How is strength?
Source: Anabolics E-Book Edition by William Llewellyn 2011Avoid Aromatase Inhibitors. Aromatase-inhibiting drugs counter estrogenic side effects by preventing the production of estrogen in the body. While an effective practice, they also deprive the body of a hormone that is important to cardiovascular health. In particular, estrogen supports the production of good (HDL) cholesterol, which means that aromatase inhibitors may inadvertently increase the cardiovascular strain of a steroid cycle. If estrogenic side effects are apparent and a reduction or elimination of the offending steroid(s) is not considered an option, the SERM (Selective Estrogen Receptor Modulator) drug Nolvadex could be used instead. This drug offers partial estrogenic action in the liver, which may allow
it to counterer estrogenic side effects without the same negative shift in cholesterol.
Are you referring to me? If so, I have no idea what you mean.Your second sentence answered your question... And i'll take decades of peoples advice over a random guy on a forum no offense
That he's gyno proneAre you referring to me? If so, I have no idea what you mean.
Devildog_ is gyno prone? I didn't see that mentioned anywhere in this thread. Even if so, I would choose Nolvadex over an AI. There have been many, many studies showing tamoxifen is helping at reducing/treating gyno. Then, you have the positive effects of keeping HDL high while on Nolva, while AI's reduce that advantage completely and cause LDL to skyrocket.That he's gyno prone
He didn't. He said that you answered the question about why use an AI with your second sentence. Which mentions being gyno prone.Devildog_ is gyno prone? I didn't see that mentioned anywhere in this thread. Even if so, I would choose Nolvadex over an AI. There have been many, many studies showing tamoxifen is helping at reducing/treating gyno. Then, you have the positive effects of keeping HDL high while on Nolva, while AI's reduce that advantage completely and cause LDL to skyrocket.
I still don't follow what you mean exactly. If this is someone's first cycle, they'll have no idea if they're sensitive to estrogen and thus prone to gyno. I typically recommend someone keep an AI on hand during their first cycle, but there's no need to take it ED or EOD to reduce estrogen, because estrogen is a good compound to have circulating in the body during a cycle.He didn't. He said that you answered the question about why use an AI with your second sentence. Which mentions being gyno prone.
This is his first injectable cycle. He has run Trest and DMZ at least once.I still don't follow what you mean exactly. If this is someone's first cycle, they'll have no idea if they're sensitive to estrogen and thus prone to gyno. I typically recommend someone keep an AI on hand during their first cycle, but there's no need to take it ED or EOD to reduce estrogen, because estrogen is a good compound to have circulating in the body during a cycle.
Source: Anabolics E-Book Edition by William Llewellyn 2011 (This version of the above text was quoted from the Anabolics 9th Edition, which for some strange reason is listed as selling for $900 on Amazon. But the $10 eBook version of the text is well worth the purchase too. I guess I have a very expensive book in my possession, it's even autographed by the author himself!)We must, however, not be led into thinking that estrogen serves no benefit. It is actually a desirable hormone in many regards. Athletes have known for years that estrogenic steroids are the best mass builders, but it is only recently that we are finally coming to understand the underlying mechanisms why. It appears that reasons go beyond the simple size, weight, and strength increases that one would attribute to estrogen-related waterretention, with this hormone actually having a direct effect on the process of anabolism. This is manifest through increases in glucose utilization, growth hormone secretion, and androgen receptor proliferation.
Glucose Utilization and Estrogen
Estrogen may playa very important role in the promotion of an anabolic state by affecting glucose utilization in muscle tissue. This occurs via an altering of the level of available glucose 6-phosphate dehydrogenase, an enzyme directly tied to the use of glucose for muscle tissue growth and recuperation. More specifically, G6PD is a vital part of the pentose phosphate pathway, which is integral in determining the rate nucleic acids and lipids are to be synthesized in cells for tissue repair. During the period of regeneration after skeletal muscle damage, levels of G6PD are shown to rise dramatically, which is believed to represent a mechanism for the body to enhance recovery when needed. Surprisingly, we find that estrogen is directly tied to the level of G6PD that is to be made available to cells in this recovery window. The link between estrogen and G6PD was established in a study demonstrating levels of this dehydrogenase enzyme to rise after administration of testosterone propionate. The investigation further showed that the
aromatization of testosterone to estradiol was directly responsible for this increase, and not the androgenic action of this steroid. The non-aromatizable steroids dihydrotestosterone and fluoxymesterone were tested alongside testosterone propionate, but failed to duplicate the effect of testosterone. Furthermore, the positive effect of testosterone propionate was blocked when the aromatase inhibitor 4-hydroxyandrostenedione (formestane) was added, while 17-beta estradiol administration alone caused a similar increase in G6PD to testosterone propionate.The inactive estrogen isomer 17* alpha estradiol, which is unable to bind the estrogen receptor, failed to do anything. Further tests using testosterone propionate and the anti-androgen flutamide showed that this drug also did nothing to block the positive action of testosterone, establishing it as an effect independent of the androgen receptor.
Estrogen and GH/IGF·l
Estrogen may also play an important role in the production of growth hormone and IGF-1. IGF-1 (insulin like growth factor) is an anabolic hormone released in the liver and various peripheral tissues via the stimulus of growth hormone (See Drug Profiles: Growth Hormone).
IGF-1 is responsible for the anabolic activity of growth hormone such as increased nitrogen retention/protein synthesis and cell hyperplasia (proliferation). One of the first studies to bring this issue to our attention looked at the effects of the anti-estrogen tamoxifen on IGF-1 levels, demonstrating it to have a suppressive effect. A second, perhaps more noteworthy, study took place in 1993, which looked at the effects of testosterone replacement therapy on GH and IGF-1 levels alone, and compared them to the effects of testosterone combined again with tamoxifen. When tamoxifen was given, GH and IGF-l levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300 mg of testosterone enanthate weekly to cause a slight IGF-l increase in normal men. Here the 300 mg of testosterone ester caused an elevation of estradiol levels, which would be expected at such a dose. This was compared to the effect of the same dosage of nandrolone decanoate; however, this steroid failed to produce the same increase. This result is quite interesting, especially when we note that estrogen levels were actually lowered when this steroid was given. Yet another demonstrated that GH and IGF-l secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to
suppress GH and IGF-l secretion.
Estrogen and the Androgen Receptor
It has also been demonstrated that estrogen can increase the concentration of androgen receptors in certain tissues. This was shown in studies with rats, which looked at the effects of estrogen on cellular androgen receptors in animals that underwent orchiectomy (removal of testes, often done to diminish endogenous androgen production). According to the study, administration of estrogen resulted in a striking 4800/0 increase in methyltrienolone (a potent oral androgen often used to reference receptor binding in studies) binding in the levator ani muscle. The suggested explanation is that estrogen must either be directly stimulating androgen receptor production, or perhaps diminishing the rate of receptor breakdown. Although the growth of the levator ani muscle is commonly used as a reference for the anabolic activity of steroid compounds, it is admittedly a sex organ muscle, and different from skeletal muscle tissue in that it possesses a much higher concentration of androgen receptors. This study, however, did look at the effect of estrogen in fast-twitch skeletal muscle tissues (tibialis anterior and extensor digitorum longus) as well, but did not note the same increase as the levator ani. Although discouraging at first glance, the fact that estrogen can increase androgen receptor binding in any tissue remains an extremely significant finding, especially in light of the fact that we now know androgens to have some positive effects on muscle growth that are mediated outside of muscle tissue.
Estrogen and Fatigue
"Steroid Fatigue" is a common catchphrase these days, and refers to another important function of estrogen in both the male and female body, namely its ability to promote wakefulness and a mentally alert state. Given the common availability of potent third-generation aromatase inhibitors, bodybuilders today are (at times) noticing more extreme estrogen suppression than they had in the past. Often associated with this suppression is fatigue. Under such conditions, the athlete, though on a productive cycle of drugs, may not be able to maximize his or her gains due to an inability to train at full vigor.This effect is sometimes also dubbed "steroid lethargy." The reason is that estrogen plays an important supporting role in the activity of serotonin. Serotonin is one of the body's principle neurotransmitters, vital to mental alertness and the sleep/wake cycle. Interference with this neurotransmitter is also associated with chronic fatigue syndrome, so we can see how vital it is to fatigue specifically. Estrogen suppression in menopause has also been associated with fatigue, as has the clinical use of newer (more potent) aromatase inhibitors like anastrozole, letrozole, exemestane, and fadrozole in some patients. These things may be important to consider when planning your next cycle. Although not everyone notices this problem when estrogen is low, for those that do, a little testosterone or estrogen can go a long way in correcting this. It is also of note that the use of strictly non-aromatizable steroids sometimes causes this effect as well, likely due to the suppression of natural testosterone production (cutting off the main substrate
used by the male body to make estrogen).
Anti-Estrogens and the Athlete
So what does this all mean to the bodybuilder looking to gain optimal size? Basically I think it calls for a cautious approach to the use of estrogen maintenance drugs if mass is the key objective (things change, of course, if we are talking about cutting). Obviously, anti-estrogens should be used if there is a clear need for them due to the onset of estrogenic side effects, or at the very least, the drugs being administered should be substituted for nonestrogenic compounds. Gynecomastia is certainly an unwanted problem for the steroid user, as are noticeable fat mass gains. But if these problems have not presented themselves, the added estrogen due to a cycle of testosterone or Dianabol, for example, might indeed be aiding in the buildup of muscle mass, or keeping you energetic. An individual confident they will notice, or are not prone to getting, estrogenic side effects, may therefore want to hold off using estrogen maintenance drugs so as to achieve the maximum possible gains in tissue mass
As we mentioned already, testosterone is a substrate for the aromatase enzyme and converts to E2. A female hormone. Here too demonisation has made E2 the enemy. And yet again we are overlooking several factors. First of all, bloat, fat gain and gyno occur only at very high concentrations of E2, something we should be able to avoid if we are sane with our doses. And if not, we have numerous anti-aromatase drugs at our disposal, of which I favour Mesterolone (Proviron ) as it is a DHT analogue, will increase free testosterone and does not block E2 entirely in low doses, so we still reap the benefits. So what are the benefits of E2 ? Well, estrogen enhances gluconeogenesis (use of glucose for tissue repair and energy storage) , increases the release of human Growth Hormone and can increase androgen receptor upregulation (E2 makes testosterone more effective as an androgen)
Anyone who makes the choice to run AAS will always have to test the waters with an aromatizing compound and determine whether or not we are sensitive. Although it's wise to keep an rx anti-estrogen on hand during our first cycle, not just for PCT but for emergencies like gyno or if you feel you're getting too much bloat, I also recommend having finasteride on hand during a first cycle for the same reason. It just doesn't make sense to just run an anti-estrogen throughout an entire first cycle because you're scared of a compound in which you don't have any idea how you'll react to it.This is his first injectable cycle. He has run Trest and DMZ at least once.
Although estrogen has been linked to BPH, in reality the truth is much harder to figure out. What causes it is essentially still a mystery.
http://www.ncbi.nlm.nih.gov/pubmed/12032329Benign prostatic hyperplasia (BPH) is a disease of unknown etiology ...
This may very well be true, but remember, we are looking at acute raising of estrogen levels, not chronic. 8-12 weeks is not a chronic estrogen increase. These types of studies are looked at for women who are using estrogen replacement therapy for years, not an AAS user who runs testosterone for a short period. However, I do recommend in many, many threads that AAS users buy and use a blood pressure monitor daily to keep track of their BP levels. Androgens can increase BP highly, even without the addition of estrogen.
I just had to laugh at this one "Irritable Men Syndrome"
AIs have more negatives than positives when comparing to SERMs.For every positive there is a negative. For a few extra pounds and some strength, I don't feel like excess estrogen is worth it. Is some good yes. But Nolva doesn't provide that balance. An AI at the PROPER dose does.
Sir, you seem to be having a hard enough time managing your OTC cycle. Maybe you should take some of this guy's advice. And the irritable syndrome was simply to make a point. Emotional roller-coaster is no fun with high E2.Anyone who makes the choice to run AAS will always have to test the waters with an aromatizing compound and determine whether or not we are sensitive. Although it's wise to keep an rx anti-estrogen on hand during our first cycle, not just for PCT but for emergencies like gyno or if you feel you're getting too much bloat, I also recommend having finasteride on hand during a first cycle for the same reason. It just doesn't make sense to just run an anti-estrogen throughout an entire first cycle because you're scared of a compound in which you don't have any idea how you'll react to it.
Although estrogen has been linked to BPH, in reality the truth is much harder to figure out. What causes it is essentially still a mystery.
http://www.ncbi.nlm.nih.gov/pubmed/12032329
It's also been theorized that VEGF, a signal protein is solely responsible for BPH formation. VEGF doesn't seem to be activated by testosterone or estrogen, but more likely by DHT, which is what has been the most accepted theory of BPH formation for a long time (eg: high DHT levels cause prostate growth, this is why drugs like finasteride and dutasteride are prescribed for treatment of BPH, as opposed to anti-estrogens)
http://www.ncbi.nlm.nih.gov/pubmed/14673953
http://www.ncbi.nlm.nih.gov/pubmed/12201932
But, this is getting way off topic.
This may very well be true, but remember, we are looking at acute raising of estrogen levels, not chronic. 8-12 weeks is not a chronic estrogen increase. These types of studies are looked at for women who are using estrogen replacement therapy for years, not an AAS user who runs testosterone for a short period. However, I do recommend in many, many threads that AAS users buy and use a blood pressure monitor daily to keep track of their BP levels. Androgens can increase BP highly, even without the addition of estrogen.
You can read my entire writeup on helping to prevent cardiovascular problems on cycle in this thread here: http://anabolicminds.com/forum/steroids/281497-cycle-heart-support.html#post5370240
I just had to laugh at this one "Irritable Men Syndrome" View attachment 135840
AIs have more negatives than positives when comparing to SERMs.
No worries bro it actually brought some good life to this thread. Nice to have someone in my corner is well.Sorry Devildog, I'm done with it. Keep up the good work bro. Feeling good? Keep doing what you're doing!!
Some dude's just want to argue and bring you down. This guy having a bad enough time managing a PH cycle and wants to come in here and tell you what to do. GTFO
Bear in mind I'm using a completely new experimental compound with one study titled "Prohormone supplement 3-hydroxy-5-androst-1-en-17-one enhances resistance training gains but impairs user health".Sir, you seem to be having a hard enough time managing your OTC cycle.
Are there any actual studies showing elevated estrogen cycles in men lead to depression/irritation/etc? The site you quoted that from is a site that SELLS TESTOSTERONE REPLACEMENT THERAPY. So, I wouldn't say they are the most reliable source on the subject.Maybe you should take some of this guy's advice. And the irritable syndrome was simply to make a point. Emotional roller-coaster is no fun with high E2.
I don't come here to brag about my gains or use them to justify because I've put on X amount of weight I know more about something than someone else. That kind of braggadocio just makes you sound arrogant. Size & strength ≠ knowledge.You seem to just like to argue, you get lost in the conversation (I've seen it a couple times), and it's your way or no way. I've put on nearly 40lbs. of LBM in 2.5 years and have used an AI every time. AT THE PROPER DOSE. NO ONE IS SUGGESTING CRUSHING ESTROGEN
Link me to it and I'll take a look.I think you need to get on Daniel's BP and E2 protocol, your cycle would probably go way smoother bud.
I don't like to come here and just spout off like I'm some kind of badass pro who comes to forums to challenge people in things I know nothing about but pretend like I do, but if you think I don't know what I'm talking about, then I'll just give you a few of my credentials.No worries bro it actually brought some good life to this thread. Nice to have someone in my corner is well.
I feel great and the gains are great. I'm not gonna take the advice of some random schmuck over years and years of people studying and saying something else.
Last thing I want is gyno so eff this guy.
Broscience
Broscience is the predominant brand of reasoning in bodybuilding circles where the anecdotal reports of jacked dudes are considered more credible than scientific research.
Broscience in action:
"Bro, you gotta slam 40-60 grams of waxy maize plus 20 grams of BCAA within 7 seconds of finishing your last set of squat rack curls. Otherwise, you'll go straight catabolic."
No idea what you're referring to here. The right study on what? Are you trying to be facetious or sarcastic?Because you couldn't find the right study I guess.
If you say so. I'd call that easy way out of trying to prove your point.And I can't debate with you, you miss the point of things if they weren't completely spelled out.
Sure didn't sound that way.i.e. Me explaining my gains while using an AI. It was not meant to brag.
If you give up on an argument, there's really nothing more I can say or do. But all I saw from you was you claiming you made gains while using AIs, two mostly irrelevant studies on the subject, and one completely spurious article. If that's the best you got, then I'd say that's a pretty poor way of validating your claims.But like I said I'm done in this guys' log. You're right, I'm wrong, the end.
I contend it's totally possible I'm wrong, but I don't come at this argument with anecdotal evidence. Peer reviewed studies > anecdotal evidence 100% of the time.Respect for the Demon Haunted World Reference. You'll see by my profile I'm a Sagan fan. And a science advocate. But there's more to this than this study or that. And while you may say my claim of gains comes off as arrogant, I call you out on your own cognitive dissonance.
Maybe if Dma378 wants, we could start a new thread on this topic in the Anabolics section with what we've posted so far and continue it from there so we won't clog up this guy's log anymore.Get the **** off my thread already *******
That's your prerogative. All I ask is you keep an open mind and take the time to read the stuff I've posted, especially from William Llewellyn, who I consider one of the leading experts in the field of AAS.I appreciate your input pogue and you're name haha but I disagree with what you're saying and will not be switching anything up.
Dat der Cell-TechMy fitness director asked me what I was taking today
Told him creatine and proper diet, he didn't believe me hahaDat der Cell-Tech
Ahahahahhahaha never will ever get old hahahaDat der Cell-Tech
If it's good enough for Ronnie, well then...Ahahahahhahaha never will ever get old hahaha
Speaking of classic quotes I've been getting consistent and deep chest pumps for the first time in years, "it's like I'm always cumming." Lmao