[Nipply Russel]

Boom. Thanks for chiming in. But I'm not following - due to the formatting, I can't tell which bits you've pasted from your sources and which ones are your comments on the subject, but does this one...

Pueraria mirifica needs liver activation for the chromene compound miroestrol/deoxymiroestrol to become active...it has to activate certain enzymes to become biologically active. 

...mean that liver metabolism is necessary then? If so, does that mean that my only option to to take PM orally, take a blood thinning supplement (like Rutin) and take my chances? If so, that's not great news.

[Lotus]

Boom. Thanks for chiming in. But I'm not following - due to the formatting, I can't tell which bits you've pasted from your sources and which ones are your comments on the subject, but does this one...

Pueraria mirifica needs liver activation for the chromene compound miroestrol/deoxymiroestrol to become active...it has to activate certain enzymes to become biologically active. 

...mean that liver metabolism is necessary then? If so, does that mean that my only option is to take PM orally, take a blood thinning supplement (like Rutin) and take my chances? If so, that's not great news.

Ah, I see. I compose offline, without quotations, it's just less hassle. The liver activation is from me, but comes from science studies. 

No, not necessarily the only option. As I recommended and try the suppository method. The fast metabolism via water/PM 
is too fast..maybe puts oneself at higher risk for side effects. We want a slow approach that will have meaningful results, and hopefully no side effects. The first pass metabolism eliminates 90% of supplements. Your plan will have a liver activation...that's a plus because they'll be more PM there to use. Do use a fatty acid for making a DIY suppositories, like coconut oil/ or olive oil. YouTube has some good videos on the how too. Just search DIY rectal suppository. Just remember, there is such a thing as micronized rectal estradiol suppository...so you're on the right track.

Apologies on the format. Hope this helps

[Isabela]

You can find a lot of opposing results in clinical trials from pubmed for a same subject..
I've been used PM topically for a long time, this is clearly giving me breast tenderness and I had some limited growth.
Breast grow is not only induced by estrogen, growth factor is involved and no one knows exactly how to grow breast tissue in vivo, today women are still going for breasts implants surgeries.
PM is coming from herbs, I guess tissue from animals will be more likely to have an effect humans.
Humans and animals are growing same organs, those organs are working the same way, plants is a totally different story.
I have ordered both ovary and mammary caps, it will be pretty interesting to get that tissues running in the bloodstream bypassing liver and digestion process, this should have a much better effect on the organs of a man than tissue from plants.

[Sylvia Coco]

Very interesting topics have been raised about it, it is a pleasure to read it.
I have a question about people with blood clotting problems. Is this method of using PM safer for the circulatory system?

[Nipply Russel]

Very interesting topics have been raised about it, it is a pleasure to read it.
I have a question about people with blood clotting problems. Is this method of using PM safer for the circulatory system?

That's what we're hoping. Suppository and transdermal dosing of pharmaceutical hormones is claimed to produce a significantly lower likelihood of clots, although suppository dosing isn't as well-researched, simply because it's considered to be less favorable than the popular patch method. It would stand to reason that PM could be "more safely" taken using the suppository.

As I understand it (and I'm pretty dense), Lotus is saying that liver activation is required when taking PM, but suppositories ARE liver-activated. But she is stating that a slow-release fatty acid-based suppository is best. That's a bit of a drag, but it is what it is.

Stating the above for (hopeful) clarification.

For me, I either need to pursue the suppository route or take Rutin for blood thinning and take my chances...or discontinue use altogether.

[Sylvia Coco]

Thank you for your answer.
You write about Rutin - I am taking warfarin and my blood is very thin. Do you think I'm safe and can take PM?

[thegirl1951]

Thank you for your answer.
You write about Rutin - I am taking warfarin and my blood is very thin. Do you think I'm safe and can take PM?

CoCo,

Warfarin is a complicated drug that has a complex chemistry according to my hematologist.  It interacts with many different foods and drugs.   If you are taking warfarin and don't have your own INR measuring machine I would be very careful about taking any herbs that may interact with warfarin without talking to your doctor.   I take two different kinds of anticoagulants (warfarin and 

Plavix .  Platvix is an antiplatelets drug that works differently than warfarin.  

Your health is at stake. 

Just my two cents.

[christin14]

The suppository method seems interesting. It sounds like PM could be more effective at lower doses. If I am reading this correctly, the recommendation would be to melt cocoa butter and then add the PM powder and mix. From the searching I did, it looks like you would need the following:

Suppository molds
https://www.amazon.com/Reusable-Supposit...B072Q5XVBN

Suppository applicators
https://www.amazon.com/Sephure-Supposito...op?ie=UTF8

I currently have Ainterol 500mg capsules. Do we have any idea how many mg of PM should be in each suppository? 250mg or 500mg? Should it be once a day, twice a day?

