rHGH Guide

rHGH Guide
According to studies in the New England Journal of Medicine GH use will:
Shed Bodyfat, Increase Muscle Tone; Boost your Energy, Strength, and Endurance
Reduce Wrinkles and Create Tighter, Smoother Skin; Help you Sleep Better, Improve Sex Drive and Performance, Improve Immune and Heart Function, Bone Density, Healing Time and Cholesterol, Improve Brain Function, Memory and Mental Focus

Wow! Sure sounds like a wonder drug to me! Yeah right, anyway here is some real world information for bodybuilders. Somatropin (rHGH) is produced by the pituitary gland and is responsible in adolescence for growth of tissues, protein deposition, and the breakdown of sub-q fat stores. As we age, growth hormone levels decrease but still remain active in the body, releasing in cycles during the day. Synthetic growth hormone used exogenously by bodybuilders is a 191 chain sequence of amino acids that replicates the bodies natural production of growth hormone.

Growth hormone has been in use by bodybuilders since the early 1980’s, though at this time, HGH was being extracted from the pituitary glands of cadavers and had enormous side effects, most prominently Creutzfeldt Jacob disease. This is a rare and fatal brain disease, it need not be discussed here since it is not possible in synthetic forms of rHGH, but if you want more info just run a search in google. rHGH stimulates growth in most body tissues which is due to an increase in cell number rather than cell size. This includes muscle tissue as well as internal organs, hence the dreaded GH gut.

Use of growth hormone by bodybuilders will cause increased muscle size, localized and overall bodyfat loss, increased protein synthesis, increased glucose output by the liver, increased insulin resistance and lowered thyroid output. Stored fats will be used as a primary fuel source, thus the body fat loss.

So is rHGH the wonder drug everyone lusts after? It certainly is beneficial but not for everyone. You must be willing to take risks to achieve maximum benefits from its use, as well as substantial financial investment. Do it right the first time or don’t do it at all! You will achieve faster and greater growth from cycles of steroids than with GH, though once you reach a plateau, not many products work better.

Ok, so now you have decided that this is the drug for you and you are ready to try it, so what next? Well here are some general guidelines to follow for maximal results from GH use:

Daily injections are a must to maintain stable blood levels as GH has a very short life span in the body. It will peak almost immediately after injection and will clear the body with a half-life of only 20-30 minutes. It is best injected first thing in the morning upon rising to raise levels that are very low from sleeping, and immediately after training. I do not recommend injecting before bed as many bodybuilders do, since that is the time of day that your body will release naturally high levels of growth hormone, and exogenous use will only block that release. If you take it in the morning when levels are low, after training when levels are depleted and then let your body release while sleeping, you are getting one extra release for free! GH is best taken long term, short cycles do not maximize the benefits of muscle cell increase, only fat loss. Here is how I take my GH for maximum benefits:

6iu ed injected sub-q, preferably in the stomach
3iu injected upon rising, 3iu injected immediately post-workout
10iu insulin taken 30 minutes after GH injection
25mcg cytomel ed
use of androgens such as testosterone

The timing of GH and insulin injections is critical. If insulin is injected before the GH, your pancreas will stop release of insulin monitoring due to the exogenous source. GH when injected will mobilize stored glycogen release which will turn into glucose for energy. This will cause a rapid rise in blood sugar levels that will not shut down or stop rising due to the feedback loop being momentarily cut off. You will go hyperglycemic and end up in the hospital. You must first inject your GH, then the insulin; this will cause a rise in glucose release by the GH and will be controlled and shuttled into muscle tissue for repair by the later injection of insulin.
Use of cytomel or some type of T3 hormone is critical since GH use will severely lower thyroid levels. Small exogenous sources are necessary to maintain normal levels and 25 mcg ed is sufficient. This will also aid in body fat loss by maintaining proper thyroid functioning.
Use of androgens is also necessary due to the promotion of anabolism by increasing muscle size that benefits the new cell number increase by the GH. Remember GH will not directly cause muscle cell size increase, just the number of cells, therefore, androgens are necessary to increase size. Testosterone or trenbolone are both highly androgenic and perfect for out stack.

One myth that needs to be cleared up: high doses of GH use and the 5 on 2 off program. First, if you find that you are not achieving results off of 4-6iu ed, than something else is the problem, not your dose. The use of high doses if primarily cause by heat damage to the protein chain causing denatured proteins. This will decrease the effect and you must use higher doses to achieve the same effect. Other reasons for high dose use are; fake gh, not using insulin, cytomel or test, poor diet, improper timing schedule and the 5 on 2 off. This program was recommended by dealers as a way to move product by offering a lower cost cycle. No doctor in the world would recommend this protocol, Peak blood concentrations are reached in 2-6 hours after injection, and therefore, multiple daily injections are necessary to achieve stable release schedule and results. If you take your last injection Friday afternoon, and then not again till Monday morning, then you have negated all effects offered by the 6 hour concentratio. Yes, you will achieve results using a 5 on 2 off program, but not as well as if you inject ed. It’s your money; I can only tell you how to optimize use.

Side effects of GH use include; carpal tunnel syndrome, tingling in the extremities, numbness in the hands and feet, increased organ growth, decreased insulin reception, acromegaly but only in extreme dose use, and decreased thyroid output causing fat accumulation. If you find that you are experiencing any of the above side effects, lower your dose immediately. This is especially important with carpal tunnel. If you feel like your wrists are hurting then lower the dose until pain subsides. You do not want to have that surgery, trust me.

GH is a fantastic product, beneficial for many reasons. Most people will experience thinning of the skin, increased vascularity, fat loss, permanent increases in muscle size due to the cell number increase, and overall feelings of wellness. You will probably need less sleep and feel supercharged all day long. I highly recommend GH use, but only when you have the money to do it right. 4-6 month cycles are optimal, year round if you are over age 35. If you have anything of benefit to add to this thread, feel free to contribute or PM me.

This was posted in the "Very Basix Question on T3/ GH" thread by Mr. Vic. All thanks go to him. But I was wondering if you had any input, especially the final conclusion at the very end of the artice: "If you’ve been using GH without T4, you’ve been wasting half your money – and if you’ve been using it with T3, you’ve been wasting your time. Start using T4 with your GH, and you’ll finally be getting the full results from your investment."

Thyroid Hormone + Growth Hormone
(IF you aren’t using T4 with your GH, you’re not doing it right)
By Anthony Roberts with James Daemon, PhD.

 

Quite some time ago, I wrote a book on Anabolics, and since then, I’ve received quite a bit of feedback on it. Some of the information contained in the book is based on the 50-60 profiles I completed for Steroid.com’s main page. As a result, I get feedback on certain portions of the book from people who have read them online.

