The Sane cycle : safe and effective use of steroids

[Big Cat]

This is my first outline, still very rough and basic and missing one or two essential elements, of the sane cycle. A project I have been working on in past months to outline a steroid/diet/supplementation plan that allows you to stay healthy, increase your health and still add a nominal amount of LEAN mass to your frame while maintaining of lowering fat.

Any and all comments are extremely welcome.

Introduction

It has long been my goal to demonstrate that steroid use cannot only occur without causing any harm, it can actually benefit us in lengthening our life-span and increasing our quality of life. Since in essence, steroids have never led to the death of any person, and that they are far less lethal than most over the counter products, such as plain aspirin, they should really be legal. And since they are prescription medication, any use of these products should occur under medical supervision. But hey, some idiots did make them illegal and good luck finding a doctor that will help you, much less one that actually knows what he is talking about.

That is why I set out to write this. It is in no way complete, it is merely a quick rundown of several facts and the safest conclusions I could make based on them. But it should empower you to convince your health-care provider to help you, and educate him on how to do so.

Many people who have known me throughout my quest to refute the dangers of steroid use have asked me for help in proving these facts to sceptics and laymen, and this is EXTREMELY difficult because of the large amount of propaganda they have had to endure over past years. This may still be a tad too scientific for the dumber individuals, but may serve as a tool to educate smarter friends and relatives. And I hope that it may do so.

Cycle duration

For cycle duration I have chosen 12 weeks. Its rather arbitrary and its certainly not something you should consider absolute fact. A cycle doesn't have to be 12 weeks to be safe. But we have ample evidence to suggest that with proper post-cycle, full HPTA recovery can be made in less than 50 days (1) , and since most people do not like to play pincushion and employ for the majority long-acting products, 12 weeks is sufficiently long to reap all the benefits of your cycle and get adequate gains.

As a rule we will use equal time off as on. So after the cycle (post-cycle not included) you will stay off 12 weeks. Recovery should be established in less than 50 days, so technically after 2 months you could already safely start another cycle, but since physiology is not linear math and not everyone will be able to complete the cycle and post-cycle as per the instructions, we should offer ourselves some leeway. So we will cycle on 12 weeks, then stay off 12 weeks before recommencing

Product Choice

We need to be realistic about the products we use as well. I could outline all sorts of magnificent exotic cycles, but chances that you will be able to find all the needed products without taking a second mortgage on your house or get swindled by less than reputable dealers is slim. Therefore we opt for the more available products. First of all we will exclude products that are no longer made or are extremely hard to find, that includes drostanolone (Masteron), quinbolone (anabolicum vister), mibolerone (cheque drops), formebolone (esiclene), clostebol (megagrisevit), MENT, methandriol, metribolone, furazabol (miotolan), Norethandrolone (Nilevar), ethylestronol (orabolin), Stenbolone, oxabolone (steranabol), etc.

Of what's left, we need to make a selection. Halotestin is out. Too androgen mediated, too liver toxic. Trenbolone and nandrolone (Deca-Durabolin, Laurabolin, Durabolin) are excluded because they are too suppressive. Andriol because it is ineffective, oxandrolone (Anavar) because a useful dose (75+ mg per day) is too expensive, and Methenolone (Primobolan) because of its price. Primo is a decent androgen, but seems to have no other mode of action.
Most of these products would have been excluded for other reasons anyway, with the possible exception of trenbolone and oxandrolone.

We will also exclude methandrostenolone (Dianabol) and oxymetholone (Anadrol). While these are useful drugs at the beginning of a cycle, especially as far as bulk and strength, they fall outside of what we are looking for : a long term cycling plan with relatively lean results. On top of that I want to make a case for stanozolol (Winstrol/Stromba) and I do not feel comfortable recommending the use of two orals, due to liver toxicity (even though liver toxicity is a tad exaggerated, but then that just allows us more leeway with the Winstrol).

That leaves us with three products : testosterone, boldenone (equipoise) and stanozolol (Winstrol/Stromba). Can you build an effective cycle with clean and proper results, with only these three substances? Of course you can. But before we delve into that, let me defend my choice of products.

In defense of testosterone

Apart from being the most effective steroid, it's also the sanest choice with regards to health. It makes sense that by administering the exogenous variant of our prime androgen, we will not allow anything in the body that would normally occur to fall into disuse, nor allow anything that would normally not happen to occur. Because a lot of studies and conclusions are based on findings with testosterone, we can only safely make these assumptions about testosterone. That is why we not only use it, it will be the base for our cycle. And it should be for any health-conscious cycle.

Testosterone is the most effective steroid commercially available today. This observed in the real world, since even with the necessary bulk, testosterone increases lean body mass more than any other steroid we have access to. More than the stronger androgens, and more than the stronger estrogens. That is because testosterone has a very diverse mode of action. Testosterone is the most present androgen in the body. Its also the most important endogenous androgen in muscle tissue. But everywhere else in the body, that role is put aside for Dihydrotestosterone (DHT). Now DHT is a reduced version of testosterone with a saturated A-ring (steroids are lipophillic, 19-carbon, 4-ring structures made from cholesterol). These other tissues are rich in an enzyme called 5-alpha-reductase. When testosterone binds to this enzyme, its 4,5-double bond is broken and two hydrogen atoms (hence dihydro) attached to the spaces that are freed on the A-ring. DHT is a much more potent androgen, roughly three times the affinity of testosterone for the androgen receptor.

Many people regard DHT as the enemy, because among these androgen-specific tissues are the scalp (aggravating a genetic tendency to hair loss) and the skin (causing outbreaks of acne). But in fact DHT is more than that to us. Since it is the prime androgen in nerve tissue, it will be imperative to have ample DHT levels for optimal neuromuscular response. This is why many people taking the 5-alpha-reductase inhibitor finasteride (Proscar) find that their strength does not increase, or even decreases. Secondly we tend to forget that DHT is a potent anti-aromatase. The aromatase enzyme is the enzyme that converts testosterone to the estrogen estradiol (E2). As we will discuss next, E2 certainly has its benefits as well, but too high a concentration will result in excess adipose storage and more water retention (bloat). Certainly we don't need this if it can be avoided. Since this is a long term plan, we are in no way planning to walk around like the 'stay puffed marshmallow man'?. By blocking the 5-alpha reductase we have a shift towards aromatization of testosterone, because there is more testosterone available (not converted to DHT) and there are more aromatase enzymes (not taken up by DHT). This could in turn lead to problems with feminization and gynocomastia (breast growth in men). So as you can see, DHT is quite important in this equation.

A more important issue is perhaps the prostate. Prostate cancer is a disease of modern society. And steroid use has been known to cause or aggravate Benign prostate hypertrophy, a growth stage of the prostate gland in middle-aged men. Because the prostate is androgen specific, DHT is often named as the culprit. But the latest research determines that estrogen is in fact the causative factor, although a level of androgenic action is required. Androgens have actually been preferred as a therapeutic means to treat BPH.

[Big Cat]

As we mentioned already, testosterone is a substrate for the aromatase enzyme and converts to E2. A female hormone. Here too demonization has made E2 the enemy. And yet again we are overlooking several factors. First of all, bloat, fat gain and gyno occur only at very high concentrations of E2, something we should be able to avoid if we are sane with our doses. And if not, we have numerous anti-aromatase drugs at our disposal, of which I favour Mesterolone (Proviron) as it is a DHT analogue, will increase free testosterone and does not block E2 entirely in low doses, so we still reap the benefits. So what are the benefits of E2? Well, estrogen enhances gluconeogenesis (use of glucose for tissue repair and energy storage) (2), increases the release of human Growth Hormone (3) and can increase androgen receptor upregulation (E2 makes testosterone more effective as an androgen) (4).

Lastly we consider actions not mediated by either the androgen or the estrogen receptor. This could in large part explain why testosterone is still the greatest steroid available, despite there being more potent androgens and more estrogen mediated drugs. A combination of trenbolone, a much stronger androgen, and oxymetholone (which has direct estrogenic action, without requiring aromatisation) only yields roughly the same amount of mass as equipotent or even lesser doses of testosterone. Why ? Well this brings us back to the point I raised about using a base that is equal to the endogenous alternative. Because certain processes may not be activated by these bastard hormones. One study (5) showed that testosterone had more effect in ductal branching in prostate tissue than did DHT, which would indicate a non-AR mechanism, since DHT is more potent at the AR, especially in the prostate. Could it be the estrogen factor ? No, because the DHT prohormone 3-alpha (5-alpha-androstan-3a,17b-diol) had the same effect as testosterone, and 3-alpha does not aromatize. So there is another mechanism in play here, which certainly supports the thesis that there is more to testosterone than merely agonism of estrogen and androgen receptors. Another study demonstrated that testosterone may upgrade beta-adrenoreceptors in vivo, through a non-AR mediated mechanism (again testosterone outperformed DHT in this area), and since administration of estrogen receptor antagonists showed no significant changes, we can also state it was not ER-mediated. The relevance of this in regards to muscular hypertrophy may be a lot greater. This did in large part determine the diet I planned with this cycle and the use of beta-adrenergic agents. So testosterone has proven beneficial in three separate fashions, and easily allows a defense of its selection.

But safety played a factor in my decision as well. Many theories about the evils of steroids were debunked these past few years, and most of the studies that disproved this long-standing anti-steroid propaganda, used testosterone as a substrate. So the only safe conclusion as far as these studies go is that TESTOSTERONE, and not steroids in general, is safe and beneficial. That is not to say the others are not as safe, but there is no proof that gives us any certainty that they are. One of the main reasons against the use of steroids has been cardiovascular risk. Several studies have looked at this closely, and not only did they determine that testosterone did not pose a heart risk (6), they also concluded that low testosterone levels induce cardio-vascular risk (7), whereas supraphysiological administration seemed to decrease the risk (8) (decreases in total cholesterol, HDL and LDL, LDL/HDL ratio and apoplipoprotein B, a marker for cardiovascular risk). In conclusion it is safe to state that testosterone is actually good for your ticker, and as normal levels of testosterone decrease with age, a good case is to be made for Hormonal Replacement therapy in the interest of cardiovascular health. Lastly testosterone was also shown to increase mental health (9), as it increased cognitive performances in older men. So testosterone cannot only promote more lean mass than any other steroid, it can also make you live longer by decreasing heart risk, and get better quality out of your remaining years by enhancing cognitive performance and fighting dementia.

