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Updated: Jan 11, 2026
An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
Published on: August 13, 2019
Adverse Cardiometabolic Impacts of Sleep Fragmentation and Estradiol Suppression: An Experimental Model of Menopause
Shadab A Rahman1,2,3, Leilah K Grant1,2,3, Aviva Y Cohn4
1Division of Sleep and Circadian Disorders, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
Context:
Risk of cardiometabolic disease increases in women transitioning to postmenopause, during which estradiol declines universally. Most of these women experience fragmentation of sleep because of nocturnal hot flashes, without a reduction in total sleep time.
Objective:
We examined the independent impact of estradiol suppression, sleep, and their combination on cardiometabolic outcomes categorized as satiety and hunger, lipid profile, cardiac vital signs, and glucoregulation.
Design:
Participants completed 5-night inpatient studies under eucaloric conditions, once during mid-follicular phase/estrogenized and again under estrogen-suppressed conditions, using the same experimental protocol both times. For all participants, sleep was unfragmented the first 2 nights and then experimentally fragmented without reducing total sleep time the next 3 nights.
Setting:
Inpatient intensive physiological monitoring research facility.
Participants:
Thirty-eight healthy premenopausal women.
Intervention(S):
Clinical experimental induced menopause model including GnRH agonist-induced hypoestrogenism and sleep fragmentation.
Main Outcome Measure(S):
Leptin and satiety.
Results:
Estradiol suppression significantly decreased leptin and increased lipid profiles (false discovery rate [FDR]-adjusted P ≤ .05). Sleep fragmentation significantly increased heart rate (FDR-adjusted P = .002) and trended to increase fasting glucose (FDR-adjusted P = .08). Estradiol suppression and sleep fragmentation worsened individual cardiometabolic outcomes by (median, interquartile range) 4.0% (1.5%, 6.3%) from normalized baseline values. Sleep fragmentation worsened a composite cardiometabolic index derived from individual clinical cardiometabolic measures by an additional 103% over estradiol suppression alone.
Conclusion:
Independent of aging, there are significant adverse changes in cardiometabolic health induced by core components of the transition to postmenopause, including novel effects of sleep fragmentation, a modifiable target.
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