CoChat
Sign Up
Cited by 218Tryptophan and brain disordersTreatment of Major DepressionStress Responses and Cortisol

The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.

Elevated C-Reactive Protein in Patients With Depression, Independent of Genetic, Health, and Psychosocial Factors: Results From the UK Biobank

Pitharouli, Maria C., Hagenaars, Saskia P., Glanville, Kylie P., Coleman, Jonathan R.I., Hotopf, Matthew, Lewis, Cathryn M., Pariante, Carmine M.·2021·American Journal of Psychiatry
DOI 10.1176/appi.ajp.2020.20060947
Open this paper in CoChat — free account

Abstract

OBJECTIVE: The authors investigated the pathways (genetic, environmental, lifestyle, medical) leading to inflammation in major depressive disorder using C-reactive protein (CRP), genetic, and phenotypic data from the UK Biobank. METHODS: This was a case-control study of 26,894 participants with a lifetime diagnosis of major depressive disorder from the Composite International Diagnostic Interview and 59,001 control subjects who reported no mental disorder and had not reported taking any antidepressant medication. Linear regression models of log CRP level were fitted to regress out the effects of age, sex, body mass index (BMI), and smoking and to test whether the polygenic risk score (PRS) for major depression was associated with log CRP level and whether the association between log CRP level and major depression remained after adjusting for early-life trauma, socioeconomic status, and self-reported health status. RESULTS: CRP levels were significantly higher in patients with depression relative to control subjects (2.4 mg/L compared with 2.1 mg/L, respectively), and more case than control subjects had CRP levels >3 mg/L (21.2% compared with 16.8%, respectively), indicating low-grade inflammation. The PRS for depression was positively and significantly associated with log CRP levels, but this association was no longer significant after adjustment for BMI and smoking. The association between depression and increased log CRP level was substantially reduced, but still remained significant, after adjustment for the aforementioned clinical and sociodemographic factors. CONCLUSIONS: The data indicate that the "genetic" contribution to increased inflammation in depression is due to regulation of eating and smoking habits rather than an "autoimmune" genetic predisposition. Moreover, the association between depression and increased inflammation even after full adjustment indicates either the presence of yet unknown or unmeasured psychosocial and clinical confounding factors or that a core biological association between depression and increased inflammation exists independently from confounders.

Overview

Integrity signals

Registry

Crossref · 10.1176/appi.ajp.2020.20060947

Cites

51 of 51 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Show all 51 references

Cited by

Sorted by citations

Items 201–218 of 218

Related

See all

Metadata

Authors
Pitharouli, M. C., Hagenaars, S. P., Glanville, K. P., Coleman, J. R. I., Hotopf, M., Lewis, C. M., & Pariante, C. M.
Affiliations
National Health Service (GB)
ORCID
Venue
American Journal of Psychiatry
Publisher
American Psychiatric Association Publishing
Published
2021-06
Volume
178
Issue
6
Pages
522-529
ISSN
  • 0002-953X (ISSN-L)
  • 1535-7228
DOI
10.1176/appi.ajp.2020.20060947
OpenAlex
W3161566379
Cited by
218
References
51
Citations by year
2026: 42 · 2025: 34 · 2024: 41 · 2023: 41 · 2022: 36 · 2021: 24
FWCI
11.81
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
  • Research Portal (King's College London) (submittedVersion)
Funders
Medical Research Council (MR/S015132/1, MR/N015746/1, MC_PC_17228)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
major depressive disorder, C-reactive protein, low-grade inflammation, polygenic risk score, genetic predisposition to depression, smoking, body mass index, early trauma, socioeconomic status
MeSH terms
Adverse Childhood Experiences, C-Reactive Protein, Depressive Disorder, Major, Major Depressive Disorder, Female, United Kingdom, Health Status, Humans, Inflammation, Male, Middle Aged, Psychology, Smoking, Social Class, Linear Models, Case-Control Studies, Biological Specimen Banks, Genetic Predisposition to Disease

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review