Hence my case for using testosterone as a base of our safe cycle.

What type of testosterone?

There are many different types of testosterone. Long esters, short esters, methyltest, andriol, and mixes like Sustanon and Omnadren. First of all we need to state that methyltest is not testosterone. The 17-alpha-methylation makes quite a few alterations. It will express less androgen binding, lower conversion to mestanolone (Methyl-DHT), and despite lower aromatization, also a heavier amount of estrogenic action because it converts to methyl-DHT, a much stronger and efficient type of estrogen. So methyltestosterone is not a valid choice. Andriol uses a rather ineffective delivery system based on lipophillic absorption in the ductus thoracicus of the lymphatic system. Fine in theory, but appears to be less effective than hoped, and the amounts needed to make andriol of use to us are not affordable.

We will also include Sustanon and Omnadren, these are combinations of long and short esters (structures attached to slow the release of the compound into the blood), usually injected over wide time-spans. This creates a very unstable blood-level, contrary to popular belief. Imagine if you will a product of 3 esters, one that releases over 3 days, one that releases over 6 days and one that releases over 9 days. 100 mg of each injected once every 9 days. The first three days the first ester would release 100 mg of testosterone. The second ester would release 50 mg and the last ester would release 33.3 mg of testosterone. The next three days the first is already gone, the second releases only 50 mg and the last only 33.3 mg. And on the last three days only 33.3 mg of testosterone from the last ester is released. At the beginning I have the massive dose of 183.3 mg in my blood, and at the end only 33.3 mg, you do the math.

The saner thing to do is to use a single ester and inject as soon as levels taper off to levels upon injection. The three most widely used esters and their frequency of injection are propionate (every 2 days), enanthate (every 6-7 days) and cypionate (every 7 days). There is also the longer undecanoate, but that is rather hard to find, and the esterless suspension. The latter is great for mass, but seems to cause a great deal of water retention and needs to be injected once or twice a day, which is not wishful for a long term plan. So which of these should we use ?

Well, the propionate is my first choice, because its release patterns seems to be the most beneficial in keeping water weight under control, and it clears faster than the other two allowing for faster recuperation. For lean gains, I would certainly make the choice for propionate, also because it has a lighter, shorter ester and thus more testosterone per mg. But not many people appreciate injecting every 2 days, and with the concomitant use of boldenone undecylenate the fast clearance time seems to be a non-factor. So if you can tolerate a little more water weight, enanthate or cypionate allow for weekly injections.

In defense of Boldenone

Boldenone differs from testosterone only in that it has an extra double-bond on it's a-ring at the 1 position. This changes the conformation of the A-ring and its affinity for certain structures. As such it is only half as androgenic as testosterone because of lower affinity to the androgen receptor, and it does not form a more potent androgen in androgen-specific tissue, because it has particularly low affinity for the 5-alpha-reductase enzyme (10) (that converts test to DHT). Even though its conversion product is quite potent (1-testosterone).

Boldenone's affinity for the aromatase is roughly reduced by the same percentage, and so it only creates about half as much estrogen. So in essence, boldenone offers us many of the same characteristics that testosterone does, but because of its lessened affinity poses less of a threat for the acute, visible side-effects. So by dividing our doses over testosterone and boldenone, we can reduce both acute and long-term side-effects.

Boldenone is patented as a veterinary drug, but the high demand has made a wide range of affordable human grade products available to us and the use of boldenone is now quite wide-spread among recreational athletes. It is touted as the successor to the mighty Deca-Durabolin. Deca is nandrolone decanoate. Nandrolone has the benefit of being deactivated by the 5-alpha-reductase enzyme and being even less of a threat for acute androgenic side-effects. But alas, it is a very suppressive hormone that severely interferes with endogenous production of testosterone and it has been concluded that both nandrolone (11) and several of its metabolites (12) exhibit progestagenic activity (which causes gyno through estrogen mediated pathways) and seems to cause more bloat because it acts as an aldosterone agonist (13), reabsorbing more salts from the urinary tract. On top of that it seems to have a terrible effect on our libido (can you say limp dick ?).

[Big Cat]

Boldenone gives us none of the aforementioned problems, and despite being a much, much weaker androgen than nandrolone, it seems to exhibit the same level of anabolism in vivo. Which again points in the direction of the non-AR and non-ER mediated pathways to muscular hypertrophy we discussed with testosterone. Boldenone offers two other distinct benefits that have been noted by many a user, despite lack of scientific backing so far. The first is that boldenone seems to increase the appetite. This too is most likely a non-AR mechanism, since many of its inactive metabolites like androstadiendione exhibit the same property and to the same extent, but in low doses. This could be crucial since we steroids can build our muscles, but they need something to build with. That something is amino acids derived from our protein intake, hence our high-protein diets. But to have ample amino acids left to build muscle, we must first eat sufficient calories, more calories than our maintenance of metabolism requires. And in that case it can be of huge benefit to increase your appetite.

The second advantage is that it causes an uncharacteristic rise in aerobic fitness. It is well known that androgen binding increases Erythropoetin release from the kidneys, which increases red blood cell count. Red blood cells carry oxygen through the blood stream, so we have a greater aerobic capacity. But boldenone seems to exhibit an increase in aerobic capacity, far greater than its androgenic affinity would allow us to suspect. Which is probably why this veterinary hormone gained so much human attention in the first place. Along with the increase in respiratory capacity from beta-adrenrgic stimulation (discussed later in this article) could lead us to new heights in any type of sports we practice that require endurance.

So in light of its safety and efficacy, the choice for boldenone as our secondary drug is a quite easy one.

In defense of Stanozolol

Stanozolol is a methylated drug. That means it can be taken orally and be quite effective, but also displays a certain level of liver toxicity. We need to reexamine these findings, toxicity is often overstated and it was found (14) that many cases where liver toxicity was determined based on aminotransferase levels were false positives when we looked at the CGT levels. Nonetheless some care should be taken. In general we advise no more than 6-8 weeks on any hepatoxic drug within normal doses (for stanazolol that is 50-100 mg per day) when taken orally and up to 10 weeks when injected (50-75 mg per day). After that ample time should be given to the liver to recover.

Stanozolol has no 3-keto group, which is in most cases essential for androgen binding. So it is far from the heavy androgen some would have you believe it is. But it does appear to exhibit good binding in some places. Like its parent, DHT, it seems to reduce some aromatase activity and it may guard against some progestagenic binding (15) as well (from nandrolone or trenbolone) although it is unlikely its affinity for the PR is strong enough to play a crucial role in that. It has been suggested that stanozolol may have good binding to the microsomal AR, which may explain its benefits as far as energy utilization. Both aerobic and anaerobic, stanozolol seems to exhibit a large increase in performance. Strength and explosiveness increase, and athletes seem to tire less fast. It has therefore been a favourite of many runners, both in shorter and longer distances. The main use here for us will then also be to assist in the maintaining and gaining of strength, rather than sheer mass, although its light anti-aromatase properties will also aid us in attaining a more fat-free body.

One reason, with regards to safety, why I chose to include stanozolol and not a more potent bulk-up agent as the oral component of this cycle, is because of its effects on tendons. It has long been a concern that steroid usage causes tendon damage. Directly it doesn't of course, but as muscle size increases and strength increases, so does pressure on tendons. And since the tendons do not have a large degree of vascularity they cannot adapt as quickly as the muscle. Repeated strain causes microtrauma, and when enough microtraumata have built up, eventually the tendon will rupture. Stanozolol however, has been found to increase collagen synthesis (16) where testosterone did not. Collagen is a key component in fibrous tissue such as cartilage and tendons, and may therefore offer us the bonus effect of maintaining tendon health or even repairing damage of microtrauma, and keep our cartilage healthy so we can resist the pressure on our joints.

The Goal and the diet

The goal we are pursuing with this, is to create a stable long-term plan for cycling steroids that will not only not jeopardize our health, but actually improve it. The reason we choose to use steroids however is to look better or perform better. It would therefore be unwise for a long-term plan to include excess body-fat, too much water retention etc. On the other hand, muscle growth is reliant on sufficient calories.

[Big Cat]

Our primary goal is to eat enough. If we consider what we do in a day and the calories we need to achieve that, we need to eat at the very least 20% more to see sufficient growth. Preferably 30% more. Our secondary goal is to keep fat off. The prime mover there is insulin. Insulin stores glucose in the muscle as glycogen and increases the shuttling of nutrients into fat cells. So naturally our goal is to keep insulin low. Insulin is a very anabolic hormone, but that does not mean we cannot achieve growth without it. In order to keep insulin low, we need to eat as little as possible high-glycemic carbs. Any type of carbs that contain glucose (and can therefore increase insulin rapidly) must be avoided. That increases most types of pasta, white bread, an excess amount of starches like potatoes, anything that has added sugar in it, regular table sugar, dextrose, maltodextrin, maltose and several oligosaccharides. A little fruit here and there is fine, as fructose does not appear to be so drastic in insulin levels, and low Glycemic carbs are fine as well (such as the lactose in milk and such). Our diet will probably be moderate to low-carb because of this. More importantly our diet should be high protein. Because first of all protein is what we require to build muscle. Secondly because the body can burn protein, but most likely will not if other means are available. And since we will be manipulating our beta-adrenergic system, we will have plenty of free fatty acids at our disposal. That means the amount of protein in our diet needs to be so great that with it we are eating at least 20% above maintenance, and without it we are eating at least 20% below maintenance. I would keep fat around 20-25% of your diet (from clean sources of course) and then fill the rest in as you please : high-protein and no high GI carb sources.

Because this will allow us to keep insulin low, we cannot only keep fat off, we can also maximally manipulate the beta-adrenergic system, meaning we could potentially lose fat, or at least lower body-fat percentage by keeping fat off and increasing lean body mass.

The take home message : A high-protein diet that contains little or no high GI carb sources, and that meets the demand of being at least 20% over maintenance (around 18 kcals per pound of bodyweight, but that is just an estimate).

