————————

1. Prisoner’s original protocol?

2. Prisoner later mentioned adding in AI or SERM use?

3. Prisoner mentioned being able to taper other AAS besides just test? (Something about masteron comes to mind).

4. Bushy mentioned adding peptides?

5. Anything outside of the above “standard” protocols?

Link to the original site

The usual stuff:

- You should be at least 21. No sense messing up your endocrine system, seeing as for all intents and purposes, PH’s are anabolic steroids.
- You should have training and nutrition under your belt. Like AAS, these compounds are NOT a magic pill.

Just popping a few capsules a day won’t net any magic results, but training hard, eating right and popping these pills can help you gain a few more pounds than you normally might.
- If you have access to AAS, use the AAS. Better gains, less (negative) sides.

I’m a 19 year old guy who cant put on weight…

Stop. Notice your age. In mathematical terms it looks like this:
19 < 21 = NO PH’s
Eat more. Sleep More. You will be able to gain weight. But pro-hormones may dramatically affect your body’s ability to produce and utilize testosterone in the future. Pro-hormones will act in a manner not unlike AAS, and will produce the same negative sides (with a few bonus negative sides thrown in for fun).

What is a PH?

A pro-hormone is a substance that is a precursor to a hormone, usually having minimal hormonal effect by itself. The term has been used in medical science since the middle of the 20th century. Examples of natural, human pro-hormones include pro-insulin and pro-opiomelanocortin.

How does this help me, the bodybuilder?

Well, when Anabolic Steroids were made illegal, many supplement companies made the move to circumvent this by creating precursors to a common anabolic steroids (like good old Testosterone). Even Biotest did this, and released the product known as MAG-10:

http://www.T-Nation.com/…g10s_here_3&cr=

Sweet! Where do I get this stuff?

Here’s the thing… you can’t. Not the good stuff anyway. In 2004, Premier Warlord George W. Bush signed the Anabolic Steroid Control Act of 2004 which made AAS and pro-hormones illegal. Unfortunately, a lot of the world has this idea that the FDA knows what they’re doing… so a lot of other countries have banned them too.

What?! Then why the hell did you made this thread you bastard?

Well here’s the thing: the ban only lists specific pro-hormones. Supplement companies are trying to keep one step ahead by creating different pro-hormones and of course - designer anabolic steroids. These are usually methylated anabolic steroids that have flown under the radar.

Some examples are:

- Epistane (also known as Havoc)
- Superdrol/Masterdrol
- Help me out guys, list some more!

This sounds too good to be true… whats the catch?

There’s a few:

1. A lot of these aren’t likely to be legal for too long.
2. Pro-hormones haven’t been tested as well as regular anabolic steroids. Simply put, we know about most (if not all) the side effects of AAS. We don’t know much about pro-hormones.
3. They are almost ALWAYS methylated anabolic steroids (like Epistane) which will be hard on the liver.
4. Gains are actually better with AAS.

Then wouldn’t AAS be a better option?

Yes. Unfortunately, not everyone has access to a supplier and for them, pro-hormones may well be the only choice.

Will I still need a PCT? And what is a PCT?

Post Cycle Therapy. A necessary part of hormone manipulation, which allows your body to return to its normal levels. Any large amount of exogenous testosterone will result in some form of shutdown, and you need to get your balls back in action! Most people will recommend Nolvadex run at 40/40/20 or something similar. Each case is different, and it’s up to you to do the research.

Most people will recommend Tamoxifen as part of your PCT, but it will vary from product to product. The usual PCT will consist of:

Week 1: 40mg Tamoxifen ED
Week 2: 40mg Tamoxifen ED
Week 3: 20mg Tamoxifen ED

Plus assorted cycle support products, such as Himalaya’s Liv 52.

So is it cool to stack Superdrol, Pheraplex and Trenadrol as my first stack?

No with a side of possibly. Generally its better to try running a non methylated pro-hormones first, and then step up to the methylated compounds second, due to the fact they’re harder on the body/liver than the non methyl’s. “Bridging” methyl’s (running one into the other) is in a quick phrase, somewhat nuts.

