Evidence map›Paper›PMID 30762873›Full record

ReviewClinical and experimental immunology2019

Depressive symptoms in inflammatory bowel disease: an extraintestinal manifestation of inflammation?

C D Moulton, P Pavlidis, C Norton, S Norton, C Pariante, B Hayee, N Powell

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical and experimental immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 2 pooled it
8.9field-weighted citation impact, top 2% 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

57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 97 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

7 authors at 2 institutions in 1 country.

C D MoultonDepartment of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.ORCID 0000-0003-0880-4495
P PavlidisCentre for Inflammation Biology and Cancer Immunology, King's College London, London, UK.
C NortonFlorence Nightingale Faculty of Nursing, Midwifery and Palliative Care, King's College London, London, UK.
S NortonHealth Psychology, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
C ParianteDepartment of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
B HayeeDepartment of Gastroenterology, King's College Hospital NHS Foundation Trust, London, UK.
N PowellCentre for Inflammation Biology and Cancer Immunology, King's College London, London, UK.
King's College London · GBKing's College Hospital NHS Foundation Trust · GB

Funding

Department of HealthMedical Research Council G108/603Medical Research Council MR/J002739/1Medical Research Council MR/N029488/1
6 · The paper itself

Abstract

Depressive symptoms are reported by more than 20% of people with inflammatory bowel disease (IBD), while sleep difficulties and fatigue are even more common. Co-morbid depressive symptoms predict a poor IBD course, including increased risk of relapse and surgery, which is inconsistently improved by psychological treatments. Rather than being distinct systems, there is compelling evidence for bidirectional communication between gut and brain, driven by neural, metabolic, endocrine and inflammatory mediators. An emerging concept is that depressive symptoms may be mechanistically linked to excess inflammation and dysregulation of the gut-brain axis. Given the close link between the intestinal microbiota and host immune responses, patients prone to shifts in their intestinal microbiome, including smokers, those with poor diet and early life stress, may be exposed to exaggerated immune responses. Excess inflammation is associated with brain changes (depressive symptoms, fatigue, sleep difficulties) and worsening gastrointestinal symptoms, which are exacerbated by psychological distress. Equally, treatments both for depressive symptoms and IBD provide opportunities to break this cycle by reducing the causes and effects of inflammation. As well as addressing potential risk factors such as smoking and diet, treatments to alter the microbiome may reduce depressive symptoms. Observational evidence suggests that anti-inflammatory treatments for IBD may improve co-morbid depressive symptoms correlating with reduction in inflammation. With a growing range of treatments targeting inflammation centrally, peripherally and in the gut, IBD provides a unique model to understand the interplay between brain and gut in the pathogenesis of depressive symptoms, both in IBD and in the whole population.

Indexed as

DepressionInflammatory Bowel DiseasesAnimalsBrainChronic DiseaseComorbidityGastrointestinal MicrobiomeHumansInflammationRisk Factorsdepressive symptomsgut-brain-axisinflammationinflammatory bowel diseasemicrobiome

Identifiers

PMID30762873
PMCPMC6693970
OpenAlexW2911476667

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.