The actual cycle

Now we need to put the cycle together. Below I will outline one good way to use these products and then offer some explanations to my reasoning. I will also already include the post-cycle regimen, even though we will discuss that at a later point in time.

Week 1-12 : Testosterone enanthate / cypionate 400-500 mg/week
Or : Testosterone propionate 150 mg every other day

Week 1-2 : Boldenone Undecylenate 600-800 mg/week
Week 3-12 : Boldenone Undecylenate 300-400 mg/week
Week 6-13 : Stanozolol 50-100 mg/day
Week 12-14 : HCG 3000/3000/1500/1500 IU / 5days
Week 12-17 : Tamoxifen Citrate 20 mg/day
Week 14-15 : Clomiphene Citrate 100 mg/day
Week 16-17 : Clomiphene Citrate 50 mg/day
Week 14-15 : (Spironolactone) 50 mg/day

Week 7-18 : Beta-adrenergic mix with ephedrine (as described below).

You may notice the dose of boldenone is larger the first two weeks, that's because longer esters tend to need some time to accumulate before showing their best effects, and by front-loading with a higher dose, we can achieve accumulation faster and see results sooner. I ran the stanozolol a week longer in this example, which should be fine considering it would take at least 2 weeks after the cycle to clear all boldenone, so the stanazolol beyond this point should cause no further suppression.

The patterns for post-cycle will be discussed at a later time.

Post-cycle discussion

Post-cycle has been touted as critical in the process of complete and total recovery. Here too I'm basing myself on certainties from a few studies and making my conclusions accordingly. That is why I offer the advice I offer. This does not mean you should conclude that anything else will necessarily be detrimental, but I cannot guarantee as good an outcome.

The choice of a Tamoxifen/clomiphene/spironolactone combination

The choice for a tamoxifen/Clomiphene combo is primarily because of two factors. Only one relevant study (1) came up as far as recovery after a stack of products (testosterone and nandrolone) was used for twelve weeks, utilized HCG and both clomiphene and tamoxifen to achieve a complete recovery of the HPTA to acceptable levels in 45 days. The second reason is the raging war over which is the better post-cycle drug, clomiphene or tamoxifen has lead to several conclusions. The first is that while 150 mg of clomiphene and 20 mg of tamoxifen have lead to roughly a similar increase in LH levels (17) , but that with the high dosing of clomiphene over time there are certain disadvantages. Such as that it may damage eyesight and may act as a weak estrogen (18) in undesirable places (like the pituitary). So using tamoxifen alongside it will allow us to lower the dose and decrease the chance of these side-effects and add the distinct benefit that Tamoxifen (being the stronger of the two) will prevent the clomiphene from exerting any much influence at the pituitary, and that it will increase LH responsiveness to GnRH (17) where Clomiphene does not. Clomiphene is still used as it seems to offer other advantages, such as an increase in SHBG (19), which may seem like a bad thing at first, but which may decrease androgen-related negative feedback and may thus be in our advantage.

Regardless of the final outcome I feel I have settled the dispute, at least in my own head. Why bother figuring it out when we can use both, limit any negative effects and reap the proven benefits of full recovery ? I used to run tamoxifen slightly less long than clomiphene, but given the suppressive effects of the latter at the pituitary, I later decided it wiser to continue running tamoxifen as long as the clomiphene.

[Big Cat]

The addition of spironolactone is one of personal choice. It is a systemic anti-androgen that will reduce androgen-related negative feedback. Lack of androgens may also increase a loss of muscle tissue however, so whether or not you run it and for how long I leave up to you. I can only offer you personal findings, no studies. But in my experience the use of spironolactone during the first two weeks of clomiphene treatment offered a significant advantage in the amount of recovery post-cycle without any significant amount of muscle loss. But since I have no actual verifiable data on this, I will not attempt to push this too hard. The use of clomiphene alone should already aid in this by increase SHBG.

The use of HCG and the things you need to know

Human Chorionic Gonadotrophin acts as an LH analogue. That means it plays no active role in increasing hypothalamic or pituitary activity after suppression, but that it will act on LH receptors such as in the Leydig cells and activate the process of natural manufacture of testosterone and estrogen in the testes. This may counter or help quicker recovery of any testicular atrophy that may have occurred during a cycle, and since it increases the capacity to produce natural hormones, will also in the end speed up recovery because the response to increase LH will be greater.

What you do need to realize is that because it acts as LH, high doses of lengthy use will decrease receptor affinity for LH and increase negative feedback, thus countering the purpose of the post-cycle. For that reason it is not used during, but rather after the cycle, and intermittent rather than continually. Since it will also increase estrogen directly and via aromatase conversion, further shutdown may be created but this should in large part be covered by your co-administration of Tamoxifen and Clomiphene. Because of its inhibitory effects on the hypothalamic-pituitary axis, we will use it during the last part of the cycle and the weeks following, when the steroids have not yet cleared our body. And cease use several weeks prior to cessation of the Clomiphene/Tamoxifen combo so as not to let it interfere with our recovery at the hypothalamus and pituitary.

I should also inform you that practical experience has taught me that while most people respond better to the intermittent administration as described above, some have responded better to more frequent administration (ED [every day] to every three days).

Ephedrine and the point of beta-adrenergic stimulation

I have been referring to the beta-adrenergic system all throughout this article and I know a lot of you are dying to find out what the hell I'm talking about. Most of you who know the term beta-adrenergic have heard in relation to certain fat loss supplements. And that will be a key part of what we discuss here. But beta-adrenergic stimulation offers both catabolic benefits (lipolysis in adipocytes) and anabolic benefits (increased protein synthesis in muscle tissue). Naturally our high calorie diet will prohibit us from losing a great deal of fat and in most cases we may not lose any. But if we can prevent adding fat, the consequent increase in lean muscle tissue will lower our body-fat percentage favourably.

I will explain the mechanism of the beta-adrenergic system in a minute, but first we need to understand that we have beta-adrenoreceptors on fat cells, that will initiate the release of fatty acids for oxidation (fat loss) and that we also have them on muscle cells, where they will increase protein synthesis (20). That means muscular hypertrophy will be greater with adequate caloric intake while restricting fat loss. The combination should result in a lower body-fat percentage since lean body mass will increase and fat storage remains status quo.

The beta-adrenergic system in a nutshell

Imagine the end of a nerve, then a space and then a fat cell (adipocyte). The space between the nerve and the adipocyte is called the synapse or the synaptic space. The nerve stimulates the adipocyte via electrical charges (ion streams) or neurotransmitters. Among the neurotransmitters is a hormone called noradrenaline (NA). When NA is released into the synapse, it has several receptors it can bind to on the adipocyte. They are classified into two categories, alpha and beta. The alpha receptors will inhibit fat loss (or protein synthesis in the muscle cell) while the beta receptors will increase fat loss (or protein synthesis in the muscle cell).

When a beta-receptor is engaged it will release a stimulatory G-protein into the cell, the alpha variation will release an inhibitory G-protein into the cell. These proteins will activate or deactivate the enzyme adenylate cyclase which splits ATP molecules into cyclic AMP (cAMP) molecules. cAMP is what we call the second messenger, the transporter of the signal in the cell. Without cAMP stimulation would not occur. cAMP activates the catalytic subunit of protein Kinase A, which activates Hormone sensitive Lipase (HSL) by phosphorylating it to HSL-P. HSL-P in turn will initiate a three step process by which it removes fatty acids that are bound to an alcohol function (normal storage of fat is triglycerides). These free fatty acids can be transported outside the cell by certain proteins and then used as fuel for the body, completing the oxidation of fat.

[Big Cat]

In muscle cells the process is similar, with stimulation, cAMP etc, but will obviously differ in the last few steps, leading to protein synthesis.

Beta agonists and the diet : losing fat AND gaining muscle?

The main regulator of the system is insulin, which has the exact opposite effect as noradrenaline. So obviously we will have to keep insulin under control as much as possible. That will allow us to use the beta-adrenergic system to its maximum potential. Now noradrenaline has been touted as anti-catabolic, but this effect is observed because it causes protein synthesis and thus less protein is released from the cell to be burned. The effect is in other words anabolic. Which is why it may serve us as far as increasing lean muscle mass, especially since we have demonstrated effectively that testosterone and most likely boldenone will upregulate beta-adrenoreceptors. By using beta stimulators later in the cycle and post-cycle (provided adequate calories in diet) we can insure maximum muscle gain and muscle maintenance post-cycle, while keeping the fat off.

Because we need to eat a certain amount of calories to grow it is unrealistic to expect a great deal of fat loss capacity from the use of these products. But it should go a long distance in preventing the addition of further fat mass, which, combined with a significant increase in lean body mass, will decrease body-fat percentage. However, some fat loss is not unthinkable, since we are eating a high protein diet and the body will prefer the available free fatty acids, especially if we can bring them into circulation.

Ephedrine Hcl

Our first goal in this endeavour should be to have a product that stimulates noradrenaline. Now some may think it is wiser to opt for other methods of fat loss, but DNP, T3 and corticosteroids will make it increasingly difficult to preserve lean mass. Other still may prefer that the use of stronger specific beta-2 or beta-3 agonists like clenbuterol, salbutamol, albuterol or octopamine should be used, but because of their potency they will quickly render the beta-adrenergic system useless, and only make use of part of the available systems to us (either beta-2 or beta-3 instead of both). The beta-2 receptor is most certainly the prime mobilizer here, where the beta-3 only has minimal if any activity, but has been deemed crucial to continuation of cathecholamine responses under sustained sympathetic activity (21). Most likely it maintains a certain amount of beta-adrenergic stimulation, but without increasing metabolism, so as to spare calories but continue the use of fatty acids for survival. As much as 40% of the activity of ephedrine has been attributed to the beta-3 stimulatory effects (22).

Since ephedrine acts by increasing natural noradrenaline release, it serves our purpose the best. It is also the more natural approach and less taxing on our system than some other fat loss preparations (T3 causes rebound by TSH shutdown, clenbuterol is very strong in increasing heart rate, and the list goes on). As opposed to more specific beta-2 agonists such as the likes of clenbuterol, ephedrine actually seems to have improved effects on thermogenisis after continual use (23). Ephedrine Hcl is our best choice here, although some will no doubt opt for standardized preparations using ma huang. This herb, depending on preparation will contain more or less than the actual 8% ephedra from dose to dose and is hence unreliable. If this is the only thing available to you, it is better than nothing however, but pure ephedrine Hcl should be preferred.

