Thread: Using clomid in place of Nolva

For PCT-Clomid is my choice.

Yeah but im wondering if I can use clomid for on cycle gyno flare. I have read that 50 to 100mg is when it is effective. How long would one use that dose and would I just use it till gyno subsides? Any opinions ? Thanks

Originally Posted by BigBoiH

Yeah but im wondering if I can use clomid for on cycle gyno flare. I have read that 50 to 100mg is when it is effective. How long would one use that dose and would I just use it till gyno subsides? Any opinions ? Thanks

Sorry about that. I have never experienced gyno. If I did I think I'd look to Letro.

Use Letro for gyno if their is a lump.

If it isn't a lump yet, use nolva, not clomid.

Originally Posted by BigBoiH

Yeah but im wondering if I can use clomid for on cycle gyno flare. I have read that 50 to 100mg is when it is effective. How long would one use that dose and would I just use it till gyno subsides? Any opinions ? Thanks

Clomid does NOTHING for gyno, NOTHING. It is used in PCT to help restart your natural testosterone production, nothing else.

For gyno you need to be using and A/I not a SERM. An A/I would be aromasin, arimidex, letro.

You need BOTH for PCT. The A/I should also be used during the cycle and throughout the PCT.

Originally Posted by CT

... The A/I should also be used during the cycle and throughout the PCT.

..and it wouldn't hurt to run an AI a few weeks after. Test can keep aromatizing up to 5 half-lifes.

For enanth, this is like 70 days.

Originally Posted by Tyler3295

..and it wouldn't hurt to run an AI a few weeks after. Test can keep aromatizing up to 5 half-lifes.

For enanth, this is like 70 days.

No not really, seeing that you do need some estrogen for libido and healthy joint function and by 45 days it's pretty much minimal at best. I guess you could if you wanted to. I know guys who run an A/I year round if they are on gear or not.

For gyno, I'd use nolva.

Originally Posted by Walnutz

For gyno, I'd use nolva.

I always use an A/I, and no gyno problems. Better to prevent than wait for problems. Adex or aromasin always does the trick for me. If I ever did get a lump, I'd use the strong stuff (Letro).

Do you still need to run an AI on a cycle of a non aromatizing compound?

Originally Posted by mystictrunks

Do you still need to run an AI on a cycle of a non aromatizing compound?

That's a good question, I'm going to say no, but everyone is different. I guess if you were running primo, mast and winstrol why would you really need one?

Good post.

Originally Posted by CT

No not really, seeing that you do need some estrogen for libido and healthy joint function and by 45 days it's pretty much minimal at best. I guess you could if you wanted to. I know guys who run an A/I year round if they are on gear or not.

Yeah, but I'd rather run aromasin for a week or two after PCT than to get post-PCT gyno. :/

Of course, I am gyno-prone and have had that happen..

Originally Posted by CT

Clomid does NOTHING for gyno, NOTHING. It is used in PCT to help restart your natural testosterone production, nothing else.

For gyno you need to be using and A/I not a SERM. An A/I would be aromasin, arimidex, letro.

You need BOTH for PCT. The A/I should also be used during the cycle and throughout the PCT.

Nolva and clomid both are serms. But people still use nolva for gyno symptoms. I will be running adex @ .5mg eod. I think I found my own answer doing a little more research. I can use clomid but most choose nolva because it only takes 20-40mg of nolva compared to 100-150 of clomid. And Nolva can help HPTA production the same as clomid. They both stimulate the heightened release of GnRH and LH output.

