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Thread: SERM/AI Definition

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    LuvMuhRoids's Avatar
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    SERM/AI Definition

    Selective Estrogen Receptor Modulator (SERM) Compounds that bind with estrogen receptors and exhibit estrogen action in some tissues and anti-estrogen action in other tissues. The ideal SERM would deliver all the benefits of estrogen without the adverse effects. ex: Clomiphene Citrate (Marketed as Clomid or Serophene). Tamoxifen (Marketed as Nolvadex).

    Aromatise Inhibitor (AI) Aromatase inhibitors exhibit a very different mechanism of action than SERM’s. Aromatase inhibitors prevent the conversion of androgens into estrogen in fat, muscle, breast, and brain. ex: Anastrazole (brand name Arimidex ). FEMARA (letrozole tablets).

    NOTE: Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor. In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). LH output by the pituitary will be increased as a result, which in turn can increase the level of testosterone by the testes.

    Although these two are related anti-estrogens, they appear to act very differently at different sites of action. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary.

    by William Llewellyn


    SERM:
    Clomid, stimulates the hypophysis to release more gonadotropin so that
    a faster and higher release of follicle stimulating hormone aud
    luteinizing hormone occurs. This results in an increase of the body's
    own testosterone production. Clomid is a synthetic estrogen, however
    it does also work as an anti-estrogen. How does it work? Because it is
    a weak synthetic estrogen, it will bind to the estrogen receptor (ER)
    and not cause any problems. At the same time the increase in estrogen
    from steroids are blocked from attaching to the ER.

    Nolvadex, is very comparable to Clomid, behaves in the same manner in
    all tissues, and is a mixed estrogen agonist/antagonist of the same
    type as Clomid. The two molecules are also very similar in structure.
    It is not correct that Nolvadex reduces levels of estrogen: rather, it
    blocks estrogen from estrogen receptors and, in those tissues where it
    is an antagonist, causes the receptor to do nothing.

    Cyclofenil, similar to HCG and Clomid in action. This drug is most
    commonly used to increase endogenous testosterone levels after a cycle
    in an attempt to avoid a hard crash while waiting for your hormone
    levels to naturally balance. Similar to HCG and Clomid, cyclofenil
    seems to quickly and effectively raise natural levels. Cyclofenil is
    an estrogen that works as an anti-estrogen as well as a testosterone
    booster.

    AI:
    Femara, (letrozole tablets) for oral administration contain 2.5 mg of
    letrozole, a nonsteroidal aromatase inhibitor (inhibitor of estrogen
    synthesis). Letrozole is a nonsteroidal competitive inhibitor of the
    aromatase enzyme system; it inhibits the conversion of androgens to
    estrogens.

    Cytadren, (aminoglutethimide) at moderate doses, is a fairly effective inhibitor of aromatase and a weak inhibitor of desmolase (an enzyme needed for the
    production of all steroids), and at higher doses becomes an effective
    inhibitor of desmolase. It is therefore useful when using aromatizable
    steroids, though it is not the drug of choice for this purpose.

    Aromasin, tablets for oral administration contain 25 mg of exemestane,
    an irreversible, steroidal aromatase inactivator. Exemestane is
    chemically described as 6-methylenandrosta-1,4-diene-3,17 -dione.

    Anastrozole,(Arimidex) is the aromatase inhibitor of choice. The drug
    is appropriately used when using substantial amounts of aromatizing
    steroids, or when one is prone to gynecomastia and using moderate
    amounts of such steroids. It is manufactured by Zenica Pharmaceuticals
    and was approved for use in the United States at the end of Dec 1995.

    Proviron, is also an estrogen antagonist which prevents the
    aromatization of steroids. Unlike the antiestrogen Nolvadex which only
    blocks the estrogen receptors (see Nolvadex) Proviron already prevents
    the aromatizing of steroids. Therefore gynecomastia and increased water
    retention are successfully blocked. Since Proviron strongly suppresses
    the forming of estrogens no re-bound effect occurs.

    Teslac,is unique in its effectiveness as an antiestrogen. Like
    Proviron, it prevents the aromatizing process of the steroids from the
    basis. Thus, Teslac prevents almost completely the introduction of more
    estrogens into the blood and subsequent bonding with the estrogen
    receptors.

    6-OXO, contains a naturally occurring aromatase inhibitor that is devoid of any direct hormonal or prohormonal activity (androgenic or estrogenic). It is what science refers to as a "suicide inhibitor" of aromatase.