Yohimbine Hcl

Yohimbine is quite critical in the equation. It acts as a potent alpha-adrenoreceptor blocker (strong on alpha2, mild on alpha1). The alpha receptors inhibit adenylate cyclase activity in the cell, increase its breakdown and thus prohibit fat loss. In normal people with normal diets, there is a certain level of adrenergic action. But noradrenaline seems to have greater affinity for alpha receptors, so not enough beta receptors get filled to cause fat loss / protein synthesis. By increasing the noradrenaline release we have already filled all alpha receptors and a greater number of beta-receptors. But if we could block the alpha receptors, then that would lead not only to more potency from the existing noradrenaline / beta-latches, but it would create MORE noradrenaline / beta-latches since less NA is taken up by the alpha receptors. Thus a major strike in the right direction.

A second factor we need to consider is the alpha-2 receptor concentration on our nerve as well, which, when activated, will increase the re-uptake of noradrenaline into the nerve. By blocking this receptor we prevent re-uptake and again, more NA is available to us. So yohimbine interferes with the NA's auto-regulated negative feedback loop by acting as an alpha receptor antagonist, pre-synaptic and post-synaptic.

This is also very crucial in fat loss or prevention of fat gain in predisposed areas (abdomen and obliques in men, gluteo-femoral region in women), because these area's have adipocytes that are extremely rich in alpha receptors, but rather poor in beta receptors (ever tried getting rid of those love handles ?).

Caffeine

Apart from the well-documented findings that the combination of ephedrine and caffeine far outperformed either alone (24) in terms of lipolysis, caffeine acts very distinctly as a phospho-diesterase inhibitor. PDE's are released in the cell as a response to continual beta-adrenergic stimulation and commences the breakdown of cAMP and creates adenosine from it. Adenosine travels outside the cell and has its own receptor, that acts very similarly to the alpha-receptor to block adenylate cyclase activity and stop fat loss. Caffeine has also been shown to prevent this process by blocking the adenosine receptor and seems to offer some benefit in preventing noradrenaline reuptake (25), like yohimbine does. Possibly via the same mechanism (adenosine receptor blockade).

Caffeine also decreases insulin sensitivity, further helping to assure maximal aid in preserving and enhancing the beta-adrenergic system, and possibly helping to prevent wrong doing from eventual lapses in our diet.

Lastly caffeine is a potent diuretic and will reduce water retention in the body, offering us a leaner and more striated appearance.

[Big Cat]

Forskolin

Forskolin is product derived from the coleus forskohlii plant that has been shown to upregulate the activity of the enzyme adenylate cyclase, which we have previously shown to be important as it creates cAMP accumulation needed for the second messenger response to beta-adrenergic stimulation. While forskolin by itself may have a null effect (it was previously used to lower blood pressure where beta-adrenergic stimulation should increase blood pressure), it should have various useful effects to us. In combination with these other products cAMP accumulation will further decrease any effect from prostaglandins and adenosine receptor stimulation, or alpha2-regulated inhibition. This allows a stable environment for second messenger transport.

Guggulsterones

Guggulsterones are an age-old Ayurvedic medicine touted to increase thyroid activity. This has nothing to do with the beta-adrenergic system, and at first may seem rather obsolete. Continual fat loss and lower calorie diets have been known to cause a starvation response whereby T4 to T3 conversion is lowered and the opposite conversion increased to lower thyroid activity and thus slow metabolic rate. This occurs so that we do not use our entire fat supply in just a few days and can stay alive longer under starvation conditions. Now ephedrine has been shown to actually upgrade T4 to T3 conversion or at the very least lower the opposite reaction (23).

But this latter occurrence has been attributed to the continual alpha-receptor stimulation that ephedrine would display under normal conditions, but since we use an alpha-receptor blocker it is unlikely we will be able to make as much use of this benefit, and so the addition of Guggul is advisory, as it has been shown to increase T4 to T3 conversion (26).

Most likely, to avoid early beta-2 phosphorylation we will add yohimbine at a later stage, and should add guggul at the same time. [Guggulsterones used in the studies showing T3 increase were the E&Z extract]

Acetyl-L-Carnitine

After HSL-P has released fatty acids they just sit there basically. They require protein transport to get them into circulation where they can be used as fuel. If not, and under the high caloric diet we have outlined this is most likely, they will simply be re-esterified again. This is why we do not expect any fat loss. But just to give nature a helping hand we might add some Acetyl-L-Carnitine (ALC), one of the proteins used to transport fatty acids. Adding too much has no use as supra-physiological amounts have shown little to no benefit, but adding some may increase any possible downregulation of the transport systems and increase the likelihood that some actual fat is used.

Putting it all together

So what sort of doses and what sort of dosing pattern do we need ? Well I won't bore you with the details, but this particular mix has been most effective :

Product Per dose
Ephedrine Hcl 12.5 mg
Caffeine 100 mg
Yohimbine Hcl 3 mg
Forskolin 20-30 mg
Acetyl-L-Carnitine 200 mg
Guggulsterones 30 mg

You can opt to take 1 dose 6 times per day, roughly every 2.5 hours, or 2 doses 3 times per day, roughly every 5 hours. This is preferably taken between meals when it is most likely there is least insulin interference and most chance of any additional calories being burned that are not from food. For people who have a tendency to get jittery on ephedrine and are bothered by this, I suggest the first dosing pattern which has lower peak doses. For most people I would recommend the 3 a day dosing pattern however.

Use the Ephedrine/Caffeine/Forskolin/ALC combo for the full outlined twelve weeks, then add the yohimbine and guggul the last 6 weeks. For those wishing to do so, the last two weeks clenbuterol can be added to emphasize the fat loss effect.

More Dietary and supplementary Implications in regards to mass gain on-cycle and maintenance post-cycle.

It is imperative that the high-calorie diet is maintained at the very least through week 17. The chance of losing muscle when protein synthesis is kept high and no caloric deficit needs to be filled will severely decrease the chance of losing lean body mass. That goes without saying. It also goes without saying that this diet should be spread out over 5-6 meals daily in order to keep metabolism and nutrient supply high. But there are certain things we can do to enhance our chances as well.

Leptin management

Leptin has been hailed as the new miracle discovery in fat loss. It's a hormone that seems to regulate the amount of fat to muscle that is burned when glycogen is not available to meet energy demands. Leptin seems to be exponentially higher in obese individuals than in leaner specimen. So being lean and staying lean, our leptin levels are not to our advantage. Leptin levels are marked by higher cAMP breakdown and greater adenosine interference. So thanks to caffeine and forskolin we can sort of inhibit the effect of our low leptin on interfering with the use of fat for fuel, but we can also implicate other measure of supplementation.

Normally I might recommend Vitamin E, which has been shown to elevate leptin levels (27) slightly. But since Vitamin E seems to lower blood clotting and this effect can be enhanced by steroid use, it is never advisory to take large amounts of vitamin E while on a steroid cycle. If you have some in your multi-vitamin, lets say no more than 30-40 units, I doubt it will be a problem, but more than that may not be safe.

That leaves only two other products proven to elevate leptin, and since nicotine (28) is highly addictive and goes against our health-conscious approach, that leaves us only with zinc (29) . The addition of the highly available zinc aspartate may offer us some benefits in keeping leptin levels higher and is worthwhile in our supplementation regimen.

[Big Cat]

Magnesium

This mineral is so versatile in its use to us, that it seems unlikely that I could mention it under anything other than its own paragraph. First of all it needs to be mentioned that many athletes are deficient in magnesium, and that this deficiency is hard to detect since magnesium is stored mostly in interstitial space and intracellularly (30), and not so much in blood where it is measured. Blood levels appear to be rather constant despite deficiency.

Now magnesium is necessary for proper muscle contraction (31), glycolysis (use of blood sugar, effectively lowering glycogen increasing efficiency of the beta-adrenergic system), protein synthesis, preventing cardio-vascular disease, improved cellular metabolism, and creatine storage. As such taking supplemental magnesium in a fairly large dose will be beneficial to us.

ZMA

Since we recommend both the intake of zinc and magnesium, it may be wise to opt for a ZMA supplement, that contains 30 mg of chelated zinc and 450 mg of chelated magnesium. Since both can be hindered in absorption by calcium (32), and bodybuilders often eat calcium-rich foods, it is better to take them together during a time when the stomach is relatively empty (at least 60 minutes after the last meal) and without calcium present. The time of day preferentially near sleeping time as Zinc has beneficial effects in maintaining optimal testosterone levels and resting recovery, so this is the time of greatest activity.

Creatine

Creatine has been the age-old supplement in bodybuilding, from high meat intake to the latest fad in creatine-enhancement supplementation. However, it appears plain old micronized creatine is still your best bet. The efficacy increase of most of these hyped up supplements is so small it in no way makes up for the price increase. Why do we recommend creatine here ? Well mostly energy supply during the late end of the cycle and the post-cycle. Glycogen will be low due to our low intake of high-GI carbs and enhanced glycolysis through supplementation. Therefore added creatine may be able to restore our ATP losses to some degree, at least for anaerobic activity like weight training, so we have ample energy at all times. By having increased magnesium intake we should be able to increase creatine storage as well. Transport of creatine into the cell will be somewhat limited in the absence of insulin, but should in no way be a problem. Considering the length of time we will use this and the minimal input we expect from it, it makes little sense to load the creatine. Taking 3 grams of creatine 45 minutes prior and again immediately after our workouts should be more than sufficient.

Vitamin B complex

Here too the benefits to be had are multiple. B-vitamins have common characteristics that include enhancing the circulation, allowing for a better oxygen supply and more energy, helps with blood formation and metabolizes carbohydrates. That means once again a valuable contribution to our goal of adding lean mass to the frame. B-vitamins are water-soluble and readily depleted, so making sure we have optimal levels on a daily basis is needed. A B-Vitamin complex that supplies a 100-1000% of the daily needed amounts is recommended.

