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Clin Endocrinol (Oxf). 2018 Oct;89(4):514-525. doi: 10.1111/cen.13797. Epub 2018 Jul 23.

Oestradiol level, oestrogen receptors, and mortality in elderly men: The three-city cohort study.

Author information

1
Paris-Saclay University, Paris-South University, UVSQ, Center for Research in Epidemiology and Population Health, INSERM, Villejuif, France.
2
Service de Génétique Moléculaire, Pharmacogénétique et Hormonologie, Hôpitaux Universitaires Paris Sud, AH-HP, CHU Bicêtre, France.
3
INSERM UMR_S U1185, Fac Med Paris Sud, Univ. Paris Sud, Université Paris-Saclay, Le Kremlin Bicêtre, France.
4
University Bordeaux, INSERM, Bordeaux Population Health Research Center, UMR 1219, CHU Bordeaux, Bordeaux, France.
5
INSERM, University of Montpellier, Neuropsychiatry: Epidemiological and Clinical Research, Montpellier, France.

Abstract

CONTEXT:

Although endogenous oestradiol, generally considered as the female hormone, has been little investigated in men, it could play a role in men's health, mortality in particular. The influence of oestrogen receptors (ER) genetic polymorphisms on this relationship has never been studied.

DESIGN AND PARTICIPANTS:

The Three-City cohort study included (1999-2001) 3650 men ≥65 years who were followed for mortality over 12 years. At baseline, total oestradiol (tE2) was measured and ER genotyped in a random subsample of 472 men without hormonal treatment. Free oestradiol (fE2) was estimated using Vermeulen and Södergard algorithms.

MAIN OUTCOME:

Mortality data were obtained from death certificates. We used inverse probability weighted Cox models to examine the association of oestradiol with all-cause and cause-specific mortality and its interaction with ER genetic polymorphisms.

RESULTS:

A total of 183 men died over the follow-up (cardiovascular disease (CVD), n = 44; cancer, n = 57; other causes, n = 82). After adjustment, there was a quadratic relationship of all-cause mortality with tE2 and fE2 (P-quadratic = 0.04 and 0.05, respectively), with higher mortality for the top and bottom tertiles compared to the middle one. These associations were stronger for CVD mortality (P-quadratic = 0.01 and 0.02 for tE2 and fE2, respectively) and disappeared for cancer mortality. There was no evidence of an interaction of oestradiol with any ER polymorphisms on all-cause mortality.

CONCLUSION:

In elderly men, we showed a nonlinear association of tE2 and fE2 with all-cause mortality. These quadratic relationships were stronger for CVD mortality and did not exist for cancer mortality. ER genetic polymorphisms did not modify this association.

KEYWORDS:

ageing; cancer mortality; cardiovascular mortality; genetic polymorphisms; risk; sex hormone

PMID:
29935032
DOI:
10.1111/cen.13797

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