Share this article on:

Lipids, estrogen status, and coronary heart disease risk in women


Section Editor(s): Wenger, Nanette K.; Drinkwater, Barbara L.

Medicine & Science in Sports & Exercise: January 1996 - Volume 28 - Issue 1 - p 13,14
Roundtable Discussion

Serum lipid and lipoprotein levels are well-established risk factors for the development of coronary heart disease (CHD)(3). Whereas low-density lipoprotein (LDL) cholesterol levels have been identified as the major lipoprotein that alters CHD risk(5), elevated triglycerides carried in the very-low-density lipoproteins (VLDL), and reduced high-density lipoprotein(HDL) cholesterol levels also independently increase cardiovascular risk in women (9). All lipid risk factors are dynamic and are influenced by age, body weight, physical activity, diet, and hormone status(7). These influences allow for a multidisciplinary approach to improve dyslipidemia and hence reduce the prevalence of CHD among women.

Increasing age is associated with higher total and LDL cholesterol levels(10). Premenopausal women have lower LDL cholesterol levels than same aged men. Several cross sectional studies have observed a 30 mg·dl-1 higher LDL level in men age 50 compared with men age 20 yr. For women, the age-related difference is less prominent until the perimenopausal years, when much higher LDL cholesterol levels are observed. In the postmenopausal years, women have higher LDL cholesterol levels than same aged men. The age-related increase in LDL levels is blunted with postmenopausal estrogen replacement therapy.

Whereas overweight premenopausal women have clearly higher LDL cholesterol levels than lean premenopausal women, overweight perimenopausal women and postmenopausal women have LDL levels similar to lean same aged women(4). However, for all ages, excess body weight is universally associated with higher serum triglyceride levels and lower HDL cholesterol levels. Some observational studies have suggested that the waist-to-hip ratio best correlates with the deleterious lipid effects of body weight (2). However, most individuals with high waist-to-hip ratios have excess body weight, so this ratio may not provide a more sensitive measure of obesity than simple weight or weight adjusted for height alone (6).

Physical activity can indirectly and directly alter lipid levels(3,5). In general, women who are more physically active have leaner body weights than women who are inactive, and some of the indirect, beneficial effects of exercise on lipid levels may be due to the effect of exercise on reducing body fat. Women who exercise at training levels experience a direct effect of exercise on lipids: i.e., an increase in HDL cholesterol levels. However, if training is intense enough to create an anovulatory state, the beneficial effects of training exercise on HDL may be blunted.

Two dietary factors account for the majority of the LDL cholesterol raising potential of the diet: saturated fatty acids and dietary cholesterol(3,5). Women may experience an additional lipoprotein change with dietary therapy. If total dietary fat intake falls below 25% of calories, a significant reduction in HDL cholesterol levels can occur. This reduction may not confer an increased risk for cardiovascular disease, since women living in countries consuming low fat diets also have lower HDL cholesterol levels; these countries have low rates of CHD.

Another factor that alters lipid levels in women is estrogen status(11). In the perimenopausal years, as ovarian function declines, LDL levels increase. Cross sectional studies report lower LDL levels in postmenopausal women who take estrogen replacement therapy compared with women not on estrogen therapy. Clinical trials have proven that estrogen replacement therapy reduces LDL cholesterol levels. Unopposed estrogen replacement therapy also raises HDL cholesterol levels; combined estrogen/progestin regimens either raise slightly or have no effect on HDL cholesterol levels.

There is a growing body of evidence suggesting that estrogen replacement therapy may not only reduce the incidence of CHD in healthy women(12), but may also reduce the risk for subsequent events in women with established CHD (1,8). In these studies, the benefits of estrogen therapy appear to augment the well-established benefits of LDL reduction alone.

Lipid risk factors do not operate in a vacuum. Risk factors are multiplicative and small deleterious changes in one risk factor can promote CHD risk if these small changes are accompanied by deleterious changes in other risk factors. Hence, excess body weight can raise blood pressure, raise LDL cholesterol levels, raise triglyceride levels, raise blood sugar levels, and raise uric acid levels, as well as lower HDL cholesterol levels. Whereas some of these changes may be associated with only a minor increase in risk, the multiplication of small increases in risk can lead to even greater impact on overall cardiovascular risk.

Back to Top | Article Outline


1. American College of Sports Medicine Position Stand. Physical activity, physical fitness, and hypertension. Med. Sci. Sports Exerc. 15:i-x, 1993.
2. Bjorntorp, P. Abdominal fat distribution and disease: an overview of epidemiological data. Ann. Med. 24:15-18, 1992.
3. Denke, M. A. Diet and lifestyle modification and its relationship to atherosclerosis. Med. Clin. North Am. 78:197-223, 1994.
4. Denke, M. A., C. T. Sempos, and S. M. Grundy. Excess body weight: an under-recognized contributor to dyslipidemia in white American women. Arch. Intern. Med. 154:401-410, 1994.
5. The Expert Panel. Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel II). J.A.M.A. 269:3015-3023, 1993.
6. Garn, S. M., T. V. Sullivan, and V. Hawthorne. Evidence against functional differences between “central” and“peripheral” fat. Am. J. Clin. Nutr. 47:36-39, 1988.
7. Godsland, I. F., B. A. Wynn, D. Crook, and N. E. Miller. Sex, plasma lipoproteins, and atherosclerosis: prevailing assumptions and outstanding questions. Am. Heart J. 114:1467-1503, 1987.
8. Kane, J. B., M. J. Mallow, T. A. Ports, N. R. Phillips, J. C. Diehl, and R. J. Havel. Regression of coronary atherosclerosis during treatment of familial hypercholesterolemia with combined drug regimens.J.A.M.A. 264:3007-3012, 1990.
9. Kannel, W. B. Relevance of blood lipids in the elderly: the Framingham Study. Cardiovasc. Risk Factors 2:170-179, 1992.
10. The Lipid Research Clinics Program Epidemiology Committee. Plasma lipid distributions in selected North American populations: the Lipid Research Clinics Program Prevalence Study. Circulation 60:427-439, 1979.
11. Sacks, F. M. and B. W. Walsh. The effects of reproductive hormones on serum lipoproteins: unresolved issues in biology and clinical practice. Ann. N. Y. Acad. Sci. 592:272-285, 1990.
12. Stampfer, M. Estrogen replacement therapy in coronary heart disease: a quantitative assessment of the epidemiologic evidence.Prev. Med. 20:47-63, 1991.
Back to Top | Article Outline

Section Description

Exercise and Cardiovascular Disease Risk in Women: Interaction with Selected Endocrine Factors

This mongraph is based on the proceedings of an ACSM Roundtable entitled“Exercise and Cardiovascular Disease Risk in Women: Interaction with Selected Endocrine Factors,” held June 21-22, 1994, in Indianapolis, Indiana.

The Exercise and Cardiovascular Disease Risk in Women: Interaction with Selected Endocrine Factors Roundtable was funded through a grant from Wyeth-Ayerst Laboratories.

©1996The American College of Sports Medicine