hackskii

Febuary 2006, Muscular Development

Boosting Testosterone via Aromatase Inhibition by Dan Gwartney, MD

Double-dipping is a term used in the business world and refer to situations that provide additional revenue with no addition work. An example of double-dipping is a waste recycler charging a customer to pick up sorted trash (paper, aluminum, etc.) and then selling the materials to a recycling plant for additional income. Though the extra income rarely doubles the amount of money generated, it always improves the companies bottom line. Wise business operators always look for ways to double-dip. In many cases, the benefits go even further. Consider the waste company- not only have they generated two sources of income from the same operation, but they’ve decreased they’re cost by not having to pay dump fees for recycled waste.

Double-Dipping In Bodybuilding
There are rare opportunities for double-dipping in bodybuilding as well. Human growth hormone (GH) offers double-dipping effects of both fat burning and building lean mass. Clenbuterol has a mildly anabolic effect, but is also a potent thermogenic agent. Clearly, combining both anabolic and lipolytic (fat reducing) effects has made both of these drugs extremely popular among bodybuilders.
There’s another double-dipping opportunity that’s often overlooked. In part, this is due to the relatively new entrance of the latest generation of this class of products. Supply also effects their popularity; as well, they don’t provide as much bang for the buck as anabolic steroids. Regardless, this class of drug is still highly regarded and sought after among more experienced and sophisticated bodybuilders.
The class of drugs is aromatase inhibitors. Aromatase is a complex of enzymes that convert androgens (testosterone, androstenedione and many anabolic steroids) into estrogenic hormones. Estrogens are hormones that impart female characteristics, increase bone density, affect blood clotting and promote fat and water retention. Most bodybuilders are familiar with some of the effects with estrogens, causing bloating or gynecomastia (the development of breast tissue under the male nipple). There are two primary estrogens, estradiol and estrone, with estradiol (E2) being the more active of the two forms.
Prior to the development of the latest aromatase inhibitors, bodybuilders had few choices for reducing the estrogenic load of a cycle. Often, they tailored their cycles to include both aromatizing and non-aromatizing steroids, tapering down on the amount of the more effective (relative to mass and strength) aromatizing steroids if bloating arose. In preparation for competition, aromatizing steroids were often removed from the cycle to improve the hardened appearance onstage. If gynecomastia appeared, there were few effective options. Cytadren (aminoglutethimide) is a non-specific inhibitor of steroid formation. Though it was usually regarded as being a cortisol suppressing agent, it also had moderate anti-aromatase activity at low doses. Nolvadex (tamoxifen) is a mixed estrogen agonist-antagonist. Though tamoxifen did reduce gynecomastia in some cases, it worsened it in others. Tamoxifen also increases sex hormone binding globin, reducing the bioavailability or steroid hormones; it’s also been noted to increase estrogen levels ironically. Clomid (clomifene citrate) also works at the level of the estrogen receptor, but it’s use was usually reserved for restoring natural testosterone production at the end of a cycle.

Age-Related Testosterone Declines
Through medical science has no interest in bodybuilding, many discoveries relate to the sport. In the matter of aromatase inhibition, breast cancer research has been extremely valuable. Breast cancers are typically responsive to female sex hormones (estrogens and progesterone). Therapies that reduce estrogen levels in the body and especially tumors, have been actively investigated and developed by the pharmaceutical industry. This has resulted in the development of effective anti-aromatase drugs. Several drugs in this class have been developed, including the most recent generation of aromatase inhibitors, anastrazole and letrozole.
Bodybuilders are familiar with anastrazole and letrozole by the trade names Arimidex and Femera. Arimidex is more commonly encountered and has been used with great effectiveness in treating steroid-induced gynecomastia. It’s also believed to provide a tighter, harder appearance. Femera is less commonly encountered but is believed to be slightly more effective for the steroid-using bodybuilder.
Though most recent research on these drugs relates to breast cancer therapy, there have been several interesting studies on aromatase inhibition in human males. One such study was published in the Journal of Clinical Endocrinology and Metabolism, reporting some very interesting results. There were also several comments in the discussion that hold potential value to bodybuilding, though that aspect wasn’t addressed for obvious reasons.
The purpose of this study was to test whether the age-related decline in testosterone is due to an increased suppressive effect of estrogens on the hypothalamic-pituitary axis. To briefly review, natural testosterone production is regulated via a negative-feedback loop, involving the testes and two regions of the brain- the hypothalamus and the pituitary gland. Testosterone production occurs in the testes under the stimulation of a protein hormone released from the pituitary called leutinizing hormone (LH). LH, in turn, is released from the pituitary under stimulation from of the hypothalamic hormone called gonadotropin-releasing hormone (GnRH). The hypothalamus is called the master gland because it monitors the body and regulates the activity of the endocrine glands and by means of its releasing hormones. In the case of testosterone, when the hypothalamus detects that androgen levels are too high, it temporarily shuts down GnRH release. When GnRH levels drop, the pituitary stops releasing LH and the testes are no longer stimulated to produce testosterone. Once the testosterone levels drop, GnRH surges, causing LH and subsequently testosterone levels to pick back up. For reasons not clearly understood, the body isn’t designed to maintain a steady level, even level of testosterone. Rather it produces testosterone in wave-like surges, with peaks and valleys in the blood levels of testosterone. Even more interesting is the fact that the hypothalamus doesn’t only detect testosterone, but it’s metabolites estradiol and dihydrotestosterone (DHT).


