Re: Transdermal vs oral estrogen and clots

[Guest guest]

I would invite those in this discussion to delineate what estrogen they are writing about, is it human estrogens or pharmaceutical estrins and progestins -- these are important distinctions for the physiological response to endogenous hormones is very different from exogenous and pharmaceutical synthetic and artificial hormones, and even bio-identical exogenous hormones. If we continue to conflate what is manufactured versus what occurs in nature within our bodies in our 'scientific dialog' we cannot in truth consider our dialogue or our findings valid. I refer you to Tom Hilgers thoughts on this matter.

Geraldine Matus, HRHP, Ph.D CandidateDirector and Academic DeanJustisse-Healthworks for Womenwww.justisse.ca info@...

10145 - 81 AvenueEdmonton, AB. T6E 1W91-   1-1- (Fx)Behind every wise woman are many other wise women.

 

There are a number of studies that show transdermal estrogen does not cause increased storke, etc unlike oral estrogen,. Here are three references out of a dozen.

 

1. The main one is from the huge EPIC study in France of more than 100,000 women.

 

Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:3071-3078

" Effects of Oral and Transdermal Estrogen/Progesterone Regimens on Blood Coagulation and Fibrinolysis in Postmenopausal Women

A Randomized Controlled Trial "

Pierre-Yves Scarabin et al.

.. " The oral estrogen group was associated with a significant decrease in both mean tissue-type plasminogen (t-PA) concentration and plasminogen activator inhibitor (PAI-1) activity and a significant rise in global fibrinolytic capacity (GFC) compared with the two other groups. A transdermal estrogen regimen had no significant effect on PAI-1, t-PA, and GFC levels. There were no significant changes in mean values of fibrinogen, factor VII, von Willebrand factor, protein C, fibrin D-dimer, and plasminogen between and within the three groups. We conclude that oral estrogen/progesterone replacement therapy may result in coagulation activation and increased fibrinolytic potential, whereas opposed transdermal estrogen appears without any

substantial effects on hemostasis. Whereas these results may account for an increased risk of venous thromboembolism in users of oral postmenopausal estrogen, they emphasize the potential importance of the route of estrogen administration in prescribing hormone replacement therapy to postmenopausal women, especially to those at high risk of thrombotic disease. "

 

2. Another - the ESTHER study involved thousands of women,

Circulation. 2005;112:3495-3500,

Cardiovascular Disease in Women:Hormone Therapy and Venous Thromboembolism Among

Postmenopausal Women; Impact of the Route of Estrogen Administration and Progestogens:

nne Canonico, et al

for the Estrogen and Thromboembolism Risk (ESTHER) Study Group

 

3. and another study

Arterioscler Thromb Vasc Biol. 2003 Sep 1;23(9):1671-6. Epub 2003 Jul 17.

Differential effects of oral and transdermal estrogen/progesterone regimens on sensitivity to activated protein C among postmenopausal women: a randomized trial.

Oger E, et al. SARAH Investigators.

 

D

 

 

 

[Guest guest]