Putting together supplementation

On workout days we will use 3 grams of creatine about 45 minutes before the workout, and again, with a post-workout protein shake (note : no weight gainers or added carbs) within 30 minutes of completing training, from week 1 through week 13.

The rest of our supplementation is taken throughout the cycle and post-cycle : 1 dose of B-vitamins with breakfast, 1 dose of ZMA on an empty stomach between before last and last meal of the day, in the absence of calcium. Last meal should be taken prior to bed.

Protein shakes should be used as deemed necessary to increase protein and/or calorie intake at any time during the day. Protein shakes are preferably a combination of casein and whey, mixed in milk.

Other worthwhile supplementation, but certainly not necessary, are dessicated liver tablets, CLA and omega-3 and 6 fatty acids to improve cholesterol profile.

The use of an anti-aromatase

Some may not be satisfied with just the lean results from using testosterone propionate, boldenone undecylenate, stanozolol and a beta-adrenergic cocktail on a low-carb, high protein diet. The aromatization from the testosterone/boldenone may still be too much to cope with. In that case an anti-aromatase drug can be added. But we should first point out that blocking the aromatization of these steroids will result in a lower HDL/LDL cholesterol ratio and thus has implications as far as cardio-vascular risk.

If an anti-aromatase product is used, I recommend proviron over femara or arimidex, even though the latter are stronger. Proviron is milder and does allow for some estrogen, which gives us the increased benefits mentioned under the header "in defense of testosterone" previously while still reducing over-all levels a bit which decreases water retention and visceral fat accumulation.

Now testosterone/boldenone lower subcutaneous fat primarily where the beta-adrenergic cocktail will reduce visceral fat first and then subcutaneous fat. So they are highly synergistic. By blocking the aromatase you will increase visceral fat burning because you stop estrogen's anabolic effect on visceral fat stores. I would only add Proviron if you note a tad too much water retention or if you experience signs of gynocomastia (male breast growth). Start with 25-50 mg and do not increase unless deemed absolutely necessary. At this dose you can run the proviron week 1-13, if you have to increase it, consider decreasing it again when problems desist.

What about the side-effects that will occur?

Acute side-effects have been put into the background because they pose no threat to our health and existence per se. But since they are often visible, we still care to address them as best as we can :

Gyno

When nipples get itchy or swollen and you fear gyno may begin to set in, you should use the proviron as outlined above. In the acute stage, running some 20-40 mg Nolvadex the first 3-4 days may offer relief as well. Again, any longer is not advisable since we do depend on estrogen for certain effects such as Growth Hormone increases and androgen receptor upregulation.

Hair loss

Hair loss via steroid use is a pre-existing genetic condition. If you do not have it all the steroids in the world won't affect your hair. If you do have it however, then its an inevitable fact and sad to be the one to say it, but you might as well deal with it while you can still get the body to compensate for it.

I highly advise against the two standard treatments, which are the administration of either a 5-alpha-reductase blocker or an anti-androgen. That the latter is a bad idea I needn't point out. Using an anti-androgen would entirely defeat the purpose of using androgenic steroids. Among this class of drugs is spironolactone (aldactone). That the former is a bad idea may not be known to most. First of all since stanozolol is DHT derivative and boldenone has no high affinity for the 5AR, using a 5AR inhibitor would not affect these drugs. It would only stop the conversion of testosterone to DHT. Now we already mentioned the negative effects resulting from less DHT including less strength, lower neuromuscular response and increased chance of estrogenic side-effects (too much estrogen works against us because of its effects on gluconeogenisis).

So you might try topical remedies such as minoxidil hair sprays or something if you believe that sort of thing would work, but stay away from finasteride (proscar, propecia) and spironolactone (aldactone).

Liver damage

Liver damage is often overstated. We do use a liver taxing drug (stanozolol) so we do need to address this. Oftentimes the negative effect of oral steroids on the liver have been quoted because of elevated aminostransferase values, which are indeed a partial indicator for liver damage. However these levels will rise as a result of muscular damage from training as well and offer us no conclusion as to the actual negative effect. For that purpose it is essential that when you have bloodwork done, you ask the doctor to check creatine kinase and CGT levels as well. If the former is higher than normal and the latter remains unchanged then no liver damage has occurred. If the opposite is true and CK is normal and CGT is elevated, then liver damage has occurred.

If it does occur then the use of milk thistle (sylibum marianum) or Picrorohiza (33) is recommended. Both appear to have a good effect on liver regeneration. Because some of the activities of these products may be mediated by enhancing cytochrome P-450 activity, it Is not recommended that you take them as a precautionary measure. Instead, have blood levels checked for the aforementioned values once every 3 weeks while taking stanozolol and if deemed necessary, add them to your supplementation regimen

Loss of Libido

Since we use testosterone as a base, this will not be problem. Additional use of proviron would further stimulate libido, so it is actually possible your libido may be phenomenally higher than normal.

Acne

Get over yourself, these are zits, they pose no threat to your health. Proper skin care and OTC medication can be used if it makes you feel better, but avoid the use of prescription medication like anti-biotics and Accutane at all costs, as these products are far more taxing on your liver than stanozolol. So in the interest of your health prescription medication for acne is not advisable.

If you get acne so bad that it really ruins your life : DON'T USE STEROIDS !!!!

[Big Cat]

Virilisation

If you are a a man : who cares ?
If you are a woman : DON'T USE STEROIDS !!!!

Prostate hypertrophy

No link between steroids and prostate cancer has ever been demonstrated, however with age a condition known as benign prostate hypertrophy can occur. Since we previously determined estrogen to be the causative factor and that androgens can actually be used as therapy to counter BPH, adding proviron at 50 mg/day should limit your risk of this. If you already have BPH or other prostate problems : DON'T USE STEROIDS !!!!

Appendix : Working with your doctor

As we mentioned before, steroid use should occur under medical supervision. With this document you are capable of interpreting a lot of data. So this may be a good time to point out what sort of data you will need from your doctor. I would advise, as I do to all my athletes, that you have blood work done every 3 weeks while on and several weeks after the cycle, starting with the week before the cycle. The following data should be collected :

Suppression and recovery are examined based on levels of LH, FSH, DHEA, androstenedione and testosterone. During the cycle blood levels of testosterone and androstenedione should rise, as other decline and post-cycle a reverse tendency should be noted.

Liver damage is based on aminotransferase values (ALT, AST) as well as Creatine Kinase (CK) and gamma-glutamyltransferase (CGT). When CGT is elevated we can speak of liver damage. If it is significantly elevated use of milk thistle and cessation of use for stanozolol is recommended. If CGT is not elevated, CK levels may explain why ALT and AST are elevated.

Thyroid activity is measured with levels of TSH, T4 and T3. TSH levels should not be affected at any time during this cycle since no exogenous thyroid hormone is used. The amount of T4 and T3 are crucial as both steroid use and yohimbine use will suppress T4 to T3 conversion, and guggul should counter that to some extent. This is why it may be wise to keep an eye on this as well. It can't hurt and if you are having blood checked anyway, can't see why you wouldn't have this checked

Lastly, cholesterol values. Total cholesterol and HDL/LDL ratio should be examined. During the cycle HDL/LDL-ratio should remain normal and total cholesterol should lower, unless you are using proviron, then HDL/LDL ratio may drop. After the cycle and complete recovery, values should restore themselves.

Peter "Big Cat" van Mol

References

http://www.medibolics.com/ScallyVergelAstractHPGA.pdf

Aromatization of androgens to estrogens mediates increased activity of glucose 6-phosphate dehydrogenase in rat levator ani muscle. Endocrinol 106(2):440-43 1980

and

The pentose phosphate pathway in regenerating skeletal muscle. Biochem J 170: 17 1978

Activation of the somatotropic axis by testosterone in adult males: Evidence for the role of aromatization. Weissberger and Ho. J Clin Endocrinol Metab 76 (1993) 1407-12.

Modulation of the cytosolic androgen receptor in striated muscle by sex steroids. Rance, Max. Endocrinol 115 (1984) 862-6

Foster BA, Cunha GR. Efficacy of various natural and synthetic androgens to induce ductal branching morphogenesis in the developing anterior rat prostate.
Endocrinology. 1999 Jan;140(1):318-28.

Sader MA, Griffiths KA, McCredie RJ, et al. Androgenic Anabolic Steroids and arterial structure and function in male bodybuilders. J Am Coll Cardiol 2001 ; 37(1): 224-230

Zmuda JM, Cauley JA, Kriska A, et al. Longitudinal relationship between endogenous testosterone and cardiovascular disease risk-factors in middle-aged men. Am J Epidemiol 1997; 146(8): 609-617 (13-year follow-up of former Multiple Risk Factor intervention Trial participants)

Diekerman RD, McConathy WJ, Zachariah NY. Testosterone , sex-hormone binding globuline, lipo-proteins and vascular disease risk. J Cardiovasc Risk 1997; 4(5-6): 363-366

Moffat SD, Zonderman AB, Metter EJ, Blackman MR, Harman SM, Resnick SM. Testosterone Supplementation Therapy for Older Men: Potential Benefits and Risks.J Am Geriatr Soc. 2003 Jan;51(1):101-115.

Schanzer, Donike , metabolism of boldenone in man : gas chromatographic/mass spectrometric identification of urinary excreted metabolites and determination of excretion rates, Bol Mass Spec 21, 1992, 3-16

Clark SW, Sweet F, Warren JC., Synthesis and use of affinity-labeling steroids for interceptive purposes., Am J Obstet Gynecol 1975 Mar 15;121(6):864-73


Hochberg RB, Hoyte RM, Rosner W., E-17 alpha-(2-[125I]iodovinyl)-19-nortestosterone: the synthesis of a gamma-emitting ligand for the progesterone receptor., Endocrinology 1985 Dec;117(6):2550-2

and

Traish AM, Williams DF, Wotiz HH., Binding of (3H)7 alpha,17 alpha-dimethyl-19-nortestosterone (mibolerone) to progesterone receptors: comparison with binding of (3H)R5020 and (3H)ORG2058., Steroids 1986 Feb-Mar;47(2-3):157-73

Sekihara H, Ohsawa N, Kosaka K., Biochem Biophys Res Commun 1980 Mar 28;93(2):495-500


Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ. Anabolic steroid-induced hepatotoxicity: is it overstated? Clin J Sport Med. 1999 Jan;9(1):34-9.