Originally Posted by BigBoiH

I had made an order and there is one thing that I forgot to ask about. I have been doing research on clomid and why to use it over nolva. I decided that I would go with clomid.Every one says have nolva on hand just in case during cycle signs of gyno. I have been wondering about if you have in cycle signs of gyno, how would you run clomid on cycle to fight effects. Can it give the same if not better effects? I am sorry I didnt consider this ahead of time. I can order some nolva if need be. And no I am not asking this on cycle, just preparing for all situations when my package does arrive.
Thanks ahead of time, gang!
BigBoiH

I think at this point most people are sold on the use of Nolvadex (Tamoxifen Citrate) instead of Clomid for post cycle therapy (PCT), since both compete estrogen at the receptor site, both increase serum test levels, and both drugs may also alter blood lipid profiles favorably (6). But since 20mgs of Tamoxifen is equal to 150mgs of clomid for purposes of testosterone elevation, FSH and LH, but Tamoxifen doesn’t decrease the LH response to LHRH (6) I think most people agree to Nolvadex’s superiority for PCT.


... more studies related to gyno

Metabolism. 1986 Aug;35(8):705-8.

Treatment of gynecomastia with tamoxifen: a double-blind crossover study.

Parker LN, Gray DR, Lai MK, Levin ER.

Benign asymptomatic or painful enlargement of the male breast is a common problem, postulated to be due to an increased estrogen/testosterone ration or due to increased estrogenic or decreased androgenic stimulation via estrogen or androgen receptor interactions. Treatment at present consists of analgesic medication or surgery. However, treatment directed against the preponderance of estrogenic stimulation would seem to represent a more specific form of therapy. In the present double-blind crossover study, one-month courses of a placebo or the antiestrogen tamoxifen (10 mg given orally bid) were compared in random order. Seven of ten patients experienced a decrease in the size of their gynecomastia due to tamoxifen (P less than 0.005). Overall, the decrease for gynecomastia for the whole group was significant (P less than 0.01). There was no beneficial effect of placebo (P greater than 0.1). Additionally, all four patients with painful gynecomastia experienced symptomatic relief. There was no toxicity. The reduction of breast size was partial and may indicate the need for a longer course of therapy. A followup examination was performed in eight out of ten patients nine months to one year after discontinuing placebo and tamoxifen. There were no significant changes from the end of the initial study period except for one tamoxifen responder who developed a recurrence of breast tenderness after six months, and one nonresponder who demonstrated an increase in breast size and a new onset of tenderness after ten months. Therefore, antiestrogenic treatment with tamoxifen may represent a safe and effective mode of treatment for selected cases of cosmetically disturbing or painful gynecomastia.


Tamoxifen treatment for pubertal gynecomastia

By Derman O, Kanbur NO, Kutluk T.
Section of Adolescent Medicine, Department of Pediatrics,
Hacettepe University Faculty of Medicine, 06100 Ankara-Turkey.
We evaluated the efficacy of the tamoxifen treatment in 37 patients with pubertal gynecomastia. All had distinct, easily palpable breast swellings with a diameter of over three cm. Pain, tenderness, and swelling associated with gynecomastia were reported by six patients. Eight of the patients were obese. One patient also suffered from varicocele. Pain and size reduction was seen in all patients with tamoxifen treatment. No long-term side effects of tamoxifen were observed. The dose of tamoxifen was increased in three patients due to poor response. Two of the treatment group had recurrence problem at follow-up. We did not need to refer any patient to surgery. Tamoxifen treatment is relatively non-toxic, may be beneficial and we think it should be considered for pubertal gynecomastia.

some kind of gyno that I personally prefer

Originally Posted by Tyler3295

Yeah, but I'd rather run aromasin for a week or two after PCT than to get post-PCT gyno. :/

Of course, I am gyno-prone and have had that happen..

Oh yeah, I totally agree with you. You should always run an A/I to the end of your PCT. I think a lower dose E2-3D is usually best after 1-2 weeks.

I think I misread your first post, sorry.

Originally Posted by BigBoiH

Nolva and clomid both are serms. But people still use nolva for gyno symptoms. I will be running adex @ .5mg eod. I think I found my own answer doing a little more research. I can use clomid but most choose nolva because it only takes 20-40mg of nolva compared to 100-150 of clomid. And Nolva can help HPTA production the same as clomid. They both stimulate the heightened release of GnRH and LH output.

Right they are both SERMS. Nolva decreases IGF-1 and natural GH output so why would anyone choose that when they are trying to recover? It's counterproductive.

