PDA

View Full Version : I need to know cem tamox dosage



jjpeters4
09-21-2010, 04:20 PM
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.

pyes
09-21-2010, 05:43 PM
http://www.twolvesblog.com/images/stories/wh-double-facepalm.jpg

Dude, your whole cycle is wacky.

unclem
09-22-2010, 04:24 AM
u need clomid for pct. arimidex or aromasin for on hand in case gyno arrives.

pyes
09-22-2010, 05:09 AM
u need clomid for pct. arimidex or aromasin for on hand in case gyno arrives.

you should've had this stuff before cycling.

Du
09-22-2010, 07:16 AM
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.

jjpeters4
09-22-2010, 07:27 AM
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.

Du
09-22-2010, 07:37 AM
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.

pyes
09-22-2010, 07:41 AM
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 :)

Du
09-22-2010, 08:06 AM
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...

ersin.konuk
09-22-2010, 08:08 AM
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.....

Du
09-22-2010, 08:43 AM
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.

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.

References

1 Vermeulen A., Comhaire F., Hormonal effects of an anti-estrogen, tamoxifen, in normal and oligospermic men, Fertil. Ster. 29 (1978) 320-27

2 Bruning PF, Bronfer JMG, Hart AAM, Jong-Bakker M, tamoxifen, serum lipoproteins and cardiovascular risk, Br. J. Cancer 1988 Oct, 58 (4) 497-9

source - Anabolic Steroids, Bodybuilding Discussion Forums (http://www.steroidology.com/forum/)

ersin.konuk
09-22-2010, 10:33 AM
:clapping:good read thanx that should clear everything up........

BigBoiH
09-22-2010, 01:03 PM
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[i]. 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.

Du
09-22-2010, 01:24 PM
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




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.

BigBoiH
09-22-2010, 02:44 PM
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.

Du
09-22-2010, 03:14 PM
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-.

jjpeters4
09-22-2010, 05:20 PM
well said Du!