It’s an all out assault that’s usually attempted by someone with some decent pro-hormone experience under his belt. Most people will tell you NOT to run two methyl’s at one time, as it is a great way to kill off your liver.

If I take more of these than recommended will I have a heart attack?

Probably not, however as pro-hormones are relatively untested, it is suggested people start small and work up to a level that they feel comfortable with.

You could take twice the dosage, in theory but depending on the product that might just land you in the hospital. The effects WILL NOT double if you double the dose, you reach a point of diminishing returns where your body literally cannot process the amount of material you’ve ingested.

Most likely your sides will double, meaning you’ll earn a neato nickname like “Pizza Face” or “The Pillsbury Dough Boy” from increased skin oil or water retention respectively. For a first time out you should read the back of the bottle and stick to those parameters.

It is generally recommended to take the capsules will some sort of fat. One option is to down Fish Oil capsules (or Flameout) with each dose.

Will this show up in a drug test?

Yes and no. If you’re being tested for anabolic anabolic steroids, then yes, they will show up. If you’re being drug tested for a job odds are they’re looking for narcotics, hallucinogens, and most importantly weed.

How much/What do I have to eat?

Everyone is different. There’s a section called ‘Supplements & Nutrition’. Post there. More importantly, what are you doing this cycle for? Are you cutting or bulking? That all factors into diet requirements.

I’m going to go out partying with my friends and knock back a few. Is it cool to drink on these?

HELL NO. If you’re running a methylated cycle you liver is already taking a pretty beating, adding alcohol to that mix is NOT a good way to go. Not to mention the fact that alcohol basically stops protein synthesis entirely, which negates even taking the pro-hormones (or AAS) in the first place.

While non-methyl cycles are easier on the liver drinking alcohol is a great way to stuff up your diet and reduce your gains.

So I finished my cycle, can I start one tomorrow?

No.

Minimum time frame between cycles: Cycle + PCT + “Normalization Period” = Ready for your next cycle. What the hell is a normalization period? It’s however long your body needs to get back to where it was hormonally before you overloaded it with pro-hormones on cycle and then with anti-estrogen’s in PCT.

Your body will also use this period of time to do a little house cleaning on your cell receptors in your body making the next cycle as effective as the last one. The normal time will be at least the length of your PCT.

*********************************************

Pro-hormone “Traits”

The difference between “wet” and “dry” anabolic steroids/phs is water retention. Water retention is caused by estrogen conversion through aromatase.

WET:
- M1,4ADD
- Pheraplex
- M1T (and subsequent legal variants/clones)
- *Superdrol

DRY:
- Bold (Being reviewed by DEA for possible banning)
- Epistane (AKA Havoc)
- Tren
- *Superdrol
- Halodrol
- Winztrol (banned?)
- Furazadrol
- Prop

STRENGTH:
- Tren (Being reviewed by DEA for possible banning as we speak)
- Superdrol
- M1T(and legal clones)
- Pheraplex and clones (Being reviewed by DEA for possible banning as we speak)
- M14ADD

Pro-hormone Classification

Steroids are classified under 2 categories. Class I has a strong binding to the androgen receptor. Class II does not bind to the androgen receptors, rather it works through other means in the body.

Cliff’s notes of the above statement:

Class I = binds to androgen receptor
Class II = does not

These pro-hormone classifications are based on their steroid counterparts. If there are any revisions needed PLEASE post so below. If that goes unnoticed, PM me.

Class I

Boldenone based - 1,4AD & Bold
Progestin based - (similar to trenbolone) - Trenadrol & Trenaplex
Dienolone based - (again similar to tren) - Mdien
Mepitiostane (Thioderon) based - Epistane & Clones (like Havoc & so on so forth)
Desoxymethyltestosterone/DMT (Madol) based phs - Pheraplex & clones
Testosterone
DHT (Dihydrotestosterone) based phs - M5AA

Class II

Masteron (Dromostanolone) based - Superdrol & Clones
Oral Turinabol (Dehydrochlormethyltestosterone) based - Halodrol & Clones
Dianabol (methandrostenolone) based - M1,4ADD, M1T, 1-T, Methyl XT
Winstrol (stanozolol) based - Winztrol, Orastan-A, Furaguno, etc
Furazabol (miotolan) based - Furazadrol etc
Progesterone based - Revolt, Propadrol, Max LMG
Clostebol based - Chlorodrol, Oxyguno
4-AD

