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Hepa-Merz 5g/10ml konc.inf.tirp.10ml N10
Anotacija 

Hepa - Merz
Veiklioji medžiaga - L - ornitin - L - aspartatas.
Infuzijų tirpalo koncentratas ilgalaikei intraveninei infuzijai.

Vartojimo informacija. Prašom skaityti atidžiai!
SUDĖTIS
Vienoje 10 ml ampulėje yra 5,0 g L - ornitin - L - aspartato.
Vartojimas
Vaistas vartojamas sunkioms ūminėms ir lėtinėms kepenų ligoms, pavyzdžiui,
kepenų cirozei, riebalinei kepenų distrofijai, hepatitui intensyviai gydyti, kai yra padidėjęs amoniako kiekis kraujyje; jis labai tinka prasidedančiam sąmonės sutrikimui gydyti, taip pat sąmonei sutrikus (įvykus komai).
KONTRAINDIKACIJOS
Hepamerco negalima vartoti, jei yra sunkių inkstų funkcijos sutrikimų
(inkstų nepakankamumas), pavyzdžiui, kai kreatinino kraujo serume yra
daugiau kaip 3 mg/100 ml.
ŠALUTINIS POVEIKIS
Pavieniais atvejais atsiranda virškinamojo trakto sutrikimų (pykinimas,
vėmimas), kurie sumažinus vaisto dozę arba infuzijos greitį paprastai
praeina, todėl dėl jų vaisto vartojimo nutraukti nereikia.
Dozavimas ir vartojimo būdas
Jeigu nepaskirta kitaip, gydant ūminį kepenų uždegimą (hepatitą), reikia
infuzuoti 1 - 2 ampules per dieną, gydant lėtinį kepenų uždegimą ir kepenų
cirozę - 2 - 4 ampules per dieną.
Prasidėjus sąmonės sutrikimui (prekomai) ir sąmonei pritemus (įvykus
komai), priklausomai nuo ligonio būklės per 24 valandas reikia infuzuoti
iki 8 ampulių, maksimalus infuzijos greitis - 5 g per valandą.
Hepamercą galima maišyti su įprastiniais infuzijų tirpalais, tačiau kad
jis tiktų infuzuoti į veną, 500 ml infuzijų tirpalo negalima tirpinti
daugiau kaip 6 ampulių infuzijų tirpalo koncentrato.
Ypatingi nurodymai
Vartojant dideles dozes, reikia kontroliuoti šlapalo kiekį kraujo serume
ir šlapime.
Jeigu kepenų funkcija žymiai susilpnėjusi, siekiant išvengti virškinamojo
trakto sutrikimų (pykinimo, vėmimo), infuzijos greitį reikia nustatyti
individualiai.
Hepamerco infuzijų tirpalo koncentrato nevartoti, pasibaigus jo tinkamumo
laikui.
Vaistą laikyti vaikams neprieinamoje vietoje!
Merz + Co. GmbH & Co . 6000 Frankfurt/ Main 1
_____________________________________________________________________
PAKUOTĖ
10 ampulių, kurių kiekvienoje yra 10 ml infuzijų tirpalo koncentrato.
Savybės
Hepamerco sudėtyje esantis L - ornitin - L - aspartatas amoniaką padaro
nekenksmingą, šlapalo cikle didindamas jo sintezę. Be to, jis detoksikuoja
ir ekstrahepatinį amoniaką audiniuose.

Už vertimo tikslumą atsakau
Doc. A.Milašius
Tekstą redagavo V.Jurkienė

Hepatil 500mg/5ml inj.N10
Anotacija 

Tvirtinu
Valstybines vaistu kontroles tarnybos viršininkas
V. Budnikas
1999m.
Informacija vartotojui

