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Thread: Estrogen Will It Effect My Gains
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Estrogen Will It Effect My Gains
ESTROGEN
Will it effect my gains ?
BY Merc.
When you talk about testosterone you also usually hear words like , estrogen and aromatase ..
Most people that use AAS understand that testosterone converts to estrogen ( via the aromatase enzyme) this causes problems like bloating , gyno as well as other sides .. People have been posting alot about using AI's and asking about how estrogen relates to gains.
Well estrogen is important in building muscle. Estrogen has been connected to increasing GH and IGF-1 . Testosterone's effects are dependent on aromatization to esterogen ..
If you look at what they give cattle to put on mass its estradiol. If they use only One compound to put mass on they use estradiol ( Anthony Roberts did a radio interview on this recently) .. Estrogen's role is an important one .. You hear of alot of people that use AI's reporting that thier gains are greatly reduced . The AI's reduce thier estrogen levels too much which effects Growth factors( GH , IGF) and reduces thier gains.
I have a buddy that had done 2 cycles. The first using test E at 500 mg every week with Adex at 0.5 EOD.. For his second cycle he used 600 mg of Cyp every week with 40 mg of Dbol everyday for a kick start and Adex at 0.5 EOD.. He ate right and trained right on both of his cycles .. He was not gaining on his cycles like he should have been ( and yes his gear was legit ).. I had told him about estrogen's role in building muscle.. He listened but didn't really understand everything about it .. I explained it again and he started to catch on to what I was explaining.. This was at the end of his second cycle.. He made an appointment with his Doc and asked him if he could order some blood work .. The doctor ordered a total testosterone and total estrogen blood test.. His estrogen was extremely low.. He then finished his cycle and did a proper pct and took time off to recover ..
Than he did another cycle using Dbol, Test E 600 mg per week, no AI . This time around he totally transformed his body . People that didn't see him in a few months didn't even recognize him. He went to the doctor again and asked for blood work while he was on cycle ( wk 7 I think) .. This time his estrogen was high ( something like 300 ng/ml, 120 ng/ml or less is in range).. His strength was through the roof and he said that there was a great sense of well being and that his energy level was way up. There were no real sides that where experienced. I saw him alot while he was on cycle and he never really looked bloated.
If you do a search on here you will see that alot of people are reporting that AI's are effecting thier gains .. I think AI's are a important compound to consider using, but keep in mind that estrogen's role is a important one .
Gyno also needs estrogen to form ( as well as progesterone, GH and IGF). So you also need to take into consideration that too much estrogen can cause problems....
Well there has been a lot of people asking if taking an AI will effect gains so I wanted to write this to give a little bit of input on estrogen's effects on building muscle..Last edited by Merc..; 02-04-2008 at 10:49 PM. Reason: changed font
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10-25-2007, 08:50 PM #2
Very informative Merc... and at just the right time for me. I have all my AI's and SERM's on hand and i know what to look for. i think i'm going to lay off all of them for a bit and see what happens. i don't know why i was so paranoid to begin with... i went damn near 18 weeks my first cycle with no AI's until the very end... my gains werer phanominal compared to this cycle, which i am using arimidex or letro eod in very small amounts (.15mg/dose). thanks again
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10-25-2007, 08:51 PM #3
im one of the unlucky ones that if i dont take an AI my nipples kill me. I dont want man boobies..
nice post merc
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10-25-2007, 09:32 PM #4
nice post merc. I never use anything while bulking, unless it is to control gyno. I still have not figured out the right balance for cutting though. If i take arim I dont get the water and estrogen fat gains, but I dont gain muscle and feel horrible and flat, if I dont take anything it is just the opposite.
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10-25-2007, 09:34 PM #5
good post merc!!!
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10-25-2007, 10:13 PM #6New Member
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Originally Posted by 305GUY
great post!
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Originally Posted by 305GUY
What doses of test do you use ?
Merc.
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Originally Posted by buffgator
Merc.
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10-25-2007, 11:04 PM #9
i dunno what doses he uses but i have the same problem. i HAVE to take ridiculous amounts of either letro or adex to control it...... never use more than 450mg test/ same of deca
Last edited by 5ifthCitizen; 10-25-2007 at 11:09 PM.
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Bump
Merc.
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10-26-2007, 08:26 AM #11Anabolic Member
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Originally Posted by Merc.
