Ask Michael Scally: Why Use Both Clomid and Nolvadex Together for PCT?

[jackiebigmur]

yeah, that makes sense. So the serm helps with the natural t production helping the overall balance until the estrogen returns to a normal level? I guess it's all about getting things back to normal. thanks

 

[Jeton]

I am going to respond. Tonight I should have a chance to go by my university's library and get the full text of the study in question. From all the other references I've posted, however, I think it's clear that men (at least those who identify as heterosexual) do NOT normally exhibit estrogen priming. And in those who do identify as homosexual, there very well may be estrogen priming, though it's stil totally unclear how clomid administration would impact on that.

much obliged, of course i'm very curious to see it.opcorn:

He won't acknowledge you unless you kick him in his tiny little balls. And they are not shut down either!!!![)]

u've seen them up close, haven't u!

 

[OhNoYo]

yeah, that makes sense. So the serm helps with the natural t- production helping the overall balance until the estrogen gets to a normal level? I guess it's all about trying to get everything back to normal. Thanks

No, that's not how it works at all. SERM stands for selective estrogen receptor modulator. It acts like estrogen in some receptors at specific tissues, but blocks estrogen receptors (ER) in other tissues, so estrogen can't bind to them, ultimately inactivating those receptors temporarily. Provided below is a the wikipedia link discussing SERMs that u mite find useful...

[ame="http://en.wikipedia.org/wiki/Selective_estrogen_receptor_modulator"]Selective estrogen receptor modulator - Wikipedia, the free encyclopedia@@AMEPARAM@@/wiki/File:Tamoxifen_Raloxifen_nci-vol-2738-300.jpg" class="image"><img alt="" src="http://upload.wikimedia.org/wikipedia/commons/thumb/c/ca/Tamoxifen_Raloxifen_nci-vol-2738-300.jpg/220px-Tamoxifen_Raloxifen_nci-vol-2738-300.jpg"@@AMEPARAM@@commons/thumb/c/ca/Tamoxifen_Raloxifen_nci-vol-2738-300.jpg/220px-Tamoxifen_Raloxifen_nci-vol-2738-300.jpg[/ame]

 

[Conciliator]

Ok Jetson. Get ready... this is going to be a long one. I found the study in question and scanned it in. You can download it [ame="http://rapidshare.com/files/381466646/Sexual_differentiation_of_gonadotrophin_secretion__sexual_orientation_and_gender_role_behavior.pdf"]here[/ame]. The bad news is that this is a review paper, not the study for which we wanted to examine the methods. They explain in the abstract, "In clinical studies, we were able to induce a positive estrogen feedback on LH secretion in most intact homosexual men in clear-cut contrast to intact hetero- or bisexual men." Fortunately, the full text tells us what those clinical studies are. They're mentioned in this excerpt:

In addition, a positive estrogen feedback could be evoked in homosexual men in contrast to heterosexual men. This finding suggested that homosexual men may possess, at least in part, a more female-differentiated brain based on an androgen deficiency during brain differentiation [12]. In view of this finding, which was clearly confirmed most recently by Gladue et al. [13], a world-wide dispute was started about the question whether prenatal sex hormone levels or postnatal psychosocial learning processes may be more important for sexual differentiation of the brain, sexual orientation, gender role behaviour and gender identity.

So references 12 and 13 are the two clinical studies in which this difference between heterosexuals and homosexuals was ostensibly found. Reference 12 is this study.It's interesting to note that it's been cited by 127 other papers, showing that it's been highly influential. Unfortunately, I don't have access to this paper either online or at the library. We glean some details when we look at the abstract, though:

A positive estrogen feedback effect was also induced in intact homosexual men in contrast to intact heterosexual and bisexual men. Thus in 21 homosexual men an intravenous injection of 20 mg Presomen (Premarin) produced a significant decrease of serum LH levels followed by an increase above initial LH values. In 20 heterosexual and in five bisexual men, by contrast, intravenous estrogen administration, while producing a significant decrease of the serum LH level, was not followed by an increase above the initial LH values.

