First run with primo added to test blast e2?

[mindgame1516]

Just a little back information I’ve been running trt 160mg a week. My test usually sits right around high mid high 900s and my e2 =29

If im at 200mgs a week my test levels are total test-1200ng and my E2-39ng

If I blast 500mg test alone I need telismarting, atenelol and an AI. My blood pressure shoot up to hypertensive state with out an arb and beta blocker. I’ve also never got my labs pulled on an actual blast to see me E2 bc it’s the same dr that knows im on TRT. So I never wanted to go for blood while on a blast.

I’m adding Primo E 150mg 2x a week @300week
My Test E im doing 225mg 2x aweek @450weekly

40mg telismartan
25 mg atenolol

I pinned yesterday and def felt that my blood pressure shot up today. In a total feels a boners way but when my BP shoots up my tinnitus gets real bad(ringing in ears) I checked bp it was 139/83 83 hr. Not terrible but def higher then 2 days ago I took started telsmartin and a arb block and notably feel better prob from the fast actin aten. My next thing im not looking forward is to finding the sweet spot for primo to test ratio. I know everyone is different and everyone’s body reacts in a different way. So im looking to add to the board on sharing my experience with it and look forward to hearing some of you vets with expierence with primo

What’s your guys that have ran primo experience on dosage ratios??

Also woke up and my shirt was damp as fuck does it make you sweat at night?

 

[mindgame1516]

What's your question?

Sorry re edited the last part

 

[Mongo966]

I used to run them at around 1:1. Usually something like 250mg test 200 primo. I never had much in the way of side effects aside from primo slamming my lipid profile which is the reason I tend not to run it any more. Never had nightsweats from primo.

 

[lilhawk]

Yeah I sweat a lot all the time on primo, especially when first starting it. Primo is my favorite drug by far, as far as E2 goes it crushes mine, but never have to use an ai no matter what I take. Currently doing 200 primo 400 test weekly along with GH. If dieting I will bump the primo up to 500 and keep test the same.

 

[mindgame1516]

Yeah I sweat a lot all the time on primo, especially when first starting it. Primo is my favorite drug by far, as far as E2 goes it crushes mine, but never have to use an ai no matter what I take. Currently doing 200 primo 400 test weekly along with GH. If dieting I will bump the primo up to 500 and keep test the same.

Do you feel a difference in E2 sides when you bring the primo up from 200 to 500?

 

[Jin23]

Just a little back information I’ve been running trt 160mg a week. My test usually sits right around high mid high 900s and my e2 =29

If im at 200mgs a week my test levels are total test-1200ng and my E2-39ng

If I blast 500mg test alone I need telismarting, atenelol and an AI. My blood pressure shoot up to hypertensive state with out an arb and beta blocker. I’ve also never got my labs pulled on an actual blast to see me E2 bc it’s the same dr that knows im on TRT. So I never wanted to go for blood while on a blast.

I’m adding Primo E 150mg 2x a week @300week
My Test E im doing 225mg 2x aweek @450weekly

40mg telismartan
25 mg atenolol

I pinned yesterday and def felt that my blood pressure shot up today. In a total feels a boners way but when my BP shoots up my tinnitus gets real bad(ringing in ears) I checked bp it was 139/83 83 hr. Not terrible but def higher then 2 days ago I took started telsmartin and a arb block and notably feel better prob from the fast actin aten. My next thing im not looking forward is to finding the sweet spot for primo to test ratio. I know everyone is different and everyone’s body reacts in a different way. So im looking to add to the board on sharing my experience with it and look forward to hearing some of you vets with expierence with primo

What’s your guys that have ran primo experience on dosage ratios??

Also woke up and my shirt was damp as fuck does it make you sweat at night?

There has been a surge of topics around primo and e2 lately. Your's is probably the 5th to surface in the last 2 weeks or so.

Primo lowers estrogenic signaling and it's action is rather complicated and as of yet not completely defined. It does not only prevent aromatization of testosterone to estrogens, but it also blocks estrogens action at the receptor (tissue specific) and probably has other ways of negatively interacting with the whole estrogen signaling cascade, ie. lowering ER function via second messenger systems, etc

What does this mean? It means that serum E2 readings don't tell the whole story in regards to your total estrogenic load, ie. you might have in range E2 but at the same time experience some specific low estrogen effects - night sweats being such an example.

This is one of those instances where serum e2 readings wont tell you the whole picture and to a certain extent you have to go by observable effects.