Estrogen roles thrue the GH, IGF pathway, would then be insignificant, Even when using a strong AI.
Is there other pathways that estrogen could be anabolic ?
There seems to be easier to recover from a cycle when using an AI though, its very possible that high estrogen levels could harm the leydig cells...
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10-26-2007, 08:33 AM #12
Good Info. Thanks Merc
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10-26-2007, 09:09 AM #13Associate Member
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Yea Merc, I'm with 305 guy too..if i dont use ai's my nipples hurt. I do know what you mean the role of estrogen. I'm on a current cycyle and im using less ai then ususal and my gains are so much better. nipples are sensitive still and im on letro.
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Originally Posted by vitor
I would like to get some feedback from people who used GH and an AI in thier cycle ?
Merc.
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10-26-2007, 09:52 AM #15
awesome as always merc, thanks
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Originally Posted by pgilligan10
Merc.
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10-26-2007, 11:31 AM #17
good post merc.
whats your opinion on AI's during pct? i have found great sucess with them...
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10-26-2007, 11:46 AM #18Originally Posted by anhukem
Originally Posted by Merc.
ive tried armidex .5mg EOD but i notice on the day i dont take it my nips really bother me.
i've also tries .5mg ED which works great for my nips but really affects my sex drive negatively.
My perfect dose is .25mg ED which controls nipple ssoreness quite well but if some how i put pressure on my nip is when my nip kills me!
OFF TOPIC: does anyone else not like the new board format where if a new post quotes an old one, the new one goes straight up to the old post. maybe i'm weird. lol
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good read merc....
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Originally Posted by number twelve
I am on HRT now but when I did pct I used Hookers protocol..
Merc.
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10-26-2007, 12:19 PM #21Anabolic Member
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One thing that is for sure; higher estrogen levels on a cycle will make you hold more water and glycogen(this will be less pronounced the leaner you are). If someone is 15%bf or higher chances are there will be significant more water stored in fat-cells, when estrogen levels go up.
Since this will increase scaleweight and bodysize, people will often mistakenly think they are gaining more...But higher scaleweight doesnt need to mean more LBM. So, not using an AI can sometimes give you an false impression of gains...
But the question remains: Is Estrogen anabolic thrue another pathway than by increasing levels of gh/igf?
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10-26-2007, 12:37 PM #22
I would love to not take AI's...but I have to...or here come man titties.
I wish I wasn't gyno prone.... I would most certainly make better gains.
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10-26-2007, 12:40 PM #23Anabolic Member
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Originally Posted by football2007
If you take nolva, yust replace that with GH at a suitable dosage, to make up for the decrease nolva will make in igf levels.
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10-26-2007, 12:43 PM #24
I'm using NPP at the moment...so using nolva is kinna outta the question.
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Originally Posted by vitor
4-androstenedione ..
Merc.
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10-26-2007, 12:53 PM #26
very informative post merc.
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10-26-2007, 01:41 PM #27Originally Posted by Merc.
tried letro from .5 to 1.5mg/day. helps the gyno about 80-90%.
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10-26-2007, 01:54 PM #28
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Originally Posted by mr newbreed
Nolva increases PgR and gives more for the 19 nors ( trens) metabolites to bind to and can possibly increase your chances of getting gyno..
Merc.
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10-26-2007, 02:09 PM #30
so leave it alone?.if gyno was to start what would i be using
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Originally Posted by mr newbreed
Some people dont have any problem when using nolva with 19 nors but almost everyone I know has had problems..
You could use letro or adex...
Also could look into using caber....
Merc.
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10-26-2007, 03:07 PM #32
whats caber bro,ive never heard it...and what ml should i run the letro?
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Originally Posted by mr newbreed
Also
You could try like .25 mg ED or EOD on the Letro .. You might have to mess with the dose to see what works best for you..
