Evidence map›Paper›PMID 21485745›Full record

ArticleDialogues in clinical neuroscience2011

Inflammation in depression: is adiposity a cause?

Richard C Shelton, Andrew H Miller

Open access · diamondAbstract read
In one paragraph

Article in Dialogues in clinical neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 21% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.

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4 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Richard C SheltonDepartment of Psychiatry, Vanderbilt University School of Medicine, Nashville, Tennessee 37212, USA. richard.shelton@vanderbilt.edu
Andrew H Miller
Emory University · USVanderbilt University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mounting evidence indicates that inflammation may play a significant role in the development of depression. Patients with depression exhibit increased inflammatory markers, and administration of cytokines and other inflammatory stimuli can induce depressive symptoms. Mechanisms by which cytokines access the brain and influence neurotransmitter systems relevant to depression have also been described, as have preliminary findings indicating that antagonizing inflammatory pathways may improve depressive symptoms. One primary source of inflammation in depression appears to be adiposity. Adipose tissue is a rich source of inflammatory factors including adipokines, chemokines, and cytokines, and a bidirectional relationship between adiposity and depression has been revealed. Adiposity is associated with the development of depression, and depression is associated with adiposity, reflecting a potentional vicious cycle between these two conditions which appears to center around inflammation. Treatments targeting this vicious cycle may be especially relevant for the treatment and prevention of depression as well as its multiple comorbid disorders such as cardiovascular disease, diabetes, and cancer, all of which have also been associated with both depression and inflammation.

Indexed as

AdiposityInflammationAdipose TissueAnimalsAntidepressive AgentsAnti-Inflammatory AgentsBrainCytokinesDepressionHumansModels, BiologicalNeurotransmitter AgentsAntidepressive AgentsAnti-Inflammatory AgentsCytokinesNeurotransmitter Agents

Identifiers

PMID21485745
PMCPMC3181969
OpenAlexW1928617315

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.