@Type-IIx wrote an article not long ago on this topic, you might want to take a look: Primobolan / Equipoise Crashed my E2 – Help! - MESO-Rx

The tissue selectivity of it's anti estrogenic signaling just adds to the complexity of subjectively judging your actual estrogen signaling. It makes it really hard to determine if your levels are where you want them to be. Night sweats for example, is primo having a substantial anti estrogenic in your hypothalamus, resulting in night sweats, or is primo having some sort of an antagonistic effect on estrogens function of dilating and constricting blood vessels? Is what's happening something you should worry about and possibly remedy via increasing exogenous T administration to increase estrogen conversion? But will now the extra estrogen be detrimental in other tissues where primo doesn't have a huge antagonistic effect? ...

In regards to your query; my personal experience with primo is more or less negative. Loss of libido, anxiety, night sweats, etc. I don't like it and hence don't use it.

 

[Type-IIx]

There has been a surge of topics around primo and e2 lately. Your's is probably the 5th to surface in the last 2 weeks or so.

Primo lowers estrogenic signaling and it's action is rather complicated and as of yet not completely defined. It does not only prevent aromatization of testosterone to estrogens, but it also blocks estrogens action at the receptor (tissue specific) and probably has other ways of negatively interacting with the whole estrogen signaling cascade, ie. lowering ER function via second messenger systems, etc

What does this mean? It means that serum E2 readings don't tell the whole story in regards to your total estrogenic load, ie. you might have in range E2 but at the same time experience some specific low estrogen effects - night sweats being such an example.

This is one of those instances where serum e2 readings wont tell you the whole picture and to a certain extent you have to go by observable effects.

@Type-IIx wrote an article not long ago on this topic, you might want to take a look: Primobolan / Equipoise Crashed my E2 – Help! - MESO-Rx

The tissue selectivity of it's anti estrogenic signaling just adds to the complexity of subjectively judging your actual estrogen signaling. It makes it really hard to determine if your levels are where you want them to be. Night sweats for example, is primo having a substantial anti estrogenic in your hypothalamus, resulting in night sweats, or is primo having some sort of an antagonistic effect on estrogens function of dilating and constricting blood vessels? Is what's happening something you should worry about and possibly remedy via increasing exogenous T administration to increase estrogen conversion? But will now the extra estrogen be detrimental in other tissues where primo doesn't have a huge antagonistic effect? ...

In regards to your query; my personal experience with primo is more or less negative. Loss of libido, anxiety, night sweats, etc. I don't like it and hence don't use it.

Good to see you, Jin. I feel like I haven't seen you around much lately.

I will make one minor correction: there is no evidence of metenolone's acting antiestrogenically at the receptor level (as a SERM or ER antagonist), but rather, preventing tissue uptake of estrogens. A minor quibble, but it's been a widely promulgated myth so far as I can tell that metenolone possesses indirect AI effects by metabolites, and I have at least raised contrary evidence for until more data is provided or published – if not rebutted outright – the purported findings of Dr. Todd Lee & Kurt Havens, Ph.D. cand. here: [link].

There is associative data to suggest that metenolone may (i.e., likely) act as an AI, provided in the very link that you provided to my article above, as well as here: [link]. It's important to note that while metenolone is actually unsaturated (an oversight on my part), since it is a 1-ene, it is 5-reduced & nonaromatizable like all of the AAS possessing antiaromatase activity tested (select endogenous metabolites of testosterone). All five C19 steroids – DHT, 5α-androstanedione, 3α-diol, 3β-diol, & 5β-androstane-3,17-dione competitively inhibited aromatase (i.e., reduced T ⇒ E₂) at 10-fold higher concentrations than T. The percentage reductions (-%Δ) in estradiol accumulation were:
* 73.3% (5α-androstanedione) > 60.4% (DHT) > 49.1% (3β-diol) > 35.0% (5β-androstane-3,17-dione) > 24.3% (3α-diol)

It may also inhibit 17β-HSD1, known to decrease E2 & increase DHT, as I believe that 1-testosterone ("DHB") does (explaining its principal metabolite, DHT, despite already being 5α-reduced) and that DHT has been known to do, albeit as a weak substrate.

 

[Type-IIx]

Good to see you, Jin. I feel like I haven't seen you around much lately.

I will make one minor correction: there is no evidence of metenolone's acting antiestrogenically at the receptor level (as a SERM or ER antagonist), but rather, preventing tissue uptake of estrogens. A minor quibble, but it's been a widely promulgated myth so far as I can tell that metenolone possesses indirect AI effects by metabolites, and I have at least raised contrary evidence for until more data is provided or published – if not rebutted outright – the purported findings of Dr. Todd Lee & Kurt Havens, Ph.D. cand. here: [link].

