ArticleMedicine2026
From lipid profiles to disease onset: Triglycerides as predictive biomarkers in endometriosis.
Article in Medicine, 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
4 authors.
Funding
Abstract
Dyslipidaemia is related to endometriosis, but it is not known which lipid component is most relevant, and whether the observed correlation reflects the causal relationship. The relationship between triglycerides (TG) and endometriosis is studied through population research, and Mendelian randomization (MR) is used to evaluate the genetic evidence consistent with the causal relationship. We analyzed 2345 women from National Health and Nutrition Examination Survey 1999 to 2006 to assess lipid profiles and self-reported clinician-diagnosed endometriosis. Survey-weighted multivariable logistic regression was used with progressive covariate adjustment. Lipid-lowering medication use was additionally considered to address treatment-related confounding. For causal inference, 2-sample MR was conducted using genome-wide significant instruments for TG from large genome-wide association study resources and endometriosis summary statistics from FinnGen. Sensitivity analyses included assessments of heterogeneity and horizontal pleiotropy, as well as leave-one-out analyses. In the cross-sectional analysis, higher TG levels were associated with higher odds of endometriosis after multivariable adjustment. Compared with the lowest TG quartile, the highest quartile showed increased odds (odds ratio = 1.71, 95% confidence interval: 1.01-2.89). In MR analyses, genetically predicted TG was associated with endometriosis with consistent direction across methods; the inverse variance weighted estimate was odds ratio = 1.25 (95% confidence interval: 1.11-1.40). No statistically significant associations were observed for total cholesterol, low-density lipoprotein, or high-density lipoprotein. Subgroup analyses did not suggest clear effect heterogeneity by age, body mass index, or major metabolic comorbidities. In National Health and Nutrition Examination Survey 1999 to 2006, elevated TG was associated with higher odds of endometriosis. Two-sample MR provided genetic evidence consistent with a causal contribution of lifelong higher TG to endometriosis risk. These findings warrant confirmation in prospective cohorts and interventional studies before translation into clinical prevention strategies.
Indexed as
Identifiers
What Socratic 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 Socratic graph.