Common Cures and treatments for Gyno

[biggiesmallz]

Article Outline

References
A selective estrogen receptor modulator (SERM) is a compound that can act as an estrogen agonist or antagonist, depending on the specific target tissue (1). At present, four SERMs are approved for clinical use: clomiphene, raloxifene, tamoxifen, and toremifene. Most of the unique pharmacology of SERMs can be explained by three interactive mechanisms: [1] differential estrogen-receptor expression in a given target tissue, [2] differential estrogen-receptor conformation on ligand binding, and [3] differential binding to the estrogen receptor of coregulator proteins (2) and (3).

In women, SERMs have been shown to increase gonadotropin circulating levels, which are based on the estrogen antagonistic properties of SERMs at the hypothalamic and pituitary level (4). In addition, it has been shown that the estrogen agonist activity of SERMs in the liver causes a significant increase of sex hormone***8211;binding globulin (SHBG) levels (2) and (3).

There have been relatively few studies of SERMs in males. Tamoxifen citrate was introduced 30 years ago as an empiric treatment for idiopathic oligozoospermia because of its stimulatory action on gonadotropin secretion and its postulated direct effects on Leydig cell function and 5***945;-dihydrotestosterone production in seminiferous tubules and epididymis (5). As a result, the administration of tamoxifen led to a twofold increase in spermatozoa concentration. However, this particular SERM has not been shown to induce any marked changes in motility and morphology (6) and (7).

The effect of treatment with tamoxifen citrate on cumulative achievement of pregnancy over a long period of time is similar to that of assisted reproductive techniques (ART) (8) and (9). On the basis of these results (6), (10) and (11), tamoxifen citrate was proposed by a World Health Organization working committee as the first line of treatment for idiopathic oligozoospermia (12).

In a recent study, we have shown that the administration of toremifene, at a dose of 60 mg, once daily, for a period of 3 months in men with idiopathic oligozoospermia is also associated with significant improvements in sperm count and in motility and morphology as well, mediated by increased gonadotropin secretion and possibly a direct beneficial effect of toremifene on the testes. Notably, these findings were indicative of a better testicular exocrine response to treatment in men whose partners achieved pregnancy (22%) compared with those partners who did not (13).

The present study was designed to evaluate, compare, and contrast the effects of three selective estrogen receptor modulators (SERMs), namely, tamoxifen, toremifene, and raloxifene, on the hypothalamic-pituitary-testicular axis in subfertile men with idiopathic oligozoospermia. To the best of our knowledge, no previous study has compared the effects of the three most commonly used SERMs on the hypothalamic-pituitary-testicular axis in men with idiopathic oligozoospermia.

We recruited 284 consecutive subfertile men with idiopathic oligozoospermia, aged 20 to 51 years (mean ± standard deviation [SD] 33.88 ± 4.90 years) from the fertility center of our department for a period comprising the last 3 years. All men were characterized as subfertile because their partners had been unsuccessful in achieving pregnancy for a period of more than 12 months although their partners did not show any of the known causes of female subfertility.

Idiopathic oligozoospermia was defined as quantitative and/or qualitative aberrations of sperm variables according to World Health Organization criteria (12). Men with known or demonstrable causes of oligozoospermia (varicocele, infections, autoimmunity, stress, chromosomal abnormalities, environmental factors, or epididymitis) as well as azoospermic men and men with higher than normal follicle-stimulating hormone (FSH) levels were excluded. All men were examined by the same physician (an endocrinologist).
Careful clinical examination showed that all men had complete development of the secondary sex characteristics, with a mean testicular volume (±SD) of 17.45 ± 3.80 cm3. Total testicular volume was assessed by comparison with a standard value on orchidometry. None of the men had received any medication during the 6-month period preceding the study.

The first 94 men received tamoxifen as monotherapy at a dose of 20 mg daily for a period of 3 months. Consecutively, 99 men received toremifene at a dose of 60 mg daily for the same period, and 91 men received raloxifene at a dose of 60 mg daily for 3 months. At baseline and at the end of the first, second, and third months of treatment, blood samples were collected at 9 am after an overnight fast. All samples were centrifuged immediately, and serum was stored at ***8211;70°C until assayed (within 6 months) for FSH, luteinizing hormone (LH), and testosterone. At baseline and at the end of the third month, we performed semen analysis, and the sperm concentration, spermatozoal motility, and normal sperm forms were determined.

View attachment 554523

All participants were properly informed about the purpose of the study and gave written informed consent. The study was approved by the ethics committee of the hospital.

We measured FSH and LH using the immunoradiometric assay (IRMA) kits from Biosource Technologies (Fleurus, Belgium). Total testosterone was measured by enzyme-linked immunosorbent assay (ELISA; testosterone enzyme immunoassay test kit, LI7603; Linear Chemicals, Barcelona, Spain).
Statistical analysis was performed with SPSS statistical software, v. 15.0 (SPSS Inc., Chicago, IL). Two-tailed statistical significance was set at 5%. The normality of distribution was assessed with the Kolmogorov-Smirnov test. Values that did not fit the normal distribution were log-transformed. Means were compared at baseline with Student's t-test and during treatment with general linear model (GLM)-based two-way repeated measures analysis of (co)variance (AN[C]OVA); time (treatment) was set as the within-groups factor and treatment group (tamoxifen vs. toremifene vs. raloxifene) as the between-subjects factor.

The FSH levels (before and during the 3-month treatment period) in men of the three groups are presented in Table 1. The FSH levels were increased in the men of all three groups (F = 163.05, P<.001), with the greater increase to be observed at the end of the first month of treatment (P<.001). A statistically significant interaction was observed (F = 57.42, P<.001) overall and for each time interval separately. The increase in FSH levels was greater in men from the tamoxifen and toremifene groups compared with men from the raloxifene group, resulting in statistically significantly higher FSH levels in men from the first two groups compared with those in the raloxifene group at the end of the first, the second, and the third months of treatment (P<.05). Moreover, a statistically significant increase of FSH levels was observed in men from the toremifene group at the end of the second and the third months of treatment (P<.001); in men from the raloxifene group, FSH levels were decreased at the end of the second and increased at the end of the third month of treatment (P<.001).

The LH levels (before and during the 3-month treatment period) in men from all three groups are presented in Table 1. The LH levels were increased in the men from all three groups (F = 122.43, P<.001), with the greater increase observed at the end of the first month of treatment (P<.001). A statistically significant interaction was observed (F = 20.05, P<.001) overall and for each time interval separately. The LH increase in men from the tamoxifen and toremifene groups compared with men from the raloxifene group was greater at the first month, resulting in higher LH levels in the tamoxifen and toremifene groups compared with the raloxifene group at the end of the first, second, and third months of treatment (P<.05). No statistically significant increase of LH levels was observed in men from the tamoxifen or raloxifene groups at the end of the first month of treatment; however, a statistically significant decrease of LH levels was observed in men from the toremifene group at the end of the second month, and an increase of LH levels was noticed at the end of the third month of treatment (P<.001). The LH levels were higher in men from the tamoxifen group compared with those of men in the toremifene group at the end of the first, second, and third months of treatment (P<.001).