Hepatilio injekcijų tirpalas
Ornithini Aspartas
Ornitino aspartatas
Vaisto sudetis
L-ornitino L-aspartatas ir injekciju vanduo.
Savybes ir poveikis
Hepatilio veiklioji medžiaga L-ornitino L-aspartatas yra junginys,
padarantis nuodus organizme nekenksmingus. Jis ypac veiksmingas sutrikus
kepenu veiklai, kai organizme kaupiasi amoniako, t.y. medžiagos,
sukeliancios neurotoksini poveiki, perteklius. Medikamentas veikia šlapalo
sintezes ciklo reakcijas ir kepenu lastelese vykstancia glutamino sinteze.
Ornitinas dalyvauja šlapalo sintezes ciklo reakcijose ir jas aktyvina, be
to, iš aspartato sintetinami pirimidinai, kuriuos organizmas suvartoja
nukleorugšciu sintezei pažeistose kepenu lastelese.
Medikamentas nesutrikdo organizmo elektrolitu bei rugšciu ir šarmu
pusiausvyros.
INDIKACIJOS
* Sunki kepenu liga, del kurios gali atsirasti encefalopatija (pvz.,
piktnaudžiavimo alkoholiu, virusu ar kitokiu priežasciu sukeltas kepenu
pažeidimas).
* Kepenu veiklos nepakankamumo sukelta encefalopatija, kepenu koma arba
bukle prieš ja.
KONTRAINDIKACIJOS
* Sunkus inkstu veiklos nepakankamumas (kreatinino koncentracija didesne
negu 3 mg%).
* Neštumo ir žindymo laikotarpis.
* Amino rugšciu apykaitos sutrikimas, pvz., del fermentu trukumo.
Rekomenduojamos atsargumo priemones
Jei kepenu veikla labai sutrikusi, doze reikia mažinti (pvz., vartoti puse
iprastines dozes), priešingu atveju gali sutrikti virškinamojo trakto veikla.
Saveika su kitais vaistais
Saveikos su vaistais ir kitokiomis medžiagomis nepastebeta.
Dozavimas ir vartojimo budas
Medikamento doziu intervalas labai platus. Dažniausiai rekomenduojamas
toliau nurodytas dozavimas.
Vyresniems negu 7 metu pacientams reikia 2 kartus per diena i vena letai
suleisti arba sulašinti po 0,5 g (viena ampule) preparato. Tokia doze
reiketu vartoti 3-4 savaites. Jei liga sunki, per diena galima injekuoti net
4 ampules.
Jaunesniems negu 7 metu vaikams reikia vartoti puse suaugusio žmogaus dozes.
Gydymo trukme priklauso nuo ligos eigos.
ŠALUTINIAI POVEIKIAI
Pavieniais atvejais sutrinka virškinamojo trakto veikla (atsiranda pykinimas
ir vemimas) bei pasireiškia alergine odos reakcija.
Žinotina!
Prieš pradedant vartoti preparato, reikia patikrinti, ar nepasibaiges ant
pakuotes nurodytas tinkamumo laikas. Jei jis pasibaige, medikamenta vartoti
draudžiama.
Preparata reikia laikyti tamsioje, vaikams neprieinamoje vietoje.
Pakuote
Dežute, kurioje yra 10 ampuliu. Vienoje ampuleje (5 ml) yra 0,5 g
veikliosios medžiagos.
Gamintojas
AB farmacijos fabrikas "Pliva Krakow",
ul. Mogilska 80,
31 - 546 Krokuva, Lenkija.
Spec. redaktorius - doc. A. Milašius
Teksta redagavo V. Jurkiene

Ne draudziami, o parduodami su receptu.

Paskutinį kartą taisė Antana5 (2008-09-17 19:01)

Ar šiuos preparatus galima vartot kaip alternatyvą Tribulus Terrestris papildams?Ir iš kur būtų galima gauti šių preparatų?

o tas tamoxifen citrate ne tas pats ten kur vaistinej parsiduoda tamoxifenas ?

o po trumpo prohormono kurselio kokia doze ir kiek laiko to tamoxifeno gerti ?

Masteron as an Anti-Estrogen

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

by Anthony Roberts, Author of Anabolic Steroids - The Ultimate Research Guide

Discussion of pharmaceutical agents below is presented for information only. Nothing here is meant to take the place of advice from a licensed health care practitioner. Consult a physician before taking any medication.

I know it must seem like I sit around all day trying to find new uses for old drugs, but in this case, nothing could be further than the truth. Before I get into how and why you can use Masteron as an Anti-Estrogen, I?ll tell you a bit about where this idea came from, and why I?m telling you about it. And yes, this works in real life, not just on paper - I?ve used it and seen it used for this purpose successfully by several athletes.

A few years ago, I wrote my first piece on Masteron (Drostanolone Propionate), and discovered what its clinical use actually was: Reduction of breast cancer tumors, and as hormonal treatment of breast cancer. Well?the long version of that is that Masteron is an androgenic, anabolic steroid, used as an agent used to prevent or inhibit the growth of cancerous tumors.

Then, in one of those weird "duh" moments, I realized that gynocomastia, mastectomy, and Masteron all had that similar word root. You?d think that having an English degree would have helped me notice this fact sooner?anyway, I wrote the profile and didn?t think much about it anymore. I was then contacted by the owner of an underground lab, and asked why Masteron was always produced with a propionate ester, and whether it would be ok with a longer ester. This began another long period of research for me into Masteron. Well, I found out that Masteron would be fine with a longer ester, but I actually had a chance to test it out with that particular ester before it hit the market...I was still standing after 3 weeks on it, so it was produced en masse (as a side note that particular Underground Lab still produces it and it?s one of their better selling products).