Reference 13 is to this study by Gladue et al. It was published in the highly prestigious journal Science. It's been cited by 154 papers, making it even more influential than the other. Fortunately, I have access to this one online. I made it available for download [ame="http://rapidshare.com/files/381460855/Neuroendocrine_Response_to_Estrogen_and_Sexual_Orientation.pdf"]here[/ame]. What we learn from the full text is how the two groups of men were differentiated into heterosexual and homosexual. We read that "All subjects were objectively classified a priori into behaviorally distinct categories of sexual orientation (9)." Footnote 9 gives us all the details, the most important of which are the following:

To be included in the homosexual sample, men had to have had erotic fantasies exclusively or primarily involving male partners since puberty (a rating of 5 to 6 on the Kinsey scale of sexual orientation) [A. C. Kinsey, W. B. Pomeroy, C. E. Martin, Sexual Behavior in the Human Male (Saunders, Philadelphia, 1948)]. Similarly, genital experiences had to have exclusively or primarily involved a male since puberty. Individuals included in the heterosexual sample reported having had erotic fantasies about and genital sexual contact with persons of only the opposite sex since puberty (Kinsey rating of 0). Thus, there was no overlap in fantasies or behavior between the heterosexual and homosexual samples. Groups were matched for comparable age distributions (range, 21 to 37; median age, 26). A clinical interview was used to classify all volunteers, the records being reviewed under blind conditions by all three authors. Subjects were included for analysis only if consensus was obtained as to their Kinsey ratings. This was especially critical for the integrity of the homosexual sample. Homosexuality is a term that covers a wide range of childhood and adult experiences. To establish a group of fairly exclusively homosexual men, it was essential to distinguish volunteers having exclusively homosexual desires, interests, and experiences lifelong from men having such characteristics intermittently, periodically, or only recently.

This quote from the end of the paper is also very relevant to your question:

These findings are based on a particular subset of homosexual men and may not apply to all male homosexuals. While recent surveys show that 75 percent of the male homosexual population claims to be exclusively homosexual (a Kinsey rating of 6), the respondents were asked to describe their orientation and activities for only the preceding 12 months (15). According to Kinsey (9), 4 percent of the male homosexual population meet criteria for lifelong homosexual orientation. In our study the two groups of men were selected such that they represented the opposite ends of the spectrum of sexual orientation, in order that any subtle differences in neuroendocrine responsiveness might be detected. The homosexual men in this study reported a longterm pattern of sexual behavior and fantasies involving male partners. Whether a differential neuroendocrine response is present in men of less exclusive homosexual orientation is an open question.

The findings in this study with respect to estrogen priming and the LH response were as follows

Examination of individual response patterns showed a greater variability among the homosexual men than among the heterosexual men. If we consider a positive estrogen feedback response of LH to be a change in LH at 72 or 96 hours that exceeds mean baseline values for all men by more than 2 standard deviations, then 9 of the 14 homosexuals exceeded this criterion, compared to 0 of the 17 heterosexual men (P = 0.0001, Fisher's Exact Test) and 11 of the 12 heterosexual women (89 percent) (P = 0.104). Note that, while the number of homosexual men responding is similar to that of women, the magnitude of the response is clearly dissimilar (Fig. 1). Comparing a response only 1 standard deviation above baseline, 11 of the homosexual men exceeded this criterion and only one heterosexual man (P = 0.000044). Hence, although not all the homosexual men studied showed an enhanced response of LH to estrogen compared to the heterosexual men, significantly more did.

And interestingly, even though the homosexual men showed an increase in LH in response to estrogen, they showed suppressed testosterone levels just like the heterosexual men who had their LH levels lowered by the estrogen. The researchers surmised that the LH spike may have desensitized leydig cells, but I find that explanation to be lacking.

I think this paper and "reference 12" (above) corroborate the references that I posted at the start of this thread that heterosexual men (at least those who strongly identify themselves as such) demonstrate no estrogen priming, just negative and suppressive feedback from estrogen.

-Conciliator

 

[Conciliator]

He won't acknowledge you unless you kick him in his tiny little balls. And they are not shut down either!!!![)]

Misrepresenting things yet again! You know darn well that you were sucking them, not kicking them

 

[Jeton]

ok now itt's MY turn to play for time, it's almost 5am n i need to finish folding enuff laundry for my fiance to let me go to sleep...will chase down ur links later today....

 

[Michael Scally MD]

According to a study published in the April 29 issue of the journal Neuron, "the male hormone testosterone doesn't work in ways that had been assumed when it comes to masculinizing the brain during development and making males behave a certain way when they're adults." Working with mice, researchers "found that estrogen...can be derived from circulating testosterone in males. In the brain, this testosterone-derived estrogen can control many behaviors that are typically linked to males." In mice, estrogen appears to masculinize "the neural circuits for mating, fighting, and territory marking."


