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Thread: Clomid or Nolva

  1. #1
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    Clomid or Nolva

    Okay so I kinda stuck this question in with one of my other posts but never got a answer to it so i figured I would give it it's own special post. I'm towards the end of DMZ stack (DMZ) being the main compound and as ya'll know it's some pretty harsh s***. I got clomid and nolva on hand and would run the clomid 100/50/50/50 and nolva at 20s across the board but extend it for 6 weeks. Should I go with both of them? Just one? If so which one? Would yall reccomend running a natural t booster with it or a product such as recycle or revolution? Honestly I think anything past nolva and clomid will be overkill however I am simply gathering other peoples thoughts on the matter because this will probably be my last cycle of anything for a good while. Would like to try and roll natty for a little longer. Any thoughts are welcome.

  2. #2
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    Both Bro if you read the pct section they will explain why.Research before you put things into your body.This way you will know wat to expect.

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    Quote Originally Posted by songdog View Post
    Both Bro if you read the pct section they will explain why.Research before you put things into your body.This way you will know wat to expect.
    Already read it. Thats why I asked on here because all the PH guys just say to run one of em and something like Recycle or Revolution. And yall say completely different. But from my "research" it looks like doing both at those doses should make me good?

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    Quote Originally Posted by jcrutche View Post
    Already read it. Thats why I asked on here because all the PH guys just say to run one of em and something like Recycle or Revolution. And yall say completely different. But from my "research" it looks like doing both at those doses should make me good?
    No offense but you obviously didn't read everything. Like snogdog said if you read everything you would know why you should run both and wouldn't be asking this question. I'm just saying!!!

  5. #5
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    Use both, better to be on the safe side.

  6. #6
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    I would use both. i always use both in all my PCT protocols. 4 weeks clomid: 100/100/50/50 Nolva: 40/40/20/20

  7. #7
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    Both at the dosages you said would be the way to go IMO. If you have liquid from arr the only diff i would make is run the clomid at 70/35/35/35

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    Okay awesome. Thanks for all the help guys. Don't really know why i asked if i should use both cause I was going to anyways hah. But yeah mainly I was just wondering about the dosages and whether I should use anything else along with them. Oh, and yes I am using liquid, not tabs.

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    Run Both

  10. #10
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    I have Clomid and was about to use it but was put off by this:

    http://forums.steroid.com/showthread...T#.UMFzIKWjOJU

    Did a Nolva only PCT.

    I'm sure there are many of us who don't know whats correct...

  11. #11
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    I believe this article was originally contributed to this forum by my friend JimmyInk'd


    The following explains why it is prudent to use BOTH nolvadex and clomid together in your PCT . It is by Dr Scally - probably the foremost expert in the United States on this topic.

    Med Hypotheses. 2009 Jun;72(6):723-8. Epub 2009 Feb 23.

    Anabolic steroid -induced hypogonadism--towards a unified hypothesis of anabolic steroid action.

    Tan RS, Scally MC.

    Source
    HPT/Axis Inc., 1660 Beaconshire Road, Houston, TX 77077, USA.

    Abstract

    Anabolic steroid-induced hypogonadism (ASIH) is the functional incompetence of the testes with subnormal or impaired production of testosterone and/or spermatozoa due to administration of androgens or anabolic steroids . Anabolic-androgenic steroid (AAS), both prescription and nonprescription, use is a cause of ASIH. Current AAS use includes prescribing for wasting associated conditions. Nonprescription AAS use is also believed to lead to AAS dependency or addiction. Together these two uses account for more than four million males taking AAS in one form or another for a limited duration. While both of these uses deal with the effects of AAS administration they do not account for the period after AAS cessation. The signs and symptoms of ASIH directly impact the observation of an increase in muscle mass and muscle strength from AAS administration and also reflect what is believed to demonstrate AAS dependency. More significantly, AAS prescribing after cessation adds the comorbid condition of hypogonadism to their already existing chronic illness. ASIH is critical towards any future planned use of AAS or similar compound to effect positive changes in muscle mass and muscle strength as well as an understanding for what has been termed anabolic steroid dependency. The further understanding and treatments that mitigate or prevent ASIH could contribute to androgen therapies for wasting associated diseases and stopping nonprescription AAS use. This paper proposes a unified hypothesis that the net effects for anabolic steroid administration must necessarily include the period after their cessation or ASIH.