Altering Ratios
The researchers designed a study whereby they could measure whether older men were more sensitive to estrogen suppression of testosterone production as compared to young men. To test this, they measured several hormones, including LH and testosterone (T) in two groups of men, old versus young. It’s known that T production decrease with age, resulting in a 50 percent reduction of bioavailability T. It’s believed that this reduction is due to cellular changes in the regulatory function of the brain and the increased negative feedback (or suppression). It’s also known that aromatase activity increases with age and overall fat content increases, combining to maintain estrogen levels even in the face of decreasing T levels. This results in remarkably lower T:E ratio, with E representing estradiol levels. This altered ratio is likely responsible for many other changes experienced by men with age.
Initially, it appeared as though there was little difference between the two groups, as the older and younger men had similar LH and total T values. However, the older men had much higher sex hormone biding globin (SHBG), which traps circulating T, keeping it from being metabolized, but also preventing it from having and biological activity. This resulted in significantly lower free or bioavailability T level and markedly lower free T:free E ratios.
The subjects were then given 2.5 milligrams per day of leptosome (Femera) for 28 days and retested. The aromatase inhibitor produced “a remarkable and comparable elevation” of both GnRH and T in both groups. Letrozole increased LH and T 339 percent and 146 percent respectively in the younger group; LH and T increased 323 percent and 99 percent in the older group. Letrozole also reduced E levels by 46 percent in young men, and 62 percent in the older subjects. SHBG also dropped significantly in both groups, with the T:E and free T:free E ratios rising sharply in response.
Despite robust response to aromatase inhibition, the study failed to show any evidence in older men experiencing greater suppressive effect of estrogen on natural estrogens on natural testosterone production. In fact younger men demonstrated a greater response to aromatase inhibition relative to the suppressive effects of estrogens on the hypothalamus and pituitary gland. While it remains to be seen what accounts for the hormonal changes older men experience, it’s clear that inhibiting aromatase might restore some of the youthful hormonal values.

“Natural” Supraphysiologic Testosterone Levels
Thus far, the study has been valuable in that it clearly demonstrates that healthy men, both young and old, can safely tolerate short-term aromatase inhibition and experience hormonal changes that would be beneficial to those involved in bodybuilding. As noted earlier, there were several comments in the discussion that are note worthy of further regard.
One issue that impaired the study, but was very noteworthy was the observation that the effect of letrozole persisted for much longer than anticipated. Subjects were originally scheduled to have a 14-washout period, where they didn’t receive either drug or placebo before beginning the second phase of the study. However, after the 14-day break, it was discovered that the subjects who received letrozole were still experiencing the effects of the drug with markedly higher T. This is somewhat surprising , as letrozole has a half-life of approximately 2.5 days, so one would presume 14 days would be sufficient to eliminate the drug from the system. It’s possible that the daily dose regimen allows levels to build up higher than anticipated. In fact, a separate study looking at obese men with low T levels showed that 2.5 mg given three times a week was sufficient to restore normal T levels. It’s possible that letrozole wouldn’t need to be dosed daily to provide adequate protection against aromatization.
The degree of T elevation experienced by the younger and older men was quite pronounced. In fact, both groups ended up with T levels at or above the upper limit of normal for young men. This would suggest that suppressing aromatase could allow a steroid-free bodybuilder to experience “natural” supraphysiologic testosterone levels. This would be roughly equivalent to receiving 250 to 300 milligrams or testosterone enanthate per week.
Though the goal of aromatase inhibition is to reduce estrogen conversion of androgens, it’s not necessary to completely remove estrogens from the body. There are case reports of men and women who were born without and aromatase activity due to genetic mutation. These individuals are not particularly robust specimens. They are typically very tall (due to a failure to close growth plates of the bone), have fragile skeletons due to low bone mineral density and in the case of males, are fully mature sexually. Females experience pubertal failure with virilization (male characteristics- facial hair, clitor*****ly, etc). Males also have a macroorchidism, a term describing abnormally large testes. Thus, complete suppression of aromatase would not be of benefit to the bodybuilder long term.
Fourtunately, the degree of suppression appeared to be only partial in the letrozole study. Both groups still retained 40 to 50 percent of their original estrogen levels, though it remains to be seen if such values would lead to an increased risk of osteoporosis.