So here I was with all of this research on Masteron and nothing to do with it. Well, after I took another look at the compound, a couple of things struck me. The first that struck me is that Masteron is made for women! Yeah?go back and read that again if you have to. Masteron is one of the few steroids that were actually created with women in mind, not men, and it?s the one that most people tell women to avoid! And the other thing that I noticed right away was that it is used for treatment of breast cancer. In particular, it?s used for the treatment of estrogen dependant breast tumors. By now, I?m sure you see where I?m going with this?Nolvadex is used clinically for this same purpose, as is Arimidex, Femera, Aromasin (a steroidal Aromatase Inhibitor), and Teslac (a steroid, technically). That?s some good company to be in, if you?re a steroid. But interestingly, Teslac is actually a steroid also, and Aromasin is a Steroidal Aromatase Inhibitor. So why can?t a "real" steroid do the same job at preventing breast cancer? Well, the answer is that it can!

To understand why Masteron can be used as an anti-estrogen, first we need to know that it?s derived from DHT. Why is this important?

This is important because DHT directly inhibits estrogenic activity on tissues. It is possible that it does this, possibly by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen receptor binding. Either way, it has multiple hypothesized mechanisms of action in some tissues. It has also been hypothesized that DHT actually suppresses estrogen?s effects not by inhibition of synthesis of estrogen receptor, but by (get ready?big words coming up) decreasing estrogen-induced RNA transcription at some point after the actual estrogen receptor binding has occurred. This means, in much simpler terms, that the estrogen gets to the receptor, but just doesn?t do its job (1). This means you can take steroids that convert to estrogen (called aromatizable steroids) and not worry about that estrogen possibly making you retain water, gain fat, or watch "Desperate Housewives." Also, this could mean that the antiestrogenic effect of DHT is mediated by an androgen receptor mediated mechanism. In fact, DHT has been shown to prevent the estrogen-dependent augmentation of the progesterone receptor in human breast cancer cells. And, not to be redundant, but it?s important to remember that virtually all of the anti-estrogens we use to control gyno and water retention are also used to treat breast cancer. So, now we know have observed that androgens are capable of inhibiting both the estrogenic induction and the ongoing stimulation of PRc synthesis, but have no apparent effect upon basal concentrations of this receptor. Dihydrotestosterone (DHT) demonstrates a very high degree of inhibition of estrogen in human breast cancer cells. (2). But it?s not just DHT that does this; its metabolites have been shown to inhibit aromatization itself; DHT, androsterone, and 5alpha-androstandione are all potent inhibitors of the formation of estrone from androstenedione. In fact, it's so potent at reducing estrogen that transdermal DHT gel applied to the affected area has been used to treat gynocomastia (3). DHT is such a potent anti-estrogen that it been even been used to increase height in children with short stature, and since it?s been determined that this increase is not due to GH-mediated effects, it was strongly suggested that DHT?s anti-estrogenic effects are the mechanism by which it can increase height (4) Of course, I suspect I don?t need to tell you that DHT is structurally incapable or converting to estrogen?

So all of this tells us that DHT will certainly have beneficial effects on keeping our estrogen in check, but what about Masteron? Can it be used as effectively? Well, let?s take a look at what Masteron actually is, relative to DHT. But before we can do that, I think a quick explanation of DHT is in order first. Don?t worry; I?ll make it as brief and painless as possible.

DHT is actually the result of testosterone interacting with the 5alpha-reductase (5a-R) enzyme. This enzyme is present in the scalp, prostate, external genitalia, and other places. As far as I can see, it apparently exists for the sole purpose of converting a steroid with a double bond between carbon 4 and carbon 5 to one with a single bond between them, and subsequently adding a hydrogen atom to each carbon. This process is called (of course) 5alpha-reduction.


+

5a-Reductase

=

Testosterone

Dihydrotestosterone

So now we know how testosterone becomes Dihydrotestosterone. And everything would be great if this is the only thing that happened to our good old friend testosterone, because as you may already know, DHT is a far more potent androgen than testosterone. But, unfortunately, this is not the end of the story, because DHT is largely deactivated by the enzyme 3-alpha Hydroxysteroid Dehydrogenase (3bHSD), which is mainly present in skeletal muscle.

