Evidence map›Paper›PMID 35690664›Full record

ArticleScientific reports2022

Reduced arterial elasticity after anabolic-androgenic steroid use in young adult males and mice.

H S Melsom, C M Heiestad, E Eftestøl, M K Torp, K Gundersen, A K Bjørnebekk, P M Thorsby, K O Stensløkken, J Hisdal

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

H S Melsom *Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
C M Heiestad *Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway. c.m.heiestad@medisin.uio.no.
E EftestølDepartment of Biosciences, Faculty of Mathematics and Natural Sciences, University of Oslo, Oslo, Norway.
M K TorpInstitute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway.
K GundersenDepartment of Biosciences, Faculty of Mathematics and Natural Sciences, University of Oslo, Oslo, Norway.
A K BjørnebekkThe Anabolic Androgenic Steroid Research Group, Oslo University Hospital, Oslo, Norway.
P M ThorsbyBiochemical Endocrinology and Metabolism Research Group, Hormone Laboratory, Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway.
K O StensløkkenInstitute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway.
J HisdalInstitute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
University of Oslo · NOOslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-doses of anabolic-androgenic steroids (AAS) is efficient for building muscle mass, but pose a risk of cardiovascular side effects. Little is known of the effect of AAS on vasculature, but previous findings suggest unfavorable alterations in vessel walls and vasoreactivity. Here, long-term effect of AAS on vascular function and morphology were examined in male weightlifters, and in a mimicking animal model. Arterial elasticity and morphology were tested with ultrasound, pulse wave velocity (PWV) and carotid intima media thickness (cIMT) in 56 current male AAS users, and 67 non-exposed weightlifting controls (WLC). Female mice were treated with testosterone for 14 days and echocardiography were applied to evaluate vascular function and morphology. Male AAS users had higher PWV (p = 0.044), reduced carotid artery compliance (p = 0.0005), and increased cIMT (p = 0.041) compared to WLC. Similar functional changes were found in the ascending aorta of mice after 7- (p = 0.043) and 14 days (p = 0.001) of testosterone treatment. This animal model can be used to map molecular mechanisms responsible for complications related to AAS misuse. Considering the age-independent stiffening of major arteries and the predictive power of an increase in PWV and cIMT, the long-term users of AAS are at increased risk of severe cardiovascular events.

Indexed as

Carotid Intima-Media ThicknessPulse Wave AnalysisAnimalsCarotid ArteriesElasticityFemaleMaleMiceTestosteroneTestosterone

Identifiers

PMID35690664
PMCPMC9188580
OpenAlexW4282923699

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.