Not Pro-hormones…

AMS’s (Advanced Muscle Science) products - test boosters
Testabolan is not a prohormone, it is an ecdysterone, tribulus, oglio peptide product.
Superdrol NG - Prasterone = DHEA, Methyl Xanthine = Caffine, Aprodine HCL = Pseudoephedrine Hydrochloride, ATD - test booster/aromatase inhibitor

I would like to add that Mass Tabs is a prosteroid - 2a, 17a-dimethyl 17b-hydroxy 5a-androstan-1-ene-3-one however since its close to about 3-4 anabolic steroids/other prohormone compounds out there, I can’t classify it. I would guess its a class II though.

Stacking

If you plan on stacking two pro-hormones at the same time, the best combination are class I mixed with a class II. For example SD/Bold, Halo/Tren, M1T/Prop, and so on…

Here’s why:
When you take a class I/class I stack, you’re theoretically limiting your body’s ability to suck up the little steroid molecules you’re pumping into it. Think of it like a burger joint parking lot at lunchtime. There are no parking spots available, and you’re stuck lying in line wait for a spot to open up.

However, with a class I/class II combination while one pro-hormone floats around binding to the androgen receptor, the other little guy is busy attaching itself to other parts of the body to encourage growth.

**************************************

Now this post is far from complete. This is where that whole audience participation thing comes in. Chime in peeps!

Link to the original site

(more…)

ShareThis

Link to the original site

Gynecomastia, or gynaecomastia, is the development of abnormally large mammary glands in males resulting in breast enlargement, which can sometimes cause secretion of milk. The term comes from the Greek gyne (stem gynaik-) meaning “woman” and mastos meaning “breast”.

The condition can occur physiologically in neonates (due to female hormones from the mother), in adolescence, and in the elderly. In adolescent boys the condition is often a source of distress, but for the large majority of boys whose pubertal gynecomastia is not due to obesity, the breast development shrinks or disappears within a couple of years.

The causes of common gynecomastia remain uncertain, although it has generally been attributed to an imbalance of sex hormones or the tissue responsiveness to them; a root cause is rarely determined for individual cases.

Breast prominence can result from hypertrophy of breast tissue, chest adipose tissue and skin, and is typically a combination. Breast prominence due solely to excessive adipose is often termed pseudogynecomastia or sometimes lipomastia.

Gynecomastia should be distinguished from work hypertrophy of the pectoralis muscles caused by much exercise, e.g. swimming.

Some Causes:

Physiologic gynecomastia (also called Turcios Disease) occurs in neonates, at or before puberty and with aging. Many cases of gynecomastia are idiopathic, meaning they have no clear cause.

Potential pathologic causes of gynecomastia are: medications including hormones, increased serum estrogen, decreased testosterone production, androgen receptor defects, chronic kidney disease, chronic liver disease, HIV treatment, and other chronic illness.

Gynecomastia as a result of spinal cord injury and refeeding after starvation has been reported. In 25% of cases, the cause of the gynecomastia is not known.

Medications cause 10-20% of cases of gynecomastia in post-adolescent adults. These include cimetidine, omeprazole, spironolactone, imatinib mesylate, finasteride and certain antipsychotics.

Some act directly on the breast tissue, while others lead to increased secretion of prolactin from the pituitary by blocking the actions of dopamine (prolactin-inhibiting factor/PIF) on the lactotrope cell groups in the anterior pituitary.

Androstenedione, used as a performance enhancing food supplement, can lead to breast enlargement by excess estrogen activity. Medications used in the treatment of prostate cancer such as antiandrogens and GnRH analogs can also cause gynecomastia. Marijuana use is also thought by some to be a possible cause; however, published data is contradictory.

Increased estrogen levels can also occur in certain testicular tumors, and in hyperthyroidism. Certain adrenal tumors cause elevated levels of androstenedione which is converted by the enzyme aromatase into estrone, a form of estrogen. Other tumors that secrete hCG can increase estrogen.

A decrease in estrogen clearance can occur in liver disease, and this may be the mechanism of gynecomastia in liver cirrhosis. Obesity tends to increase estrogen levels.

Decreased testosterone production can occur in congenital or acquired testicular failure, for example in genetic disorders such as Klinefelter Syndrome. Diseases of the hypothalamus or pituitary can also lead to low testosterone.

Abuse of anabolic androgenic anabolic steroids (AAS) has a similar effect. Mutations to androgen receptors, such as those found in Kennedy disease can also cause gynecomastia.

Although stopping these medications can lead to regression of the gynecomastia, surgery is sometimes necessary to eliminate the condition.

Repeated topical application of products containing lavender and tea tree oils among other unidentified ingredients to three prepubescent males coincided with gynecomastia; it has been theorised that this could be due to their estrogenic and antiandrogenic activity.

However, other circumstances around the study are not clear, and the sample size was insignificant so serious scientific conclusions cannot be drawn.

Treatment:

Treating the underlying cause of the gynecomastia may lead to improvement in the condition.

Patients should talk with their doctor about revising any medications that are found to be causing gynecomastia; often, an alternative medication can be ft avoids gynecomastia side-effects, while still treating the primary condition for which the original medication was found not to be suitable due to causing gynecomastia side-effects (e.g., in place of taking spironolactone the alternative eplerenone can be used.)

Selective estrogen receptor modulator medications, such as tamoxifen and clomiphene, or androgens or aromatase inhibitors such as Letrozole are medical treatment options, although they are not universally approved for the treatment of gynecomastia.

Endocrinological attention may help during the first 2-3 years. After that window, however, the breast tissue tends to remain and harden, leaving surgery (either liposuction, gland excision, skin sculpture, reduction mammoplasty, or a combination of these surgical techniques) the only treatment option.

Many American insurance companies deny coverage for surgery for gynecomastia treatment on the grounds that it is a cosmetic procedure.

Radiation therapy is sometimes used to prevent gynecomastia in patients with prostate cancer prior to estrogen therapy. Compression garments can camouflage chest deformity and stabilize bouncing tissue bringing emotional relief to some. There are also those who choose to live with the condition.

Possible treatment for Gyno using Letro:

SERM - Selective estrogen receptor modulator. These drugs work by binding to the estrogen receptors and flooding them in a sense, making it difficult (but not impossible by any means) for estrogen to bind to the receptors and thus prevent the onset of estrogen related side effects.

Most common forms: Tamoxifen (Nolvadex), Clomiphene (Clomid)
AI - Aromatise Inhibitor. These drugs work by inhibiting the aromatization of estrogen. This means that in effect AI’s prevent androgens from converting to estrogen, again, making it difficult (but not impossible) for estrogen to reach receptor sites.

Most common forms: Anastrozole (l-dex, a-dex), Exemestane (aromasin), Femera (letrozole). For our purpose of reversing gyno we are interested in Letro.

Letro and your sex drive:
Letrozole will suppress your sex drive. This is another reason why it is so important to act on preventing gyno as soon as possible. Since we all know that Test should be run in every cycle this will cancel out the effect of sex drive suppression.

Running letro to prevent gyno:
If you decide to run estrogen protection while on cycle (and it’s suggested that you do unless you are aware that you do not require it), you can run either a SERM or an AI.

Letro will be the most powerful AI you can use, it will inhibit 98+% of estrogen using a dose as low as .25mg and even lower. This is why I suggest you do not use a dose higher than .50mg while on cycle just trying to prevent estrogen related side effects.

You will want to start running the letro approximately 2 weeks before you begin your cycle to allow it to fully stabilize in your blood. It’s been said that letro takes up to 60 days to stabilize, I don’t know if I buy into this for the reason that some have reversed gyno after using letro for only 1 week. Still to be safe, it’s recommended to start it before your cycle as stated above.

If you do decide to run letro there is absolutely no need to run another AI or SERM. Do not make the mistake of thinking more is better. Think of it this way; if letro is preventing the conversion of androgens to estrogen than there is no estrogen, what would the purpose of a SERM be when there is no estrogen to bind to the receptors? Nolva will only take away from the effectiveness of letro.

