Testosterone - 2000mg/week

[RA]

impressive you found it!
for pct nolva, then he talked separate for the cycles about letro and adex.
good memory!

you are dangerous ...lol...........

[305GUY]

Honestly i may never touch test again.

[guest589745]

It implies you should suck it up, go with the grain and used the testo.

Oh yea my bad, lemme go shoot some more real quick lol.

[RA]

Again (although I feel that in that particular case the user could probably/maybe get away with a Nolva only PCT...I still feel "my" PCT is optimal, and would be my reccomendations)...in that thread, I do not reccomend a nolva only PCT. All I'm doing is saying that Nolva is superior SERM for PCT than Clomid.

Nowhere in that entire thread do I say (or imply) anything to support your original contention that I reccomend a Nolva only PCT. Nothing in that thread really supports your claim that I said what you are attributing to me.

I support Nolva over Clomid, which is not the same as a Nolva only PCT. You keep providing evidence that I prefer nolva to clomid, but nothing that says I support Nolva alone (although I can only imagine that in some specific instances I would).

Honestly, the links you're providing to support your claims, aren't doing that at all.

Ok, I can say with 100% certainty that I was not the only one on the board with the impression that you were pushing nolva only pcts but if you want to run away from it now thats fine.

[*Narkissos*]

blah blah blah... decimate words instead of ideas.. arrives at nothing.

Thread continues in circles.

Honestly hooker...

[oswaldosalcedo]

this theory of nolva only for pct,it fall down with me,cos i have 8-12 pg/ml of estradiol (pre,in,post cycle),i dont need nolva is clomid what I need.
again, everybody need blood work.

we have to be careful with the over-generalizations

[taiboxa]

this theory of nolva only for pct,it fall down with me,cos i have 8-12 pg/ml of estradiol (pre,in,post cycle),i dont need nolva is clomid what I need,for example.
again, everybody need blood work.

[oswaldosalcedo]

estradiol normal levels 10-50 pg/ml.

[Property of Steroid.com]

Bad example Hooker.. I'm looking for the 'bad and dangerous advice' you alluded to.. and i think you need to dig deeper.


I guess i'd be putting myself out on a limb here as you'll wave your wand and pull out a study to support your position... but i disagree with your statement: "suppression has little to do with the metabolites produced" ..Furthermore you conceded that the metabolites are "intrinsically supressive". Is that not a paradox?

In the course of my research i came accross soil (manure treated)/flesh (post slaughter etc.) studies that stated that the metablites of trenbolone are biologically active for months post excretion. What bearing does this have on the athlete's suggested use of a compound? Maybe none... maybe as much/little as the rat and in vivo studies that most of the bodybuilding world's articles are based on.

/end babbling

What am i saying?

Unless you can state conclusively (i.e. without a doubt), then your views are speculation. Further, even if you CAN state conclusively... there was no 'bad advice' given on the thread you so poorly used as your example.

I disagree. I think that by claiming that absurd dosages of compounds can be managable, then citing how they can be managed, the onus of proof lies with him to verify his claims. Tai is claiming that he has used absurd dosages, and that anyone else can, simply by management of bloodwork. I asked him to show us said bloodwork, and he can't...I think that calls into question the safety of his dosages. And I think that, to be frank, his claim (in that same thread) that Halo is not as toxic as winstrol ought to be challenged as well. Where's the bloodwork proof of that one?

And the fact that metabolites can be intrinsically suppressive has no bearing on whether they actually are produced in high enough amounts to support Tai's claim that they in fact are. No Paradox there, as the burden of proof lies with him, not myself. To verify his claims, he needs to prove that metabolites are produced in a quantity that has been shown to be high enough to induce suppression, and then he needs to explain why his theory poses a better model than the inverse mirror image of blood plasma levels vs/ suppression provided by the Minto et. al studies I referenced earlier. I provided strong evidence for my claims that blood plasma levels are the factor most influencing suppression. He presented a counter claim that it's metabolites. HE also provided no proof supporting his claim. Now, burden of proof lies with him disproving me and showing reasons that the Minto studies on Nandrolone are not sufficient to support my claims, or are not as strong as his evidence to the contratry.

Tai is making claims (and he, of course has bloodwork to verify them, right?) and I'm asking for proof. Burden of proof, lies with him, not myself. None of the assumptions or eliptical arguments he relies on have strengthened his claims yet. It's not an arument, it's me explaining why he's wrong...not seeing it for what it is, doesn't turn it into an argument...regardless of what color someone's name is.

In terms of my ideas needing conclusive proof, otherwise they are speculation, that's not correct either. Theories are not proven, at all, and are still designated as theories, even if they've been shown to be true innumerable times. Ever hear of the "theory of relativity"?

[taiboxa]

i would like to retract my claims and provide them as theorys w/o any conceivable evidence just to end this thread k thnx.

[Property of Steroid.com]

Ok, I can say with 100% certainty that I was not the only one on the board with the impression that you were pushing nolva only pcts but if you want to run away from it now thats fine.

Maybe I was...I honestly don't recall, and that's why I asked you to provide me with a link....to freshen up my memory. But in light of the links provided, I'm inclined to think that my preference for Nolva over Clomid has been misinterpreted by many (you among them) to be representitive of something that it is not.

[Property of Steroid.com]

i would like to retract my claims and provide them as theorys w/o any conceivable evidence just to end this thread k thnx.

Stating that you have bloodwork proving your point is not a "theory"....it's a verifiable claim that you have something in your posession. Stating that you have bloodwork showing that halo is less toxic than winstrol is not a theory...it's a claim as to the posession of certain items (bloodwork).

"I have $100" is not a theory, it's a statement of posession. You are saying you have bloodwork providing proof of your (absurd) claims. I asked to see it. You can't provide it. I call bullshit. I honestly don't even think you run the doses you're claiming you do, and in the absence of any bloodwork, I certainly don't believe that you have successully and safely managed their side effects; and I believe it to be a dangerous practice for you to mislead members in that way.

[RA]

Maybe I was...I honestly don't recall, and that's why I asked you to provide me with a link....to freshen up my memory. But in light of the links provided, I'm inclined to think that my preference for Nolva over Clomid has been misinterpreted by many (you among them) to be representitive of something that it is not.

Could be but I typed in your name and nolva as a key word and got 21 results. I dare say youve mentioned nolva more than that...so im guessing some were deleted?

[oswaldosalcedo]

accept errors is a normal thing.

[*Narkissos*]

Every thread hooker posts on veers substantially off topic.

[Property of Steroid.com]

Could be but I typed in your name and nolva as a key word and got 21 results. I dare say youve mentioned nolva more than that...so im guessing some were deleted?

Try using google cache. It keeps a log of every time something is posted (semi-permanently) on the internet for over 2 weeks. By using google cache, you can find every time I've ever mentioned Nolvadex on Steroid .com, in the last 5 years, whether it's been removed from the board or not.

This way you can see if I've mentioned it within the context you're saying I did, without fear that it's been removed from here.

[Property of Steroid.com]

Every thread hooker posts on veers substantially off topic.

It's my sincere hope that even though threads veer off topic, the general level of knowledge of everyone reading the thread improves.

Think about it...for several years, there were many paradigms and axioms that everyone on the boards subscribed to. And through dialogue, we've advanced (and sometimes changed for the better), those paradigms and axioms.

That tradition should be upheld, even if it makes people uncomfortable.

It's often quarrelsome, and pugnacious...but that's how the advancement of knowledge has to be sometimes.

I forget who said it (it was carved in stone at the library of the university I attended), but I always thought it to be a good sentiment to describe my attitude:

"Let no man ever fear to speak the truth, or dare to speak a falsehood"

[taiboxa]

Stating that you have bloodwork proving your point is not a "theory"....it's a verifiable claim that you have something in your posession. Stating that you have bloodwork showing that halo is less toxic than winstrol is not a theory...it's a claim as to the posession of certain items (bloodwork).

"I have $100" is not a theory, it's a statement of posession. You are saying you have bloodwork providing proof of your (absurd) claims. I asked to see it. You can't provide it. I call bullshit. I honestly don't even think you run the doses you're claiming you do, and in the absence of any bloodwork, I certainly don't believe that you have successully and safely managed their side effects; and I believe it to be a dangerous practice for you to mislead members in that way.

[oswaldosalcedo]

Every thread hooker posts on veers substantially off topic.

really .............lol.................

just kidding.

[taiboxa]

i like paradigms, my dad and i would go to kansas to hunt them in the winter!

[oswaldosalcedo]

...................... i.e. factual information about anabolic steroid pharmacology, pharmacokinetics, pharmacodynamics, etc... then I'll say that the most informed voice here would be mine.........................

Arrogance?

[*Narkissos*]

It's my sincere hope that even though threads veer off topic, the general level of knowledge of everyone reading the thread improves.

If only your posts were geared towards improving the 'general knowledge of everyone reading'.. as opposed to digging up and sharing dirt with crude abandon.

Arrogance?

Understatement of the century.

[Property of Steroid.com]

If only your posts were geared towards improving the 'general knowledge of everyone reading'.. as opposed to digging up and sharing dirt with crude abandon.

If only that kind of voice were listened to.

[Swifto]

****ing hell Anthony, the shit does follow you. After reading the thread again. Here and other boards.

I would start banging on about how you seem to attack every post/reply and blame it on your attitude etc...But I think its a little late for that at 28 years old.

No flame...But it amazes me to say the least.

[dsmdrew]

after reading this thred i through anthonys book that i bought away! now i know he is full of shit!

[fLgAtOr]

after reading this thred i through anthonys book that i bought away! now i know he is full of shit!

Despite what you may think of him, he's responsible for more input to this site than you are.

Until you contribute a little more, keep your nose out of where it doesn't belong.

[BG]

Despite what you may think of him, he's responsible for more input to this site than you are.

Until you contribute a little more, keep your nose out of where it doesn't belong.

Yes I agree. He's very knowledgable and has ton tons for the AAS community.

[goose]

Despite what you may think of him, he's responsible for more input to this site than you are.

Until you contribute a little more, keep your nose out of where it doesn't belong.

I have to Believe in MR roberts...I just spent 250$ on his product.

You got to remember this is a guy that was on Personal terms with Nandi.

I`m just not sure how good he is at rugby,I was in the under 18 England team,back in the day.

This is an example how great Nandi was:

Wannabebig: Why do you think Deca has been touted as one of, if not the most suppressive androgen?

Nandi: Deca's reputation as being highly suppressive to the Hypothalamic-Pituitary-Testicular Axis (HPTA) is probably deserved, but Trenbolone may be even more suppressive. Unfortunately there is not much research to rely on here so we are forced to speculate to some degree. There are several reasons that could explain Deca's ability to shut down the HPTA relatively strongly. First, the decanoate ester is very long lived. By this I mean because of its hydrophobicity (insolubility in water or plasma) it has a tendency to diffuse very slowly out of the injection site into the plasma where the ester is removed from the nandrolone molecule. I like to refer people to the study by Minto et al to see this depicted graphically in Figure 1 from the Pharmacology website.

As Fig.1 shows, it takes over a month for nandrolone plasma levels to return to zero after a single injection of Deca. Figure 3 in the same study shows that plasma levels of endogenous testosterone levels are a virtual mirror image of plasma nandrolone levels, with testosterone

The above mentioned ability of Deca and other androgens to suppress natural testosterone production by acting to disrupt GnRH signaling is the third reason Deca is quite suppressive. The presence of androgen receptors in the GnRH secreting neurons has been demonstrated in a number of studies (see 4,5 for example) and it is believed that androgens act directly on these receptors to disrupt GnRH pulse signaling. As most readers are aware, nandrolone binds to the AR with a greater affinity than does testosterone, so this may be another factor in nandrolone being more suppressive than other steroids . However, as (4) points out, DHT could possibly be the active androgen in the hypothalamus. If this is the case, one might expect testosterone, via its conversion to DHT, to be more suppressive at the hypothalamic level. This clearly requires more research.

Deca also aromatizes to some degree, and since estrogens are quite suppressive, this certainly could contribute to Deca's ability to shut a person down compared to nonaromatizing steroids. On the other hand, testosterone aromatizes quite readily and the resulting elevated estrogen levels contribute significantly to HPTA suppression. Moreover, by suppressing testosterone production, which is a superior substrate for aromatase, Deca has been shown to either lower estrogen levels or leave them unchanged. So aromatization is the least likely mechanism for Deca's HPTA suppression.

In a recent issue of Mind & Muscle I described in an article entitled Understanding Androgen Actions how different androgens and anabolic steroids, after binding to the androgen receptor, preferentially bind to different genes:

Quoting from the article,

"[There is] evidence for the existence of distinct steroid specific target gene transcription profiles following AR activation (3). In other words, the structures of androgen responsive genes vary in such a way that some genes are more readily activated by certain androgens than by others. The set of genes readily switched on by a given androgen determines the net physiological effect of that androgen."

This is most likely the best explanation for the suppressive nature of Deca: due perhaps simply to the shape or charge distribution of the molecule, after binding to the androgen receptor (AR), the Deca/AR complex preferentially binds to genes that regulate LH and/or GnRH production, the net result being a decrease in the production of either or both of those hormones.

Wannabebig: What's the most effective method using Clomid to recuperate post-cycle?

Nandi: Everyone seems to have his or her pet dosing regimen here.

What I typically suggest is something like Clomid 300mg per day for the first 2 or 3 days, then 10days of 100mg and than ten days of 50mg. No doubt many people will take issue with this schedule, and if someone has a dosing regimen that seems to work for them, they should stick to it.

In my opinion the dosing schedule is not so important as is the need to accompany the Clomid with HCG either on a regular basis during the cycle, or towards the end of the cycle and extending into the post cycle recovery period, or simply at the end of the cycle. For example, a lot of guys at cuttingedgemuscle (CEM) are running 1000 IU/day of hCG for 10 days post cycle with either Clomid or Nolvadex . Again, opinions vary as to the most effective protocol and unfortunately we have little if any science to fall back on. After using Clomid and HCG primarily as post cycle ancillaries, I'm now still using Clomid in the traditional way after a cycle, but employing weekly injections of HCG throughout the cycle to (hopefully) reduce testicular atrophy. As most readers know, HCG acts like LH, stimulating the testicular Leydig cells. Probably more than anything else, testicular atrophy is what prolongs recovery. Studies have shown that post cycle, the pituitary recovers much more quickly than do the testes. In fact, after the pituitary has recovered several weeks post cycle, pituitary LH secretion becomes supraphysiological, presumably as the body tries to stimulate the still atrophied testes (6). If we can reduce the atrophy by keeping the testes "primed" with HCG recovery should be quicker.

Getting back on topic, there is another reason I believe Clomid is important post cycle. This is strictly my theory and I admit I have no proof to back it up. I have noticed though from a number of studies, as well as from blood work posted by members, that Sex Hormone Binding Globulin (SHBG) remains low for many weeks (16 in some studies) after a cycle. SHBG levels control total test levels. Low SHBG means low total testosterone. Clomid acts as an estrogen in that it elevates SHBG. When clomid is used post cycle, the body will sense that testosterone is low relative to SHBG, and boost test production. (Technically what I believe will happen is that the elevated SHBG will lower free test levels by binding up more free test, blocking any suppressive effect of this test at the hypothalamic level. Lower free test also means lower aromatization into highly suppressive estrogen. Both effects should speed recovery.)

Wannabebig: Why has testosterone been suggested as the "safest" drug to use?

Nandi: There are several things we need to look at when we talk about the safety of a drug. One topic I see discussed more and more often on my board and others is the effect of AAS on a person's cholesterol profile. Maybe we're all getting a little older and are more concerned about cardiovascular health. There is a wealth of data showing that oral 17 alpha alkylated steroids (Winstrol is often cited as a particularly bad culprit) are more effective at lowering HDL cholesterol, the good cholesterol, than are other injectable steroids. According to one study, it took 600 mg per week of testosterone enanthate administration before there was a statistically significant drop in HDL (7). On the other hand, as little as 6 mg/day of Winstrol can lower HDL by 33% (8). What about testosterone versus other injectables, like nandrolone? Unfortunately there is a lack of data on the effects of high doses of nandrolone on cholesterol. What studies that are out there typically use 100 to 200 mg per week. The results of these studies are variable. Some done in subjects with compromised health, such as HIV or dialysis patients, show a trend of decreasing HDL. Other studies in healthy individuals show little if any effect on cholesterol (9). So testosterone may or may not be special compared to other injectables as far as cholesterol goes. I think we can conclude though that testosterone is safer than orals.

Liver toxicity is probably the second most discussed health issue. Again, most bodybuilders know that oral AAS tend to raise liver enzyme values at much lower doses than do injectable steroids. We run into the same problem here comparing testosterone to other injectables as we did when addressing cholesterol. There is a lack of research on high doses of drugs other than test.

Wannabebig: What about the ongoing consensus by users that Testosterone should be used as a base for a cycle?

Nandi: As far as using testosterone as a base for a cycle, I'm not convinced it is any better than other injectables like Deca or Equipoise . And let's not forget our female readers for whom test might be a poor choice for a base because of its relative androgenicity. If a person chose to use something other than test around which to build their cycle, I would recommend throwing in some test however, if for no other reason than to help maintain libido. The advocates of building a cycle around test usually cite its ability to elevate DHT levels, which probably helps fuel aggression and allows for more intense training sessions, and its aromatisation to estrogen, which elevates liver derived IGF-1.

I would counter these arguments by the observation that many bodybuilders make excellent gains while using test with an antiestrogen and/or finasteride, which blocks DHT production. Researchers are beginning to realize that the local production of IGF-1 within skeletal muscle by androgens is probably more important for muscle growth than is hepatically derived IGF-1, and other steroids, like Deca, are capable of inducing this local IGF-1 production (10). On the other hand, people certainly make terrific gains from test, so from an empirical standpoint, it is an excellent choice for a base around which to build a cycle. As an advocate of the KISS principle, I confess to being perplexed by the number of different drugs some bodybuilders use in a cycle. If someone asked me what would be my choice for a "favourite cycle", I would say test and tren , or EQ and tren. Nothing else is needed, in my opinion. We'll get some critical feedback from readers on this point, I'm sure. I do see a definite trend among members on various boards using less orals out of concerns for health. I think that is a positive movement.

Wannabebig: The D-Bol bridge theory claims that at the suggested dose of 10 mg each morning the HTPA will not be suppressed. Is there any truth to this?

Nandi: None whatsoever that I have ever seen. I would say to the people making this claim that the burden is on them to present some evidence that bridging does NOT suppress the HPTA. There is ample evidence that very low doses of Dianabol and Anavar , two drugs often cited as being good for bridging, significantly suppress the HPTA. Advocates of bridging counter this fact with the claim that while that may be true, the studies where the HPTA was suppressed do not specify at which time of the day the drugs were taken. The claim made by bridging advocates is that LH and testosterone levels are highest in the morning, and if one were to take say 10 mg of dbol so that plasma dbol levels peaked at the same time plasma test levels peaked, the body would somehow fail to notice the extra plasma androgen and hence there would be no suppression. There is just no evidence the body works this way.

There are other points to consider as well. The observation that testosterone peaks in the AM is true in the majority of young people, but not in all. And as we age, this AM peak is blunted and the pattern becomes one of a series of rather uniform peaks throughout the 24-hour period. (In fairness to bridging advocates some very recently published data are at odds with this previously widespread reported loss in the diurnal fluctuations in testosterone with aging [11].) There is tremendous individual variation in in the timing of these peaks and troughs. We also talked above about how androgens can act directly on the hypothalamus to block LH and testosterone production. Not enough is know about the temporal relationship between hypothalamic GnRH pulses, LH production, and test secretion to conclude that taking dbol when test peaks will have no effect on the GnRH signal(s) responsible for that peak. Moreover, some research has shown that 5 and 10 mg of dbol administered daily can reduce endogenous testosterone by 66 and 73% respectively, WITHOUT depressing LH, leaving open the possibility that the dbol is having a direct effect on testicular testosterone production without any hypothalamic or pituitary action. So we may not even fully understand all the mechanisms by which dbol (and other AAS) affects testosterone production (12). Lacking a complete knowledge of androgen actions, how can re reasonably conclude bridging does not suppress endogenous testosterone production?

If someone wants to stay "on" all the time and call it bridging, that is fine and is his or her choice. I just don't think they should try to justify the practice by claiming it is not suppressive of the HPTA or of endogenous testosterone production. I'm not making a value judgement here. There may not even be any serious health consequences to taking low doses of something like dbol between cycles, but on the other hand there in fact may be health implications. We saw above, for example, how very low doses of certain oral AAS can have dramatic effects on HDL. Steroids have traditionally been cycled to help avoid any long-term detrimental health effects associated with their use. Now we have certain individuals essentially advocating being "on" all the time, and using what are potentially the most dangerous steroids, 17 alpha alkylated orals, for this purpose. Am I overstating potential risks? Perhaps, but since there is little research to guide us, I'd rather err on the side of caution. If an individual wants to bridge, that is their business, but I don't think they should jump on the soapbox encouraging others to do so.

Wannabebig: Often times you hear people talking about taking a break from taking steroids so their receptors can clean out otherwise their gains will come to a halt. Is this another myth?

Nandi: Receptors are continually being degraded and remanufactured in cells, so they never really clog up and require cleaning.
I think this is a sort of fanciful way of talking about receptor upregulation/downregulation, which is a complex topic. "Do gains slow because receptors downregulate (decrease in number and/or sensitivity) during a cycle?" is probably a more accurate way of posing the question. There are conflicting data in this regard. Short-term in vitro and in vivo studies generally show that androgens upregulate the androgen receptor (AR) in skeletal muscle. For example, in humans given 15 mg of oxandrolone daily for 5 days, the skeletal muscle AR density nearly doubled (13). When exposed to testosterone in vitro, skeletal muscle AR expression increased significantly (14).

In longer-term studies the picture is somewhat different. One study looked at AR expression in androgen treated sedentary rats vs nontreated exercised rats over 8 weeks. The androgen treated rats showed a decrease in the number of receptors, whereas the exercise trained rats showed an increase. (15) Unfortunately, the authors failed to address the question of interest to bodybuilders, and that would be the combined effects of exercise and androgen use on skeletal muscle AR regulation.

In long term studies in humans we get yet a different picture. In work conducted by Sheffield-Moore et. al., (16) older men were supplemented with testosterone so as to bring their testosterone levels into the mid to high physiological range. Androgen receptor expression had more than doubled after one month of treatment, yet by 6 months had returned to baseline. If this downregulation occurs when supraphysiological doses of testosterone are used, it could very well explain why gains tend to slow during a long cycle.

So, unfortunately the data are equivocal. The definitive experiment of combining supraphysiological AAS with resistance training and looking at AR regulation does not appear to have been carried out yet. Would exercise combined with AAS maintain increased AR expression, or would the addition of exercise serve to offset the AAS induced AR downregulation observed in the study by Bricout et al? Do the extremely high doses of AAS used by bodybuilders lead to more or less downregulation ( or even upregulation ) compared to what was seen by Sheffield-Moore et al? These are just a couple of questions that require further research, and could lead to answers on why exercise combined with AAS use is so much more productive than simply using steroids alone when it comes to building muscle mass.

[Property of Steroid.com]

You got to remember this is a guy that was on Personal terms with Nandi.

Don't know if you picked up my book, but I dedicated it to him. The dedication is actually the part of the book that I'm most proud of.

[RA]

Yes I agree. He's very knowledgable and has ton tons for the AAS community.

You dont need to point that out....he does it enough himself

[Swifto]

This threads till going...

[oswaldosalcedo]

and this gem?

Quote: HOOKER
Anabolic Review Steroid Profile: Equipoise (Boldenone Undeclynate)

--------------------------------------------------------------------------------

Equipoise

Boldenone Undeclynate
(1,4-androstadiene-3-one,17b-ol)
Molecular Weight(base): 286.4132
Molecular Weight (ester): 186.2936
Formula (base): C19H26O2
Manufacturer: Various
Effective Dose (Men): 200-600mgs/week
Effective Dose (Women): 50-100mgs/week
Active life: 15 days
Detection Time: Up to 5 months
Anabolic/ Androgenic ratio: 100:50


.............................. evident on internet message boards today, where many will advise against including both of them in a cycle because “they act the same way.”

The 1-2 double bond that Eq has is responsible for many of it’s characteristics. First of all, it act to slow aromatization (conversion into estrogen). The best estimate is that it does so at roughly half the rate of testosterone (1). This is the best number I’ve found in studies. Athletes almost never report estrogenic side effects with Eq, even when the dose is up to a gram per week. Side effects caused by estrogen.include oily skin, acne, and gynocomastia, and as I said, those are usually not found from Eq. Virilization (development of male sexual characteristics in women) is almost never seen with this compound, when reasonable doses are used by female athletes. This is one of the few injectable compounds which could be successfully be used by female athletes and bodybuilders, and isn’t often faked.

That double bond is also responsible for Eq’s resistance for being changed by the 5- 5-Alpha-reductase enzyme (2)(3). This enzyme converts a small amount of Boldenone into Dihydroboldenone, which is a very potent androgen (7x as anabolic as testosterone)(4). As I said though, such a small amount of it is converted that it’s really of no concern to most athletes taking Eq. This factor, plus it's low aromatisation rate mean athletes don't need to consider using ancillaries with Eq.............................


acne from estrogen! ................lol...............
there are other gems, of course.

[BajanBastard]

Acne, oily skin and gyno not caused by elevated levels of estrogen?

[IBdmfkr]

The only other thread with 5pages of useless info was the Hall of Shame thread I created.

This thread puts it to shame with the all the back and forth bickering..
You Internet tough guys are too much.

[Property of Steroid.com]

Acne, oily skin and gyno not caused by elevated levels of estrogen?

I'm fairly certain that they are, though clinical data is conflicting with regards to acne. Non-aromatizing androgens also produce all of the above, except for the gyno most of the time...although A50 can produce all of the above, and doesn't aromatize. With the use of AIs, people tend to find less of most, if not all, of those issues are lessened. That leads me to believe that estrogen is, at least in part, responsible for contributing to those side effects. Androgen levels, without the estrogen can also do it.

Also....take a look at teenage girls, who typically have elevated estrogen...acne typically follows. And...how many postmenopausal women have acne? Almost none. Inductively, I feel there's strong inductive as well as deductive evidence to conclude that estrogen contributes to all of those side effects.

[fLgAtOr]

I'm fairly certain that they are, though clinical data is conflicting with regards to acne. Non-aromatizing androgens also produce all of the above, except for the gyno most of the time...although A50 can produce all of the above, and doesn't aromatize. With the use of AIs, people tend to find less of most, if not all, of those issues are lessened. That leads me to believe that estrogen is, at least in part, responsible for contributing to those side effects. Androgen levels, without the estrogen can also do it.

Also....take a look at teenage girls, who typically have elevated estrogen...acne typically follows. And...how many postmenopausal women have acne? Almost none. Inductively, I feel there's strong inductive as well as deductive evidence to conclude that estrogen contributes to all of those side effects.

I have found this to be true in my personal experience.

This is also a reason why some people are avoiding clomid.

EDIT:
When my gyno symptoms were at their worst, so was my acne.

[oswaldosalcedo]

I'm fairly certain that they are, though clinical data is conflicting with regards to acne. Non-aromatizing androgens also produce all of the above, except for the gyno most of the time...although A50 can produce all of the above, and doesn't aromatize. With the use of AIs, people tend to find less of most, if not all, of those issues are lessened. That leads me to believe that estrogen is, at least in part, responsible for contributing to those side effects. Androgen levels, without the estrogen can also do it.

Also....take a look at teenage girls, who typically have elevated estrogen...acne typically follows. And...how many postmenopausal women have acne? Almost none. Inductively, I feel there's strong inductive as well as deductive evidence to conclude that estrogen contributes to all of those side effects.

i said acne,not gyno,post the scientific evidence.

[BajanBastard]

I'm fairly certain that they are, though clinical data is conflicting with regards to acne. Non-aromatizing androgens also produce all of the above, except for the gyno most of the time...although A50 can produce all of the above, and doesn't aromatize. With the use of AIs, people tend to find less of most, if not all, of those issues are lessened. That leads me to believe that estrogen is, at least in part, responsible for contributing to those side effects. Androgen levels, without the estrogen can also do it.

Also....take a look at teenage girls, who typically have elevated estrogen...acne typically follows. And...how many postmenopausal women have acne? Almost none. Inductively, I feel there's strong inductive as well as deductive evidence to conclude that estrogen contributes to all of those side effects.

Exactly this was my line of thinking as well.


Oswald i think it's up to you to post something to prove this wrong buddy.

[fLgAtOr]

Exactly this was my line of thinking as well.


Oswald i think it's up to you to post something to prove this wrong buddy.

This may not be the end-all-be-all answer. But I believe that it plays a role. I think DHT also plays a role in acne as well...I think some have used Nizoral for skin problems before.

[oswaldosalcedo]

Exactly this was my line of thinking as well.


Oswald i think it's up to you to post something to prove this wrong buddy.

a lot my friend,I have studied this topic.