# STEROIDS FORUM > PCT (POST CYCLE THERAPY) >  Nolvadex vs. Clomid for PCT

## WhiteTiger

It seems like everyday questions concerning PCT pop up, and weather one should use either Clomid or nolva or a combo of both. I hope that this article written by BigCat may help to clear up some misconceptions.

While practically similar compounds in structure, few people ever really consider Clomid and nolva to be similar. Its not just a common myth in steroid circles, but even in the medical community. This misconception originates from their completely different uses. Nolvadex is most commonly used for the treatment of breast cancer in women, while Clomid is generally considered a fertility aid. In bodybuilding circles, from day one, Clomid has generally been used as post-cycle therapy and Nolvadex as an anti-estrogen.

But as I intend to demonstrate this is in essence the same. I believe the myth to have originated because nolva is clearly a more powerful anti-estrogen, and the people selling Clomid needed another angle to sell the stuff, so it was mostly used as a post-cycle aid. But few users really understand how Clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids . After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up. Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody's best interest to bring back natural test as soon as humanly possible. Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That's basically how the mechanism works, nothing more, nothing less.

Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall estrogen with 20-40 mg a day, than Clomid can in doses of 100-150 mg a day. A noteworthy difference. Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it. As such they will occupy the receptor and keep it from binding estrogens. This means they do not actively work to reduce estrogen in the body like Proviron , Viratase or arimidex would (by competing for the aromatase enzyme), but that it blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to.

This has advantages and disadvantages. The disadvantage is that when use is discontinued, the estrogen level is still the same and new problems will develop much sooner. The advantage is that it works much faster and has results sooner than with an aromatase blocker like Proviron or arimidex. Therefor, when problems such as gynocomastia occur during a cycle of steroids one will usually start 20 mg/day of nolva or 100 mg/day of Clomid straight away, in conjunction with some Proviron or arimidex. The proviron or arimidex will actively reduce estrogen while the Clomid or Nolvadex will solve your ongoing problem straight away. This way, when use is discontinued there is no immediate rebound.

So which one should you use? Well personally, I'd have to say Nolvadex. Both as an on-cycle anti-estrogen and a post-cycle therapy. As an anti-estrogen its simply much stronger, demonstrated by the fact that better results are obtained with 20-40 mg than with 100-150 mg of Clomid. For post-cycle, this plays a key role as well. It deactivates rebound estrogen much faster and more effective. But most importantly, Nolvadex has a direct influence on bringing back natural testosterone, where as Clomid may actually have a slight negative influence. The reason being that tamoxifen (as in Nolvadex) seems to increase the responsiveness of LH (luteinizing hormone) to GnRH (gonadtropin releasing hormone), whereas Clomid seems to decrease the responsiveness a bit1.

Another noteworthy fact about Nolvadex is that it acts more potently as an estrogen in the liver. As you remember, I mentioned that clomiphene and tamoxifen are basically weak estrogens. Well, tamoxifen is apparently still quite potent in the liver. This offers us the positive benefits of this hormone in the liver, while avoiding its negative effects elsewhere in the body. As such Nolvadex can have a very positive impact on negative cholesterol levels2 in the body, and therefore too should be considered a better choice than Clomid. It will not solve the problem of bad cholesterol levels during Steroid use , but will help to contain the problem to a larger degree.

Another reason why I promote the use of Nolvadex over Clomid post-cycle (as if being 3-4 times stronger and having more of a direct effect on restoring natural test wasn't enough) is because it's a lot safer. Not just because it improves lipid profiles, but also because it simply doesn't have the intrinsic side-effects that Clomid has. Clomid causes more acne for sure, but that's mainly because you need to use a 3-4 times higher dose. But Clomid seems to also affect the eyesight. Long-term Clomid therapy causes irreversible changes in eyesight3 in users. Irreversible. For me that alone is reason enough to prefer Nolvadex.

Lastly, one should be aware that use of these compounds can reduce the gains made on steroids. Nolvadex more so than Clomid, simply because it is stronger. Estrogen is responsible for a number of anabolic factors such as increasing growth hormone output, upgrading the androgen receptor and improving glucose utilization. This is why aromatizing steroids like testosterone are still best suited for maximum muscle gain. When reducing the estrogen levels, we therefore reduce the potential gains being made. For this reason one may opt to try Clomid during a cycle instead of Nolvadex. Although I would imagine that the problem that needed solved would be of more concern, in which case nolva remains the weapon of choice. It's a plain fact that there is a high correlation between gains and side-effects. Either you go for maximum gains and tolerate the side-effects, or you reduce the side-effects, and with it the gains. That's life, nothing is free.

Stacking and Use:

If problems of Gynocomastia or other estrogen related symptoms tend to pop up during a cycle the use of 20-30 mg of Nolvadex or 100 mg of Clomid daily should easily contain the problem, and be used until a few days after the problem subsides. For best results and the least amount of problems upon cessation it is best stacked with Proviron (50 mg) or arimidex (0.5 mg) for this duration as well. Its not advised that these products be ran concomitantly with the steroid for the entire duration of the stack, as this will reduce your gains. Instead cease the usage of anti-estrogens once the problem is contained, and should the problem resurface, simply recommence the use of the products in the same manner as described above.

Once a cycle of steroids is concluded one should always initiate a post-cycle therapy to help bring back natural testosterone as soon as possible. This will help you to retain the mass you gained. How this is done depends highly on the type of steroid used. If only orals were used, therapy should start immediately, even the last day of the stack. If short-acting esters or water-based injectables were used, therapy should commence within 4-7 days after last injection, and if long-acting esters were used then it should commence 1.5 to 2 weeks after the last injection was given. The length of the therapy will vary as well, from 3-5 weeks. The longer acting the product was, the longer therapy should be continued to make sure all suppressive factors are cleared before use of Clomid/Nolvadex is discontinued.

For best results, it is best stacked with HCG (Human Chorionic gonadotrophin), which functions as an LH analog and can help bring testicle size back up. HCG use starts the last week of a cycle, and on from there every 5-6 days (usually 1500-3000 IU) and discontinued 1.5 to weeks prior to the cessation of Nolvadex/clomid. The reason being that HCG itself is also suppressive of natural testosterone and should be out of the body before therapy is over, or it will inhibit natural testicle function. But I can not stress enough that HCG possibly plays a more important role in post-cycle therapy than clomid/Nolvadex. For Clomid and Nolvadex, doses are usually tapered down. Its best to start with 40-50 mg of Nolvadex or 150 mg of Clomid for the first week or the first two weeks, and then finish the program with 20-25 mg of Nolvadex or 100 mg of Clomid for an additional two weeks.