[Lotus]

Very interesting topics have been raised about it, it is a pleasure to read it.
I have a question about people with blood clotting problems. Is this method of using PM safer for the circulatory system?

That's what we're hoping. Suppository and transdermal dosing of pharmaceutical hormones is claimed to produce a significantly lower likelihood of clots, although suppository dosing isn't as well-researched, simply because it's considered to be less favorable than the popular patch method. It would stand to reason that PM could be "more safely" taken using the suppository.

As I understand it (and I'm pretty dense), Lotus is saying that liver activation is required when taking PM, but suppositories ARE liver-activated. But she is stating that a slow-release fatty acid-based suppository is best. That's a bit of a drag, but it is what it is.

Stating the above for (hopeful) clarification.

For me, I either need to pursue the suppository route or take Rutin for blood thinning and take my chances...or discontinue use altogether.

Hi Nipply & Sylvia, (Nipply my friend, you're far from dense). 

Over the years I've seen about a dozen cases of DVT being reported from PM use (at BN), even 1 case is way too many. So why is this happening?, here's my take:

Systemic inflammation (stemming from oxidative stress) can lead to thrombosis. Some years ago we had a thread helping people make sense of their hormone test results. What I found was users of PM had higher white blood cell count, indicating inflammation. Too much estrogen stimuli can lead to DVT. I still see people talking about taking 3,000mg of PM. This is an unnecessary risk to one's health, no matter how healthy the individual is. In cis-women only 250mg (or even 100mg) is recommended because of how it extends their menstrual cycle...plus a few other things. 1,000 to 1,500 is all I'd personally take if I was still on PM. Obesity and lack of exercise can be another risk factor. 

From the study below progesterone was found to inhibit the action of thrombin by 10-15%. Personally speaking progesterone cream should be included on day one if you're taking PM...or BO. We need that extra protection from progesterone when starting NBE. I would suggest vitamin D3 as it helps to reduce inflammation lowering the risk of thrombosis...go with vitamin D3 w/organic olive oil. I take 10,000 iu. 

Nipply (or anyone else) chose the route that's best for you. This information is to provide you with some options to consider. I will be introducing a new Breast Growing plan soon that will be a lower risk option. Feel free to ask questions. 

Listed Science:

Chronic Stress Facilitates the Development of Deep Venous Thrombosis
https://www.hindawi.com/journals/omcl/2015/384535/


Progesterone metabolites rapidly stimulate calcium influx in human platelets by a src-dependent pathway
Peter F Blackmore. Steroids. 2008 Aug.

Abstract
The effects of several steroids and their metabolites were examined for their ability to rapidly alter intracellular free calcium ([Ca(2+)](i)) in the anucleate human platelet. Earlier studies suggested that steroids had direct and rapid non-genomic effects to alter platelet physiology. The rationale for performing this study was to investigate the signal transduction events being activated by steroids. Super-physiologic concentrations (1.0-10.0microM) of beta-estradiol and several estradiol metabolites and analogs potentiated (approximately twofold) the action of thrombin to elevate [Ca(2+)](i) in platelets, whereas 10.0microM progesterone inhibited the action of thrombin by 10-15%. Progesterone and beta-estradiol by themselves did not affect [Ca(2+)](i). Progesterone metabolites can achieve high blood concentrations. Some progesterone metabolites, particularly those in the beta-conformation, were potent stimulators of Ca(2+) influx and intracellular Ca(2+) mobilization in platelets. They activated phospholipase C because their ability to increase [Ca(2+)](i) was inhibited by the phospholipase C inhibitor U-73122. The ability of pregnanediol and collagen to increase [Ca(2+)](i) was inhibited by the src tyrosine kinase inhibitor PP1, whereas the actions of thrombin and thapsigargin to increase [Ca(2+)](i) were not affected by PP1. The effects of progesterone metabolites to increase [Ca(2+)](i) were observed with concentrations as low as 0.1microM. Pregnanolone synergized with thrombin to increase [Ca(2+)](i). It is hypothesized that human platelets possess receptors for progesterone metabolites. These receptors when stimulated will activate platelets by causing a rapid increase in [Ca(2+)](i). Pregnanolone, isopregnanediol and pregnanediol were the most effective stimulators of this newly identified src-dependent signal transduction system in platelets. Progesterone metabolites may regulate platelet aggregation and hence thrombosis in vivo.


