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- W2182000519 abstract "The timing hypothesis posits that exogenous estrogen plus progestin (E+P) hormone therapy (HT) is generally beneficial when initiated in proximity to the final menstrual period, but this benefit decreases and can lead to increased risk when initiated six to ten years later. This concept has been put forward to explain the discrepancies across randomized clinical trials assessing HT for prevention of cardiovascular disease. Similarly, while postmenopausal estrogen alone therapy (E) is associated with a slight decrease in breast cancer, this decrease is not found with E+P. The timing hypothesis, therefore, provides guidance for future clinical care of menopausal women but does not address the underlying physiologic basis or mechanistic difference in either the timing or the HT regimen. However, longitudinal epidemiological data collected from mid-aged women and experimental studies in nonhuman primates provide additional information that may permit the associations found in population-based studies to hypothesize a causal pathway. Using the Bradford-Hill criteria for evoking causality, it is possible to posit that the increased incidence in cardiovascular disease and breast cancer during the menopausal transition induced under the influence of endogenous cyclic estrogen and progesterone, which leads to increased adrenal steroid production, is recapitulated by imposing exogenous E+P following the return of the adrenal to a pre-transition status." @default.
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- W2182000519 date "2014-01-01" @default.
- W2182000519 modified "2023-09-24" @default.
- W2182000519 title "A Mechanistic Hypothesis to Explain the Timing Hypothesis" @default.
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