AIFM Aromatest Inhibitor for Men Now Available

[lionhead]

Just got a HELL OF RASH on both my fore arms....
noticed irritation from the solution in the beginning and stoppep applying now 5 days later both my forearms have humungous rashes on them.... itchy as hell... got some antihistamins to calm things down will wait to see what will happen then ill post more info.

 

[SWALE]

Estrogen is rapidly dropping during post cycle therapy (pct). By the time the post cycle therapy (pct) takes hold, it is already at levels which do not suppress the HPTA. Therefore an Aromatase inhibitor (AI) is not appropriate during that time, as administering same can not otherwise but induce the untoward effects of hypoestrogenemia. This unnecessarily extends the time of cardiovascular plaque deposition, amongst others.

I think a distinction needs to be made regarding the phrase "post cycle therapy (pct)". I refer to the time when serum androgen levels are roughly what 200mg of test per week produces. HPTA stimulation through estrogenic suppression--whether via direct antagonism or estrogen production control--is overcome by androgenic supression until then. Until that time--which can be weeks after your last Anabolic Androgenic Steroids (AAS) injection--you are still "on". Therefore, an Aromatase inhibitor (AI) could, and should, be used until then. We also have to keep in mind that it takes about 2.5 half-lives to establish steady serum levels of medications.

As you know, I have always been in favor of controlling estrogen during the cycle, as I have been for continual Human Chorionic Gonadotropin (HCG) administration. it is therefore not much elevated at the end of the cycle, so Aromatase inhibitor (AI) use during that time is completely unwarranted.

There is NO "clinical and anecdotal evidence that supports use of AI's during post cycle therapy (pct)". It is all anecdotal, combined with the extrapolation--frequently unwarranted--from studies under completely different experimental conditions. And, as I said, those who truly understand the pathways, and how the body functions, do not believe introducing powerful endocrine disrupters--especially during a time of rapid androgen deceleration--helps normalize the system. The same could be said of finasteride.

What evidence exists that "oestrogen rebound does not occur with suicidal AI's", please?

I am very much interested in the possibilities your new product brings.

 

[macro]

note- not reccomending Aromatase inhibitor (AI) treatment alone (though some do)

during PCT, SERMS are being used so endogenous estrogen (for the reasons you elucidated- blood lipids, etc) is not particularly useful and local aromatization may yield suppression.



agree that the studies are not duplicative, however they are relevant.

Diabetes Obes Metab. 2005 May;7(3):211-5. Related Articles, Links


Letrozole normalizes serum testosterone in severely obese men with hypogonadotropic hypogonadism.

de Boer H, Verschoor L, Ruinemans-Koerts J, Jansen M.

Department of Internal Medicine, Ziekenhuis Rijnstate, Wagnerlaan 55, 6800 TA Arnhem, The Netherlands. hdeboer@alysis.nl

BACKGROUND: Morbid obesity is associated with increased estradiol production as a result of aromatase-dependent conversion of testosterone to estradiol. The elevated serum estradiol levels may inhibit pituitary LH secretion to such extent that hypogonadotropic hypogonadism can result. Normalization of the disturbed estradiol-testosterone balance may be beneficial to reverse the adverse effects of hypogonadism. AIM: To examine whether aromatase inhibition with Letrozole can normalize serum testosterone levels in severely obese men with hypogonadotropic hypogonadism. PATIENTS AND METHODS: Ten severely obese men, mean age 48.2 +/- 2.3 (s.e.) years and body mass index 42.1 +/- 2.6 kg/m(2), were treated with Letrozole for 6 weeks in doses ranging from 7.5 to 17.5 mg per week. RESULTS: Six weeks of treatment decreased serum estradiol from 120 +/- 20 to 70 +/- 9 pmol/l (p = 0.006). None of the subjects developed an estradiol level of less than 40 pmol/l. LH increased from 4.5 +/- 0.8 to 14.8 +/- 2.3 U/l (p < 0.001). Total testosterone rose from 7.5 +/- 1.0 to 23.8 +/- 3.0 nmol/l (p < 0.001) without a concomitant change in sex hormone-binding globulin level. Those treated with Letrozole 17.5 mg per week had an excessive LH response. CONCLUSION: Short-term Letrozole treatment normalized serum testosterone levels in all obese men. The clinical significance of this intervention remains to be established in controlled, long-term studies.

