Cholesterol and atherosclerosis: modulation by oestrogen

Purpose of review Oestrogens are important modulators of lipid metabolism, inflammation and vascular homeostasis. Endogenous oestrogens contribute to the low prevalence of atherosclerotic vascular disease in premenopausal women with intact ovarian function, and cessation of oestrogen production following menopause increases cardiovascular risk. Orally administered oestrogens such as postmenopausal hormone therapy increase HDL and reduce LDL cholesterol levels, and they increase triglyceride levels. Current guidelines do not recommend postmenopausal hormone therapy for cardiovascular prevention. Recent findings Recent clinical studies have suggested potential benefits of natural oestrogen or selective oestrogen receptor modulators on cardiovascular outcomes, effects that are associated with lipid profile improvements. In contrast to earlier studies such as the Women's Health Initiative, the Heart and Estrogen/Progestin Replacement Study or the Estrogen Replacement and Atherosclerosis trial, in which investigators used hormone mixtures derived from horse urine (misleadingly named 'conjugated oestrogens' with unknown activity on oestrogen receptors), triphasic oestrogen therapy started early after menopause as primary prevention study protocol improved outcome. New studies suggest therapeutic potential of natural oestrogens and certain selective oestrogen receptor modulators to reduce coronary artery disease risk in postmenopausal women. Summary Endogenous oestrogens are important regulators of lipid metabolism and inhibit inflammation, vascular cell growth and plaque progression in premenopausal women. The recent trials warrant further studies, which should also determine how much of the potential benefits are due to improvements of lipid metabolism.