    L-Dex, same as arimidex or anastrozole; known as an AI and popular on chemical supply sites. This is the name given on chemical supply sites instead of it's original name. L-Dex meaning "Liquidex".

    There are a number of chemical research sites that sell liquid products similar to the above mentioned items. These products are the same but in liquid form such as liquid clomid, liquid nolva, liquid femera, and liquid arimidex.

    Dosage's are usually adminstered by droppers but dosage amounts per ml differ from site to site.



    Also, even though bodybuilders resort to these products in paranoia of the affects of estrogen. It is important to remember, estrogen is necessary and must be balanced not completely inhibited in the system. Below is an excellent reading about the necessity of estrogen.

    To much is bad, but estrogen in moderation is priceless!
    by William Llewellyn

    Can estrogen work to augment muscle growth? Is this hormone always unwanted when we are taking anabolic steroids? Anecdotal reports from athletes suggest that the use of estrogen maintenance drugs such as tamoxifen (anti-estrogen) or aminoglutethimide (anti-aromatase) may slightly hinder muscle mass gains during steroid therapy. An explanation or even clarification for this observation has not been easy to come by. Here I would like to take a look at the comparative effectiveness of certain aromatizable and non-aromatizable drugs, as well as the possible mechanism in which estrogen can play a beneficial role to the athlete.

    The Androgen Receptor
    All anabolic/androgenic steroids promote muscle growth primarily via the cellular androgen receptor (abbreviated as AR in this article). The steroid attaches to and activates the androgen receptor, which ultimately gives the cell an order to increase protein synthesis. This process is well understood. But it has been suggested that other mechanisms may foster muscle growth during steroid therapy as well, which lie outside of the androgen receptor. One way this is evidenced is by the fact that steroids displaying a high affinity for the AR in muscle tissue do not always promote an equally high level of muscle growth. In other words, anabolic potency does not always correspond perfectly to receptor affinity. Clearly there are some disparities that lead into question whether or not the androgen receptor is the only thing at work concerning growth.

    Testosterone, Nandrolone and Methenolone
    Testosterone is without question one of the most effective steroids for building muscle mass available to athletes. However it does not have the highest affinity for the androgen receptor compared to some other steroids. For example, it has been shown that by eliminating the 19-methyl group (nandrolone) the affinity of the steroid for the androgen receptor is greatly enhanced[i]. Nandrolone thus displays approximately 2-3 times greater affinity for the androgen receptor compared to testosterone, yet its ability to promote muscle growth seems to be considerably lower than testosterone at an equal dosage. One discussed possibility for this occurrence is the reduced androgenic potency of nandrolone. While testosterone converts to the more active steroid dihydrotestosterone (3-4 times greater AR affinity) upon interaction with the 5-alpha reductase enzyme in various androgenic target tissues such as the skin, scalp, prostate, CNS and liver, nandrolone drops to a third of its original potency by converting to the weak steroid dihydronandrolone[ii]. However this action is very site specific, and in muscle tissue nandrolone dominates as the active form of the steroid. Therefore this explanation may not suffice.

    Nandrolone also differs from testosterone in its ability to be converted by the aromatase enzyme to estradiol (an active estrogen). In comparison, nandrolone aromatizes at approximately 20% of the rate testosterone does, and as such is not known as a very estrogenic steroid. It is likewise favored when reduced estrogenic side effects such as water retention, fat deposition and gynecomastia are desired. However athletes know that there is a trade off with the reduced tendency for nandrolone to promote side effects, in that it is a less anabolic steroid. With its known high affinity for the AR in muscle tissue, could this suggest that estrogen may also be a key mediator of muscle growth?

    When we look at Primobolan ® (methenolone) we see a similar trend. Methenolone is at least as good a binder of the androgen receptor as testosterone. By some accounts it is on par with nandrolone[iii]. However it is known to be much weaker than both steroids at promoting muscle growth. We know that methenolone does not interact with 5-alpha reductase, and as such its affinity for the AR does not increase or decrease in androgen target tissues. This would logically seem like a more favorable trait for anabolism over the weakening we see with nandrolone. However methenolone is a markedly weaker anabolic, and requires relatively high doses to promote growth. This also brings into question the role of 5-alpha reductase in promoting an anabolic state. Perhaps the fact that Primobolan® is a non-aromatizable steroid is more relevant.