For our purposes here, we?re only going to be concerned with one particular action of this enzyme. It can either converts a steroid with a keto group on position 3 of the steroid to one with a hydroxy group in that position, thus converting DHT is to androstanediol. This conversion is part of reason DHT alone has not proven to be a very effective muscle builder, as androstanediol is not going to be very anabolic at all. If you look off to the left of the following molecular diagram, and compare it to the one above for DHT, you?ll notice that the "O" (oxygen) has been replaced with an "HO" (hydrogen + oxygen) at the third position:

Androstanediol

3bHSD is present all over the body (as is 5a-R, for the most part), but is found in especially high concentrations in the scalp and prostate, and it?s even possible that its actions on DHT will exacerbate male pattern baldness in the former tissue. Also, it?s worth noting that DHT is the androgen responsible for development of external genitalia. This is most likely the reason that women experience a temporary clitoral hypertrophy when they use the often recommended steroids (Primobolan, Anavar, Winstrol, etc?) in excessive doses. In an interesting aside, I find it really interesting that the most typical steroids recommended are the most likely to cause clitoral enlargement and other possible androgenic effects. But on the bright side, in my experience with female athletes, that first effect is most welcome...actually, topical DHT can even be used to treat Microphalia (extremely tiny genitalia) in males (5). This last fact, if you?ve ever wondered, is the type of information discussed behind closed doors by of owners and staff of "private/invite-only" anabolic steroid boards and forums?for obvious reasons?

Ok, so now you know what DHT is, where it comes from, what it can do, and why it?s not a particularly potent anabolic when used alone. Here?s what Masteron is, relative to its parent compound, DHT. Masteron is an injectable steroid that is simply the DHT molecule which has been altered to be 2alpha-Methyl-DHT?you can see this modification by comparing the DHT molecule above with the following Masteron one, and paying special attention to the left hand side again, and the "H3C" modification:


Masteron, aka Drostanolone Propionate

This 2-alpha-methyl alteration makes it much more potent anabolic, although it?s still only about 60% as anabolic as testosterone and a quarter as androgenic. I?m going to speculate that these ratings make it not the most potent anabolic in the world, but its anti estrogenic effects plus its ability to increase aggression make it a very nice pre-contest addition. This is also where we get the absurd rumor that Masteron won?t do anything for you unless you?re already at a very low body-fat percentage. This is not true at all. No matter what body-fat percentage you?re at going to get a nice anti-estrogenic effect from Masteron, as well as some nice aggression and strength in the gym - the former and latter are both known as "non-genomic" effects, and are a result of the strong Central Nervous System stimulatory effects of Masteron, which is very common with DHT derived steroids. Basically, if you?re fat, and you take something that increases aggression and has anti-estrogenic effects (Halotestin and Arimidex, lets say), you wouldn?t expect to get huge and ripped. It?s the same thing with Masteron. Now, what if you add in Arimidex and Halotestin to a pre-contest cycle, you?ll get harder and look better. That?s exactly what?ll happen if you add Masteron into a Pre-contest cycle. It?s not that you have to be at some random body-fat percentage to get results from it, but you?ll need to be at that lower body-fat percentage to "see" those results. Again, if you?re fat and take Halo and Arimidex, you aren?t going to look much better?think of Masteron in similar terms, but it won?t work as well for aggression as Halotestin, and won?t be as good for combating estrogen as Arimidex. Gauged against either one of them alone, Masteron will likely make you look much harder and lift more weight. But if you are looking to do a low dosage cycle with a minimal amount of compounds in it, a simple Testosterone (propionate) and Masteron cycle may be exactly what you are looking for. On a personal note, that is a cycle that I use very frequently, at about 100mgs of each, shot every other day.

But has Masteron actually lived up to my claims for being an anti-estrogen? Yes. From 1968 to 1972, a decent sized study was conducted on Masteron, in a group of premenopausal women with breast cancer. About a third responded well to Masteron (6). This is because of its anti-estrogenic effects, clearly- though it doesn?t perform as well as Arimidex, Letrozole, or Aromasin. If you?re not running huge amounts of aromatizable steroids, this is a very good choice to add into your cycle. If you?re doing large amounts of those compounds, then you need to use a traditional anti-estrogen as your ancillary compound of choice. But if you?re running well under a gram of aromatizable steroids, Masteron will likely be all the anti-estrogen you need. This number comes from my person experience, as well as others I?ve interviewed.

Now, as a bit of an addendum, I?d like to address the use of Masteron in women. Lets get this straight: Masteron was developed for women. Okay? Got me? If you? ve been paying attention up to this point, you already know that Masteron is intended for females and is derived from the same root (DHT) as most other steroids commonly used and recommended for female athletes (Primobolan, Anavar, Winstrol, etc?are all derived from DHT). And, another shocking fact is that Masteron has a lower androgenic rating than almost every other commonly recommended steroid used by female athletes. Anavar has a rating of 24 compared to oral testosterone and Masteron has a rating of 25 compared to testosterone, expressed as a percent (so yes that means 24% and 25% respectively).

Basically, Masteron works as a hormonal therapy for breast cancer and has been shown to be a useful and safe agent for females of all age groups, even though it may appear to be less effective then other possible therapies in postmenopausal patients (6). It is, therefore, very safe for women. Masteron is certainly no less safe than Anavar or Primobolan for women, as long as it?s used with something resembling a degree of respect and intelligence.