Cabergoline
From Wikipedia, the free encyclopedia
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Cabergoline
Systematic (IUPAC) name
N-[3-(Dimethylamino)propyl]-N-[(ethylamino)carbonyl]- 6-(2-propenyl)-8g-ergoline-8-carboxamide
or
1-[(6-allylergolin8ß-yl)- carbonyl]-1- [3-(dimethylamino)propyl]-3-ethylurea
Identifiers
CAS number 81409-90-7
ATC code G02CB03 N04BC06
PubChem 54746
DrugBank APRD00836
Chemical data
Formula C26H37N5O2
Mol. mass 451.604 g/mol
Pharmacokinetic data
Bioavailability First-pass effect seen; absolute bioavailability unknown
Protein binding Moderately bound (40% to 42%); concentration- independent
Metabolism Hepatic, predominately via hydrolysis of the acylurea bond or the urea moiety
Half life 63-69 hours (estimated)
Excretion Urine (22%), feces (60%)
Therapeutic considerations
Pregnancy cat. C(US)
Legal status ℞-only(US)
Routes Oral
Cabergoline (brand names Dostinex® and Cabaser®), a lysergic acid amide derivative, is a potent dopamine receptor agonist on D2 receptors.[1] It also acts on dopamine receptors in lactophilic hypothalamus cells to suppress prolactin production in the pituitary gland. It is frequently used as a second-line agent in the management of prolactinomas when bromocriptine is ineffective.
Contents [hide]
1 Pharmacokinetics
2 Carcinogenity
3 Uses
4 Off-label/recreational uses
5 Contraindications and precautions
6 Pregnancy and lactation
7 Side effects
7.1 Valvular heart disease
8 Interactions
9 Dosage
10 References
[edit] Pharmacokinetics
Following a single oral dose, resorption of cabergoline from the gastrointestinal (GI) tract is highly variable, typically occurring within 0.5 to 4 hours. Ingestion with food does not alter its absorption rate. Human bioavailability has not been determined since the drug is intended for oral use only. In mice and rats the absolute bioavailability has been determined to be 30 and 63 percent, respectively. Cabergoline is rapidly and extensively metabolized in the liver and excreted in bile and to a lesser extent in urine. All metabolites are less active than the parental drug or inactive altogether. The human elimination half-life is estimated to be 63 to 68 hours in patients with Parkinson's disease and 79 to 115 hours in patients with pituitary tumors.
[edit] Carcinogenity
In rodents a dose-dependent increase in malignant tumors has been found. The correlation is thought to be species specific. No clinical data exists on carcinogenity in humans.
[edit] Uses
Monotherapy of Parkinson's disease in the early phase.
Combination therapy, together with levodopa and a decarboxylase inhibitor such as carbidopa, in progressive-phase Parkinson's disease.
Adjunctive therapy of prolactin-producing pituitary gland tumors (microprolactinomes).
In some countries also: ablactation and dysfunctions associated with hyperprolactinemia (amenorrhea, oligomenorrhea, anovulation, and galactorrhea).
[edit] Off-label/recreational uses
It has at times been used as an adjunct to SSRI antidepressants as there is some evidence that it counteracts certain side effects of those drugs, such as reduced libido and anorgasmia. It also has been suggested online that it has a possible recreational use in reducing or eliminating the male refractory period. It is also used by bodybuilders to control gynecomastia caused by elevated prolactin levels caused by use of Nandrolones.
[edit] Contraindications and precautions
Hypersensitivity to ergot derivatives
Pediatric patients (no clinical experience)
Severely impaired liver function or cholestasis
Co-medication with drugs metabolized mainly by CYP P450 such as erythromycin and ketoconazole, because increased plasma levels of cabergoline may result (althoug cabergoline undergoes minimal CYP450 metabolism).
Cautions: severe cardiovascular disease, Raynaud's Disease, gastroduodenal ulcers, active gastrointestinal bleeding, hypotension.
[edit] Pregnancy and lactation
Pregnancy: Approximately 100 female patients became pregnant under therapy with cabergoline for hyperprolactinemic conditions. The incidence of spontaneous abortions and congenital abnormalities was comparable to nontreated patients. Nevertheless, women wishing to become pregnant should wait a period of four weeks after discontinuation of cabergoline. Patients becoming pregnant under therapy should terminate cabergoline immediately, if possible.
Lactation: In rats cabergoline was found in the maternal milk. Since it is not known if this effect also occurs in humans, breastfeeding women should not be treated.
[edit] Side effects
Approximately 200 patients with newly diagnosed Parkinson's disease participated in a clinical study of cabergoline monotherapy. Seventy-nine (79) percent reported at least one side effect. These side effects were chiefly mild or moderate:
GI tract: Side effects were extremely frequent. Fifty-three percent of patients reported side effects. Very frequent: Nausea (30%), obstipation (22%), and dry mouth (10%). Frequent: Gastric irritation (7%), vomiting (5%), and dyspepsia (2%).