J Clin Endocrinol Metab. 2005 Oct;90(10):5717-22. Epub 2005 Jul 26. Related Articles, Links


Comparative assessment in young and elderly men of the gonadotropin response to aromatase inhibition.

T'Sjoen GG, Giagulli VA, Delva H, Crabbe P, De Bacquer D, Kaufman JM.

Department of Endocrinology, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium. guy.tsjoen@ugent.be

CONTEXT: Aging in men is associated with a decline in serum testosterone (T) levels. OBJECTIVE: Our objective was to assess whether decreased T in aging might result from increased estradiol (E2) negative feedback on gonadotropin secretion. DESIGN AND SETTING: We conducted a comparative intervention study (2004) in the Outpatient Endocrinology Clinic, Ghent University Hospital. PARTICIPANTS: Participants included healthy young and elderly men (n = 10 vs. 10). INTERVENTIONS: We used placebo and letrozole (2.5 mg/d) for 28 d, separated by 2 wk washout. MAIN OUTCOME MEASURES: We assessed changes in serum levels of free E2, LH, and FSH, free T, SHBG, and gonadotropins response to an i.v. 2.5-microg GnRH bolus. RESULTS: As assessed after 28 d of treatment, letrozole lowered E2 by 46% in the young men (P = 0.002) and 62% in the elderly men (P < 0.001). In both age groups, letrozole, but not placebo, significantly increased LH levels (339 and 323% in the young and the elderly, respectively) and T (146 and 99%, respectively) (P value of young vs. elderly was not significant). Under letrozole, peak LH response to GnRH was 152 and 52% increase from baseline in young and older men, respectively (P = 0.01). CONCLUSIONS: Aromatase inhibition markedly increased basal LH and T levels and the LH response to GnRH in both young and elderly men. The observation of similar to greater LH responses in the young compared with the elderly does not support the hypothesis that increased restraining of LH secretion by endogenous estrogens is instrumental in age-related decline of Leydig cell function.

 

[SWALE]

It is important when analyzing a scientific study to not only assertain what the study tells us, but also (and sometimes moreso) what it does NOT. The two studies you provide are cases in point.

The first one looks at obese diabetic men, not the hypogonadotropic hypogonadism iatrogenically induced in those coming off from a steroid cycle. No comparison is made between use of SERM-class drugs, or whether a SERM/AI post cycle therapy (pct) is preferable to a SERM-only post cycle therapy (pct) (which is what the true question is here). Even more importantly, no investigation is made into the increased health risks of hypoestrogenemia (which extends to risks of the Anabolic Androgenic Steroids (AAS) cycle when it occurs), as it was not a goal of the study.

The second study was conducted on men who not only were NOT hypogonadotropic, but were actually HYPERgonadotropic. For this, and other reasons, this one definitely should not be included in anyone's arguement in this thread.

It is common knowledge that estrogen inhibits the HPTA. It is also well established that aromatase inhibition elevates gonadotropins. But that does not mean it is better to use AI's during post cycle therapy (pct), or a SERM/AI combination during post cycle therapy (pct), than lone SERM administration. It is my professional opinion, as a physician who works almost exclusively in hormonal modulation, with years of experience in this area, that use of AI's during post cycle therapy (pct) is a mistake (for this and other reasons I have detailed in this very thread).

Let's briefly return to my previous statement from my last post:

"There is NO "clinical and anecdotal evidence that supports use of AI's during post cycle therapy (pct)". It is all anecdotal, combined with the extrapolation--frequently unwarranted--from studies under completely different experimental conditions."

