Part 1
The A B C's of anti e's
Ok. I'll admit it. I didn't know much about anti-estrogens and their ilk before I started researching this article. And I'll admit another thing: I didn't care. I knew that 10mgs of Nolvadex per day was all I ever needed to not get gyno, though 50 mgs/day of Clomid seemed to work the same for me. Cytadren (remember that stuff?) worked for me also, at 250mgs/day, but it seemed to make me more prone to joint pain and problems. HCG worked best for me when I shot 500i.u. every other day post cycle for about 3 weeks. Arimadex was too expensive. AND THAT'S ALL I NEEDED TO KNOW!
Now nobody uses Cytadren anymore. We have affordable Arimadex (Anastrozole) in liquid form. We have Femera. And I had work to do to catch up.
In the long run, I wasn't that interested in what all this other stuff did because I already knew what worked for me. Well, keep reading and you'll find out why I was wrong, what my new plan is for during a cycle and post-cycle recovery, and some other interesting stuff about not getting any side effects from roids. Here we go!
So, first things first. Some steroids convert to estrogen. This is through the aromatase enzyme, and is called (duh) aromatization. When this happens you can get side effects associated with having too much estrogen, including bloating, gynocomastia, acne, and so on. Some steroids on the other hand, have progesteronic activity (deca, for example actually fits into the progesterone receptor with 20% the efficiency of actual progesterone!) (Cancer Res 1978 Nov;38(11 Pt 2):4186-98). The symptoms (acne, etc...) are the more or less the same for progesteronic and estrogenic effects. Note that I didn't say that these other steroids convert to progesterone, but rather that they have progesteronic effects. That's because the steroid is able to act on the progesterone receptor without conversion to another substance. Hence, on my old bulking cycle of 600mgs per week of Deca and my 750mgs per week of Test, anti-estrogens would only help with the aromatization of the test and not the progesteronic activity of the Deca I'm was taking. Know what else? Here are a bunch of other compounds that don't aromatize significantly (thats good news) activity and hence don't need any amount of anti-estrogens: Methenolone, Stanozolol, Dromostanolone, Oxandrolone, Mesterolone, Stenbolone, and Trenbolone (though it acts on the Progesterone Receptor with 60% the efficiency of progesterone itself, according to the last study I cited). Taking a big dose of any of these? Anti -estrogens won't help much if at all, per se, but keeping estrogen levels low is still a good idea. Remember, estrogen still has a role to play, even sides, in ways we don't fully understand yet. Not only that but if you take progesteronic gear and use nolvadex, you may be at an increased risk for progesteronic sides, as nolvadex may increase progesterone receptors (Gynecol Oncol. 1999 Mar;72(3):331-6.).
What can you do?
Well, the easy answer is to take bromocriptine (parlodel) at 2.5 to 5mg every day. Bromocriptine is one of those drugs that the life-extention crowd were very big on a few years ago. It is an anti-parkinsons medication which causes higher levels of the neurotransmitter dopamine, with side effects being an increased sex drive, possible curbing of appetite, possible stimulation of CNS, and fat loss. It's also indicated for some forms of male hypogonadism (yeah, so it may increase test levels on its own!). However, what we're interested in here is that it can be used to lower prolactin and progesterone. [Side note: A few tabs of Cabergoline per day will also lower prolactin and improve sexual function. I just couldn't figure out where else this would fit into this article.] Back to Bromo...it sounds almost perfect, right? Well, unfortunately, bromocriptine is also used to treat acromegaly (too much GH produced by the pituitary), and ergo may lower GH levels in your body! Fortunately, the dosage needed to halt overproduction of GH in your body is 10-20mgs/day, so we're safe with our amount necessary to stop from growing breasts from too much deca.and yes, all the cool fat burning, sex drive, and nootropic "side effects" happen at 2.5-5mgs/ day doses. As a side note, taking 25mcg of T3 or maybe 50-100mcgs of T4 may be effective for eliminating some if not all of the chance of getting gyno from tren. And yeah, I have the research to back that statement up, but it involves another page of reading about TRH, TSH, the negative feedback loop involved with low levels of T4 stimulating TRH, blah blah blah. Trust me, you don't care about the reasons why this works, just that it does. If you're doing tren, take some T3 and you'll get increased fat-burning, no gyno, and more maybe even anabolism. So if I were cutting up, tren, T3 (25mcgs), and bromo would all be part of my stack , and I'd expect to get really cut really fast (of course, there's other cool drugs I'd add into that mix.clen, test, etc.but this is about anciliaries, not a cutting cycle).
Another idea to reduce progesterone is to take RU486 (yeah, the pregnancy drug). This drug has anti-progesteronic effects, and in women 600mgs totally plocks progesterone. Don't even think about taking this dose, though.I'd reccomend taking around 50 mgs a day and working your way up. Remember, cortisol is also decreased with RU486, so sore joints may be a problem. Considering this, bromo's cool secondary effects, and price, I'd consider bromocriptine a better choice.
So what steroids do aromatize? Here some offenders: Testosterone, Methandrostenolone, Fluoxymesterone, (only in high enough doses).I'm sure you see a patern and you get the idea..And Deca...yeah it even aromatizes, besides being a progestin, though not much.
Everyone still with me?
Okay, so what are some drugs that inhibit aromatization? Cytadren (aminoglutethemide), at 250-500mgs per day will do the trick, as will Arimidex at .5-1mg per day (more about Arimidex later, and remember, this is all dependant on what doses of aromatizing drugs you're taking). Cytadren also limits the conversion of test to DHT, which may help eliminate any hair loss during a cycle. [Finesteride (Propecia = 1mg tabs, Proscar = 5mg tabs) has similar effects with regards to halting some of DHT's negative effects.]. Cytadren may also slightly inhibits test production, so that kinda turns me off to it. Especially when other drugs actually increase test production and will prevent side effects more effectively. Unfortunately, cytadren has a really short life, and it ideally should be taken 2-3x a day. That plus its cortisol inhibiting effects (and the sore joints you get from that) don't make it really ideal for me. On the bright side, Cytadren may (theoretically) improve blood lipid profiles. Finasteride, can be compared with cytadren, as it also has the added benefit of eliminating some 5-AR (5-Alpha Reductase), which can cause both male pattern baldness as well as acne. Reducing 5-AR will reverse 5-AR inspired hypertrophy of the sebaceous glands and cause a reduction in acne (Skin Pharmacol. 1997;10(5-6):288-97.), as well as help with hair loss caused by the conversion (via 5-AR) of testosterone to DHT (Expert Opin Pharmacother. 2004 Apr;5(4):933-40). I would never take this stuff without another ancillary, as it can also (rare) cause gyno.
What else can we do to avoid side effects? Well, we can block the receptors that the estrogen attaches itself to, thus causing the side effects. Clomid (Clomiphine Citrate) and Nolvadex (Tamoxifen) will do this. As these drugs are selective in their activity, they are estrogenic to certain receptors (blood lipid profiles are favorably enhanced by the estrogenic action of these drugs), and antiestrogenic to others (they are anti-estrogenic in terms of their action on breast tissue, for example.and yes I know that Nolvadex is actually a weak estrogen that blocks out the competing stronger estrogens with regards to attaching to the receptors in breast tissue.I'm trying to keep things relatively simple, though). Generally Nolvadex is cheaper than Clomid, and thus more often used.
Now dig this: According to William LLewellyn, studies conducted in the late 1970's at the University of Ghent in Belgium used Nolvadex for 10 days at a dosage of 20mg daily, which increased serum testosterone levels to 142% of baseline, on par with the effect of 150mg of Clomid daily for the same duration! Depending on what you read into this, I'd say that Nolvadex is a superior buy for post-cycle recovery. That being said, Nolvadex is good, but not quite perfect, as it lowers IGF-1 levels. Post-cycle, though, when I'm worried about returning test-levels to normal, I'm not too worried about IGF-1 levels. Though, personally, I've found testicular atrophy during a cycle is attenuated to a greater degree by Clomid. So besides competing with estrogen at the receptor, these drugs both increase serum test levels, and both drugs may also alter blood lipid profiles. I couldn't find the studies W.L. mentioned, but still found that 20mgs of tamoxifen is equal to 150mgs of clomid for purposes of testosterone elevation, FSH and LH, but tamixifen did not decrease the LH response to LHRH (Fertil Steril. 1978 Mar;29(3):320-7.). Thus, I'd still reccomend Nolv over clomid. Actually, I think nolvadex is far superior to clomid for most purposes.
As Nolvadex isn't actually an anti-aromatase, but rather a competitor for the receptor site, and seeing as it increases test levels so much, I'd say that it's actually a better post-cycle drug than Clomid (which wreaks havoc on my eyesight, due to it's Occular Toxicity.and Nolvadex has some of that property, but in my experience doesn't mess with my eyesight as much). At least I know that it's what I'll be using post-cycle, even despite its effects on IGF-1. And it's important to remember that IGF levels play an important role in Breast Cancer (which is what many of our ancillary drugs were developed for), so many of them will decrease IGF levels, as that is desirable for breast cancer survival.
Cyclofenil (remember that drug?) will do just about everything with regards to halting estrogen's binding to receptors that the other two drugs I just discussed will do, but helps LH production to a greater degree. Lowering your LH (in addition to having an adverse effect on the general recovery of your entire hormonal system) will also contribute to estrogenic-type effects. Raising LH = Good. Lowering LH = Bad. Most people take a tab or 2 per day of this stuff, in any case. There's better stuff on the market, though.
Now onto Femara (AKA Letrozole), which is more effective than Arimidex in it's ability to pass thru the cell membrane of lipid (fat) cells and inhibit the activity of aromatase -- Arimidex is just over 80% effective at inhibiting aromatase, Femara is around 95-97% Levels of estrogen are totally undetectable in any patients taking Letrozole, and it has even been used to increase testosterone to normal levels (from sub-normal ones) and increase LH, FSH and SHBG (Epilepsy Behav. 2004 Apr;5(2):260-3). Other than that, both of these drugs stop the process of aromatization, rather than just blocking (competing for, if you prefer) the receptors as Clomid and Nolvadex do. An effective dose of Letrozole is 1-2.5 mg/day (I use 1mg/day), but be forewarned, it can kill your sex drive, and could decrease IGF levels. On the other hand, I've seen studies where it increases IGF levels. Also worth noting is that there's a rebound effect when you come off Letrozol. What can I say? Letrozole's effects on serum lipids (cholesterol, both HDL and LDL) are, in the words of one researcher: "inconsistent. "And compared with Aromasin and Arimidex, In non-cellular systems, letrozole is 2-5 times more potent than anastrozole and exemestane in its inhibition of the aromatase enzyme and activity, and in cellular systems it is 10-20x more potent! Letrozole (2.5mg daily) also achieved a much greater suppression of the plasma concentrations of both estrone and estrone sulphate (estrogens) than anastrozole (1mg daily) and a greater inhibition of in vivo aromatization also (sorry for the geek-speak.it's over for now.). ( J Steroid Biochem Mol Biol. 2003 Oct;87(1):35-45.) Exemestane can also cause androgenic sides (Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S.)(1. J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 2. J Steroid Biochem Mol Biol 1997 Nov-Dec;63(4-6):261-7). I've used Letrozole, and it cleared up my minor gyno lumps, to the point that they are totally gone now.
How about Aromasin? Well, its totally different than everything else we've looked at so far. Aromasin (exemestane) it is a aromatase inactivator (AI)...It actually makes estrogen receptors useless. Instead of just inhibiting production (as an anti-aromatase would do) it cuts off production totally. Aromasin can effectively prevent about 90-95% of estrogen conversion. Oddly, this compound can actually increase IGF levels (Anticancer Res. 2003 Jul-Aug;23(4):3485-91).Worth noting is that Aromasin may possibly be less harsh on blood lipids (having no effect: J Clin Endocrinol Metab. 2003 Dec;88(12):5951-6. ) than some of the other compounds mentioned here (with the exception of Nolvadex which may actually improve HDL & LDL in some cases: Br J Cancer. 2004 Aug 2;91(3):476-81.). Though it has also been shown to have an undesirable effect on blood lipids in some cases.
Lets talk about Arimadex (Anastrozole), now. From the research I've done, this seems to be one of the best ancillaries around and I'll tell you why. First off, 'dex is an aromatase inhibitor (AI.remember what that is?). 1mg per day of this stuff (J Clin Endocrinol Metab 2000 Jul;85(7):2370-7, "Estrogen Suppression in Males") was shown to decrease estrogen by 50% and increase testosterone levels by 58%. LH and FSH also went up slightly. The test increase didn't happen at a dose of .5 per day, but estrogen suppression was the same. Anastrozole also raises IGF1 and shows a trend towards increasing IGF2 (J Steroid Biochem Mol Biol. 2002 Apr;80(4-5):411-8) BTW, literature provided by the original maker of Arimadex states that stable blood plasma concentrations of the compound are achieved after 7 consecutive 1mg daily doses. All of that plus the usual blood lipid changes we've seen with most of the anciliaries we've looked at! Anyway, that's a pretty hefty decrease in estrogen, even at .5mg/day.
For my money, if I wanna stop aromatization during a cycle, I'm gonna use Arimadex at .5mgs per day or Letrozole at 1mg/day. They are perfect during-cycle ancillaries. Unfortunately, you need to take Anastrozole for a week to get a steady level of it in your blood (same thing goes for Exemestane), wheras you need to take Letrozole for 60 days to get a steady blood plasma level. Though Anastrozole has a life of 41-48 hours, and exemestane has a life of 27 hours, Letrozole has a whopping 2-4 day (!) life (Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S.).
What about HCG (Human Chorionic Gonadotropin)? For starters, it increases (stimulates) endogenous (natural) testosterone production. It's ideal for post-cycle. I've found personally that 500IU every other day or even every day, post-cycle works best for me. Incidentally, this is the PDR (and Dan Duchaine's) reccomendation. In one study I looked at, 6000IU of HCG elevated test levels for 6 days. That's why a lot of people recommend taking it every 3-5 days. I'd have more stable blood levels, though if I shot it more frequently .remember, it's non-estrified and a water-based injectable, after all. In that same study I read, 1500IU of HCG shot test levels up between 250 and 300%. Again, though, I'd be more comfortable with the more stable and slow increase. Also, keep in mind that HCG suppresses FSH and LH production and has been anecdotally linked to gyno. Thus, it (in combination with Nolvadex) is ideal for post-cycle recovery.when gyno is not as much of an issue (due to the nolvadex and the cessation of other compounds), but restoring natural test levels is.
SO.lets review:
During a cycle (because I ALWAYS use test in my cycles), I think it's a good idea to use Arimadex at .5-1mg per day, or Letrozole at 1-2.5mgs/day, to take care of aromatization, thus preventing side effects related to estrogen. If I'm using gear that has progesteronic side effects , I'm gonna avoid nolvadex, and I'm gonna have to throw in some Bromocriptine at 2.5-5mgs every day, especially when I'm using lots of Tren (and perhaps trying to get cut), because I'd want the added "side effects" we already discussed from the Bromo, and I'd thrown in that T3 as well. When I'm all done with the cycle, Nolvadex (at 10-20mgs/day for a month) post cycle, plus 500-1000 IU of HCG every other day (for 2-3 weeks) will help restore test levels to normal. Clomid at 50mgs per day will .umm..keep or return your nuts to a normal size, and will have anti-estrogenic and pro-gonadotropic effects. I used to like it during a cycle to keep my nuts big. Sorry, there's no really polite way to say that stuff about keeping your nuts normal.... But in any case, I'd run the Clomid for about 2 weeks of the start of PCT if this was a concern, or during the cycle...possibly for the last 2 weeks, if you want. I used to use it quite alot, myself, during a cycle (at 50-100mgs/day). Although I've been shying away from it recently due to the relative inexpensiveness of other, better compounds...and the fact that clomid messes with my vision.
So there it is. I hope this answers some questions for everyone and helps you to make decisions concerning ancillaries in your next cycle.
Addendum:
One thing you won't be using in your next cycle, however, it Falsodex. It's new to our little world of AAS users, and one injection per month can give you all the anti-estrogen and anti-progesterone effects you need!
Falsodex is an estrogen receptor antagonist, which has no agonist effects at all. What it does is downregulates Estrogen Receptors (kinda like how Clen DownRegulates your beta receptors....so you get decreased effects from the stuff). Basically, it binds to the Estrogen Receptor more strongly then Tamoxifen, but still has no estrogen agonist effects. Here's the interesting part:
The resultant downregulation of your Estrogen Receptors from the use of Falsodex results in decreased _expression of the Progesterone Receptor as well! Tamoxifen, as we all know, can increase the sides from progesteronic drugs because of an increase in progesterone receptor _expression. So you can take this stuff as both an anti-estrogen and an anti-progestin! No more buying Arimidex or whatever, and Bromocriptine! Sweet, huh?
But here's the part that really gave me a hard-on:
As I said earlier, it is administered via an IM injection of 250mgs once per month! And at that dose, it has have most if not all of the same estrogen lowering effects of 1mg/day of Arim or 2.5mgs per day of Letrozole, but has the added benefits of lowering progesterone receptor _expression.
(Br J Cancer. 2004 Mar;90 Suppl 1:S15-8)
(Drugs. 2004;64(6):633-48.)
(J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):209-12)
Now, I dont agree with the clomid keeping your nuts during cycle and some other things but I do like this article alot.
The A B C's of anti e's
Ok. I'll admit it. I didn't know much about anti-estrogens and their ilk before I started researching this article. And I'll admit another thing: I didn't care. I knew that 10mgs of Nolvadex per day was all I ever needed to not get gyno, though 50 mgs/day of Clomid seemed to work the same for me. Cytadren (remember that stuff?) worked for me also, at 250mgs/day, but it seemed to make me more prone to joint pain and problems. HCG worked best for me when I shot 500i.u. every other day post cycle for about 3 weeks. Arimadex was too expensive. AND THAT'S ALL I NEEDED TO KNOW!
Now nobody uses Cytadren anymore. We have affordable Arimadex (Anastrozole) in liquid form. We have Femera. And I had work to do to catch up.
In the long run, I wasn't that interested in what all this other stuff did because I already knew what worked for me. Well, keep reading and you'll find out why I was wrong, what my new plan is for during a cycle and post-cycle recovery, and some other interesting stuff about not getting any side effects from roids. Here we go!
So, first things first. Some steroids convert to estrogen. This is through the aromatase enzyme, and is called (duh) aromatization. When this happens you can get side effects associated with having too much estrogen, including bloating, gynocomastia, acne, and so on. Some steroids on the other hand, have progesteronic activity (deca, for example actually fits into the progesterone receptor with 20% the efficiency of actual progesterone!) (Cancer Res 1978 Nov;38(11 Pt 2):4186-98). The symptoms (acne, etc...) are the more or less the same for progesteronic and estrogenic effects. Note that I didn't say that these other steroids convert to progesterone, but rather that they have progesteronic effects. That's because the steroid is able to act on the progesterone receptor without conversion to another substance. Hence, on my old bulking cycle of 600mgs per week of Deca and my 750mgs per week of Test, anti-estrogens would only help with the aromatization of the test and not the progesteronic activity of the Deca I'm was taking. Know what else? Here are a bunch of other compounds that don't aromatize significantly (thats good news) activity and hence don't need any amount of anti-estrogens: Methenolone, Stanozolol, Dromostanolone, Oxandrolone, Mesterolone, Stenbolone, and Trenbolone (though it acts on the Progesterone Receptor with 60% the efficiency of progesterone itself, according to the last study I cited). Taking a big dose of any of these? Anti -estrogens won't help much if at all, per se, but keeping estrogen levels low is still a good idea. Remember, estrogen still has a role to play, even sides, in ways we don't fully understand yet. Not only that but if you take progesteronic gear and use nolvadex, you may be at an increased risk for progesteronic sides, as nolvadex may increase progesterone receptors (Gynecol Oncol. 1999 Mar;72(3):331-6.).
What can you do?
Well, the easy answer is to take bromocriptine (parlodel) at 2.5 to 5mg every day. Bromocriptine is one of those drugs that the life-extention crowd were very big on a few years ago. It is an anti-parkinsons medication which causes higher levels of the neurotransmitter dopamine, with side effects being an increased sex drive, possible curbing of appetite, possible stimulation of CNS, and fat loss. It's also indicated for some forms of male hypogonadism (yeah, so it may increase test levels on its own!). However, what we're interested in here is that it can be used to lower prolactin and progesterone. [Side note: A few tabs of Cabergoline per day will also lower prolactin and improve sexual function. I just couldn't figure out where else this would fit into this article.] Back to Bromo...it sounds almost perfect, right? Well, unfortunately, bromocriptine is also used to treat acromegaly (too much GH produced by the pituitary), and ergo may lower GH levels in your body! Fortunately, the dosage needed to halt overproduction of GH in your body is 10-20mgs/day, so we're safe with our amount necessary to stop from growing breasts from too much deca.and yes, all the cool fat burning, sex drive, and nootropic "side effects" happen at 2.5-5mgs/ day doses. As a side note, taking 25mcg of T3 or maybe 50-100mcgs of T4 may be effective for eliminating some if not all of the chance of getting gyno from tren. And yeah, I have the research to back that statement up, but it involves another page of reading about TRH, TSH, the negative feedback loop involved with low levels of T4 stimulating TRH, blah blah blah. Trust me, you don't care about the reasons why this works, just that it does. If you're doing tren, take some T3 and you'll get increased fat-burning, no gyno, and more maybe even anabolism. So if I were cutting up, tren, T3 (25mcgs), and bromo would all be part of my stack , and I'd expect to get really cut really fast (of course, there's other cool drugs I'd add into that mix.clen, test, etc.but this is about anciliaries, not a cutting cycle).
Another idea to reduce progesterone is to take RU486 (yeah, the pregnancy drug). This drug has anti-progesteronic effects, and in women 600mgs totally plocks progesterone. Don't even think about taking this dose, though.I'd reccomend taking around 50 mgs a day and working your way up. Remember, cortisol is also decreased with RU486, so sore joints may be a problem. Considering this, bromo's cool secondary effects, and price, I'd consider bromocriptine a better choice.
So what steroids do aromatize? Here some offenders: Testosterone, Methandrostenolone, Fluoxymesterone, (only in high enough doses).I'm sure you see a patern and you get the idea..And Deca...yeah it even aromatizes, besides being a progestin, though not much.
Everyone still with me?
Okay, so what are some drugs that inhibit aromatization? Cytadren (aminoglutethemide), at 250-500mgs per day will do the trick, as will Arimidex at .5-1mg per day (more about Arimidex later, and remember, this is all dependant on what doses of aromatizing drugs you're taking). Cytadren also limits the conversion of test to DHT, which may help eliminate any hair loss during a cycle. [Finesteride (Propecia = 1mg tabs, Proscar = 5mg tabs) has similar effects with regards to halting some of DHT's negative effects.]. Cytadren may also slightly inhibits test production, so that kinda turns me off to it. Especially when other drugs actually increase test production and will prevent side effects more effectively. Unfortunately, cytadren has a really short life, and it ideally should be taken 2-3x a day. That plus its cortisol inhibiting effects (and the sore joints you get from that) don't make it really ideal for me. On the bright side, Cytadren may (theoretically) improve blood lipid profiles. Finasteride, can be compared with cytadren, as it also has the added benefit of eliminating some 5-AR (5-Alpha Reductase), which can cause both male pattern baldness as well as acne. Reducing 5-AR will reverse 5-AR inspired hypertrophy of the sebaceous glands and cause a reduction in acne (Skin Pharmacol. 1997;10(5-6):288-97.), as well as help with hair loss caused by the conversion (via 5-AR) of testosterone to DHT (Expert Opin Pharmacother. 2004 Apr;5(4):933-40). I would never take this stuff without another ancillary, as it can also (rare) cause gyno.
What else can we do to avoid side effects? Well, we can block the receptors that the estrogen attaches itself to, thus causing the side effects. Clomid (Clomiphine Citrate) and Nolvadex (Tamoxifen) will do this. As these drugs are selective in their activity, they are estrogenic to certain receptors (blood lipid profiles are favorably enhanced by the estrogenic action of these drugs), and antiestrogenic to others (they are anti-estrogenic in terms of their action on breast tissue, for example.and yes I know that Nolvadex is actually a weak estrogen that blocks out the competing stronger estrogens with regards to attaching to the receptors in breast tissue.I'm trying to keep things relatively simple, though). Generally Nolvadex is cheaper than Clomid, and thus more often used.
Now dig this: According to William LLewellyn, studies conducted in the late 1970's at the University of Ghent in Belgium used Nolvadex for 10 days at a dosage of 20mg daily, which increased serum testosterone levels to 142% of baseline, on par with the effect of 150mg of Clomid daily for the same duration! Depending on what you read into this, I'd say that Nolvadex is a superior buy for post-cycle recovery. That being said, Nolvadex is good, but not quite perfect, as it lowers IGF-1 levels. Post-cycle, though, when I'm worried about returning test-levels to normal, I'm not too worried about IGF-1 levels. Though, personally, I've found testicular atrophy during a cycle is attenuated to a greater degree by Clomid. So besides competing with estrogen at the receptor, these drugs both increase serum test levels, and both drugs may also alter blood lipid profiles. I couldn't find the studies W.L. mentioned, but still found that 20mgs of tamoxifen is equal to 150mgs of clomid for purposes of testosterone elevation, FSH and LH, but tamixifen did not decrease the LH response to LHRH (Fertil Steril. 1978 Mar;29(3):320-7.). Thus, I'd still reccomend Nolv over clomid. Actually, I think nolvadex is far superior to clomid for most purposes.
As Nolvadex isn't actually an anti-aromatase, but rather a competitor for the receptor site, and seeing as it increases test levels so much, I'd say that it's actually a better post-cycle drug than Clomid (which wreaks havoc on my eyesight, due to it's Occular Toxicity.and Nolvadex has some of that property, but in my experience doesn't mess with my eyesight as much). At least I know that it's what I'll be using post-cycle, even despite its effects on IGF-1. And it's important to remember that IGF levels play an important role in Breast Cancer (which is what many of our ancillary drugs were developed for), so many of them will decrease IGF levels, as that is desirable for breast cancer survival.
Cyclofenil (remember that drug?) will do just about everything with regards to halting estrogen's binding to receptors that the other two drugs I just discussed will do, but helps LH production to a greater degree. Lowering your LH (in addition to having an adverse effect on the general recovery of your entire hormonal system) will also contribute to estrogenic-type effects. Raising LH = Good. Lowering LH = Bad. Most people take a tab or 2 per day of this stuff, in any case. There's better stuff on the market, though.
Now onto Femara (AKA Letrozole), which is more effective than Arimidex in it's ability to pass thru the cell membrane of lipid (fat) cells and inhibit the activity of aromatase -- Arimidex is just over 80% effective at inhibiting aromatase, Femara is around 95-97% Levels of estrogen are totally undetectable in any patients taking Letrozole, and it has even been used to increase testosterone to normal levels (from sub-normal ones) and increase LH, FSH and SHBG (Epilepsy Behav. 2004 Apr;5(2):260-3). Other than that, both of these drugs stop the process of aromatization, rather than just blocking (competing for, if you prefer) the receptors as Clomid and Nolvadex do. An effective dose of Letrozole is 1-2.5 mg/day (I use 1mg/day), but be forewarned, it can kill your sex drive, and could decrease IGF levels. On the other hand, I've seen studies where it increases IGF levels. Also worth noting is that there's a rebound effect when you come off Letrozol. What can I say? Letrozole's effects on serum lipids (cholesterol, both HDL and LDL) are, in the words of one researcher: "inconsistent. "And compared with Aromasin and Arimidex, In non-cellular systems, letrozole is 2-5 times more potent than anastrozole and exemestane in its inhibition of the aromatase enzyme and activity, and in cellular systems it is 10-20x more potent! Letrozole (2.5mg daily) also achieved a much greater suppression of the plasma concentrations of both estrone and estrone sulphate (estrogens) than anastrozole (1mg daily) and a greater inhibition of in vivo aromatization also (sorry for the geek-speak.it's over for now.). ( J Steroid Biochem Mol Biol. 2003 Oct;87(1):35-45.) Exemestane can also cause androgenic sides (Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S.)(1. J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 2. J Steroid Biochem Mol Biol 1997 Nov-Dec;63(4-6):261-7). I've used Letrozole, and it cleared up my minor gyno lumps, to the point that they are totally gone now.
How about Aromasin? Well, its totally different than everything else we've looked at so far. Aromasin (exemestane) it is a aromatase inactivator (AI)...It actually makes estrogen receptors useless. Instead of just inhibiting production (as an anti-aromatase would do) it cuts off production totally. Aromasin can effectively prevent about 90-95% of estrogen conversion. Oddly, this compound can actually increase IGF levels (Anticancer Res. 2003 Jul-Aug;23(4):3485-91).Worth noting is that Aromasin may possibly be less harsh on blood lipids (having no effect: J Clin Endocrinol Metab. 2003 Dec;88(12):5951-6. ) than some of the other compounds mentioned here (with the exception of Nolvadex which may actually improve HDL & LDL in some cases: Br J Cancer. 2004 Aug 2;91(3):476-81.). Though it has also been shown to have an undesirable effect on blood lipids in some cases.
Lets talk about Arimadex (Anastrozole), now. From the research I've done, this seems to be one of the best ancillaries around and I'll tell you why. First off, 'dex is an aromatase inhibitor (AI.remember what that is?). 1mg per day of this stuff (J Clin Endocrinol Metab 2000 Jul;85(7):2370-7, "Estrogen Suppression in Males") was shown to decrease estrogen by 50% and increase testosterone levels by 58%. LH and FSH also went up slightly. The test increase didn't happen at a dose of .5 per day, but estrogen suppression was the same. Anastrozole also raises IGF1 and shows a trend towards increasing IGF2 (J Steroid Biochem Mol Biol. 2002 Apr;80(4-5):411-8) BTW, literature provided by the original maker of Arimadex states that stable blood plasma concentrations of the compound are achieved after 7 consecutive 1mg daily doses. All of that plus the usual blood lipid changes we've seen with most of the anciliaries we've looked at! Anyway, that's a pretty hefty decrease in estrogen, even at .5mg/day.
For my money, if I wanna stop aromatization during a cycle, I'm gonna use Arimadex at .5mgs per day or Letrozole at 1mg/day. They are perfect during-cycle ancillaries. Unfortunately, you need to take Anastrozole for a week to get a steady level of it in your blood (same thing goes for Exemestane), wheras you need to take Letrozole for 60 days to get a steady blood plasma level. Though Anastrozole has a life of 41-48 hours, and exemestane has a life of 27 hours, Letrozole has a whopping 2-4 day (!) life (Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S.).
What about HCG (Human Chorionic Gonadotropin)? For starters, it increases (stimulates) endogenous (natural) testosterone production. It's ideal for post-cycle. I've found personally that 500IU every other day or even every day, post-cycle works best for me. Incidentally, this is the PDR (and Dan Duchaine's) reccomendation. In one study I looked at, 6000IU of HCG elevated test levels for 6 days. That's why a lot of people recommend taking it every 3-5 days. I'd have more stable blood levels, though if I shot it more frequently .remember, it's non-estrified and a water-based injectable, after all. In that same study I read, 1500IU of HCG shot test levels up between 250 and 300%. Again, though, I'd be more comfortable with the more stable and slow increase. Also, keep in mind that HCG suppresses FSH and LH production and has been anecdotally linked to gyno. Thus, it (in combination with Nolvadex) is ideal for post-cycle recovery.when gyno is not as much of an issue (due to the nolvadex and the cessation of other compounds), but restoring natural test levels is.
SO.lets review:
During a cycle (because I ALWAYS use test in my cycles), I think it's a good idea to use Arimadex at .5-1mg per day, or Letrozole at 1-2.5mgs/day, to take care of aromatization, thus preventing side effects related to estrogen. If I'm using gear that has progesteronic side effects , I'm gonna avoid nolvadex, and I'm gonna have to throw in some Bromocriptine at 2.5-5mgs every day, especially when I'm using lots of Tren (and perhaps trying to get cut), because I'd want the added "side effects" we already discussed from the Bromo, and I'd thrown in that T3 as well. When I'm all done with the cycle, Nolvadex (at 10-20mgs/day for a month) post cycle, plus 500-1000 IU of HCG every other day (for 2-3 weeks) will help restore test levels to normal. Clomid at 50mgs per day will .umm..keep or return your nuts to a normal size, and will have anti-estrogenic and pro-gonadotropic effects. I used to like it during a cycle to keep my nuts big. Sorry, there's no really polite way to say that stuff about keeping your nuts normal.... But in any case, I'd run the Clomid for about 2 weeks of the start of PCT if this was a concern, or during the cycle...possibly for the last 2 weeks, if you want. I used to use it quite alot, myself, during a cycle (at 50-100mgs/day). Although I've been shying away from it recently due to the relative inexpensiveness of other, better compounds...and the fact that clomid messes with my vision.
So there it is. I hope this answers some questions for everyone and helps you to make decisions concerning ancillaries in your next cycle.
Addendum:
One thing you won't be using in your next cycle, however, it Falsodex. It's new to our little world of AAS users, and one injection per month can give you all the anti-estrogen and anti-progesterone effects you need!
Falsodex is an estrogen receptor antagonist, which has no agonist effects at all. What it does is downregulates Estrogen Receptors (kinda like how Clen DownRegulates your beta receptors....so you get decreased effects from the stuff). Basically, it binds to the Estrogen Receptor more strongly then Tamoxifen, but still has no estrogen agonist effects. Here's the interesting part:
The resultant downregulation of your Estrogen Receptors from the use of Falsodex results in decreased _expression of the Progesterone Receptor as well! Tamoxifen, as we all know, can increase the sides from progesteronic drugs because of an increase in progesterone receptor _expression. So you can take this stuff as both an anti-estrogen and an anti-progestin! No more buying Arimidex or whatever, and Bromocriptine! Sweet, huh?
But here's the part that really gave me a hard-on:
As I said earlier, it is administered via an IM injection of 250mgs once per month! And at that dose, it has have most if not all of the same estrogen lowering effects of 1mg/day of Arim or 2.5mgs per day of Letrozole, but has the added benefits of lowering progesterone receptor _expression.
(Br J Cancer. 2004 Mar;90 Suppl 1:S15-8)
(Drugs. 2004;64(6):633-48.)
(J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):209-12)
Now, I dont agree with the clomid keeping your nuts during cycle and some other things but I do like this article alot.