My recommendations for female use of this compound would be to start between 10-25mgs every third day, and increase dosages from there if no side effects are experienced. At those dosages, I suspect no side effects would be experienced, and I?d be comfortable saying none will be experienced up through 20mgs, injected every other day.

So there you have it. A totally new way to look at an old friend - Masteron - it?s useful as an anti-estrogen as well as an anabolic, and can certainly be safely used by both Men as well as women.


About The Author

Anthony Roberts has been researching anabolic steroids for over a decade and is the author of the new book, Anabolic Steroids: Ultimate Research Guide. He began his research at the age of seventeen while he was a competitive martial artist, ultimately winning a silver medal in his state martial arts tournament in the black belt division. His firsthand experience in steroids began after he switched sports and began playing rugby, in which he ultimately made two consecutive appearances at the hooker position in the national collegiate all-star games.

Netrinkit straipsnio sio Sita ateiti reikes paverst kai notebook isigysiu

Taboo rašė:

Pasitvirtina visi faktai apie masteron kaip apie antiestrogena..
Tapo vienu mano megiamiausiu prepu

Vienintelis minusas - norint palaikyti reikiama doze gaunasi mazumele brangokai. Svarsciau apie masteron'a savo ziemos bulkinge kaip apie anti-e bet 40ml sueitu kaip niekas jei laikyt panasiai 400mg per savaite.

woolf rašė:

Kolegos patarkit ka ir kiek reiktu pasiimti issivalymui nuo:
30ml fenilo?
20ml propiko?
20ml masterio?
20ml winio?

Buciau dekingas, jei kazkuris parasytumet, kokio vaisto ir kokio kiekio jo reiketu.

6 sav, proviron tamoxifen ir laiko hcg tikrai nesiulysiu

Ka patartumėt naudot atsistatymui po decos ir sustos kurso?

Paskutinį kartą taisė manodarbai2 (2008-12-15 12:28)

http://forums.steroid.com/showthread.php?t=198848
I am starting this thread after tons of reading, and taking advice from the more prominent members from various boards. I just wanted to summarize a bunch of useful threads here, bringing it together in one post and simplifying the popular substances used to control estrogen/progesterone/cortisol and restore natural test levels. Ill go over the compounds briefly, and summarize at the end of the post. I'd like to thank Anthony Roberts for his input on this thread. A few definitions before you start :

SERM's (Selective Estrogen Receptor Modulator) : These block certain estrogen receptors, ***ending on the drug, and dont actually lower estrogen in the blood. Estrogen is left to circulate with nowhere to go. Because of this, SERMS have a positive effect on cholesterol levels. They have a negative effect on IGF-1, so if bulking, only take them if totally necessary. They are good at blocking gyno. Commonly used during PCT, and less often used while cycling. A SERM like nolvadex is widely used in PCT to help kickstart the HPTA back to normal function, in conjunction with other beneficial drugs. To learn how this works, please refer to Anthony Roberts PCT in the PCT section.

AI's (Aromatase Inhibitors) : There are 2 types of AI's. Type I (suicide inhibitor) attaches to the aromatase enzyme and permanently disables it. Type II compete for the enzyme, but dont destroy it. Both are effective at lowering estrogen substantially. Both are commonly used during both cycling and PCT. Used mainly when low estrogen levels are desired, like contest preparation/cutting. Beware that lowering estrogen with strong AI's can have a negative effect on cholesterol levels and low estrogen levels can lead to sore joints, cause your losing estrogens anti-inflammitory effect. Can also have a negative impact on your libido. Estrogen has an important role in mass building and joint health, as noted below where "estrogen" is explained.

RI's (Reductase Inhibitors) : These drugs stop the conversion of testosterone into DHT wherever 5-alpha reductase enzymes are present. RI's work by blocking the action of the 5-alpha. There are 2 5a's. Type I 5a and Type II 5a. Different RI's block one or both of these 5a's. The main reason someone uses RI's is to stop hairloss. They are common anti hairloss drugs. The problem is, when you block the dht conversion, there are less androgens available and may reduce your gains. Sometimes people report less strength, aggression and drive to train.

