Secular trends of body mass index in <scp>N</scp>orth <scp>I</scp>ndian children with <scp>T</scp>ype 1 diabetes do not support the <scp>A</scp>ccelerator <scp>H</scp>ypothesis

Dayal, Devi; Samprathi, Madhusudan; Jayaraman, Dhaarani; Kohat, Dilesh; Bhalla, Anil Kumar

doi:10.1111/cen.12941

Cited by 8 publications

(10 citation statements)

References 21 publications

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“…Dayal et al (22) recently reported that there was no association between BMI and age at diagnosis in North Indian children with new-onset type 1 diabetes. In addition, it has been reported that the incidence of type 1 diabetes continued to rise in 2001-2008 in Australian youth aged 10-18 years, while the incidence of type 2 diabetes remained steady (23).…”

Section: Prevalence Of Diabetic Nephropathymentioning

confidence: 98%

Prevalence of Diabetes and Diabetic Nephropathy in a Large U.S. Commercially Insured Pediatric Population, 2002–2013

Jick

Breitenstein

et al. 2015

Diabetes Care

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OBJECTIVE To estimate the prevalence of diabetes and diabetic nephropathy in a large population of U.S. commercially insured patients aged <18 years from 2002 to 2013. RESEARCH DESIGN AND METHODS Using the U.S. MarketScan Commercial Claims and Encounters Database, we identified 96,171 pediatric patients with diabetes and 3,161 pediatric patients with diabetic nephropathy during 2002–2013. We estimated prevalence of pediatric diabetes overall, by diabetes type, age, and sex, and prevalence of pediatric diabetic nephropathy overall, by age, sex, and diabetes type. RESULTS The annual prevalence of diabetes in the whole pediatric population increased from 1.86 to 2.82 per 1,000 during 2002–2013: 1.48 to 2.32 per 1,000 for type 1 diabetes and 0.38 to 0.67 per 1,000 for type 2 diabetes in 2002–2006 and then 0.56 to 0.49 per 1,000 thereafter. The annual prevalence of diabetic nephropathy in pediatric patients with diabetes increased from 1.16 to 3.44% for all cases and 0.83 to 2.32% for probable cases only in 2002–2013. Prevalence of diabetes and diabetic nephropathy was highest in patients aged 12 to <18 years. While prevalence of type 1 diabetes was higher in male than in female youth, prevalence of type 2 diabetes and diabetic nephropathy was higher in female than in male youth. There was no difference in prevalence of diabetic nephropathy by diabetes type. CONCLUSIONS The prevalence of diabetes and diabetic nephropathy increased in the U.S. MarketScan commercially insured pediatric population from 2002 to 2013. The prevalence of diabetes and diabetic nephropathy markedly increased starting at age 12 years.

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Section: Prevalence Of Diabetic Nephropathymentioning

confidence: 98%

Prevalence of Diabetes and Diabetic Nephropathy in a Large U.S. Commercially Insured Pediatric Population, 2002–2013

Jick

Breitenstein

et al. 2015

Diabetes Care

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“…4 Our own study conducted in an ethnically different patient population and aimed at testing the AH in a developing country setup, demonstrated no association between BMI and age at diagnosis. 5 This was despite the fact that the prevalence of overweight and obesity in children has shown a significant average increase of 3% in our country during the time frame of our study. 6,7 Furthermore, the incidence of T1D at our hospital has also shown a significant increase over a similar time span.…”

mentioning

confidence: 59%

Brakes on the accelerator: the journey of accelerator hypothesis from “the missing link” to “an evolving concept”