When someone takes the time to send an e-mail to Steroid.com or AnabolicBooks LLC, they’re screened, and eventually some of them make their way to my e-mail account. AnabolicBooks LLC is publisher- a little known fact is that my book is actually wasn’t edited by me, nor do I own the rights to any of it. When they forward an e-mail to me, I typically consider it very carefully, and reply to the original sender. If amendments or additions are useful for anything I’ve previously written (readers frequently send me recently published studies), I typically reply and thank the person for their help.

This time, something odd happened. I was forwarded an e-mail from AnabolicBooks, and the reader seemed to know what he was talking about, but (I thought) mistaken about interactions between Growth Hormone and Thyroid medication. I took a look at the e-mail, and knew that I could quickly find a study that I had saved previously, to send to the reader, to verify that the claims in my work on GH were sound.

In this particular case- James Daemon, PhD- was the reader, and was correct in his assessment of the interaction between thyroid hormone and Growth Hormone. And, in direct contradiction, so was I. Thyroid medication decreases the anabolic effect of Growth Hormone. And it increases it.
Huh?

There’s some leaps here, because research in some of the necessary areas is sketchy (or not done yet), but if you read the entirety of this article, you’ll learn how to get a significantly more gains from Growth Hormone, for pennies a day, by the addition of a readily available (and cheap) addition to it. And yeah, it’s a drug you can get anywhere on the ‘net, very easily. And no, it’s not a steroid.
In fact, I’ll go so far as to say you’re throwing away a substantial portion of your gains from growth hormone if you are not using this drug with it.

Ok…I’ll explain things a bit further. First, a brief explanation of Thyroid Hormone as well as Growth Hormone may be necessary.

Your thyroid gland secretes two hormones that are going to be of primary importance in understanding Thyroid/ GH interaction. The first is thyroxine (T4) and the second is triiodothyronine (T3). T3 is frequently considered the physiologically active hormone, and consequently the one on which most athletes and bodybuilders focus their energies on. T4, on the other hand, is converted in peripheral tissue into T3 by the enzymes in the deiodinase group, of which there are three types- the three iodothyronine deiodinase either catalyze the initiation (D1, D2) or termination (D3) of thyroid hormone effects. The majority of the body's T3 (about 80%) comes from this conversion via the first two types of deiodinase, while conversion to an inactive state is accomplished by the third type.

It’s important to note that not all of the body’s T4 is converted to T3, however- some remains unconverted. The secretion of T4 is under the control of Thyroid Stimulating Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlled through release of Thyrotropin Releasing Hormone which is produced in your hypothalamus. So, when T3 levels go up, TSH secretion is suppressed, due to the body’s self regulatory system known as the “negative feedback loop” . This is also the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. However, it should be noted that thyroid stimulating hormone (like all other hormones) can not work in a vacuum. TSH also requires the presence of Insulin or Insulin-like Growth Factor to stimulate thyroid function (1) When thyroid hormone is present without either insulin or IGF-1, it has no physiological effect (ibid).

Most people think that T3 is just a physiologically active hormone that regulates bodyfat setpoint and has some minor anabolic effects, but in actuality, in some cases of delayed growth in children, T3 is actually too low, while GH levels are normal, and this has a growth limiting effect on several tissues (2) This could be due to T3’s ability to stimulate the proliferation of IGF-1 mRNA in many tissues (which would, of course, be anabolic), or it could be due to the synergistic effect T3 has on GH, specifically on regulation of the growth hormone gene. Although it is largely overlooked in the world of performance enhancement, regulation of the growth hormone response is predominantly determined by positive control of growth hormone gene transcription which is proportional to the concentration of thyroid hormone-receptor complexes, which are influenced by T3 levels. (3)

At this point, just to give you a better understanding of what’s going on, I think it’s prudent to also give a brief explanation of Growth Hormone ( GH) as well.

Your body’s GH is regulated by many internal factors, such as hormones and enzymes. hormones. A change in the level of your body’s GH output begins in the hypothalamus with somatostatin (SS) and growth hormone-releasing hormone (GHRH). Somatostatin exerts its effect at the pituitary to decrease GH output, while GHRH acts at the pituitary to increase GH output. Together these hormones regulate the level of GH you have in your body. In many cases, GH deficiency presents with a low level of T3, and normal T4(
4). This is of course because conversion of T4-T3 is partially dependant on GH (and to some degree GH stimulated IGF-1), and it’s ability to stimulate that conversion process of T4 into T3.

Interestingly, the hypothalamus isn’t the only place where SS is contained; the thyroid gland also contains Somatostatin-producing cells. This is of interest to us, because in the case of the thyroid, it’s been noted that certain hormones which were previously thought only to govern GH secretion can also influence thyroid hormone output as well. SS can directly act to inhibit TSH secretion or it may act on the hypothalamus to inhibit TRH secretion. So when you add GH into your body from an outside source, you are triggering the body into releasing SS, because your body no longer needs to produce its own supply of GH…and unfortunately, the release of SS can also inhibit TSH, and therefore limit the amount of T4 your body produces.
But that’s not the only interaction we see between the thyroid and Growth Hormone.
As we learned in high-school Biology class, the body likes to maintain homeostasis, or “normal” operating conditions. This is the body’s version of the status quo, and it fights like hell to maintain the comfort of the status quo (much like moderators on most steroid discussion boards). What we see with thyroid/ GH interplay is that physiological levels of circulating thyroid hormones are necessary to maintain normal pituitary GH secretion, due to their directly stimulatory actions. However, when serum concentrations of thyroid hormone increase above the normal range we see an increase in hypothalamic somatostatin action, which suppresses pituitary GH secretion and overrides any stimulatory effects that the thyroid hormone may have had on GH. The suppression of GH secretion by thyroid hormones is probably mediated at the hypothalamic level by a decrease in GHRH release(5).
In addition, as IGF-I production is increased in the hypothalamus after T3 administration and T3 may participate in IGF-1 mediated negative feedback of GH by triggering either increased somatostatin tone and/or decreased GHRH production (6). IGF, interestingly, has the ability to mediate some of T3’s effects independent of GH, but not to the same degree GH can (7.) In fact, IGF-I production is increased in the hypothalamus after T3, administration it may plausibly participate in negative feedback by triggering either increased somatostatin tone and/or decreased GHRH production. So we know that GH lowers T4 (more about this in a sec), but an increase in T3 upregulates GH receptors (8) as well as IGF-1 receptors (9,10).