Reducing Side Effects, Increasing Testosterone
The authors compared the results of other aromatase inhibition studies in males, using either anastrazole (Arimidex) or leptosome (Femera). The estrogen-reducing effect seen in this study is in agreement with other letrozole studies. While anastrozole also has potent estrogen lowering effect, it’s potency is less than that of letrozole. Comparing several studies, using different dosing schedules, it appears that letrozole is capable of lowering estrogen levels 40 to 60 percent, while anastrozole (commonly dosed at one milligram per day)lowered estrogen 30 to 50 percent. It’s important to note that these figures represent blood levels and there’s some debate as to the importance of tissue levels, rather than circulating levels of estrogen. Even in that regard, letrozole is considered superior.
Also discussed were the comparable results between letrozole and clomiphene citrate (Clomid). Clomid is used at the end of cycles to aid in restoring natural testosterone production. In considering this comment, and the fact that Femera (letrozole) is used in some fertility drug procols, it appears that letrozole could be used in place of clomid for off-cycle recovery. This would be particularly beneficial when used along with human chorionic gonadotropin (hCG), as hCG is known to raise estrogen levels in men, eve as they are attempting to restore their testosterone producing ability.
An unrelated study suggested another mechanism whereby aromatase inhibition helps resolve feminizing side effects. In studying the cellular effects of aromatase inhibitors verses timeline on breast cancer cells, it was determined that aromatase inhibition led to a reduction or progesterone receptors in the tissue. In contrast, tamoxifen increased progesterone receptor density. Progesteron is another female steroid hormone, and is believed by some to be due for the uncommon cases of nandrolone-induced gynecomastia.It remains unclear as to why older men suffer the hormonal changes associated with age. Certainly, it is known that older men have higher aromatase activity and greater fat mass leading to higher estrogen levels, higher SHBG leading to lower bioavailability of T, functional and cellular changes in the testes and brain leading to less orderly signaling and lower T response, and a greater degree of inhibition by DHT and T.
Though enhanced estrogenic suppression of the hypothalamus and pituitary isn’t the culprit causing older men to have lower testosterone and T:free E ratios, by suppressing estrogen formation through aromatase inhibition, many of the changes are corrected. For the bodybuilder, this is of significant note, as it proves once again the utility of class of drug for the steroid using bodybuilder and offers the non-steroid using bodybuilder an option to consider for increasing testosterone to mildly supraphsiologic levels. Aromatase inhibitors are on the banned substance list for the IOC (Olympics), so competitive athletes need to be aware of organizational restrictions.
Aromatase inhibitors give bodybuilders a chance to double-dip as the drug reduces estrogenic side effects and increases testosterone levels. By reducing SHBG, testosterone and other steroids would have a greater bioavailability though they would clear the system more quickly. Gynecomastia, water retention and fat accumulation could be more easily controlled.
While these effects are clearly attractive to bodybuilders, they also hold value to aging men. Hopefully, in the interest of the growing aging population, further research will be conducted to investigate the role of this class of drugs in combating the ravages of aging and age-associated diseases .

I think the author has some errors in here but I do like the article. I highlighted some of the stuff I liked in it.

