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Cancer Causes Control. 2020 Apr;31(4):309-320. doi: 10.1007/s10552-020-01280-6. Epub 2020 Feb 25.

Endogenous estradiol and inflammation biomarkers: potential interacting mechanisms of obesity-related disease.

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Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.
Nell Hodgson Woodruff School of Nursing, Emory University, Atlanta, GA, USA.
Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.
Pharmacogenetics Laboratory, Faculty of Pharmacy, Centre Hospitalier Universitaire (CHU) de Québec Research Center, Laval University, Quebec City, QC, Canada.
HPV Immunology Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc, Frederick, MD, USA.



Disentangling the effects of endogenous estrogens and inflammation on obesity-related diseases requires a clearer understanding of how the two biological mechanisms relate to each other.


We studied 155 healthy postmenopausal women not taking menopausal hormone therapy enrolled in the Prostate Lung Colorectal and Ovarian (PLCO) screening cancer trial. From a baseline blood draw, we measured endogenous estradiol and 69 inflammation biomarkers: cytokines, chemokines, adipokines, angiogenic factors, growth factors, acute phase proteins, and soluble receptors. We evaluated the estradiol-inflammation relationship by assessing associations across different models (linear, ordinal logistic, and binary logistic) using a variety of estradiol classifications. We additionally investigated the estradiol-inflammation relationship stratified by baseline obesity status (BMI < 30 stratum and BMI > 30 stratum).


Associations of estradiol with 7 inflammation biomarkers met p < 0.05 statistical significance in linear and ordinal models: C-reactive protein (CRP), adiponectin, chemokine (C-X-C motif) ligand-6, thymus activation-regulated chemokine, eosinophil chemotactic protein, plasminogen activator inhibitor-1, and serum amyloid A. The positive association between estradiol and CRP was robust to model changes. Each standard deviation increase in endogenous estradiol doubled a woman's odds of having CRP levels higher than the study median (odds ratio 2.29; 95% confidence interval 1.28, 4.09). Estradiol was consistently inversely associated with adiponectin. Other estradiol-inflammation biomarker associations were not robust to model changes.


Endogenous estradiol appears to be associated with CRP and adiponectin; the evidence is limited for other inflammation biomarkers.


Cytokines; Endogenous estradiol; Inflammation; Obesity; Serum biomarkers


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