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## randomizer

Great read, very informative, cheers.

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## WhiteTiger

Glad you liked it!

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## 1000_DaysAsTheLion

cool article, thanks for posting

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## bigpapabuff

very good read, pct just as important as the cycle.

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## WhiteTiger

Yep, I think more members need to read this!

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## Fit N Fun

Hmmmm, lots of well written information, however Tamoxifen taken on its own for a month does very little for my balls. Add in Clomid and my balls grow huge within 10 or 12 days.

So my experience differs with the authours, you might say that ball size has nothing to do with recovery, my feeling is that it is very important.

FWIW my PCT is :-

Week 1, 50mg Clomid + 40mg Tamoxifen 
Week 2 to 5, 25mg Clomid + 20mg Tamoxifen 

For my last PCT, I added in the following compounds as suggested by Swifto.

Tribulus (Sopharma) 1g/ED
Ashwagandha RE 2g/ED9 weeks

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## WhiteTiger

I see, what about having the HCG during cycle to prevent the atrophy, would Nolva do the PCT then without the unwanted side of clomid?

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## Fit N Fun

I always take HCG or in the case of my last cycle "Low dose Naltrexone" to keep my HPTA functioning - big thread about this if you search for Naltrexone.

The PCT I use is the Gold standard, check for threads on here by Swifto, he is the guru on PCT

Tamoxifen on its own does not do it for me, Its Clomid that appears to me to make all the difference, at least on ball size.

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## Fit N Fun

Just read the above guide again and have to disagree with the statements BigCat made about HCG use.

HCG & Naltrexone should be used throughout your cycle and not into your PCT.

The advice above is to use HCG at the end of the cycle to within 1.5 weeks of the end of PCT, this will provide testosterone through stimulating the testes and will not encourage the hypothalamus (HPTA) to come back to life.

By the way, Low dose Naltrexone maintains HPTA activity throughout your cycle and is IMHO the most important and most effective way to limit the negative effects of Steroid use .

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## WhiteTiger

Nice. Yes I have read the entries by Swifto, alll good stuff there. I just wanted to see what people thought of using Nolvadex without Clomid.

Thanks for your replies.

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## Swifto

I like Tore and Tamox, but thats me.

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## FONZY007

would like to use tore, Hmmm hearing alot about. But like fit states IM worried more about ball size to gauge me whats going on with my body.

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## GotNoBlueMilk

Clomid is better for stiumating LH levels:

Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro, E. Y. Adashi, A. J. Hsueh, T. H. Bambino and S. S. Yen, AJP - Endocrinology and Metabolism, Vol 240, Issue 2 125-E130

The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. 

Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. 

*Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH* release at a concentration of 10(-7) M. Furthermore, *tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH*. Our findings suggest that *Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.*

This is why Clomid is prescribed over Nolva for male fertility issues. It raises LH levels better, and through a different route than Nolva. This is also why many swear by Colimd for PCT. It simply does more. The sides may suck, but it does more. 

Two more things. Can't lay my hands on the studies, but it turns out the best dose for Clomid is 25 mg/ED. Higher amounts are actually counter productive in raising LH. This of course assumes pharamcy grade and not research chemical grade. The study was also done on the average joe, so if you are bigger and using research chemicals you may want to go to 35-50 mg/ED. Not 100 though.

Finally, another study showed that mixing Nolva and Clomid was also counter productive. So except for the 1 week you overlap while switching from Clomid to Novla, you don't want to take them together. It is counter productive to do so.

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## FONZY007

taking clomid and nolva together counter productive first time I heard that.

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## Lemonada8

pre-double post

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## Lemonada8

> Two more things. Can't lay my hands on the studies, but it turns out the best dose for Clomid is 25 mg/ED. Higher amounts are actually counter productive in raising LH. This of course assumes pharamcy grade and not research chemical grade. The study was also done on the average joe, so if you are bigger and using research chemicals you may want to go to 35-50 mg/ED. Not 100 though.
> 
> Finally, another study showed that mixing Nolva and Clomid was also counter productive. So except for the 1 week you overlap while switching from Clomid to Novla, you don't want to take them together. It is counter productive to do so.



Where did you see those 2 things? I disagree with both of those statements, and ive done prolly alot more indepth research then most on this topic

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## GotNoBlueMilk

Basically, both Nolva and Clomid compete for the E2 receptors. If Nolva beats Clomid to a receptor, then Clomid can't enhance the GnRH-stimulated release of gonadotropin. So based on this line of reasoning, we should not mix Nolva and Clomid unless you are weaning from Clomid to Nolva.

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## Lemonada8

To make that kind of claim with a drug you need to get into pk vs pd of the drug... Can u link the studies plz

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## shennen

what the f.....

im currently using nolva and clomi 20/35mg ed........
is this actually hurting my recovery?

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## freakinhuge

I like to use both, always worked for me. Clomid 70/35/35/35 nolva 40/20/20/20

Use what works best for you.

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## mike1991

very good read.

so im looking into doing a cycle of test e and looking for advice of how i should go with my PCT on a daily basis? how often and how much dosage can you guys recommend?

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## GotNoBlueMilk

Geeze, I feel like I just walked into a church and said that there is no such thing as creation. I'm not saying any such thing.

No, taking both does not hurt your recovery. No, using both does not invalidate PCT. Using both is simply counter productive. Using both together is better than using just Nolva, but not as good as using Clomid alone. Read the explinations and this is rather obvious. If you want to use 20 products all at once use them. If it works for you then it works. 

I'm just saying what works best. Now go do what your faith dictates.

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## GotNoBlueMilk

> To make that kind of claim with a drug you need to get into pk vs pd of the drug... Can u link the studies plz


I already did, in the very first post. I have even *highlighted* the relevant parts. You now have to read and understand exactly what is being said and the implications. It says Clomid is better at a LH release, and that Nolva and Clomid compete for the same receptors. Conclusion: if a needed receptor is occupied by Nolva, Clomid cannot occupy it and therefore Clomid will not attach and exert a greater amount of LH reponse than the Nolva that does occupy the receptor. I really can't explain this any more simply.