Human estrogens are currently not available for clinical use to the best of my knowledge.  They only occur endogenously and are, therefore, in my opinion not within the “mix†for discussion.  We have pharmaceutical hormones which can be derived from many sources, some synthetic and some listed as “natural†but to the best of my knowledge the chemical equivalent of human estrogen and progesterone does not “occur†naturally; then there are the “so called†bio-identical hormones which are the “same†chemical composition of naturally endogenous human hormones, ie estrone, estriol and estradiol and progesterone.  These all need to be “made†from something, either a natural source or a synthetic source since they do not occur on their own naturally.  There is always some much confusion on these issues.  There is a difference on how they are metabolized.  There is not a difference, once metabolized, on their end point function and side effects.  All estrogens inc rease the risk of breast cancer and blood clots; within the human body there are “balances†which occur in nature and with other hormones and cell receptivity that differentiate one’s “natural†risk of getting cancer, i.e. the generally acceptably rate of breast cancer in a women is 1/8 if she lives till 90; the other 7 women all make all the same hormones but don’t get breast cancer because of other confounding factors like family history, age of first full term delivery, breast feeding and body weight etc.  This discussion, I assume, is about consuming some type of exogenouse hormone whether bioidentical, “derived from natural sources “ (but still compounded or synthesized by a person to be consumed or used) or synthetic.  From: nfpprofessionals [mailto:nfpprofessionals ] On Behalf Of Geraldine MatusSent: Sunday, December 11, 2011 11:26 AMTo: nfpprofessionals Subject: Re: Transdermal vs oral estrogen and clots I would invite those in this discussion to delineate what estrogen they are writing about, is it human estrogens or pharmaceutical estrins and progestins -- these are important distinctions for the physiological response to endogenous hormones is very different from exogenous and pharmaceutical synthetic and artificial hormones, and even bio-identical exogenous hormones. If we continue to conflate what is manufactured versus what occurs in nature within our bodies in our 'scientific dialog' we cannot in truth consider our dialogue or our findings valid. I refer you to Tom Hilgers thoughts on this matter. Geraldine Matus, HRHP, Ph.D CandidateDirector and Academic DeanJustisse-Healthworks for Womenwww.justisse.ca info@...10145 - 81 AvenueEdmonton, AB. T6E 1W91- 1-1- (Fx)Behind every wise woman are many other wise women. There are a number of studies that show transdermal estrogen does not cause increased storke, etc unlike oral estrogen,. Here are three references out of a dozen. 1. The main one is from the huge EPIC study in France of more than 100,000 women. Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:3071-3078 " Effects of Oral and Transdermal Estrogen/Progesterone Regimens on Blood Coagulation and Fibrinolysis in Postmenopausal Women A Randomized Controlled Trial " Pierre-Yves Scarabin et al.. " The oral estrogen group was associated with a significant decrease in both mean tissue-type plasminogen (t-PA) concentration and plasminogen activator inhibitor (PAI-1) activity and a significant rise in global fibrinolytic capacity (GFC) compared with the two other groups. A transdermal estrogen regimen had no significant effect on PAI-1, t-PA, and GFC levels. There were no significant changes in mean values of fibrinogen, factor VII, von Willebrand factor, protein C, fibrin D-dimer, and plasminogen between and within the three groups. We conclude that oral estrogen/progesterone replacement therapy may result in coagulation activation and increased fibrinolytic potential, whereas opposed transdermal estrogen appears without any substantial effects on hemostasis. Whereas these results may account for an increased risk of venous thromboembolism in users of oral postmenopausal estrogen, they emphasize the potential importance of the route of estrogen administration in prescribing hormone replacement therapy to postmenopausal women, especially to those at high risk of thrombotic disease. " 2. Another - the ESTHER study involved thousands of women, Circulation. 2005;112:3495-3500, Cardiovascular Disease in Women:Hormone Therapy and Venous Thromboembolism Among Postmenopausal Women; Impact of the Route of Estrogen Administration and Progestogens: nne Canonico, et al for the Estrogen and Thromboembolism Risk (ESTHER) Study Group 3. and another study Arterioscler Thromb Vasc Biol. 2003 Sep 1;23(9):1671-6. Epub 2003 Jul 17. Differential effects of oral and transdermal estrogen/progesterone regimens on sensitivity to activated protein C among postmenopausal women: a randomized trial. Oger E, et al. SARAH Investigators. D

[Guest guest]

Was this very large study funded by vested interests?Sent from my iPhone

There are a number of studies that show transdermal estrogen does not cause increased storke, etc unlike oral estrogen,. Here are three references out of a dozen.

1. The main one is from the huge EPIC study in France of more than 100,000 women.

Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:3071-3078

"Effects of Oral and Transdermal Estrogen/Progesterone Regimens on Blood Coagulation and Fibrinolysis in Postmenopausal Women

A Randomized Controlled Trial"

Pierre-Yves Scarabin et al.

