possible uses for Nolva... besides PCT

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    Question possible uses for Nolva... besides PCT


    could tamoxiphen be used in a cycle all by itself, not PCT, maybe as a hardening agent/ anti-catabolic supplement during a cutting cycle? I'm just thinking about other uses it could have outside it's most common use for PCT.

    BTW, this is just a theoretical question.

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    Let me give my psychic 8 ball a shake... All signs point to no.
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    Unless your body is predisposed to making more estro than the average guy I would say no. Anti catabolic? Unlikely
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    Nolva is too strong to use in this way anyway IMO. 6-OXO or AromaZap would tend to do the same thing and have fewer sides (making a guess here). Still, I would say proper diet and rest (sleep at least 8 hours a day) would affect cortisol levels (and therefore muscle catabolism) more than an anti-e.
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    I'd be willing to bet nolva used on a person with a fully functional HPTA would raise testosterone levels anywhere from 100-300ng/dl at 40mg/day, would also make you more vascular through less water retention. I would imagine a decent anticatabolic effect just by having more test, and the only sides I can see are your balls weighing you down and your girlfriend getting mad for making a bigger mess in bed. Just my 2 cents.
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    Quote Originally Posted by supersoldier
    I'd be willing to bet nolva used on a person with a fully functional HPTA would raise testosterone levels anywhere from 100-300ng/dl at 40mg/day, would also make you more vascular through less water retention. I would imagine a decent anticatabolic effect just by having more test, and the only sides I can see are your balls weighing you down and your girlfriend getting mad for making a bigger mess in bed. Just my 2 cents.
    hahaha
    oh god you just made a nolva only cycle sound way too good to the newbs on this board
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    If you are looking for a straight anti-catabolic for cutting or between cycles, try a transdermal 7-oxo DHEA. I threw 10g into 8oz of T-gel, it's the same as FL7 but almost twice as potent & much cheaper. I find it very effective for that purpose.
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    Quote Originally Posted by supersoldier
    I'd be willing to bet nolva used on a person with a fully functional HPTA would raise testosterone levels anywhere from 100-300ng/dl at 40mg/day, would also make you more vascular through less water retention. I would imagine a decent anticatabolic effect just by having more test, and the only sides I can see are your balls weighing you down and your girlfriend getting mad for making a bigger mess in bed. Just my 2 cents.
    yeah, that's kind of what I was thinking...
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    Quote Originally Posted by supersoldier
    I'd be willing to bet nolva used on a person with a fully functional HPTA would raise testosterone levels anywhere from 100-300ng/dl at 40mg/day, would also make you more vascular through less water retention. I would imagine a decent anticatabolic effect just by having more test, and the only sides I can see are your balls weighing you down and your girlfriend getting mad for making a bigger mess in bed. Just my 2 cents.
    Nolva can actually cause water retention.

    "In fact as I mentioned to you those drugs are really SERMS: estrogenic in some tissues and antiestrogenic in others. I did a little research on the two mechanisms whereby estrogen induces water retention (increases in antidiuretic hormone, or AVP, and aldosterone) and discovered that for AVP, tamoxifen is actually an agonist, just like estrogen, so should enhance water retention by that route:

    Updated Note: Here is one showing no effect on renin and sodium excretion with tamoxifen. So the increase in AVP should lead to water retention from nolva since there is no effect on the renin-aldosterone system:"

    http://www.ncbi.nlm.nih.gov/entrez/...9&dopt=Abstract


    You could proably just use flax oil and zinc to get the same rise in testosterone.
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    an article about losing fat/cutting at bb.com says to use nolva as part of a fat loss program. maybe someone can dig it up.
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    Quote Originally Posted by Bobo
    Nolva can actually cause water retention.

    "In fact as I mentioned to you those drugs are really SERMS: estrogenic in some tissues and antiestrogenic in others. I did a little research on the two mechanisms whereby estrogen induces water retention (increases in antidiuretic hormone, or AVP, and aldosterone) and discovered that for AVP, tamoxifen is actually an agonist, just like estrogen, so should enhance water retention by that route:

    Updated Note: Here is one showing no effect on renin and sodium excretion with tamoxifen. So the increase in AVP should lead to water retention from nolva since there is no effect on the renin-aldosterone system:"

    http://www.ncbi.nlm.nih.gov/entrez/...9&dopt=Abstract


    You could proably just use flax oil and zinc to get the same rise in testosterone.
    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.

    http://www.mindandmuscle.net/content/page-72.html

    "Nolvadex, used for 10 days at a dosage of 20mg daily, increased serum testosterone levels to 142% of baseline" taken from the same article... if this is true, it could be a good product to use for people seeking mild anabolism with minimal side effects... maybe for a month to break a plateau, or during times of heavy stress (pshycological) that can significantly lower testosterone levels.
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    I have read Bills articles many times but this has no bearing on what I stated at all. It doesn't matter that Clomid and Nolva have anti-estrogenic properties in the hypothalamus and pituitary. Its a fact they raise LH levels which in turn raise testosterone. Thats not the point. THe point being if you are looking for a hardening agent Nolva can cause water retention because its effect on AVP. Flax oil and zinc can do the same thing withouth being an agonist to water retention.