    Estrogen and GH/IGF-1
    To date the most common explanation for why anti-estrogens may be slightly counterproductive to growth in the sports literature has been the suggestion that estrogen plays a role in the production of growth hormone and IGF-1. IGF-1 (insulin like growth factor 1, formerly known as somatomedin C) is of course an anabolic product released primarily in the liver via GH stimulus. IGF-1 is responsible for the growth promoting effects (increased nitrogen retention, cell proliferation) we associate with growth hormone therapy. We do know that women have higher levels of growth hormone than men, and also that GH secretion varies over the course of the menstrual cycle in direct correlation with estrogen levels[iv]. Estrogen is likewise often looked at as a key trigger in the release of GH in women under normal physiological situations.

    It is also suggested that the aromatization of androgens to estrogens in men plays an important role in the release and production of GH and IGF-1. This was evidenced by a 1993 study of hypogonadal men, comparing the effects of testosterone replacement therapy on GH and IGF-1 levels with and without the addition of tamoxifen[v]. When the anti-estrogen tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300mg of testosterone enanthate weekly (which elevated estradiol levels) to cause a slight IGF-1 increase in normal men, whereas 300mg weekly of nandrolone decanoate (a poor substrate for aromatase that caused a lowering of estradiol levels in this study) would not elevate IGF-1 levels[vi]. Yet another study shows that GH and IGF-1 secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1 secretion, presumably due to its strong anti-estrogenic/gonadotropin suppressing action[vii]. All of these studies seem to support a direct, estrogen-dependant mechanism for GH and/or IGF-1 release in men. It is difficult to say at this point just how important estrogen is to IGF-1 production as it relates to the promotion of anabolism in the steroid using athlete, however it remains an interesting subject to investigate.

    Glucose Utilization and Estrogen
    Estrogen may play an even more vital role in promoting an anabolic state by affecting glucose utilization in muscle tissue. This occurs via an altering the level of available glucose 6-phosphate dehydrogenase. G6PD is an important enzyme in the support anabolism, as it is directly tied to the use of glucose for muscle growth and recuperation[viii] [ix]. During the period of regeneration after skeletal muscle damage, levels of G6PD are shown to rise dramatically. G6PD enzyme plays a vital role in what is known as the pentose phosphate pathway, and as such this rise is believed to enhance the PPP related process in which nucleic acids and lipids are synthesized in cells; fostering the repair of muscle tissue.

    A 1980 study at the University of Maryland has shown that levels of glucose 6-phosphate dehydrogenase rise after administration of testosterone propionate , and further that the aromatization of testosterone to estradiol is directly responsible for this increase.[x] In this study neither dihydrotestosterone nor fluoxymesterone could mimic the affect of testosterone propionate on levels of G6PD, an affect that was also blocked by the addition of the potent anti-aromatase 4-hydroxyandrostenedione to testosterone. 17-beta estradiol administration caused a similar increase in G6PD, which was not noticed when its inactive estrogen isomer 17-alpha estradiol (unable to bind the estrogen receptor) was given. An anti-androgen could also not block the positive action of testosterone. This study provides one of the first palatable explanations for a direct and positive effect of estrogen on muscle tissue.

    What does this all mean?
    It is a long held belief among athletes that estrogen maintenance drugs can slightly hinder muscle gains during steroid therapy with a strong aromatizable steroid such as testosterone. Whether or not we have plausibly explained this remains to be seen, however the above evidence certainly does provide strong support for a direct and positive affect of estrogen on growth. Does this mean we should abandon estrogen maintenance drugs? I don’t think that should be the case. It is important to remember that estrogen can deliver many unwanted effects such as increased water retention, fat deposition and the development of female breast tissue when it becomes too active in the male body. Clearly if we plan a high-dose cycle with an aromatizable steroid, anti-estrogens will be an important inclusion. However we cannot ignore the suggestion of using estrogen maintenance drugs only when they are necessary to combat visible side effects during mild to moderately dosed cycles, especially if bulk is the ultimate goal of the athlete.

    References
    1. Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men. Vermeulen, Comhaire. Fertil and Steril 29 (1978) 320-7

    2. Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro. Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Am J Physiol 1981 Feb;240(2):E125-30

    3. The effect of clomiphene citrate on sex hormone binding globulin in normospermic and oligozoospermic men. Adamopoulos, Kapolla et al. Int J Androl 4 (1981) 639-45
    Last edited by LuvMyRoids; 02-10-2005 at 12:00 AM.

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    Good post, LMR. I've seen too many posts lately that have said some thing like "should I use Ldex or nolva?......I know they're the same thing, but....."
    They certainly are not the same thing. The two complement each other very well, and I'd recommend anyone using test to use .25mg/day of Ldex and 10mg/day of nolva. You don't use anti e's JUST because you don't want gyno. In fact that's not even the primary reason. You want to control (not eliminate) estrogen, and keep it at reasonable (but usually still well above) normal physiological levels. This will prevent excessive bloat, which in turn prevents excessive elevation of BP.

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    Mr. Sparkle's Avatar
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    Thats a good read. I agree that there is a lot of confusion on this subject...

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    its is important to note that SERMS (tamox and clomi) have very different tissue activity profiles

    The AI's have different suppression and tissue affinities as well.

    thus they are not interchangeable and you can get very different effects by switching among them ie AI to AI and SERM to SERM.

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    powerlifter's Avatar
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    Nice post Bro - einstein is right - people do lump the compounds together

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    Thanks guys. I had to post up something explaining what AI's and SERM's were because the term is used so much here. A lot of users and members here dont understand the difference let alone the explanation or term of these two words. Pheedno is definitely one that uses these words interchangably through his advice and I think members dont understand what we mean by SERM and AI.

    I imagine this thread will get buried in the archives and we will still have to explain this to the new members every other day but least it's in the archives for search.
    JaneDoe likes this.

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    Quote Originally Posted by LuvMyRoids
    Thanks guys. I had to post up something explaining what AI's and SERM's were because the term is used so much here. A lot of users and members here dont understand the difference let alone the explanation or term of these two words. Pheedno is definitely one that uses these words interchangably through his advice and I think members dont understand what we mean by SERM and AI.

    I imagine this thread will get buried in the archives and we will still have to explain this to the new members every other day but least it's in the archives for search.
    Sure hope it doesn't get buried - should be a sticky because explains it in clear easy - to - understand language - just my opinion

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    Vote for sticky??

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    sticky

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    Quote Originally Posted by macrophage69alpha
    its is important to note that SERMS (tamox and clomi) have very different tissue activity profiles

    The AI's have different suppression and tissue affinities as well.

    thus they are not interchangeable and you can get very different effects by switching among them ie AI to AI and SERM to SERM.
    Bingo!

    I will post up a thread difinitively specifying the differences in action as well as the differences in tissue selectivity tomorrow. The SERMs are explained(to an extent) in my PCT protocol thread over at WCB(which I'll post here shortly) but a thread detailing the differences is necessary

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    Quote Originally Posted by Pheedno
    Bingo!

    I will post up a thread difinitively specifying the differences in action as well as the differences in tissue selectivity tomorrow. The SERMs are explained(to an extent) in my PCT protocol thread over at WCB(which I'll post here shortly) but a thread detailing the differences is necessary
    Sounds good Bro

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    Yep, that's where I got the idea from. That site has a good section on reference and explanation to PCT. Since we discuss PCT here frequently and mention SERM and AI so much it would be beneficial to AR and its members. Good deal thanks Pheedno.
    Quote Originally Posted by Pheedno
    Bingo!

    I will post up a thread difinitively specifying the differences in action as well as the differences in tissue selectivity tomorrow. The SERMs are explained(to an extent) in my PCT protocol thread over at WCB(which I'll post here shortly) but a thread detailing the differences is necessary

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    LMR - he has already got that post he was talking about started !!! Pheedno - da man !

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    Yah I see it. Was hoping he would post here and make my thread a sticky....sigh
    Quote Originally Posted by powerlifter
    LMR - he has already got that post he was talking about started !!! Pheedno - da man !

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    Quote Originally Posted by LuvMyRoids
    Yep, that's where I got the idea from. That site has a good section on reference and explanation to PCT. Since we discuss PCT here frequently and mention SERM and AI so much it would be beneficial to AR and its members. Good deal thanks Pheedno.
    Actually bro, since you have this already started, you can add the specifics to this thread and we'll stick it. I don't mind laying out another thread detailing the above at all, but if your interested in finishing it up here, then by all means

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    Quote Originally Posted by Pheedno
    Actually bro, since you have this already started, you can add the specifics to this thread and we'll stick it. I don't mind laying out another thread detailing the above at all, but if your interested in finishing it up here, then by all means
    WHOO HOO - HURRAY FOR LMR !!!!!

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    sticky............
    The answer to your every question

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    Ok I know exactly what you mean now. Im going to finish this up tomorrow. Thanks pheedno.
    Quote Originally Posted by Pheedno
    Not a copy a paste bro. I'm talking about specifics to the class(both SERM and AI)
    Basically a list which gives an overview of the more common meds we use
    SERMS:
    Nolva-
    Clomid-

    AI's:
    Anastrozole
    Letrozole
    Exemestane-(which is actually an inactivator but would be a feasible addition)

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    bump, it's done

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    bumping this for all to read. Nice job...very comprehensive.

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    I would like to add that I am not fond of William Llewellyn's comparison of tamox vs clomid; as I think he ignores the duration times in studies when concluding that tamox is a superior SERM in recovering HPTA.
    I am of the opinion that tamox's selective nature binds it to breast, bone, and liver ERs over the pituitary, while clomid is selective towards hypothalamus & pituitary(also the ovary, endometrium, vagina, and cervix), which also accounts for the de-sensitization to GnRH.
    Tamox will work at stimulating LH, but IMO, will require longer durations and doses exceeding the norm-20mg, if it is not paired with clomid; and better yet, an AI

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    bump.

    xxample

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    Thanks for the awesome post, I had lots of my questions answered by reading this...

    RR

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    brilliant read

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    i was reading this great thread and encountered a contradiction. Can someone please enlighten me on this issue.

    "When the anti-estrogen tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone."

    as we know tamoxifen is a serm.
    (SERM) Compounds that bind with estrogen receptors and exhibit estrogen action in some tissues and anti-estrogen action in other tissues. The ideal SERM would deliver all the benefits of estrogen without the adverse effects. ex: Clomiphene Citrate (Marketed as Clomid or Serophene). Tamoxifen (Marketed as Nolvadex ).

    the serm prevents the estrogen from going to a certain tissue, but does not prevent its production as AIs do. Then how come a serm lowered GH and IGF-1(since there is estrogen flowing through the body)?
    Last edited by std4; 11-20-2006 at 05:21 AM.

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    awsome post, Im new to the site and this is a great base for finding out about PCT and AI's Thanks man

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    Great Info. I know its old thread but thanks for posting.

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    Great post, it's hard to find high quality information nowadays. Please keep posting more information.

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    lets see if ive got this correct use letro during cycle and use nolva after cycle.

    is that correct?????

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    You didn't need tu bump this to get an answer

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    Quote Originally Posted by ChuckLee View Post
    You didn't need tu bump this to get an answer
    sorry i just like to make sure that ive got it 100% correct.

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    is it ok to inject letro because the anabolic review research is selling a 90 day supply of injectable letro for just $105.

    it should be ok for me to ask because anabolic review research is one of the sponsors of this forum they have an ad banner at the top of the screen.

    and if it is ok to inject letro do you just inject it like you would with steroids .

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    No it is not injectable letro, its a buy 2 get 1 free deal. so 3 bottles of letro for $105. Letro is not inejctable its oral only.

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    Quote Originally Posted by legobricks View Post
    No it is not injectable letro, its a buy 2 get 1 free deal. so 3 bottles of letro for $105. Letro is not inejctable its oral only.
    but its sold in liquid bottles does that mean you should mix 1ml of it with a small glass of water then drink it?????

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    ggoyal is offline Junior Member
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    it's also flavored ig u hadn't noticed(sign it's oral)

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    Quote Originally Posted by ggoyal View Post
    it's also flavored ig u hadn't noticed(sign it's oral)
    it doesnt say its flavoured or that its oral???

    http://www.ar-r.com/shop/product_inf...products_id=42

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    I believe it does in the picture but the picture links are not working.

    Yes its oral, but i believe lion is having problems shipping to the uk at the moment.

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    Quote Originally Posted by shifty_git View Post
    I believe it does in the picture but the picture links are not working.

    Yes its oral, but i believe lion is having problems shipping to the uk at the moment.
    ok thanks what is lion and why are they having problems shipping to the uk???

    does this mean i cant buy letro from the anabolic research site or even syringes from them????

  39. #39
    Kiltedguard is offline New Member
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    Great post. I know I'm Necroposting, but this really cleared some things up for me. I'm my reasearch I've always tried to suppress purly to avoid gyno in my test subject. These actually add a bit more depth into the entire thing and allow for some fine tuning. Thanks!!

  40. #40
    Gym Jones's Avatar
    Gym Jones is offline New Member
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    This was useful data. Thank you. Adding to my research notes

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