ArticleMetabologia2026
Smoking, GAD65 autoimmunity, genetic susceptibility to type 1 diabetes and incident adult-onset diabetes in the EPIC-InterAct case-cohort study.
Article in Metabologia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aims/hypothesis: Smoking increases the risk of type 2 diabetes, but its role in autoimmune diabetes remains unclear. We investigated whether smoking is associated with being GAD65 autoantibody (GAD65Ab) positive or the risk of progressing to diabetes. We also assessed its interaction with genetic susceptibility to type 1 diabetes. Methods: We used data from the EPIC-InterAct case-cohort study including 11,161 incident cases of adult-onset diabetes and 14,922 subcohort participants. Logistic regression was used to estimate odds ratios (ORs) for being GAD65Ab positive at baseline by smoking status. Hazard ratios (HRs) of diabetes by baseline smoking and GAD65Ab status were estimated using Prentice-weighted Cox regression. Two- and three-way interactions between smoking, GAD65Ab status and a type 1 diabetes genetic risk score (T1D-GRS) were assessed by attributable proportion due to interaction (AP). Results: There was no evidence that smoking was associated with being GAD65Ab positive (OR 1.00, 95% CI 0.82, 1.22 current vs never smoking), but among GAD65Ab-positive participants current smokers were more likely to progress to diabetes than never smokers (HR 1.40, 95% CI 1.03, 1.90) and there was an interaction between being GAD65Ab positive and heavy smoking for diabetes risk (AP 0.32, 95% CI 0.15, 0.49 ≥ 15 pack-years vs never smoking). Three-way interaction between heavy smoking, being GAD65Ab positive and the highest T1D-GRS tertile was also observed (combined HR 7.30, 95% CI 5.17, 10.31; AP 0.46, 95% CI 0.23, 0.70). Conclusions/interpretation: While smoking may not be associated with being GAD65Ab positive, it may increase the risk of progressing to diabetes in GAD65Ab-positive individuals and in those with genetic susceptibility to type 1 diabetes. Graphical Abstract: Supplementary Information: The online version contains supplementary material available at 10.1007/s44357-026-00003-9.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.