    PMID: 19231088 [PubMed - indexed for MEDLINE]

    Future treatments:
    A treatment goal of HPTA restoration will have its basis in the regulation and control of testosterone production. The HPTA has two components, both spermatogenesis and testosterone production.
    In males, luteinizing hormone (LH) secretion by the pituitary positively stimulates testicular testosterone (T) production; follicle-stimulating hormone (FSH) stimulates testicular spermatozoa production. The pulsatile secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus stimulates LH and FSH secretion. In general, absent FSH, there is no spermatozoa production; absent LH, there is no testosterone production. Regulation of the secretion of GnRH, FSH, and LH occurs partially by the negative
    feedback of testosterone and estradiol at the level of the hypothalamo-pituitary. Estradiol has a much larger, inhibitory effect than testosterone, being 200-fold more effective in suppressing LHsecretion [57–61].


    In the case of ASIH, where the individual suffers from functional hypogonadism and the belief for eventual return of function, treatment is directed at HPTA restoration. A medical quandary for physicians presented with hypogonadal patients secondary to AAS administration is there is currently no FDA approved drug to restore
    HPTA function. Standard treatment to this point has been testosterone replacement therapy (TRT), human chorionic gonadotropin (hCG ), conservative therapy (‘‘watchful waiting” or ‘‘do nothing”), or off-label prescribing of aromatase inhibitors or selective estrogen receptor modulators (SERM).

    The primary drawback of testosterone replacement and hCG administration is that this therapy is infinite in nature. These treatments will remedy the signs and symptoms associated with hypogonadism, but do not alleviate the need for a life-long commitmentto therapy. Further, administration serves to further HPTA suppression.

    Conservative therapy (‘‘watchful waiting” or ‘‘do nothing”) is the probably worst case option as this does nothing to treat the patient with ASIH. Also, conservative therapy will have the undesirable result of the nonprescription AAS user to return to AAS use as a means to avoid ASIH signs and symptoms.

    The aromatase inhibitors demonstrate the ability to cause an elevation of the gonadotropins and secondarily serum testosterone [62]. The administration of SERMs is a common treatment in attempts to restore the HPTA because they increase LH secretion from the pituitary that leads to increased local testosterone production
    [63–67].

    Guay has used clomiphene citrate as therapy for erection dysfunction and secondary hypogonadism. Patients received clomiphene citrate 50 mg per day for 4 months in an attempt to raise their testosterone level [68]. Clomiphene has been reported in a case study to reverse andropause secondary to anabolic–androgenic steroid use [69]. The patient received clomiphene citrate 50 mg twice per day in an attempt to raise his testosterone level. The patient when followed up after two months had a relapse,
    tiredness and loss of libido, after discontinuing clomiphene citrate. There are case study reports demonstrating the effectiveness of the combination of clomiphene and tamoxifen in HPTA restoration after stopping AAS administration [70–73].
    Clomiphene is a mixture of the trans (enclomiphene) and is (zuclomiphene) enantiomers, which have opposite effects upon the estradiol receptor [74]. Enclomiphene is an estradiol antagonist, while zuclomiphene is an estradiol agonist. The addition of tamoxifen to clomiphene might be expected to increase the overall antagonism of the estradiol receptor.


    This excerpt from an interview with Dr Scally:

    "Clomiphene is an antiestrogen, which decreases the estrogen effect in the body. It has a dual effect by stimulating the hypothalamic pituitary area and it has an antiestrogenic effect, so that it decreases the effect of estrogen in the body. Tamoxifen is more of a strict antiestrogen, it decreases the effect of estrogen in the body, and potentiates the action of clomiphene. Tamoxifen and clomiphene citrate compete with estrogen for estrogen receptor bind¬ing sites, thus eliminating excess estrogen circulation at the level of the hypothalamus and pituitary, allowing gonadotropin production to resume. Administering them together produces an elevation of LH and secondar¬ily gonadal sex hormones. " Dr Michael Scally

  12. #12
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    Quote Originally Posted by MickeyKnox View Post
    I believe this article was originally contributed to this forum by my friend JimmyInk'd


    The following explains why it is prudent to use BOTH nolvadex and clomid together in your PCT . It is by Dr Scally - probably the foremost expert in the United States on this topic.

    Med Hypotheses. 2009 Jun;72(6):723-8. Epub 2009 Feb 23.

