scholarly journals Seasonal Variation in Month of Diagnosis of Polish Children with Type 1 Diabetes - A Multicenter Study

2018 ◽  
Vol 127 (05) ◽  
pp. 331-335 ◽  
Author(s):  
Agnieszka Szypowska ◽  
Anna Ramotowska ◽  
Marta Wysocka-Mincewicz ◽  
Artur Mazur ◽  
Lucyna Lisowicz ◽  
...  

Abstract Aim The seasonal variation of incidence of type 1 diabetes (T1D) theory supports the hypothesis that environmental factors play a role in the onset of the disease. The aim of this study is to assess seasonality of month of diagnosis in children with T1D in Poland. Material and methods the study group consisted of 2174 children from eastern and central Poland diagnosed with T1D between 2010 and 2014. Analysis was performed in different age groups, based on place of residence (rural/urban area) and depending on sex. Results We noted significant seasonality in the incidence of T1D with a peak in diagnosis of diabetes in January and the minimum rate in June. A total of 423 (19%) children were diagnosed in the warmest months (June to August with a mean temperature of 16.8°C) compared to 636 (29%) recognised in the coldest months (December to February with a mean temperature of −1.6°C), OR 0.57 95%CI [0.51-0.67], p<0.0001. We noted a more flat seasonal pattern in children 0-4 years of age compared with subjects 5–17 years old with a week correlation of trend comparison between both groups, r=0.69, p=0.001. Similar seasonal variation in the incidence of T1D was noted in children from urban and rural setting. For girls, seasonal pattern peaks were observed one month earlier as compared to boys. Conclusions Seasonal variation in incidence of T1D diagnosis of Polish children supports the role of different environmental factors in diabetes onset. The majority of children were diagnosed with diabetes in autumn and winter.

2020 ◽  
Vol 11 ◽  
Author(s):  
Sandra Dedrick ◽  
Bharathi Sundaresh ◽  
Qian Huang ◽  
Claudia Brady ◽  
Tessa Yoo ◽  
...  

2013 ◽  
Author(s):  
P. Osborn ◽  
C. A. Berg ◽  
A. E. Hughes ◽  
P. Pham ◽  
D. J. Wiebe

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 317-OR
Author(s):  
BARDEES FODA ◽  
MATTHEW H. FORSBERG ◽  
ASHLEY E. CIECKO ◽  
KEVIN W. MUELLER ◽  
ARON GEURTS ◽  
...  
Keyword(s):  

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Gerry K. Schwalfenberg

This paper looks at the environmental role of vitamin D and solar radiation as risk reduction factors in autoimmune disease. Five diseases are considered: multiple sclerosis, type 1 diabetes, rheumatoid arthritis, autoimmune disease of the thyroid, and inflammatory bowel disease. Clinical relevant studies and factors that may indicate evidence that autoimmune disease is a vitamin D-sensitive disease are presented. Studies that have resulted in prevention or amelioration of some autoimmune disease are discussed. An example of the utility of supplementing vitamin D in an unusual autoimmune disease, idiopathic thrombocytic purpura, is presented.


Author(s):  
Tiantian Yue ◽  
Fei Sun ◽  
Faxi Wang ◽  
Chunliang Yang ◽  
Jiahui Luo ◽  
...  

AbstractThe methyl-CpG-binding domain 2 (MBD2) interprets DNA methylome-encoded information through binding to the methylated CpG DNA, by which it regulates target gene expression at the transcriptional level. Although derailed DNA methylation has long been recognized to trigger or promote autoimmune responses in type 1 diabetes (T1D), the exact role of MBD2 in T1D pathogenesis, however, remains poorly defined. Herein, we generated an Mbd2 knockout model in the NOD background and found that Mbd2 deficiency exacerbated the development of spontaneous T1D in NOD mice. Adoptive transfer of Mbd2−/− CD4 T cells into NOD.scid mice further confirmed the observation. Mechanistically, Th1 stimulation rendered the Stat1 promoter to undergo a DNA methylation turnover featured by the changes of DNA methylation levels or patterns along with the induction of MBD2 expression, which then bound to the methylated CpG DNA within the Stat1 promoter, by which MBD2 maintains the homeostasis of Th1 program to prevent autoimmunity. As a result, ectopic MBD2 expression alleviated CD4 T cell diabetogenicity following their adoptive transfer into NOD.scid mice. Collectively, our data suggest that MBD2 could be a viable target to develop epigenetic-based therapeutics against T1D in clinical settings.


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