Hormone replacement therapy, HRT, in early menopause may slow progression of cardiovascular disease.

“Hormone Replacement therapy in early menopause is important to decrease the bone loss following menopause. I have posted several articles on this website related to osteoporosis. Post-menopausal women not taking hormone replacement lose 60% of their total bone mass between menopause and 60 years of age.

Now another benefit is reported. The study below shows slowing of atherosclerosis by taking hormone replacement.

It is important to know what replacement is most safe. Also know the safety advantages of vaginal or topical HRT versus oral hormone placement. The metabolism is different when taking a medical orally than transcutaneous. Vaginal HRT with estriol elevates estriol a little and transiently if it elevates blood levels at all.

Testosterone is another hormone loss in menopause. Its involvement in bone loss and atherosclerosis has not been as extensively tested. The research available that I found does not report a significant risk of  testosterone replacement to keep the normal pre-menopausal blood level.

This finding is so important in my view that I posted the abstract of the original article just below the announcement in the popular press.

If you know women in the age group to be peri-menopausal please tell them the news.” Bill Chesnut, MD

To go back to New Health News: https://billchesnutmd.com/new-health-news

Starting HRT in early menopause may slow progression of cardiovascular disease, study indicates

The Wall Street Journal (3/30, Beck, Subscription Publication) reports the findings of a 643-patient study published in the New England Journal of Medicine study add to the evidence that beginning hormone replacement therapy (HRT) in early menopause may be protective against cardiovascular disease.

The NPR (3/30, Bichell) “Shots” blog reports that in the study, investigators “directly tested the effect of starting hormone therapy within the first six years after menopause, versus the effect of starting 10 years or more after menopause.” After five years, researchers found that “women who started hormones within six years of menopause had artery walls that thickened a little more slowly than the women on the placebo, whereas the extra estrogen did not seem to slow thickening in the group that started the hormone therapy later.”



Vascular Effects of Early versus Late Postmenopausal Treatment with Estradiol

Howard N. Hodis, M.D., Wendy J. Mack, Ph.D., Victor W. Henderson, M.D., Donna Shoupe, M.D., Matthew J. Budoff, M.D., Juliana Hwang-Levine, Pharm.D., Yanjie Li, M.D., Mei Feng, M.D., Laurie Dustin, M.S., Naoko Kono, M.P.H., Frank Z. Stanczyk, Ph.D., Robert H. Selzer, M.S., and Stanley P. Azen, Ph.D., for the ELITE Research Group*

N Engl J Med 2016; 374:1221-1231March 31, 2016DOI: 10.1056/NEJMoa1505241



Data suggest that estrogen-containing hormone therapy is associated with beneficial effects with regard to cardiovascular disease when the therapy is initiated temporally close to menopause but not when it is initiated later. However, the hypothesis that the cardiovascular effects of postmenopausal hormone therapy vary with the timing of therapy initiation (the hormone-timing hypothesis) has not been tested.


A total of 643 healthy postmenopausal women were stratified according to time since menopause (<6 years [early postmenopause] or ≥10 years [late postmenopause]) and were randomly assigned to receive either oral 17β-estradiol (1 mg per day, plus progesterone [45 mg] vaginal gel administered sequentially [i.e., once daily for 10 days of each 30-day cycle] for women with a uterus) or placebo (plus sequential placebo vaginal gel for women with a uterus). The primary outcome was the rate of change in carotid-artery intima–media thickness (CIMT), which was measured every 6 months. Secondary outcomes included an assessment of coronary atherosclerosis by cardiac computed tomography (CT), which was performed when participants completed the randomly assigned regimen.


After a median of 5 years, the effect of estradiol, with or without progesterone, on CIMT progression differed between the early and late postmenopause strata (P=0.007 for the interaction). Among women who were less than 6 years past menopause at the time of randomization, the mean CIMT increased by 0.0078 mm per year in the placebo group versus 0.0044 mm per year in the estradiol group (P=0.008). Among women who were 10 or more years past menopause at the time of randomization, the rates of CIMT progression in the placebo and estradiol groups were similar (0.0088 and 0.0100 mm per year, respectively; P=0.29). CT measures of coronary-artery calcium, total stenosis, and plaque did not differ significantly between the placebo group and the estradiol group in either postmenopause stratum.


Oral estradiol therapy was associated with less progression of subclinical atherosclerosis (measured as CIMT) than was placebo when therapy was initiated within 6 years after menopause but not when it was initiated 10 or more years after menopause. Estradiol had no significant effect on cardiac CT measures of atherosclerosis in either postmenopause stratum. (Funded by the National Institute on Aging, National Institutes of Health; ELITE ClinicalTrials.gov number, NCT00114517.)