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Scott


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craigybabes

thanks for that scott ill have to remember that mate! lol

Lord Lucan

yet agian another facinating post by hascks so does that mean that test boosters with estrogen inhibitors would be like double dipping because they stop the aromising of test to estrogen? and if yes does that mean taking them on and post cycle would increase the mass that you retain?

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hackskii

Actually I dont think taking AI's during PCT is a good idea at all.
I think this could drive down estrogen too low and cause some bone loss, lipid profile problems, compromise immune system, but yes I have read femera, adex, both can raise test levels if taken PCT but I dont think this is the way to go.

But, almost anything that lowers estrogen in men will raise testosterone because estrogen is part of the negative feedback loop that influences testosterone production.
Clomid and nolvadex will too but I think at even higher levels than an AI.
Nolvadex can lower IGF-1 production and also raise SHBG where you will have less free test.

That william Llewellyn dude that wrote anabolics 2006 book along with Swale both agree that you can run into problems using a AI during PCT.

I just kind of like the article even though I think there are some errors in it but I didnt write it, I just posted it
I have another one I might post, it is pretty good too.

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Scott


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hackskii

Anti-Estrogens Report Card

By J @ AG-GUYS

Remember when you were in school, and you got a report card? If you were like me, you dreaded that time of the semester. I typically got passing grades and on occasion a failing grade that would mean I had to pull straight A’s for the next half of the year in order to avoid repeating a class. What does this have to do with anything?

Well I was trying to figure out a way to rate the most commonly used anti-estrogens on the market, and the best way I can think of is to do a report card for them. Why a report card? Well…because it’s pretty easy to understand, first of all. You can be in first place in a race and that’s good, but “1st” on a scale of 1-10 is bad…so lets ditch the number system. I mean…hell…we all know what an “A+” is (or at least, in theory we do), and if you’re anything like me, you certainly know what an “F” is also. So I’m going to rate the most popular anti-estrogens that are available on the market today, with the all-too-familiar school grading system of A - F.

Also, I’d like to state right off the bat that I’m going to mainly be addressing the most commonly discussed and used ancillary compounds on the market today, for use during a cycle. Basically, if you can easily obtain it, you’ll be reading about it in this piece. Sooo….that means if you’re “old school” and are looking for a detailed description of Cytadren or Teslac, you’re out of luck.

So why do we need anti-estrogens? Well, certain anabolic steroids convert to estrogen - this is via the aromatase enzyme, and is called aromatization. This is probably the cause of most of the side effects we experience like bloating, gynocomastia, (possibly) acne, and a host of other side effects we’d rather avoid. Estrogen can also cause additional growth, however, as well as having immunostimulating effects and is beneficial for healthy joints- so it’s important to note that we don’t want to eliminate all estrogen from our bodies.

Anyway, before I get into it, I’m going to have to explain a bit about different types of Anti-Estrogens, ok? First we’ll take a look at SERMs, which stands for “Selective Estrogen Receptor Inhibitor.” There are basically two drugs in this class that we’re going to look at, namely Clomid (Clomiphene Citrate) and Nolvadex (Tamoxifin Citrate).

Basically both of these drugs have the ability to act as an estrogen agonist (or activator, in simpler- though less precise- terms) in some tissue and as an antagonist (inactivator), in others. I’ll get into the specific actions of both of them shortly.

The other class of medications I’m going to explain is Aromatase Inhibitors. Aromatase Inhibitors basically prevent the aromatase enzyme from doing its job. AIs are classified into two types: type I, also known as suicidal or noncompetitive inhibitors; and type II, known as competitive inhibitors. Aromasin and ATD are in the first category, while Arimidex and Letrozole are in the second. Both type I & II mimic substrates (essentially androgens), and can compete with it for access to the binding site on the actual enzyme (aromatase). After this initial binding, the next step is where things begin to differ for the two different types of AI’s. Once a noncompetitive inhibitor has bound, the enzyme initiates a sequence of what’s called hydroxylation, and hydroxylation produces an unbreakable covalent bond between the inhibitor and the enzyme protein. This is important because now, enzyme (aromatase) activity is permanently blocked; even if all of the unattached inhibitor is removed, and now, enzyme activity can only be restored by new enzyme synthesis. Type II AI’s or competitive inhibitors, on the other hand, reversibly bind to the active enzyme site, and one of two effects is had: no enzyme activity is triggered, or the enzyme is somehow triggered without effect. The type II inhibitor can then actually disassociate from the enzyme, eventually allowing renewed competition between the inhibitor and the substrate for binding to the site (estrogen synthesis).

