Evidence map›Paper›PMID 37667866›Full record

ArticleClinical endocrinology2024

Genetically predicted plasma cortisol and common chronic diseases: A Mendelian randomization study.

Wei-Hsuan Lee, Susanna C Larsson, Angela Wood, Emanuele Di Angelantonio, Adam S Butterworth, Stephen Burgess, Elias Allara

Open access · hybridAbstract read
In one paragraph

Article in Clinical endocrinology, 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.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
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

7 authors at 2 institutions in 3 countries.

Wei-Hsuan LeeBritish Heart Foundation, Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
Susanna C LarssonUnit of Cardiovascular and Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0003-0118-0341
Angela WoodBritish Heart Foundation, Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
Emanuele Di AngelantonioBritish Heart Foundation, Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
Adam S ButterworthBritish Heart Foundation, Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
Stephen BurgessBritish Heart Foundation, Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
Elias AllaraBritish Heart Foundation, Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.ORCID 0000-0002-1634-8330
University of Cambridge · GBUppsala University · SE

Funding

British Heart Foundation CH/12/2/29428British Heart Foundation RG/13/13/30194British Heart Foundation RG/18/13/33946Medical Research Council MC_UU_00002/7Wellcome Trust 100114Wellcome Trust 204623/Z/16/Z
6 · The paper itself

Abstract

objectiveCushing's syndrome is characterized by hypercortisolaemia and is frequently accompanied by comorbidities such as type 2 diabetes, hypertension, osteoporosis, depression and schizophrenia. It is unclear whether moderate but lifelong hypercortisolaemia is causally associated with these diseases in the general population. We aimed to address this research gap using a Mendelian randomization approach.

methodsWe used three cortisol-associated genetic variants in the SERPINA6/SERPINA1 region as genetic instruments in a two-sample, inverse-variance-weighted Mendelian randomization analysis. We obtained summary-level statistics for cortisol and disease outcomes from publicly available genetic consortia, and meta-analysed them as appropriate. We conducted a multivariable Mendelian randomization analysis to assess potential mediating effects.

resultsA 1 standard deviation higher genetically predicted plasma cortisol was associated with greater odds of hypertension (odds ratio: 1.12; 95% confidence interval [CI]: 1.05-1.18) as well as higher systolic blood pressure (mean difference [MD]: 0.03 SD change; 95% CI: 0.01-0.05) and diastolic blood pressure (MD: 0.03 SD change; 95% CI: 0.01-0.04). There was no evidence of association with type 2 diabetes, osteoporosis, depression and schizophrenia. The association with hypertension was attenuated upon adjustment for waist circumference, suggesting potential mediation through central obesity.

conclusionThere is strong evidence for a causal association between plasma cortisol and greater risk for hypertension, potentially mediated by obesity.

Indexed as

Cushing SyndromeDiabetes Mellitus, Type 2HypertensionOsteoporosisChronic DiseaseGenome-Wide Association StudyHumansHydrocortisoneMendelian Randomization AnalysisObesityPolymorphism, Single NucleotideHydrocortisonechronic diseasescortisolhypertensionmajor mental illnessMendelian randomizationosteoporosistype 2 diabetes

Identifiers

PMID37667866
PMCPMC7615603
OpenAlexW4386438478

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.