    "However, in the presence of the nuclear oestrogen receptor antagonist tamoxifen (10 microM), E2 still produced an inhibition of Cl- secretion...We conclude that E2 inhibits colonic Cl- secretion via a non-genomic pathway that involves intracellular Ca2+ and PKC. It is possible that this gender-specific mechanism contributes to the salt and water retention associated with high E2 states.

    http://www.jphysiol.org/cgi/content/full/530/1/47


    If you want a better alternative use an AI as it has been shown to have a much favorable effect on water retention (letro, dex, 6-OXO)
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    Quote Originally Posted by lancelot
    an article about losing fat/cutting at bb.com says to use nolva as part of a fat loss program. maybe someone can dig it up.
    More myths.

    Estrogen makes a person fat, doesn’t it? Well, women do have a higher body fat content in general than do men, especially in the gluteofemoral (hips and buttocks) region. Is estrogen really the cause of this gender dimorphism in adiposity? Probably not. In fact, there are a wealth of data that implicate estrogen as both an anorectic and antiadipogenic hormone. It is much more likely that progesterone is the culprit in supporting higher levels of gluteofemoral fat in women (1). The model described in (1) has progesterone as the lipogenic hormone. Before menopause, both estrodiol and progesterone are secreted by the ovaries. After menopause, estrone becomes the primary circulating estrogen produced from aromatization of adrenal androgens (primarily the aromatization of androstenedione to estrone by adipose tissue), while progesterone levels drop dramatically since adrenal production of progesterone is minimal.

    In premenopausal women, progesterone increases lipoprotein lipase activity, which is greater in the gluteofemoral region, while estrogen suppresses it. Lipoprotein lipase is the body’s primary fat storage enzyme; it is responsible for allowing fats to leave the circulation and enter adipocytes. The progesterone wins out however and before menopause, women tend to have more gluteofemoral fat and less abdominal fat.

    Why do women have more gluteofemoral fat while men have more central (abdominal) fat? One popular theory is that women hold fat in the gluteofemoral region where it is far removed from the liver and has fewer fat mobilizing enzymes/more fat retaining enzymes than in men. Men hold fat in the visceral and abdominal subcutaneous region where it is closer to the liver and richer in fat mobilizing enzymes. Proximity to the liver is a factor because the portal circulation connects abdominal fat deposits directly to the liver. Free fatty acids released from abdominal deposits can act directly on the liver to promote gluconeogenesis, providing the body with a ready supply of glucose for “fight or flight” situations.

    From an adaptational viewpoint, women's fat is designed to be stored until needed for lactation and child rearing. Men's fat on the other hand is designed to be readily mobilized for fight or flight situations during defense and hunting. This theory may be a bit simplistic as well as sexist; but it does make sense to some degree.

    Most likely the notion of estrogenic fat originated from the belief that estrogen upregulates alpha 2 receptors in fat cells, retarding lipolysis. This may be just one facet of estrogen’s actions. If one looks at the net result of estrogen’s effects, to quote a leading expert in the field


    “Testosterone and GH inhibit LPL and stimulate lipolysis markedly. Oestrogens seem to exert net effects similar to those of testosterone.” (2)

    For example, animal studies have shown that testosterone promotes alpha 2 adrenoreceptor mediated antilipolytic activity, just as it promotes beta adrenoreceptor mediated lipolysis.

    Interestingly, recent research has even attributed at least part of testosterone's fat burning properties to its local aromatization to estradiol (3). For instance when testosterone is administered along with an aromatase inhibitor, LPL activity increases, showing that the testosterone itself is devoid of any ability to lower LPL. (4)

    There are a number of animal studies where estradiol administration led to significant weight and fat loss. Citing just one, for example:


    "The administration of 17 beta-estradiol (500 micrograms/kg, 2 or 4 weeks) to male rats significantly reduced the body weight...Basal lipolysis and adrenaline-induced lipolysis [due to increase in HSL action] were also significantly enhanced in the epididymal adipose tissue from the male rat treated either with 7 mg/kg estradiol 12 h ahead or with 500 micrograms/kg estradiol for 2 weeks. These results indicate that estradiol exerts strong effects on metabolism of the adipose and these effects seems to be mediated through cyclic-AMP." (5)


    This research indicates that in addition to the abovementioned inhibition of LPL, estrogen also stimulates the lipolytic enzyme hormone sensitive lipase.

