ArticleBMC geriatrics2024
Causal linkage of Graves' disease with aging: Mendelian randomization analysis of telomere length and age-related phenotypes.
Article in BMC geriatrics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Autoimmune thyroid disease and human health: a systematic review of Mendelian randomization studies.Frontiers in immunology · 2025Pooled it
- The mechanisms, epidemiology, and clinical implications of thyroid hormones and age-related macular degeneration: a narrative review.Frontiers in medicine · 2026Review
- Global, regional, and national burden of autoimmune disease in older adults (≥60 years) from 1990 to 2021: Results from the Global Burden of Disease Study 2021.The journal of nutrition, health & aging · 2025Article
- Identification of Risk Loci for Radiotherapy-Induced Tinnitus and Hearing Loss Through Integrated Genomic Analysis.International journal of molecular sciences · 2025Article
- Causal relationship between circulating immune cells and the risk of esophageal cancer: a Mendelian randomization study.Discover oncology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundAging is an irreversible progressive decline in physical function. Graves' disease (GD) is a common cause of hyperthyroidism and is characterized by elevated levels of the thyroid hormone (TH). High TH levels are associated with aging and a shortened lifespan. The causal relationship between GD and aging has yet to be investigated.
methodsWe used genome-wide association study (GWAS) datasets and Mendelian randomization (MR) analysis to explore the causal link between GD and aging. To assess the statistical power of instrumental variables (IVs), F-statistics and R
resultsF-statistics of the five IVs were greater than 10, and the R
conclusionsGD accelerates the occurrence of age-related phenotypes including TL, senile cataracts, age-related hearing impairment, COPD, and sarcopenia. In contrast, there are no causal linkages between GD and facial aging, age-related macular degeneration, or Alzheimer's disease. Further experimental studies could be conducted to elucidate the mechanisms by which GD facilitates aging, which could help slow down the progress of aging.
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Registered trials
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