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Please show me a study of Clomid decreases estrogen in male

mojo

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Besides Bill Robert, I cannot find a single study that clomiphene citrate decreases estorgen in our body.


Both clomiphene citrate and tamoxifen are estrogen receptor blockers that have been suggested as empiric treatments for male infertility. By preventing the important negative feedback of estrogens to the pituitary and hypothalamus, LH/FSH pulsatile release and GnRH stimuli are augmented. Since FSH is important for spermatogenesis, it is possible that increased FSH release may further enhance sperm production. Increased LH release also results in higher serum testosterone levels that are converted peripherally as well as in the liver to estrogens. Since men with idiopathic infertility have normal testosterone levels, by definition, the increased FSH, LH and testosterone that result from clomiphene or tamoxifen treatment may boost testosterone and estrogen levels above normal levels. This increased estrogen production may be detrimental to normal sperm production and should be avoided. Therefore, all patients considered for empiric therapy should be counselled to have early and frequent testosterone and estradiol levels to monitor treatment.

More importantly, the effect of anti-estrogens on fertility for men with idiopathic subfertility are unimpressive. A partial list of series of patients treated in controlled series with clomiphene citrate is presented below. Although sperm concentration may increase on treatment, little to no effect on sperm motility or pregnancy rates occurs. A significant number of patients may have a dramatic decline in sperm production on empiric therapy. Patients should be aware of these minimal benefits and possible risks prior to treatment. Common side effects of clomiphene citrate include visual disturbances, weight gain or loss, changes in libido, gastrointestinal or neurological disturbances as well as skin changes. Initial doses should probably be only 12.5-25 mg/day if this treatment is chosen, to avoid excessive serum testosterone levels.



I have even found studies that clomid after binding to selective estrgen site, the brain will even trigger more estorgen release due to clomid tricking the brain to think it is not enough estorgen in our system.

I find I even bloat up more on clomid, more water retenion.
 

Ozmrolympia

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Mojo how are you buddy!!

My experience has been that Clomid is a very harsh drug. I can answer your above question from personal experience.

Over the last few years i have juiced quite heavy going over 3 grams per week on most cycles. This led to my LH/FSH levels falling below the normal acceptable level and thus i was advised to start HCG therapy which i did. Unfortunately i took a friends advice and also started clomiphene therapy. That was a huge mistake.

Firstly i developed gyno from clomiphene which means that it converts to estrogen in the body or attaches itself to the estrogen receptors. Whatever the case, i developed gyno and eventually had it surgically removed.

Using blood tests, i also saw a significant increase in my estradiol levels while on clomiphene. Werid but true!

Add to this acne that takes 3 months to dissapear and severe mood swings, depression for me and you could understand why i hate the stuff.

Arimidex dosnt work for me eigther, only nolvadex.
 

Johan

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Oz do you use nolva instead of clomid then for post cycle recovery??
 

preist943

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could not find a study that u asked for but here is the most info i could find from my files i have from the net hope this will help somewhat








Clomid and Nolvadex



Pharmaceutical Name: Clomiphene (as citrate)
Effective dose: 100-150 mg/day orally

Available Doses: 25 and 50 mg tabs

Pharmaceutical Name: Tamoxifen (as citrate)
Effective dose: 20-40 mg / day orally

Available Doses: 10,20,30 and 40 mg tabs



Characteristics:

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.

Lastly, one should be aware that use of these compound 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 mg of Nolvadex or 150 mg of Clomid for the first week or the first two weeks, and then finish the program with 20 mg of Nolvadex or 100 mg of Clomid.

References

1 Vermeulen A., Comhaire F., Hormonal effects of an anti-estrogen, tamoxifen, in normal and oligospermic men, Fertil. Ster. 29 (1978) 320-27

2 Bruning PF, Bronfer JMG, Hart AAM, Jong-Bakker M, tamoxifen, serum lipoproteins and cardiovascular risk, Br. J. Cancer 1988 Oct, 58 (4) 497-9







--------------------------------------------------------------------------------
 

mojo

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preist943, thanks for the article.
Looks like both AusMro and Preist943 both agree with me, clomid being poor choice of anti-estrogen.
 

Big A

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Of course it's a poor choice. Just think of it this way. Clomid, by affecting your HPTA, it makes you realease testosterone. Testosterone aromatizes very easily, so more estrogen.
 

wolverine

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Weird, because clomid works great for me. As soon as I feel my nips getting tender I start the clomid at 100mg/day and in a few days it's gone. I don't think clomid actually decreases circulating estrogen, but since it is a weak estrogen itself it binds better to the receptor yet does not have the full effect of estrogen (such as causing gyno.) If you are to take arimidex along with it, or even aromasin if you can get it, you would have a double whammy in the clomid binding to the receptor while that arimidex/aromasin would inhibit the aromatase enzyme. Keep in mind that aromasin completely inhibits the enzyme once attached, unlike arimidex which is considered a "reversable" inhibitor.
 