Dayal

Muthuvel

2017

Int J Sci Rep

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CONTEXTThe accelerator hypothesis (AH) proposed by the late Prof Terence Wilkin attempts to unite the type 1 (T1D) and type 2 diabetes (T2D) by obesity driven insulin resistance (IR) and tends, in part, to explain the rising incidence of T1D by a parallel increase in the incidence of obesity.1 Since its inception in 2001, several studies have been conducted across the world to test the validity of AH. The results of these studies have shown considerable variability with some studies confirming and others refuting or showing neutrality to the key proposals of AH. This brief communication discusses the journey of AH over the last 16 years in the light of data accumulated from studies that aimed to test relevance and applicability of AH in diverse patient populations. KEY PREDICTIONS AND CONTROVERSIESThe AH proposes that all the three processes or accelerators i.e. IR, autoimmunity and genetic predisposition that result in presentation of diabetes (either type 1 or 2) are driven by excess weight gain, which is thought to be "the missing link" between the two types of diabetes.1 In particular, IR associated with recent weight gain is considered the main accelerator of pancreatic β-cell apoptosis that leads to earlier onset of T1D in individuals at genetic risk. The acceleration of diabetes and its presentation at a younger age will, ABSTRACTThe incidence of Type 1 diabetes (T1D) has increased significantly over the past few decades but the causes for this increase are poorly understood and hence the strategies for preventing T1D are difficult to design. T1D is characterised by autoimmune destruction of pancreatic β-cells resulting in insulin deficiency as opposed to Type 2 diabetes (T2D) characterised by weight driven insulin resistance (IR). The accelerator hypothesis (AH), proposed by the late Prof Terence Wilkin in 2001 offers an alternative mechanism for T1D and a different approach to prevention of T1D. This hypothesis considers both T1D and T2D as one and proposes that obesity driven IR is the key factor that may lead to either type of diabetes. It thus offers an easy explanation for the increasing worldwide incidence of childhood diabetes which is paralleled by the increase in childhood obesity rates. However, one of the key predictions of AH that the obesity related IR accelerates the onset of diabetes and hence heavier children should develop diabetes at a younger age, has remained a matter of debate since the hypothesis was first proposed. Since the inception of AH, the results of a number of studies which aimed at testing the hypothesis in diverse patient populations have shown support or opposed this key prediction. This article discusses the relevance of AH in the context of data from these studies.

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“…On the other hand, there are some concerns that high BMI might reflect heavier extent of insulin resistant and thus leading to the overload of β‐cell and then eventually accelerate the worsening of β‐cell function . Indeed, the “accelerator” or “overload” hypotheses had been proposed long ago, and researchers hold the thought that higher BMI might be the “accelerator” for T1D progression, but the reported results were conflicting …”

Section: Introductionmentioning

confidence: 99%

Complicated curve association of body weight at diagnosis with C‐peptide in children and adults with new‐onset type 1 diabetes

Gong

Zhong

et al. 2020

Diabetes Metabolism Res

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Aim: To investigate the association of body mass index (BMI) or BMI z-score (BMIz) at diagnosis with β-cell function in new-onset type 1 diabetes (T1D) patients in children and adults.Methods: This was a retrospective cohort study; 256 children (<18 years) and 245 adults (≥18 years) with less than 1-year duration were recruited and followed for 4 years with an interval of 12 months. Smooth curve fitting, a two-piecewise linear model, and Cox proportional hazards models were utilized to investigate the influence of BMI/BMIz on C-peptide levels.Results: Heavier patients (BMIz ≥ −1 in children and BMI in adults ≥20.2 kg/m 2 ) had greater C-peptide with a complicated J curve in all age groups after adjustment for age of onset, sex, and disease duration. Moreover, after 4 years of follow-up, patients with higher BMI/BMIz had a lower risk of β-cell failure (HR = 0.7; 95% CI, 0.6-1.0; P = .026). However, no association was found between baseline BMI/BMIz at diagnosis and C-peptide rate of decline during 1 year follow-up.Conclusion: Association between BMI/BMIz and C-peptide in T1D followed a complicated J curve pattern, and heavier patients had greater C-peptide at diagnosis and a lower risk of β-cell failure at 4 years, suggesting that baseline BMI is a useful predictor for β-cell function in patients with T1D.

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Secular trends of body mass index in North Indian children with Type 1 diabetes do not support the Accelerator Hypothesis

Abstract: There was no association between BMI SDS and age at diagnosis in children with new onset T1D. Further studies are needed to test whether the accelerator hypothesis is relevant in developing countries.

Cited by 8 publications

References 21 publications

Prevalence of Diabetes and Diabetic Nephropathy in a Large U.S. Commercially Insured Pediatric Population, 2002–2013

Prevalence of Diabetes and Diabetic Nephropathy in a Large U.S. Commercially Insured Pediatric Population, 2002–2013

Brakes on the accelerator: the journey of accelerator hypothesis from “the missing link” to “an evolving concept”

Complicated curve association of body weight at diagnosis with C‐peptide in children and adults with new‐onset type 1 diabetes

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