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## GotNoBlueMilk

I should add, I have a bias against Nolva to begin with because it is carcinogen: http://potency.berkeley.edu/chempage...20CITRATE.html

Rat experiments show Nolva produces DNA adducts while Clomid does not. I haven't seen the experiments reproduced in humans, though. Just have the UC Berkely site info.

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## Swifto

> Clomid is better for stiumating LH levels:
> 
> Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro, E. Y. Adashi, A. J. Hsueh, T. H. Bambino and S. S. Yen, AJP - Endocrinology and Metabolism, Vol 240, Issue 2 125-E130
> 
> The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. 
> 
> Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. 
> 
> *Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH* release at a concentration of 10(-7) M. Furthermore, *tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH*. Our findings suggest that *Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.*
> ...


1. Its in vitro and this has not been seen in vivo. I'd raher a study in vivo any day of the week.

2. I'm not a rat.

3. Have you seen comparable studies on Tamox/Clomid testing this exact MOA, as it actaully shows the opposite and Tamox shows a sensitising effect on the pituitary. Clomid shows the opposite.

4. If you're thinking about estrogen priming. It does not happen in males, but only female rodents and female subjects. Not such phenomenom has been seen in males.




> I already did, in the very first post. I have even *highlighted* the relevant parts. You now have to read and understand exactly what is being said and the implications. It says Clomid is better at a LH release, and that Nolva and Clomid compete for the same receptors. Conclusion: if a needed receptor is occupied by Nolva, Clomid cannot occupy it and therefore Clomid will not attach and exert a greater amount of LH reponse than the Nolva that does occupy the receptor. I really can't explain this any more simply.


Explain to me in a comparable study Tamoxifen exerted a larger LH release from the pituitary than Clomid did? 




> I should add, I have a bias against Nolva to begin with because it is carcinogen: http://potency.berkeley.edu/chempage...20CITRATE.html
> 
> Rat experiments show Nolva produces DNA adducts while Clomid does not. I haven't seen the experiments reproduced in humans, though. Just have the UC Berkely site info.


So is estrogen.

Clomid is actually more estrogenic than Tamoxifen is. It is an agonist in more tissues, so one would assume its also a carcinogen.

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## Lemonada8

In males clomid decreases responsiveness to LH over time, while tamox increases it. 
Clomid has a higher affnity for the ER than tamox does. So they arent gonna "compete" and both only occupy about 40% of the total ER in the body even with increasing doses. so by combining them you arent losing any efficacy.
also, you cant rely on studies on ovariectomized rats, they were female rats that had their ovaries removed. They dont have the same hormonal profile due to the lack of the Y chromosome. the development is much different than male humans. 
however the rat issue is not that big of a deal
Using SERMs have also been shown to reduce the amount of total ER in the body, which after a cycle would be elevated.

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## Swifto

> In males clomid decreases responsiveness to LH over time, while tamox increases it. 
> Clomid has a higher affnity for the ER than tamox does. So they arent gonna "compete" and both only occupy about 40% of the total ER in the body even with increasing doses. so by combining them you arent losing any efficacy.
> also, you cant rely on studies on ovariectomized rats, they were female rats that had their ovaries removed. They dont have the same hormonal profile due to the lack of the Y chromosome. the development is much different than male humans. 
> however the rat issue is not that big of a deal
> Using SERMs have also been shown to reduce the amount of total ER in the body, which after a cycle would be elevated.


Looks like you've just gone into more detail (I couldnt be bothered, it was late) with the points I just made above. Thanks.

How did you come to the conclusion "Comid has a higher affinity for the ER than Tamox"? Thats a general statement and it will vary in tissue selection. Seeing as Tamox is much more of an antagonist that Clomid is, even in generalised terms, I dont think thats correct.

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## GotNoBlueMilk

> In males clomid decreases responsiveness to LH over time, while tamox increases it. 
> Clomid has a higher affnity for the ER than tamox does. So they arent gonna "compete" and both only occupy about 40% of the total ER in the body even with increasing doses. so by combining them you arent losing any efficacy.
> also, you cant rely on studies on ovariectomized rats, they were female rats that had their ovaries removed. They dont have the same hormonal profile due to the lack of the Y chromosome. the development is much different than male humans. 
> however the rat issue is not that big of a deal
> Using SERMs have also been shown to reduce the amount of total ER in the body, which after a cycle would be elevated.


I'm sorry, I thought everyone had a basic understanding of LH. It is manufactured in the pituitary, so I am only talking about pituitary ER. And specifically, I am pointing out that Clomid is better for LH stiumulation in PCT than Nolva because of the GnRH quality. 

Ovaries, ER receptors in breast tissue, how many ER they occupy in the total ER count of the body, overall ER receptor count in the body as a whole, is irrelevant to my point and post. 

And I never said to use Clomid for extended periods of time. I never even said when to use it. I simply pointed out it is more efficient for GnRH and LH production because of the GnRH component. This makes it beneficial in PCT and more suited to raising LH than Nolva. It's the same concept as Triptorelin, which also is a GnRH. Nolva simply increases LH by blocking ER receptors in the pituitary. Clomid blocks the receptors and also acts as a GnRH. This GnRH property gives a long-term benefit to LH levels. Not on the same level as Triptorelin, but better nontheless. Oh, and you can't mix Triptorelin with Nolva either, and for the same reason.

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## Swifto

> I'm sorry, I thought everyone had a basic understanding of LH. It is manufactured in the pituitary, so I am only talking about pituitary ER. And specifically, I am pointing out that Clomid is better for LH stiumulation in PCT than Nolva because of the GnRH quality. 
> 
> Ovaries, ER receptors in breast tissue, how many ER they occupy in the total ER count of the body, overall ER receptor count in the body as a whole, is irrelevant to my point and post. 
> 
> And I never said to use Clomid for extended periods of time. I never even said when to use it. I simply pointed out it is more efficient for GnRH and LH production because of the GnRH component. This makes it beneficial in PCT and more suited to raising LH than Nolva. It's the same concept as Triptorelin, which also is a GnRH. Nolva simply increases LH by blocking ER receptors in the pituitary. Clomid blocks the receptors and also acts as a GnRH. This GnRH property gives a long-term benefit to LH levels. Not on the same level as Triptorelin, but better nontheless. Oh, and you can't mix Triptorelin with Nolva either, and for the same reason.


No, you're wrong.

Tamoxifen sensitises the pituitary to GnRH, which means there will be a bigger LH surge, when compared to Clomid.

As shown here: _Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro. Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Am J Physiol 1981 Feb;240(2):E125-30_ 

Clomid does not behave like estrogen in the pituitary in male subjects (estroge priming), only female.

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## Lemonada8

> Looks like you've just gone into more detail (I couldnt be bothered, it was late) with the points I just made above. Thanks.
> 
> How did you come to the conclusion "Comid has a higher affinity for the ER than Tamox"? Thats a general statement and it will vary in tissue selection. Seeing as Tamox is much more of an antagonist that Clomid is, even in generalised terms, I dont think thats correct.


its all about dissociation constants. the lower the stronger binding it is to the receptor

DIFFERENTIAL DEPLETION OF CYTOPLASMIC
HIGH AFFINITY OESTROGEN RECEPTORS AFTER
THE in vivo ADMINISTRATION OF THE
ANTIOESTROGENS, CLOMIPHENE, MER-25 AND TAMOXIFEN 

Attachment 117152Attachment 117152

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## GotNoBlueMilk

> its all about dissociation constants. the lower the stronger binding it is to the receptor
> 
> DIFFERENTIAL DEPLETION OF CYTOPLASMIC
> HIGH AFFINITY OESTROGEN RECEPTORS AFTER
> THE in vivo ADMINISTRATION OF THE
> ANTIOESTROGENS, CLOMIPHENE, MER-25 AND TAMOXIFEN 
> 
> Attachment 117152Attachment 117152


Again, this is great if you are looking for a SERM that does a better job of blocking E receptors in the entire body. For PCT and stimulating the body's production of testosterone via LH excretion, we do not care about that. I don't think anyone considers Clomid better than Nolva for gyno protection. But I am not discussing that at all. So arguing that Nolva is better for PCT because it is better at preventing gyno is not a valid arguement.

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## GotNoBlueMilk

> No, you're wrong.
> 
> Tamoxifen sensitises the pituitary to GnRH, which means there will be a bigger LH surge, when compared to Clomid.
> 
> As shown here: _Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro. Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Am J Physiol 1981 Feb;240(2):E125-30_ 
> 
> Clomid does not behave like estrogen in the pituitary in male subjects (estroge priming), only female.


Funny, you quote the same study as in my initial post but you fail to read the study or the post. I have copied the releveant paragraph here and highlighted the relevent section one more time:

*Tamoxifen*, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, *was without effect on the GnRH-stimulated LH release* at a concentration of 10(-7) M. Furthermore, *tamoxifen*, unlike Clomid,* caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH*. Our findings suggest that *Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin*.

You have the correct study, you just didn't read it correctly.

It's time to move on. I certainly am.

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## Swifto

> Funny, you quote the same study as in my initial post but you fail to read the study or the post. I have copied the releveant paragraph here and highlighted the relevent section one more time:
> 
> *Tamoxifen*, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, *was without effect on the GnRH-stimulated LH release* at a concentration of 10(-7) M. Furthermore, *tamoxifen*, unlike Clomid,* caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH*. Our findings suggest that *Clomid and its Enclomid isomer, unlike tamoxifen , exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin*.
> 
> You have the correct study, you just didn't read it correctly.
> 
> It's time to move on. I certainly am.


Dont move on.

This article is wrong then I assume?

Your going on what the abstract states (which can be dangerous in my experience) and William Lwellyn is going on the full paper. 

Have you read the full paper yet?
_

Nolvadex VS. Clomid



Clomid, Nolvadex and Testosterone Stimulation
By William Llewellyn


I have received a lot of heat lately about my preference for Nolvadex over Clomid, which I hold for all purposes of use (in the bodybuilding world anyway); as an anti-estrogen, an HDL (good) cholesterol-supporting drug, and as a testosterone-stimulating compound. Most people use Nolvadex to combat gynecomastia over Clomid anyway, so that is an easy sell. And for cholesterol, well, most bodybuilders unfortunately pay little attention to this important issue, so by way of disinterest, another easy opinion to discuss. But when it comes to using Nolvadex for increasing endogenous testosterone release, bodybuilders just do not want to hear it. They only seem to want Clomid. I can only guess that this is based on a long rooted misunderstanding of the actions of the two drugs. In this article I would therefore like to discuss the specifics for these two agents, and explain clearly the usefulness of Nolvadex for the specific purpose of increasing testosterone production.



Clomid and Nolvadex

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 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.

Studies conducted in the late 1970's at the University of Ghent in Belgium make clear the advantages of using Nolvadex instead of Clomid for increasing testosterone levels (1). Here, researchers looked the effects of Nolvadex and Clomid on the endocrine profiles of normal men, as well as those suffering from low sperm counts (oligospermia). For our purposes, the results of these drugs on hormonally normal men are obviously the most relevant. What was found, just in the early parts of the study, was quite enlightening. Nolvadex, used for 10 days at a dosage of 20mg daily, increased serum testosterone levels to 142% of baseline, which was on par with the effect of 150mg of Clomid daily for the same duration (the testosterone increase was slightly, but not significantly, better for Clomid). We must remember though that this is the effect of three 50mg tablets of Clomid. With the price of both a 50mg Clomid and 20mg Nolvadex typically very similar, we are already seeing a cost vs. results discrepancy forming that strongly favors the Nolvadex side.



Pituitary Sensitivity to GnRH

But something more interesting is happening. Researchers were also conducting GnRH stimulation tests before and after various points of treatment with Nolvadex and Clomid, and the two drugs had markedly different results. These tests involved infusing patients with 100mcg of GnRH and measuring the output of pituitary LH in response. The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more LH will be released. The tests showed that after ten days of treatment with Nolvadex, pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with 150mg Clomid, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more LH was released before treatment). As the study with Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosterone and LH levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment Clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of Nolvadex serves only to increase pituitary sensitivity to this hormone. That is not to say Clomid won't increase testosterone if taken for the same 6 week time period. Quite the opposite is true. But we are, however, noticing an advantage in Nolvadex.



The Estrogen Clomid

The above discrepancies are likely explained by differences in the estrogenic nature of the two compounds. The researchers' clearly support this theory when commenting in their paper, "The difference in response might be attributable to the weak intrinsic estrogenic effect of Clomid, which in this study manifested itself by an increase in transcortin and testosterone/estradiol-binding globulin [SHBG] levels; this increase was not observed after tamoxifen treatment". In reviewing other theories later in the paper, such as interference by increased androgen or estrogen levels, they persist in noting that increases in these hormones were similar with both drug treatments, and state that," …a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation".

Although these two are related anti-estrogens, they appear to act very differently at different sites of action. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary. To find further support for this we can look at an in-vitro animal study published in the American Journal of Physiology in February 1981 (2). This paper looks at the effects of Clomid and Nolvadex on the GnRH stimulated release of LH from cultured rat pituitary cells. In this paper, it was noted that incubating cells with Clomid had a direct estrogenic effect on cultured pituitary cell sensitivity, exerting a weaker but still significant effect compared to estradiol. Nolvadex on the other hand did not have any significant effect on LH response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.



Conclusion

To summarize the above research succinctly, Nolvadex is the more purely anti-estrogenic of the two drugs, at least where the HPTA (Hypothalamic-Pituitary-Testicular Axis) is concerned. This fact enables Nolvadex to offer the male bodybuilder certain advantages over Clomid. This is especially true at times when we are looking to restore a balanced HPTA, and would not want to desensitize the pituitary to GnRH. This could perhaps slow recovery to some extent, as the pituitary would require higher amounts of hypothalamic GnRH in the presence of Clomid in order to get the same level of LH stimulation.

Nolvadex also seems preferred from long-term use, for those who find anti-estrogens effective enough at raising testosterone levels to warrant using as anabolics. Here Nolvadex would seem to provide a better and more stable increase in testosterone levels, and likely will offer a similar or greater effect than Clomid for considerably less money. The potential rise in SHBG levels with Clomid, supported by other research (3), is also cause for concern, as this might work to allow for comparably less free active testosterone compared to Nolvadex as well. Ultimately both drugs are effective anti-estrogens for the prevention of gyno and elevation of endogenous testosterone, however the above research provides enough evidence for me to choose Nolvadex every time.

In next month's follow-up article I will be discussing the role anti-estrogens play in post-cycle testosterone recovery. Most specifically, I will be detailing what a proper post-cycle ancillary drug program looks like, and explain why anti-estrogens alone are not effective during this window of time.


References
1. Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men. Vermeulen, Comhaire. Fertil and Steril 29 (1978) 320-7

2. Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro. Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Am J Physiol 1981 Feb;240(2):E125-30

3. The effect of clomiphene citrate on sex hormone binding globulin in normospermic and oligozoospermic men. Adamopoulos, Kapolla et al. Int J Androl 4 (1981) 639-45_

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## Lemonada8

> Again, this is great if you are looking for a SERM that does a better job of blocking E receptors in the entire body. For PCT and stimulating the body's production of testosterone via LH excretion, we do not care about that. I don't think anyone considers Clomid better than Nolva for gyno protection. But I am not discussing that at all. So arguing that Nolva is better for PCT because it is better at preventing gyno is not a valid arguement.


i agree with you on that clomid should be used in PCT, and actually gonna write up an article on it. 
but the issue i had was quoted in my first post, how did you get to the 25mg dose of clomid is best and 2) how does taking clomid and nolva together reduce the effectiveness?
clomid has a higher affnity for the pituitary receptor (previous post) so when it comes to which will bind, the clomid will usually bind first.

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## GotNoBlueMilk

> Pituitary Sensitivity to GnRH
> 
> But something more interesting is happening. Researchers were also conducting GnRH stimulation tests before and after various points of treatment with Nolvadex and Clomid, and the two drugs had markedly different results. These tests involved infusing patients with 100mcg of GnRH and measuring the output of pituitary LH in response. The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more LH will be released. The tests showed that after ten days of treatment with Nolvadex, pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with *150mg Clomid*, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more LH was released before treatment). As the study with Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosterone and LH levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment Clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of Nolvadex serves only to increase pituitary sensitivity to this hormone. That is not to say Clomid won't increase testosterone if taken for the same 6 week time period. Quite the opposite is true. But we are, however, noticing an advantage in Nolvadex.


This study is flawed in that we know higher doses of Clomid actually decrease the GnRH reponse. This is why I said above the the best dosage for Clomid is 25 mg. At this level it does not desensitize in a short period of time. Using Clomid for three weeks at the correct does should be fine.

Think about Triptolorin, at a very very small dose it stimulates LH and testosterone production; at a high dose it castrates you by shutting down GnRH. So we want to use 25 mg, not 150 mg. Again, this assumes 25 mg of clinical grade Clomid.

I'll try to dig up the study that showed maximum output is with 25 mg. It is possible I am remembering this incorrectly and the maximum dose is 50 mg. But I know it is not above 50 mg.

I have seen studies where Clomid was used for many months at 25 mg ED and showed steady LH response. There was no desensitizing. This is why docs prescribe Clomid at 25 mg ED to stimulate testosterone levels in men when their LH levels are low. The studies show this is effective, even for longterm. But it has to be lower doses because more is not better. Less is better.

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## Swifto

> This study is flawed in that we know higher doses of Clomid actually decrease the GnRH reponse. This is why I said above the the best dosage for Clomid is 25 mg. At this level it does not desensitize in a short period of time. Using Clomid for three weeks at the correct does should be fine.
> 
> Think about Triptolorin, at a very very small dose it stimulates LH and testosterone production; at a high dose it castrates you by shutting down GnRH. So we want to use 25 mg, not 150 mg. Again, this assumes 25 mg of clinical grade Clomid.
> 
> I'll try to dig up the study that showed maximum output is with 25 mg. It is possible I am remembering this incorrectly and the maximum dose is 50 mg. But I know it is not above 50 mg.
> 
> I have seen studies where Clomid was used for many months at 25 mg ED and showed steady LH response. There was no desensitizing. This is why docs prescribe Clomid at 25 mg ED to stimulate testosterone levels in men when their LH levels are low. The studies show this is effective, even for longterm. But it has to be lower doses because more is not better. Less is better.


Ok.

I often suggest 25mg/ED Clomid in PCT as it has been proven to raise serum T by 142%. The study is at the bottom of my PCT sticky. Larger doses also seem to cause more occular toxicity.

Also an advocate of Trip at a very low dose to stimulate endo. GnRH, never used it personally though.

I'd like to see this study to shed more light on this, but you raise a good point.

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## GotNoBlueMilk

Tracked down the maximum dosage stuff. 

First, we already looked at the 25 mg, long term dose of Clomid study. So we know that works and does not lead to desensitization.

*Here is the study that tested 50 mg of Clomid ED:*
Recovery of persistent hypogonadism by clomiphene in males with prolactinomas under dopamine agonist treatment, Rogerio Silicani Ribeiro and Julio Abucham, European Journal of Endocrinology, Vol 161, Issue 1, 163-169

Results: Ten patients (71%), five hyperprolactinemic and two normoprolactinemic, responded to clomiphene (testosterone >300 ng/dl). Testosterone levels increased from 201±22 to 457±37 ng/dl, 436±52, and 440±47 ng/dl at 4, 8, and 12 weeks respectively (0.001<P<0.01). Estradiol increased significantly and peaked at 12 weeks. LH increased from 1.7±0.4 to 6.2±2.0 IU/l, 4.5±0.7, and 4.6±0.7 IU/l at 4, 8, and 12 weeks respectively (0.001<P<0.05). FSH levels increased in a similar fashion. Prolactin levels remained unchanged. Erectile function improved (P<0.05) and sperm motility increased (P<0.05) in all six patients with asthenospermia before clomiphene. 
*End of Study Text*

Even though the number of subjects is low, the results are significant and conclusive. As you can see, the Testosterone response peaked at week 4 and then decreased a little but basically was the same level from week 4-12. But of special interest is that LH increased from 1.7 to 6.2 at week 4, but decreased to ~4.5 thereafter. Too bad there wasn't a shorter test interval; however, this shows that at 4 weeks or earlier desensitization occured for LH response even though administration of clomid was constant. Given the dramatic increase in LH between start and week 4, and the dramatic decrease from week 4 to 8, it is highly probable that the desensitization occured close to 4 weeks, and not 10 days.

We take the 50 mg study and compare to the long term 25 mg study to conclude that 25 mg is maximum dosage. However, if you are doing 4 weeks or less 50 mg would be fine. 

So the little voice in the back of my head that was telling me the maximum dose may be 50 mg instead of 25 is correct; We should consider 50 mg the maximum does unless we are going to do super shot cycles of Clomid. We already know from above that 150 mg desensitized LH in less than 10 days. I found a study showing the same for 100 mg based on 7 days usage. 

Given all of this, 50 mg ED for 4 weeks or less is maximum dosage when used for stimulating LH production in a PCT scenario. If going longer than 4 week, 25 mg ED would be maximum dosage.

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## WhiteTiger

Very good thread, Im glad it started this kind of discussion, this is what I was looking for. So in short what have we came to agree on?

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## GotNoBlueMilk

> So in short what have we came to agree on?


PCT is a complicated business that we truely don't fully understand!

We are forced to rely on studies that are not designed for PCT investigation. We find applicable data from studies designed for other purposes and try to figure out the best approach for PCT. Some studies fit well with our goals, others do not. In the end, we have to look at all these studies and form an option based on logic and conclusions, with some assumptionsm rather than hard facts from studies that perfectly match our needs. So 50 mg in a limited sample gives us information. 150 mg in another study gives us information. 

What we truly need is to get a large, post Mr. Olympia experiment designed and run. Take all the Mr. Olympia contestants and right after the Mr. Olympia contest start a PCT experiment that truly meets our needs. This will show the best PCT based on bodybuilders, not 45 y/o hypogondal men, 25 y/o hypogonal men with pituitary issues, etc.

Based on Swifto's pic, he has a lot better chance of getting the bodybuilding community to agree to this experiment than I do. I look more like popeye before eating spinich and don't run in the pro bodybuilder circles.

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## Swifto

> Tracked down the maximum dosage stuff. 
> 
> First, we already looked at the 25 mg, long term dose of Clomid study. So we know that works and does not lead to desensitization.
> 
> *Here is the study that tested 50 mg of Clomid ED:*
> Recovery of persistent hypogonadism by clomiphene in males with prolactinomas under dopamine agonist treatment, Rogerio Silicani Ribeiro and Julio Abucham, European Journal of Endocrinology, Vol 161, Issue 1, 163-169
> 
> Results: Ten patients (71%), five hyperprolactinemic and two normoprolactinemic, responded to clomiphene (testosterone >300 ng/dl). Testosterone levels increased from 201±22 to 457±37 ng/dl, 436±52, and 440±47 ng/dl at 4, 8, and 12 weeks respectively (0.001<P<0.01). Estradiol increased significantly and peaked at 12 weeks. LH increased from 1.7±0.4 to 6.2±2.0 IU/l, 4.5±0.7, and 4.6±0.7 IU/l at 4, 8, and 12 weeks respectively (0.001<P<0.05). FSH levels increased in a similar fashion. Prolactin levels remained unchanged. Erectile function improved (P<0.05) and sperm motility increased (P<0.05) in all six patients with asthenospermia before clomiphene. 
> *End of Study Text*
> ...


Here's one for you then...


_After looking into it, I'm amazed at what long term studies of clomiphene administration have shown. Isolated clomid administration is capable of much more than I ever imagined. Take for instance this study in which five healthy young adult men aged 26 to 33 were given 50 mg of clomiphene citrate twice a day for 8 weeks. The whole study focused on how the older men were relatively non-responsive compared to the younger men, yet the data on the young healthy men is incredible in and of itself. I'm surprised the researchers didn't even raise an eyebrow at this.

By week 8 of CC administration, the total testosterone level (Fig 2A) achieved in the young adult group was 48.2± 1.4 nmol/L (a 268% increase above baseline level). The young adult men reached a maximal nSHBG-T level (free testosterone level) (Fig 2B) of 20.6 ± 3.2 nmol/L (a 1,410% increase) after 8 weeks of CC administration. The increase in free testosterone is huge. And the beauty of it is that this is all endogenous production, due to increases in LH and FSH, which were also measured and graphed in the full study.

Full study: http://www.andrologyjournal.org/cgi/reprint/12/4/258_


http://forums.steroid.com/showthread...d#.To8uaLLX-So

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## GotNoBlueMilk

> Here's one for you then...
> 
> 
> _After looking into it, I'm amazed at what long term studies of clomiphene administration have shown. Isolated clomid administration is capable of much more than I ever imagined. Take for instance this study in which five healthy young adult men aged 26 to 33 were given 50 mg of clomiphene citrate twice a day for 8 weeks. The whole study focused on how the older men were relatively non-responsive compared to the younger men, yet the data on the young healthy men is incredible in and of itself. I'm surprised the researchers didn't even raise an eyebrow at this.
> 
> By week 8 of CC administration, the total testosterone level (Fig 2A) achieved in the young adult group was 48.2± 1.4 nmol/L (a 268% increase above baseline level). The young adult men reached a maximal nSHBG-T level (free testosterone level) (Fig 2B) of 20.6 ± 3.2 nmol/L (a 1,410% increase) after 8 weeks of CC administration. The increase in free testosterone is huge. And the beauty of it is that this is all endogenous production, due to increases in LH and FSH, which were also measured and graphed in the full study.
> 
> Full study: http://www.andrologyjournal.org/cgi/reprint/12/4/258_
> 
> ...


And this makes sense, because often older men's leydig cells do not respond to LH the same as when they were younger. This is a typical cause for low testosterone levels in older men. Also, if LH is naturally on the higher end of range, Clomid therapy is of little or no benefit.

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## GotNoBlueMilk

> Here's one for you then...
> 
> 
> _After looking into it, I'm amazed at what long term studies of clomiphene administration have shown. Isolated clomid administration is capable of much more than I ever imagined. Take for instance this study in which five healthy young adult men aged 26 to 33 were given 50 mg of clomiphene citrate twice a day for 8 weeks. The whole study focused on how the older men were relatively non-responsive compared to the younger men, yet the data on the young healthy men is incredible in and of itself. I'm surprised the researchers didn't even raise an eyebrow at this.
> 
> By week 8 of CC administration, the total testosterone level (Fig 2A) achieved in the young adult group was 48.2± 1.4 nmol/L (a 268% increase above baseline level). The young adult men reached a maximal nSHBG-T level (free testosterone level) (Fig 2B) of 20.6 ± 3.2 nmol/L (a 1,410% increase) after 8 weeks of CC administration. The increase in free testosterone is huge. And the beauty of it is that this is all endogenous production, due to increases in LH and FSH, which were also measured and graphed in the full study.
> 
> Full study: http://www.andrologyjournal.org/cgi/reprint/12/4/258_
> 
> ...


And this makes sense because older men's leydig cells often fail to respond to LH stimulation the same as when they were young. Also, if LH base levels are in the part of the range, then Clomid therapy has little if anything to offer for raising testosterone levels .

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## Swifto

> And this makes sense, because often older men's leydig cells do not respond to LH the same as when they were younger. This is a typical cause for low testosterone levels in older men. Also, if LH is naturally on the higher end of range, Clomid therapy is of little or no benefit.


Well this sure as f*ck blows a hole in your "only use Clomid for 4 weeks because of LH desensitisation" doesnt it? Dont get too caught up in LH anyway, serum T is what we want eventually.

I realise you cannot compare hypogondal males with eugondal though. 

Still.

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## GotNoBlueMilk

> Well this sure as f*ck blows a hole in your "only use Clomid for 4 weeks because of LH desensitisation" doesnt it? Dont get too caught up in LH anyway, serum T is what we want eventually.
> 
> I realise you cannot compare hypogondal males with eugondal though. 
> 
> Still.


LH tells the leydig cells to produce testosterone . So w/o LH, one has very low testosterone . For PCT, we have to watch LH if we want a permanent recovery. The shutdown LH production is what has to be recovered! Once LH is recovered testosterone is recovered. Sure we want testosterone higher, but we have to do that via LH. Any compound that raises leydig cells production of testosterone does it via LH stimulation (Clomid by blocking ER in the pitutitary and GnRH, Novla by blocking ER in the pituitary) or by mimicing LH (HCG ). So hypogondal males will not benefit from any treatment except TRT since their leydig cells no longer respond to LH very well. 

The other thing about Clomid and Triptolorin is they are a GnRH, so after a person stops using them the pitutitary keeps on producing LH if the pitutitary is healthy. We only need a few weeks of Clomid for PCT. Then we move onto something else. Non-PCT use of Clomid to reverse low testosterone, a lower dose is used for a longer time. I honestly don't know if that longer period at a lower is really beneficial or not. But it is a long period that is prescribed by docs.

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## Swifto

> LH tells the leydig cells to produce testosterone . So w/o LH, one has very low testosterone . For PCT, we have to watch LH if we want a permanent recovery. The shutdown LH production is what has to be recovered! Once LH is recovered testosterone is recovered. Sure we want testosterone higher, but we have to do that via LH. Any compound that raises leydig cells production of testosterone does it via LH stimulation (Clomid by blocking ER in the pitutitary and GnRH, Novla by blocking ER in the pituitary) or by mimicing LH (HCG ). So hypogondal males will not benefit from any treatment except TRT since their leydig cells no longer respond to LH very well. 
> 
> The other thing about Clomid and Triptolorin is they are a GnRH, so after a person stops using them the pitutitary keeps on producing LH if the pitutitary is healthy. We only need a few weeks of Clomid for PCT. Then we move onto something else. Non-PCT use of Clomid to reverse low testosterone, a lower dose is used for a longer time. I honestly don't know if that longer period at a lower is really beneficial or not. But it is a long period that is prescribed by docs.


Are you kidding me?

Go through my posts mate as I have more than a basic understanding on hypogonadism in general and post androgen administration hypogonadism. I know what f*cking LH is.

The study about is 100mg/ED for 12 weeks, the 142% figure (the abstract is at the bottom of my sticky) is done for 8 weeks. All show healthy increased testosterone levels from baseline.

My suggestion for PCT, if I advise Clomid, is 25mg/ED for 6 weeks, 50mg/ED week 1. Thats worked for me and countless others who have followed it. 

I actually prefer Tamox/Tore PCT, personally.

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## GotNoBlueMilk

> Are you kidding me?
> 
> Go through my posts mate as I have more than a basic understanding on hypogonadism in general and post androgen administration hypogonadism. I know what f*cking LH is.
> 
> The study about is 100mg/ED for 12 weeks, the 142% figure (the abstract is at the bottom of my sticky) is done for 8 weeks. All show healthy increased testosterone levels from baseline.
> 
> My suggestion for PCT, if I advise Clomid, is 25mg/ED for 6 weeks, 50mg/ED week 1. Thats worked for me and countless others who have followed it. 
> 
> I actually prefer Tamox/Tore PCT, personally.


I have seen lots of your posts and know what you understand. My comments were for clarification and benefit of others who read this and may come to the wrong conclusion that LH is irrelevant, based on your comment, "Dont get too caught up in LH anyway, serum T is what we want eventually."