    Some of the most compelling evidence for the antiadipogenic effect of estrogen in both males and females comes from studies of estrogen receptor knockout mice and humans with aromatase deficiency. Both the afflicted humans and the knockout mice exhibit obesity. A detailed look at this topic can be found here:




    I also mentioned that estrogen is a potent hunger-suppressing hormone. Research is a bit sketchier here, but the effect is thought to be due to an estrogen-induced inhibition in melanin-concentrating hormone (MCH) signaling (6). MCH is a neuropeptide found in the hypothalamus that is also thought to be involved in leptin’s regulation of appetite. Leptin, an anorectic hormone secreted from the adipose tissue, acts on the specific receptor present on its target neurons in the brain, and suppresses the expression of both MCH and its receptor. So we see that the actions of both estrogen and leptin are at least partly mediated through interactions with MCH.
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    Nice read Bobo.
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    Quote Originally Posted by NPursuit
    Nice read Bobo.
    agreed, thanks for the insight...
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    Quote Originally Posted by supersoldier
    I would imagine a decent anticatabolic effect just by having more test, and the only sides I can see are your balls weighing you down and your girlfriend getting mad for making a bigger mess in bed. Just my 2 cents.
    Clomid does that better..

    Besides, nolva by itself makes no sense as it lowers IGF-1... When you're not "on", you'll need all the natty IGF-1 your body releases..
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    One possible use of standard pct preparations is in improved recovery allowing an increase in training volume. This would then allow you to burn more fat with cardio.

    I have been looking into this and on the positive side what I have read sugest that clomiphene/tamoxifen may:

    Reduce exercise induced muscle damage and DOMS although I have seen no explanation of the mechanism for this.
    In addition it will increase endogenous testosterone production but I am unsure to what extent.

    The downside is that it may also reduce growth hormone release. I read something that indicated that as estrogen is involved in the release of GH with the clomid/nolva blocking the receptors there is a reduction in GH release.

    From another forum on a similar thread I thought this article posted by JohnnyB was very helpful:

    Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.

    Vermeulen A, Comhaire F.

    The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.



    The following sugests clomid is also useful. But I wonder how this relates to people within normal test range to start with and maybe his broken pelvis stoped him running and that is what enabled test levels to increase.

    Idiopathic hypogonadotropic hypogonadism in a male runner is reversed by clomiphene citrate.

    Burge MR, Lanzi RA, Skarda ST, Eaton RP.


    University of New Mexico School of Medicine, Department of Medicine/Endocrinology-5ACC, Albuquerque 87131, USA.

    OBJECTIVE: To assess the efficacy of estrogen antagonist therapy on the function of the hypothalamic-pituitary-testicular axis in a young male runner with significant morbidity attributable to idiopathic hypogonadotropic hypogonadism. DESIGN: An uncontrolled case study. SETTING: The outpatient endocrinology clinic of a university tertiary referral center. PATIENT(S): A 29-year-old male who has run 50 to 90 miles per week since 15 years of age and who presented with a pelvic stress fracture, markedly decreased bone mineral density, and symptomatic hypogonadotropic hypogonadism. INTERVENTION(S): Clomiphene citrate (CC) at doses up to 50 mg two times per day over a 5-month period. MAIN OUTCOME MEASURE(S): Serum concentrations of LH, FSH, and T before and after CC therapy, as well as clinical indicators of gonadal function. RESULT(S): Barely detectable levels of LH and FSH associated with hypogonadal levels of T were restored to the normal range with CC therapy. The patient experienced improved erectile function, increased testicular size and sexual hair growth, and an improved sense of well being. CONCLUSION(S): Exercise-induced hypogonadotropic hypogonadism exists as a clinical entity among male endurance athletes, and CC may provide a safe and effective treatment option for males with debilitating hypogonadism related to endurance exercise.



    This is my first post here so hello all.
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    Reducing estrogen most certainly reduces GH pulses along wiht IGF-1 (systemic). Estrogen does so many beneficial things when kept within normal levels. It will increase glyocgen storage, GH, IGF-1, strength, joint protection, etc.... Also the fisrt study is on oligospermic men so the conclusion wouldn't represent what will happen in a normal man.