Typical Male Behavior Comes From Estrogen, Too
Both male and female hormones play role in making men masculine, research shows
http://healthday.com/Article.asp?AID=638553

WEDNESDAY, April 28 (HealthDay News) -- Gender-specific behavior patterns are often chalked up to testosterone in men and estrogen in women, but a new study explains why the hormone issue isn't so clear cut.

The male hormone testosterone doesn't work in ways that had been assumed when it comes to masculinizing the brain during development and making males behave a certain way when they're adults, researchers found.

"It was known that testosterone and estrogen are essential for typical male behaviors in many vertebrate species," study senior author Dr. Nirao M. Shah, of the anatomy department at the University of California, San Francisco, said in a news release. "However, how these two hormones interact to control masculinization of the brain and behavior remained to be established."

Shah and colleagues genetically engineered mice to get rid of a pathway thought to play a role in how animals become masculinized. Yet, they found that the mutant mice still acted like males -- fighting and marking territory -- but with some differences. In particular, the extent and frequency of typical male behaviors varied between the mutant mice and the other mice.

The study, published in the April 29 issue of the journal Neuron, found that estrogen, which is virtually undetectable in the circulation of most male species, can be derived from circulating testosterone in males. In the brain, this testosterone-derived estrogen can control many behaviors that are typically linked to males.

"Our findings in conjunction with previous work suggest a model for the control of male pattern behaviors in which estrogen masculinizes the neural circuits for mating, fighting and territory marking, and testosterone and estrogen signaling generate the male typical levels of these behaviors," Shah said. "It will be interesting in future studies to identify the molecular and circuit level mechanisms that are controlled by these hormones."


Juntti SA, Tollkuhn J, Wu MV, et al. The Androgen Receptor Governs the Execution, but Not Programming, of Male Sexual and Territorial Behaviors. Neuron;66(2):260-72.
Neuron - The Androgen Receptor Governs the Execution, but Not Programming, of Male Sexual and Territorial Behaviors

Summary Testosterone and estrogen are essential for male behaviors in vertebrates. How these two signaling pathways interact to control masculinization of the brain and behavior remains to be established. Circulating testosterone activates the androgen receptor (AR) and also serves as the source of estrogen in the brain. We have used a genetic strategy to delete AR specifically in the mouse nervous system. This approach permits us to determine the function of AR in sexually dimorphic behaviors in males while maintaining circulating testosterone levels within the normal range. We find that AR mutant males exhibit masculine sexual and territorial displays, but they have striking deficits in specific components of these behaviors. Taken together with the surprisingly limited expression of AR in the developing brain, our findings indicate that testosterone acts as a precursor to estrogen to masculinize the brain and behavior, and signals via AR to control the levels of male behavioral displays.

 

[BBC3]

[)]

If you were sitting in the vicinity of my bowl of peanuts and sunflower seeds, there is not question I might have picked them up. And without a single hair on the sack, how could anyone be blamed for the honest mistake. However, I am sure I readily spit them out with the rest of the duds......... If I crunched them up too badly, I apologize. Its a good thing you have that hermaphodatic vagina under them......

Misrepresenting things yet again! You know darn well that you were sucking them, not kicking them

 

[IronCore]

Misrepresenting things yet again! You know darn well that you were sucking them, not kicking them

BOOOYOW!!!

Damn Asshat... Your my boy and all but... DAYUM!!!... You got OWNED... never thought I would see the day.. [)]


Seriously though guys... I sincerely appreciate all of the Highly valuable information you have all bestowed upon us, however, I would like for you all to remember there are some of us here that rely heavily upon the research and methods you recommend.

I for one am one of them and would certainly hate to know that I followed the wrong misguided advice and ruined my test-tickles

With that in mind, to me, it still seems logical to follow the recommend PCT established by Dr.Scally as it has a clinically proven track record... Not to say that I will not reduce my nolva dosage... But I would rather be safe than sorry...

 

[BBC3]

EDIT. No Comment.

 

[Conciliator]

According to a study published in the April 29 issue of the journal Neuron, "the male hormone testosterone doesn't work in ways that had been assumed when it comes to masculinizing the brain during development and making males behave a certain way when they're adults." Working with mice, researchers "found that estrogen...can be derived from circulating testosterone in males. In the brain, this testosterone-derived estrogen can control many behaviors that are typically linked to males." In mice, estrogen appears to masculinize "the neural circuits for mating, fighting, and territory marking."