.."The oral estrogen group was associated with a significant decrease in both mean tissue-type plasminogen (t-PA) concentration and plasminogen activator inhibitor (PAI-1) activity and a significant rise in global fibrinolytic capacity (GFC) compared with the two other groups. A transdermal estrogen regimen had no significant effect on PAI-1, t-PA, and GFC levels. There were no significant changes in mean values of fibrinogen, factor VII, von Willebrand factor, protein C, fibrin D-dimer, and plasminogen between and within the three groups. We conclude that oral estrogen/progesterone replacement therapy may result in coagulation activation and increased fibrinolytic potential, whereas opposed transdermal estrogen appears without any

substantial effects on hemostasis. Whereas these results may account for an increased risk of venous thromboembolism in users of oral postmenopausal estrogen, they emphasize the potential importance of the route of estrogen administration in prescribing hormone replacement therapy to postmenopausal women, especially to those at high risk of thrombotic disease."

2. Another - the ESTHER study involved thousands of women,

Circulation. 2005;112:3495-3500,

Cardiovascular Disease in Women:Hormone Therapy and Venous Thromboembolism Among

Postmenopausal Women; Impact of the Route of Estrogen Administration and Progestogens:

nne Canonico, et al

for the Estrogen and Thromboembolism Risk (ESTHER) Study Group

3. and another study

Arterioscler Thromb Vasc Biol. 2003 Sep 1;23(9):1671-6. Epub 2003 Jul 17.

Differential effects of oral and transdermal estrogen/progesterone regimens on sensitivity to activated protein C among postmenopausal women: a randomized trial.

Oger E, et al. SARAH Investigators.

D

[Guest guest]

Certainly, the studies show that. However, Ortho-Evra is in hot water over

higher clotting rates, despite being transdermal. Possibly due to higher dose

or dose effect... noted in epocrates database and I think a recent FDA alert.

, MD

Front Royal, VA

________________________________

From: nfpprofessionals on behalf of Davenport

Sent: Sun 12/11/2011 3:09 AM

To: nfpprofessionals

Subject: Transdermal vs oral estrogen and clots

There are a number of studies that show transdermal estrogen does not cause

increased storke, etc unlike oral estrogen,. Here are three references out of a

dozen.

1. The main one is from the huge EPIC study in France of more than 100,000

women.

Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:3071-3078

" Effects of Oral and Transdermal Estrogen/Progesterone Regimens on Blood

Coagulation and Fibrinolysis in Postmenopausal Women

A Randomized Controlled Trial "

Pierre-Yves Scarabin et al.

.. " The oral estrogen group was associated with a significant decrease in both

mean tissue-type plasminogen (t-PA) concentration and plasminogen activator

inhibitor (PAI-1) activity and a significant rise in global fibrinolytic

capacity (GFC) compared with the two other groups. A transdermal estrogen

regimen had no significant effect on PAI-1, t-PA, and GFC levels. There were no

significant changes in mean values of fibrinogen, factor VII, von Willebrand

factor, protein C, fibrin D-dimer, and plasminogen between and within the three

groups. We conclude that oral estrogen/progesterone replacement therapy may

result in coagulation activation and increased fibrinolytic potential, whereas

opposed transdermal estrogen appears without any substantial effects on

hemostasis. Whereas these results may account for an increased risk of venous

thromboembolism in users of oral postmenopausal estrogen, they emphasize the

potential importance of the route of estrogen administration in prescribing

hormone replacement therapy to postmenopausal women, especially to those at high

risk of thrombotic disease. "

2. Another - the ESTHER study involved thousands of women,

Circulation. 2005;112:3495-3500,

Cardiovascular Disease in Women:Hormone Therapy and Venous Thromboembolism Among

Postmenopausal Women; Impact of the Route of Estrogen Administration and

Progestogens:

nne Canonico

<http://circ.ahajournals.org/search?author1=nne+Canonico & sortspec=date & subm\

it=Submit> , et al

for the Estrogen and Thromboembolism Risk (ESTHER) Study Group

3. and another study

Arterioscler Thromb Vasc Biol. <http://www.ncbi.nlm.nih.gov/pubmed/12869355>

2003 Sep 1;23(9):1671-6. Epub 2003 Jul 17.

Differential effects of oral and transdermal estrogen/progesterone regimens on

sensitivity to activated protein C among postmenopausal women: a randomized

trial.