Johan

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Wolverine are you saying that aromasin shuts down aromatising for ever???
 

Animal

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Pointless

What's the point? Both are considered oestrogens. Both Nolvadex and clomid affect the LH/HPT and inthe same way, but with Nolv using 10mg and Clo using 50mg. Big deal.

Nolvadex is more site specific for breast tissue and therefore may not be as good a systemic anti-e as clomid. Nolvadex also decreases IGF-1 production.


Nolvadex, Tamoxifen Citrate, is a drug that? tehnically an estrogen. It?
classified as a mixed estrogen agonist/antagonist. It was developed for
females with breast cancer. It works by attaching to estrogen receptors (ER)
in target tissues and doing nothing. In other words, it has a benign
activity in certain tissues, so when it attaches to those ER it prevents
estrogen from attaching there and activating the receptor. In the early 80?,
Dan Duchaine started using it on himself and others in his circle because he
thought it could have the same activity in abnormal male breast tissue, he
was right. Thus Nolvadex entered the bodybuilding scene. Now lets talk about
the other things Nolvadex does, for one thing in many tissues it acts as an
estrogen, for example, the liver, this is not good. For years "experts" in
the art of performance enhancing steroid use have hypothesized that Nolvadex
caused a reduction in the production of IGF 1. Well it does, just not the
way a lot of people thought, in fact estrogen in high quantities causes a
reduction in IGF 1, and when it attaches to ER at the liver, Nolvadex acts
like an estrogen. Another common misconception is that some people think
when they are using an estrogen antagonist like Nolvadex that the amount of
estrogen in the body is being reduced, that? not the case, all of it is
still there, wreaking havoc in other ways, like increasing the ability for
the body to store macronutrients as fat and causing a reduction in IGF 1
(Nolvadex makes this event even worse). Out of all the ancillary medication
out there to use as a PREVENTATIVE measure, Nolvadex is by far the worst, in
addition to the things I have mentioned, Nolvadex also has many other
possible side effects, most of them hematological, such as greatly
increasing the possibility of venous thrombosis, and pulmonary embolism,
this is not good considering that most of the steroids we use during a mass
cycle increase red blood cell count, thus thickening the blood before the
Nolvadex is even added. Now kept in you arsenal as a medication for gyno
that has already started, Nolvadex is the best thing available to us, but if
we are using anicillaries during the cycle, we will never have a reason to
use it. And saying that it will benefit a cycle just aint so. Saying it
should be included in every cycle is BS. There are just too many things out
there that work better.
 

Animal

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And

While this is done on alcoholics, there is a control group and no rise in estradiol from higher LH levels was noted.

Authors
Martinez Riera A. Santolaria Fernandez F. Gonzalez Reimers E. Milena A.
Gomez Sirvent JL. Rodriguez Moreno F. Gonzalez Martin I.
Rodriguez Rodriguez E.
Title
Alcoholic hypogonadism: hormonal response to clomiphene.
Source
Alcohol. 12(6):581 7, 1995 Nov Dec.
Abstract
To investigate the androgen, weak androgen, estrogen, and gonadotrophin
response to clomiphene in alcoholics, we determined in 63 male patients
(25 with and 38 without liver cirrhosis) serum testosterone, sexual
hormone binding protein (SHBG), dehidroepiandrosterone, androstenedione,
LH, FSH, prolactin, and estradiol levels, on the first and the sixth day
after admission, and after a course of 8 days of clomiphene 200 mg/day.
The same test was performed on 15 healthy volunteers. Cirrhotic patients
showed decreased basal testosterone levels and a loss of the circadian
rhythm with recovery after clomiphene. Although basal testosterone levels
in noncirrhotic alcoholics did not differ from those of the controls,
there was a significant improvement after withdrawal. SHBG levels were
higher in both groups of alcoholics than in controls, pointing to a worse
degree of hypogonadism, because only the free hormone is active. Before
the clomiphene test, serum LH and FSH levels were nonsignificantly higher
in both groups of alcoholics than in the control group. After clomiphene
both LH and FSH increased. Androstenedione and estradiol showed a
(parallelism) similar behavior in alcoholic and in cirrhotic groups,
showing in both cases higher levels than in the control group, and an
increase after clomiphene, perhaps reflecting peripheral conversion of
androgens to estrogens. Because clomiphene has no effect on the adrenal
cortex, the increase of androstenedione after clomiphene points to its
testicular origin (directly or after testosterone conversion) and not to
an adrenal one. The highest serum estradiol levels were observed in
cirrhotics with ascites or gynecomastia. We have not found any relation
between serum hormone levels and alcohol intake nor with nutritional
status.
 