There is associative data to suggest that metenolone may (i.e., likely) act as an AI, provided in the very link that you provided to my article above, as well as here: [link]. It's important to note that while metenolone is actually unsaturated (an oversight on my part), since it is a 1-ene, it is 5-reduced & nonaromatizable like all of the AAS possessing antiaromatase activity tested (select endogenous metabolites of testosterone). All five C19 steroids – DHT, 5α-androstanedione, 3α-diol, 3β-diol, & 5β-androstane-3,17-dione competitively inhibited aromatase (i.e., reduced T ⇒ E₂) at 10-fold higher concentrations than T. The percentage reductions (-%Δ) in estradiol accumulation were:
* 73.3% (5α-androstanedione) > 60.4% (DHT) > 49.1% (3β-diol) > 35.0% (5β-androstane-3,17-dione) > 24.3% (3α-diol)

It may also inhibit 17β-HSD1, known to decrease E2 & increase DHT, as I believe that 1-testosterone ("DHB") does (explaining its principal metabolite, DHT, despite already being 5α-reduced) and that DHT has been known to do, albeit as a weak substrate.

I should clarify that my contention vs. Todd & Kurt is that metenolone doesn't act as a pro-drug to atamestane (1-methyl-boldione) because all published human metabolism studies of methenolone show that it maintains its 5α steroidal core. I believe that its metabolites are antiestogenic, many probably by competitive inhibition of aromatase, but so is it, the parent molecule.

 

[Jin23]

A minor quibble, but it's been a widely promulgated myth so far as I can tell that metenolone possesses indirect AI effects by metabolites, and I have at least raised contrary evidence for until more data is provided or published – if not rebutted outright – the purported findings of Dr. Todd Lee & Kurt Havens, Ph.D. cand. here: [link].

Eh, I knew I was overreaching. Yes, tissue uptake, remember your reference to synovial cells ... Do you have a working theory on the underlying's of this mechanism - is it via altering gene expression or non genomic? Or come to think of it, are you even talking about inhibiting estrogen-ER complex translocation (I just assumed) or are you simply referencing androgen AR binding lowering ER expression?

 

[Type-IIx]

Eh, I knew I was overreaching. Yes, tissue uptake, remember your reference to synovial cells ... Do you have a working theory on the underlying's of this mechanism - is it via altering gene expression or non genomic? Or come to think of it, are you even talking about inhibiting estrogen-ER complex translocation (I just assumed) or are you simply referencing androgen AR binding lowering ER expression?

Without looking closely, it probably just means that diffusion and any active transport of estrogens that might occur, doesn't. Sorry, today is my day off, total rest.

 

[Black90tsi]

I don't have any input on your primo question. But in my experience your doctor doesn't get the test results of bloodwork you purchase outside of the dr's prescriptions. If you go to one of the online bloodwork sites and order your own bloodwork the results only go to you as the person who ordered the tests. Even going to the same place to get your bloods drawn and analyzed your dr still shouldn't get them.

If you're really worried about it then order bloods from a lab other than the one that you use for your trt dr. If you go to LabCorp for your trt bloodwork then find an online place that uses quest for drawing/analyzing. Or vice versa. My experience is using quest for both. My dr only gets the results of the stuff he orders tests for. Not what I do on my own. Even though I can see all of the results on the MyQuest app when I look.

 

[BlazinDayz]

Good to see you, Jin. I feel like I haven't seen you around much lately.

I will make one minor correction: there is no evidence of metenolone's acting antiestrogenically at the receptor level (as a SERM or ER antagonist), but rather, preventing tissue uptake of estrogens. A minor quibble, but it's been a widely promulgated myth so far as I can tell that metenolone possesses indirect AI effects by metabolites, and I have at least raised contrary evidence for until more data is provided or published – if not rebutted outright – the purported findings of Dr. Todd Lee & Kurt Havens, Ph.D. cand. here: [link].