This brings me to my next point. Do not listen to anyone who tells you to bump up your nolvadex to 60+mg ED if you get gyno. I have no idea where this idea started but I have seen it suggest far too many times recently.

Nolvadex will do nothing to reverse your gyno, let me make that clear IT WILL DO NOTHING FOR GYNO. If you are running nolva as your anti-e and start to develop gyno than sure you can bump the dosage a small amount to try to prevent it from progressing further, but letrozole must begin ASAP.

It is very important that you begin taking letrozole immediately, the longer your wait the more risk you take in not being able to reverse it.

How do I know if I have gyno?
If you have developed gyno you will have a lump behind your nipple. It will be fairly hard, and it will be tender to touch.

Running letro to reverse gyno:
I am going to go over the three different scenarios which people could fit into. Remember regardless of what scenario you are in it is important that you begin taking the letro ASAP.

1. Already using an anti-e aside from letro.
2. Already using letro @ a dose of .25mg or .50mg ED.
3. Not running any estrogen protection.

1.
Day 1: .25mg Letro + anti-e*
Day 2: .50mg Letro
Day 3: 1.0mg Letro
Day 4: 1.5mg Letro
Day 5: 2.0mg Letro
Day 6: 2.5mg Letro **

2.
Day 1: .50mg Letro
Day 2: 1.0mg Letro
Day 3: 1.5mg Letro
Day 4: 2.0mg Letro
Day 5: 2.5mg Letro **

3.
Day 1: .50mg Letro
Day 2: 1.0mg Letro
Day 3: 1.5mg Letro
Day 4: 2.0mg Letro
Day 5: 2.5mg Letro **

*Regardless of the anti-e you are using it is important to still use it for the first day you begin letro as the letro will not have taken any effect and you by no means want your body to be without any protection when gyno is already prevalent.

** You will remain at this dose until gyno symptoms subside. Once you believe your gyno is gone it is important to stay at this dose for another 4-7 days to ensure all traces are gone. It’s recommended that people with a bf% over 15 stay on for a week as it may be harder to judge completely whether the lump is completely gone.

Once this period is over it will be important to taper letro down slowly rather than coming off it completely. Regardless of which manner you tapered up your dose you will all taper down in the same fashion.

Day 1: 2.0mg
Day 2: 1.5mg
Day 3: 1.0mg
Day 4: .50mg***
Day 5: .25mg
***You can remain at this dose or go down further to .125mg. It is really up to you at this point. They are both very common maintenance doses as an anti-e while on cycle. Personally, most have stayed with .25mg and never had a problem.

Letro and the estrogen rebound:
With your estrogen being completely inhibited there is a definite estrogen rebound as your body tries to re-stabilize the testosterone:estrogen balance. We can prevent this rebound effect by supplementing further with another AI or SERM.

So, it’s suggested that when you are coming to the end of your cycle you will more than likely be using Nolva in your PCT so just make sure that you begin taking nolva the last day you are going to take your letro and then continue on as you would with regular PCT.

This now leads us into the question of reversing gyno while not on cycle. There are a few things to remember here. You have already waited longer than you should have, and your sex drive will be shot.

You can use tribulus or another natural test booster to help you in this scenario but I can’t guarantee the effectiveness. Just follow gyno reversal protocols 2 or 3. When coming off again you must taper and begin using nolvadex to prevent any rebound effect that may occur.

How much nolvadex should you use if you are not going into PCT and running this off cycle? I suggest starting at 20mg ED for a week and then lowering it to 10mg for another week and then coming off completely.

Other Links:

http://www.gynecomastia.org/
http://www.plasticsurgery.org/…FTOKEN=44259626
http://www.gynecomastia.com/

Credits due to C-Bino, Wikipedia, Gynecomastia.org, WebMD, eMedicine.com, Familydoctor.com, and Gynecomastia.com

Link to the original site

Link to the original site

Link to the original site

Link to the original site

(more…)

ShareThis

Link to the original site

(more…)

ShareThis

Link to the original site

Link to the original site