Testosterone levels (before and during the 3-month treatment period) in men from the three groups are presented in Table 1. Testosterone levels were increased in men from all three groups (F = 190.52, P<.001). A statistically significant interaction was observed (F = 38.83, P<.001) overall and for each time interval separately. In the tamoxifen group, testosterone levels were increased during the first and the second month but were decreased during the third month of treatment, although they remained higher than baseline levels (P<.001). In the toremifene group, testosterone levels were also increased at the end of the first month (P<.001) but with no further changes, resulting in statistically significant lower levels at the end of the second and the third months compared with those of the tamoxifen group (P<.05). In contrast, in the raloxifene group, a less marked increase of testosterone levels was observed at the end of the first month (P<.05) and a gradual decrease to baseline levels thereafter, resulting in lower levels compared with those in the other two groups at the end of the first, second, and third months of treatment (P<.01).

Three selective estrogen receptor modulators (SERMs), namely, tamoxifen, toremifene, and raloxifene, were compared in terms of their effect on the hypothalamic-pituitary-testicular function of men with idiopathic oligozoospermia. The study design was based on substantial evidence concerning the beneficial effects of tamoxifen (8), (9) and (12) and toremifene (13), separately, in this particular population of subfertile men. To the best of our knowledge, no comparative study has been published so far.

Serum FSH and LH (see Table 1) levels were increased after administration of tamoxifen at a dose of 20 mg daily and toremifene at a dose of 60 mg daily. This increase was basically observed during the first month of treatment. This finding indicates that these specific SERMs have a stimulatory effect on hypophyseal gonadotropin secretion due to their well-known antiestrogenic properties (3), (14) and (15).

In the raloxifene group, the gonadotropin increase was significantly less marked. It seems that the antiestrogenic action of tamoxifen and toremifene on hypophyseal gonadotropin secretion is more potent than that of raloxifene. It has to be noted that a statistically significant increase in gonadotropin levels had been observed with the double dose of raloxifene (120 mg daily) in a previous study in elderly men (60 to 70 years old) (16). Therefore, it seems quite likely that the potency of SERM action depends on both the dosage and the endogenous gonadotropin levels.

Tamoxifen and toremifene administration induced a statistically significant increase in total testosterone levels as well. The increased gonadotropin secretion could be the reason for this observed increase in testosterone levels 1 L. Plouffe Jr. and S. Siddhanti, The effect of selective estrogen receptor modulators on parameters of the hypothalamic-pituitary-gonadal axis, Ann NY Acad Sci 949 (2001), pp. 251***8211;258. View Record in Scopus | Cited By in Scopus (11)(1) and (3). It should be noted though that tamoxifen has also been reported to have direct stimulating effects on Leydig cell function (17) and 5***945;-dihydrotestosterone production in seminiferous tubules and epididymis (5) and (18).

Moreover, in a recent report (13), toremifene administration led to a statistically significant increase in both testosterone production and sperm quality. This improvement in testicular function is apparently mediated by both increased gonadotropin secretion and a direct beneficial effect on the testes. In the raloxifene group, a less marked increase in testosterone levels was observed at the end of the first month as well as a gradual decrease to levels that did not differ from baseline. This difference could be attributed to the milder stimulatory effect of raloxifene on hypophyseal gonadotropin secretion.

Our study has shown that the antiestrogenic effects of SERMs at the hypothalamic level result in a significant increase of gonadotropin levels, which is more marked for tamoxifen and toremifene compared with raloxifene. The increase in SHBG levels should be attributed to the estrogenic properties of tamoxifen and toremifene at the liver; in contrast, raloxifene seems to exert an antiestrogenic effect. The greater increase in testosterone levels after administration of tamoxifen and toremifene compared with raloxifene should be attributed to the greater stimulation of gonadotropin secretion, although a direct effect on the testis cannot be excluded.

I think that's all of it, just copied and pasted from closest relevant source I could find. I know there's abstracts of it through pubmed and the like

The effect of selective estrogen receptor modulator administration on the hypothalamic-pituitary-testicular axis in men with idiopathic oligozoospermia.
Tsourdi E, Kourtis A, Farmakiotis D, Katsikis I, Salmas M, Panidis D.
Source

Second Department of Obstetrics and Gynecology, Division of Endocrinology and Human Reproduction, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Abstract

This study evaluates, compares, and contrasts the effects of three selective estrogen receptor modulators (SERMs), namely, tamoxifen, toremifene, and raloxifene, on the hypothalamic-pituitary-testicular axis in 284 consecutive subfertile men with idiopathic oligozoospermia using three therapeutic protocols: [1] tamoxifen, 20 mg, once daily (n = 94); [2] toremifene, 60 mg, once daily (n = 99); and [3] raloxifene, 60 mg, once daily (n = 91). The antiestrogenic effects of SERMs at the hypothalamic level result in a statistically significant increase of gonadotropin levels, which is more marked for tamoxifen and toremifene compared with raloxifene.

PMID:
18692782
[PubMed - indexed for MEDLINE]


And also here's some following renditions of the study from ergolog and ironmagazine;

Ergolog:
ergo-log.com/nolvabest.html

IronMag:
ironmagazine.com/2013/nolvadex-best-t-booster-of-the-serms/

 

[biggiesmallz]

Also if my diction is unclear somewhere feel free to point it out. I don't claim to know everything, in fact I think part of my problem may be referencing things with different words which I feel like I don't have a complete personal understanding of in the first place;

For example; When referring to "estrogen" I do understand that there are various forms of it, but for the purposes of gyno reference I assume that E2 aka Estradiol is the one we're basically worried about, which is most commonly referenced as "Estro or Estrogen or is simply signified by E when speaking of E:T ratios and such as they relate to that understanding, correct me if I'm wrong. And on that same note, what exactly is measured on the female hormonal panel? is it this same form of estrogen?

When I refer to other forms of estrogen, that understanding comes from reading an article about DIM and how it's allegedly effective at getting rid of cancerous forms of estrogen (again, correct me here if I'm wrong as well) Thanks again brother

 

[Austinite]

So, let's see if I understood you guys correctly, because I still feel like somewhere either my basic foundational information is wrong.


What I meant by "all-around-SERM" is that it's multi-faceted, meaning not only is it effective at promoting healthy testosterone production through stimulating the HPT axis, but is also very effective at blocking estrogen from binding to estrogen receptors, and/or for treatment of gynecomastia.

