae that are often present at symptomatic onset (eg, glucose toxicity, stress response, etc).”
The authors state this as an assumption.
Intervention before a critical threshold of remnant β-cell mass is lost would avoid several sequelae that are often present at symptomatic onset.
“This concept is based on studies in animal models of type 1 diabetes, where earlier interventions seem to be more efficacious, and the belief that intervention before a critical threshold of remnant β-cell mass is lost would avoid several sequelae that are often present at symptomatic onset (eg, glucose toxicity, stress response, etc).”
The paper relies on this without support.
Type 1 diabetes begins long before symptomatic onset.
“Additional modifications that could improve the applicability of type 1 diabetes research include changes in clinical trial design (eg, adaptive trial design),156 identifying more practical therapies (in terms of finance and delivery of public health care), better defining disease heterogeneity,147 utilising animal models of type 1 diabetes more effectively,127 and applying the concept that type 1”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“sustained near-normoglycemia is associated with fewer chronic complications and better quality of life [1,2,3].”
From Does Resistant Starch Formed by Cooling Pasta Decrease the Postprandial Glycemic Response in Type 1 Diabetes? A Randomized Single-Blind Crossover Study (2026) · cites this paper as [2]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Destruction of the insulin-producing pancreatic beta cells due to an immune-associated or environmental insult results in type 1 diabetes [5].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [5]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Type 1 diabetes mellitus (T1DM) is an autoimmune disorder in which immune cells destroy insulin-producing β-cells of the pancreas, resulting in little to no insulin production1.”
From The epidemiology of type 1 diabetes mellitus in older adults (2025) · cites this paper as [1]
Experimental — accuracy not yet measuredIn the citing paper
“T1D is more “severe” than T2D, as ~90% of beta-cells are destroyed by autoimmunity, which results in vastly reduced insulin levels.108”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [108]
In the citing paper
“a consensus model has emerged in which type 1 diabetes is envisaged to result from the selective destruction of beta cells by immune cells infiltrating the islets of Langerhans [1–3, 8, 9].”
From Islet cell hyperexpression of HLA class I antigens: a defining feature in type 1 diabetes (2016) · cites this paper as [2]
Citations
Cites
Diagnosis and Classification of Diabetes Mellitus
American Diabetes Association (2010) · Diabetes Care · doi:10.2337/dc11-s062 · Cited by 14,094
IDF Diabetes Atlas: Global estimates for the prevalence of diabetes for 2015 and 2040
Ogurtsova, K., Fernandes, J. D. D. R., Huang, Y., Linnenkamp, U., Guariguata, L., Cho, N. H., Cavan, D. A., Shaw, J. E., & Makaroff, L. (2017) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2017.03.024 · Cited by 7,138
Shapiro, A. M. J., Lakey, J. R. T., Ryan, E. A., Korbutt, G. S., Toth, E., Warnock, G. L., Kneteman, N. M., & Rajotte, R. V. (2000) · New England Journal of Medicine · doi:10.1056/nejm200007273430401 · Cited by 5,237
Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes
(2005) · New England Journal of Medicine · doi:10.1056/nejmoa052187 · Cited by 5,138
IDF Diabetes Atlas: Global estimates of the prevalence of diabetes for 2011 and 2030
Whiting, D. R., Guariguata, L., Weil, C., & Shaw, J. E. (2011) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2011.10.029 · Cited by 4,018
Diagnosis and Classification of diabetes mellitus
Rossi, G. (2014) · Diapedia.org eBooks · doi:10.14496/dia..20 · Cited by 3,212
International Expert Committee report on the role of the A1c assay in the diagnosis of diabetes
The International Expert Committee (2009) · Diabetes Care · doi:10.2337/dc09-9033 · Cited by 3,185
Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease
Ueda, H., Howson, J. M. M., Esposito, L., Heward, J., Snook, Chamberlain, G., Rainbow, D. B., Hunter, K. M. D., Smith, A. N., Di Genova, G., et al. (2003) · Nature · doi:10.1038/nature01621 · Cited by 2,175
Patterson, C. C., Dahlquist, G. G., Gyürüs, E., Green, A., & Soltész, G. (2009) · The Lancet · doi:10.1016/s0140-6736(09)60568-7 · Cited by 1,854
Eisenbarth (1986) · doi:10.1056/nejm198605223142106 · Cited by 1,659
Self-citation
Research works printed but not linked: 1
- Keenan, 2010, Residual insulin production and pancreatic ss-cell turnover after 50 years of diabetes: Joslin Medalist Study, Diabetes, 59, 2846, 10.2337/db10-0676 · DOI · Paper page
Cited by
Sorted by citations
Comorbidity: a network perspective
Cramer, A. O. J., Waldorp, L. J., van der Maas, H. L. J., & Borsboom, D. (2010) · Behavioral and Brain Sciences · doi:10.1017/s0140525x09991567 · Cited by 1,575
DiMeglio, L. A., Evans-Molina, C., & Oram, R. A. (2018) · The Lancet · doi:10.1016/s0140-6736(18)31320-5 · Cited by 1,561
Katsarou, A., Gudbjörnsdottir, S., Rawshani, A., Dabelea, D., Bonifacio, E., Anderson, B. J., Jacobsen, L. M., Schatz, D. A., & Lernmark, Å. (2017) · Nature Reviews Disease Primers · doi:10.1038/nrdp.2017.16 · Cited by 1,475
The Role of Inflammation in Diabetes: Current Concepts and Future Perspectives
Tsalamandris, S., Antonopoulos, A. S., Oikonomou, E., Papamikroulis, G.-A., Vogiatzi, G., Papaioannou, S., Deftereos, S., & Tousoulis, D. (2019) · European Cardiology Review · doi:10.15420/ecr.2018.33.1 · Cited by 1,381
Cao, H., Duan, L., Zhang, Y., Cao, J., & Zhang, K. (2021) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-021-00830-x · Cited by 1,380
Metadata
- Authors
- Atkinson, M. A., Eisenbarth, G. S., & Michels, A. W.
- Affiliations
- University of Florida Health (US)
- Corresponding author
- Atkinson, Mark A
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2014-01
- Volume
- 383
- Issue
- 9911
- Pages
- 69-82
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- PMC
- PMC4380133
- OpenAlex
- W2062573090
- Cited by
- 2,931
- References
- 251
- Citations by year
- 2026: 223 · 2025: 238 · 2024: 287 · 2023: 266 · 2022: 258 · 2021: 271 · 2020: 256 · 2019: 221 · 2018: 234 · 2017: 196 · 2016: 144 · 2015: 143 · 2014: 83
- FWCI
- 14.90
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (K08DK095995)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- type 1 diabetes, pathogenesis, natural history (disease), disease heterogeneity, disease prediction, pancreatic pathology, insulin pump, continuous glucose monitoring, insulin therapy, diabetes complications, diabetes management
- MeSH terms
- Diabetes Mellitus, Type 1, Humans, Hypoglycemic Agents, Insulin, Islets of Langerhans, Pancreas, Artificial
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-27, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-27 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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