Animal

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Just in case

Those aren't enough to show that IGF is affect by nolvadex.

http://www.google.com/search?q=cach...CS/SECTION15/55.pdf+tamoxifen+citrate+and+IGF 1&hl=en

http://www.intouchlive.com/journals/oncology/o9812d.htm
The effects of the steroid hormones differ by organ site. The mitotic rate of the endometrial cells lining the uterus is stimulated by
estrogen and inhibited by progestins. Breast tissue undergoes cell proliferation and loss in concert with the ovaries’ cyclic
production of estrogen and progesterone.[115] The role of estrogen as a primary stimulant of breast cell proliferation, which
contributes to the development of breast cancer, is supported by epidemiologic studies, animal studies, and clinical trials.[112,114]
In addition, the simultaneous presence of progesterone probably further increases the rate of breast cell proliferation.[112]
Although progesterone has inhibitory effects on the endometrium, evidence is accumulating that it increases the rate of cell division
in breast tissue beyond that of estrogen alone.[118] Because the combined presence of estrogen and progesterone in oral
contraceptives has stimulatory effects on breast cell proliferation, a protective effect against breast cancer is not anticipated, nor
has such an effect been seen.[116,118]
Tamoxifen citrate is a nonsteroidal compound that exerts both estrogen agonistic and antagonistic effects. Acting as an
antiestrogen in the breast, tamoxifen increases breast cell growth inhibitory factors, such as transforming growth factor beta
(TGF beta) and reduces stimulatory factors, such as

transforming growth factor alpha (TGF alpha) and insulin like growth factor 1 (IGF 1).[147,148] Estrogen stimulates the growth
of breast tumor cells by increasing the levels of growth stimulatory factors, such as TGF alpha.[147,148]
 

wolverine

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Johan said:
Wolverine are you saying that aromasin shuts down aromatising for ever???
Only for the aromatase enzyme it attaches to. If new enzymes are produced and aromasin is not present in the body, then you will have conversion.
 

xcelbeyond

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Animal!

Glad to see you found time and made your way over here bro!

For those that don't know A, he's one of the most knowledgeable bros online. His "sometimes" brash demeanor oftentimes offends others, but he really does make an attempt to help everyone - so keep that in mind.

Animal - do you think you can post that info on the effect of Nicotine here?

xcelbeyond
 
Last edited:

xcelbeyond

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Re: nicotine

Animal said:
You can post it.
I would post but it's one of the few "great" posts that I didn't save!! It got sooo damn long I never bothered to. Then, when I thought about copying it, it fell off the end at the old Fina board.

xcelbeyond
 
Last edited:

MikeS

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ANIMAL IS HERE!

Another brilliant addition to the board. Thanks for stopping by bro.
I may be repeating what has already been said; but my summary is this. Nolvadex and clomid are similar products - but both have different affinity to certian receptor sites. Clomid shows more efficient in antagonizing the HPTA estro receptors, and nolv the receptors in breast tissue. Where else one is more effective in other receptor areas is of less concern to us. Wheather this is shown in research has not been mentioned, but in real life BB practice, the results speak for themselves. I also agree with the fact ALL anti estros/blockers affect anabolic results. So I personally like to attempt to find that fine line of using just enough anti estros, and not too much. I use 50mg clomid 3x wk along with .25mg arimidex 2x wk. And certainly the clomid does help combat HPTA suppression throughout the cycle. I also use it post cycle with HCG.
 

hyper

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Yea, good to see you Animal!

Interesting post. Good reading!
 

Sanjac

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Someone posted that arimidex is a reversible inhibitor of aromatase. Available research shows that the enzyme:substrate complex is stable for 40 days. THIS IS IRREVERSIBLE for all intents and purposes. Aromasin is unlikely to show any different behavior than arimidex for the "normal" user.

BTW, new enzyme molecules are generated by the body every day.

SJ
 

Animal

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letrozole

letrozole has been shown in studies not to mess with IGF-1 levels.

Oh, that long nicotine post, I didn't save it, either. All I have is what's on my board on the 'nicotine and ghrelin' thread at www.animalkits.be
 

xcelbeyond

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Re: letrozole

Animal said:
letrozole has been shown in studies not to mess with IGF-1 levels.
I was going through old posts and dug this one up. Can anyone on this statement?

xcel
 

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