As can be previously stated, and due to the ability of GH to convert inactive T4 into active T3, GH administration in healthy athletes shows us an entirely predicatble increase in mean free T3 (fT3), and a decrease in mean free T4 (fT4) levels.(11)

Interaction between GH, IGF-I, T3, and GC. GH stimulates hepatic IGF-I secretion and local production of growth plate IGF-I, and exerts direct actions in the growth plate. Circulating T3 is derived from the thyroid gland and by enzymatic deiodination of T4 in liver and kidne.. The regulatory 5'-DI and 11ßHSD type 2 enzymes may also be expressed in chondrocytes to control local supplies of intracellular T3 and GC. Receptors for each hormone (GHR, IGF-IR, TR, GR) are expressed in growth plate chondrocytes.

So, with the use of GH, what we see is an increased conversion of T4-T3, and possible inhibition of Thyroid Releasing Hormone by Somatostatin, and therefore even though T3 levels may rise, there is no increase in T4 (logically, we see a decrease). Now, as we’ve seen, GH is HIGHLY synergistic with T3 in the body, and as a mater of fact, if you’ve been paying any attention up until this point, you’ll note that the limiting factor on GH’s ability to exert many of it’s effects, is mediated by the amount of T3 in the body.

As noted before, T3 enhances many effects of GH by several mechanisms, including (but not limited to): increasing IGF-1 levels, IGF-1 mRNA levels, and finally by actually mediating the control of the growth hormone gene transcription process as seen below:

Comparison of the kinetics of L-T3-receptor binding abundance to changes in the rate of transcription of the GH gene.(3)

As you can see, T3 levels are directly correlative to GH gene transcription. The scientists who conducted the study which provided the graph above concluded that the amount of T3 present is a regulatory factor on how much GH gene transcription actually occurs. And gene transcription is what actually gives us the effects from GH. This last fact really seems to shed some light on why we need T3 levels to be supraphysiological if we’re going to be using supraphysiological levels of GH, right? Otherwise, the GH we’re using is going to be limited by the amount of T3 our body produces. However, since we’re taking GH, and it is converting more T4 into T3, T4 levels are lowered substantially, and this is the problem with GH. and may actually be THE limiting factor on GH…if we assume that at least some of GH’s effects are enhanced by thyroid hormone, and specifically T3, then what we are looking at is the GH that has been injected is being limited by a lack of T3. But that doesn’t make sense, because if we use T3 + GH, we get a decrease in the anabolic effect of GH.

This is where Mr. Daemon, who had contacted me via an e-mail to my publisher, about Thyroid + GH interaction, was able to shed some light on things. You see, I knew that it couldn’t just be the actual presence of enough T3 along with the GH that was limiting GH’s anabolic effect, because, simply adding T3 to a GH cycle will reduce the anabolic effect of the GH (12.).

Originally, he had said to me that T3 was synergistic with GH, wheras I said that T3 actually reduced the anabolic effects of GH- now I realize we were both correct. Logically this presents a bit of a problem, which I believe can be solved. This came from reading several studies provided to me by Dr.Daemon. the trend I was seeing was that even when Growth Hormone therapy was used, T3 levels needed to be elevated in order to treat several conditions caused by a lack of natural growth hormone. And even if the patient was on GH, T3 levels still needed to be elevated. And what I noticed was that those levels were elevated successfully by using supplemental T4 but not T3.

Here’s why I think this is:

Additional T3 is not all that’s needed here. What’s needed is the actual conversion process of T4-T3, and the deiodinase presence and activity that it involves. This is because Local 5'-deiodination of l-thyroxine (T4) to active the thyroid hormone 3,3',5-tri-iodothyronine (T3) is catalyzed by the two 5'-deiodinase enzymes (D1 and D2). These enzymes not only “create” T3 out of T4, but actually regulates various T(3)-dependent functions in many tissues including the anterior pituitary and liver. So when there is an excess of T3 in the body, but normal levels of T4, the body’s thyroid axis sends a negative feedback signal., and produces less (D1 and D2) deiodinase, but more of the D3 type, which signals the cessation of the T4-T3 conversion process, and is inhibitory of many of the synergistic effects that T3 has! Remember, Type 3 iodothyronine deiodinase (D3) is the physiologic INACTIVATOR of thyroid hormones and their effects (13) and is well known to have independent interaction with growth factors (which is what GH and IGF-1 are).(14) This is because with adequate T4 and excess T3, (D1 and D2) deiodinase is no longer needed for conversion of T4 into T3, but levels of D3 deiodinase will be elevated. When there is less of the first two types of deidinase, it would seem that the T3 which has been converted to T4 can not exert it’s protein sparing (anabolic effects), as those first two types are responsible for mediation of many of the effects T3 has on the body. This seems to be one of the ways deiodinase contributes to anabolism in the presence of other hormones.

All of this would explain why anecdotally we see bodybuilders who use T3 lose a lot of muscle if they aren’t using anabolics along with it- they’re not utilizing the enzyme that would regulate some of T3’s ability to stimulate protein synthesis, while they are simultaneously signaling the body to produce an inhibitory enzyme (D3). And remember, for decades bodybuilders who were dieting for a contest have been convinced that you lose less muscle with T4 use, but that it’s less effective for losing fat when compared with T3? Well, as we’ve seen, without something ( GH in this case) to aid in the conversion process, it would clearly be less effective! Since the deiodinase enzyme is also located in the liver, and we see decreased hepatic nitrogen clearance with GH + T3, it would seem that the D3 enzyme is exerting it’s inhibitory effects, but in the absence of the effects of the first two deiodinase enzymes, it remains unchecked and therefore not only limits the GH’s nitrogen retention capability.

In other words, if we have enough to GH in our body aid in supraphysiological conversion of T4 into T3, but we already have the too much (exogenous) T3, the GH is not going to be converting any excess T4 into T3 after a certain point- which would be a limiting factor in GH’s anabolic effects, when coupled with the act that we’ve allowed the D3 enzyme to inhibit the T3/ GH synergy that is necessary.

As further evidence, when we look at certain types of cellular growth (the cartilage cell in this case) we see that GH induced rises in IGF-I stimulates proliferation, whereas T3 is responsible for hypertrophic differentiation. So it would seem that in some tissues, IGF-1 stimulates the synthesis of new cells, while T3 makes them larger. In this particular case, The fact that T4 and (D1) deiodinase is am
active component in this system is noted by the authors. They clearly state (paraphrasing) that: “T4 is is converted to T3 by deiodinase (5'-DI type 1) in peripheral tissues…[furthermore] GH stimulates
conversion of T4 to T3 , suggesting that some effects of GH
may involve this pathway.” The thing I want you to notice is that the authors of this paper state that the that the conversion PATHWAY is probably involved, and not the simple presence of T3. (15 )

Also, that same study notes that T3 has the ability to stimulates IGF-I and expression in tissues that whereas GH has no such effect (ibid).