The beneficial effects that tamoxifen has on testosterone production I deduced from this study, which I assume all of you have seen; 3 month greek study done on testosterone production with raloxifene,torem,and nolva

View attachment 554521


This is also why I mentioned that raloxifene does not seem to be a good candidate for the purpose of recovering testosterone levels solely; it simply is not as effective at doing so out of all of our other options. So, perhaps I don't have the most complete understanding of the functions of raloxifene in relation to gonadatrophin production, would welcome any enlightening input there.



Also, as far as this business of "rebound gyno", being on other boards I've seen virtually the same repetitive reaction of guys taking a PCT for a standard 4-6 week oral cycle with nonaromatizeable compounds, and then some time post SERM post cycle therapy (pct), say a month or two or three down the road, the end up getting symptoms of rebound gyno.... hence the development of the understanding that it must be caused by estrogen, and that running a mild suicidal Aromatase inhibitor (AI) with the SERM (something like 6-oxo, or Arimistane or even Aromasin) should basically get rid of this further development. Yet, you have stated;



Now, you specifically advise against the approach of running an Aromatase inhibitor (AI) outside of direct cycle use, and further state that Post Cycle recovery should only include SERM treatment (this, for the cases of short oral cycles, say 4-6 weeks, where Human Chorionic Gonadotropin (HCG) use would simply be impractical or unnecessary). Did I understand you correctly? And why is that?

Also, it has been my understanding that SERMs elevate circulating estrogen, so I don't see how the possibility of estrogen rebound post-SERM use is avoided if we only use SERM treatment during post cycle therapy (pct). Even on the basic level, SERMs artificially raise testosterone production to or slightly above baseline in most cases, which means more conversion to estrogen during a time when your T:E ratio is already off-balanced to favor Estradiol (in the cases when you have just finished a cycle and your endogenous T production is practically nil). So it makes sense to me that SERMs can potentiate further production of estrogen, bringing it further off balance, leading further into gynecomastia land. Or is my understanding somewhere flawed? Thanks.

Also, you had mentioned above that torem and tamox are not even close when it comes to comparison of function, yet their chemical structure is very similar, I understand they are not the same, but I assumed they were close given that fact. Also I've seen numerous studies where Torem ended up being slightly more effective than Tamox at reversing or regressing developing gyno. (hence my suggestion in the OP that Ralox, nolva and torem are practically interchangeable when it comes to the application of gyno treatment, ralox being the more favored one obviously) I can find some and post here for reference if want, or if you are also familiar with the general knowledge then I would appreciate a comment on Toremifene's proper use. For me personally I've noticed my body just takes well to it for PCT purposes, but didn't have it on hand when I had my gyno flare up so used nolva instead.

You also said Adex at 1mg daily is ludicrous.. I sort of understand that, but at the time it was corrective measure that was the issue. So I had been taking it at 1mg weekly as preventive measure, and then about 4 months down the road the lumps crept up. I waited another 2 months or so before I did anything about them. Here's another thing I'm fuzzy on; you said that SERM treatment for the purposes of gyno reversal would generally take longer than 2-6 weeks, but I was able to reverse my lumps with nolva/adex/lil bit of letro within a matter of 3 weeks completely. So I assume the responsible drugs were the adex and letro? and less so the nolva?

Those are the basic fuzzy misunderstandings and misconceptions that I can think of at the moment, thanks again for your time and input

No. I never said hCG would be impractical during post cycle therapy (pct). I said hCG is a terrible idea. Impractical would tend to be acceptable in some cases. There are no cases where hCG is acceptable post cycle when used by an individual who is not under care for a restart.

There are 2 ways that could potentially desensitize Leydig Cells:

1. Prolonged LH deprivation: When you inject steroids, your LH production is halted at the pituitary, remember? So if you continue in a suppressed state for weeks upon weeks, your Leydig Cells could potentially become unresponsive, or desensitized. It is possible to reverse desensitization of the cells, but that has been proven to be quite a difficult task. So when you use hCG on cycle, the mimicked LH analog will maintain stimulation of Leydig cells so that you don't run the risk of rendering them useless. This level of maintenance will ensure a much healthier and speedy recovery and one of the most important reasons to use hCG on cycle.

2. Over stimulation/supplying of Leydig cells: There is no reason to use more than 500 IU of hCG at one time. And certainly not a good idea to run even that dose on a daily basis. You do not have an unlimited-ever-flowing-supply of Leydig cells. There is only so much stimulation hCG can do. What happens when you dose hCG really high, is that you're increasing intra-testicular estrogen. So you're thinking that you could use an aromatase inhibitor in that case, right? Nope. AI's are not effective treatment for intra-testicular e2. Furthermore; high doses is a surefire way to desensitize Leydig Cells. So we have a double whammy here. And this is just another reason to use hCG on cycle, and not "blast" hCG post cycle leading up to and/or during post cycle therapy (pct).

hCG is suppressive. Since we know that hCG mimics LH, then we know that in the presence of exogenous LH, the pituitary gland will not produce LH. which one is natural? The one I just induced by using hCG, or the one coming from the pituitary? The pituitary of course! So why? Why on earth would you want to suppress your pituitary with hCG when you're trying to recover?! Are we clear on this one?

For the sake of preventing another debate, Rich Piana is clueless. I know many nonsensical theatrics stem from him.

As for an Aromatase inhibitor (AI), when would it be necessary post cycle? This goes back to your original post regarding ratios. You're merely creating an imbalance. While I stated in the original reply that you cannot create a balance on cycle due to supraphysiological serum testosterone, this is not the case during post cycle therapy (pct). And in fact, you would create an imbalance. How many estrogen combating drugs do you need? Your experience with 6-Oxo is fine, but that is not what we're discussing here.

Look, I've already done my research and I know that you're a long lasting members of a Prohormone board (which is where the original posted was copied from). You need to understand that the ideology of a "Knowledgeable member" at the prohormone board will never mesh with that of a steroid board. This would simply be a never ending battle.

Chemical structures? Can you explain a chemical structure? Because I can cite every metabolic pathway for any of the serms. Which ALL share similar pathways with the exception of Raloxifene. Tamox is in fact merely identical to Nolvadex (if we're talking chemical structures). They vary when nolvadex is moved to its metabolite; endoxifen via P450 pathway. Same with Clomiphene by the way...

There is nothing wrong with Torem for post cycle therapy (pct). I have no idea once again where I might have said that. It's closer to Clomiphene than it is Tamoxifen. Clomid and Nolva for post cycle therapy (pct), or Torem and Nolva would generally suffice. Not Torem and clomid. Your experience is not something that needs to be dissected. You used too many compounds and attempting to analyze each, and which one actually offered most benefit is a cumbersome task. No way I would dive into that arena. This would be like eating 3 different exotic foods and attempting to find out which one caused poisoning.

Your gynecomastia prevention in a few weeks with Adex caused a rebound, as you admittedly stated your lumps appeared later on. So in fact, you did not prevent gynecomastia. So I'm not sure why we're talking about the period in which it takes to reverse gynecomastia. Had you used Nolvadex, there would never have been a rebound. the preventative measure you took was merely a mask, abused by high doses of arimidex.

Your second round, where you attempted reversal is not relevant. Again, there are no studies done on using 3 compounds for the sake of reversal. Of course if you demolish (unsafely) your e2 it would lessen the lumps. You're citing random studies, but not once have you mentioned your own blood work. I'm entirely confused by this, or simply blind.

You have to understand that you could be hypersensitive, which in fact could yield speedy results to any compound. Although you're using outrageous doses. This is not healthy. Refer back to my example of killing a fly with a baseball bat. these methods are never, under any circumstances, in any scenario, ever discussed among endocrinologists and/or urologists. Because it is simply unacceptable and unethical to put a patient through any of this. An attempt at a study would leave the ethics committee furious.

Try not to over think this stuff. Use proven, recently studied methods on men, not women; as we differ. And certainly nt studies on mice. lastly, no need to reference anything done in the 70's. We are far too advanced to reference what we did in the 70's for most cases. Some things were never even discovered until recently, such as hepcidin, which was discovered in 2000, and it's suppression from steroids causes excess RBC production. Before that, we merely speculated. Not telling you not to research, but try to stay current with some of the research.

 

[biggiesmallz]

I see... well put, and yes we are absolutely clear on the Human Chorionic Gonadotropin (HCG). Also just to clarify I never suggested that you said torem was not an acceptable means for post cycle therapy (pct). All I was hoping to understand is why you failed to mention it in your original reply as an acceptable form of treatment for gyno (your very first reply only refers to nolva or raloxifene).

As far as the studies, I don't know what to tell you honestly; I haven't been in this game that long, and the only studies that were available to me for understanding through direct contact were the older studies... so I have to build a base somewhere, right? This is actually the first opportunity to clarify some of the flaws inherent in that age-old approach (from those foundational studies) after all it was from learning of that past material, that we now know what we know in the first place. I admit I simply don't have up-to-date information, that's part of why I came here in the first place. For what it's worth all of your input has been greatly appreciated, since it may shed some light on some of the other less up-to-date ways that I come across on the daily which are parroted as "the right way to do things" on the forums I frequent which you're familiar with.

On that same note, just for personal benefit for absolute clarification;

You are saying that the best actual treatment option for gyno would be:
1. Preventive measure of Aromatase inhibitor (AI) run during the cycle if needed (with testosterone, for example, or other aromatizing compounds)
2. Corrective measure of SERM treatment (ralox or nolva) if it pops up

And for off-cycle, or in cases of Post-cycle (so PCT or post-PCT) treatment of gyno should be limited to SERM-only treatment? And no rebound should occur, bloodwork verification a must.

The reason I haven't gotten any bloodwork to discuss is because my personal position and situational circumstances simply don't give me constant access to it (in transition between jobs and lacking transportation) so I'm left to kind of use my own best judgement and the best information I have available to me to steer my way through my own medical treatment (prior military service injuries, hence the need for anabolics... hospital only offered me support braces and percocets, both of which are utterly useless)

In a perfect world, I understand clearly exactly what you're saying, and do understand the significance of needing to get bloodwork consistently, and will do so towards the end of this run and probably around PCT and post PCT time the best I can manage within my own ability. But, this situation came up, so it was an attempt at trying to tackle the problem at hand and in the process the hope was also to help others gain clearer understanding of it themselves.

In any case, long story short, I thoroughly appreciate all of your gracious input and clarity, harder to find that from where I came from. I'm sure you're also familiar with the ridiculous level of magical broscientists that frequent those prohormone boards, I was just trying not to get caught in the same loop. Thanks again

 

[Austinite]

^ I didn't mention Torem because I did not disagree with you. I only quoted what I disagreed with originally.

You are saying that the best actual treatment option for gyno would be:
1. Preventive measure of Aromatase inhibitor (AI) run during the cycle if needed (with testosterone, for example, or other aromatizing compounds)
2. Corrective measure of SERM treatment (ralox or nolva) if it pops up

Yes. Aromatase inhibitor (AI) on cycle, and if you are hypersensitive, you can use Nolvadex on cycle at 10 to 20mg daily, and it would aid in estrogen rebound prevention as well.

Ralox or nolva for reversal of existing gynecomastia is the safe and effective way of treatment without adverse effects for majority of human males.

 

[heavyiron]

Good discussion here guys!

 

[biggiesmallz]

^o, hai! I guess you've already been here, so no introduction is necessary, welcome to the chat

Austinite, quick clarification if I may;

There are 2 ways that could potentially desensitize Leydig Cells:

1. Prolonged LH deprivation: When you inject steroids, your LH production is halted at the pituitary, remember? So if you continue in a suppressed state for weeks upon weeks, your Leydig Cells could potentially become unresponsive, or desensitized. It is possible to reverse desensitization of the cells, but that has been proven to be quite a difficult task. So when you use hCG on cycle, the mimicked LH analog will maintain stimulation of Leydig cells so that you don't run the risk of rendering them useless. This level of maintenance will ensure a much healthier and speedy recovery and one of the most important reasons to use hCG on cycle.

2. Over stimulation/supplying of Leydig cells: There is no reason to use more than 500 IU of hCG at one time. And certainly not a good idea to run even that dose on a daily basis. You do not have an unlimited-ever-flowing-supply of Leydig cells. There is only so much stimulation hCG can do. What happens when you dose hCG really high, is that you're increasing intra-testicular estrogen. So you're thinking that you could use an aromatase inhibitor in that case, right? Nope. AI's are not effective treatment for intra-testicular e2. Furthermore; high doses is a surefire way to desensitize Leydig Cells. So we have a double whammy here. And this is just another reason to use hCG on cycle, and not "blast" hCG post cycle leading up to and/or during PCT.

Now, I understand the proper usage of Human Chorionic Gonadotropin (HCG) on-cycle... generally advised at 250iu bi-weekly, sometimes at 500iu bi-weekly, but from the source I came across they referenced a study that basically said there's marginal benefit from Human Chorionic Gonadotropin (HCG) when pinning 250 vs 500 bi-weekly, so with that understanding I don't see the need to pin more than 250. That said, is there some limited duration to which Human Chorionic Gonadotropin (HCG) should be used on-cycle?

What I mean here is that generally standard AAS cycles are no more than 16 weeks, for the most part. I have been on mine for about 5 months, and am probably going to extend it another 2-3 months or so to get as much physical recovery/reconstruction out of it as possible. That said, I stopped pinning the Human Chorionic Gonadotropin (HCG) a couple of months ago because I also heard conflicting information on long-term Human Chorionic Gonadotropin (HCG) use can possibly desensitize lydig cells to natural LH response. Any truth to that? And given that scenario, what would be the optimal usage of Human Chorionic Gonadotropin (HCG) in this particular situation?

I understand these are probably "newbie" questions to you in a way, and I'm sorry to have to make you repeat that which for you I assume is basic knowledge at this point, but it would be easier for me to just have everything out in a more interactive way completely, than to have to track down every piece just for tid-bits of clarification.

The other thing I wanted to ask you about, is you mentioned nolva and clomid actually work synergistically towards the re-establishment of testosterone production and spermagenesis when combined together in a PCT protocol, would the same synergy hold true for torem and clomid? Was planning to use this in post cycle when I get to it.

And what are your thoughts on using triptorehlin (gonadotropin-releasing hormone agonist) at 100micrograms to start off the post cycle therapy (pct), then followed by the double-SERM combo for full recovery? Too much polymedicating? Unnecessary? Or potentially useful? Thanks again, that's all the personally-relevant loose ends I could think of at the moment

 

[DreDay187]

^o, hai! I guess you've already been here, so no introduction is necessary, welcome to the chat

Austinite, quick clarification if I may;


Now, I understand the proper usage of Human Chorionic Gonadotropin (HCG) on-cycle... generally advised at 250iu bi-weekly, sometimes at 500iu bi-weekly, but from the source I came across they referenced a study that basically said there's marginal benefit from Human Chorionic Gonadotropin (HCG) when pinning 250 vs 500 bi-weekly, so with that understanding I don't see the need to pin more than 250. That said, is there some limited duration to which Human Chorionic Gonadotropin (HCG) should be used on-cycle?

What I mean here is that generally standard AAS cycles are no more than 16 weeks, for the most part. I have been on mine for about 5 months, and am probably going to extend it another 2-3 months or so to get as much physical recovery/reconstruction out of it as possible. That said, I stopped pinning the Human Chorionic Gonadotropin (HCG) a couple of months ago because I also heard conflicting information on long-term Human Chorionic Gonadotropin (HCG) use can possibly desensitize lydig cells to natural LH response. Any truth to that? And given that scenario, what would be the optimal usage of Human Chorionic Gonadotropin (HCG) in this particular situation?

I understand these are probably "newbie" questions to you in a way, and I'm sorry to have to make you repeat that which for you I assume is basic knowledge at this point, but it would be easier for me to just have everything out in a more interactive way completely, than to have to track down every piece just for tid-bits of clarification.

The other thing I wanted to ask you about, is you mentioned nolva and clomid actually work synergistically towards the re-establishment of testosterone production and spermagenesis when combined together in a PCT protocol, would the same synergy hold true for torem and clomid? Was planning to use this in post cycle when I get to it.

And what are your thoughts on using triptorehlin (gonadotropin-releasing hormone agonist) at 100micrograms to start off the post cycle therapy (pct), then followed by the double-SERM combo for full recovery? Too much polymedicating? Unnecessary? Or potentially useful? Thanks again, that's all the personally-relevant loose ends I could think of at the moment

The objective with hCG is to maximize stimulation of the testes so their original mass is recovered more quickly than if we relied solely on physiological LH production. It is important that hCG not be overused. Testicular sensitization to this hormone is a delicately regulated mechanism. When hCG is taken for too long or at too high a dosage, the LH receptor can become desensitized.355 This can actually interfere with recovery of hypothalamic-pituitary-testicular axis.

Excerpt From: Llewellyn, William. ***8220;Anabolics.***8221;

Proc Natl Acad Sci U S A. 1981 Oct;78(10):6309-13.
Desensitization to gonadotropins in cultured Leydig tumor cells involves loss of gonadotropin receptors and decreased capacity for steroidogenesis.
Freeman DA, Ascoli M.
Abstract
The ability of human choriogonadotropin (hCG) to regulate its receptors and target cell responses has been studied in a clonal strain of cultured Leydig tumor cells (MA-10). Exposure of the MA-10 cells to hCG results in decrease in hCG binding activity which is dependent on time and the concentration of hCG. This decrease is due to a change in the number of receptors rather than in the affinity of the receptors, and it is accompanied by a corresponding reduction in the ability of hCG to stimulate steroidogenesis. Exposure of the MA-10 cells to hCG also resulted in a reduction of the steroidogenic responses to cholera toxin and 8-Br-adenosine cyclic 3',5'-monophosphate. The hCG-induced loss of steroidogenic responses to these stimuli seems to be due to the stimulation of steroidogenesis rather than to the decrease in hCG receptors because it also can be induced when steroidogenesis is stimulated with cholera toxin or 8-Br-adenosine 3',5'-monophosphate under conditions such that the number of hCG receptors is not reduced.
PMID: 6273862 [PubMed - indexed for MEDLINE] PMCID: PMC349028

On-Cycle:

Bodybuilders and athletes may also administer Human Chorionic Gonadotropin throughout a steroid cycle, in an effort to avoid testicular atrophy and the resulting reduced ability to respond to LH stimulus. In effect, this practice is used to avoid the problem of testicular atrophy, instead of trying to correct it later on when the cycle is over. It is important to remember that the dosage needs to be carefully monitored with this type of use, as high levels of hCG may cause increased testicular aromatase expression (raising estrogen levels),771 and also desensitize the testes to LH.772 As such, the drug may actually induce primary hypogonadism when misused, greatly prolonging, not improving, the recovery window. Current protocols for the use of hCG in this manner involve administering 250 IU subcutaneously every 3rd or 4th day throughout the length of the steroid cycle. Higher doses may be necessary for some individuals, but st no point should exceed 500 IU per injection.

These on-cycle hCG protocols were developed by Dr. John Crisler, a well-known figure in the anti-aging and hormone-replacement field, for use with his testosterone replacement therapy (TRT) patients.

Excerpt From: Llewellyn, William. ***8220;Anabolics.***8221; iBooks.

Med Biol. 1986;63(5-6):192-200.
The different mechanisms for suppression of pituitary and testicular function.
Sandow J, Engelbart K, von Rechenberg W.
Abstract
The differential mechanisms reducing androgen secretion by LHRH agonists are discussed with relevance to clinical therapy. LH secretion can be desensitised by exposure to agonists using high doses, frequent injections or sustained release/constant infusion. The desensitized pituitary is refractory to hypothalamic stimulation. Pituitary receptor suppression is associated with depletion of pituitary gonadotrophin content, and a decline of LH and FSH secretion to a basal rate. Recovery of LH responsiveness to endogenous LHRH stimulation requires restitution of gonadotrophin content (about 7 days in rats). After long-term infusions in normal men, testosterone secretion recovers within 7-10 days. The binding capacity of testicular LH/hCG receptors is reduced in rats after supraphysiological gonadotrophin stimulation, by agonists or directly by hCG, concomitantly the steroidogenic capacity of the testis in vitro is impaired. Qualitative changes in androgen biosynthesis are a marked fall in testosterone production and dose-dependent enhancement of progesterone production. After 12 months of buserelin injections, the changes in hCG-stimulated rat testes are an increased ratio of progesterone/17-OH-progesterone (inhibition of 17-hydroxylase), a reduced capacity for secretion of androstenedione and testosterone (block of 17,20-desmolase), and increased 5 alpha-pregnane-3,20-dione (this steroid inhibits the 17,20-desmolase, similarly to progesterone). After treatment, Leydig cell function recovers completely. Leydig cell hyperplasia is observed as a result of the steroidogenic changes. These findings in rats have not been observed in dogs, monkeys or in humans.(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 3010006 [PubMed - indexed for MEDLINE]

There's truth to the desensitization claims.