50mg clomid ED from day one is more than enough. 100-150mg ED is overkill.

You can do what ever you want really.

Here is a good thread about why nolva is a poor choice.
Why nolvadex is a poor choice

Originally Posted by CT

Nolva decreases IGF-1 and natural GH output so why would anyone choose that when they are trying to recover? It's counterproductive.

Do you have any evidence that nolva decreases IGF-1 and natural GH or are you just saying what you have heard before?

Not according to this:

Originally Posted by dg806

Originally from Mind and Muscle.

Clomid, Nolvadex and Testosterone Stimulation
by William Llewellyn



Introduction


I have received a lot of heat lately about my preference for Nolvadex over Clomid, which I hold for all purposes of use (in the bodybuilding world anyway); as an anti-estrogen, an HDL (good) cholesterol-supporting drug, and as a testosterone-stimulating compound. Most people use Nolvadex to combat gynecomastia over Clomid anyway, so that is an easy sell. And for cholesterol, well, most bodybuilders unfortunately pay little attention to this important issue, so by way of disinterest, another easy opinion to discuss. But when it comes to using Nolvadex for increasing endogenous testosterone release, bodybuilders just do not want to hear it. They only seem to want Clomid. I can only guess that this is based on a long rooted misunderstanding of the actions of the two drugs. In this article I would therefore like to discuss the specifics for these two agents, and explain clearly the usefulness of Nolvadex for the specific purpose of increasing testosterone production.



Clomid and Nolvadex


I am not sure how Clomid and Nolvadex became so separated in the minds of bodybuilders. They certainly should not be. 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. Both drugs do this, but for some reason bodybuilders persist in thinking that Clomid is the only drug good at stimulating testosterone. What you will find with a little investigation however is that not only is Nolvadex useful for the same purpose, it should actually be the preferred agent of the two.

Studies conducted in the late 1970's at the University of Ghent in Belgium make clear the advantages of using Nolvadex instead of Clomid for increasing testosterone levels (1). Here, researchers looked the effects of Nolvadex and Clomid on the endocrine profiles of normal men, as well as those suffering from low sperm counts (oligospermia). For our purposes, the results of these drugs on hormonally normal men are obviously the most relevant. What was found, just in the early parts of the study, was quite enlightening. Nolvadex, used for 10 days at a dosage of 20mg daily, increased serum testosterone levels to 142% of baseline, which was on par with the effect of 150mg of Clomid daily for the same duration (the testosterone increase was slightly, but not significantly, better for Clomid). We must remember though that this is the effect of three 50mg tablets of Clomid. With the price of both a 50mg Clomid and 20mg Nolvadex typically very similar, we are already seeing a cost vs. results discrepancy forming that strongly favors the Nolvadex side.



Pituitary Sensitivity to GnRH


But something more interesting is happening. Researchers were also conducting GnRH stimulation tests before and after various points of treatment with Nolvadex and Clomid, and the two drugs had markedly different results. These tests involved infusing patients with 100mcg of GnRH and measuring the output of pituitary LH in response. The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more LH will be released. The tests showed that after ten days of treatment with Nolvadex, pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with 150mg Clomid, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more LH was released before treatment). As the study with Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosterone and LH levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment Clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of Nolvadex serves only to increase pituitary sensitivity to this hormone. That is not to say Clomid won't increase testosterone if taken for the same 6 week time period. Quite the opposite is true. But we are, however, noticing an advantage in Nolvadex.



The Estrogen Clomid


The above discrepancies are likely explained by differences in the estrogenic nature of the two compounds. The researchers' clearly support this theory when commenting in their paper, "The difference in response might be attributable to the weak intrinsic estrogenic effect of Clomid, which in this study manifested itself by an increase in transcortin and testosterone/estradiol-binding globulin [SHBG] levels; this increase was not observed after tamoxifen treatment". In reviewing other theories later in the paper, such as interference by increased androgen or estrogen levels, they persist in noting that increases in these hormones were similar with both drug treatments, and state that," …a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation".

