ArticleAllergy, asthma & immunology research2026
A Risk Factor Atlas for Allergy-Related Airway Diseases: Evidence From Multi-Biobank Genetic Study.
Article in Allergy, asthma & immunology research, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeUnderstanding factors contributing to allergy-related airway diseases (AADs).
methodsWe conducted a meta-analysis of Mendelian randomization (MR) estimates from multi-biobank to investigate the effects of 83 common factors on asthma, allergic rhinitis (AR), chronic rhinosinusitis (CRS), and nasal polyps (NPs). Data for AADs were obtained from multiple independent populations including FinnGen, UK Biobank and large consortia (asthma, 137,498 cases and 1,009,466 controls; AR, 51,712 cases and 592,784 controls; CRS, 24,688 cases and 760,073 controls; and NP, 11,796 cases and 760,075 controls). The meta-analyses combining the above multi-biobank MR results were employed as our main results.
resultsGenetically proxied social isolation, smoking time and frequency, sedentary time, global and central obesity, C-reactive protein (CRP), insomnia, major depressive disorder (MDD), anxiety, attention deficit hyperactivity disorder, neuroticism, posttraumatic stress disorder (PTSD), rheumatoid arthritis (RA), atopic dermatitis (AD), type 1 diabetes (T1D), gastroesophageal reflux disease (GERD), childhood obesity, early menarche, smoking around birth, and childhood maltreatment could increase the risk of asthma. Education, higher income, cheese intake, sleep duration, high density lipoprotein cholesterol, forced expiratory volume in 1 second/forced vital capacity, well-being and ulcerative colitis were associated with a decreased risk of asthma. Social isolation, CRP, Crohn's disease, GERD, insomnia, MDD, neuroticism and AD could increase the risk of AR, whereas well-being could decrease the risk of AR. Sedentary time, MDD, anxiety, PTSD, opioid use disorder, RA, AD, T1D, hypothyroidism, and GERD could increase the risk of CRS, whereas coffee intake, apolipoprotein A1, and well-being were associated with a decreased risk of CRS. Smoking duration, RA, AD and T1D could increase the risk of NP, whereas fresh fruit intake could decrease the risk of NP.
conclusionsThis study offers potential causal evidence for AAD risk factors and provides actionable targets for primary prevention.
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.