Also, your study you say blows a hole in the 4 week max clomid usage is actually supported. If you want to split hairs, sure. For older males it turned out to be exactly 4 weeks. For younger males it was 6 weeks. So if you want to push to 6 weeks this study would support it if you are under 33.

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## Swifto

> I have seen lots of your posts and know what you understand. My comments were for clarification and benefit of others who read this and may come to the wrong conclusion that LH is irrelevant, based on your comment, "Dont get too caught up in LH anyway, serum T is what we want eventually."
> 
> Also, your study you say blows a hole in the 4 week max clomid usage is actually supported. If you want to split hairs, sure. For older males it turned out to be exactly 4 weeks. For younger males it was 6 weeks. So if you want to push to 6 weeks this study would support it if you are under 33.


I'm not splitting hairs, I guess I'm being more particular.

Your contribution to this thread has been excellent and I urge you to stick around. Good stuff.

I always like it when people formulate opinions and protocol's based on clinical data, its what I try to do.

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## WhiteTiger

So, is there a specific blood test to request end of cycle prior to pct, during pct or after? I would like to ensure my levels are optimal. The only blood tests ive had is prior cycle and mid cycle. I guess what im asking is what should i ask for and when.

My biggest concern is not ruining my chances of having kids. Any info on that?

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## jkn399

great read.

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## GotNoBlueMilk

> So, is there a specific blood test to request end of cycle prior to pct, during pct or after? I would like to ensure my levels are optimal. The only blood tests ive had is prior cycle and mid cycle. I guess what im asking is what should i ask for and when.
> 
> My biggest concern is not ruining my chances of having kids. Any info on that?


You have to remember that the goal of PCT is to get your system back to where it was pre-cycle. To determine that goal, you have to do a blood test 60 days post PCT, after all the Clomid, Nolva, DAA, or whatever you use is completely out of your system and your hormone levels have stabalized. So your final post PCT results would be compared to the prior cycle results. Make sure you are at least back to baseline. 

Consider if you get back only to 80% of baseline. Next cycle you have a lower baseline and once again you get back to only 80% of that. After several cycles you have clinically low T levels when you are not on cycle. Not a good result.

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## GotNoBlueMilk

> I'm not splitting hairs, I guess I'm being more particular.


Actually, I now have to backtrack on some of my comments and clarify. My original point is accurate, but I allowed myself to lose focus on the main point. My whole point about Clomid being better for PCT was due to it's GnRH properties. Unfortunately, the GnRH response diminishes at higher doses over time. So please bear with me so I can recap and summarize, then we will both see how the different study results are relevant in as far as they study went and what it was investigating. Swifto is focused on PCT raising testosterone as a whole, while I am more focused on one aspect of PCT which is restoring HPTA via GnRH. I consider the GnRH response key to kicking off PCT for longterm success. It is the GnRH response that makes triptorelin so great for PCT, and so risky when overused.

In the study _Clomid , Nolvadex and Testosterone Stimulation, By William Llewellyn_ that Swifto posted, it measured GnRH response using 150 mg of Clomid. It claimed that the response diminished after 7 days. My response was, of course it diminished after 7 days because the dose was too high.

However, in other studies we see that LH blood levels increase well beyond 7 days at high doses. This is because Clomid also acts as Nolva, both a SERM, in blocking estrogen receptors in the pituitary. So the pitutitary has no E2 binding at its receptors and therefore starts pumping out more LH. So as a SERM, Clomid will increase LH levels long after it has desensitized the GnRH response in the pituitary. But from what we know of a GnRH (again think about triptorelin which is the ultimate example), a little is great but once you desenstize the GnRH response bad things happen. 

So strickly looking at the GnRH response produced by Clomid, we need to do a shorter period at lower doses. Doing higher for longer periods still allows Clomid to work as a SERM and raise LH and testosterone, but it is no longer working as a GnRH and worse, it has now desensitized the GnRH response. 

For measuring the success of Clomid as a GnRH, we have to ignore any study that simply measures LH and testosterone levels . Those results have the SERM qualities of Clomid mixed in and do not measure the GnRH response. The SERM qualities of Clomid will overshadow the GnRH qualities unless the study is designed to measure the latter. Novla is far better choice as a SERM, but it lacks the GnRH response.

Where does this leave us as far as my line of thought goes?

*Use Clomid in the beginning of PCT for 3 weeks at 50 mg every day.* Switch to Nolva after that. Maybe overlap the two for a week doing Clomid 50 mg EOD for the 4th week while blood levels of Nolva increase. *Do not continue to use Clomid as a pure SERM beyond the intial period* since Nolva does attach to more receptors and has less sides. *As a SERM, Nolva is definately preferred. But for GnRH response which will benefit PCT longterm, we want to use Clomid.* 

I have to acknowledge, the 3 weeks and 50 mg values are something that lacks firm evidence in the PCT world. But studies do suggest they are good values to start with. Maybe 2 weeks or 4 weeks is good. Maybe 25 mg or 100 mg is a better dose. I don't know. But we do know for a fact that 150 mg over 7 days is too much. So we want to work lower than that, and possibly much lower.

If you don't like the sides of Clomid try adding in 150 mg of glutathione IM EOD. This does wonders for me. Some have argued this is because glutathione will enable the liver to pull the Clomid out of the body faster, reducing sides. I cannot agree with this since the clomid was doing it's job and increasing leydig cell size, despite the fact that I did 250 IU of HCG while doing Test Cyp, and for two weeks after the last Test shot I did 500 IUs EOD. I started Clomid two weeks after the last Test Cyp shot. I suspect that the small dopamine response from glutathione may be the reason sides are reduced. But aside from how I feel better, why I feel better is all speculation on my part.

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## Thesoviet666

> Hmmmm, lots of well written information, however Tamoxifen taken on its own for a month does very little for my balls. Add in Clomid and my balls grow huge within 10 or 12 days.
> 
> So my experience differs with the authours, you might say that ball size has nothing to do with recovery, my feeling is that it is very important.
> 
> FWIW my PCT is :-
> 
> Week 1, 50mg Clomid + 40mg Tamoxifen 
> Week 2 to 5, 25mg Clomid + 20mg Tamoxifen 
> 
> ...


Try clomid with a mild ai such as formadrol and daa all together, works great

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## anahny

So from my understanding Nolva works better than clomid and faster without the sides of clomid. And the only other thing clomid does is speed up testicle growth. So why not run Nolva 40/20/20/20 while taking a low dose clomid say 35mg every other day or so. Would that work?

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