    Anabolic steroid -induced hypogonadism--towards a unified hypothesis of anabolic steroid action.

    Tan RS, Scally MC.

    Source
    HPT/Axis Inc., 1660 Beaconshire Road, Houston, TX 77077, USA.

    Abstract

    Anabolic steroid-induced hypogonadism (ASIH) is the functional incompetence of the testes with subnormal or impaired production of testosterone and/or spermatozoa due to administration of androgens or anabolic steroids . Anabolic-androgenic steroid (AAS), both prescription and nonprescription, use is a cause of ASIH. Current AAS use includes prescribing for wasting associated conditions. Nonprescription AAS use is also believed to lead to AAS dependency or addiction. Together these two uses account for more than four million males taking AAS in one form or another for a limited duration. While both of these uses deal with the effects of AAS administration they do not account for the period after AAS cessation. The signs and symptoms of ASIH directly impact the observation of an increase in muscle mass and muscle strength from AAS administration and also reflect what is believed to demonstrate AAS dependency. More significantly, AAS prescribing after cessation adds the comorbid condition of hypogonadism to their already existing chronic illness. ASIH is critical towards any future planned use of AAS or similar compound to effect positive changes in muscle mass and muscle strength as well as an understanding for what has been termed anabolic steroid dependency. The further understanding and treatments that mitigate or prevent ASIH could contribute to androgen therapies for wasting associated diseases and stopping nonprescription AAS use. This paper proposes a unified hypothesis that the net effects for anabolic steroid administration must necessarily include the period after their cessation or ASIH.

    PMID: 19231088 [PubMed - indexed for MEDLINE]

    Future treatments:
    A treatment goal of HPTA restoration will have its basis in the regulation and control of testosterone production. The HPTA has two components, both spermatogenesis and testosterone production.
    In males, luteinizing hormone (LH) secretion by the pituitary positively stimulates testicular testosterone (T) production; follicle-stimulating hormone (FSH) stimulates testicular spermatozoa production. The pulsatile secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus stimulates LH and FSH secretion. In general, absent FSH, there is no spermatozoa production; absent LH, there is no testosterone production. Regulation of the secretion of GnRH, FSH, and LH occurs partially by the negative
    feedback of testosterone and estradiol at the level of the hypothalamo-pituitary. Estradiol has a much larger, inhibitory effect than testosterone, being 200-fold more effective in suppressing LHsecretion [57–61].


    In the case of ASIH, where the individual suffers from functional hypogonadism and the belief for eventual return of function, treatment is directed at HPTA restoration. A medical quandary for physicians presented with hypogonadal patients secondary to AAS administration is there is currently no FDA approved drug to restore
    HPTA function. Standard treatment to this point has been testosterone replacement therapy (TRT), human chorionic gonadotropin (hCG ), conservative therapy (‘‘watchful waiting” or ‘‘do nothing”), or off-label prescribing of aromatase inhibitors or selective estrogen receptor modulators (SERM).

    The primary drawback of testosterone replacement and hCG administration is that this therapy is infinite in nature. These treatments will remedy the signs and symptoms associated with hypogonadism, but do not alleviate the need for a life-long commitmentto therapy. Further, administration serves to further HPTA suppression.

    Conservative therapy (‘‘watchful waiting” or ‘‘do nothing”) is the probably worst case option as this does nothing to treat the patient with ASIH. Also, conservative therapy will have the undesirable result of the nonprescription AAS user to return to AAS use as a means to avoid ASIH signs and symptoms.

    The aromatase inhibitors demonstrate the ability to cause an elevation of the gonadotropins and secondarily serum testosterone [62]. The administration of SERMs is a common treatment in attempts to restore the HPTA because they increase LH secretion from the pituitary that leads to increased local testosterone production
    [63–67].

    Guay has used clomiphene citrate as therapy for erection dysfunction and secondary hypogonadism. Patients received clomiphene citrate 50 mg per day for 4 months in an attempt to raise their testosterone level [68]. Clomiphene has been reported in a case study to reverse andropause secondary to anabolic–androgenic steroid use [69]. The patient received clomiphene citrate 50 mg twice per day in an attempt to raise his testosterone level. The patient when followed up after two months had a relapse,
    tiredness and loss of libido, after discontinuing clomiphene citrate. There are case study reports demonstrating the effectiveness of the combination of clomiphene and tamoxifen in HPTA restoration after stopping AAS administration [70–73].
    Clomiphene is a mixture of the trans (enclomiphene) and is (zuclomiphene) enantiomers, which have opposite effects upon the estradiol receptor [74]. Enclomiphene is an estradiol antagonist, while zuclomiphene is an estradiol agonist. The addition of tamoxifen to clomiphene might be expected to increase the overall antagonism of the estradiol receptor.