So what are we doing when we add T3 to GH? We’re effectively shutting down the conversion pathway that is responsible for some of GH’s effects! And what would we be doing if we added in T4 instead of T3? You got it- we’d be enhancing the pathway by allowing the GH we’re using to have more T4 to convert to T3, thus giving us more of an effect from the GH we’re taking. Adding T4 into our GH cycles will actually allow more of the GH to be used effectively!

Remember, the thing that catalyzes the conversion process is the deiodinase enzyme. This is also why using low amounts of T3 would seem (again, anecdotally in bodybuilders) to be able to slightly increase protein synthesis and have an anabolic effect – they aren’t using enough to tell the body to stop or slow down production of the deiodinase enzyme, and hence .Although this analogy isn’t perfect, think of GH as a supercharger you have attached to your car…if you don’t provide enough fuel for it to burn at it’s increased output level, you aren’t going to derive the full effects. Thyroid status also may influence IGF-I expression in tissues other than the liver.So what we have here is a problem. When we take GH, it lowers T3 levels…but we need T3 to keep our GH receptor levels optimally upregulated. In addition, it’s suspected that many of GH’s anabolic effects are engendered as a result of production of IGF-1, so keeping our IGF receptors upregulated by maintaining adequate levels of T3 seems prudent. But as we’ve just seen, supplementing T3 with our GH will abolish Growth Hormone’s functional hepatic nitrogen clearance, possibly through the effect of reducing the bioavailability of insulin-like growth
factor-I (12.)

So we want elevated T3 levels when we take GH, or we won’t be getting ANYWHERE NEAR the full anabolic effect of our injectable GH without enough T3. And now we know that not only do we need the additional T3, but we actually want the CONVERSION process of T4 into T3 to take place, because it’s the presence of those mediator enzymes that will allow the T3 to be synergistic with GH, instead of being inhibitory as is seen when T3 is simply added to a GH cycle. And remember, we don’t only want T3 levels high, but we want types 1 and 2 deiodinase to get us there- and when we take supplemental T3, that just doesn’t happen…all that happens is the type 3 deiodinase enzyme shows up and negates the beneficial effects of the T3 when we combine it with GH.

And that’s where myself and Dr. Daemon ended up, after a week of e-mails, researching studies, and gathering clues.

If you’ve been using GH without T4, you’ve been wasting half your money – and if you’ve been using it with T3, you’ve been wasting your time. Start using T4 with your GH, and you’ll finally be getting the full results from your investment.

Drug Profile: Methandienone

Active Life: 6-8 hours
Drug Class: Anabolic/Androgenic Steroid (Oral)
Average Dose: Men 15-50 mg/day......Women 5-10 mg/day
Acne: Yes, especially in higher dosages
Water Retention: Yes, similar to testosterone
High Blood Pressure: Yes
Liver Toxic: Yes
Aromatization: Yes
DHT Conversion: No
Decrease HPTA function: Yes, dose and cycle length dependant

Methandienone is a derivative of testosterone, exhibiting strong anabolic and moderate androgenic properties. This compound was first made available in 1960, and it quickly became the most favored and widely used anabolic steroid in all forms of athletics. This is likely due to the fact that it is both easy to use and extremely effective. In the U.S. Dianabol production had meteoric history, exploding for quite some time, then quickly dropping out of sight. Many were nervous in the late 80's when the last of the U.S. generics were removed from pharmacy shelves, the medical community finding no legitimate use for the drug anymore. But the fact that Dianabol has been off the U.S. market for over 10 years now has not cut its popularity. It remains the most commonly used black market oral steroid in the U.S. As long as there are countries manufacturing this steroid, it will probably remain so.

Similar to testosterone and Anadrol 50, Methandienone (other known as Dianabol) is a potent steroid, but also one which brings about noticeable side effects. For starters methandienone is quite estrogenic. Gynecomastia is often a concern during treatment, and may present itself quite early into a cycle (particularly when higher doses are used). At the same time water retention can become a pronounced problem, causing a notable loss of muscle definition as both subcutaneous water and fat build. Sensitive individuals may therefore want to keep the estrogen under control with the addition of an anti-estrogen such as Nolvadex and/or Proviron. The stronger drugs Arimidex, Femara, or Aromasin (antiaromatase) would be a better choice if available.

In addition, androgenic side effects are common with this substance, and may include bouts of oily skin, acne and body/facial hair growth. Aggression may also be increased with a potent steroid such as this, so it would be wise not to let your disposition change for the worse during a cycle. With Dianabol there is also the possibility of aggravating a male pattern baldness condition. Sensitive individuals may therefore wish to avoid this drug and opt for a milder anabolic such as Deca-Durabolin. While Dianabol does convert to a more potent steroid via interaction with the 5-alpha reductase anzyme (the same enzyme responsible for converting testosterone to dihydrotestosterone), it has extremely little affinity to do so in the human body's. The androgenic metabolite 5alpha dihydromethandrostenolone is therefore produced only in trace amounts at best. Therefore the use of Proscar/Propecia would serve no real purpose.

Being moderately androgenic, Methandienone is really only a popular steroid with men. When used by women, strong virilization symptoms are of course a possible result. Some do however experiment with it, and find low doses (5mg) of this steroid extremely powerful for new muscle growth. Whenever taken, Methandienone (dianabol) will produce exceptional mass and strength gains. It's effectiveness is often compared to other strong steroids like testosterone and Anadrol 50, and it is likewise a popular choice for bulking purposes. A daily dosage of 20-40mg is enough to give almost anybody dramatic results. Some do venture much higher in dosage, but this practice usually leads to a more profound incidence of side effects. It additionally combines well with a number of other steroids. It is noted to mix particularly well with the mild anabolic Deca-Durabolin. Together one can expect an exceptional muscle and strength gains, with side effects not much worse than one would expect from Dianabol alone. For all out mass, a long acting testosterone ester like enanthate can be used. With the similarly high estrogenic/androgenic properties of this androgen, side effects may be extreme with such a combination however. Gains would be great as well, which usually makes such an endeavor worthwhile to the user. As discussed earlier, ancillary drugs can be added to reduce the side effects associated with this kind of cycle.

In order to withstand oral administration, this compound is c17 alpha alkylated. We know that this alteration protects the drug from being deactivation by the liver (allowing nearly all of the drug entry into the bloodstream), however it can also be toxic to this organ. Prolonged exposure to c17 alpha alkylated substances can result in actual damage, possibly even the development of certain kinds of cancer. To be safe one might want to visit the doctor a couple of times during each cycle to keep an eye on their liver enzyme values. Cycles should also be kept short, usually less than 8 weeks long to avoid doing any noticeable damage. Jaundice (bile duct obstruction) is usually the first visible sign of liver trouble, and should be looked out for. This condition produces an unusual yellowing of the skin, as the body has trouble processing bilirubin. In addition to the skin, the whites of the eyes may also yellow, a clear indicator of trouble. Should this occur the drug should be discontinued immediately and a doctor visited. This is usually a point where further, permanent damage can be avoided.

