Evidence map›Paper›PMID 31938470›Full record

ReviewWorld journal of diabetes2020

Current understandings of the pathogenesis of type 1 diabetes: Genetics to environment.

Adebola Matthew Giwa, Rizwan Ahmed, Zahra Omidian, Neha Majety, Kagan Ege Karakus, Sarah M Omer, Thomas Donner, Abdel Rahim A Hamad

Open access · diamondAbstract readReview
In one paragraph

Review in World journal of diabetes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 2 pooled it
5.4field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 123 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Review
  5. Experimental models in diabetes research.Laboratory animal research · 2026
    Review
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26 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 3 countries.

Adebola Matthew GiwaDepartment of Pediatrics, Johns Hopkins Medical Center, Baltimore, MD 21287, United States.
Rizwan AhmedDepartment of Pathology, Johns Hopkins Medical Center, Baltimore, MD 21205, United States.
Zahra OmidianDepartment of Pathology, Johns Hopkins Medical Center, Baltimore, MD 21205, United States.
Neha MajetyDepartment of Pathology, Johns Hopkins Medical Center, Baltimore, MD 21205, United States.
Kagan Ege KarakusSchool of Medicine, Koc University, Istanbul 34450, Turkey.
Sarah M OmerDepartment of Pathology, Johns Hopkins Medical Center, Baltimore, MD 21205, United States.
Thomas DonnerDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, United States.
Abdel Rahim A HamadDepartment of Pathology, Johns Hopkins Medical Center, Baltimore, MD 21205, United States. ahamad@jhmi.edu.
United Lincolnshire Hospitals NHS Trust · GBCreative Research Enterprises (United States) · USJohns Hopkins Medicine · USJohns Hopkins Bayview Medical Center · US

Funding

Institutional Training for PediatriciansT32HD044355 · NICHD · JOHNS HOPKINS UNIVERSITY · PI BRADY, TAMMY MCLOUGHLIN · 2003 to 2023
$4.1M
NICHD NIH HHS T32 HD044355
6 · The paper itself

Abstract

Type 1 diabetes (T1D) is an autoimmune disease that usually strikes early in life, but can affect individuals at almost any age. It is caused by autoreactive T cells that destroy insulin-producing beta cells in the pancreas. Epidemiological studies estimate a prevalence of 1 in 300 children in the United States with an increasing incidence of 2%-5% annually worldwide. The daily responsibility, clinical management, and vigilance required to maintain blood sugar levels within normal range and avoid acute complications (hypoglycemic episodes and diabetic ketoacidosis) and long term micro- and macro-vascular complications significantly affects quality of life and public health care costs. Given the expansive impact of T1D, research work has accelerated and T1D has been intensively investigated with the focus to better understand, manage and cure this condition. Many advances have been made in the past decades in this regard, but key questions remain as to why certain people develop T1D, but not others, with the glaring example of discordant disease incidence among monozygotic twins. In this review, we discuss the field's current understanding of its pathophysiology and the role of genetics and environment on the development of T1D. We examine the potential implications of these findings with an emphasis on T1D inheritance patterns, twin studies, and disease prevention. Through a better understanding of this process, interventions can be developed to prevent or halt it at early stages.

Indexed as

Diabetes preventionRole of genetics in type 1 diabetesType 1 diabetes concordanceType 1 diabetes discordanceType 1 diabetes environmentType 1 diabetes epigeneticsType 1 diabetes geneticsType 1 diabetes twin studies

Identifiers

PMID31938470
PMCPMC6927819
OpenAlexW2994833425

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.