Psychiatric disturbances and central nervous system (CNS): Altogether 51 percent of patients were affected. Very frequent: Sleep disturbances (somnolence 18%, insomnia 11%), vertigo (27%), and depression (13%). Frequent: dyskinesia (4%) and hallucinations (4%).
Cardiovascular: Approximately 30 percent of patients experienced side effects. Most frequent were hypotension (10%), peripheral edema (14%) and non-specific edema (2%). Arrhythmias were encountered in 4.8%, palpitations in 4.3%, and angina pectoris in 1.4%.
In a combinatiion study with 2,000 patients also treated with levodopa, the incidence and severity of side effects was comparable to monotherapy. Encountered side effects required a termination of cabergoline treatment in 15% of patients. Additional side effects were infrequent cases of hematological side effects, and an occasional increase in liver enzymes or serum creatinine without signs or symptoms.
As with other ergot derivatives, pleuritis, exudative pleura disease, pleura fibrosis, lung fibrosis, and pericarditis are seen. These side effects are noted in less than 2% of patients. They require immediate termination of treatment. Clinical improvement and normalization of X-ray findings are normally seen soon after cabergoline withdrawal.
The reported incidence and severity of side effects in hyperprolactinemic patients was comparable.
[edit] Valvular heart disease
In two studies published in the New England Journal of Medicine on January 4, 2007, cabergoline was implicated along with pergolide in causing valvular heart disease.[2][3] Both drugs are ergot-derived dopamine agonists, although their molecular skeletons are different. As a result of this, the FDA removed pergolide from the U.S. market on March 29, 2007.[4] Since cabergoline is not approved in the U.S. for Parkinson's Disease, but for hyperprolactinemia, the drug remains on the market. Treatment for hyperprolactinemia requires lower doses than that for Parkinson's Disease, diminishing the risk of valvular heart disease.
[edit] Interactions
No interactions were noted with levodopa or selegiline. The drug should not be combined with other ergot derivatives. Dopamine antagonists such as antipsychotics and metoclopramide inhibit the clinical action of cabergoline and should therefore not be used concomitantly. The use of antihypertensive drugs should be intensively monitored because excessive hypotension may result from the combination.
[edit] Dosage
Parkinson's disease: Monotherapy: Initial dose should be 0.5 mg daily. The usual maintenance dose is 2 to 4 mg daily. Combination therapy: Usually 2 to 6 mg daily.
Tumors of the pituitary gland and other hyperprolactinemic conditions: Initially 0.5 mg per week, slowly titrated to 4.5 mg per week, if necessary.
Ablactation: According to specific treatment scheme.
[edit] References
^ Dostinex at www.rxlist.com. Retrieved on 2007-04-27.
^ Schade, Rene; Andersohn, Frank & Suissa, Samy et al. (2007-01-04), "Dopamine Agonists and the Risk of Cardiac-Valve Regurgitation", New England Journal of Medicine 356 (1): 29-38, <http://content.nejm.org/cgi/content/full/356/1/29>
^ Zanettini, Renzo; Antonini, Angelo & Gatto, Gemma et al. (2007-01-04), "Valvular Heart Disease and the Use of Dopamine Agonists for Parkinson's Disease", New England Journal of Medicine 356 (1): 39-46, <http://content.nejm.org/cgi/content/full/356/1/39>
^ Food and Drug Administration Public Health Advisory (2007-03-29). Retrieved on 2007-Last edited by Merc..; 10-26-2007 at 10:12 PM.
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10-26-2007, 03:24 PM #34Anabolic Member
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Originally Posted by Merc.
100mg clomid ed would block the E-recepter in the chest effectively, despite what many people think of clomid as an anti-gyno agent.
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Originally Posted by vitor
Keep in mind it takes about 150 mg of clomid to accomplish what 20 mg of nolva bascially can..
Merc.
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10-26-2007, 06:55 PM #36Information
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Moved
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10-26-2007, 07:36 PM #37New Member
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great post bro, very informative
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Originally Posted by #Admin#
Merc.
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10-27-2007, 04:59 AM #39
so just to finalize,do you recomend running any AI even if there is no sign of gyno,or should it be used as and when needed?
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10-27-2007, 05:51 AM #40
good post Merc...always comin through in the clutch.
I dont need any AI's during cycle - I may use nolva to keep bloat down but thats it...PCT i always used to use clomid and nolva but this time around I am going to use Aromasin and nolva.
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