A woman’s risk of developing atherosclerosis and heart disease increases once she reaches menopause. The onset of menopause is due to the progressive decline of estrogen. Apart from serving a significant role in a woman’s reproductive health, estrogen protects bone health, keeps the lining of blood vessels strong and pliable, maintains cholesterol levels, and keeps arteries free from plaque by lowering LDL and increasing HDL cholesterol levels. Lower levels of estrogen thereby increase susceptibility to atherosclerosis, due to minimal regulation of fats, cholesterols, and other substances on artery walls.
Your body makes three types of estrogen, each of which predominates during different stages of life:
- Estradiol (E2), common in women of childbearing age, is the strongest of all three estrogens. It promotes the maturation and release of the egg and thickens the uterus lining to allow a fertilized egg to implant.
- Estriol (E3), common during pregnancy and prepares the mother for labor and breastfeeding.
- Estrone (ET), common after menopause, is the weakest of the three estrogens. Since it’s not as potent as estradiol and estriol, it causes symptoms of menopause such as hot flashes, fatigue, reduced sex drive, and depression.
Recent studies show that estradiol treatment administered within six years of the onset of menopause can improve heart health by slowing down atherosclerosis progression. Early Versus Late Intervention Trial with Estradiol (ELITE) examined this correlation with 643 healthy postmenopausal women over five years. Each participant was administered 1 mg/day estradiol or placebo either six years or ten years after menopause, and carotid intima-media thickness (CIMT) was actively monitored. CIMT is used to measure the extent of carotid atherosclerotic vascular disease by evaluating the thickness of the intima and media, two inner layers of the carotid artery. Initial findings indicate that the average CIMT decreased by 0.0034 mm per year with estradiol administration relative to the placebo treatment for the six-year group. While there were no significant findings for the ten-year group, this result shows the possible efficacy of estradiol on strengthening the carotid artery.
Dr. Karim, an associate professor of clinical preventive medicine at the University of Southern California, conducted further research to validate this correlation using additional technical measures for atherosclerosis. Results supported the CIMT data, showing that the control group had significantly more atherosclerosis than the estradiol group for early postmenopausal women, which was 0.30 per year. There were no significant differences between late post-menopausal women and control. Dr. Karim states these values are excellent news, “I think this should comfort clinicians in terms of prescribing estradiol therapy to women who don’t have any contraindications and who are within six years of menopause.”
More research still has to be done before we start prescribing estrogen as a preventive measure for heart disease. Still, in the meantime, this adds to the growing body of evidence that HRT, initiated soon after menopause starts, is safe and decreases mortality. Dr. Karim and colleagues will be conducting follow up studies to investigate lipid particles and markers of inflammation.
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