Estrogen : The first hormone we need to keep an eye on. Many AAS convert to estrogen via the aromatization process. Some AAS are worse than others. Also, estrogen spikes after a cycle. High levels of estrogen leads to gyno, water retention, fat storage etc. Estrogen plays a key role in progesterone related gyno. We either block its receptors with SERMS or reduce its production with AIs. We watch estrogen levels during a cycle and in PCT. Lowering estrogen too much will mess up your blood lipids. Letting it get out of control will cause sides like gyno, water retention etc. Estrogen plays a role in IGF-1 levels, may lower IGF-1 when blocked with a SERM. Estrogen is also beneficial hormone when bulking, promoting higher androgen receptor concentrations (!). It also is beneficial in another way - its supposed to act as an anti-inflammatory - this means blocking or reducing it too much during a heavy bulking cycle can result in injury to joints. Obviously different estrogen levels are desired for different goals, and it is not always good to block its action or its production. Usually, while bulking, estrogen is allowed to rise unless gyno or water retention (leading to high blood pressure) becomes a problem. When cutting and shedding water and lifting a little lighter (contest prep for example) estrogen is usually dropped with an AI. Proper diet and training can help the bad side effects high estrogen can have.

Progesterone : Its not so much progesterone that we watch, which is actually a healthy hormone, but progestins which may act upon its receptors. Progestins, like Tren or Deca (nor-9's), may act on its receptor or lower progesterone in the blood. Gyno and lactating are more common side effects. Some people use progesterone receptor blockers to combat this, or a prolactin production inhibitor.

Cortisol : The third hormone, the stress hormone. When elevated to long, it will store fat. Eat muscle. Cause lethargy. Moodiness. You may crave carbs by the boat load. Cortisol spikes after a cycle because AAS blocks it while on cycle, upping cortisol production and receptor sites. IMO not enough attention is payed to this. It has special functions in the body that are absolutely necessary, like its anti-inflamitory ability. However, when elevated for long periods, it turns into a muscle eating beast. The most important time to watch cortisol is after a cycle, when it spikes. There are a couple ways to help control this, explained below.

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

Now that you brushed up on some defentions, here are some useful compounds :


SERMS (Selective Estrogen Receptor Modulation)

Nolvadex (Tamoxifen Citrate) : Nolvadex is a SERM. It selectively binds to certain estrogen receptors, effectively blocking the estrogen and stopping unwanted sides such as gyno. It DOES NOT lower estro levels in the blood, it only blocks it from binding to certain receptors. It also helps your blood fat levels. It does not suppress LH, blocks desired estro receptors and helps stop HCG from desensitizing your testicles to natural LH. Nolva should be used during HCG therapy, at 20 mg a day, for the reason i just mentioned. Can be used during cycle if you see signs of gyno. Its mainly used to block the estrogen spike when you come off cycle, and should be used right through to the end until natural test levels are back. One drawback to consider about Nolva is that it may cause progesterone receptors to become more sensitive. This means that while using progestins such as Deca or Tren, you may become more sensetive to progestin related gyno.

Faslodex (Fulvestrant) : Approved for use in 2002 for breast cancer research, this drug is unlike most we have seen. It is classified as an estrogen receptor downregulator. It prevents estrogen from exerting its influence on the estrogen receptor. Similar to Nolvadex, but is not selective. It hits all estrogen receptors. It also does this to progesterone receptors to a lesser degree. It is injectable, at 250mg a month. No information on how it affects blood lipids. It is also very expensive.

Clomid (Clomiphene Citrate) : This drug is also a SERM, almost identicle to Nolva. It is said to be a weaker blocker mg for mg than Nolva. Its common use is in PCT, usually for about a month, used after HCG and all AAS esters have run out of your body. Even though it is weaker than Nolva at blocking, it is believed to be quicker at bringing HPTA back to balance. Both are commonly used during PCT. It binds to different receptors than Nolva. There is a lot of debate on this, but until there is solid proof, it may be prudent to include this in your PCT. Commonly taken at about 100mg a day.

Fareston (Toremifene Citrate) : This is a second generation SERM. Approved for use in 1997. Chemically very similar to Nolva and Clomid, it is less powerful mg for mg. Fareston may have a stronger posotive effect on your cholesterol levels. For those who find this an important issue, this is a drug of choice. Used every day at around 60mg.

Evista (raloxifene) : A newer SERM, Evista is shown to be a blocker in breast tissue, but acts as a receptor agonist in bone tissue (unlike Nolvadex). This action promotes bone density. Taken at about 60mg a day. Evista may prove to be very beneficial, as it also helps cholesterol levels (like Nolvadex). Evista is supposed to have a more powerful gyno blocking effect than Nolvadex.

Cyclofenil : Much like Nolvadex, this is also a SERM. Used at about 600mg a day, it is weaker mg for mg. A good alternative if Nolva is not available, which is usually not the case.


AI (Aromatase Inhibitors)

Teslac (Testolactone) : This is a first generation steroidal aromatase inhibitor. Like a suicide, it permanently attaches to the aromatase enzyme. Taked at a maximum of 250mg a day. It is not as strong as the newer AI's, but some people still like to use it. It can lower estrogen about 50%. Streroidal in structure, it has no anabolic effect.

