Evidence map›Paper›PMID 31230727›Full record

ArticleBiological psychiatry2019

Physician-Training Stress and Accelerated Cellular Aging.

Kathryn K Ridout, Samuel J Ridout, Constance Guille, Douglas A Mata, Huda Akil, Srijan Sen

Abstract readMulticenter Study
In one paragraph

Article in Biological psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

15 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  14. Telomeres, Trauma, and Training.Biological psychiatry · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Kathryn K RidoutDepartment of Psychiatry, Kaiser Permanente, San Jose, California; Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, Providence, Rhode Island.
Samuel J RidoutDepartment of Psychiatry, Kaiser Permanente, San Jose, California.
Constance GuilleBrain Research and Integrative Neuropsychopharmacology Division, Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, South Carolina.
Douglas A MataDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Brigham Education Institute, Boston, Massachusetts.
Huda AkilMolecular and Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan; Department of Psychiatry, University of Michigan, Ann Arbor, Michigan.
Srijan SenMolecular and Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan; Department of Psychiatry, University of Michigan, Ann Arbor, Michigan. Electronic address: srijan@umich.edu.

Funding

Mobile Technology to Identify Behavorial Mechanisms Linking Genetic Variation and DepressionR01MH101459 · NIMH · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SEN, SRIJAN · 2013 to 2023
$6.4M
NIMH NIH HHS R01 MH101459
6 · The paper itself

Abstract

backgroundStress is a key precipitant for many common diseases, but established biological markers to track stress and guide investigations into mechanisms linking stress and disease are lacking. Cross-sectional studies have identified correlations between stress and telomere attrition, but no large, longitudinal studies examining the impacts of chronic stress on telomere length exist. Residency training for physicians is a well-established stressful experience and can be used as a prospective stress model.

methodsIn a longitudinal cohort study of 250 interns (first-year residents) at 55 United States hospital systems serving during the 2015-2016 academic year, we examined associations between measures of the residency experience and saliva-measured telomere attrition.

resultsTelomere length shortened significantly over the course of internship year, from mean ± SD of 6465.1 ± 876.8 base pairs before internship to 6321.5 ± 630.6 base pairs at the end of internship (t

conclusionsThis work implicates telomere attrition as a biologically measurable consequence of physician training, with the magnitude of attrition associated with workload. Identification of an objective, biological sequela of residency stress may help to facilitate the development of effective interventions. Further, the findings implicate telomere attrition as an objective biomarker to follow the pathologic effects of stress, in general.

Indexed as

Cellular SenescenceInternship and ResidencyOccupational StressTelomere HomeostasisTelomere ShorteningAdultCross-Sectional StudiesFemaleHumansLongitudinal StudiesMaleNeuroticismPhysiciansUnited StatesYoung AdultAgingEducationGraduateMedicalResidencyTelomere

Identifiers

PMID31230727
PMCPMC6788968

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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.