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Does Phera armoitize?

Justing2

Member
Ive had one problem with gyno in the past but only from mdrol. I was thinking of doing a phera/epi bridge but then someone told phera can armoitize. Is that true. I took phera twice before the mdrol and never had a problem but since the mdrol I still have a very small lump. I was able to get it smaller by using letro. Should I avoid Phera now even though it didn't bother me before?
 
given my history with it do you think I would be ok using it again? Like I said Ive taken it twice with no problems.
 
But do you think With the little gyno I have left from mdrol Id be ok running phera now seeing that Phera has never bothered me with gyno before.
 
I was a fool when I did mdrol and only used reveristol as my pct. 2 months later boom I had two painful lumps in my nipples. This time around I have nolva for my pct. Im going to keep some letro on hand this time for my phera/epi bridge should anything go wrong. Maybe even does .25mg's every 3 days. I heard that works.
 
wtf! it seems like everyone on here has gyno or they think they do?? if your doing ur pct right you shouldnt hava problem with gyno, am i correct? i know i never have!

Actually gyno can flare up even with a proper PCT. Can flare up on cycle even when there isnt really a reason for it to. A lot of people that have run tren 19 nor usually get prolactin based gyno on cycle or post cycle unless you use a prolactin antagonist... Now, there are some people that believe they do, but really dont (mind playing tricks on them)...
 
P-Plex does not aromatize and it is not "wet" because of sodium in the diet. P-Plex as well as M-Drol suppress SHBG to the point where endogenous estrogen can be freed up, sometimes causing symptoms associated withexcess estrogen. Having a SERM on hand is the best solution, as an AI will not address estrogen that has already been formed and is being freed due to SHBG being suppressed too low--however an AI would help with newly formed estrogen, e.g., through the aromatization of testosterone formed during PCT. However, AIs are tricky to use in my opinion and people tend to suppress estrogen too low, which can cause a whole host of problems.

How suseptable one is to this SHBG effect will largely determine what, if any, estrogen related side effects you may encounter with P-Plex or M-Drol.


Crowbar
 
So in my case are you saying that if something does flare up I would be better adding some nolva into the mix rather than Letro? Sorry Im bad at the AI thing.Never had to worry about it before.
 
Justing2, yes I'd just use some low-dose Nolva if you start to encounter problems--maybe 10-20 mg. EOD, you'll have to adjust as needed.

Crowbar
 
Thank you so much crowbar!! 1 more question. I just did about 2 months of letro to shrink the gyno I got from mdol. I started taking nolva 3 days ago. how long should I wait before I start taking the Phera?
Thanks again!
 
Actually gyno can flare up even with a proper PCT. Can flare up on cycle even when there isnt really a reason for it to. A lot of people that have run tren 19 nor usually get prolactin based gyno on cycle or post cycle unless you use a prolactin antagonist... Now, there are some people that believe they do, but really dont (mind playing tricks on them)...

I've ran "tren" before and didn't get prolactin gyno and didn't use a prolactin antagonist. Others have too. Of course, some people have gotten gyno, so YMMV. I had post-pct bloodwork done and my prolactin levels were quite low (but normal).

A prolactin antagonist isn't necessary at all IMO. It is an option, but I think there are better options for people using very high doses of 19-nor's or that are prone to gyno. Even though they are effective for 19-nor's, most prolactin antagonists have pretty severe side effects.

You won't develop prolactin gyno if your estrogen is kept low, even if your prolactin is elevated, so letro works quite well to prevent all types of gyno, and can be used to treat gyno symptoms from 19-nor and other steroid families alike (test, DHT). Arimidex is better as an on cycle preventative since it is no so d@mn strong as letro but letro can be used at .25mg e3d or so if desired. Higher doses of letro (tapering down) followed by nolva (tapering down) for the estrogen rebound has been used numerous times successfully to halt gyno symptoms in their tracks and "cure" gyno given that not too much time has elapsed.

I think most people have no idea how much more dangerous prolactin antagonists are versus aromatase inhibitors.
 
P-Plex does not aromatize and it is not "wet" because of sodium in the diet. P-Plex as well as M-Drol suppress SHBG to the point where endogenous estrogen can be freed up, sometimes causing symptoms associated withexcess estrogen. Having a SERM on hand is the best solution, as an AI will not address estrogen that has already been formed and is being freed due to SHBG being suppressed too low--however an AI would help with newly formed estrogen, e.g., through the aromatization of testosterone formed during PCT. However, AIs are tricky to use in my opinion and people tend to suppress estrogen too low, which can cause a whole host of problems.

How suseptable one is to this SHBG effect will largely determine what, if any, estrogen related side effects you may encounter with P-Plex or M-Drol.


Crowbar

Any diet high in sodium while on cycle will tend to promote or worsen water retention. Some steroids also bind to the glucocorticoid and mineralocorticoid receptors and directly cause water retention by affecting sodium levels. Cortisol levels can be suppressed by any steroid on cycle and if severe enough, then the body will just compensate by releasing more cortisol (-->more water retention).

Mdrol and Phera are most likely potent inhibitors of 11-beta hydroxylase which results in significant water retention within the muscle (no subcutaneous "bloat" but the water is there). Inhibition of 11-BH can also suppress cortisol production while increasing production of DHEA which in turn can directly stimulate estrogen receptors. So plenty of gyno ingredients here.

Phera and Mdrol are both considered to be strong androgens and due to their effects on SHBG, they can easily upset the androgen-estrogen ratio and invite gyno until androgen levels return to normal.

Any androgen with a high binding affinity for SHBG can bump off bound estrogen so that it becomes free, circulating estrogen. Again, helping to set the stage for gyno (rarely is gyno caused by 1 thing; it needs cofactors).

It's true that an AI cannot eliminate a just-unbound-from-SHBG "puddle" of estrogen on the fly, but if one were to use an AI throughout the cycle, little to no new estrogen would be formed and possibly bound only to be bumped into the circulating state later. So an AI could be used to prevent gyno when using highly SHBG bound steroids; you would run it the duration of the cycle of course. The only real need for a SERM then would be for PCT and the estrogen rebound from using an AI on cycle. Of course, you could use a SERM like you said, but their safety profile doesn't make me comfortable enough to use them on cycles (PCT is plenty of SERM-time for me; AIs are much safer).

I have a friend that uses arimidex every cycle all the way into PCT along with HCG (real AAS user) and he has never had any issues with gyno and he has never used a SERM b/c he doesn't need them. He has used the whole range of AAS too, so the specific compound really doesn't matter in a gyno context if you keep estrogen low.
 
So do you think arimidex would be my best option to use during my cycle to prevent my old gyno from getting worse?
 
wtf! it seems like everyone on here has gyno or they think they do?? if your doing ur pct right you shouldnt hava problem with gyno, am i correct? i know i never have!

gotta watch the estrogen rebound after PCT, thats what got me. controlled it a bit too much.
 
Dumbhick, I don't disagree with most of what you said except Ais being safer than SERMS. People routinely get themselves into trouble using Ais. For one thing, without proper testing it is VERY easy to suppress estrogen too low using Ais--and this carries a host of problems. People often see estrogen as an absolute negative, when in reality it has positive atributes as well. For example, Clomid will act as an estrogen antagonist at the breast tissue, but as an estrogen agonist at the bone and in terms of endothilial function and cholesterol levels; whereas Ais can, and will, send your blood lipids into the ****ter! If you want an expert opinion on this see what Seth Roberts has to say about the use of Ais.

Of course your points concerning steroids in general are valid, nevertheless my point remains that the primary reason people experience gyno from substance such as P-Plex and M-Drol THAT DON"T AROMATIZE is because of their effects on SHBG. Also, Ais will do nothing to address the estrogen that was already there (and bound to SHBG) long before you ever statred your cycle, through the natural aromitization of testosterone. This estrogen is now going to be unbound with the use of P-Plex or M-Drol. If you're sensitive to the effects of estrogen you will need a SERM to control this.

As to the use of Ais on cycle, I used "real" AAS before things began getting too ****in sketchy legally. Back when I ran cycles there was never this obsession with Ais like there is today. Guys used low-dose SERMS on cycle with intermittent Hcg, followed by Clomid tapered down during PCT--that's it. Ocassionally some guys would use low-dose Ais on cycle--but not often. Surprisingly--or not--guys weren't developing "gyno" left and right like they seem to today!


Crowbar
 
Dumbhick, I don't disagree with most of what you said except Ais being safer than SERMS. People routinely get themselves into trouble using Ais. For one thing, without proper testing it is VERY easy to suppress estrogen too low using Ais--and this carries a host of problems. People often see estrogen as an absolute negative, when in reality it has positive atributes as well. For example, Clomid will act as an estrogen antagonist at the breast tissue, but as an estrogen agonist at the bone and in terms of endothilial function and cholesterol levels; whereas Ais can, and will, send your blood lipids into the ****ter! If you want an expert opinion on this see what Seth Roberts has to say about the use of Ais.

Of course your points concerning steroids in general are valid, nevertheless my point remains that the primary reason people experience gyno from substance such as P-Plex and M-Drol THAT DON"T AROMATIZE is because of their effects on SHBG. Also, Ais will do nothing to address the estrogen that was already there (and bound to SHBG) long before you ever statred your cycle, through the natural aromitization of testosterone. This estrogen is now going to be unbound with the use of P-Plex or M-Drol. If you're sensitive to the effects of estrogen you will need a SERM to control this.

As to the use of Ais on cycle, I used "real" AAS before things began getting too ****in sketchy legally. Back when I ran cycles there was never this obsession with Ais like there is today. Guys used low-dose SERMS on cycle with intermittent Hcg, followed by Clomid tapered down during PCT--that's it. Ocassionally some guys would use low-dose Ais on cycle--but not often. Surprisingly--or not--guys weren't developing "gyno" left and right like they seem to today!


Crowbar


Actually, I got most of my information from Seth Robert's Anabolic Pharmacology book (sitting on my desk right now).

I don't really agree with all of his SERM-steroid stack approaches.

I am completely aware of the negative side effects of driving estrogen too low, and the fact that many people still think that no estrogen = a good thing. Of course this is not true. One way to monitor indirectly whether your AI use is suppressing estrogen too much is to monitor your cholesterol at home using an at-home test machine and LDL, HDL, and trigylceride strips, like my friend does. If your cholesterol really starts to get out of control, beyond what is typical of steroids, then it is probably a safe assumption that you need to back off of the AI dose/frequency. And there is no substitute for on cycle and post-cycle bloodwork by a professional. Of course, few people do this...(I do)

The safety issue I mentioned had to do with the direct side effects/toxicity of AIs versus SERMs. SERMs are inherently more toxic than AIs, period, over and out. Tamoxifen is carcinogenic and has caused secondary malignancies in cancer patients. Most SERMs have varying degrees of ocular toxicity, ESP clomid, but also nolva and torem as well. The only major concern with AIs in general is to not drive estrogen so low that you develop estrogen-deficient secondary side effects such as hyperlipidemia (probably the major concern though estrogen supports sex drive and bone health, etc).

I still maintain that using an AI from start to finish on cycle will prevent gyno if done properly. I follow with a SERM, but it ends up just coinciding with PCT, so it limits the amount of time that I am on SERMs which is a good thing. I stick with this approach when needed b/c there is no way that I would ever run a SERM for 10 weeks in a row (6 week cycle + 4 week PCT). It is true that an AI cannot make estrogen that is freed from the bound state magically disappear-I think I said this above (it will circulate and can bind to the ER yes), BUT if your body does not continue to produce significant amounts of estrogen (say by using .5mg ed of arimidex for any cycle, AROMATIZING OR NOT), then significant amounts of estrogen will NOT be produced and in turn won't be newly bound by SHBG only to be released later. If the bound-estrogen pool is not being actively replenished by aromatase, then estrogen is not going to be continually dumped from SHBG into the circulating state b/c it won't even be there to be dumped after a while; perhaps after the initial dump of estrogen due to SHBG displacement-I don't know exactly when pre-cycle, bound estrogen would no longer be an issue once AI use has commenced. I think it will take more than one "spurt" of free estrogen in the circulating state to produce any symptoms of gyno.

What Seth's book doesn't tell you is much about SERM toxicity versus AI toxicity as it should. But he only spent half a page at most on each SERM and AI so what do you expect. If you want more info, read the drug mfg's monograms at Invalid Link Removed and maybe the Dark Side article on SERMs at Invalid Link Removed. AIs need to be used with care, so you can't be sloppy like most people are with SERM doses, but when used carefully I maintain that they are much safer drugs than SERMs. Greater care is needed in using AIs on non-aromatizing cycles since a smaller, less frequent dose is likely fine.

BTW, it's funny you mentioned an obsession with AIs today. What I have seen on this forum lately has been an unhealthy obsession with SERMs (get a SERM, get clomid, u need nolva, serm, google serm, etc). They might be "safer" for Joe Blow who doesn't know what bloodwork is but knows what Clomid is (to some extent, being a moron and all). I've also seen an obsession with prolactin antagonists (get cab, get bromo, get p5p, get a job, etc) and I can refer you to your own book reference to remind you that Seth Roberts is pretty adamant about not using them due to their severe side effects. Not only him, but doctors on other forums are of a similar opinion as to their severe side effects not being worth the risk of using them (I know you weren't arguing for/against prolactin agents, but this is just what I have seen lately). I haven't seen as much of an obsession with AIs. They are very potent unlike SERMs, so some intelligence and blood monitoring is needed obviously. Not everyone using anabolics has intelligence to spare, however.

That is my somewhat educated opinion and personal cycle approach; to each his own.
 
Dumbhick: "SERMs are inherently more toxic than AIs, period, over and out." I asked Bill Roberts his thought on this statement in order to get yet another expert opinion. I asked him if this statement was accurate in his opinion. His response follows:

"No. These drugs have been around a long time and have an excellent safety record."

He further noted that cancer patients are often maintained on these drugs for years at a time:


That actually is the one area where there is substantial concern: not that Nolvadex becomes cancer-causing, but that in some cases it loses effectiveness after about 5 years of continuous use.


Crowbar
 
The safety issue I mentioned had to do with the direct side effects/toxicity of AIs versus SERMs. SERMs are inherently more toxic than AIs, period, over and out. Tamoxifen is carcinogenic and has caused secondary malignancies in cancer patients. Most SERMs have varying degrees of ocular toxicity, ESP clomid, but also nolva and torem as well. The only major concern with AIs in general is to not drive estrogen so low that you develop estrogen-deficient secondary side effects such as hyperlipidemia (probably the major concern though estrogen supports sex drive and bone health, etc).

What Seth's book doesn't tell you is much about SERM toxicity versus AI toxicity as it should. But he only spent half a page at most on each SERM and AI so what do you expect. If you want more info, read the drug mfg's monograms at Invalid Link Removed and maybe the Dark Side article on SERMs at Invalid Link Removed. AIs need to be used with care, so you can't be sloppy like most people are with SERM doses, but when used carefully I maintain that they are much safer drugs than SERMs. Greater care is needed in using AIs on non-aromatizing cycles since a smaller, less frequent dose is likely fine.

You are entitled to your opinion and it is through disagreement that we improve our understanding. That being said, I think you might want to differentiate between something that is written from a marketing perspective to sell supplements versus an opinion of an expert in the field. PP is a good group of guys but I think that those articles on SERM toxicity are a little overblown.
 
Another point that concerns me with Ai use is that driving estrogen very low can adversely affect endothelial function.

Crowbar
 
You are entitled to your opinion and it is through disagreement that we improve our understanding. That being said, I think you might want to differentiate between something that is written from a marketing perspective to sell supplements versus an opinion of an expert in the field. PP is a good group of guys but I think that those articles on SERM toxicity are a little overblown.

Seth-Your point about marketing and opinions is well taken; the irony is that I bought your book from PP. Of course they are going to be a little slanted given that they sell supplements, but the manufacturers of the drugs aren't slanted (Invalid Link Removed) other than trying to keep their product on the market by any means necessary. Nolvadex has a black box FDA warning about the risk of secondary malignancies. Letrozole doesn't. Love your book, BTW; it's very handy and a good complement to Lewellyn's Anabolics 2009, among others.

Crowbar-I know about the too low estrogen effects of AIs; anyone who doesn't should avoid them. Thankfully that is a largely reversible effect and minimizing the use of them minimizes the effects of high cholesterol on the heart which is the primary concern in my eyes with AIs. Bone density is a concern too, but again, anabolics and orthonormal estrogen levels increase bone density (I think; don't quote me on that; don't have time to look it up), so I see this as a temporal, dose-dependent effect also. In my opinion, as long as AIs are used PROPERLY (dose, duration, whether they are even needed, regular intra and post and pre-cycle bloodwork, and maybe at home cholesterol testing), then they are safer substances than the older generation of SERMs (nolva, clomid esp). The new ones are getting better safety wise, but they haven't proven themselves in the bodybuilding arena yet and/or aren't widely available.

Secondary malignancies are not always reversible. Neither is optic neuropathy and even cataracts, the latter of which is not a rare side effect of SERMs. Rxlist.com frankly states (actually the drug mfg) that during trial X of Nolvadex, x number of people reported secondary malignancies, and 1 or 2 people died during the trial from thrombosis, etc (which is also mentioned in the black box warning). Death isn't reversible. The number of cases is low, BUT the FDA deemed that the risk was high enough to warrant their dreaded black box warning.

For your convenience: Invalid Link Removed

WARNING

For Women with Ductal Carcinoma in Situ (DCIS) and Women at High Risk for Breast Cancer: Serious and life-threatening events associated with NOLVADEX in the risk reduction setting (women at high risk for cancer and women with DCIS) include uterine malignancies, stroke and pulmonary embolism. Incidence rates for these events were estimated from the NSABP P-1 trial (see CLINICAL PHARMACOLOGY-Clinical Studies - Reduction in Breast Cancer Incidence In High Risk Women). Uterine malignancies consist of both endometrial adenocarcinoma (incidence rate per 1,000 women-years of 2.20 for NOLVADEX vs 0.71 for placebo) and uterine sarcoma (incidence rate per 1,000 women-years of 0.17 for NOLVADEX vs 0.4 for placebo)*. For stroke, the incidence rate per 1,000 women-years was 1.43 for NOLVADEX vs 1.00 for placebo**. For pulmonary embolism, the incidence rate per 1,000 women-years was 0.75 for NOLVADEX versus 0.25 for placebo**.

Some of the strokes, pulmonary emboli, and uterine malignancies were fatal.

Health care providers should discuss the potential benefits versus the potential risks of these serious events with women at high risk of breast cancer and women with DCIS considering NOLVADEX to reduce their risk of developing breast cancer.

The benefits of NOLVADEX outweigh its risks in women already diagnosed with breast cancer.

REFERENCES

*Updated long-term follow-up data (median length of follow-up is 6.9 years) from NSABP P-1 study. See WARNINGS: Effects on the Uterus-Endometrial Cancer and Uterine Sarcoma.

**See Table 3 under CLINICAL PHARMACOLOGY-Clinical Studies.

In the "real world", these substances have been used for a long time, but I see frequent complaints of vision problems from people using Clomid, though nearly all SERMs can adversely affect vision. And of course the mixed properties of Clomid make a fair portion of people girly, emotional, sex in the city, crybabies (less serious of a side effect, but not desirable either). YMMV I guess.
 
Dumbhick: "SERMs are inherently more toxic than AIs, period, over and out." I asked Bill Roberts his thought on this statement in order to get yet another expert opinion. I asked him if this statement was accurate in his opinion. His response follows:

"No. These drugs have been around a long time and have an excellent safety record."

He further noted that cancer patients are often maintained on these drugs for years at a time:


That actually is the one area where there is substantial concern: not that Nolvadex becomes cancer-causing, but that in some cases it loses effectiveness after about 5 years of continuous use.


Crowbar

You are correct that the various anti-e drugs (including AIs) tend to become less effective for cancer treatment as time goes on, often necessitating a switch from nolva to letro or vice versa.

Cancer patients may be maintained on all sorts of anti-neoplastic/anti-cancer drugs for years at a time when such use is necessitated, justified, and effective, b/c the goal is prolongation of life even in the face of the risk of 2nd-ary malignancies b/c the primary malignancy (DCIS, etc) would kill most people much faster if not treated (though sometimes the secondary malignancy ends up killing them, but they still probably lived longer than they would have without treatment). The goal is prolongation of life, not re-enlargement of your testicles.

So basically, I am saying that your comment (or Bill Roberts rather) about cancer patients being maintained on this drugs for years at a time, while true, is not relevant to the safety of their use in bodybuilding. Cancer patients don't tend to have long "shelf-lives", so what's good for the cancer patient cannot be assumed to be good for the bodybuilder. Maybe it is, maybe it isn't, but you cannot connect these two dots from Bill's true statement about their use in cancer patients (it seems to be what you are implying by including his comment which is really out of context in terms of bodybuilding). The treatment objectives are entirely different. Tamoxifen is used in high risk settings medically, so a slightly different risk/benefit assessment is used; recovering from a cycle is not a high risk setting.

I know that AIs are used to treat breast cancer medically as well, and all drugs have risks/sides; I just personally judge the risk to be less from AIs than SERMs and consequently, I limit my use of SERMs (both agents really) in length and dose and for the PCT setting only to reduce lifetime exposure.

However, there is no question that Nolvadex has carcinogenic (and genotoxic) effects; that is not an opinion either. Its carcinogenicity has been demonstrated in multiple studies and the mfg cites them accordingly.