Aromasin (Exemestane) : This drug is classified as a Type I Suicide AI. It binds to the aromatase enzyme and kills it. It is effective at lowering estrogen up to 85%. Once again, you have to watch out for your cholesterol levels. Used mainly for cutting when low estrogen levels are desired. Aromasin is shown to help bone density. Clinical doses are about 25mg a day, but it has been shown that as little as 2.5mg a day can be as effective.

Lentaron (Formestane) : A Type I Suicide AI. Lentaron is not classified as a drug, and can be sold over the counter as a suppliment. Not as strong as the third generation AIs (arimidex, femera). Can lower estrogen by about 60%. Used as an injectable, it is dosed at about 250mg every 2 weeks. Due to poor bioavailability, daily doses of oral Lentaron are about 250mg.

Arimidex (Anastrozole) : This is a widely used type II AI. It competes with estrogen for the aromatase enzyme. This effectively lowers estrogen up to 80% in the blood. Approved for use in 1995 to fight breast cancer. At doses up to 1mg a day, it has been shown to be very effective at controlling estrogen while on cycle or in PCT. It is usefull for curbing the effects that come with aromatizing AAS's while in cycle, and can be used in PCT. Nolvadex is shown to decrease the effectiveness of Arimidex when used together. In this case a suicide inhibitor may be more well suited, like in PCT. It is also called L-dex, in its liquid form.

Femera (Letrozole) : Letro is a competative Type II AI also. Also farely new compared to other compounds, it is shown to be effective at lowering estrogen by blocking the aromatase enzyme. Doses up to 2.5mg a day are used, but usually as low as .5mg a day can be just as effective. Clinical studies show Femera to lower estrogen by 75-78%, sometimes up to 95%. Once again, watch out for your blood lipids (cholesterol) to get out of whack. There may a noted rebound effect of estrogen levels that goes along with Letro use.


Cortisol Control

Cytadren (aminoglutethimide) : This drug has the ability to reduce cortisol at higher doses (1000mg a day), and act as an AI at lower doses (250mg a day). The cortisol effect is shortlived if taken for a number of consecutive days. Can lower estrogen a lot, anbout 90%. The higher dose has a long list of sides. More effective as an AI.

Mirtazapine :This is used to lower cortisol. Even though it may be effective in cortisol control, Johan has pointed out that it may cause some phycological side effects, like making you feel like a zombie. Here is a pubmed abstract for is effects on cortisol levels, among other things.http://www.ncbi.nlm.nih.gov/entrez/...1&dopt=Abstract

Cytodyne (Phosphatidylserine) : This is also used to lower cortisol, but is only effective in lowering about 30%. There are other ingredients in Cytodyne than Phosphatidylserine. Phosphatidylserine is the only real proven ingredient to lower cortisol, or so ive gathered so far. Effective at 800mg a day of PS as an ingredient.

Relacore : This over the counter cocktail of herbs and vitamins and minerals is supposed to reduce the amount of cortisol in your blood. I find it chills me out a little, however i read some places that it may raise estrogen. I used it for a bit, however I dont bother any more.

Vitamin C: At doses of about 1.5 grams a day, can have a lowering effect on elevated cortisol, not to mention its other healthy effects.


LH Repalacement Therapy - Testosterone Stimulating Drugs

HCG (Human Chorionic Gonadotropin) : HCG is a replacement for your natural LH (luteinizing hormone). LH is what your body produces to tell your testicles to produce natural testosterone. LH levels drop when using AAS (HPTA suppression). Using HCG while on cycle prevents testicular shrinkage, speeding PCT when the time comes. Using Nolva while using HCG helps stop HCG from de-sensitizing your testicles to natural LH. In my opinion, any decent cycle/PCT should include HCG. It has been suggested to me that HCG can be used throughout a cycle at 500iu E4D, but im unsure of this from practical experience. The most favorable way is to use it in the last couple weeks of your cycle at a higher dose, like 500iu ED. The trick is to end the use of HCG just as the last AAS is running out of your system. So, 3 weeks before the the last ester leaves your blood, you would start the HCG/nolva combo. HCG at about 500iu ED and Nolva 20mg ED. This is done before Nolva/aromasin (for example) PCT starts, and runs about a few weeks longer than the end of the HCG. Always include Nolva with your HCG, they work together well. Be careful not to overdose on HCG and permanently desenstize your testicles to LH. HCG has an active life of about 3 days. Vitamin E is a booster, read the next one :

Vitamin E : As Anthony Roberts pointed out to me, vitamin E increases the response to HCG. This may be useful in making the low doses of HCG we use more effective at growing back shrunken testicles. Doses can be generally 1000iu a day while using HCG.