 

[Austinite]

Now, I understand the proper usage of Human Chorionic Gonadotropin (HCG) on-cycle... generally advised at 250iu bi-weekly, sometimes at 500iu bi-weekly, but from the source I came across they referenced a study that basically said there's marginal benefit from Human Chorionic Gonadotropin (HCG) when pinning 250 vs 500 bi-weekly, so with that understanding I don't see the need to pin more than 250. That said, is there some limited duration to which Human Chorionic Gonadotropin (HCG) should be used on-cycle?


What I mean here is that generally standard AAS cycles are no more than 16 weeks, for the most part. I have been on mine for about 5 months, and am probably going to extend it another 2-3 months or so to get as much physical recovery/reconstruction out of it as possible. That said, I stopped pinning the Human Chorionic Gonadotropin (HCG) a couple of months ago because I also heard conflicting information on long-term Human Chorionic Gonadotropin (HCG) use can possibly desensitize lydig cells to natural LH response. Any truth to that? And given that scenario, what would be the optimal usage of Human Chorionic Gonadotropin (HCG) in this particular situation?

I understand these are probably "newbie" questions to you in a way, and I'm sorry to have to make you repeat that which for you I assume is basic knowledge at this point, but it would be easier for me to just have everything out in a more interactive way completely, than to have to track down every piece just for tid-bits of clarification.

The other thing I wanted to ask you about, is you mentioned nolva and clomid actually work synergistically towards the re-establishment of testosterone production and spermagenesis when combined together in a PCT protocol, would the same synergy hold true for torem and clomid? Was planning to use this in post cycle when I get to it.

And what are your thoughts on using triptorehlin (gonadotropin-releasing hormone agonist) at 100micrograms to start off the post cycle therapy (pct), then followed by the double-SERM combo for full recovery? Too much polymedicating? Unnecessary? Or potentially useful? Thanks again, that's all the personally-relevant loose ends I could think of at the moment

Alright. I don't think any of your questions are "newbie" questions. These are all things that the majority ignore because it requires thinking. However, your questions are already answered above, you simply rephrased the questions ... so myanswers will remain the same, but I'll rephrase them for the sake of the discussion.

There's only so many cells to stimulate, and the doses of 1500 weekly max, spread over 3 or more doses is sufficient enough. If long term therapy was dangerous at those doses, it would mean that our very own production would desensitize cells, doesnt make sense, does it? 250 IU is not necessarily the magic number. Your goal should be to use the least amount of hCG that works for you. Recently, discussing my concerns with the lead urologist in Houston, TX, we came to conclude that for me, as a testosterone replacement therapy (TRT) patient, my usual dose of 250 twice weekly is excessive. So we are planning on reducing the dose to 100 IU, 3 times weekly. Note that this urologist is not my doctor, but a friend and partner in a clinical trial.

Blasting hCG is unhealthy, and the increase in intratesticular E2, which cannot be managed with the commonly readily available aromatase inhibitors, is damaging.

With regards to coupling Toremifene and Clomiphene, research would yield a negative conclusion. Large emphasis on the word "research" as this is not an experienced opinion. Toremifene and clomiphene are closer to a match, which would render them FSH dominant, vs both; LH and FSH. Both of these compounds are more effective solely, at sensitizing your pituitary cells to gonadotropin releasing hormones. Nolvadex is not as impactful, although effective. Because of the reasons I mentioned earlier, Nolvadex should always be a staple in post cycle therapy (pct), and coupled with either Clomiphene or Toremifene.

I have no comments regarding triptorelin.

 

[biggiesmallz]

I see, thank you kindly All clear on the eastern front, just need to disseminate the finer adjustments to my self-proclaimed personal gyno guide
View attachment 554524


Also if anyone has any further input on triptorehlin I would be interested in its proper application. Experientially I've found very limited information on it, I do know the case that its advocation "sprung up" from, but after digging into bloodwork on various forums I wasn't able to find any relevant consistency in it's application. So either the product sourcing is unstable, or the product itself is not a consistent means of stimulating HPTA production (warning labels of possible chemical castration aside)

 

[Austinite]

heh, at one point I thought gynecomastia was prolactin induced

 

[Maintenance Man]

I know I've said it before but sometimes I feel like the Lawnmower Man instead of Maintenance Man. This knowledge and info is tingling my synapses and neurons to the point I'm not sure how fast I can real it all in!!! This is a great discussion guys. Glad you're back Austinite. Nice to have another knowledgeable member like yourself biggiesmallz

 

[biggiesmallz]

Uno mas

how significant is impact of nolva/clomid on IGF-1 levels? (what does that even mean physiologically speaking?) I assume they recover naturally like everything else and that temporary SERM treatment for the purposes of PCT is fairly negligible in the long run, I just don't understand it's relative significance; hence my personal favoring towards torem, which AFAIK has no impact on IGF levels. Thanks

 

[DreDay187]

Uno mas

how significant is impact of nolva/clomid on IGF-1 levels? (what does that even mean physiologically speaking?) I assume they recover naturally like everything else and that temporary SERM treatment for the purposes of PCT is fairly negligible in the long run, I just don't understand it's relative significance; hence my personal favoring towards torem, which AFAIK has no impact on IGF levels. Thanks

I believe it's limited to Nolva and doesn't include clomid and as far as I have read the impact is minimal with little significance. But then there's the fact I've only seen one study so I domt know if it was even replicated or not.

 

[biggiesmallz]

Thanks, I just realized the study I saw which shows negative impact of clomid on IGF levels was done on women. No concrete evidence that this holds true for males

 

[biggiesmallz]

Thanks again guys, pleasure working with you. Hopefully this will clear out some of the circulating crap going around the places I learned from, and give a more consistent and medically founded/sound way of approaching the issue.

Austinite, your input has been simply invaluable. Thank you all for contributing, every little bit helped.

Now for some lulz

And all is right in the world again

 

[biggiesmallz]

What kind of gains can I expect on my PH/DS/AAS Cycle?

One more common question I wanted to address, kind of unrelated, but relevant to all the stuff in the OP. You guys feel free to distribute the understanding where applicable, I just see this same thing posed by everybody that starts any kind of cycle, oral or AAS.