The only way opinion factors in here is how these studies translate to bodybuilders (particularly men, though male rats are mentioned below, since mostly women were studied) using the drug for non-FDA approved purposes (not studied IOW) for varying lengths of time and at varying doses and lifetime exposures, and usually in the setting of oral and/or injectable steroid use ("abuse" as they call it).

Citing from the professional monogram Invalid Link Removed

Effects on the Uterus-Endometrial Cancer and Uterine Sarcoma
An increased incidence of uterine malignancies has been reported in association with NOLVADEX treatment. The underlying mechanism is unknown, but may be related to the estrogen-like effect of NOLVADEX. Most uterine malignancies seen in association with NOLVADEX are classified as adenocarcinoma of the endometrium. However, rare uterine sarcomas, including malignant mixed mullerian tumors (MMMT), have also been reported. Uterine sarcoma is generally associated with a higher FIGO stage (III/IV) at diagnosis, poorer prognosis, and shorter survival. Uterine sarcoma has been reported to occur more frequently among long-term users ( ≥ 2 years) of NOLVADEX than non-users. Some of the uterine malignancies (endometrial carcinoma or uterine sarcoma) have been fatal.

In the NSABP P-1 trial, among participants randomized to NOLVADEX there was a statistically significant increase in the incidence of endometrial cancer (33 cases of invasive endometrial cancer, compared to 14 cases among participants randomized to placebo (RR=2.48, 95% CI: 1.27-4.92). The 33 cases in participants receiving NOLVADEX were FIGO Stage I, including 20 IA, 12 IB, and 1 IC endometrial adenocarcinomas. In participants randomized to placebo, 13 were FIGO Stage I (8 IA and 5 IB) and 1 was FIGO Stage IV. Five women on NOLVADEX and 1 on placebo received postoperative radiation therapy in addition to surgery. This increase was primarily observed among women at least 50 years of age at the time of randomization (26 cases of invasive endometrial cancer, compared to 6 cases among participants randomized to placebo (RR=4.50, 95% CI: 1.78-13.16). Among women ≤ 49 years of age at the time of randomization there were 7 cases of invasive endometrial cancer, compared to 8 cases among participants randomized to placebo (RR=0.94, 95% CI: 0.28-2.89). If age at the time of diagnosis is considered, there were 4 cases of endometrial cancer among participants ≤ 49 randomized to NOLVADEX compared to 2 among participants randomized to placebo (RR=2.21, 95% CI: 0.4-12.0). For women ≥ 50 at the time of diagnosis, there were 29 cases among participants randomized to NOLVADEX compared to 12 among women on placebo (RR=2.5, 95% CI: 1.3-4.9). The risk ratios were similar in the two groups, although fewer events occurred in younger women. Most (29 of 33 cases in the NOLVADEX group) endometrial cancers were diagnosed in symptomatic women, although 5 of 33 cases in the NOLVADEX group occurred in asymptomatic women. Among women receiving NOLVADEX the events appeared between 1 and 61 months (average=32 months) from the start of treatment.

In an updated review of long-term data (median length of total follow-up is 6.9 years, including blinded follow-up) on 8,306 women with an intact uterus at randomization in the NSABP P-1 risk reduction trial, the incidence of both adenocarcinomas and rare uterine sarcomas was increased in women taking NOLVADEX. During blinded follow-up, there were 36 cases of FIGO Stage I endometrial adenocarcinoma (22 were FIGO Stage IA, 13 IB, and 1 IC) in women receiving NOLVADEX and 15 cases in women receiving placebo [14 were FIGO Stage I (9 IA and 5 IB), and 1 case was FIGO Stage IV]. Of the patients receiving NOLVADEX who developed endometrial cancer, one with Stage IA and 4 with Stage IB cancers received radiation therapy. In the placebo group, one patient with FIGO Stage 1B cancer received radiation therapy and the patient with FIGO Stage IVB cancer received chemotherapy and hormonal therapy. During total follow-up, endometrial adenocarcinoma was reported in 53 women randomized to NOLVADEX (30 cases of FIGO Stage IA, 20 were Stage IB, 1 was Stage IC, and 2 were Stage IIIC), and 17 women randomized to placebo (9 cases were FIGO Stage IA, 6 were Stage IB, 1 was Stage IIIC, and 1 was Stage IVB) (incidence per 1,000 women-years of 2.20 and 0.71, respectively). Some patients received post-operative radiation therapy in addition to surgery. Uterine sarcomas were reported in 4 women randomized to NOLVADEX (1 was FIGO IA, 1 was FIGO IB, 1 was FIGO IIA, and 1 was FIGO IIIC) and one patient randomized to placebo (FIGO 1A); incidence per 1,000 women-years of 0.17 and 0.04, respectively. Of the patients randomized to NOLVADEX, the FIGO IA and IB cases were a MMMT and sarcoma, respectively; the FIGO II was a MMMT; and the FIGO III was a sarcoma; and the one patient randomized to placebo had a MMMT. A similar increased incidence in endometrial adenocarcinoma and uterine sarcoma was observed among women receiving NOLVADEX in five other NSABP clinical trials.

Carcinogenesis
A conventional carcinogenesis study in rats at doses of 5, 20, and 35 mg/kg/day (about one, three and seven-fold the daily maximum recommended human dose on a mg/m²basis) administered by oral gavage for up to 2 years) revealed a significant increase in hepatocellular carcinoma at all doses. The incidence of these tumors was significantly greater among rats administered 20 or 35 mg/kg/day (69%) compared to those administered 5 mg/kg/day (14%). In a separate study, rats were administered tamoxifen at 45 mg/kg/day (about nine-fold the daily maximum recommended human dose on a mg/m² basis); hepatocellular neoplasia was exhibited at 3 to 6 months.