I'm not sure how novel this idea is. The paper from 1987 that I scanned in yesterday says: "In this context, it should be noted that natural and synthetic estrogens can exert paradoxical, i.e. androgen-like effects on male-type brain differentiation [16]. Several findings suggest that endogenous and exogenous androgens are even aromatized in the brain to estrogens - at least in part - for male-type brain differentiation [17]."

Also Dr. Scally, when you have a chance, could you please respond to the questions I raised in these two posts?
https://thinksteroids.com/community/posts/687817
https://thinksteroids.com/community/posts/687859

 

[Conciliator]

I for one am one of them and would certainly hate to know that I followed the wrong misguided advice and ruined my test-tickles

With that in mind, to me, it still seems logical to follow the recommend PCT established by Dr.Scally as it has a clinically proven track record... Not to say that I will not reduce my nolva dosage... But I would rather be safe than sorry...

The problem with this line of reasoning is that it assumes that nolva doesn't have a clinically proven track record, which is not true. One of the largest and most recent studies on the topic compared the effects of tamoxifen (nolva) to the newer generation SERMs toremifene and raloxifene. They looked specifically at HPTA endpoints, using relatively large study groups. After one and two months of treatment (the length of most PCT), tamoxifen was superior to toremifene and raloxifene at increasing LH and testosterone levels. For example, after two months of toremifene at 60mg/day, LH increased from 4.05 to 5.05 and test increased from 498.96 to 709.79. In contrast, nolva at 20mg/day increased LH from 4.54 to 7.73 and test from 496.59 to 835.06. Nolva alone clearly does a good job at restoring the HPTA.

 

[BBC3]

Hey ConciBoy. I see you are making regular reference to toremifene since I brought it to the board's attention a few months back. Anyway, I remember you were curious about the information I posted referring to the fact that Toremifene shrank the prostate and seminal vessels due to the E2 Blockade specific to the prostate (speculatively). WHat did you ever turn up?? Did you find any independent studies on this? Or is that all manufacturer hubbub.

The problem with this line of reasoning is that it assumes that nolva doesn't have a clinically proven track record, which is not true. One of the largest and most recent studies on the topic compared the effects of tamoxifen (nolva) to the newer generation SERMs toremifene and raloxifene. They looked specifically at HPTA endpoints, using relatively large study groups. After one and two months of treatment (the length of most PCT), tamoxifen was superior to toremifene and raloxifene at increasing LH and testosterone levels. For example, after two months of toremifene at 60mg/day, LH increased from 4.05 to 5.05 and test increased from 498.96 to 709.79. In contrast, nolva at 20mg/day increased LH from 4.54 to 7.73 and test from 496.59 to 835.06. Nolva alone clearly does a good job at restoring the HPTA.

 

[Conciliator]

Hey ConciBoy. I see you are making regular reference to toremifene since I brought it to the board's attention a few months back.

You give yourself too much credit. My mention of toremifene has absolutely nothing to do with you bringing it up a few months ago. I talked about it on Meso before you were even a member here and the first two times you had the word "toremifene" in a post was when you were quoting me saying it.

Anyway, I remember you were curious about the information I posted referring to the fact that Toremifene shrank the prostate and seminal vessels due to the E2 Blockade specific to the prostate (speculatively). WHat did you ever turn up??

I didn't turn up anything. That whole discussion demonstrated how you make statements that are misleading and unsupported. First, you say "Thats right, a reduction is estrogen actually reduces prostate size." And then you ask Solo47, "Does it not interest you at all that the Serm I referred to will shrink your prostate??" You're making statements of fact, that in humans toremifene "actually reduces prostate size" and that it "will shrink your prostate." So I call you out for the evidence. And what does it amount to? http://www.fareston.com/pdfs/Prescribing_Info.pdf excerpt in the prescribing info under the heading "Carcinogenesis, Mutagenesis, and Impairment of Fertility":

Toremifene produced impairment of fertility and conception in male and female rats at doses ?25.0 and 0.14 mg/kg/day, respectively (about 3.5 times and 1/50 the daily maximum recommended human dose on a mg/m2 basis). At these doses, sperm counts, fertility index, and conception rate were reduced in males with atrophy of seminal vesicles and prostate.

So you take a single reference from a study in rats and then start telling humans, as a matter of fact, that it'll have the same effect. Needless to say, you can't make extrapolations like that. At the very least, say there's tentative evidence in rats or the possibility that it may occur in humans, but don't go around making statements of fact like there's some established effect in humans. You have no idea if toremifene will decrease the prostate size in humans and you have no business telling people that it will.