This is a wonderful question to consider, that applies to many other areas of life, not just bodybuilding, so let's take a look at it;

What can I expect to gain? Or, what is a realistic expectation?

Nothing, truth be told. Do not expect anything! What do I mean by this? Basically put, any and all of your expectations are going to be wrong. All expectations are wrong, because all expectations are unnatural. If you expect a specific result, there is EVERY CHANCE that you will be frustrated. Expectation, in it's nature, leads to frustration... in it's very nature.
I'm just uncovering the fallacy... how many times have you expected something to happen, and something completely different happened alltogether... then u're left frustrated. The frustration is because of expectation. The outcome of expectation is frustration, so frustration is reactive of expectation...

Just the way things are. If we drop expectation tho, then everything that happens is unexpected, adds to the mystery And then 5lbs, or 10lbs, or 15lbs, everything is equally appreciated cuz you get what you get, there's no expectation so there's no frustration, then whatsoever happens is just dandy. Then it's just a pure experience.

we don't have to do anything with frustration, we simply need to understand what expectation is properly... so let's take a look at that;

What is expectation?

Your expectation is always for a specific result; one specific desired effect out of all potential effects possible. If your expectation gets fulfilled, then you will be happy. But if it does not, then you will feel cheated somewhere and will be frustrated with life because it's not going according to your expectations. And expectations are rarely fulfilled... Let's take a look at why, with a quick example;

Example; Let's assume that you have heard, from all over the world, that hazlenuts are the best nuts in the world. You've never tried a hazlenut before, but since everyone seems to be making the same statement, you wanna see if there is any truth to it. So, you decide you're going to grow your own hazelnut tree. So you spend 2 thousand dollars, and 2 years of labor growing and nurturing this tree. Your only desire is to try one hazelnut, pure and natural, to see what everyone is talking about... So when the harvest time finally comes around, you pick the first nut you come to, and you expect it to have nuts... you're very excited, you go to your kitchen, get a nutcracker, and break the nut open... and lo and behold;

IT'S A DUD!!

View attachment 554534


IT'S EMPTY. BECAUSE YOU WERE EXPECTING A NUT, YOU ARE GOING TO BE PISSED OFF AND FRUSTRATED, AND MAY CURSE THE WHOLE TREE OUT OF THAT FRUSTRATION.

The thing is, your expectation was NOT unrealistic... it simply wasn't according to the way life functions. All expectations are for a specific result, for a desired effect... for one potential possibility of fruit from the tree of nature. But the tree itself does not live according to your expectations, the tree provides both... good nuts, and the occasional empty bad nut; this is just the way things are. Now, if you were expecting a good nut, and you get an empty dud, you will be pissed off, curse the tree, and curse the whole world for lying to you. You may burn the tree and tell all your friends off... but, if you didn't have any expectations, and you opened a nut, saw it was empty, saw the facticity of it, you wouldn't be frustrated because you had no expectations in the first place, you just wanted to see what it was... so you move on to the next nut on the tree, and lo and behold;

View attachment 554533

EUREKA! The holy grail of hazelnuts! Full, whole, and actual The tree is capable of providing both, but the tree does so unrelated to your expectations. So to expect any specific desired result, is simply setting yourself up for a possible frustration. Either expect ALL possible results, or drop expectation all together.

Do YOU think it's reasonable to expect 15 lbs? what happens when you hit 14.7 lbs, or 12.3 lbs? or if you have to go on some trip halfway through and never get a chance to finish the 6 weeks? or a thousand and one other things that can happen in life in a moment's notice?


So then how am I supposed to lift bro?


To answer this question, a 15 lb gain would depend on a ton of factors from food intake, to training and rest, to personal physiology (none of which are guaranteed to provide you that 15 lbs). Some guys take tbol for 6 weeks and gain 20 lbs, other guys can't seem to gain 5. So, does that put the supplement in question? or the person? I've tried tbol, so I can tell you the supplement is certainly not in question... it does SOMETHING. The rest just boils down to what you do with the supplement. So again, am I going to tell you that it's a realistic and guaranteed expectation to have for 15lbs? No, no one in their right mind would tell you that. It's a possibility, sure. From possibility, to actuality, the process would depend on you and your circumstances, and what you do with it all.


That's all I got, thanks again folks

 

[biggiesmallz]

Austinite, just wanted to add one more thing;

You are absolutely correct with your information, it's very accurate, but one point you were only HALF correct on... your baseball bat analogy. The thing is, I understand the reason for your suggestions of low dosing and minimal possible effective dosage, because YOU, my dear friend, are hypersensitive to the substances. I completely understand that, and there is nothing wrong with that, but given that consideration we are also missing the other half of the population.

When you said 2.5mg pharma-grade letro will destroy you, I understand the reason behind that statement... because generally speaking pure-letro protocols are pure hell, they crush all estrogen in the entire system, they leave your "dick string in the dirt" so-to-speak, scuse the language but it's relevant to the point; libido is nonexistent. Joints dry out, and overall general lethargy from depletion of estrogen, as well as possible weight fluctuations are all no bueno.

However, on that same note, I agree with you that estrogen SHOULD NOT BE CRUSHED. But neither are you absolutely right either, in some cases, for people that are not as hypersensitive, a mild Aromatase inhibitor (AI) may very well be beneficial in conjunction with SERM treatment to effectively regress and eliminate gyno. I for one have access to pharmaceutical grade Letro, and Nolva, and Arimidex, those were the ones I used in my "experiment"... all medical-grade stuff from overseas, I know because I just back-tracked and triple checked the labs that make them. One is an Israeli medical center, another one is in Turkey, and one in India... but they're all valid medical facilities with good standing.

My point is, not everyone has the same sensitivity to certain compounds, and as you mentioned, there is no standard dosing. The trick, then, is to find the RIGHT amount, and the right drugs, that are applicable to the specific individual case in question. Some people may be perfectly fine with just a SERM. Others may also need a mild Aromatase inhibitor (AI). Saying 30mg daily of Ralox is fine for everybody is simply making a blanket statement that is not true, it will not hold water everywhere. Some people may need 60mg. Others may need to add a small amount of Aromatase inhibitor (AI) to it just for the purposes of reducing the lump. Bloodwork is absolutely VITAL in establishing whether or not an Aromatase inhibitor (AI) would be needed in order to facilitate the best proper approach without crushing estrogen entirely.

So basically I'm not saying you are wrong, I'm saying you are half-correct. You need both; the sledgehammer and the feather. Sometimes in life you absolutely need to use the sledgehammer, and other times it's essential to feather the situation. Everything is situational, but the proper and creative balance of both is absolutely essential.

I'd like to wholeheartedly thank you one last time for the insight you've given me, it's truly priceless, even the medical knowledge aside. Keep on keeping on brother, respect

 

[Austinite]

Austinite, just wanted to add one more thing;

You are absolutely correct with your information, it's very accurate, but one point you were only HALF correct on... your baseball bat analogy. The thing is, I understand the reason for your suggestions of low dosing and minimal possible effective dosage, because YOU, my dear friend, are hypersensitive to the substances. I completely understand that, and there is nothing wrong with that, but given that consideration we are also missing the other half of the population.

When you said 2.5mg pharma-grade letro will destroy you, I understand the reason behind that statement... because generally speaking pure-letro protocols are pure hell, they crush all estrogen in the entire system, they leave your "dick string in the dirt" so-to-speak, scuse the language but it's relevant to the point; libido is nonexistent. Joints dry out, and overall general lethargy from depletion of estrogen, as well as possible weight fluctuations are all no bueno.

However, on that same note, I agree with you that estrogen SHOULD NOT BE CRUSHED. But neither are you absolutely right either, in some cases, for people that are not as hypersensitive, a mild Aromatase inhibitor (AI) may very well be beneficial in conjunction with SERM treatment to effectively regress and eliminate gyno. I for one have access to pharmaceutical grade Letro, and Nolva, and Arimidex, those were the ones I used in my "experiment"... all medical-grade stuff from overseas, I know because I just back-tracked and triple checked the labs that make them. One is an Israeli medical center, another one is in Turkey, and one in India... but they're all valid medical facilities with good standing.

My point is, not everyone has the same sensitivity to certain compounds, and as you mentioned, there is no standard dosing. The trick, then, is to find the RIGHT amount, and the right drugs, that are applicable to the specific individual case in question. Some people may be perfectly fine with just a SERM. Others may also need a mild Aromatase inhibitor (AI). Saying 30mg daily of Ralox is fine for everybody is simply making a blanket statement that is not true, it will not hold water everywhere. Some people may need 60mg. Others may need to add a small amount of Aromatase inhibitor (AI) to it just for the purposes of reducing the lump. Bloodwork is absolutely VITAL in establishing whether or not an Aromatase inhibitor (AI) would be needed in order to facilitate the best proper approach without crushing estrogen entirely.

So basically I'm not saying you are wrong, I'm saying you are half-correct. You need both; the sledgehammer and the feather. Sometimes in life you absolutely need to use the sledgehammer, and other times it's essential to feather the situation. Everything is situational, but the proper and creative balance of both is absolutely essential.

I'd like to wholeheartedly thank you one last time for the insight you've given me, it's truly priceless, even the medical knowledge aside. Keep on keeping on brother, respect

There is no such thing as joints "drying out". You would collapse if that ever happened.

Biggie, I urge you to refrain from using examples you're not experienced with. Earlier, you only mentioned UGL related products. Now suddenly your "experiment" involved pharmaceutical. It is beginning to seem that you are no longer playing devil's advocate as it would have been the first thing to mention when I spoke of the variations between UGL and pharmaceutical. Unless I missed it somehow. I provided you with several studies, one indicating a 385 microgram daily dose in extremely obese hypogonadal men. Obesity carries an extreme amount of aromatase enzymes.

Here's another tip. Unless you purchased your product with a prescription, it is not pharmaceutical grade. Can you tell me what brands you used? Do you happen to have any on hand where you can share images? I ask because there are 1000's upon 1000's of UGL's that provide so called pharmaceutical gear, when in fact it is merely a label. Many folks mistake UGLs for pharmacies, such as Unigen/Genesis. It's been referred to as a pharm grade product when in fact it is nothing but UGL.

Israeli pharmacies are not regulated. You can walk into any pharmacy in Israel and purchase aromatase inhibitors. Same with it's neghbor; the Hashemite kingdom of Jordan. And Syria, Lebanon, Kuwait and Egypt. Again, unless you are doctor-prescribed, as I am, you have absolutely no possible way of verifying grade. (Unless you had a mass spec performed for 1000 dollars) This entire pharm grade term is used far too loosely today by everyone.

I am not hypersensitive. Had I been hypersensitive then a dose of 0.25 mg of arimidex would also cause issues for me and make it difficult to manage e2, that is far from the truth. Some folks may be hypersensitive, but this is generally observed in very low body fat, well below 9%, which is uncommon.

From letrozole, Bone problems can occur, edema, hyperchlesteroemia, elevated bilirubin, elevated liver enzymes, lymphopenia and a host of other issues that may occur with these abusive doses. We're not going to defy any laws here, the power of letrozole cannot be denied as it's visible in its very actions. It's not comparable to any other compound on a mg basis.

Depleting E2 is not limited to sexual side effects:

- Osteoporosis (weakened bones) ; (long-term low levels)
- Fatigue
- Lethargy
- Skin quality diminishes
- Depression
- Poor sense of wellbeing & poor quality of life
- Anxiety & panic attacks
- Depression
- Erectile dysfunction
- Loss of balance/instability/dizziness
- Respiratory related concerns
- Irritability
- Low libido
- Insomnia

There is no denying the dose. You can attempt to debunk the ideology all day long, but until you've been prescribed, the efforts are fruitless, while appreciated. The leading testosterone therapy endocrinologist and urologists avoid letrozole as an e2 control method for a reason. Letrozole was never, not once mentioned in any of the seminars at ENDO2011, 2012 or 2013. Not one time.

I am the biggest devil's advocate, especially with physicians. This one, I can't challenge. Too many doctors and far too much evidence lead me to now only believe, but to understand how this compound works. (the real compound). It's damaging to mineralocorticoids and disruptive to isoprenos on the way to steroid-genesis pathway.

It takes many years to understand a compound and its metabolites, I assure you, I wouldn't be able to make an assessment based on no experience and a few reads on the internet.

 

[biggiesmallz]

I mentioned liquid dosing in the OP because most people only have direct access to Research Chem grade solutions, and chrisotpherm's quote was regarding that dosing.

My personal use was purchased from the Ukraine, from everything I can tell it's medical grade. Again, without a spectroanalysis I cannot confirm that it's to the same potency regarding what you're referring to, but it's also not liquid-grade research chemicals either.

It's not essential for me to prove or disprove my medications... I mean, I can certainly take pictures, the letro tabs are round, the 1mg adex tabs are small squares, nolva is the same size as the letro tabs at 10mg per tab... that's not the point here, the point is that ALL of the drugs have their proper applications and uses, and you're right that it's absolutely ESSENTIAL to get those uses right medically-speaking, with the smallest dosage that is applicable to the situation at hand, all I'm saying is that they ALL play their part. I understand the warning labels and exactly what you're saying... don't get me wrong, we have zero misunderstanding regarding the proper medical application of these drugs and their possible detrimental side effects if not properly used. I'm just saying to completely negate the use of Aromatase Inhibitors from the purposes of Gyno treatment is too narrow-minded and one sided, only bloodwork should be the final standard when making that decision since every case is unique and individual, and the aromatase process equally as unique and specific to the individual in question.