It's pretty common on the Boards for guys to throw studies up which are irrelevant to the points being made. The trained scientific mind would not do so, or at least offers/concedes, up front, limited applicability to the arguement at hand.

 

[Iron Gladiator]

There is NO "clinical and anecdotal evidence that supports use of AI's during PCT". It is all anecdotal, combined with the extrapolation--frequently unwarranted--from studies under completely different experimental conditions. And, as I said, those who truly understand the pathways, and how the body functions, do not believe introducing powerful endocrine disrupters--especially during a time of rapid androgen deceleration--helps normalize the system. The same could be said of finasteride.

Swale, I am a little confused here. I have read a number of your informative posts and I have decided to use nolvadex solely for PCT, which to my understanding should start after my last Anabolic Androgenic Steroids (AAS) shot. It is also my understanding that AI's, Human Chorionic Gonadotropin (HCG) is only used during the cycle. You commented on finasteride, I am currently taking Proscar during my cycle, should I discontinue its use during PCT? If I decide to continue to use Proscar, at what point should I start using it again, after PCT? During my next cycle? And what are the reasons for this? What about anti-cortisol during PCT?

Thanks

 

[macro]

at least offers/concedes, up front, limited applicability to the arguement at hand.

"agree that the studies are not duplicative, however they are relevant."

 

[macro]

Even more importantly, no investigation is made into the increased health risks of hypoestrogenemia (which extends to risks of the Anabolic Androgenic Steroids (AAS) cycle when it occurs), as it was not a goal of the study.

essentially irrelevant in a SERM/AI based post cycle therapy (pct). Even if you were to run the Aromatase inhibitor (AI) days past the last dose of nolva, its would still not be an issue due to extended nolva half life.

in solely Aromatase inhibitor (AI) based, it certainly might be an issue. though this could be mitigated by a lesser dose (milder oestrogenic suppression)

 

[SWALE]

I'm sure others get the points made.

 

[macro]

hmmm.... ok.

 

[SWALE]

Are you saing that you think running a SERM-class drug while E levels have been driven too low with an Aromatase inhibitor (AI) somehow automatically protects the body from the ravages of same?

 

[macro]

Are you saing that you think running a SERM-class drug while E levels have been driven too low with an Aromatase inhibitor (AI) somehow automatically protects the body from the ravages of same?

yes, SERMS are essentially a form oestrogen replacement therapy, though to what extent depending on the individual SERM. Their activity profiles are not identical.

 

[SWALE]

Macro--SERM's are not "estrogen replacement". Taking one actually has little resemblance to the effects of endogenously produced estrogen. Here's a hint: look at your pathways.

 

[Senri]

just rehashing for some questions. When do the effects come in that your estrogen is getting low, im only getting increased libido, im not so sure of strength yet. Im wondering of taking clomid after i finish the bottle use 50mg a day for one week or two weeks (weigh 167lbs) whats the verdict im unsure of when for effecient test boost.

 

[macro]

Macro--SERM's are not "estrogen replacement". Taking one actually has little resemblance to the effects of endogenously produced estrogen. Here's a hint: look at your pathways.

SERM just means selective estrogen receptor modulator. thier effects can range from those of faslodex almost a pure blocker, to those with both antagonist and agonist effects like nolva and clomid, to almost pure estrogen agonists like PPT (1,3,5-tris(4-hydroxyphenyl)-4-propyl-1H-pyrazole) (ERalpha agonist).


you can expect to see development of more selective estrogen agonists for menapausal HRT. (note- nolva is currently used, though its profile is not ideal)

 

[macro]

just rehashing for some questions. When do the effects come in that your estrogen is getting low, im only getting increased libido, im not so sure of strength yet. Im wondering of taking clomid after i finish the bottle use 50mg a day for one week or two weeks (weigh 167lbs) whats the verdict im unsure of when for effecient test boost.

they may never come, if you use moderate aromatase inhibitor levels for you. individual "need" to suppress aromatase varies. also the "catch point" at which E suppression is too much is quite varied.

