Evidence map›Paper›PMID 35634363›Full record

ArticleCurrent opinion in endocrine and metabolic research2022

Cause or consequence? Understanding the role of cortisol in the increased inflammation observed in depression.

Nare Amasi-Hartoonian, Luca Sforzini, Annamaria Cattaneo, Carmine Maria Pariante

Open access · hybridAbstract read
In one paragraph

Article in Current opinion in endocrine and metabolic research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. CD4The journal of headache and pain · 2026
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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

4 authors at 3 institutions in 2 countries.

Nare Amasi-HartoonianInstitute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychological Medicine, London, UK.
Luca SforziniInstitute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychological Medicine, London, UK.
Annamaria CattaneoDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy.
Carmine Maria ParianteInstitute of Psychiatry, Psychology and Neuroscience, King's College London, Department of Psychological Medicine, London, UK.
King's College London · GBCentro San Giovanni di Dio Fatebenefratelli · ITSouth London and Maudsley NHS Foundation Trust · GB

Funding

Medical Research Council G108/603Medical Research Council MR/N029488/1Medical Research Council MR/S003444/1Wellcome Trust 104025
6 · The paper itself

Abstract

Glucocorticoids such as cortisol are a class of steroid hormones that play an important role in co-ordinating the body's response to stress. Elevated cortisol levels and increased inflammation have frequently been reported in patients with depression. The currently accepted "glucocorticoid resistance" model posits this increased inflammation as a consequence of reduced sensitivity to cortisol's putative anti-inflammatory action. However, opposing evidence has accumulated that supports a more recent model, which instead proposes that cortisol possesses immune potentiating properties and may thus directly cause the increased inflammation seen in depression. Despite all of this, a clear explanation of the neuroendocrine mechanism that contributes to the development of depression is still lacking and thus requires further investigation in improved future studies.

Indexed as

cortisolglucocorticoid receptorglucocorticoid resistanceHypothalamic-pituitary-adrenal axisinflammationmajor depressive disorder

Identifiers

PMID35634363
PMCPMC7612780
OpenAlexW4225293157

What OpenQuestion holds

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Registered trials

None linked

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.