Progesterone Control

Lilopristone, Onapristone: These are progesterone blockers also, said to be safer and possibly more effective than RU-486 when it comes to progesterone blocking. They were developed after RU-486 in an attempt to make more effective, less harsh drugs to block progesterone.

Dostinex (Cabergoline), Bromo (Bromocriptine), B-6 : These are used for Deca/Tren gyno sides. This type of gyno is related to progesterone and its receptors. Tren/Deca may act on the progesterone receptor, as they are progestins, and may increase prolactin in the blood (causing lactating). These drugs stop production of prolactin at the pituitary gland. Controlling estrogen levels with an AI also helps here, as progestins themsleves haven't been proven to cause gyno.

RU-486 (Mifepristone - abortion pill) : This drug has the ability to block estrogen, progesterone AND cortisol. It may or may not be very well tolerated, but I would like to find out more about it, as it is used in the bodybuilding world. In PCT it is used to block cortisol and progesterone. A powerful drug that may turn out to be a good choice, but i need more evidence and feedback from experience useing RU-486. Check out this thread i have going if you would like to learn more about it :
http://forums.steroid.com/showthread.php?t=180912


RI's (5a Reductase Inhibitors)

Proscar (Finasteride) : This is primarily a Type II 5-alpha blocker. This means that when you are taking a high dose of testosterone, the resulting conversion of test to DHT in certain parts of the body become to high for ones own comfort, mainly hairloss and prostate enlargement. This is where the type II 5a enzymes are mainly found. This will not work against AAS that are already highly androgenic by design, without conversion. AAS like Tren will still exhibit high androgenic properties. Used at doses up to 5mg a day.

Avodart (Dutasteride) : Like Proscar but newer and more effective at blocking the effects of DHT in not only the scalp and prostate (which are Proscar's main strengths) but also in the skin, effectively reducing acne. This is because Avodart will block both Type I and Type II 5-alpha enzymes, covering more of the problem areas due to DHT. Available in .5mg softgels, this is an effective dose. Approved for use in 2002.


Fat Burning, Anti-Catabolic

Clen (Clenbuterol) : Clenbuterol is a bronchodilator. Everyone knows clen is used to burn fat. Why am I listing it here in a PCT thread? Well, for its anti-catabolic properties. Clen may lower the effect of AAS while on cycle, so I personally dont use it while cycling. It does, however, have an effect on cortisol levels. While on cycle, cortisol is not to much of a problem if you eat right. AAS use increases cortisol production, and increases receptor sites. This means that when you finish a cycle, cortisol spikes along with estrogen. This is a part of the "crash" that is often overlooked. People have reported that blocking cortisol in PCT speeds along fat loss. Clen is supposed to have a blocking effect on cortisol. So, along side of its ability to burn fat, it is anti catabolic in it ability to block cortisol until desired hormone levels are achieved in PCT. For me, it makes sense to use clen in PCT until desired hormone levels are achieved, as it also burns away fat in the process.



SUMMARY and RECOMMENDATIONS

All AAS can supress the HPTA, even in small doses, thus lowering natural LH. Factors that affect ones ability to recover quickly are genetics, cycle length or steroid type. Some AAS will shut you down hard and fast, some not so bad. Some lucky people can rebound quickly without medications, but many need it to avoid a crash and losing muscle/gaining fat. It is in our best interest to use the appropriate medications in the CORRECT doses to keep sides down (like bloat), grow quickly and keep quality mass when we are done our cycles. Most of us can get away with using 2 or 3 compounds to keep sides to a minimum, rebound quickly, and keep gains we worked hard for. Higher levels of AAS (and therefore higher estrogen/progestins) may require more intense hormone control and heavier PCT. Remember, we are aiming to level out estrogen, progesterone, cortisol and testosterone. In PCT, we are trying to achieve equilibrium of the HPTA, getting FSH (follicle stimulating hormone) and LH (luteinizing hormone) back to normal. Keeping our hard earned gains is obviously our first priority.

In short, we generally use :

AI's - While on cycle to "dry up" or lower estrogen because of a persons sensetivity to it (if needed). Used in PCT for the same reason and to help get back to homeostasis. Usually used with a SERM in PCT.

SERM's - to block estrogen while on cycle (if needed) or to help kickstart the HPTA during PCT (most common use). Usually used with an AI in PCT.

HCG - To prevent testicular shrinkage during a cycle, or to encourage them to grow back more quickly. Usually used with an AI and SERM in PCT as the last AAS run out of your body, and stopped a few weeks before your SERM and AI.

Keep in mind these are generally accepted guidelines and everyone has their own preferences. I hope this post helps out, as i wrote it for beginners who are having a hard time searching through the massive amount of info... this thread will be updated as often as i learn something new... feel free to offer suggestions. Enjoy!

nu antanas teisus,pilnas googlas,ire man jokios naudos is jos:rolleyes: