In a well controlled study esterified estrogen
has a .92 risk of venous thrombosis (less than the control group)!!!
Esterified Estrogens and Conjugated Equine Estrogens and the Risk of Venous Thrombosis
Nicholas L. Smith,
PhD; Susan R. Heckbert, MD, PhD; Rozenn N. Lemaitre, PhD; Alex P. Reiner, MD, MPH; Thomas Lumley, PhD; Noel S. Weiss, MD, DrPH; Eric B. Larson, MD, MPH; Frits R. Rosendaal, MD; Bruce M. Psaty, MD, PhD
Context Clinical trial evidence
indicates that estrogen therapy with or without progestins increases venous thrombotic risk. The findings
from these trials, which used oral conjugated equine estrogens, may not be generalizable to other estrogen
Objective To compare risk of
venous thrombosis among esterified estrogen users, conjugated equine estrogen users, and nonusers.
Setting, and Participants This population-based, case-control study was conducted at a large health maintenance
organization in Washington State.
Cases were perimenopausal and postmenopausal women aged 30 to 89 years who sustained a first venous
thrombosis between January 1995 and December 2001 and controls were matched on age, hypertension status, and calendar
Measure Risk of first venous thrombosis in relation to current use of esterified or conjugated equine estrogens,
with or without concomitant progestin. Current use was defined as use at thrombotic event for cases and a
comparable reference date for controls.
Results Five hundred eighty-six
incident venous thrombosis cases and 2268 controls were identified. Compared with women not currently
using hormones, current
users of esterified estrogen had no increase in venous thrombotic risk (odds ratio [OR], 0.92; 95% confidence
interval [CI], 0.69-1.22). In contrast, women currently taking conjugated equine estrogen had an elevated risk (OR, 1.65;
95% CI, 1.24-2.19). When analyses were restricted to estrogen users, current users of conjugated equine estrogen
had a higher risk than current users of esterified estrogen (OR, 1.78; 95% CI, 1.11-2.84). Among conjugated
equine estrogen users, increasing daily dose was associated with increased risk (trend P value
= .02). Among all estrogen users, concomitant progestin use was associated with increased risk compared
with use of estrogen alone (OR, 1.60; 95% CI, 1.13-2.26).
Conclusion Our finding that
conjugated equine estrogen but not esterified estrogen was associated with venous thrombotic risk needs
to be replicated and may have implications for the choice of hormones in perimenopausal and postmenopausal women.
Author Affiliations: Departments of Epidemiology (Drs Smith,
Heckbert, Reiner, Weiss, and Psaty), Medicine (Drs Lemaitre and Psaty), Biostatistics (Dr Lumley), and Health Services (Dr
Psaty), University of Washington, Seattle; Center for Health Studies, Group Health Cooperative, Seattle, Wash (Drs Heckbert,
Larson, and Psaty); and Leiden University Medical Center, Leiden, the Netherlands (Dr Rosendaal).
e.g. women who didn't take it seem to have had—on average—a 70%
higher relative risk of dementia). This is consistent with research that hormone therapy improves
executive and attention processes in postmenopausal women. . . . . A recent large well-designed randomized controlled trial
recently showed that increased breast cancer risk applies only to those women who take progesterone analogues (as was done
in the WHI) but not to those taking progesterone itself.
Comparative effects of oral esterified estrogens with and without methyltestosterone on endocrine profiles and dimensions
of sexual function in postmenopausal women with hypoactive sexual desire
Fertility and Sterility, Volume 79, Issue
6, Pages 1341-1352
In some women, a decline in sexual interest accompanies a relative androgen insufficiency after
menopause. We sought to characterize the hormonal effects of the combination of oral esterified estrogens and methyltestosterone
and to investigate whether this regimen improves hypoactive sexual desire.
Double-blind randomized trial.
Healthy volunteers in a multicenter research environment.
Postmenopausal women taking estrogen therapy who were experiencing hypoactive sexual desire.
4 months of treatment with 0.625 mg of esterified estrogens (n = 111) or the combination of
0.625 mg of esterified estrogens and 1.25 mg of methyltestosterone (n = 107).
Main outcome measure(s)
Baseline and end-of-study measurements of total and bioavailable testosterone and sex hormone–binding
globulin (SHBG), and mean change in level of sexual interest or desire as rated on the Sexual Interest Questionnaire.
Treatment with the combination of esterified estrogens and methyltestosterone significantly
increased the concentration of bioavailable testosterone and suppressed SHBG. Scores measuring sexual interest or desire and
frequency of desire increased from baseline with combination treatment and were significantly greater than those achieved
with esterified estrogens alone. Treatment with the combination was well tolerated.
Increased circulating levels of unbound testosterone
and suppression of SHBG provide a plausible hormonal explanation for the significantly improved sexual functioning in women
receiving the combination of esterified estrogen and methyltestosterone.
J Reprod Med. 1998 Oct;43(10):847-56.
RESULTS: Estrogen-androgen therapy significantly improved sexual sensation
and desire after four and eight weeks of double-blind treatment in comparison to previous estrogen therapy and postplacebo
baseline assessments. . . . CONCLUSION: Sexual desire, satisfaction and frequency in postmenopausal women taking hormonal
therapy were improved significantly by combined estrogen-androgen therapy but not by estrogen or estrogen-progestin therapy.
Sexual function improved with estrogen-androgen therapy even though circulating estrogen levels were lower than those measured
during previous estrogen therapy. This leads to the conclusion that androgens play a pivotal role in sexual function but that
estrogens are not a significant factor determining levels of sexual drive and enjoyment.
Conclusion Our finding that
conjugated equine estrogen but not esterified estrogen was associated with venous thrombotic risk
needs to be replicated and may have implications for the choice of hormones in perimenopausal and postmenopausal