ReviewBMC medicine2012
Depression and sickness behavior are Janus-faced responses to shared inflammatory pathways.
Review in BMC medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 282 papers, 4 of them syntheses that pooled 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.
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.
Who cites it
282 citing papers in PubMed, 4 syntheses or guidelines pooled it.
- Exercise and depression symptoms in chronic kidney disease patients: an updated systematic review and meta-analysis.Renal failure · 2024Pooled it
- Pooled it
- Gut dysbiosis in severe mental illness and chronic fatigue: a novel trans-diagnostic construct? A systematic review and meta-analysis.Molecular psychiatry · 2022Pooled it
- Peripheral Alterations in Cytokine and Chemokine Levels After Antidepressant Drug Treatment for Major Depressive Disorder: Systematic Review and Meta-Analysis.Molecular neurobiology · 2018Pooled it
- Trial
- Early attachment disruption differentially enhances multiple signs of microglia activation in the prefrontal cortex, hippocampus, and preoptic area of periadolescent guinea pigs.Behavioural brain research · 2027Article
- Article
- Psychotropic Drugs: A Promising Non-Antibiotic Agent to Combat Multi-Drug-Resistant Microorganisms.Drug development research · 2026Review
- Unifying the hallmarks of major depression through neuroimmune-metabolic-oxidative (NIMETOX) dysregulation: a mechanistic systems framework.Cellular & molecular immunology · 2026Review
- Thymus Involution across the Human Menstrual Cycle.bioRxiv : the preprint server for biology · 2026Article
- Investigating the Phytochemical Constituents, Anti-Inflammatory, and Neuropharmacological Activities of Podocarpus neriifolius Leaves Through FT-IR, GC-MS, Experimental Studies, Molecular Docking, and Molecular Dynamics Simulations.Pharmacology research & perspectives · 2026Article
- Lower insulin resistance in Chinese patients with severe major depressive disorder: associations with the inflammatory response.BMC psychiatry · 2026Article
- From parasite-induced immune activation to neuroinflammation and behavioral dysfunction: convergent mechanisms across protozoa and helminths: a review.Journal of neuroinflammation · 2026Review
- Sex-dependent modulation of social distance by lipopolysaccharide-induced inflammation in mice.Translational psychiatry · 2026Article
- Review
- Age-Specific Association Between the Dietary Inflammatory Index and Depression Among Patients With Chronic Kidney Disease.Food science & nutrition · 2026Article
- Article
- Clinical Factors and Serum Biomarkers Associated With Major Depressive Disorder in Adolescents With and Without Nonsuicidal Self-Injury: A Comparative Cross-Sectional Study.Alpha psychiatry · 2026Article
- The kynurenine pathway in depression and schizophrenia: convergent signals, divergent states, and clinical signatures.EXCLI journal · 2026Review
- The emerging role of T cells in depression.Frontiers in psychiatry · 2026Review
222 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers.
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Registered trials
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.