The role of oxidative stress and antioxidants in male fertility
https://pubmed.ncbi.nlm.nih.gov/24578993/

[Heaven's Night]

Very interesting topics have been raised about it, it is a pleasure to read it.
I have a question about people with blood clotting problems. Is this method of using PM safer for the circulatory system?

That's what we're hoping. Suppository and transdermal dosing of pharmaceutical hormones is claimed to produce a significantly lower likelihood of clots, although suppository dosing isn't as well-researched, simply because it's considered to be less favorable than the popular patch method. It would stand to reason that PM could be "more safely" taken using the suppository.

As I understand it (and I'm pretty dense), Lotus is saying that liver activation is required when taking PM, but suppositories ARE liver-activated. But she is stating that a slow-release fatty acid-based suppository is best. That's a bit of a drag, but it is what it is.

Stating the above for (hopeful) clarification.

For me, I either need to pursue the suppository route or take Rutin for blood thinning and take my chances...or discontinue use altogether.

Hi Nipply & Sylvia, (Nipply my friend, you're far from dense). 

Over the years I've seen about a dozen cases of DVT being reported from PM use (at BN), even 1 case is way too many. So why is this happening?, here's my take:

Systemic inflammation (stemming from oxidative stress) can lead to thrombosis. Some years ago we had a thread helping people make sense of their hormone test results. What I found was users of PM had higher white blood cell count, indicating inflammation. Too much estrogen stimuli can lead to DVT. I still see people talking about taking 3,000mg of PM. This is an unnecessary risk to one's health, no matter how healthy the individual is. In cis-women only 250mg (or even 100mg) is recommended because of how it extends their menstrual cycle...plus a few other things. 1,000 to 1,500 is all I'd personally take if I was still on PM. Obesity and lack of exercise can be another risk factor. 

From the study below progesterone was found to inhibit the action of thrombin by 10-15%. Personally speaking progesterone cream should be included on day one if you're taking PM...or BO. We need that extra protection from progesterone when starting NBE. I would suggest vitamin D3 as it helps to reduce inflammation lowering the risk of thrombosis...go with vitamin D3 w/organic olive oil. I take 10,000 iu. 

Nipply (or anyone else) chose the route that's best for you. This information is to provide you with some options to consider. I will be introducing a new Breast Growing plan soon that will be a lower risk option. Feel free to ask questions. 

Listed Science:

Chronic Stress Facilitates the Development of Deep Venous Thrombosis
https://www.hindawi.com/journals/omcl/2015/384535/


Progesterone metabolites rapidly stimulate calcium influx in human platelets by a src-dependent pathway
Peter F Blackmore. Steroids. 2008 Aug.

Abstract
The effects of several steroids and their metabolites were examined for their ability to rapidly alter intracellular free calcium ([Ca(2+)](i)) in the anucleate human platelet. Earlier studies suggested that steroids had direct and rapid non-genomic effects to alter platelet physiology. The rationale for performing this study was to investigate the signal transduction events being activated by steroids. Super-physiologic concentrations (1.0-10.0microM) of beta-estradiol and several estradiol metabolites and analogs potentiated (approximately twofold) the action of thrombin to elevate [Ca(2+)](i) in platelets, whereas 10.0microM progesterone inhibited the action of thrombin by 10-15%. Progesterone and beta-estradiol by themselves did not affect [Ca(2+)](i). Progesterone metabolites can achieve high blood concentrations. Some progesterone metabolites, particularly those in the beta-conformation, were potent stimulators of Ca(2+) influx and intracellular Ca(2+) mobilization in platelets. They activated phospholipase C because their ability to increase [Ca(2+)](i) was inhibited by the phospholipase C inhibitor U-73122. The ability of pregnanediol and collagen to increase [Ca(2+)](i) was inhibited by the src tyrosine kinase inhibitor PP1, whereas the actions of thrombin and thapsigargin to increase [Ca(2+)](i) were not affected by PP1. The effects of progesterone metabolites to increase [Ca(2+)](i) were observed with concentrations as low as 0.1microM. Pregnanolone synergized with thrombin to increase [Ca(2+)](i). It is hypothesized that human platelets possess receptors for progesterone metabolites. These receptors when stimulated will activate platelets by causing a rapid increase in [Ca(2+)](i). Pregnanolone, isopregnanediol and pregnanediol were the most effective stimulators of this newly identified src-dependent signal transduction system in platelets. Progesterone metabolites may regulate platelet aggregation and hence thrombosis in vivo.


The role of oxidative stress and antioxidants in male fertility
https://pubmed.ncbi.nlm.nih.gov/24578993/

Reading the stuff above makes me to rethink what I'm doing... Along with experience on how I feel after more than one cycle without taking breaks. I wish I understood all this better.