ArticleInternational journal of women's health2026
Does Depression Increase the Risk of Endometriosis? A Combined Population‑Based and Laboratory Study.
Article in International journal of women's health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Endometriosis is a chronic, estrogen-dependent inflammatory disorder that causes substantial pain and infertility. Observational studies have reported higher rates of multiple psychiatric disorders among individuals with endometriosis; however, confounding and reverse causation limit causal interpretation. Methods: We performed bidirectional two-sample Mendelian randomization (MR) analyses using genome-wide association study (GWAS) summary statistics from European-ancestry populations to test causal relationships between genetic liability to depression, anxiety, insomnia, bipolar disorder, schizophrenia, and endometriosis. Instrumental variables were selected using genome-wide significance thresholds and linkage disequilibrium clumping, and robustness was evaluated using MR Egger regression, the weighted median method, and mode-based estimators, together with heterogeneity and pleiotropy tests. To assess biological coherence, SH-SY5Y cells were differentiated into sympathetic neuron-like cells, norepinephrine was quantified by enzyme-linked immunosorbent (ELISA) assay, and paracrine effects on 12Z endometriotic epithelial cells were examined using CCK-8 assays. Transcriptomic profiling was followed by Gene Ontology (GO) enrichment, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, and protein-protein interaction (PPI) network analysis. Results: Forward-direction MR supported an association between genetic liability to depression and increased endometriosis risk, whereas anxiety, insomnia, bipolar disorder, and schizophrenia showed no robust causal evidence. Reverse-direction MR did not support endometriosis genetic liability as a causal driver of psychiatric disorders. In vitro, sympathetic neuron-like differentiation increased norepinephrine secretion and enhanced 12Z cell proliferation, with stronger effects under conditioned-medium exposure. Enrichment analyses identified immune-related pathways, with prominent enrichment in Ras signaling, phosphatidylinositol 3 kinase and protein kinase B signaling, mitogen-activated protein kinase signaling, and cyclic adenosine monophosphate signaling. Conclusion: These findings suggest that depression may contribute to endometriosis susceptibility and are supported by complementary in vitro and transcriptomic evidence.
Indexed as
Identifiers
What OpenQuestion holds
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.