Now that SERMs have been explained as well as AI’s, we can see how each of them rates on my “on-cycle report card.”

Clomid

Clomid is a drug given to women as a fertility aid, which acts by binding to the estrogen receptor and thereby blocking estrogen from doing the same in some tissues. It can bind to breast tissue, and prevent estrogen from binding there to cause gynocomastia -although it is not nearly as effective as nolvadex. It can also stimulate the HPTA (Hypothalamic-Pituitary-Testicular-Axis), and stimulates LH (Luteinizing Hormone) and FSH (Follicle Stimulating Hormone). LH and FSH stimulate the release of testosterone. Unfortunately, Clomid does this only weakly, and there are much better ancillary products on the market. It works, but I think Nolvadex is much better.

Final Grade: C-


Nolvadex

Nolvadex is a Selective Estrogen Receptor Modulator. This means that it acts on the Estrogen receptor (called the "ER" but having nothing to do with George Clooney or Anthony Edwards). Now, this also means that it acts as an estrogen in some tissues which acts as an anti-estrogen in some tissues.

The estrogen receptor's ligand binding domain is just of a number of amino acid sequences "folded" into a series of helixes, which have the ability to change conformation. Different stimuli (such as Nolvadex) are well documented to have the ability to change the conformation of a very important helix (helix 12, for those keeping score at home).

When estradiol binds the ER, this particular helix takes on a conformation that allows DNA transcription to mRNA, and estrogenic effects are then expressed in the body. When Nolvadex (Tamoxifen) binds to it, the antagonist changes the shape of this helix in such a way that it now folds (or bends) in such a way to prevent proper binding of estrogen, and subsequent transcription of DNA to mRNA.

Sadly, if you take progesteronic (I made that word up) steroids 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). So besides competing with estrogen at the receptor, these drugs both increase serum test levels, and both drugs may also alter blood lipid profiles. With regards to Clomid and Nolvadex, I’ve found some research that indicates that 20mgs of tamoxifen is equal to 150mgs of clomid for purposes of testosterone elevation, FSH and LH, but tamoxifen did not decrease the LH response to LHRH (Fertil Steril. 1978 Mar;29(3):320-7). Interestingly, Nolvadex can even be used in small doses just as effectively as larger doses, when it comes to sperm indices and spermatogenesis. (“Effect of lower versus higher doses of tamoxifen on pituitary-gonadal function and sperm indices in oligozoospermic men”. Dony JM, Smals AG, Rolland R, Fauser BC, Thomas CM.) So in this case, we can actually use much lower doses than the egregiously recommended 40-60mgs/day. 5mgs a day seems to be as effective as 20, with regards to basal or LHRH stimulated gonadotropin and testosterone response or the E2/T ratio (Ibid).

So that makes Nolvadex great for preventing gyno, and superb for Post Cycle Therapy even at lower dosages, but not my favorite Ancillary product during a cycle, unless I need to help my lipid profile or just prevent gyno. I give nolvadex a …

Final Grade: B-


Aromasin

Aromasin basically is an aromatase inactivator...It actually makes estrogen receptors useless in a sense, because it inhibits the aromatase enzyme from creating more estrogen. This is like having a wall socket but no radio to plug into it…kind of useless, right? Instead of just inhibiting production (as a Type-II anti-aromatase would do) it irreversibly cuts off estrogen production from the enzyme it attaches to. Aromasin can also cause androgenic sides, so it’s not ideal for women, however. It’s not particularly harsh on cholesterol, and can be effectively used with Nolvadex. I’ve seen studies indicating that it reduces estrogen in your body by about 80%, possibly making it too strong, for maximum gains and staying healthy on a long (12 weeks or more) cycle. Aromasin, at 20mgs/day, will raise your testosterone levels by about 60%, and will even help out your free to bound testosterone ratio by lowering your body’s levels of Sex Hormone Binding Globulin (SHBG), by roughly 20% (The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 12 5951-5956)…It’s perfect for use in PCT, for many other reasons (it interacts more favorably with Nolvadex than other AIs). But it’s not 100% what we want during a cycle…for this reason, I give it a strong…

Final Grade: B+


Arimidex

From the research I've done, this seems to be the best ancillary compound around for use on a cycle. First off, 1mg per day of this stuff (J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 ) was shown to decrease estrogen by about 50% and increase testosterone levels by 58%. That’s a level of estrogen suppression I’m very comfortable with on virtually any cycle. Interestingly, that same study showed that those results were had with .5mgs/day as well. So, since you can elevate testosterone, lower estrogen (but not excessively), and keep healthy joints and lipids, and do this at a half mg per day, I give this my highest rating for an ancillary product to use on a cycle…

Final Grade: A


Letrozole

Letrozole is another type II (competitive) AI. Letrozole is actually a lot more effective than Arimidex in its ability to pass thru the cell membrane of lipid (fat) cells as well as inhibit the activity of aromatase. In some studies, circulating estrogen levels are totally undetectable in most patients taking Letrozole, and just like Arimidex, it has even been used in specific cases to increase testosterone to normal levels (from sub-normal ones) and increase LH, and FSH (Epilepsy Behav. 2004 Apr;5(2):260-3). Unfortunately, it does this too well, and although it cleared up my minor gyno lumps, and has been shown to do this in animal studies as well (J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):27-34. Aromatase overexpression transgenic mice model: cell type specific expression and use of letrozole to abrogate mammary hyperplasia without affecting normal physiology.). This got my gyno lumps to the point that they are totally gone now, prolonged use lowered my immune system and gave me joint problems (due to a lack of estrogen). It’s very strong, and maximum inhibition of aromatase in one study was found to happen in women at tiny 100mcg doses (J Clin Endocrinol Metab. 1995 Sep;80(9):2658-60.)If you aren’t on a cutting cycle, training for a contest, or trying to clear up some gyno, Letrozole is not for you. Still, it’s the most potent Aromatase Inhibitor on the market today, so I’ll cautiously give it a …

Final Grade: B


ATD

ATD is one of those products that’s getting a lot of press lately, as it’s become available from a couple of nutritional companies. I’ve seen studies showing that it can reduce estrogen levels heavily with a dose of 1-1.25mgs, twice daily.

After ten days, 84% estrogen inhibition was achieved with ATD in primates (J Clin Endocrinol Metab. 1993 Apr;76(4):988-95.), but not much of an increase in testosterone, as we see with other AIs. This is probably because, as some scientists speculated, ATD may act simultaneously as an androgen receptor blocker and as an aromatization inhibitor. In other words, ATD may prevent Testosterone from binding to androgen receptors, and thus negate some of the anabolic effects of steroids (Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis.Kaplan ME, McGinnis MY.
Department of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029) In light of the fact that ATD seems to be a bit too strong on stopping estrogen (though it undeniably inhibits aromatase), and can most likely make the steroids you take on a cycle less effective, I give ATD a…

Final Grade: D


So, in summary, I believe Arimidex (Liquidex or Anastrozole) to be the best ancillary product for use on most of the cycles that I see posted on the internet, or talked about in my gym.

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Scott


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Littleluke

quality post!

jugganaut

I concur, quality post.
How about AI with clen? Safe?

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hackskii

Are you thinking this for dieting purposes?
During a cycle or not on a cycle?

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Scott


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Cheater2K

Very intresting, i did find Nolva didnt work at all for me, i used armidex on my last 2 cycles, to which it did make a huge difference, even at 1mg EOD

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jugganaut

hackskii, Im thinking not on a cycle, and Im not really dieting, im just eating in moderation. AI's as I've read should decrease the estrogen in my body, which should lead to an increase in testosterone, and thats would be a good thing for me since im 31 and i know my test levels wouldnt be the same as it was 10yrs ago. But increased natural test can do soo much, so I figure clen will help me burn more fat. Any logic to my thinking?

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hackskii

Yah, taking an AI outside a cycle can make your estrogen receptors very sensitve and when you come off you might get gyno.

Another thing, some bone loss has been associated with AI's, women with breast cancer take adex and there is known bone loss.

Estrogen supports your lipid profile so taking lets say femera might raise LDL's and lower HDL's which raising bad cholesterol and lowering good cholesterol might not be the best idea.

I am sure for short periods of time this might not be all that bad but it can kill libido too.
Good bye sex drive.
So, estrogen is not bad only if it is excessive or if the ratio of testosterone to estrogen is not right.

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Scott


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jugganaut

You can win can you! I'll stick with my clen for now and leave the AI alone.

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Captain Hero

bump to read later

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