Granulosa cell ovarian tumors and interstitial cell testicular tumors were observed in two separate mouse studies. The mice were administered the trans and racemic forms of tamoxifen for 13 to 15 months at doses of 5, 20 and 50 mg/kg/day (about one-half, two and five-fold the daily recommended human dose on a mg/m² basis).

Mutagenesis
No genotoxic potential was found in a conventional battery of in vivo and in vitro tests with pro- and eukaryotic test systems with drug metabolizing systems. However, increased levels of DNA adducts were observed by 32P post-labeling in DNA from rat liver and cultured human lymphocytes. Tamoxifen also has been found to increase levels of micronucleus formation in vitro in human lymphoblastoid cell line (MCL-5). Based on these findings, tamoxifen is genotoxic in rodent and human MCL-5 cells.
 
Again I quote:

Dumbhick: "SERMs are inherently more toxic than AIs, period, over and out." I asked Bill Roberts his thought on this statement in order to get yet another expert opinion. I asked him if this statement was accurate in his opinion. His response follows:

"No. These drugs have been around a long time and have an excellent safety record."

He further noted that cancer patients are often maintained on these drugs for years at a time:


That actually is the one area where there is substantial concern: not that Nolvadex becomes cancer-causing, but that in some cases it loses effectiveness after about 5 years of continuous use.


I think you have to look at not only who is most at risk for these side effects but also a concept related to NNT (number needed to treat)--a little "trick" that pharmaceutical companies often play in order to make a drug seem more effective. At any rate, the incidence of these side effects is, in fact, quite low in comparison to the number of people using the drugs. Pharmaceutical warnings are by their nature often conservative--after all pharmaceutical companies and doctors have to cover their asses against lawsuits also.

Finally, the negative effects of low estrogen on endothelial function is nothing to be dismissed, and nothing which--aside from sophisticated and impractical tests for the average steroid user--is not discernable.

Crowbar


Crowbar
 
Of course Nolva will be associated with an increase--however small in the real world-of uterine cancer as Nolva is an estrogen antagonist in certain tissues, e.g., the breast, and an estrogen agonist in other tissue, e.g., the uterus. However, since as males we do not have a uterus, this is pointless.

Also, look at the ridiculous dosages used in the last study you quote--5, 20, and 35 mg./kg/day for 2 years!!!

Crowbar
 
ANY hepatotoxic substance administered at ridiculous dosages for 2 straight years is going to increase the incidence of hepatic carcinomas.

Crowbar
 
I am familiar with NNT.

Again I quote:

Carcinogenesis
A conventional carcinogenesis study in rats at doses of 5, 20, and 35 mg/kg/day (about one, three and seven-fold the daily maximum recommended human dose on a mg/m²basis) administered by oral gavage for up to 2 years) revealed a significant increase in hepatocellular carcinoma at all doses. The incidence of these tumors was significantly greater among rats administered 20 or 35 mg/kg/day (69%) compared to those administered 5 mg/kg/day (14%). In a separate study, rats were administered tamoxifen at 45 mg/kg/day (about nine-fold the daily maximum recommended human dose on a mg/m² basis); hepatocellular neoplasia was exhibited at 3 to 6 months.

Granulosa cell ovarian tumors and interstitial cell testicular tumors were observed in two separate mouse studies. The mice were administered the trans and racemic forms of tamoxifen for 13 to 15 months at doses of 5, 20 and 50 mg/kg/day (about one-half, two and five-fold the daily recommended human dose on a mg/m² basis).

Obviously you didn't read half of what I posted (I read your posts), so I shifted the bold parts around to clarify your erroneous responses.

Else you would have noted that in one of the studies with rats/mice, several tumor types were manifest in a dose and time dependent manner. The equivalent human doses ranged from ONE-HALF (that is not mega-dosing; mega-dosing is what the typical bodybuilder does with a SERM for PCT) the recommended max human daily dose to TWO and FIVE times the max. The time range 13-15 months.

Separate study: 9x the recommended max; liver cancer manifested at 3-6 months.

Men don't have uterine structures? GTFO. I know that. But to assume that those studies (which aren't even all of the mfg studies I cited) have no relevance to men is jumping to a conclusion, and one that you can't support (studies forthcoming?).

Quoting from Eric's biased paper at PP.com (the studies themselves which are cited probably aren't biased though it is hard to say if they are representative b/c little research has focused on men and the use of SERMs):

In 1996, the International Agency for Research on Cancer (IARC) concluded that tamoxifen clearly promotes uterine cancer in humans – at a standard 20mg/day dose. (16,23,42) This is due to tamoxifen acting as an estrogen agonist in the uterus, presumably from the 4-hydroxytamoxifen metabolite, which triggers abnormal growth of the uterus and the formation of cancer causing DNA adducts. (33, 40)

Contrary to popular thought, these implications are quite scary for a male when we realize the male equivalent to the uterus is the prostate – which differentiates from the same embryonic cell line, shares the same oncogene, Bcl-2, and high concentration of estrogen receptors. In fact, there is no reason to assume that tamoxifen would not initiate the same cancerous growth in the prostate. (60-62) It is no wonder that tamoxifen failed as a treatment for prostate carcinoma. (43)

Note: This same risk would be applicable to Clomid, which has also been linked to uterine cancer and ovarian hyper-stimulation. (18, 19, 57, 59)
 
ANY hepatotoxic substance administered at ridiculous dosages for 2 straight years is going to increase the incidence of hepatic carcinomas.

