The influence of nutrients on the increased risk of developing endometriosis
This paper examines how nutrient deficiencies and excesses influence endometriosis risk by affecting gene expression and disease susceptibility.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
This paper reviews how nutrient deficiencies and excesses may influence endometriosis risk through mechanisms such as effects on gene expression and epigenetic regulation (narrowly framed as nutrigenomics/early environmental programming). It synthesizes evidence that dietary-related changes can alter susceptibility to disease, with endometriosis discussed alongside broader nutrient–epigenetic–health pathways, and cites prior work on specific nutrients and related biological processes (e.g., oxidative stress and inflammatory pathways). A key limitation is that the paper is not an original study with new patient data, and the mechanistic links are presented across heterogeneous literature rather than tested in a single standardized study. This paper is centrally about endometriosis — focusing on how nutrients and diet-related mechanisms may increase the risk of developing endometriosis.
Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works
Abstract
Full text
7,243 characters
· extracted from
oa-doi-fallback
· click to expand
Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.
My notes (saved in your browser only)
Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works
Condition tags
Citation neighborhood
Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.
References (25)
- Angiogenic Factors in Endometriosis via openalex
- A Promise in the Treatment of Endometriosis: An Observational Cohort Study on Ovarian Endometrioma Reduction by N-Acetylcysteine via openalex
- Diagnostic delay in women with pain and endometriosis via openalex
- Effects of Vitamin D on Endometriosis-Related Pain: A Double-Blind Clinical Trial via openalex
- Evaluation of the Relationship between Endometriosis and Omega-3 and Omega-6 Polyunsaturated Fatty Acids via openalex
- Impact of endometriosis on quality of life and work productivity: a multicenter study across ten countries via openalex
- Menstrual physiology: implications for endometrial pathology and beyond via openalex
- Nutritional aspects related to endometriosis via openalex
- Preliminary Study of Quercetin Affecting the Hypothalamic‐Pituitary‐Gonadal Axis on Rat Endometriosis Model via openalex
- Pyrvinium pamoate induces in-vitro suppression of IL-6 and IL-8 produced by human endometriotic stromal cells via openalex
- Reactive Oxygen Species Controls Endometriosis Progression via openalex
- Regression of Endometrial Implants by Resveratrol in an Experimentally Induced Endometriosis Model in Rats via openalex
- Sulforaphane Attenuates Endometriosis in Rat Models Through Inhibiting PI3K/Akt Signaling Pathway via openalex
- The association of food consumption and nutrient intake with endometriosis risk in Iranian women: A case-control study via openalex
- Theories on the Pathogenesis of Endometriosis via openalex
- W4387447602 via openalex
- W1968486602 via openalex
- W1977087590 via openalex
- W1993852804 via openalex
- W2029860792 via openalex
- W2076900231 via openalex
- W2110486307 via openalex
- W2890757392 via openalex
- W3106849331 via openalex
- W1824231381 via openalex
Cited by (1)
Source provenance
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00