 

[macro]

Macro--SERM's are not "estrogen replacement". Taking one actually has little resemblance to the effects of endogenously produced estrogen. Here's a hint: look at your pathways.

follow up on SERM's as estrogen replacement

: Drugs. 2006;66(2):191-221. Links
Emerging selective estrogen receptor modulators: special focus on effects on coronary heart disease in postmenopausal women.Vogelvang TE, van der Mooren MJ, Mijatovic V, Kenemans P.
Department of Obstetrics and Gynecology, Project Aging Women, Institute for Cardiovascular Research-Vrije Universiteit, VU University Medical Center, Amsterdam, The Netherlands.

Menopause, regardless of age at onset, is associated with a marked increase in coronary heart disease (CHD) risk. On the basis of epidemiological studies that demonstrated mainly positive effects of postmenopausal hormone therapy on CHD as well as on risk markers of CHD, it has been suggested that CHD could be prevented in postmenopausal women with long-term hormone therapy. However, since the publications of the Heart and Estrogen/progestin Replacement Study and the Women's Health Initiative trial, prescription of hormone therapy for the prevention of CHD has become controversial. Major efforts have been made to identify alternatives for hormone therapy. Compounds suggested have included selective estrogen receptor modulators (SERMs), which represent a class with a growing number of compounds that act as either estrogen receptor agonists or antagonists in a tissue-specific manner. This pharmacological profile may offer the opportunity to dissociate favourable estrogenic effects on the bone and cardiovascular system from unfavourable stimulatory effects on the breast and endometrium. Two SERMs presently on the market are tamoxifen and raloxifene. The only data available regarding the effects of tamoxifen on cardiovascular events in postmenopausal women are from breast cancer trials. These trials found fewer fatal myocardial events in women randomly assigned to tamoxifen compared with women assigned to placebo. Raloxifene is a second-generation SERM that has been shown to prevent osteoporotic fractures, is safe for the endometrium and holds high promise for the prevention of breast cancer. The effect of raloxifene on CHD is still uncertain. On the basis of the MORE (Multiple Outcomes of Raloxifene Evaluation) trial, raloxifene may offer some protection to women with CHD or to those who are at high risk of CHD. Proof that raloxifene reduces the risk of CHD requires a clinical trial with hard clinical endpoints. Such a study is currently underway. Next-generation SERMs taken into clinical development include idoxifene, droloxifene, ospemifene, arzoxifene, acolbifene/EM-800, levormeloxifene, lasofoxifene, bazedoxifene and HMR 3339. The aim is to find a compound with the ideal profile, that is, alleviation of climacteric symptoms and prevention of osteoporotic fractures, but without an adverse effect on the breast and endometrium, and no negative effect or even a beneficial effect on the cardiovascular system and the brain. Currently, limited data are available with regard to these next-generation SERMs and CHD. Nevertheless, some of these novel agents provide arguments for continuing the search for an ideal SERM.

 

[Senri]

they may never come, if you use moderate aromatase inhibitor levels for you. individual "need" to suppress aromatase varies. also the "catch point" at which E suppression is too much is quite varied.

so you suggest use the body out or buy 6oxo and stack it with this till the bottle finishes then go about using clomid?

 

[macro]

1. never reccomend 6oxo. if you want to use another oral Aromatase inhibitor (AI), reccomend aromasin.
2. if you want to take clomid for a week and take a break from AIFM (or even use them together) thats fine.

if you are looking to add something to AIFM to improve pumps and gains.
PureCEE

if you are looking for OTC steroidals- generally dont reccomend most of them because they have a fairly unknown binding profile and no toxicity studies (methylated orals in particular). Though to be fair some of them are potent steroids, though IMO many of them are very toxic.

 

[macro]

^^

 

[Colin297]

BUMP

can i please have some info on AIFM?

Can it work to lower estrogen all over the body

Where is it applied?

And where can i get it?


Thanks