It is also interesting to note that methandienone is structurally identical to boldenone (EQ), except that it contains the added c17 alpha alkyl group discussed above. This fact makes clear the impact of altering a steroid in such a way, as these two compounds appear to act very differently in the body. The main dissimilarity seems to lie in the tendency for estrogenic side effects, which seems to be much more pronounced with Dianabol. Equipoise is known to be quite mild in this way, and users therefore commonly take this drug without any need of an anti-estrogen. Dianabol is much more estrogenic not because it is more easily aromatized, as in fact the 17 alpha methyl group and c1-2 double bond both slow the process of aromatization. The problem is that methanmdienone converts to l7alpha methylestradiol, a more biologically active form of estrogen than regular estradiol. But Dianabol also appears to be much more potent in terms of muscle mass compared to boldenone, supporting the notion that estrogen does play an important role in anabolism. In fact boldenone and methandienone differ so much in their potencies as anabolics that the two are rarely though of as related. As a result, the use of Dianabol is typically restricted to bulking phases of training while Equipoise is considered an excellent cutting or lean-mass building steroid.

The half-life of PureDbol is only about 3 to 4 hours, a relatively short time. This means that a single daily dosage schedule will produce a varying blood level, with ups and downs throughout the day. The user likewise has a choice, to either split up the tablets during the day or to take them all at one time. The usual recommendation has been to divide them and try to regulate the concentration in your blood. This however, will produce a lower peak blood level than if the tablets were taken all at once, so there may be a trade off with this option. The steroid researcher Bill Roberts also points out that a single-episode dosing schedule should have a less dramatic impact on the hypothalamic-pituitary-testicular axis, as there is a sufficient period each day where steroid hormone levels are not extremely exaggerated. I tend to doubt hormonal stability can be maintained during such a cycle however, but do notice that anecdotal evidence often still supports single daily doses to be better for overall results. Perhaps this is the better option. Since we know the blood concentration will peak about 1.5 to 3 hours after administration, we may further wonder the best time to take our tablets. It seems logical that taking the pills earlier in the day, preferably some time before training, would be optimal. This would allow a considerable number of daytime hours for an androgen rich metabolism to heighten the uptake of nutrients, especially the critical hours following training.

Drug Profile: Ephedrine

Ephedrine
Generic name: Efedrin Hydrochloride
Ephedrine

pack: 5 amps, 25mg/ml

Ephedrine is a stimulant drug, belonging to a group of medicines known as sympathomimetics. Specifically it is both an alpha and beta adrenergenic agonist (you may remember Clenbuterol is a selective beta-2 agonist). In addition, ephedrine enhances the release of norepinephrine, a strong endogenous alpha agonist. The action of this compound is notably similar to that of the body's primary adrenergic hormone epinephrine (adrenaline), which also exhibits action toward both alpha and beta receptors. When administered, ephedrine will notably increase the activity of the central nervous system, as well as have a stimulatory effect on other target cells. This will produce a number of effects beneficial to the athlete. For starters, the user's body temperature should rise slightly as more free fatty acids are produced from the breakdown of triglycerides in adipose tissue (stimulating the metabolism). This should help the user shed subcutaneous body fat stores, enhancing the look of definition in the physique. The anabolic effectiveness of steroids may also be increased with this substance (mildly), as the metabolic rate is a measure of fat, protein and carbohydrate conversion by the body. An enhanced metabolic state could clearly hasten the deposit of new muscle mass.

This stimulant effect of this drug will also increase the force of skeletal muscle contractions. For this reason ephedrine is commonly used by powerlifters before a competition, as the resultant (slight) strength and energy increase can clearly improve the weight totals on major lifts. It may also provide a notable mental edge, as the user is more energetic and better able to concentrate on the tasks ahead. Many recreational weight lifters find this effect particularly welcome, and use 25-50mg of this stimulant as a regular adjunct to their training sessions. The user often feels capable of attacking the weights with much more intensity while taking ephedrine, and leaves the gym knowing they will have had a more productive workout. It is important that this compound not be used continuously for this purpose, as its effect will diminish as the body becomes accustomed to the drug. In most instances the user will take the drug only two or three times per week, usually on those days personally "important" (like chest day). The athlete is also wise to take a break (one to two months) from ephedrine treatment after several weeks have past, so as to continue receiving the optimal effect from this drug. While the strength boosting effect of this drug is noteworthy, the primary application for ephedrine remains to be as a cutting agent. The athlete will generally take this drug a few times daily during dieting phases of training, at a dosage of 25 to 50mg per application. The widely touted stack of ephedrine (25-50mg), caffeine (200mg) and aspirin (300mg) is shown to be extremely potent for fat loss. In this combination, the ephedrine and caffeine both act as notable thermogenic stimulants. The added aspirin also helps to inhibit lipogenesis by blocking the incorporation of acetate into fatty acids. The athlete will be sure this stack is working by noticing an increase in body temperature, usually a degree or so (not an uncomfortable raise). This combination is taken two to three times daily, for a number of consecutive weeks. It is discontinued once the user's body temperature drops back to normal, a clear sign these drugs are no longer working as desired. At this point increasing the dosages would not prove very efficient. Instead a break of several weeks should be taken, so that this stack may once again work at an optimal level.

Ephedrine can produce a number of unwelcome side effects that the user should be aware of. For starters, the stimulant effect can produce shaky hands, tremors, sweating, rapid heartbeat, dizziness and feelings of inner unrest. Often these effects subside as the user becomes more accustomed to the effect of this drug, or perhaps the dosage is lowered. In general, those negatively impacted by caffeine would probably not like the stronger effects of ephedrine. The mental and physical state produced by this drug is also quite similar to that seen with Clenbuterol, so those who find little discomfort with this treatment should (presumably) be fine with this item (and vice versa). While taking this drug one may also endure a notable loss of appetite, usually a welcome effect when dieting. Ephedrine is in fact a popular ingredient in combination (prescription) appetite suppressants. The user may further notice headaches and an increase in blood pressure with regular use of ephedrine. Those suffering from thyroid dysfunctions, high blood pressure or cardiac irregularities should also not be taking this drug, as it will certainly not mix well with such conditions.



As of late there is much discussion about the future availability of ephedrine. This is due to that fact that ephedrine tablets are used as the primary base for the manufacture of methamphetamine. This is you know is an illegal drug, made and sold illicitly. The structure of these two compounds is notably similar, as only a few chemicals are needed to change ephedrine into "meth". Since ephedrine is currently an over-the-counter product, underground manufacturers can easily obtain it. A trend involving large volume retail purchases for OTC ephedrine products has been developing, and many states are taking notice of it. With the widespread increase of amphetamine addiction (and related crime) ephedrine may soon join the list of federally controlled substances. While some states have already taken action to restrict the sale of this stimulant, federal action would probably be required in order have a major impact on availability. Even if a particular state is aggressively preventing the sale of these products, a thriving mail-order market still exists to fill the demand. Thumbing through the back pages of many national magazines should make this clear, as we notice advertisements for companies which ship ephedrine tablets out by the thousand.

Drug Profile: Clomiphene Citrate

Clomiphene Citrate
Generic name: Clomiphen Citrate
PureClomid 50
pack: 20 tablets 50mg/tabl

Active Life: 5-7 days
Drug Class: Selective Estrogen Receptor Modulator (Oral)
Average Dose: Men 50-100 mg/day
Acne: Yes
Water Retention: No
High Blood Pressure: Rare
Liver Toxic: Low
Aromatization: None
Decrease HPTA function: No, used to restore it
Strong gonadotropin stimulator/mild anti-estrogen

Clomid® is the commonly referenced brand name for the drug clomiphene citrate. It is not an anabolic steroid, but a prescription drug generally prescribed to women as a fertility aid. This is due to the fact that clomiphene citrate shows a pronounced ability to stimulate ovulation. This is accomplished by blocking/minimizing the effects of estrogen in the body. To be more specific Clomid is chemically a synthetic estrogen with both agonist/antagonist properties, and is very similar in structure and action to Nolvadex. In certain target tissues it can block the ability of estrogen to bind with its corresponding receptor. Its clinical use is therefore to oppose the negative feedback of estrogens on the hypothalamic-pituitary-ovarian axis, which enhances the release of LH and FSH. This of course can help to induce ovulation.

For athletic purposes, Clomid does not offer a tremendous benefit to women. In men however, the elevation in both follicle stimulating hormone and (primarily) luteinizing hormone will cause natural testosterone production to increase. This effect is especially beneficial to the athlete at the conclusion of a steroid cycle when endogenous testosterone levels are depressed. If endogenous testosterone levels are not brought beck to normal, a dramatic loss in size and strength is likely to occur once the anabolics have been removed. This is due to the fact that without testosterone (or other androgens), the catabolic hormone cortisol becomes the dominant force affecting muscle protein synthesis (quickly bringing about a catabolic metabolism). Often referred to as the post-steroid crash, it can quickly eat up much of your newly acquired muscle. Clomid can play a crucial role in preventing this crash in athletic performance. As for women, the only real use for Clomid is the possible management of endogenous estrogen levels near contest time. This can increase fat loss and muscularity, particularly in female trouble areas such as this hips and thighs. Clomid however often produces troubling side effects in women (discussed below), and is likewise not in very high demand among this group of athletes.

Male users generally find that a daily intake of 50-100 mg (1-2 tablets) over a four to six week period will bring testosterone production back to an acceptable level. A very common regime of dosing is; 300 md/day 1, 100 mg/day for days 2-11, and 50 mg/day for days 12-21. This raise in testosterone should occur slowly but evenly throughout the period of intake. Since an immediate boost in testosterone is often desirable, many prefer to combine Clomid with HCG (Human Chorionic Gonadotropin) for the first week or two after the steroids have been removed. The kick-start from HCG also helps to restore the normal ability for the testes to respond to endogenous LH, which may be hindered for some time after the cycle is ended due to a prolonged state of inactivity. Once the HCG is stopped, the user continues treatment with Clomid alone. HCG should not be used for longer than two or three weeks though, as the resulting increased testosterone and estrogen levels may again initiate negative feedback inhibition at the hypothalamus. When planning your ancillary drug program, it is also important to remember that injectable steroids can stay active for a long duration. Using ancillary drugs the first week after a long acting injectable like Sustanon has been stopped may prove to be wholly ineffective. Instead, the athlete should wait for two to three weeks, to a point where androgen levels will be diminishing. Here the body will be primed and ready to restore testosterone production.

Clomid and HCG are also occasionally used periodically during a steroid cycle, in an effort to prevent natural testosterone levels from diminishing. In many instances this practice can prove difficult however, especially when using strong androgens for longer periods of time. There is also no exact method for using the two drugs in this manner. Some have experimented by periodically administering small doses of HCG along with one or two tablets of Clomid, perhaps for a few days at a stretch followed by a longer break. An on/off schedule would be implemented; for fear that this combination may lose some effectiveness if used continuously for this purpose. This method of intake may prove to be effective, although it is really much more feasible to stimulate testosterone production after the cycle than to try and maintain it for the long duration during.

In addition to helping with the post-cycle testosterone crash, this drug can also help with elevated estrogen levels during a steroid cycle. A high estrogen bevel puts an athlete in serious risk of developing gynecomastia, which is an obvious unwanted side effect. With the intake of Clomid, the athlete can hopefully reduce his risk for developing gynecomastia. The estrogen "blocking" properties of Clomid appear to be slightly weaker than Nolvadex in comparison however, which is why it is not usually thought of as an equal substitute for estrogen maintenance. Of course both drugs have similar actions in the body. and are relatively interchangeable for this purpose. Clomid can likewise also be used as a maintenance anti-estrogen throughout the duration of steroid cycle with good confidence, just as is done with Nolvadex. In most instances this will prove equally sufficient, the drug effectively minimizing the activity of estrogen in the body and warding off gyno and excess water/fat retention. Unfortunately just as with Nolvadex this is not always the case however, and many find it necessary to addition another anti-estrogenic drug. The most common adjunct is Proviron, an oral DHT used to competitively lower aromatase activity and raise the androgen to estrogen ratio. The Clomid/Nolvadex and Proviron combination is extremely effective, although we could alternately replace them both with a more specific aromatase inhibitor such as Arimidex,Femara, or Aromasin. While stronger at combating estrogen in most cases, these drugs are also typically much more costly.

As for toxicity and side effects, Clomid is considered a very safe drug. Bodybuilders seldom report any problems, but listed possible side effects do include hot flashes, nausea, dizziness, headaches and temporarily blurred vision. Such side effects usually only appear in females however, as they feel the effects of estrogen manipulation much more readily than men. While female athletes can clearly gain some benefit from this substance, estrogen manipulation is probably not the most comfortable way to go about cutting up. Should it still be used for such purposed and side effects do become pronounced, the drug of course is to be discontinued and (at least) a break taken from it.

Clomiphene citrate is widely available on the black market in a variety of brand names as well as generic tabs and liquid versions.

Drug Profile: Tamoxifen citrate

Generic name: Tamoxifen citrate
PureGear
pack: 60 tabletes 20mg/tabl

Active Life: 5-7 days
Drug Class: Selective Estrogen Receptor Modulator (Oral)
Average Dose: 10-30 mg/day
Acne: Yes
Water Retention: No
High Blood Pressure: Rare
Liver Toxic: low

Nolvadex®, is the trade name for the drug tamoxifen citrate, it is a non-steroidal agent that demonstrates potent anti-estrogenic properties. The drug is technically an estrogen agonist/antagonist, which competitively binds to estrogen receptors in various target tissues. With the tamoxifen molecule bound to this receptor, estrogen is blocked from exerting any action, and an anti-estrogenic effect is achieved. Since many forms of breast cancer are responsive to estrogen, the ability of tamoxifen citrate to block its action in such cells has proven to be a very effective treatment. It is also utilized successfully as a preventative measure, taken by people with an extremely high familial tendency for breast cancer. While Nolvadex is effective against estrogen, it is not our strongest available remedy. We now have the drugs Arimidex, Femara, and Aromasin available to us, which notably prevents estrogen from being manufactured in the first place. Altering the effect of estrogen in the female body can cause a level of discomfort, so anti-estrogens are most bearable when used after the point of menopause. Since Nolvadex is milder in comparison, it is more widely applicable and usually the first treatment option.

As discussed earlier, an enzyme in the male body (aromatase) is capable of altering testosterone to form estradiol. The structure of estrogen is actually quite similar to testosterone, so its presence in the male body is not all that remarkable. Since this same enzyme can also aromatize many anabolic/androgenic steroids, the buildup of estrogens can be an important concern during intake. High levels can cause a number of unwanted side effects, a primary worry being gynecomastia or the development of female breast tissue in men. This can be first noticed by the appearance of swelling or a small lump under the nipple. If left to progress it can turn into a very unsightly development of tissue, often irreversible without surgery. Estrogen can also lead to an increase in the level of water retained in the body. The result here can be a notable loss of definition, the muscles beginning to look smooth and bloated due to the retention of subcutaneous fluid. Fat storage may also be increased as estrogen levels rise. This hormone is in fact the primary reason women have a higher body fat percentage, and different fat distribution (hips/thighs) than men. Individuals sensitive to the effects of estrogen will usually be sure to have an anti-estrogen on hand when taking problematic steroids, so as to minimize the impact of related side effects.

This drug also shows the ability to increase production of FSH (follicle stimulating hormone) and LH (luteinizing hormone) in the male body. This is accomplished by blocking negative feedback inhibition caused by estrogen at the hypothalamus and pituitary, which fosters the release of the mentioned pituitary hormones. This of course is also the function of Clomid and cyclofenil. Since a higher release of LH can stimulate the Leydig's cells in the testes to produce more testosterone, Nolvadex can have a positive impact on one's serum testosterone level. This "testosterone stimulating" effect is an added benefit when preparing to conclude a steroid cycle (post cycle therapy or PCT). Since most anabolic/androgenic steroids will suppress endogenous testosterone production, Nolvadex can help restore a balance in hormone levels. Nolvadex should be preferred over Clomid for this purpose in fact, as side by side it is clearly the stronger agent. It has also been shown to increase LH responsiveness to Gonadotropin Releasing Hormone after time, while Clomid slightly lowers this sensitivity as the drug is used for several weeks..

In some cases the use of only an estrogen antagonists such as Nolvadex or Clomid may be sufficient for testosterone stimulating purposes, particularly when halting the use of a milder or shorter steroid program (which should have a less pronounced impact on the hormonal system). With stronger cycles most option to enhance the stimulating effect of these drugs with HCG, a hormone that mimics the action of LH. HCG use provides an excessive level of stimulation to the testes, which in essence may shock them out of a prolonged state of inactivity. In such a condition the Leydig's cells may not be producing a normal amount of testosterone, even though the normal release of gonadotropins has been achieved. Nolvadex can be tricky at this point. Remember it only blocks the effect of estrogen that is present in the body. If it is removed at a time when estrogen levels are still unusually high, related side effects can quickly become a pronounced problem. Since HCG not only increases the production of testosterone but also enhances the rate of aromatization in the testes, anti-estrogens should not be discontinued until at least a couple of weeks after HCG is discontinued. The result otherwise of course could be many unwanted side effects that were previously under control. When using Nolvadex to ward off the effects of estrogen during the cycle, it should similarly not be removed until the user is confident that hormone levels are well under control. With a drug such as Sustanon, this may mean continuing it for several weeks after the last shot.

A typical daily dosage for men is in the range of 10 to 30mg, the amount would be dependent on the level of effect desired. It is advisable to begin with a low dosage and work up, to avoid taking an unnecessary amount. The time in which Nolvadex is started also relies on individual needs of the user. If an athlete with a known sensitivity to estrogen is starting a strong steroid cycle, Nolvadex should probably be added soon after the cycle had been initiated. If estrogen is probably not going to be a major problem during the cycle (but will likely be after), Nolvadex is administered around the time exogenous steroid levels will drop. It will be continued for some weeks after, until the point when natural testosterone is thought to be at an acceptable level. As mentioned HCG is often used at this point as well (see related profile for more detail). Women have also utilized Nolvadex in an effort to reduce the effect of their own endogenous estrogens. This can lower body fat concentrations, especially in stubborn areas like the hips and thighs. This is of course risky, as manipulating the effect of estrogen can become uncomfortable in women. Side effects like hot flashes, menstrual irregularities and a variety of complications with the reproductive system are all possible.

When looking for a stronger anti-estrogenic effect, Proviron can make a good addition to Nolvadex. Although this compound is technically an androgen, it may have a pronounced effect on the production of estrogen in the body. Its mode of action is therefore very different than that of Nolvadex. While Nolvadex only blocks the binding ability of free-floating estrogen, Proviron can minimize the creation of it. With each drug attacking estrogen via a different mechanism, we have a very synergistic combination. A daily intake of 20-30mg Nolvadex and 25-50mg Proviron can be extremely effective when dealing with a strong estrogenic cycle. Women often avoid adding Proviron to Nolvadex treatment (thought often it is still used to enhance fat loss), for fear of developing virilization symptoms (Proviron is an oral DHT). Virilizing effects can occur very quickly once there has been a dramatic rise in the activity of androgens (intensified by a decrease in estrogen activity), so at a minimum women should be careful with such a combination.

Of great interest also is that Nolvadex is an estrogen agonist in the liver, capable of activating the estrogen receptor and mimicking the actions of this sex hormone in this region of the body. As such it can have a markedly positive impact on HDL (good) cholesterol values, as does estrogen. Many similarly use this drug to counter some of the negative consequences of steroid use in regards to cholesterol values and cardiac risk, as steroids often suppress HDL and raise LDL levels considerably. in some instances an athlete is able to maintain a very favorable HDL/LDL cholesterol ratio, to spite the use of a moderate dosage (400mg weekly) of an injectable like testosterone or nandrolone. It would be foolish to think however that Nolvadex would be a sufficient remedy with the heavy use of c-l7alpha alkylated orals or extremely high dosed cycles in general.

It has been reported by many however that Nolvadex seems to slightly reduce to gains made during a steroid cycle. It appears that many androgenic/anabolic steroids will exhibit their most powerful anabolic effect when accompanied by a sufficient level of estrogen. This may be one reason why gains made with a strong androgen like testosterone are usually much more pronounced than when using an anabolic that aromatizes to a lower degree. It therefore seems like good advice to be aware of how much Nolvadex is actually needed before committing to it during a cycle. Many people in fact find it unnecessary, even when utilizing problematic compounds such as testosterone or Dianabol. Others however find they are troubled by water retention and gynecomastia, even with milder anabolics like Deca-Durabolin and Equipoise. The estrogenic response to steroid use is very individual, and may be influenced by factors such as age and body fat percentage (adipose tissue is a primary site of aromatization).

Nolvadex is certainly the most popular anti-estrogen used by athletes today, no doubt because it is simply an effective product. It is also widely manufactured, and easy to obtain. Since there never seems to be a lack of supply, there is little incentive to manufacture a counterfeit product. All of the various generics forms of this drug are no doubt trustworthy. Women should remember to be very cautious when considering the use of Nolvadex, as they are usually very sensitive to changes in the activity of estrogen. Men looking for a stronger anti-estrogenic effect may want to consider using Arimidex, Femara, or Aromasin , three powerful new anti-aromatase compounds. They are much more effective for estrogen control.

Intermediate Cutting Cycle: Stack 1

If you're anything like me, you took a look at the title of this article and wondered what an intermediate is. It's relatively easy to figure out what a beginner is, because chances are if you haven't done steroids, you already know that you're a beginner. And if you've been using steroids for nearly a decade (as I have), you would probably have assumed you would need an advanced cycle. But if you fall in this grey area in the middle, then you're probably wondering what kind of cycles you need.

Well, I'm going to set up some guidelines to figure out whether you're an intermediate, ok? You're an intermediate if you've been lifting for at least 3 years and have done at least 3 cycles. And I think, to make my definition of intermediate a little easier to understand, I'll also suggest that you need to have done at least 3 different anabolic steroids, and stacked them in at least one of your cycles.

If you've done all of the above then you are (at least) an intermediate steroid user, and the cycle I'm going to outline here is for you. So let's take a look at a sample intermediate cutting cycle, and then I'll give you the reasoning behind it.

Week	PureProp 100	PureTren Ace 100	PureStan 10	PureNolvadex 20	Vitamin B-6
1	100 mg EOD	100 mg EOD		10 - 20 mg ED	200 mg ED
2	100 mg EOD	100 mg EOD		10 - 20 mg ED	200 mg ED
3	100 mg EOD	100 mg EOD		10 - 20 mg ED	200 mg ED
4	100 mg EOD	100 mg EOD		10 - 20 mg ED	200 mg ED
5	100 mg EOD	100 mg EOD		10 - 20 mg ED	200 mg ED
6	100 mg EOD	100 mg EOD		10 - 20 mg ED	200 mg ED
7	100 mg EOD	100 mg EOD		10 - 20 mg ED	200 mg ED
8	100 mg EOD	100 mg EOD		10 - 20 mg ED	200 mg ED
9	100 mg EOD	100 mg EOD	4 0 mg ED	10 - 20 mg ED	200 mg ED
10	100 mg EOD	100 mg EOD	4 0 mg ED	10 - 20 mg ED	200 mg ED
11	100 mg EOD	100 mg EOD	4 0 mg ED	10 - 20 mg ED	200 mg ED
12	100 mg EOD		4 0 mg ED	10 - 20 mg ED	200 mg ED
13			4 0 mg ED	10 - 20 mg ED	200 mg ED
14			4 0 mg ED	10 - 20 mg ED	200 mg ED
15	Clomid Therapy	Clomid Therapy		10 - 20 mg ED	200 mg ED
16	Clomid Therapy	Clomid Therapy		10 - 20 mg ED	200 mg ED
17	Clomid Therapy	Clomid Therapy		10 - 20 mg ED	200 mg ED

Ok, so what we have here is a cutting cycle that uses low(ish) amounts of anabolics. A cycle like this, which makes use of short estered products like PureProp 100 and PureTren A 100 will produce noticeable results almost immediately. Since this is a cutting cycle, I'll assume some kind of calorie deficit. This is important because the body is a lot more sensitive to androgens when there's a hypocaloric state & this is why bodybuilders who are dieting for contests seem to be able to do astonishing things with their bodies on relatively small amounts of anabolic steroids.

The testosterone in this cycle has a very short ester, meaning it is released into the body very rapidly after it is injected - and is therefore usually injected every day or every other day. Testosterone stacks well with anything, and produces a nice anabolic (muscle building) effect, in addition to a distinct androgenic effect. Naturally, both of these effects will work together to help you achieve a significant increase in weight-load capacity, and a gain in Body weight.

Since you're going to have to inject the testosterone propionate every other day anyway, you may as well include another product that has a similar ester length. For a cutting cycle, that would probably mean using Trenbolone Acetate. It's often used by bodybuilders before contests for its hardening abilities and fat metabolizing qualities. It is highly androgenic and does not aromatize, it makes a great cutting drug. It stacks well with anything, including Anavar, which is our final compound in this cycle.

Stanozolol does not convert to estrogen at all, so water retention is quite low with this steroid (if there's any) and gynocomastia is never reported. It is very popular for addition into a cutting cycle and provides a nice ending for this cycle, over the last four weeks, where the user may have reached a plateau in body fat loss. It's also very good at helping users retain or even gain strength when calories are low or at just maintenance level

Clenbuterol or Ephedrine can be added into a cycle like this also, if more fat loss is needed. Clenbuterol is typically used at a dose of 20-120mcgs/day in divided doses, and Ephedrine is typically used at a dose of 20mgs 3x a day.

PureClomid Therapy

	Day 1	Day 2	Day 3	Day 4	Day 5	Day 6	Day 7
Week 1	300 mg	100 mg	100 mg	100 mg	100 mg	100 mg	100 mg
Week 2	100 mg	100 mg	100 mg	100 mg	50 mg	50 mg	50 mg
Week 3	50 mg	50 mg	50 mg	50 mg	50 mg	50 mg	50 mg

Nolvadex should be kept on hand in case you start to feel signs of gyno throughout the cycle.

Legend: ED - Every Day , EOD - Every Other Day