 

[Michael Scally MD]

The problem with this line of reasoning is that it assumes that nolva doesn't have a clinically proven track record, which is not true. One of the largest and most recent studies on the topic compared the effects of tamoxifen (nolva) to the newer generation SERMs toremifene and raloxifene. They looked specifically at HPTA endpoints, using relatively large study groups. After one and two months of treatment (the length of most PCT), tamoxifen was superior to toremifene and raloxifene at increasing LH and testosterone levels. For example, after two months of toremifene at 60mg/day, LH increased from 4.05 to 5.05 and test increased from 498.96 to 709.79. In contrast, nolva at 20mg/day increased LH from 4.54 to 7.73 and test from 496.59 to 835.06. Nolva alone clearly does a good job at restoring the HPTA.

I made the point early on, which was apparently overlooked or misunderstood that it is important to evaluate drugs for the study population. The study you cite is NOT restoring the HPTA. Take a gander at the baseline. The only defect is spermatogenesis, not T. These patients have a normal HPTA as far as sex hormones. BTW: What was the E2? The E2 level is a factor, correct!!! While it might seem plausible to translate the results to other populations, it is NOT as you state, "Nolva alone clearly does a good job at restoring the HPTA." [I have never needed to use an SERM in a patient with a baseline of LH 4.54 and T 496. Clearly, not a PCT (post AAS) clinical context. Can you say, "Whoops!" ]

Further, there are few studies I am readily aware of using tamoxifen in the testosterone deficient patient. There are a number, many more than tamoxifen, of studies using clomiphene for hypogonadism. As you said yourself, you have anecdotal information that is essentially worthless. This is what you appear to be promoting.

Again, I have said repeatedly, over and over, their is an argument for SERMs/AI in PCT (POST AAS). I would like to see well-controlled studies. I am not enamored with the combination of clomiphene/tamoxifen. I do know it works and published. My experience when used singly was poor. I would like to see studies using each alone (and other drugs) for PCT.

In fact, the company I set up plans on using a single SERM so I want it to be a success rather than anything that might be attributable to the combination. Finally, stop the mental masturbation! The only way to see of the PCT works is to get laboratory confirmation. So, if you have a PCT idea, go for it. just be sure to get checked.

 

[OhNoYo]

I just have 1 ? & 1 statement...

Question is, how long has the BEEF between Con & BBC3 been going on and what was it first over?

My statement is that I feel this thread will be going on for quite a long time! It's great to see intellects like Dr. Scally & Con discuss things in such extensive detail. Mr. Roberts, care to join them?! opcorn:

 

[Conciliator]

I made the point early on, which was apparently overlooked or misunderstood that it is important to evaluate drugs for the study population. The study you cite is NOT restoring the HPTA. Take a gander at the baseline. The only defect is spermatogenesis, not T. These patients have a normal HPTA as far as sex hormones. BTW: What was the E2? The E2 level is a factor, correct!!! While it might seem plausible to translate the results to other populations, it is NOT as you state, "Nolva alone clearly does a good job at restoring the HPTA." [I have never needed to use an SERM in a patient with a baseline of LH 4.54 and T 496. Clearly, not a PCT (post AAS) clinical context. Can you say, "Whoops!" ]

I should have said "stimulating," not "restoring." I realize this study was not in a population suffering from hypogonadism. What I would ask, however, is why the results would not be highly relevant when we consider, particularly in cases where hCG was used to maintain testicular function, that stimulation of GnRH and LH production is the endpoint we care about? Is there any reason to think that eugonadal men would have a differential response to nolva at brain ERs compared to hypogonadal men? I think not. Just as studies have shown that nolva and clomid increase LH and testosterone in eugonadal men, they've shown they also increase LH and testosterone in hypogonadal men.

Further, there are few studies I am readily aware of using tamoxifen in the testosterone deficient patient.

Would you mind posting the ones that you're aware of?

There are a number, many more than tamoxifen, of studies using clomiphene for hypogonadism.

This says nothing about the comparative effectiveness, just the traditional medical use. As William Llewellyn argues:

I am not sure how Clomid and Nolvadex became so separated in the minds of bodybuilders. They certainly should not be. Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor. In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). lh - leutenizing hormone - output by the pituitary will be increased as a result, which in turn can increase the level of testosterone by the testes. Both drugs do this, but for some reason bodybuilders persist in thinking that Clomid is the only drug good at stimulating testosterone. What you will find with a little investigation however is that not only is Nolvadex useful for the same purpose, it should actually be the preferred agent of the two.