Ellis AJ, Cawston TE, Mackie EJ., The differential effects of stanozolol on human skin and synovial fibroblasts in vitro: DNA synthesis and receptor binding., Agents Actions 1994 Mar;41(1-2):37-43

and

Brestel EP, Thrush LB., The treatment of glucocorticosteroid-dependent chronic urticaria with stanozolol., J Allergy Clin Immunol 1988 Aug;82(2):265-9

Falanga V, Greenberg AS, Zhou L, Ochoa SM, Roberts AB, Falabella A, Yamaguchi Y. Stimulation of collagen synthesis by the anabolic steroid stanozolol. J Invest Dermatol 1998 Dec;111(6):1193-7.

Vermeulen, Comhaire. Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men. Fertil and Steril 29 (1978) 320-7

Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro. Am J Physiol 1981 Feb;240(2):E125-30

Adamopoulos, Kapolla et al. The effect of clomiphene citrate on sex hormone binding globulin in normospermic and oligozoospermic men. Int J Androl 4 (1981) 639-45

Astrup A, Buemann B, Christensen NJ, Toubro S, et al. The effect of ephedrine/caffeine mixture on energy expenditure and body composition in obese women. Metabolism 1992 Jul;41(7):686-688

Langin D, Tavernier G, Lafontan M. Regulation of beta 3-adrenceptor expression in white fat cells. Fundam Clin Pharmacol 1995; 9:97.

Liu YL, Toubro S, Astrup A, Stock MJ. Contribution of beta 3-adrenoceptor activation to ephedrine-induced thermogenesis in humans. Int J Obes Relat Metab Disord 1995 Sep;19(9):678-685

Astrup A, Lundsgaard C, Madsen J, Christensen NJ. Enhanced thermogenic responsiveness during chronic ephedrine treatment in man. Am J Clin Nutr. 1985 Jul; 42(1): 83-94.

And

Astrup A, Madsen J, Holst JJ, Christensen NJ The effect of chronic ephedrine treatment on substrate utilization, the sympathoadrenal activity, and energy expenditure during glucose-induced thermogenesis in man. Metabolism 1986 Mar;35(3):260-265

Dulloo AG, Miller DS, The thermogenic properties of ephedrine / methylxanthine mixtures: Human studies. Int J Obes 1986; 10: 467-81

Kalsner S, Frew RD, Smith GM., Mechanism of methylxanthine sensitization of norepinephrine responses in a coronary artery. Am J Physiol 1975 Jun;228(6):1702-1707

Tripathi, YB., et al: Thyroid stimulating action of Z-Guggulsterone obtained from commiphora mukul. Planta Medica Feb;(1):78-80,1984

and

Tripathi, Y.B., et al: Thyroid stimulatory action of (Z)-Guggulsterone: Mechanism of action. Planta Medica 54 (4): 271-277, 1988

And

Panda, Sunanda, et al: Gululu (Commiphora Mukul) induces triiodothyronine production: Possible involvement of lipid peroxidation. Life Sciences 65(12):PL 137-141, 1999

Isermann B, Bierhaus A, Tritschler H, Ziegler R, Nawroth PP. alpha-Tocopherol induces leptin expression in healthy individuals and in vitro. Diabetes Care 1999 Jul;22(7):1227-8

Eliasson B, Smith U. Leptin levels in smokers and long-term users of nicotine gum. Eur J Clin Invest 1999 Feb;29(2):145-5

Chen MD, Song YM, Lin PY. Zinc may be a mediator of leptin production in humans. Life Sci 2000 Apr 21;66(22):2143-9

Shils ME. Magnesium. In: Brown ML,ed. Present Knowledge in Nutrition, 6th ed. Washington, DC: International Life Sciences Institute Nutrition Foundation, 1990: 224-232.

P. Wester. "Magnesium," Am J Clin Nutr 45 suppl (1987): 1305-1312.

E. Hamilton, S. Gropper, The Biochemistry of Human Nutrition (St. Paul, MN: West publishing, 1987).

Luper S. A review of plants used in the treatment of liver disease: part 1. Altern Med Rev. 1998 Dec;3(6):41

[Big Cat]

please only messages to the point ...

[maxwells_revenj]

excellent post big cat, learned quite a bit, as always.

-max

[raybravo]

So what are the benefits of E2 ? increases the release of human Growth Hormone (3)
yeah even ive heard of estrogen increasing gh , now we know that gh lowers activity lipoprotein lipase in fat tissue thus preventing fat storage , while there is also this notion of estrogen being anabolic to adipose tissue . so my question is that to what extent are these 2 things cancelling each other out ?

[raybravo]

yohimbine is supressing t4 to t3 conversion ? to what extent would this be happening if a man is say using 400 mcg t4 and alongside running 20 mcg yohimbine hcl ? and how much would the equation change upon the addition of guggulsterones ?

[Big Cat]

Originally posted by raybravo
yeah even ive heard of estrogen increasing gh , now we know that gh lowers activity lipoprotein lipase in fat tissue thus preventing fat storage , while there is also this notion of estrogen being anabolic to adipose tissue . so my question is that to what extent are these 2 things cancelling each other out ?

Well lets put it this way : we have no use for excess estrogen either. Many other things in this plan should sufficiently minimize the effect on neoglucogenisis, so it should not pose a major problem in this example, but obviously in larger amounts or more insulin prone diets, we will notice an anabolic effect on adipose tissue.

[raybravo]

it has been concluded that both nandrolone (11) and several of its metabolites (12) exhibit progestagenic activity (which causes gyno through estrogen mediated pathways) and seems to cause more bloat because it acts as an aldosterone agonist (13), resorbing more salts from the urinary tract
very good point made , increasing estrogen and aldosterone agonist , last thing we want to preserve some muscle definition !
makes u wonder why some of the old pros even used it while dieting !

[Big Cat]

Originally posted by raybravo
yohimbine is supressing t4 to t3 conversion ? to what extent would this be happening if a man is say using 400 mcg t4 and alongside running 20 mcg yohimbine hcl ? and how much would the equation change upon the addition of guggulsterones ?

I have no exact data on this but I would not overestimate the strength of guggul in negating that effect. I believe guggul to be effective in negating that effect to some extent, giving us more leeway with metabolism, but I do not seriously expect T3 levels to be in the high normal range.

Supraphysiological levels of T4 may shift the balance in your favour however, but would supress TSH and cause rebound upon cessation.

[raybravo]

bc , what effect would arimi or femera have on shbg levels ?? if its increasing shbg levels , then one more reason to go with proviron during a cycle .

[raybravo]

bc , pretty hard to consume around 20 cals a pound and still maintain low insulin levels keeping the beta-adrenergic stimulation still active to the stuf we wud be using . how do we go about this !? seems pretty impractical man .

[raybravo]

since the tendons do not have a large degree of vascularity they cannot adapt as quickly as the muscle. Repeated strain causes microtraumata, and when enough microtraumata have built up, eventually the tendon will rupture. Stanozolol however, has been found to increase collagen synthesis (16) where testosterone did not. Collagen is a key component in fibrous tissue such as cartilage and tendons, and may therefore offer us the bonus effect of maintaining tendon health or even repairing damage of microtrauma, and keep our cartilage healthy so we can resist the pressure on our joints.

but what about winny lowering cortisol levels ? that would cause some joint pain wouldnt it ? atleast from most people's practical experiences , it does seem to cause some joint pain , but what u posted is interesting , so wondering where both of these match , increased collagen synthesis and lowered cortisol receptor binding .

[raybravo]

another thing , how is clen increasing heart rate without being a b1 receptor agonist bro ?

[Big Cat]

Originally posted by raybravo
bc , pretty hard to consume around 20 cals a pound and still maintain low insulin levels keeping the beta-adrenergic stimulation still active to the stuf we wud be using . how do we go about this !? seems pretty impractical man .

Not really, avoid candies, soda's, pasta's and additional sugar. Fructose does not appear to have a major impact on insulin release, so this is doable.

[Big Cat]

Originally posted by raybravo
but what about winny lowering cortisol levels ? that would cause some joint pain wouldnt it ? atleast from most people's practical experiences , it does seem to cause some joint pain , but what u posted is interesting , so wondering where both of these match , increased collagen synthesis and lowered cortisol receptor binding .

Cortisol would have to be drastically low for that to occur and I don't see that happening on a low-insulin diet.

[Big Cat]

Originally posted by raybravo
another thing , how is clen increasing heart rate without being a b1 receptor agonist bro ?

Mainly b2 is responsible for heart rate increases. only the b3 seems to be devoid of such activity.

[raybravo]

the beta-3 only has minimal if any activity, but has been deemed crucial to continuation of cathecholamine responses under sustained sympathetic activity (21). Most likely it maintains a certain amount of beta-adrenergic stimulation, but without increasing metabolism, so as to spare calories but continue the use of fatty acids for survival. As much as 40% of the activity of ephedrine has been attributed to the beta-3 stimulatory effects (22).
another thing to add here , which i found in lyle mcdonald's book , brown adipose tissue (in which b3 receptors are found primarily) can grow larger like any other tissue if chronically stimulated by such things as ephedrine etc . (1)
an increase thus in brown adipose tissue would increase the thermogenic response to those same stimuli .
(1)Duggalo AG ,ephedrine ,xanthine and prostaglandin inhibitors :actions and interactions in the stimulation of thermogenesis . int J obes (1993)17 (suppl .1) S 35-S40 .

[raybravo]

also bc , what are ur thoughts on using hcg mid cycle , lets say start of week 6(day 36) , one shot of 3000 iu and another after 5 days of the same dose , i'm thinking this should help better post cycle recovery . ur thoughts on this bro ?

[Big Cat]

Originally posted by raybravo
also bc , what are ur thoughts on using hcg mid cycle , lets say start of week 6(day 36) , one shot of 3000 iu and another after 5 days of the same dose , i'm thinking this should help better post cycle recovery . ur thoughts on this bro ?

