Rapidly rising incidence of childhood type 1 diabetes in Chinese population: epidemiology in Shanghai during 1997–2011

Zhao, Zuohui; Sun, Chengjun; Wang, Chunfang; Пин, Ли; Wang, Wei; Ye, Jun; Gu, Xuefan; Wang, Xiaodong; Shen, Shuixian; Zhi, Deng; Lu, Zhongyang; Ye, Rong; Cheng, Ruoqian; Li, Xi; Li, Xiaojing; Zheng, Zhangqian; Zhang, Miaoying; Luo, Feihong

doi:10.1007/s00592-014-0590-2

Cited by 63 publications

(63 citation statements)

References 36 publications

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“…The more recent longitudinal data sets from Shanghai 10 and Zhejiang, 11 combined with the threefold increase since 2000 of per capita milk consumption in urban China, 12 also give credence to a link with a component of milk. Accordingly, the ecological epidemiological data, although not proving causation, provide powerful evidence that A1 β-casein is a causal factor in the pathogenesis of type 1 diabetes.…”

Section: Introductionmentioning

confidence: 93%

“…In Shanghai, the incidence among children aged ⩽15 years increased at a rate of 14.2% per year between 1997 and 2011, from a low baseline of 1.5 per 100 000 in 1997–2001 to 5.5 per 100 000 in 2007–2011. 10 In Zhejiang, a major city south of Shanghai at an earlier stage of economic development, the mean incidence in adolescents aged ⩽19 years increased at a rate of 12.0% per year, from 1.22 per 100 000 in 2007 (age standardised) to 2.48 per 100 000 in 2013. 11 The greatest increase in Zhejiang was in children aged <5 years with a rate of 33.61% per year.…”

Section: Introductionmentioning

confidence: 99%

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A1 beta-casein milk protein and other environmental pre-disposing factors for type 1 diabetes

Chia

McRae

Kukuljan³

et al. 2017

Nutr. Diabetes

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Globally type 1 diabetes incidence is increasing. It is widely accepted that the pathophysiology of type 1 diabetes is influenced by environmental factors in people with specific human leukocyte antigen haplotypes. We propose that a complex interplay between dietary triggers, permissive gut factors and potentially other influencing factors underpins disease progression. We present evidence that A1 β-casein cows’ milk protein is a primary causal trigger of type 1 diabetes in individuals with genetic risk factors. Permissive gut factors (for example, aberrant mucosal immunity), intervene by impacting the gut’s environment and the mucosal barrier. Various influencing factors (for example, breastfeeding duration, exposure to other dietary triggers and vitamin D) modify the impact of triggers and permissive gut factors on disease. The power of the dominant trigger and permissive gut factors on disease is influenced by timing, magnitude and/or duration of exposure. Within this framework, removal of a dominant dietary trigger may profoundly affect type 1 diabetes incidence. We present epidemiological, animal-based, in vitro and theoretical evidence for A1 β-casein and its β-casomorphin-7 derivative as dominant causal triggers of type 1 diabetes. The effects of ordinary milk containing A1 and A2 β-casein and milk containing only the A2 β-casein warrant comparison in prospective trials.

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Section: Introductionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

A1 beta-casein milk protein and other environmental pre-disposing factors for type 1 diabetes

Chia

McRae

Kukuljan³

et al. 2017

Nutr. Diabetes

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show abstract

“…a hundredfold that of China) [47]. In countries with a lower incidence of type 1 diabetes, the increase in incidence has been more marked [48] whereas in high-prevalence countries it may have decelerated [49]. In parallel with a globally increased prevalence, the proportion of individuals with type 1 diabetes having the high-risk HLA-DR3/4 - DQ2/8 genotype has decreased [50].…”

Section: Environmental Factorsmentioning

confidence: 99%

Early prediction of autoimmune (type 1) diabetes

2017

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Underlying type 1 diabetes is a genetic aetiology dominated by the influence of specific HLA haplotypes involving primarily the class II DR-DQ region. In genetically predisposed children with the DR4-DQ8 haplotype, exogenous factors, yet to be identified, are thought to trigger an autoimmune reaction against insulin, signalled by insulin autoantibodies as the first autoantibody to appear. In children with the DR3-DQ2 haplotype, the triggering reaction is primarily against GAD signalled by GAD autoantibodies (GADA) as the first-appearing autoantibody. The incidence rate of insulin autoantibodies as the first-appearing autoantibody peaks during the first years of life and declines thereafter. The incidence rate of GADA as the first-appearing autoantibody peaks later but does not decline. The first autoantibody may variably be followed, in an apparently non-HLA-associated pathogenesis, by a second, third or fourth autoantibody. Although not all persons with a single type of autoantibody progress to diabetes, the presence of multiple autoantibodies seems invariably to be followed by loss of functional beta cell mass and eventually by dysglycaemia and symptoms. Infiltration of mononuclear cells in and around the islets appears to be a late phenomenon appearing in the multiple-autoantibody-positive with dysglycaemia. As our understanding of the aetiology and pathogenesis of type 1 diabetes advances, the improved capability for early prediction should guide new strategies for the prevention of type 1 diabetes.Electronic supplementary materialThe online version of this article (doi:10.1007/s00125-017-4308-1) contains a slideset of the figures for download, which is available to authorised users.

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“…The incidence and prevalence of type 1 diabetes (T1D) appear to be increasing in a variety of populations, with rates in Asian populations appearing to have lagged behind those in European populations . However, most regions studied have shown a progressive increase in T1D over the past few decades, with the suggestion that prevalence levels will continue to grow .…”

mentioning

confidence: 99%