    This excerpt from an interview with Dr Scally:

    "Clomiphene is an antiestrogen, which decreases the estrogen effect in the body. It has a dual effect by stimulating the hypothalamic pituitary area and it has an antiestrogenic effect, so that it decreases the effect of estrogen in the body. Tamoxifen is more of a strict antiestrogen, it decreases the effect of estrogen in the body, and potentiates the action of clomiphene. Tamoxifen and clomiphene citrate compete with estrogen for estrogen receptor bind¬ing sites, thus eliminating excess estrogen circulation at the level of the hypothalamus and pituitary, allowing gonadotropin production to resume. Administering them together produces an elevation of LH and secondar¬ily gonadal sex hormones. " Dr Michael Scally
    Damn. You just dropped some knowledge on my ass. Thanks much. And to everyone else for the help.

  13. #13
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    Quote Originally Posted by [h=2
    Nolvadex vs. Clomid for PCT[/h]
    It seems like everyday questions concerning PCT pop up, and weather one should use either Clomid or nolva or a combo of both. I hope that this article written by BigCat may help to clear up some misconceptions.

    While practically similar compounds in structure, few people ever really consider Clomid and nolva to be similar. Its not just a common myth in steroid circles, but even in the medical community. This misconception originates from their completely different uses. Nolvadex is most commonly used for the treatment of breast cancer in women, while Clomid is generally considered a fertility aid. In bodybuilding circles, from day one, Clomid has generally been used as post-cycle therapy and Nolvadex as an anti-estrogen.

    But as I intend to demonstrate this is in essence the same. I believe the myth to have originated because nolva is clearly a more powerful anti-estrogen, and the people selling Clomid needed another angle to sell the stuff, so it was mostly used as a post-cycle aid. But few users really understand how Clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids . After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up. Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody's best interest to bring back natural test as soon as humanly possible. Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That's basically how the mechanism works, nothing more, nothing less.

    Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall estrogen with 20-40 mg a day, than Clomid can in doses of 100-150 mg a day. A noteworthy difference. Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it. As such they will occupy the receptor and keep it from binding estrogens. This means they do not actively work to reduce estrogen in the body like Proviron , Viratase or arimidex would (by competing for the aromatase enzyme), but that it blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to.

    This has advantages and disadvantages. The disadvantage is that when use is discontinued, the estrogen level is still the same and new problems will develop much sooner. The advantage is that it works much faster and has results sooner than with an aromatase blocker like Proviron or arimidex. Therefor, when problems such as gynocomastia occur during a cycle of steroids one will usually start 20 mg/day of nolva or 100 mg/day of Clomid straight away, in conjunction with some Proviron or arimidex. The proviron or arimidex will actively reduce estrogen while the Clomid or Nolvadex will solve your ongoing problem straight away. This way, when use is discontinued there is no immediate rebound.

    So which one should you use? Well personally, I'd have to say Nolvadex. Both as an on-cycle anti-estrogen and a post-cycle therapy. As an anti-estrogen its simply much stronger, demonstrated by the fact that better results are obtained with 20-40 mg than with 100-150 mg of Clomid. For post-cycle, this plays a key role as well. It deactivates rebound estrogen much faster and more effective. But most importantly, Nolvadex has a direct influence on bringing back natural testosterone, where as Clomid may actually have a slight negative influence. The reason being that tamoxifen (as in Nolvadex) seems to increase the responsiveness of LH (luteinizing hormone) to GnRH (gonadtropin releasing hormone), whereas Clomid seems to decrease the responsiveness a bit1.

    Another noteworthy fact about Nolvadex is that it acts more potently as an estrogen in the liver. As you remember, I mentioned that clomiphene and tamoxifen are basically weak estrogens. Well, tamoxifen is apparently still quite potent in the liver. This offers us the positive benefits of this hormone in the liver, while avoiding its negative effects elsewhere in the body. As such Nolvadex can have a very positive impact on negative cholesterol levels2 in the body, and therefore too should be considered a better choice than Clomid. It will not solve the problem of bad cholesterol levels during Steroid use , but will help to contain the problem to a larger degree.