As you said yourself, you have anecdotal information that is essentially worthless. This is what you appear to be promoting.

How is the study anecdotal? It was a randomized clinical study with statistical analysis.

Again, I have said repeatedly, over and over, their is an argument for SERMs/AI in PCT (POST AAS). I would like to see well-controlled studies.

I'd like to see more as well. We need more studies in hypogonadal patients. And we especially need some studies directly comparing tamoxifen and clomiphene, which appear to be the most effective SERMs at the HPTA.

I am not enamored with the combination of clomiphene/tamoxifen. I do know it works and published. My experience when used singly was poor. I would like to see studies using each alone (and other drugs) for PCT.

As I asked before, "Did you happen to collect data on the three different groups (i.e. clomid, nolva, and clomid+nolva)? Do you have baseline test levels and final LH and/or test levels after a given treatment period? Or were your observations concerning nolva alone and clomid alone more casual than that? Either way, I really do value your experience. I'm just curious as to how systematically the three different protocols were tested and compared to each other."

 

[Conciliator]

I just have 1 ? & 1 statement...

Question is, how long has the BEEF between Con & BBC3 been going on and what was it first over?

It probably started around here, when there were so many ridiculous things that BBC3 had said and that I had argued against that I could start making lists.

 

[BBC3]

Well you did not start harping on it and bringing it up until recently anyway. UNTIL I POINTED IT OUT, you were completely unaware of the E2 blockade demostrating reduction in prostate and assoc. size etc.. Period. You are as obtuse as common work of others you live by. You have remained completely adverse to the idea that E2 may indeed harm the prostate, and even moreso than androgens, so dont try to deny your position now. You will never know how hard I work to develop your tiny little imagination..... Its a chore but someone....etc.... God help your spawn. What will they get for christmas. A membership to pub med on line......

Regarding the RATs. It just so happens that research on every drug man uses starts there. There are enough similarities to draw the line. DON'T pretend there are not. Yes I asked Solo, because it is a SERM used for Humans. The proof is in. E2 is bad for the prostate, so enough. Your babble is only documenting the weakness of your narrow little mind. Solo has clearly, as many of us here have, spent his days experimenting with drugs. He can make the decision. He is wise enough to interpret what I said as meaning "give it a shot".

I am thinking maybe we should submit you to microsoft and have them develop an artificial intelligence engine based on you. Or maybe they already did??!![)] Clitface...

You give yourself too much credit. My mention of toremifene has absolutely nothing to do with you bringing it up a few months ago. I talked about it on Meso before you were even a member here and the first two times you had the word "toremifene" in a post was when you were quoting me saying it.
I didn't turn up anything. That whole discussion demonstrated how you make statements that are misleading and unsupported. First, you say "Thats right, a reduction is estrogen actually reduces prostate size." And then you ask Solo47, "Does it not interest you at all that the Serm I referred to will shrink your prostate??" You're making statements of fact, that in humans toremifene "actually reduces prostate size" and that it "will shrink your prostate." So I call you out for the evidence. And what does it amount to? http://www.fareston.com/pdfs/Prescribing_Info.pdf excerpt in the prescribing info under the heading "Carcinogenesis, Mutagenesis, and Impairment of Fertility":So you take a single reference from a study in rats and then start telling humans, as a matter of fact, that it'll have the same effect. Needless to say, you can't make extrapolations like that. At the very least, say there's tentative evidence in rats or the possibility that it may occur in humans, but don't go around making statements of fact like there's some established effect in humans. You have no idea if toremifene will decrease the prostate size in humans and you have no business telling people that it will.

 

[BBC3]

The beef started a long time ago when I noticed what an arrogant and confrontational bastard he was. I could not resist. I challenged him at a fairly ignorant stage of my studies. Whether I was right or wrong, it seemed to bring me immense satisfaction. He was a fairly weak contender at the time regardless of what he may try to claim. I knew nothing.

Perhaps, I just enjoy stroking his jackass fur coat in the wrong direction. He seems to like it..[)]

By the way. His sense of humor. Yep that was me. I gave him that. I know not much, but I didn't have much to work with...

I just have 1 ? & 1 statement...

Question is, how long has the BEEF between Con & BBC3 been going on and what was it first over?

My statement is that I feel this thread will be going on for quite a long time! It's great to see intellects like Dr. Scally & Con discuss things in such extensive detail. Mr. Roberts, care to join them?! opcorn: