# I need to know cem tamox dosage



## jjpeters4 (Sep 21, 2010)

Whats up guys, I'm currently running a 4 week mdrol cycle @ 10/20/20/20 and my pct is cel's tamox. I planned on running 20/20/10/10 for the tamox, I just wanted to know if cel's tamox is regular pharm grade, if not tell me a good dosage for pct......Thanks guys.


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## pyes (Sep 21, 2010)

Dude, your whole cycle is wacky.


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## unclem (Sep 22, 2010)

u need clomid for pct. arimidex or aromasin for on hand in case gyno arrives.


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## pyes (Sep 22, 2010)

unclem said:


> u need clomid for pct. arimidex or aromasin for on hand in case gyno arrives.


 
you should've had this stuff before cycling.


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## Du (Sep 22, 2010)

jjpeters4 said:


> Whats up guys, I'm currently running a 4 week mdrol cycle @ 10/20/20/20 and my pct is cel's tamox. I planned on running 20/20/10/10 for the tamox, I just wanted to know if cel's tamox is regular pharm grade, if not tell me a good dosage for pct......Thanks guys.




I don't know why everyone is all over Clomid over Nolva lately; drives me nuts. I think your dosing looks fine, even, good. Im not familiar with mdrol, but I assume that dosage is what the label reads?

In any case, your question is regarding the Nolva; I think the dosing is pretty good. I do not think you'll *need* an AI as mentioned by others in this thread, but do make sure to have some extra Nolva in hand incase gyno pops up while on cycle. (Who knows, maybe you're prone to it.) You could always buy more now, it'll arrive by the time you need it for PCT.


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## jjpeters4 (Sep 22, 2010)

Thanks for the educated reply  Du, I did alittle reading up on the pct's, most studies I read, said that nolva was better for gyno and boosted test levels higher. As for the mdrol cycle, I did alot of study there too, it seemed when people dosed @ 30mg or higher, they started getting the most sides.


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## Du (Sep 22, 2010)

jjpeters4 said:


> Thanks for the educated reply  Du, I did alittle reading up on the pct's, most studies I read, said that nolva was better for gyno and boosted test levels higher. As for the mdrol cycle, I did alot of study there too, it seemed when people dosed @ 30mg or higher, they started getting the most sides.




I can't speak for the Mdrol, but you're spot on with your comments on Nolva. I'd choose it over Clomid any day.


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## pyes (Sep 22, 2010)

Du said:


> I don't know why everyone is all over Clomid over Nolva lately; drives me nuts. I think your dosing looks fine, even, good. Im not familiar with mdrol, but I assume that dosage is what the label reads?
> 
> In any case, your question is regarding the Nolva; I think the dosing is pretty good. I do not think you'll *need* an AI as mentioned by others in this thread, but do make sure to have some extra Nolva in hand incase gyno pops up while on cycle. (Who knows, maybe you're prone to it.) You could always buy more now, it'll arrive by the time you need it for PCT.


 
The reason I am sticking with clomid is because VIC (IMO one of the top 3 smartest users on here) says clomid over nolva. He even frowns upon nolva as a pct. As well as many other vets here. I am just learning from my mentors


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## Du (Sep 22, 2010)

pyes said:


> The reason I am sticking with clomid is because VIC (IMO one of the top 3 smartest users on here) says clomid over nolva. He even frowns upon nolva as a pct. As well as many other vets here. I am just learning from my mentors




I'd love to read why...


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## ersin.konuk (Sep 22, 2010)

Every thing i read says nolva blocks test and when i used nolva it messed with my sight bad so i use arimasin now, in my own exspiriance it works better for me.....


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## Du (Sep 22, 2010)

ersin.konuk said:


> Every thing i read says nolva blocks test and when i used nolva it messed with my sight bad so i use arimasin now, in my own exspiriance it works better for me.....




Interesting.... have a read of this. I believe it was originally written by Big Cat. So, if he did, it's a pretty reliable source of info.






> *Nolvadex vs. Clomid for PCT*
> 
> 
> 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.
> ...


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## ersin.konuk (Sep 22, 2010)

good read thanx that should clear everything up........


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## BigBoiH (Sep 22, 2010)

You know I posted that about 1 week ago in a question and this is what I got:

Look at the dates of the research done, enough said.  Here is a CURRENT article from the same person.

First, most people who have been educated by way of the boards over the  last 8 years DON'T use Nolva. Bill Llewellyn, author of Anabolics 2008,  has changed his stance on Nolva recently after endorsing it's use for 9  years.Interesting read from William LLewelyn
Estrogen is not the enemy

*Aromatizable Androgens and Anabolism:
The Role of Estrogen in Muscle Growth
by William Llewellyn *

Can estrogen work to augment muscle growth? Is this hormone always  unwanted when we are taking anabolic steroids? Anecdotal reports from  athletes suggest that the use of estrogen maintenance drugs such as  tamoxifen (anti-estrogen) or aminoglutethimide (anti-aromatase) may  slightly hinder muscle mass gains during steroid therapy. An explanation  or even clarification for this observation has not been easy to come  by. Here I would like to take a look at the comparative effectiveness of  certain aromatizable and non-aromatizable drugs, as well as the  possible mechanism in which estrogen can play a beneficial role to the  athlete. 

*The Androgen Receptor *
All anabolic/androgenic steroids promote muscle growth primarily via the  cellular androgen receptor (abbreviated as AR in this article). The  steroid attaches to and activates the androgen receptor, which  ultimately gives the cell an order to increase protein synthesis. This  process is well understood. But it has been suggested that other  mechanisms may foster muscle growth during steroid therapy as well,  which lie outside of the androgen receptor. One way this is evidenced is  by the fact that steroids displaying a high affinity for the AR in  muscle tissue do not always promote an equally high level of muscle  growth. In other words, anabolic potency does not always correspond  perfectly to receptor affinity. Clearly there are some disparities that  lead into question whether or not the androgen receptor is the only  thing at work concerning growth. 

*Testosterone, Nandrolone and Methenolone *
Testosterone is without question one of the most effective steroids for  building muscle mass available to athletes. However it does not have the  highest affinity for the androgen receptor compared to some other  steroids. For example, it has been shown that by eliminating the  19-methyl group (nandrolone) the affinity of the steroid for the  androgen receptor is greatly enhanced_. Nandrolone thus displays  approximately 2-3 times greater affinity for the androgen receptor  compared to testosterone, yet its ability to promote muscle growth seems  to be considerably lower than testosterone at an equal dosage. One  discussed possibility for this occurrence is the reduced androgenic  potency of nandrolone. While testosterone converts to the more active  steroid dihydrotestosterone (3-4 times greater AR affinity) upon  interaction with the 5-alpha reductase enzyme in various androgenic  target tissues such as the skin, scalp, prostate, CNS and liver,  nandrolone drops to a third of its original potency by converting to the  weak steroid dihydronandrolone[ii]. However this action is very site  specific, and in muscle tissue nandrolone dominates as the active form  of the steroid. Therefore this explanation may not suffice. 

Nandrolone also differs from testosterone in its ability to be converted  by the aromatase enzyme to estradiol (an active estrogen). In  comparison, nandrolone aromatizes at approximately 20% of the rate  testosterone does, and as such is not known as a very estrogenic  steroid. It is likewise favored when reduced estrogenic side effects  such as water retention, fat deposition and gynecomastia are desired.  However athletes know that there is a trade off with the reduced  tendency for nandrolone to promote side effects, in that it is a less  anabolic steroid. With its known high affinity for the AR in muscle  tissue, could this suggest that estrogen may also be a key mediator of  muscle growth? 

When we look at Primobolan® (methenolone) we see a similar trend.  Methenolone is at least as good a binder of the androgen receptor as  testosterone. By some accounts it is on par with nandrolone[iii].  However it is known to be much weaker than both steroids at promoting  muscle growth. We know that methenolone does not interact with 5-alpha  reductase, and as such its affinity for the AR does not increase or  decrease in androgen target tissues. This would logically seem like a  more favorable trait for anabolism over the weakening we see with  nandrolone. However methenolone is a markedly weaker anabolic, and  requires relatively high doses to promote growth. This also brings into  question the role of 5-alpha reductase in promoting an anabolic state.  Perhaps the fact that Primobolan® is a non-aromatizable steroid is more  relevant. 

*Estrogen and GH/IGF-1 *
To date the most common explanation for why anti-estrogens may be  slightly counterproductive to growth in the sports literature has been  the suggestion that estrogen plays a role in the production of growth  hormone and IGF-1. IGF-1 (insulin like growth factor 1, formerly known  as somatomedin C) is of course an anabolic product released primarily in  the liver via GH stimulus. IGF-1 is responsible for the growth  promoting effects (increased nitrogen retention, cell proliferation) we  associate with growth hormone therapy. We do know that women have higher  levels of growth hormone than men, and also that GH secretion varies  over the course of the menstrual cycle in direct correlation with  estrogen levels[iv]. Estrogen is likewise often looked at as a key  trigger in the release of GH in women under normal physiological  situations. 

It is also suggested that the aromatization of androgens to estrogens in  men plays an important role in the release and production of GH and  IGF-1. This was evidenced by a 1993 study of hypogonadal men, comparing  the effects of testosterone replacement therapy on GH and IGF-1 levels  with and without the addition of tamoxifen[v].* When the anti-estrogen tamoxifen was given, GH and IGF-1 levels were notably suppressed*,  while both values were elevated with the administration of testosterone  enanthate alone. Another study has shown 300mg of testosterone  enanthate weekly (which elevated estradiol levels) to cause a slight  IGF-1 increase in normal men, whereas 300mg weekly of nandrolone  decanoate (a poor substrate for aromatase that caused a lowering of  estradiol levels in this study) would not elevate IGF-1 levels[vi]. Yet  another study shows that GH and IGF-1 secretion is increased with  testosterone administration on males with delayed puberty, while  dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1  secretion, presumably due to its strong anti-estrogenic/gonadotropin  suppressing action[vii]. All of these studies seem to support a direct,  estrogen-dependant mechanism for GH and/or IGF-1 release in men. It is  difficult to say at this point just how important estrogen is to IGF-1  production as it relates to the promotion of anabolism in the steroid  using athlete, however it remains an interesting subject to investigate.  

*Glucose Utilization and Estrogen*
Estrogen may play an even more vital role in promoting an anabolic state  by affecting glucose utilization in muscle tissue. This occurs via an  altering the level of available glucose 6-phosphate dehydrogenase. G6PD  is an important enzyme in the support anabolism, as it is directly tied  to the use of glucose for muscle growth and recuperation[viii] [ix].  During the period of regeneration after skeletal muscle damage, levels  of G6PD are shown to rise dramatically. G6PD enzyme plays a vital role  in what is known as the pentose phosphate pathway, and as such this rise  is believed to enhance the PPP related process in which nucleic acids  and lipids are synthesized in cells; fostering the repair of muscle  tissue. 

A 1980 study at the University of Maryland has shown that levels of  glucose 6-phosphate dehydrogenase rise after administration of  testosterone propionate, and further that the aromatization of  testosterone to estradiol is directly responsible for this increase.[x]  In this study neither dihydrotestosterone nor fluoxymesterone could  mimic the affect of testosterone propionate on levels of G6PD, an affect  that was also blocked by the addition of the potent anti-aromatase  4-hydroxyandrostenedione to testosterone. 17-beta estradiol  administration caused a similar increase in G6PD, which was not noticed  when its inactive estrogen isomer 17-alpha estradiol (unable to bind the  estrogen receptor) was given. An anti-androgen could also not block the  positive action of testosterone. This study provides one of the first  palatable explanations for a direct and positive effect of estrogen on  muscle tissue. 

*What does this all mean? *
It is a long held belief among athletes that estrogen maintenance drugs  can slightly hinder muscle gains during steroid therapy with a strong  aromatizable steroid such as testosterone. Whether or not we have  plausibly explained this remains to be seen, however the above evidence  certainly does provide strong support for a direct and positive affect  of estrogen on growth. Does this mean we should abandon estrogen  maintenance drugs? I don’t think that should be the case. It is  important to remember that estrogen can deliver many unwanted effects  such as increased water retention, fat deposition and the development of  female breast tissue when it becomes too active in the male body.  Clearly if we plan a high-dose cycle with an aromatizable steroid,  anti-estrogens will be an important inclusion. However we cannot ignore  the suggestion of using estrogen maintenance drugs only when they are  necessary to combat visible side effects during mild to moderately dosed  cycles,especially if bulk is the ultimate goal of the athlete. _​


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## Du (Sep 22, 2010)

BigBoiH said:


> You know I posted that about 1 week ago in a question and this is what I got:
> 
> Look at the dates of the research done, enough said.  Here is a CURRENT article from the same person.
> 
> ...


​

If the idea of nolva being bad is what you got out of that article, I would suggest a re-read. Nowhere in there is there any comparison of Clomid vs Tamox, which is the topic of this discussion.

This essay is supporting the idea of limited anti E's while on PCT; not of Clomid over Nolva.


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## BigBoiH (Sep 22, 2010)

Umm actually I was agreeing with you and posting what someone wrote to me and was interested in your opinions, so I dont have to re-read jack. Also the topic of the convo  is a tamox dosage.


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## Du (Sep 22, 2010)

BigBoiH said:


> Umm actually I was agreeing with you and posting what someone wrote to me and was interested in your opinions, so I dont have to re-read jack. Also the topic of the convo  is a tamox dosage.




Ha, I read too fast, sorry about that.

My opinions, well... I guess I roundabout got to it in my last one; I still stand by Nolva over Clomid. The article itself really doesn't knock Nolva over Clomid, it simply suggests backing off the Anti E (whichever you may choose) unless you need it, as judged by physical appearance. 

Personally, unless I were able to get frequent (and I mean frequent) bloodwork to assess hormone levels, then I'd stick with avoiding gyno via use of an anti-.


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## jjpeters4 (Sep 22, 2010)

well said Du!


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