Crowbar

Not necessarily. Alcohol is acutely hepatotoxic and can be administered at ridiculous doses for 2 straight years and if stopped, then perfectly normal liver function is possible. Just ask a college student who stopped being an alkie when he graduated. It takes much longer for Alcohol to manifest its really nasty effects on the liver though it can spike your enzymes in the short term.

Alcohol is an obvious one. So is tylenol-but tylenol doesn't cause liver cancer; it can cause liver failure secondary to glutathione depletion or poor liver health or coadministration with alcohol or other drugs over time.

However, there are lots of RX drugs that (LOTS) increase liver enzymes in some of the patients during the study and yet there is no mention of hepatic carcinomas. Read up.

The usual outcome of hepatotoxic substances over time is jaundice, hepatitis, and perhaps cirrhosis. Only cirrhosis could even be close to being called a carcinoma (though it isn't per se).

Few studies have been performed, but no studies have ever definitively linked steroid use (oral 17aa and/or injectable) to an increased risk of cancer, even though they do appear to have this property on paper ("activation of oncogenes" to quote Seth's book).

In fact, Nolvadex has both non-malignant liver effects and malignant liver effects, and there does not appear to be a link between the two of them. If there is a link, then it was not studied. But I think that your statement is just incorrect.

Effects on the liver: Liver cancer
In the Swedish trial using adjuvant NOLVADEX 40 mg/day for 2-5 years, 3 cases of liver cancer have been reported in the NOLVADEX-treated group vs. 1 case in the observation group (See PRECAUTIONS- Carcinogenesis). In other clinical trials evaluating NOLVADEX, no cases of liver cancer have been reported to date.

One case of liver cancer was reported in NSABP P-1 in a participant randomized to NOLVADEX.

Effects on the liver: Non-malignant effects
NOLVADEX has been associated with changes in liver enzyme levels, and on rare occasions, a spectrum of more severe liver abnormalities including fatty liver, cholestasis, hepatitis and hepatic necrosis. A few of these serious cases included fatalities. In most reported cases the relationship to NOLVADEX is uncertain. However, some positive rechallenges and dechallenges have been reported.

In the NSABP P-1 trial, few grade 3-4 changes in liver function (SGOT, SGPT, bilirubin, alkaline phosphatase) were observed (10 on placebo and 6 on NOLVADEX). Serum lipids were not systematically collected.
 
again, ABSOLUTELY IRRELEVANT to the time frames under which bodybuilders use SERMS. Show me ONE study using reasonable dosages and reasonable time frames that indicates an increase in ANY form of tumors in males.

Crowbar
 
Yes, again, ANY hepatotoxic substance will INCREASE--not insure--an elevated risk for hepatic carcinomas--including alcohol.

Crowbar
 
You also did not address the issue of compromised endothelial function, nor the fact the the increased incidence of carcinomas is very low in relation the the actual number of people using these drugs in the real world.

Crowbar
 
again, ABSOLUTELY IRRELEVANT to the time frames under which bodybuilders use SERMS. Show me ONE study using reasonable dosages and reasonable time frames that indicates an increase in ANY form of tumors in males.

Crowbar

P.364-Anabolic Pharmacology

16 week cycle of Deca, Nolva (30mg/day-BTW the recommended max daily dose for cancer is 20mg/day), and Finasteride. Follow that with one of Seth's PCT recommendations, such as switching to Clomid and run that for another 3-4 weeks (or stay with Nolva which gives you 20 weeks or 5 months at 1.5 times the recommended max human dose for 1 cycle). No studies needed that haven't already been cited.

You could probably fit 3x 5 month cycles of Nolva at 1.5 times the max human dose in the span of 2 years if you were so inclined. That would be 15 months of use in 2 years time at 1.5 times the recommended max dose. That makes the following study seem relevant, according to your definition at least.

Granulosa cell ovarian tumors and interstitial cell testicular [I think testicles imply male mice] tumors were observed in two separate mouse studies. The mice were administered the trans and racemic forms of tamoxifen for 13 to 15 months at doses of 5, 20 and 50 mg/kg/day (about one-half, two and five-fold the daily recommended human dose [that's 20mg/day for humans] on a mg/m² basis).

Now...if you could just produce a study that indicates that the non-malignant hepatotoxic effects of Nolvadex are what causes the increased incidence of hepatocellular carcinoma...some of what you just said might make sense. It has to be exact; otherwise, it will be "ABSOLUTELY IRRELEVANT" (lol). I think it is the estrogenic effects of nolvadex that cause the increased risk of hepatocellular carcinoma if anything (personal guess).

If you could support your generalizations and conclusions with something besides capital letters, I might be more inclined to agree with you on some points.

I've wasted enough of my life on this now pointless back and forth banter. At the end of the day, you will take what you want and I will take what I want (just an observation, not the point). I am not here to convince anyone that the tooth fairy doesn't exist; you are entitled to your own opinions and beliefs as am I. I do respectfully disagree with several of your unsubstantiated generalizations in context, and I dislike that you ask for studies and references and dismiss them when provided, and yet provide none of your own to support your sweeping generalizations, comments, and dismissals. I do think you made a few valid points about 5 posts ago, to your credit.


-----------------------------------------------------------------


To the OP, this thread is about Phera and estrogen (obviously). Most of the posts to this thread have absolutely nothing to do with your question, so I apologize for my part and will not post on this thread again. I will in fact delete all of my tug-o-war/irrelevant posts upon request so that others can focus on your actual question(s). To re-cap, I think that an AI or a SERM (or both) can be used to control the estrogenic issues associated with Phera, given that each agent is used properly. Which approach you decide upon will be up to you of course.
 