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. To find further support for this we can look at an in-vitro animal study published in the American Journal of Physiology in February 1981 (2). This paper looks at the effects of Clomid and Nolvadex on the GnRH stimulated release of LH from cultured rat pituitary cells. In this paper, it was noted that incubating cells with Clomid had a direct estrogenic effect on cultured pituitary cell sensitivity, exerting a weaker but still significant effect compared to estradiol. Nolvadex on the other hand did not have any significant effect on LH response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.



Conclusion


To summarize the above research succinctly, Nolvadex is the more purely anti-estrogenic of the two drugs, at least where the HPTA (Hypothalamic-Pituitary-Testicular Axis) is concerned. This fact enables Nolvadex to offer the male bodybuilder certain advantages over Clomid. This is especially true at times when we are looking to restore a balanced HPTA, and would not want to desensitize the pituitary to GnRH. This could perhaps slow recovery to some extent, as the pituitary would require higher amounts of hypothalamic GnRH in the presence of Clomid in order to get the same level of LH stimulation.

Nolvadex also seems preferred from long-term use, for those who find anti-estrogens effective enough at raising testosterone levels to warrant using as anabolics. Here Nolvadex would seem to provide a better and more stable increase in testosterone levels, and likely will offer a similar or greater effect than Clomid for considerably less money. The potential rise in SHBG levels with Clomid, supported by other research (3), is also cause for concern, as this might work to allow for comparably less free active testosterone compared to Nolvadex as well. Ultimately both drugs are effective anti-estrogens for the prevention of gyno and elevation of endogenous testosterone, however the above research provides enough evidence for me to choose Nolvadex every time.

In next month's follow-up article I will be discussing the role anti-estrogens play in post-cycle testosterone recovery. Most specifically, I will be detailing what a proper post-cycle ancillary drug program looks like, and explain why anti-estrogens alone are not effective during this window of time.


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

Originally Posted by BigBoiH

Do you have any evidence that nolva decreases IGF-1 and natural GH or are you just saying what you have heard before?

Not according to this:

Look at the dates of the research done, enough said. Here is a CURRENT article from the same person.

First, most people who have been educated by way of the boards over the last 8 years DON'T use Nolva. Bill Llewellyn, author of Anabolics 2008, has changed his stance on Nolva recently after endorsing it's use for 9 years.

Interesting read from William LLewelyn
Estrogen is not the enemy

Aromatizable Androgens and Anabolism:
The Role of Estrogen in Muscle Growth
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.

Look, I don't care what you do all I'm doing is giving you an opinion. You can do what you wish with it, it really doesn't matter to me.

Thanks for the article!

Originally Posted by CT

Look, I don't care what you do all I'm doing is giving you an opinion. You can do what you wish with it, it really doesn't matter to me.

Im just doing research and take a subjective stand point as I should be.
My Original question is still there, but thanks for answering the other part.

Fuck. Now i'm confused. Is the Nolva I bought going to help me hold on to my gains or not?

Originally Posted by BigBoiH

Thanks for the article!



Im just doing research and take a subjective stand point as I should be.
My Original question is still there, but thanks for answering the other part.

What's the original question? I thought that was already answered?

Originally Posted by bigboih

i had made an order and there is one thing that i forgot to ask about. I have been doing research on clomid and why to use it over nolva. I decided that i would go with clomid.every one says have nolva on hand just in case during cycle signs of gyno. I have been wondering about if you have in cycle signs of gyno, how would you run clomid on-cycle to fight effects. Can it give the same if not better effects for during cycle gyno? i am sorry i didnt consider this ahead of time. I can order some nolva if need be. And no i am not asking this on cycle, just preparing for all situations when my package does arrive.
Thanks ahead of time, gang!
Bigboih

1

Originally Posted by BigBoiH

1

So you're asking what to use instead of nolva, because I already stated that clomid does nothing for gyno.

If clomid does nothing for gyno, then I really don't understand your question.

Can you try to rephrase what you originally typed?

Use an A/I on cycle and during PCT. Use clomid during PCT ONLY.