As the first reference indicates this is a valid option, intermittent use of HCG can indeed prevent testicular atrophy. The point we need to keep our eyes on however is that we don't have a definition ofr intermittent in this case and we have not established how much HCG is too much.

I can only make the recommendations i made because I have verified them for myself on several athletes with blood work.

While we can both agree that on-cycle use is another option, I can't recommend any cycling pattern that is guaranteed to deliver the same or better results.

[raybravo]

i think longer than 3 weeks on hcg would be pushing it . but i think mid cycle hcg would be an pretty good addition u know, keeping a decent set of balls at the end of the cycle :) .

[Big Cat]

Like I said, it may very well be. But I can't advise it as a certainty.

[Pie-Bald]

Originally posted by Big Cat
So testosterone cannot only promote more lean mass than any other steroid, it can also make you live longer by decreasing heart risk, and get better quality out of your remaining years by enhancing cognitive performance and fighting dementia.

Hence my case for using testosterone as a base of our safe cycle.

[

When you speak of the above beneifts along with the others mentioned, are you refering to HRT levels of Test or levels of Test commom in steroid using bodybuilders?

[Big Cat]

Both. The study I provided here was performed on healthy young male bodybuilders using testosterone. Total cholesterol was lowered, LDL was lowered and HDL remained or was slightly lowered. The effects were slightly more beneficial for HRT type deals, but certainly were not detrimental in either case.

[NickM234]

I have a question, you say test recovers completely by 45-50 days. But it obviously wouldn't recover all at once and I feel a good deal of my test (maybe half or more) is back in a couple weeks. Would I be right to assume recovery happens quickly when the steroids first reduce to low levels, then slows down late in recovery?

[Big Cat]

Originally posted by NickM234
I have a question, you say test recovers completely by 45-50 days. But it obviously wouldn't recover all at once and I feel a good deal of my test (maybe half or more) is back in a couple weeks. Would I be right to assume recovery happens quickly when the steroids first reduce to low levels, then slows down late in recovery?

Couldn't say. In normal circumstances the first few days after levels drop significantly below baseline would initiate a good reaction, but testicular atrophy would prevent a great surge in testosterone. So I think its more gradual than that. But here we are talking about forced recovery with HCG/Clomid/Nolva and possibly aldactone, so this may not hold true

I would not be too quick to make assumptions about this.

[BSMNT732]

Excellent post, you'll have to copy and paste in the Best of forum. Im glad that you have found some time to post again.

[user43390fgui8t]

bump... amazing thread BC. Good research.

[pogue]

Originally posted by Big Cat
So you might try topical remedies such as minoxidil hair sprays or something if you believe that sort of thing would work, but stay away from finasteride (proscar, propecia) and spironolactone (aldactone).

What about topical spironolactone? Are you suggesting to stay away from all anti-androgens, or would topical be the exception?

[RetiredMod]

Big Cat you have outdone yourself again very interesting article :)

Although I have a sneaking suspicious you've been reading my thoughts... ;) The cycle I am about to start is roughly the same layout you had. I was going to run the winny at the beginning but still debating. I had tinkered with the idea of throwing in an eca stack, and was planning on the yohimburn. Think I'll take your advice and add a few other supps...basically I'll be trying this cycle out.

I noticed you said either 500mg/wk of enth/cyp or 150mg EOD of test prop, but wouldn't the test prop dosages result in taking in more testosterone due to the ester weight?

[raybravo]

Originally posted by McBain

I noticed you said either 500mg/wk of enth/cyp or 150mg EOD of test prop, but wouldn't the test prop dosages result in taking in more testosterone due to the ester weight?
150 mg prop eod is 525 mg per week , and that yeilds approximately 430 mg of base testosterone , and like 360 mg of base testosterone for both test enanthate and cypionate . so yeah , good question .

[raybravo]

Originally posted by Big Cat
Well lets put it this way : we have no use for excess estrogen either. Many other things in this plan should sufficiently minimize the effect on neoglucogenisis, so it should not pose a major problem in this example, but obviously in larger amounts or more insulin prone diets, we will notice an anabolic effect on adipose tissue.
u said in this plan it wudnt be such a big thing to think about , awright agreed .
but the question still remains unanswered , to what extent is the gh producing effect of estrogen benefitial as opposed to it being anabolic to adipose tissue .
i mean how would one realise to what extent would he want to use an anti estrogen ? cos he wouldnt want to be a bloated pig , but he would also want to make use of all the positive effects of estrogen u listed out .

[Chikara]

Great posts.
Originally posted by raybravo
another thing , how is clen increasing heart rate without being a b1 receptor agonist bro ?

It does also have a beta 1 stimulating action on the heart. Thats what you feel.

http://courses.washington.edu/chat543/cvans/ansrec.htm

[ITJ]

Excellent thread Big Cat - I wish I would have had something this detailed and informative to read when I first started learning about AAS.

I have a couple of questions:

I noticed that you suggest frontloading the EQ. If you were to use a long estered test, would it be beneficial to frontload the test also?

Why do you recommend not having any high GI carbs postworkout? I thought it was of the utmost importance to quickly replenish your depleted glycogen stores after your workout no matter what type of diet you were on - keto included. And high GI carbs help your body absorb the creatine. Also, would you consider wheat rice/pasta/bread too high GI?

Lastly, you recommend only using milk thistle if liver problems arise, which is very understandable. What about using ALA throughout the whole cycle for precautionary reasons. It is a strong antioxidant, and I am not aware of any negative reasons to not use it throughout the cycle.

Once again I would like to reiterate how much of an excellent post this is. You basically summed up most of what I have learned from reading this board and others for almost 2 years now. This should be shown to anyone seriously thinking about juicing who has not done an excess amount of research. I think this should be made a sticky or atleast copied to the best of section. Thanks Big Cat, I always enjoy reading your post,

ITJ

[Punisher007]

Great read!

Couple questions for you:

1. What's your take on norephedrine. I don't mind ephedrine...but if I can get a higher or equal amount of thermogenesis out of norephedrine with less side effects, I'd rather take that :)

2. I like your idea on running low amounts of proviron throughout the cycle..but you didn't specificy how much and when to take it.

3. I'm very interested in adding trenbolone to the cycle. I know your cycle is geared towards minimizing side effects...which is fine for a risk-averse user. In my opinion, the benefits of tren outweigh the costs. Meanwhile, you are taking HCG with nolvadex, so post cycle therapy for tren is pretty much taken care of....it just seems like adding tren would be the icing on the cake?

[gofer]

When is the book coming out?

[Big Cat]

Originally posted by raybravo
150 mg prop eod is 525 mg per week , and that yeilds approximately 430 mg of base testosterone , and like 360 mg of base testosterone for both test enanthate and cypionate . so yeah , good question .

yes it would, that's why I only propose the enanthate/cypionate for people who prefer not to inject eod, clearly stated under the header on which testosterone to use.

[Big Cat]

Originally posted by pogue
What about topical spironolactone? Are you suggesting to stay away from all anti-androgens, or would topical be the exception?

Well I have heard some supporting evidence from dio that a topical spironolactone may not have much of a systemic effect, so I suppose you could give it a try, but personally I would avoid spiro during the cycle as it is still an anti-androgen

[Big Cat]

Originally posted by McBain
Although I have a sneaking suspicious you've been reading my thoughts... ;) The cycle I am about to start is roughly the same layout you had. I was going to run the winny at the beginning but still debating. I had tinkered with the idea of throwing in an eca stack, and was planning on the yohimburn. Think I'll take your advice and add a few other supps...basically I'll be trying this cycle out.


Systemic yohimbine will have a much better effect in this regard than topical, and save you a few bucks. Just a thought.

[Big Cat]

Originally posted by raybravo
u said in this plan it wudnt be such a big thing to think about , awright agreed .
but the question still remains unanswered , to what extent is the gh producing effect of estrogen benefitial as opposed to it being anabolic to adipose tissue .
i mean how would one realise to what extent would he want to use an anti estrogen ? cos he wouldnt want to be a bloated pig , but he would also want to make use of all the positive effects of estrogen u listed out .

With a prop/bold cycle I wouldn't really imagine most people would need an anti-estrogen, but if you still felt it was too bad, you could add 25-50 mg of proviron. I would certainly add that for the enanth/cypion. But like I said, there are other factors at play that limit gluconeogenisis, so the benefits of estrogen do outweigh the negative effects.

[Big Cat]

Originally posted by ITJ
I noticed that you suggest frontloading the EQ. If you were to use a long estered test, would it be beneficial to frontload the test also?

It might, but I don't deem it necessary since its the base of the stack.

Why do you recommend not having any high GI carbs postworkout? I thought it was of the utmost importance to quickly replenish your depleted glycogen stores after your workout no matter what type of diet you were on - keto included. And high GI carbs help your body absorb the creatine. Also, would you consider wheat rice/pasta/bread too high GI?

High glycogen stores or insulemic action will prevent the beta-adrenergic system from working, as was clearly outlined in this article. That would hinder or destroy our chances of fat loss/fat preservation. Replensishing them is not a necessity, studies have shown time and time again that anaerobic athletes have no use for extra carbs in the diet. So no. Thanks to beta-adrenergic stimulation ample energy supply will come from existing carb sources and free fatty acids. Rice and whole-wheat bread are not high GI, pasta and white bread are.

Lastly, you recommend only using milk thistle if liver problems arise, which is very understandable. What about using ALA throughout the whole cycle for precautionary reasons. It is a strong antioxidant, and I am not aware of any negative reasons to not use it throughout the cycle.

It has been shown to instigate fat loss through phosphorylative uncoupling (no distinction between fat and muscle) and it may increase gluconeogenisis. Both bad ideas in this cycle. Secondly, the effects of the two products I named are supported by medical practicioners as well as several studies, while the comparative effects on ALA are still not there and probably considerably weaker.

You also chose to ignore the data about how liver damage is often misdiagnosed and that this problem will most likely not occur ...