Oger E <http://www.ncbi.nlm.nih.gov/pubmed?term=%22Oger%20E%22%5BAuthor%5D> , et

al. SARAH Investigators

<http://www.ncbi.nlm.nih.gov/pubmed?term=%22SARAH%20Investigators%22%5BCorporate\

%20Author%5D> .

D

[Guest guest]

Some commentary on the studies:Comparing apples to kumquats.Some of the studies measured blood clotting factors, but I haven't seen that they measured the blood estrogen levels. It was already clear that low doses of estrogen are safer than high doses, so I can't see the justification for these studies. They should have been comparing transdermal estrogen with no estrogen and with and without progesterone. And I haven't seen their discussion of the estrogenic properties of some of the "progestins." And the focus on venous thromboembolisms is itself an obfuscation--what about hemorrhage, dementia, depression, diabetes, etc.?"The most common dose for transdermal estrogen use was ≤50 μg/d. Approximately 15% of transdermal estrogen users received preparations delivering >50 μg/d. In current users of oral estrogen therapy, the mean dose of estradiol was 1.5 mg/d, ranging from 0.5 to 2 mg daily." Circulation. 2007; 115: 840-845, Cardiovascular Disease in Women Hormone Therapy and Venous Thromboembolism Among Postmenopausal Women Impact of the Route of Estrogen Administration and Progestogens: The ESTHER Study, nne Canonico, et al.Darcy Hemstad, RN, BSNFertility and nutrition educatorCertified BOM instructor

Was this very large study funded by vested interests?Sent from my iPhone

There are a number of studies that show transdermal estrogen does not cause increased storke, etc unlike oral estrogen,. Here are three references out of a dozen.

1. The main one is from the huge EPIC study in France of more than 100,000 women.

Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:3071-3078

"Effects of Oral and Transdermal Estrogen/Progesterone Regimens on Blood Coagulation and Fibrinolysis in Postmenopausal Women

A Randomized Controlled Trial"

Pierre-Yves Scarabin et al.."The oral estrogen group was associated with a significant decrease in both mean tissue-type plasminogen (t-PA) concentration and plasminogen activator inhibitor (PAI-1) activity and a significant rise in global fibrinolytic capacity (GFC) compared with the two other groups. A transdermal estrogen regimen had no significant effect on PAI-1, t-PA, and GFC levels. There were no significant changes in mean values of fibrinogen, factor VII, von Willebrand factor, protein C, fibrin D-dimer, and plasminogen between and within the three groups. We conclude that oral estrogen/progesterone replacement therapy may result in coagulation activation and increased fibrinolytic potential, whereas opposed transdermal estrogen appears without any

substantial effects on hemostasis. Whereas these results may account for an increased risk of venous thromboembolism in users of oral postmenopausal estrogen, they emphasize the potential importance of the route of estrogen administration in prescribing hormone replacement therapy to postmenopausal women, especially to those at high risk of thrombotic disease."

2. Another - the ESTHER study involved thousands of women,

Circulation. 2005;112:3495-3500,

Cardiovascular Disease in Women:Hormone Therapy and Venous Thromboembolism Among

Postmenopausal Women; Impact of the Route of Estrogen Administration and Progestogens:

nne Canonico, et al

for the Estrogen and Thromboembolism Risk (ESTHER) Study Group

3. and another study

Arterioscler Thromb Vasc Biol. 2003 Sep 1;23(9):1671-6. Epub 2003 Jul 17.

Differential effects of oral and transdermal estrogen/progesterone regimens on sensitivity to activated protein C among postmenopausal women: a randomized trial.

Oger E, et al. SARAH Investigators.

D