    Another reason why I promote the use of Nolvadex over Clomid post-cycle (as if being 3-4 times stronger and having more of a direct effect on restoring natural test wasn't enough) is because it's a lot safer. Not just because it improves lipid profiles, but also because it simply doesn't have the intrinsic side-effects that Clomid has. Clomid causes more acne for sure, but that's mainly because you need to use a 3-4 times higher dose. But Clomid seems to also affect the eyesight. Long-term Clomid therapy causes irreversible changes in eyesight3 in users. Irreversible. For me that alone is reason enough to prefer Nolvadex.

    Lastly, one should be aware that use of these compounds can reduce the gains made on steroids. Nolvadex more so than Clomid, simply because it is stronger. Estrogen is responsible for a number of anabolic factors such as increasing growth hormone output, upgrading the androgen receptor and improving glucose utilization. This is why aromatizing steroids like testosterone are still best suited for maximum muscle gain. When reducing the estrogen levels, we therefore reduce the potential gains being made. For this reason one may opt to try Clomid during a cycle instead of Nolvadex. Although I would imagine that the problem that needed solved would be of more concern, in which case nolva remains the weapon of choice. It's a plain fact that there is a high correlation between gains and side-effects. Either you go for maximum gains and tolerate the side-effects, or you reduce the side-effects, and with it the gains. That's life, nothing is free.

    Stacking and Use:

    If problems of Gynocomastia or other estrogen related symptoms tend to pop up during a cycle the use of 20-30 mg of Nolvadex or 100 mg of Clomid daily should easily contain the problem, and be used until a few days after the problem subsides. For best results and the least amount of problems upon cessation it is best stacked with Proviron (50 mg) or arimidex (0.5 mg) for this duration as well. Its not advised that these products be ran concomitantly with the steroid for the entire duration of the stack, as this will reduce your gains. Instead cease the usage of anti-estrogens once the problem is contained, and should the problem resurface, simply recommence the use of the products in the same manner as described above.

    Once a cycle of steroids is concluded one should always initiate a post-cycle therapy to help bring back natural testosterone as soon as possible. This will help you to retain the mass you gained. How this is done depends highly on the type of steroid used. If only orals were used, therapy should start immediately, even the last day of the stack. If short-acting esters or water-based injectables were used, therapy should commence within 4-7 days after last injection, and if long-acting esters were used then it should commence 1.5 to 2 weeks after the last injection was given. The length of the therapy will vary as well, from 3-5 weeks. The longer acting the product was, the longer therapy should be continued to make sure all suppressive factors are cleared before use of Clomid/Nolvadex is discontinued.

    For best results, it is best stacked with HCG (Human Chorionic gonadotrophin), which functions as an LH analog and can help bring testicle size back up. HCG use starts the last week of a cycle, and on from there every 5-6 days (usually 1500-3000 IU) and discontinued 1.5 to weeks prior to the cessation of Nolvadex/clomid. The reason being that HCG itself is also suppressive of natural testosterone and should be out of the body before therapy is over, or it will inhibit natural testicle function. But I can not stress enough that HCG possibly plays a more important role in post-cycle therapy than clomid/Nolvadex. For Clomid and Nolvadex, doses are usually tapered down. Its best to start with 40-50 mg of Nolvadex or 150 mg of Clomid for the first week or the first two weeks, and then finish the program with 20-25 mg of Nolvadex or 100 mg of Clomid for an additional two weeks.

    Last edited by WhiteTiger; 09-27-2011 at 06:04 PM. Reason: Typos

    What about the possible eyesight problems? I know it says long term use, but what constitutes long term use?

    The possible sides of anything we take are a risk, but irreversible eyesight damage is a pretty big deal...

  14. #14
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    From the medical evidence, empirical data, and reported BB'r experiences available, vision issues are generally kept in check with doses under 150mg. Some people can handle a lot more. I cant.

    Arguably, long term use is approx many months (6mos+)

  15. #15
    Quote Originally Posted by MickeyKnox View Post
    From the medical evidence, empirical data, and reported BB'r experiences available, vision issues are generally kept in check with doses under 150mg. Some people can handle a lot more. I cant.

    Arguably, long term use is approx many months (6mos+)
    Yeah the studies using Clomid in males is like 4-6 months at 100mgs/day and they say it has proven safe.

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