On Average.. how long does bloat [face] go away post-cycle

[cope]

In your experience..

How long does it usually take for the bloat in your face to go away and your face to slim down back to normal after a cycle?

I was on a 12 week of Test-E 750wk, Deca 500wk, Masteron 400wk..

Im 5 weeks out and still have so much bloat im gettin scared.. I still have time for it to dissipate right?

[NATE0406]

what did your pct consist of?

[cope]

what did your pct consist of?

20mg Aromasin/day [going to keep taking it until W6 PCT]

1000 Vit E
Fish Oil
Multi Vit
B-5
Glucosamine
R-ALA

Glutamine w/ protein shakes

[NATE0406]

bro that is hardly a pct. you should of done some research bro. running an AI is not a pct. you need to run a proper pct. get yourself some nolva.

[cope]

bro that is hardly a pct. you should of done some research bro. running an AI is not a pct. you need to run a proper pct. get yourself some nolva.

You sure>??

Bunch of people said id be cool with just Aromasin and no Nolva.. because they are doing the exact same thing?

[NATE0406]

who told you that?? was it on here?? if so i want to see that thread bro. imo you should always run a serm in pct. aromasin is good to run while on cycle to combat sides and help in the pct process but does not take place of nolva.

[NATE0406]

bro you where told to use a serm.
http://forums.steroid.com/showthread.php?t=330488
read the thread that you started. shifty_git cleary tells you to get yourself a serm. you need to run a proper pct.

[G4R]

bro you where told to use a serm.
http://forums.steroid.com/showthread.php?t=330488
read the thread that you started. shifty_git cleary tells you to get yourself a serm. you need to run a proper pct.

BUSTED!

[sofus99]

who told you that?? was it on here?? if so i want to see that thread bro. imo you should always run a serm in pct. aromasin is good to run while on cycle to combat sides and help in the pct process but does not take place of nolva.

Actually that isn't true.

AI's are superior to SERM's, both during cycles and as PCT.

People are just too conservative to accept the fact that newer and better anti estrogen compounds are available today. Sure, Nolvadex and even Clomid were good in the old days, when AI's weren't available. But times have changed now.

Using receptor blockers is like comparing a guy walking into a warzone wearing body armour, to a guy avoiding the warzone entirely. Just because most of the bullets don't hit you if you are wearing your body armour, it is still better to avoid them in the first place.

And since the entire idea about PCT comes down to taking advantage of the negative feedback loop that exists between estrogen and testosterone - ie. lower your estrogen and you will thereby boost your testosterone production, there really isn't any advantage to using an obsolute compound.

SERM's do still have their place though. They are superior at stopping high estrogen symptoms here and now, where it will often take some time for AI's to reach optimal effect in vivo.

[NATE0406]

Actually that isn't true.

AI's are superior to SERM's, both during cycles and as PCT.

People are just too conservative to accept the fact that newer and better anti estrogen compounds are available today. Sure, Nolvadex and even Clomid were good in the old days, when AI's weren't available. But times have changed now.

Using receptor blockers is like comparing a guy walking into a warzone wearing body armour, to a guy avoiding the warzone entirely. Just because most of the bullets don't hit you if you are wearing your body armour, it is still better to avoid them in the first place.

And since the entire idea about PCT comes down to taking advantage of the negative feedback loop that exists between estrogen and testosterone - ie. lower your estrogen and you will thereby boost your testosterone production, there really isn't any advantage to using an obsolute compound.

SERM's do still have their place though. They are superior at stopping high estrogen symptoms here and now, where it will often take some time for AI's to reach optimal effect in vivo.

riiiiiiiiiiiiiiiiittttttttttttttteeeeeeeeeeee... so i take it you where one of the ppl that help him set up that awsome pct.

[sofus99]

That's hardly a valid argument dude ;-)

If you disagree, which I can see you do, please prove me wrong.

[roid_rage]

12 weeks of test e and deca and NO HCG???? Please correct me if i'm wrong, but did not see any hcg in his cycle, nor in his pct... so eventhough you are using a AI or SERM, still for me, HCG is a must have either during cycle or including it into the PCT...

[gixxerboy1]

12 weeks of test e and deca and NO HCG???? Please correct me if i'm wrong, but did not see any hcg in his cycle, nor in his pct... so eventhough you are using a AI or SERM, still for me, HCG is a must have either during cycle or including it into the PCT...

i never use hcg and dont have any problems. HCG is over rated IMO

[smokeyd]

come on boys im interested in this debate, dont let it die now haha

[cope]

Actually that isn't true.

AI's are superior to SERM's, both during cycles and as PCT.

People are just too conservative to accept the fact that newer and better anti estrogen compounds are available today. Sure, Nolvadex and even Clomid were good in the old days, when AI's weren't available. But times have changed now.

Using receptor blockers is like comparing a guy walking into a warzone wearing body armour, to a guy avoiding the warzone entirely. Just because most of the bullets don't hit you if you are wearing your body armour, it is still better to avoid them in the first place.

And since the entire idea about PCT comes down to taking advantage of the negative feedback loop that exists between estrogen and testosterone - ie. lower your estrogen and you will thereby boost your testosterone production, there really isn't any advantage to using an obsolute compound.

SERM's do still have their place though. They are superior at stopping high estrogen symptoms here and now, where it will often take some time for AI's to reach optimal effect in vivo.

This is exactly what my research concluded.

[cope]

12 weeks of test e and deca and NO HCG???? Please correct me if i'm wrong, but did not see any hcg in his cycle, nor in his pct... so eventhough you are using a AI or SERM, still for me, HCG is a must have either during cycle or including it into the PCT...

I was going to take HCG, but couldnt get my hands on it..

[cope]

Noone even answered my question though..

I wasnt asking about PCT.

I was asking how long it takes for your bloat to go away

[gixxerboy1]

Noone even answered my question though..

I wasnt asking about PCT.

I was asking how long it takes for your bloat to go away

the bloat is probably estrogen related thats why we asked about pct

[duggadoo]

well correct me if im wrong but AI usually doesnt have any effect on bring back natural test levels and SERMs do thats why pple are prescribed clomid therapy to bring back natty test levels... so the major use of serms are to bring back natty yest level and AIs are only used to comabt the estrogen as test levels are low....

[duggadoo]

so basically you are just having low test and low estrogen if just using a AI so there for not really doin anything for the loop because there is no really stimulation to bring test levels back after discontiuing AAS(your just tryin to do it natural which will take mush longer than just adding in a serm to speed up recovery) thats why a serm is so important in a pct

[cope]

Ok, so im 5 weeks out, should i just start taking nolva for the next 2 weeks? Will that help bloat?

[cope]

My test levels and all that seem fine, which is why i ask, its only the bloat in my face that is bothering me. It is very pronounced, my face is round when it is usually.. oval?

[Stoneco|d]

drink shitload of water, cardio and hit sauna a bit

[gixxerboy1]

My test levels and all that seem fine, which is why i ask, its only the bloat in my face that is bothering me. It is very pronounced, my face is round when it is usually.. oval?

drink more water cut back on sodium

[roid_rage]

i never use hcg and dont have any problems. HCG is over rated IMO

may be you did not need to... I know ppl out there that do deca only cycles, and they did fine, but not because the did fine I'm going to recommend ppl to do deca only cycles...

HGC is a fact, it boost engenous testosterone producction by mimic LH... lal all la.... I dont even have to tell you 'cause I'm pretty sure you know what HCG does.. Now why do you say is over rated??

I did PCT's with and without HCG... and to me.. HCG is a must have...

[gixxerboy1]

may be you did not need to... I know ppl out there that do deca only cycles, and they did fine, but not because the did fine I'm going to recommend ppl to do deca only cycles...

HGC is a fact, it boost engenous testosterone producction by mimic LH... lal all la.... I dont even have to tell you 'cause I'm pretty sure you know what HCG does.. Now why do you say is over rated??

I did PCT's with and without HCG... and to me.. HCG is a must have...

The reason i say its over rated. Is ive tried pct with and without and couldnt tell any difference. So imo it wasnt needed

[cope]

drink shitload of water, cardio and hit sauna a bit

i have definitely been slacking on my water intake.
im steppin it up starting this second [pounds water bottle]

[NATE0406]

well correct me if im wrong but AI usually doesnt have any effect on bring back natural test levels and SERMs do thats why pple are prescribed clomid therapy to bring back natty test levels... so the major use of serms are to bring back natty yest level and AIs are only used to comabt the estrogen as test levels are low....

exactly.. thats why AI are more commonly ran throughout a cycle. to combat sides. serms are ment to help restore natty test production. i would like to see one study that shows that an AI can take the place of a SERM in restoring natty test production. you said before that SERM's have there place.. sure they do its called pct. AI's and SERM's have two diff functions. so no one does not take the place of the other. if that was the case then why the hell does every laid out pct that you will see on this site and every other site from ppl who know there shit always include SERM's??? if you want to run your pct's with just an AI then go for it. good luck. but i dont think that advising someone else to not include a serm in there pct is bad advice.

[roid_rage]

The reason i say its over rated. Is ive tried pct with and without and couldnt tell any difference. So imo it wasnt needed

well.. may be because it wanst need it for the cycle you made... or because that's just you... but no PCT could work fine if your testex are "dead"... and the only way to bring them back alive is with a proper administration of HCG... well, at least the best and fastest way...

[cope]

lol.. its funny how noone could just answer:

it takes me about 2 months for my bloat to go away or.. takes me 2 weeks .. etc

[TJM7275]

Cope.... its different with everyone bro. Thats a question with no right answer. Mat take you longer than it takes Gixer or me. Everyone is different dude, kinda like with gains from gear. I think Nate was just trying to help you out a bit with your PCT man. My advise is to cut you sodium intake, cardio and the sauna, but keep hydataing yourself. Good Luck man and keep us posted

[sofus99]

i would like to see one study that shows that an AI can take the place of a SERM in restoring natty test production.

Effect of aromatase inhibition on bone metabolism in elderly hypogonadal men.
Leder BZ, Finkelstein JS.

Endocrine Unit, Department of Medicine, Massachusetts General Hospital, Bulfinch 327, Fruit Street, Boston, MA 02114, USA. [email protected]

Both estrogens and androgens play important roles in skeletal development and maintenance in men. The relative importance of estrogens and androgens in male bone metabolism, however, remains undefined. Anastrozole is an oral aromatase inhibitor that decreases estrogen production and increases androgen production in men. Currently, anastrozole is being investigated as a potential agent for the treatment of hypogonadism in aging men. Because anastrozole lowers estrogen levels and raises androgen levels, its effect on bone metabolism is difficult to predict. To assess the effects of anastrozole on bone turnover, we randomized 37 elderly (ages 62-74) mildly hypogonadal men (serum testosterone <350 ng/dl) to receive either anastrozole 1 mg daily (n=12), anastrozole 1 mg twice weekly (n=11), or daily placebo (n=14) for 12 weeks. Serum gonadal steroid levels, serum and urine biochemical markers of bone turnover, serum osteoprotegerin, and total body bone mineral density were measured at baseline and week 12. Mean serum levels of total and bioavailable testosterone increased substantially in both treated groups. Specifically, mean +/- SD bioavailable testosterone levels increased from 99+/-31 ng/dl to 207+/-65 ng/dl in the group receiving 1 mg of anastrozole daily and from 115+/-37 ng/dl to 178+/-55 ng/dl in the subjects receiving 1 mg of anastrozole twice weekly ( p <0.001 vs placebo for both groups). Serum estradiol levels decreased modestly in both treated groups (from 26+/-8 pg/ml to 17+/-6 pg/ml in the daily treatment group and from 27+/-8 pg/ml to 17+/-5 pg/ml in the twice-weekly treatment group, p <0.001 vs placebo for both groups). Despite these hormonal changes, no increases in biochemical markers of bone resorption were observed. Specifically, mean serum N-telopeptide and urinary deoxypyridinoline concentrations remained stable in both treated groups over the 12-week treatment period. Similarly, serum biochemical markers of bone formation (osteocalcin and amino-terminal propeptide of type 1 collagen), serum osteoprotegerin, and total body bone mineral density did not change. These data demonstrate that although short-term administration of anastrozole decreases serum estradiol levels in elderly men with mild hypogonadism, this intervention does not adversely affect bone metabolism over a 12-week period. This lack of an effect may be due to the concomitant increase in testosterone production, the relative modest effect on estradiol production, or a combination of both factors. These results suggest that anastrozole therapy is unlikely to have an adverse effect on bone metabolism when taken over extended periods and may prove to be a valuable method of normalizing testosterone production in older men.


Effect of chronic administration of an aromatase inhibitor to adult male rats on pituitary and testicular function and fertility
KJ Turner, M Morley, N Atanassova, ID Swanston, and RM Sharpe

The aim of the present study was to evaluate the effects of the administration of a potent non-steroidal aromatase inhibitor, anastrozole, on male reproductive function in adult rats. As anastrozole was to be administered via the drinking water, a preliminary study was undertaken in female rats and showed that this route of administration was effective in causing a major decrease in uterine weight (P<0.02). In an initial study in male adult rats, anastrozole (100 mg/l or 400 mg/l) was administered via the drinking water for a period of 9 weeks. Treatment with either dose resulted in a significant increase ( approximately 10%) in testis weight and increase in plasma FSH concentrations (P<0.01) throughout the 9 weeks. Mating was altered in both groups of anastrozole-treated rats, as they failed to produce copulatory plugs. Histological evaluation of the testes from anastrozole-treated rats revealed that spermatogenesis was grossly normal. In a more detailed study, adult rats were treated with 200 mg/l anastrozole via the drinking water for periods ranging from 2 weeks to 1 year. Plasma FSH and testosterone concentrations were increased significantly (P<0.001) during the first 19 weeks of treatment. However, LH concentrations were increased only at 19 weeks (P<0.001) in anastrozole-treated rats, and this coincided with a further increase in circulating and intratesticular testosterone concentrations (P<0.05). No consistent change in inhibin-B concentrations was observed during the study. Suppression of plasma oestradiol concentrations could not be demonstrated in anastrozole-treated animals, but oestradiol concentrations in testicular interstitial fluid were reduced by 18% (P<0.01). Mating was again inhibited by anastrozole treatment, but could be restored by s.c. injection of oestrogen, enabling demonstration that rats treated for 10 weeks or 9 months were still fertile. Testis weight was increased by 19% and 6% after treatment for 19 weeks and 1 year, respectively. Body weight was significantly decreased (P<0.01) by 19 weeks of anastrozole treatment; after 1 year the animals appeared to have less fat as indicated by a 27% decrease in the weight of the gonadal fat pad. The majority of anastrozole-treated animals had testes with normal spermatogenesis but, occasionally, seminiferous tubules showed abnormal loss of germ cells or contained only Sertoli cells. Ten percent of anastrozole-treated animals had testes that appeared to contain only Sertoli cells, and one rat had 'giant' testes in which the tubule lumens were severely dilated. Morphometric analysis of the normal testes at 19 weeks showed no difference in the number of Sertoli cells or germ cells, or the percentage volumes of the seminiferous epithelium, tubule lumens and interstitium between control and anastrozole-treated rats. On the basis of the present findings, oestrogen appears to be involved in the regulation of FSH secretion and testosterone production, and is also essential for normal mating behaviour in male rats. Furthermore, these data suggest that the brain and the hypothalamo-pituitary axis are considerably more susceptible than is the testis to the effects of an aromatase inhibitor. Anastrozole treatment has resulted in a model of brain oestrogen insufficiency.


Aromatase inhibition in the dog. I. Effect on serum LH, serum testosterone concentrations, testicular secretions and spermatogenesis.

Juniewicz PE, Oesterling JE, Walters JR, Steele RE, Niswender GD, Coffey DS, Ewing LL.

Department of Population Dynamics, Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland.

Chronic treatment of intact male beagles with an orally active nonsteroidal aromatase inhibitor (4-(5,6,7,8-tetrahydroimidazo [1,5a] pyridin-5-yl) benzonitrile hydrochloride; CGS 16949; CIBA-GEIGY) at a dosage of 2.5 mg./kg. per day for six months resulted in increased (p less than 0.01) serum LH and testosterone concentrations compared to placebo-fed controls. The increases in serum LH and testosterone concentrations occurred by one week of treatment and were maintained over the six month period. Testes of CGS 16949A fed dogs obtained at termination of the experiment when perfused in vitro in the presence of a maximally stimulating concentration of LH secreted nondetectable amounts of estradiol and estrone and higher (p less than 0.01) amounts of testosterone, androstenedione and dihydrotestosterone than testes of control dogs. Despite these changes in androgen secretion there was no evidence on any effect of aromatase inhibition upon spermatogenesis. These data support the hypothesis that in the dog, estrogens play a major role in negative feedback of the hypothalamic-pituitary-testicular axis.


Effect of long-term treatment with aromatase inhibitor on testicular function of adult male bonnet monkeys (M. radiata).

Shetty G, Krishnamurthy H, Krishnamurthy HN, Bhatnagar AS, Moudgal NR.

Department of Molecular Reproduction Development and Genetics Indian Institute of Science, Bangalore, India.

The role/need for estrogen in regulating testicular function of adult male bonnet monkeys (M. radiata) has been investigated by dosing orally a group of five normal males 2.5 mgs of CGP 47645, a long-acting nonsteroidal aromatase inhibitor (AI), once every 5 days for over 150 days. Such treatment resulted in a 10-fold increment in nocturnal serum testosterone (T) levels, which were sustained for 85 days of treatment, and a twofold increment in basal serum T levels was present throughout the 150 days of treatment. Analysis of ejaculated semen showed a marked reduction (approximately 90%) in sperm counts in four out of five monkeys between Days 55-85 of treatment. During this period, the motility score also was markedly reduced from a normal score of 3-5 to 0-2. Flow cytometric analysis of testicular germ cells obtained from biopsy tissue taken on Days 63 and 120 indicated a marked reduction only in elongating/elongated spermatid population (compared to Day 0 values), suggesting inhibition in spermiogenic process. Epididymal sperm maturation also seemed effected as sperm chromatin, on flow cytometric analysis for decondensability following exposure to 5 mM dithiotreitol, showed to be in a hypercondensed state. This study thus indicates that estrogen has an important role in providing normal testicular and sperm function in the primate.


Differential Regulation of Gonadotropin Secretion by Testosterone in the Human Male: Absence of a Negative Feedback Effect of Testosterone on Follicle-Stimulating Hormone Secretion1
Frances J. Hayes, Suzzunne DeCruz, Stephanie B. Seminara, Paul A. Boepple and William F. Crowley, Jr.

Studies of sex steroid regulation of gonadotropin secretion in the human male have focused primarily on the respective site(s) of negative feedback of testosterone (T) and estradiol (E2). The use of pharmacological doses of sex steroids in these studies has precluded conclusions about the relative roles of T and E2 in gonadotropin feedback. Thus, the aims of the present study were to 1) determine the relative contributions of T vs. E2 to the sex steroid component of gonadotropin regulation, and 2) distinguish the feedback effects of T that that are direct (i.e. mediated by the androgen receptor) vs. indirect (mediated by aromatization to E2).

Two experimental interventions were used: 1) inhibition of aromatization by a selective aromatase inhibitor to examine the impact of selective E2 withdrawal; and 2) acute medical castration to examine the effect of ablating both T and E2. Sixteen normal (NL) men (mean age, 30.5 ± 2.2 yr) were studied. Nine NL subjects were treated with the aromatase inhibitor, anastrozole (10 mg, orally, daily, for 5 days). Twelve NL men underwent medical castration with ketoconazole (1-g loading dose followed by 400 mg, orally, four times a day for 5 days). Ketoconazole-treated subjects received concomitant treatment with dexamethasone (0.5 mg twice daily) to prevent the development of adrenal insufficiency. Single blood samples were drawn daily between 0800–1000 h. To ensure that dexamethasone was not altering the gonadotropin response to sex steroid ablation by a direct pituitary effect, five GnRH-deficient men (mean age, 37.6 ± 3.9 yr) underwent GnRH dose-response studies at baseline and after treatment with dexamethasone (0.5 mg twice daily).

Aromatase blockade caused significant lowering of E2 (33 ± 3 to 14 ± 1 pg/mL; P < 0.0005) with a corresponding increase in T levels (563 ± 42 to 817 ± 81 ng/dL; P < 0.05). Treatment with ketoconazole resulted in equivalent suppression of E2 (41 ± 4 to 14 ± 1 pg/mL; P < 0.0005), but also induced castrate levels of T (491 ± 28 to 40 ± 3 ng/dL; P < 0.0005). Both treatment regimens were associated with a significant increase in gonadotropin levels. For LH, the percent increase in serum levels after castration was almost 3-fold greater than that seen after selective E2 withdrawal (275 ± 23% with ketoconazole vs. 95.6 ± 21% with anastrozole; P < 0.005). Despite the divergent changes in T levels with these two maneuvers (a marked decrease after ketoconazole and a significant increase with anastrozole), the percent rise in FSH levels was similar in the two protocols (91 ± 6% vs. 71 ± 7%, respectively; P = NS). Inhibin B levels were unchanged after selective E2 withdrawal (156 ± 23 vs. 176 ± 19 pg/mL), but decreased slightly with ketoconazole (156 ± 15 to 131 ± 11 pg/mL; P < 0.05). In contrast to the effects of glucocorticoid administration on gonadotropin secretion in women, no significant changes were observed in the GnRH-deficient men treated with dexamethasone in terms of mean LH levels (19.8 ± 3.2 vs. 23.3 ± 5.4 IU/L), mean LH pulse amplitude after GnRH (16.0 ± 2.5 vs. 19.0 ± 5.1 IU/L), or mean FSH levels (8.0 ± 1.9 vs. 9.2 ± 2.4 IU/L, pre vs. post).

These studies provide evidence of differential regulation of gonadotropin secretion by T in the human male. T exerts both direct and indirect feedback on LH secretion, whereas its effects on FSH appear to be mediated largely by aromatization to E2. From these data we conclude that in terms of sex steroid feedback, E2 is the predominant regulator of FSH secretion in the human male.

[QuadPower]

Very interesting discussion on the AI and SERM aspect. I'd like to throw in my 2c and then wait for the veterans to correct me or agree with me.

AFAIK, a SERM is a selective estrogen receptor modulator. Nolva is both an agonist and an antagonist. i.e. in some tissues, it binds to the tissue AND acts as a biological estrogen as well (agonistic action, e.g. liver I think) and in other tissues, it binds to the tissue but DOES NOT provoke any biological action (i.e. antagonistic e.g. in titty tissue).

AI is an aromatase inhibitor (suicide inhibitor or otherwise). The idea is to prevent aromatization of test into estrogen in the first place, thereby preventing estrogenic sides.

From what I understand, both will have their place in PCT. Having a SERM will make sure that the excess estrogen is not binding to the receptor in the tits, so gyno cannot form. However you still have all this excess estrogen hanging around in the body (and nolva itself is also estrogenic). Therefore you have to add an AI to drop further estrogen production. The negative feedback loop tells the body that estrogen is going low, therefore it needs to produce more test so it can aromatize. So the body increases test production.

In fact, you should maybe run an AI throughout the cycle at a very low dose to keep estrogen production in check (low dose because some amount of estrogen is needed for IGF-1 production which causes growth).

Damn it is all so complex.

But to summarize, and please correct me if I am wrong:

1. Run low dose AI throughout cycle (low enough to control excess estrogen but not to inhibit IGF-1).
2. Use SERM if you start seeing signs of gyno, to bind those titty receptors and prevent gyno from forming. Also up the AI dosage in this case to reduce aromatization.
3. Use both SERM and AI in pct at dosages usually run by folks.

One question I have is, the AI will only prevent conversion of test into estrogen. How about all the estrogen that has been hanging around in they body due to this massive test dose (over 12 weeks). How does one get rid of that estrogen?

Now, who wants to be the first to flame me?

[QuadPower]

To add to what I said, HCG seems to be an excellent addition to PCT, since it will stimulate the boys into starting test production from its LH hormone effect. Also need to be careful on this (not for too long) since too much HCG for too long can desensitize the leydig cells thereby causing testicular damage...? (is this correct?)

So in my first cycle (which will be soon I hope)
I will use an AI at a low dose during cycle
SERM on hand for gyno protection
SERM + AI + HCG PCT

[bmit]

HCG is a must have for me

[Vitali]

I can't speek from experience, but don't panic. I'm sure the bloat will subside soon. You're no longer on cycle, so common sense tells you your estrogen levels should be coming down with your test levels. That said, I'd get an SERM asap if you're still concerned. That should help right away with bloating as it would with gyno.

Good luck. I'm sure you'll be fine, though.

Very interesting discussion on the AI and SERM aspect. I'd like to throw in my 2c and then wait for the veterans to correct me or agree with me.

AFAIK, a SERM is a selective estrogen receptor modulator. Nolva is both an agonist and an antagonist. i.e. in some tissues, it binds to the tissue AND acts as a biological estrogen as well (agonistic action, e.g. liver I think) and in other tissues, it binds to the tissue but DOES NOT provoke any biological action (i.e. antagonistic e.g. in titty tissue).

AI is an aromatase inhibitor (suicide inhibitor or otherwise). The idea is to prevent aromatization of test into estrogen in the first place, thereby preventing estrogenic sides.

From what I understand, both will have their place in PCT. Having a SERM will make sure that the excess estrogen is not binding to the receptor in the tits, so gyno cannot form. However you still have all this excess estrogen hanging around in the body (and nolva itself is also estrogenic). Therefore you have to add an AI to drop further estrogen production. The negative feedback loop tells the body that estrogen is going low, therefore it needs to produce more test so it can aromatize. So the body increases test production.

In fact, you should maybe run an AI throughout the cycle at a very low dose to keep estrogen production in check (low dose because some amount of estrogen is needed for IGF-1 production which causes growth).

Damn it is all so complex.

But to summarize, and please correct me if I am wrong:

1. Run low dose AI throughout cycle (low enough to control excess estrogen but not to inhibit IGF-1).
2. Use SERM if you start seeing signs of gyno, to bind those titty receptors and prevent gyno from forming. Also up the AI dosage in this case to reduce aromatization.
3. Use both SERM and AI in pct at dosages usually run by folks.

One question I have is, the AI will only prevent conversion of test into estrogen. How about all the estrogen that has been hanging around in they body due to this massive test dose (over 12 weeks). How does one get rid of that estrogen?

Now, who wants to be the first to flame me?

Dude, for me you did a great job of summarizing the whole PCT topic (- taper). Excellent work my brotha!