You also did not address the issue of compromised endothelial function, nor the fact the the increased incidence of carcinomas is very low in relation the the actual number of people using these drugs in the real world.

Crowbar

Welllll, that's true, but...

I still maintain that using an AI from start to finish on cycle will prevent gyno if done properly. I follow with a SERM, but it ends up just coinciding with PCT, so it limits the amount of time that I am on SERMs which is a good thing. I stick with this approach when needed b/c there is no way that I would ever run a SERM for 10 weeks in a row (6 week cycle + 4 week PCT). It is true that an AI cannot make estrogen that is freed from the bound state magically disappear-I think I said this above (it will circulate and can bind to the ER yes), BUT if your body does not continue to produce significant amounts of estrogen (say by using .5mg ed of arimidex for any cycle, AROMATIZING OR NOT), then significant amounts of estrogen will NOT be produced and in turn won't be newly bound by SHBG only to be released later. If the bound-estrogen pool is not being actively replenished by aromatase, then estrogen is not going to be continually dumped from SHBG into the circulating state b/c it won't even be there to be dumped after a while; perhaps after the initial dump of estrogen due to SHBG displacement-I don't know exactly when pre-cycle, bound estrogen would no longer be an issue once AI use has commenced. I think it will take more than one "spurt" of free estrogen in the circulating state to produce any symptoms of gyno.

...you never responded back to one of my counter-responses that was actually relevant to this thread (for the OP anyway). So what is your point?

I would have actually liked to have had some intelligent discussion of the bold part of the quote above from page 1 of this thread b/c I don't know how long it takes for SHBG to dump most of the bound estrogen into circulation when SHBG is highly bound/suppressed due to taking Phera for instance, and I don't know how long that initial dump of estrogen will circulate before being metabolized/reduced/whatever at which point an AI would provide efficacious estrogen control by preventing aromatasation and subsequent binding and release of any additional estrogen which should minimize any chances of gyno given that you don't get gyno the first week. That is actually why I came back to this thread. But clearly that is now water under the bridge.

No disrespect, but if you just want to argue, get married. If you are married, go argue.
 
OK, to put this in very clear perspective two experts in the field--Seth Roberts and Bill Roberts--do not buy your arguments. Now maybe you know more than they do concerning these subjects, but I highly doubt it! As a final thought, here's Bill Robert's response to your cited studies:

1) Tamoxifen is known to be estrogenic in the uterus. For this reason it is inferior for women to raloxifene, as tamoxifen can promote estrogenic uterine cancer while raloxifene cannot, or not directly anyway.

(The reason for the qualification is that in pre-menopausal women, raloxifene can increase estrogen production, confounding the issue with regard to the uterus and endometrium.)

So unless your friend has a uterus, the study is not relevant.

2) Tamoxifen has been around for decades in actual human use and is not considered to be a danger for causing cancer, other than the above which is due estrogenic activity and is not relevant to men.

But if your friend wants to be afraid of it, that's his prerogative.

He also does not know much about their use, as they are also used in women who don't have breast cancer but are thought to be at risk for it, and raloxifene is used for osteoporosis prevention or treatment.

I'd suggest giving up the idea of changing this person's mind, if you have that idea. It is ordinarily a fruitless task. I recall that in my teens and maybe early (very early) 20s I felt it was important to try to change the minds of the stubborn when they are wrong, but it didn't take long to learn how fruitless and pointless that was. When people cling to error, that is their problem, not yours or mine... this really is the best way to look at it, I'd suggest. The most it's worth is a single statement of actual relevant facts, but when this is vehemently rejected, then I'd just not bother pursuing it further, really.


Crowbar
 
P.364-Anabolic Pharmacology

16 week cycle of Deca, Nolva (30mg/day-BTW the recommended max daily dose for cancer is 20mg/day), and Finasteride. Follow that with one of Seth's PCT recommendations, such as switching to Clomid and run that for another 3-4 weeks (or stay with Nolva which gives you 20 weeks or 5 months at 1.5 times the recommended max human dose for 1 cycle). No studies needed that haven't already been cited.

Just wanted to clarify that none of the cycles (or any of the information) in my book are in any way meant to be recommendations of any drug, cycle, stack or dosage of any substance legal, illegal or otherwise. The cycles outlined are meant to be examples of current and past steroid usage by athletes.

I don't think anyone (at least not me) is saying that tamoxifen or clomid are without side effect or risk. However, AI's also have inherent risks as do unproven OTC supplements so it is up to the user to decide what risk/benefit profile is acceptable for their own purposes. Also, oral C-17 alpha alkylated AAs have been shown to cause precancerous and cancerous tumors of the liver. Just an FYI as to the relative dangers since tylenol and alcohol have been thrown out there as hepatotoxic substances.
 
No disrespect, but if you just want to argue, get married. If you are married, go argue.

To the OP, this thread is about Phera and estrogen (obviously). Most of the posts to this thread have absolutely nothing to do with your question, so I apologize for my part and will not post on this thread again. I will in fact delete all of my tug-o-war/irrelevant posts upon request so that others can focus on your actual question(s). To re-cap, I think that an AI or a SERM (or both) can be used to control the estrogenic issues associated with Phera, given that each agent is used properly. Which approach you decide upon will be up to you of course.

Seth-you are correct; I forgot that you explicitly state that you aren't recommending the use of any steroids or stacks in your book (in the preface I think). My apologies for mispresentation.
 
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