    The second study is on a hypogonadotropic man so the same arguement applies.

    Overall it was good first post. You have your thinking cap on, so welcome
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    does anyone know if women produce more GH than men (considering they produce more estrogen)?

    everything has it's "pluses" and "minuses", but overall, would running tamoxiphen or clomid alone have any use towards building muscle/losing fat, or is it better left for PCT only?
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    Good question. I remember seeing something on the comparisons and it definetly was much different. GH has many different pathways in which its raised and lowered. Let me see if I cand find it.

    Overall the effects would be minimal at best and probably the same as using zinc or flax oil in normal men.
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    Woman usually have higher levels and have a better stimulatory effect. The problem with this is woman have a much higher level of progesterone that might blunt the lipolytic effects of GH.

    Gender governs the relationship between exercise intensity and growth hormone release in young adults.

    Pritzlaff-Roy CJ, Widemen L, Weltman JY, Abbott R, Gutgesell M, Hartman ML, Veldhuis JD, Weltman A.

    Department of Human Services, General Clinical Research Center, University of Virginia, Charlottesville 22903, USA.

    We previously reported that in young adult males growth hormone (GH) release is related to exercise intensity in a linear dose-response manner (Pritzlaff et al. J Appl Physiol 87: 498-504, 1999). To investigate the effects of gender and exercise intensity on GH release, eight women (24.3 +/- 1.3 yr, 171 +/- 3.2 cm height, 63.6 +/- 8.7 kg weight) were each tested on six randomly ordered occasions [1 control condition (C), 5 exercise conditions (Ex)]. Serum GH concentrations were measured in samples obtained at 10-min intervals between 0700 and 0900 (baseline) and 0900 and 1300 (Ex + recovery or C). Integrated GH concentrations (IGHC) were calculated by trapezoidal reconstruction. During Ex, subjects exercised for 30 min (0900-0930) at one of the following intensities [normalized to the lactate threshold (LT)]: 25 and 75% of the difference between LT and rest, at LT, and at 25 and 75% of the difference between LT and peak O2 uptake. No differences were observed among conditions for baseline IGHC. To determine whether total (Ex + recovery) IGHC changed with increasing exercise intensity, slopes associated with individual linear regression models were subjected to a Wilcoxon signed-rank test. To test for gender differences, data in women were compared with the previously published data in men. A Wilcoxon ranked-sums two-tailed test was used to analyze the slopes and intercepts from the regression models. Total IGHC increased linearly with increasing exercise intensity. The slope and intercept values for the relationship between total IGHC and exercise intensity were greater in women than in men. Deconvolution analysis (0700-1300 h) revealed that, regardless of gender, increasing exercise intensity resulted in a linear increase in the mass of GH secreted per pulse and summed GH production rate, with no changes in GH secretory pulse frequency or apparent half-life of elimination. Exercise reduced the half-duration of GH secretory burst in men but not in women. Gender comparisons revealed that women had greater basal (nonpulsatile) GH secretion across all conditions, more frequent GH secretory pulses, a greater GH secretory pulse amplitude, a greater production rate, and a trend for a greater mass of GH secreted per pulse than men. We conclude that, in young adults, the GH secretory response to exercise is related to exercise intensity in a linear dose-response pattern. [b]For each incremental increase in exercise intensity, the fractional stimulation of GH secretion is greater in women than in men.
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    Quote Originally Posted by Luke530
    everything has it's "pluses" and "minuses", but overall, would running tamoxiphen or clomid alone have any use towards building muscle/losing fat, or is it better left for PCT only?
    I do not think it will help gain muscle but it might indirectly allow fat loss through greater training volumes.

    At best the clomid/tamoxifen is going to increase test levels only slight and that clomid dose in the study is high. Also the marginally increased test levels are at the expence of reduced IGF.

    Clomiphene citrate increases insulin-like growth factor binding protein-1 and reduces insulin-like growth factor-I without correcting insulin resistance associated with polycystic ovarian syndrome

    Vincenzo De Leo1,5, Antonio la Marca1, Giuseppe Morgante1, Liliana Ciotta2, Luca Mencaglia3, Antonio Cianci2 and Felice Petraglia1


    1 Department Obstetrics and Gynecology, University of Study of Siena, 2 Department Obstetrics and Gynecology, University of Study of Catania and 3 Centro Florence, Firenze, Italy

