Most doctors believe that a high dose of estrogen is risky as it can lead to hypertension, stroke and blood clots but this was only observed with non bio-identical oral estrogen. Studies have shown in men, for instance, who have prostate cancer, aged 49-91 yrs old, a
high dose of bio-identical estrogen taken non-orally, high enough to sufficiently suppress T, was SAFE and even seemed to be protective.
Cancer. 2005 Feb 15;103(4):717-23."The authors tested the safety and efficacy of transdermal estradiol (TDE), as well as the effect of therapy on hot flashes, sex hormones, the procoagulant cascade, and bone turnover in patients with AIPC."
"Patients with prostate carcinoma progressing after primary hormonal therapy received TDE" (a high dose)
"The mean (+/-95% CI) serum estradiol level
increased from 17.2
pg.mL (range, 14.8-19.6 pg/mL) to 460.7 pg/mL
(range, 334.6-586.7 pg/mL). The total testosterone level remained stable in the
anorchid range during treatment, but the free testosterone level decreased as a
result of increased sex hormone binding globulin."
"No change in factor VIII activity, F 1.2, or
resistance to activated protein C was observed, whereas a modest
decrease in the protein S level was observed. CONCLUSIONS: In
patients with APIC, TDE was well tolerated and produced a modest
response rate, but was not associated with thromboembolic
complications or clinically important changes in several coagulation
factors."
J Urol. 2005 Aug;174(2):527-33; discussion 532-3.
Transdermal estradiol therapy for prostate cancer reduces
thrombophilic activation and protects against thromboembolism."Levels of VIIa and XIIa were unaffected by transdermal estradiol therapy. Although levels of TAT III were increased in some patients at 12 months, the increase was markedly less than that observed historically with equivalent doses of oral estrogens. Levels of the inhibitory and fibrinolytic factors including protein C, protein S, APC-R, TPA and PAI-1 remained stable. Reductions in F1+F2, fibrinogen and D-Dimer levels represented a normalization from increased levels to the physiological range."
"
These results suggest that transdermal estradiol reduces
thrombophilic activation in men with advanced prostate cancer, and
protects against the risk of thrombosis."
Am J Clin Oncol. 1988;11 Suppl 2:S101-3."Serum concentrations of testosterone (T) and estradiol-17 beta (E2) were analyzed in prostatic cancer patients treated with (...) polyestradiol phosphate (PEP) i.m. every fourth week as single drug therapy during a 6 month period."
"Orchidectomy levels of T were reached within 3 weeks (...) and 3 months (...). (...), mean T levels reached the upper limit of orchidectomy values after 6 months. Accumulation of E2 occurred to mean levels 1,300-2,500 pmol/L at 6 months"
"No cardiovascular side effects occurred during single-drug PEP treatment."
Prostate 1989;14(4):389-95"Oral estrogen therapy for prostatic cancer is clinically effective
but also accompanied by severe cardiovascular side effects.
Hypertension, venous thromboembolism, and other cardiovascular
disorders are associated with alterations in liver metabolism. The
impact of exogenous estrogens on the liver is dependent on the route
of administration and the type and dose of estrogen. Oral
administration of synthetic estrogens has profound effects on
liver-derived plasma proteins, coagulation factors, lipoproteins, and
triglycerides, whereas
parenteral administration of native estradiol
has very little influence on these aspects of liver function."
J Lipid Res. 2006 Feb;47(2):349-55."This prospective pilot study of 18 men with androgen-independent prostate cancer receiving ADT measured effects of TDE on lipid and inflammatory CVD risk factors before and after 8 weeks of TDE. During treatment, estradiol levels rose 17-fold; total cholesterol, LDL cholesterol, and apolipoprotein B levels decreased. HDL2 cholesterol increased, with no changes in triglyceride or VLDL cholesterol levels. Dense LDL cholesterol decreased and LDL buoyancy increased in association with a decrease in HL activity. Highly sensitive C-reactive protein levels and other inflammatory markers did not worsen. Compared with ADT, short-term TDE therapy of prostate cancer improves lipid levels without deterioration of CVD-associated inflammatory markers and may, on longer-term follow-up, improve CVD and mortality rates."
TDE = transdermal estradiol
ADT = androgen deprivation therapy
CLIMACTERIC 2005;8(Suppl 1):3–63"In women with supraphysiological estradiol levels during treatment with implants, no adverse effects on lipid metabolism, but a reduction in LDL cholesterol and fasting insulin were observed."
Also,
Am J Obstet Gynecol. 1993 Dec;169(6):1549-53."As serum estradiol levels increased throughout each phase (maximum mean estradiol 739.8 pg/ml)"
"Down-regulation of the fibrinolytic system was observed as estradiol levels increased. However, thrombin formation did not change, thus suggesting that
elevated circulating estradiol alone does not predispose to a thromboembolic event."
J Thromb Haemost. 2014;12(3):297-305."This prospective study suggests that high endogenous concentrations of estradiol and testosterone in women and men in the general population are not associated with increased risk of VTE, DVT or PE."
Br J Obstet Gynaecol. 1990 Oct;97(10):917-21."There is some anxiety about the possible harmful sequelae of supraphysiological estradiol levels but no data are currently available to show any deleterious effects of these levels on coagulation factors, blood pressure, glucose tolerance or the occurrences of endometrial or breast cancer (Hammond et al. 1974; Thom et id. 1978; Studd B Thom 1981; Armstrong 1988)."
Consider that pregnant women have levels as high as 75,000 pg/ml (
http://cebp.aacrjournals.org/cgi/content-nw/full/12/5/452/T1) and their risk of blood clots is less than 0.2%.
Curr Opin Obstet Gynecol. 2014 Dec;26(6):469-75.« Venous thromboembolism is, in the developed world, a major cause of maternal morbidity and mortality during pregnancy or early after delivery, with a reported incidence ranging from 0.49 to 2.0 events per 1000 deliveries."
Ann Intern Med. 2005 Nov 15;143(10):697-706."Women with deep venous thrombosis or pulmonary embolism first diagnosed between 1966 and 1995, including women with venous thromboembolism during pregnancy or the postpartum period (defined as delivery of a newborn no more than 3 months before the deep venous thrombosis or pulmonary embolism event date, including delivery of a stillborn infant after the first trimester)."
« The relative risk (standardized incidence ratio) for venous thromboembolism among pregnant or postpartum women was 4.29 (95% CI, 3.49 to 5.22;P < 0.001), and the overall incidence of venous thromboembolism (absolute risk) was 199.7 per 100,000 woman-years. The annual incidence was 5 times higher among postpartum women than pregnant women (511.2 vs. 95.8 per 100,000), and the incidence of deep venous thrombosis was 3 times higher than that of pulmonary embolism (151.8 vs. 47.9 per 100,000). Pulmonary embolism was relatively uncommon during pregnancy versus the postpartum period (10.6 vs. 159.7 per 100,000). "
"Among pregnant women, the highest risk period for venous thromboembolism and pulmonary embolism in particular is during
the postpartum period." (When estrogen levels drop and are low)
Hence, most cases of DVT and PE, already quite low, are present post-partum, not during pregnancy.
Compare this with blockers/anti-androgens that aren't native to the body and can pose risks for a few. I personally prefer a high dose of E. Show this documentation to your doctor.
High E appears to pose a problem only if non bio-identical estrogen is taken.