There is associative data to suggest that metenolone may (i.e., likely) act as an AI, provided in the very link that you provided to my article above, as well as here: [link]. It's important to note that while metenolone is actually unsaturated (an oversight on my part), since it is a 1-ene, it is 5-reduced & nonaromatizable like all of the AAS possessing antiaromatase activity tested (select endogenous metabolites of testosterone). All five C19 steroids – DHT, 5α-androstanedione, 3α-diol, 3β-diol, & 5β-androstane-3,17-dione competitively inhibited aromatase (i.e., reduced T ⇒ E₂) at 10-fold higher concentrations than T. The percentage reductions (-%Δ) in estradiol accumulation were:
* 73.3% (5α-androstanedione) > 60.4% (DHT) > 49.1% (3β-diol) > 35.0% (5β-androstane-3,17-dione) > 24.3% (3α-diol)

It may also inhibit 17β-HSD1, known to decrease E2 & increase DHT, as I believe that 1-testosterone ("DHB") does (explaining its principal metabolite, DHT, despite already being 5α-reduced) and that DHT has been known to do, albeit as a weak substrate.

And it's exactly this type of quality discourse that draws me to this forum.

 

[mindgame1516]

I don't have any input on your primo question. But in my experience your doctor doesn't get the test results of bloodwork you purchase outside of the dr's prescriptions. If you go to one of the online bloodwork sites and order your own bloodwork the results only go to you as the person who ordered the tests. Even going to the same place to get your bloods drawn and analyzed your dr still shouldn't get them.

If you're really worried about it then order bloods from a lab other than the one that you use for your trt dr. If you go to LabCorp for your trt bloodwork then find an online place that uses quest for drawing/analyzing. Or vice versa. My experience is using quest for both. My dr only gets the results of the stuff he orders tests for. Not what I do on my own. Even though I can see all of the results on the MyQuest app when I look.

Where’s a good place online I can order labs

 

[Black90tsi]

Where’s a good place online I can order labs

I've used Ulta labs in the past. They use quest diagnostics for their blood draws. You just select the tests you want online, pay them bring the print out of your order you receive to the lab and hand it to the technician just like you would with Dr prescribed blood work.

 

[Badandy]

I telmisartan as well. I like it because it last longer than the losartan I previously took. The down sid I notice it takes longer to work. So if I drink to muck coffee with in the first 60- 120 minutes of taking it I get a spike in bp before the meds kick in

 

[mindgame1516]

I’m going to look up that lab company and set an appointment to get lab work next week. So far my first 2 shots @250mg test and 150mg primo. The day after my shots every hour of the day gets worse anxiety wise then I take .5mg andex and feel better a few hours later.

I’m curious if I should do the blood work with test e alone @500 to see where my e2 sits at that before adding and checking blood with other compounds. I know at my cruise dose of 150mg a week my total test levels are 950ng and E2 =36

 

[Black90tsi]

You really should wait until 4+ weeks to get the tests done. You need to give it long enough for everything to reach full saturation in your system. You can use steroidplotter.com to figure out when that will be for you.

Otherwise you're only getting a snap shot of what things look like on the way up.

 

[Mongo966]

I’m going to look up that lab company and set an appointment to get lab work next week. So far my first 2 shots @250mg test and 150mg primo. The day after my shots every hour of the day gets worse anxiety wise then I take .5mg andex and feel better a few hours later.

Do you think you might be playing tricks on yourself by overthinking the situation? It's easy to get a snowball effect going once the anxiety starts, making it worse and worse. I have decades of practice talking myself down from that shit and I still get tricked on a regular basis. Just something to think about. These drugs definitely can make us more susceptible to it, without a doubt.

 

[Jin23]

I’m curious if I should do the blood work with test e alone @500 to see where my e2 sits at that before adding and checking blood with other compounds. I know at my cruise dose of 150mg a week my total test levels are 950ng and E2 =36

This is a good idea for sure.

 

[mindgame1516]

Ok fellows I figured I would update…. Spoiler alert I don’t have labs yet. At this point I’m 3 weeks in and most likely not going to get labs until another month

The first week was a rollercoaster possibility im thinking is I’m on trt so by adding more test and primo it took time for the primo to level out. By my 3rd primo injection by e2 sides started to disappear. I’m 3 weeks in now and feel amazing well completely normal no more dick issues, e2 anxiety or moodiness not night sweats.

This is the first time I have ever blasted with out needing adex for e2 sides it almost feels like a miracle I swear. The only thing I take is telismartan for BP.

I’m 3 weeks in strength is going up every week, this week I’ve noticed a noticeable difference in muscles starting to look full and also starting to lean out. I don’t expect to much from 200mg primo, I’m more happy that I can blast @500mg test without trying to control E2 the whole time. I took before pictures and will post some mid cycle pictures

Also I’m thinking about going another 3weeks at this dose to make sure I feel stable and for e2 to feel in check and then upping the dose to 400mg primo and 700 test. But then the other part of me is like that really needed