    The induction of ovulation by clomiphene could be the result of interaction of the drug at various levels: hypothalamus, pituitary and ovary. It was demonstrated that administration of clomiphene to women with polycystic ovarian syndrome (PCOS) is accompanied by a reduction in plasma concentrations of insulin-like growth factor-I (IGF-I). IGF-I seems to have an overall negative effect on normal folliculogenesis and ovulation. The aim of the present study was to evaluate the effect of clomiphene on plasma concentrations of IGF-I and IGF binding protein (IGFBP)-1 and on insulin resistance associated with PCOS. Fifteen patients diagnosed with PCOS were recruited. Clinical diagnosis was based on chronic oligomenorrhoea or amenorrhoea and hyperandrogenaemia. Clomiphene citrate was administered at a dose of 100mg/day to all women from day 5 to day 9 of the spontaneous or medroxyprogesterone acetate (MAP)-induced menstrual cycle. Blood sampling and a 2 h oral glucose loading test (75 g) were performed the day before and after the course of clomiphene. Ovulation was confirmed in 13/15 PCOS patients. Plasma concentrations of IGF-I decreased by 31.5% (434 ± 84 versus 297 ± 71 ng/ml; P < 0.05) after 5 days of clomiphene therapy, whereas plasma concentrations of IGFBP-1 increased by ~28.1% (26.3 ± 4 versus 36.6 ± 7 ng/ml; P < 0.05). This gave a 56.5% reduction in the IGF-I:IGFBP-1 ratio (21.9 versus 9.53). No significant changes in basal plasma concentrations of fasting insulin or area under the insulin curve were observed in response to oral loading. The present results show that clomiphene does not cause changes in insulin resistance associated with PCOS but reduces plasma concentrations of IGF-I and increases those of IGFBP-1, with a consequent marked reduction in the IGF-I:IGFBP-1 ratio. Keywords: clomiphene • IGF-I • IGFBP-1 • insulin • PCOS 5 To whom correspondence should be addressed at: Department Obstetrics and Gynecology, University of Siena, Policlinico Le Scotte, viale Bracci, 53100 Siena (SI), Italy. E-mail: deleo@unisi.it


    I do not know what the IGF-I:IGFBP-1 ratio indicates but a decrease in IGF-I by 31.5% is I think a bad thing as it affects GH. I have noted this is not a normal group and it is women so maybe this does not translate, but it does confirm what people say about reduced estrogen in men causing reduced GH.

    As you say it is pluses and minuses a slight increase in test for a possible decrease in GH.

    What I am now wondering is which is more significant to muscle gain and/or fat loss, through improved recovery, GH or test. I should mention at this point that I am an endurance athlete recovery to me is not always the kind of recovery needed to lift heavy.
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    Yes it defiently a bad thing. Those binding protein inhibits the effects of circulating IGF-1. This is also why Long R3 version is much more potent. The half-life is 8-12 hours as opposed to 10-12 minutes for regular IGF-1 and it much more resistent to binding proteins.

    Test would definetly help recovery much more than GH but will hinder endurace. GH defiently will be more helpful in fat loss and much more favorable with endurance and performance while helping recovery a bit (but nothing like Test) but will take months of administration to have effect.

    If your looking for gains/lfat loss while not effecting performance or maybe increasing you might want to check out Long R3 IGF-1.
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    Quote Originally Posted by Bobo
    If your looking for gains/lfat loss while not effecting performance or maybe increasing you might want to check out Long R3 IGF-1.
    While looking into your sugestion I found a thread on letrozole
    http://www.steroidology.com/forum/showthread/t-476.html of all the pct compounds that might be the one to give a good increase to test (50%) and an increase to igf-1(25%). After all this searching and looking I think these compounds should only be used to support steroid use and not on there own. Plus if letrozole was able to be used for fat burning and muscle gain I am sure people would allready be using it for that.

    I am going the, Long R3 IGF-1 B-12, route and then some homebrew in the summer/Autumn; tren with some minimal test unless I can find some EQ.
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    I agree. The problem with using an AI is the chance for a nasty rebound once use is discontinued. As far as the IGF-1 issue, sometimes it is blown out of proportion since most of these studies show levels of hepatic IGF-1. Now usually its a good thing to have increased heptic levels but that doesn't always equate to growth (since this usually increase IGF-1BP. It seems localzied IGF-1 concetrations play a more dominant role in hyperplasia. On the other hand it seems a decrease in heptic IGF-1 levels can cause problems as this seems to cause a cascade effect in many other hormones (mainly increased cortisol).

    With your combo I guarantee you will want to eat everything in the house. Both cause increased appetite but the good thing will that you should get fairly clean LBM gains with the possibilty of fat loss. Sounds like a good plan.
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