[Big Cat]

Originally posted by Punisher007
1. What's your take on norephedrine. I don't mind ephedrine...but if I can get a higher or equal amount of thermogenesis out of norephedrine with less side effects, I'd rather take that :)

No comparative data, but the lack of metabolic stimulation would indicate it is not quite as potent. Still pure norephedrine Hcl would be considered a more stable component than ma huang, so if you can source it, it is an option.

2. I like your idea on running low amounts of proviron throughout the cycle..but you didn't specificy how much and when to take it.

Depends on the severity of the problems you have. With prop I wouldn't really advise running it until the latter stages of the cycle, with enth/cyp using 25-50 mg throughout certainly couldn't hurt.

3. I'm very interested in adding trenbolone to the cycle. I know your cycle is geared towards minimizing side effects...which is fine for a risk-averse user. In my opinion, the benefits of tren outweigh the costs. Meanwhile, you are taking HCG with nolvadex, so post cycle therapy for tren is pretty much taken care of....it just seems like adding tren would be the icing on the cake?

Jury is still out. Too little data on whether or not tren is harsh on the system or not. So couldn't comment. Tren is not estrogenic, nor does it appear to have similar non AR mediated feats like test and bold do. So its just simply a very potent AR agonist. If you can make it from raw powder sources i can't imagine there being any health problems really, as long as you run it alongside this stack and not instead of one of the components.

[Big Cat]

Originally posted by gofer
When is the book coming out?

Considering the time and agonizing concentration it took just to write this first draft, probably no time soon unless I get some help.

[raybravo]

Originally posted by Big Cat
Considering the time and agonizing concentration it took just to write this first draft, probably no time soon unless I get some help.
need voulenteers ?:D

[raybravo]

bc , btw , since ure suggesting an anti androgen (aldactone) , can we suspect a prolactin increase here ?
and can bromo be added into this cycle , i'm thinking normally not necessary as lowered estrogen levels from nolva /clomid post cycle would automatically lower prolactin but the anti androgen is giving me second thoughts . what do u think bro ?

[raybravo]

another thing i wanted to post here about u saying it approximately takes 50 days for recovery , this is a post by nandi on cem bro :
"NANDI12 :
The authors performed a similar study that went for 12 weeks (1), a cycle more like what the average AAS user employs.

At the end of the cycle, test dropped from 37 nmol/l to 5 nmol/l (compared to precycle baseline of 21 nmol/l).

Estradiol dropped from a cycle high of 0.25 nmol/l to a post cycle low of 0.04 nmol/l. Baseline pre cycle was 0.08 nmol/l. Baseline LH was 6.8 U/l while 12 weeks after the cycle ended LH had risen to 8.0 U/l while test was still depressed at 14.6 nmol/l compared to a precycle level of 21.8 nmol/l.

It takes a long time to recover from a 12 week cycle. It also shows that rather than time off equalling time on, time off needs to be considerably longer for complete recovery.

(1) Am J Sports Med 1987 Jul-Aug;15(4):357-61

Androgenic-anabolic steroid effects on serum thyroid, pituitary and steroid hormones in athletes.

Alen M, Rahkila P, Reinila M, Vihko R. "

[Big Cat]

I'm not even convinced there is that much to be feared of prolactin. The anti-androgen is for exactly that purpose : displacing androgens to avoid androgen related negative feedback.

[Big Cat]

Originally posted by raybravo
another thing i wanted to post here about u saying it approximately takes 50 days for recovery , this is a post by nandi on cem bro :
"NANDI12 :
The authors performed a similar study that went for 12 weeks (1), a cycle more like what the average AAS user employs.

At the end of the cycle, test dropped from 37 nmol/l to 5 nmol/l (compared to precycle baseline of 21 nmol/l).

Estradiol dropped from a cycle high of 0.25 nmol/l to a post cycle low of 0.04 nmol/l. Baseline pre cycle was 0.08 nmol/l. Baseline LH was 6.8 U/l while 12 weeks after the cycle ended LH had risen to 8.0 U/l while test was still depressed at 14.6 nmol/l compared to a precycle level of 21.8 nmol/l.

It takes a long time to recover from a 12 week cycle. It also shows that rather than time off equalling time on, time off needs to be considerably longer for complete recovery.

(1) Am J Sports Med 1987 Jul-Aug;15(4):357-61

Androgenic-anabolic steroid effects on serum thyroid, pituitary and steroid hormones in athletes.

Alen M, Rahkila P, Reinila M, Vihko R. "

Without post-cycle care however ...

[raybravo]

yes true , post cycle therapy wasnt done the way we bodybuilders do it probly .

and one more thing , since clomid is a SERM , can it act as an estrogen and thus elevate prolactin ??

[Big Cat]

Only in certain tissues, but the NOlvadex should prevent that since it is as strong at 20 mg than Clomid at 150 mg

[Pie-Bald]

Hey BC, what type of food ratios do you recommend? You said low to moderate carbs so does that mean something in the 30% carbs, 50% protein, 20% fat range?

[ITJ]

Thanks alot for answering my questions, but I have one more regarding hairloss - I understand that if you are predisposed to hairloss that you are going to lose it at some point anyway. However, running Test, Eq, Winny, and possibly proviron will drastically increase the rate at which you are losing hair. Would a topical anti DHT product just prevent DHT conversion in your scalp or would it eventually get into your blood and have the same effect as propecia/proscar just to a lesser degree? Basically could you still get the benefits of having DHT in your cycle, while somewhat slowing hairloss? Also, anything else that you would recommend for slowing hairloss on a cycle, while still maximizing gains?

Thanks,
ITJ

[Big Cat]

Originally posted by ITJ
Thanks alot for answering my questions, but I have one more regarding hairloss - I understand that if you are predisposed to hairloss that you are going to lose it at some point anyway. However, running Test, Eq, Winny, and possibly proviron will drastically increase the rate at which you are losing hair. Would a topical anti DHT product just prevent DHT conversion in your scalp or would it eventually get into your blood and have the same effect as propecia/proscar just to a lesser degree? Basically could you still get the benefits of having DHT in your cycle, while somewhat slowing hairloss? Also, anything else that you would recommend for slowing hairloss on a cycle, while still maximizing gains?


Dio seemed to believe that topical minoxidil would work well and made a pretty good case for it. Hasn't convinced me, but it can't hurt to try it. Especially since he backed his point quite well.

[Big Cat]

Non-aromatizing substances when used by themselves have been known to cause poor HDL/LDL ratio's and could offer potential to increase cardio-vascular risk.

[Chikara]

Originally posted by raybravo
bc , btw , since ure suggesting an anti androgen (aldactone) , can we suspect a prolactin increase here ?
and can bromo be added into this cycle , i'm thinking normally not necessary as lowered estrogen levels from nolva /clomid post cycle would automatically lower prolactin but the anti androgen is giving me second thoughts . what do u think bro ?
Spironolactone has been related to gynecomastia / galactorrhea. People who are it risk should be aware of that.

[RetiredMod]

Originally posted by Chikara
Spironolactone has been related to gynecomastia / galactorrhea. People who are it risk should be aware of that.
I assume this doesn't apply to topical spiro though? I'm pretty gyno prone and didn't notice any increased occurance of gyno when using topical spiro...but that doesn't really mean very much. Opinions?

[Yeti]

Originally posted by Big Cat
I'm not even convinced there is that much to be feared of prolactin. The anti-androgen is for exactly that purpose : displacing androgens to avoid androgen related negative feedback.

so if tren is added would bromo still need to be on hand?

[Big Cat]

No, adding trenbolone would increase androgen related negative feedback anyway and is a stupid idea in this cycle.

[raybravo]

bc , i saw this post on cem by ready2explode saying nolva acts as an estrogen in the liver , is this true ? never read this before .
also , if this is true , i guess its better on the lipid profile compared to arimi ?

[raybravo]

again , one more question about estrogen promoting fat gain , what about its upregulation of a2 receptors and reduction of circulating tsh?

[Redbrave]

raybravo,

"Another noteworthy fact about Nolvadex is that it acts more potently as an estrogen in the liver. As you remember, I mentioned that clomiphene and tamoxifen [Nolvadex] are basically weak estrogens. Well, tamoxifen is apparently still quite potent in the liver. This offers us the positive benefits of this hormone in the liver, while avoiding its negative effects elsewhere in the body."

The above is from a Big cat article, http://www.bodybuilding.com/fun/catnolv.htm

[raybravo]

oh, i have over looked that , thanx bro . anyway , if thats true , definitely better than arimi and other aromatase inhibitors for ur lipid profile .

[Big Cat]

Originally posted by raybravo
bc , i saw this post on cem by ready2explode saying nolva acts as an estrogen in the liver , is this true ? never read this before .
also , if this is true , i guess its better on the lipid profile compared to arimi ?

Yes on both counts.

[Big Cat]

Originally posted by raybravo
again , one more question about estrogen promoting fat gain , what about its upregulation of a2 receptors and reduction of circulating tsh?

Like I said, that's why estrogen is a delicate matter, something of which we need enough, but not too much.

[raybravo]

bro , estrogen also seems to be causing proliferation of preadipocytes, which can mature into fat cells, there seems to be so many conflicting things on estrogen , u need to write a detailed article on it man , cos while estrogen is causing proliferation of preadipocytes into adipocytes , estrogen is also lower levels of the enzyme lipoprotein lipase (LPL) , so using an anti aromatase is actually increase lipoprotein lipase levels ,which is obviously bad , so whats this whole deal man ? has got me confused !

[SlateDrake]

Great post BC! Very similar to what I was planning on for a summer cycle.

One question - I was also thinking about using rHGH at 4iu/day (AM and Late Afternoon). Can you see any negatives in conjunction with you thoughts above?

I was going to use the rHGH specifically for localized fat loss.

[Big Cat]

Apart from the distinct side-effects of HGH specifically, I see no fault with that. On the contrary, HGH is likely to reduce insulin sensitivity.

[SlateDrake]

Thanks BC, that's exactly what I was thinking as well.

What do you think about adding 12.5mcg or 25mcg/day of T3 to help with protein synthesis as well?

I'm not talking about a massive T3 pyramid cycle, but just running the 12.5mcg/day for the entire cycle. Do you think this would work against anything?

[Big Cat]

Originally posted by SlateDrake
Thanks BC, that's exactly what I was thinking as well.

What do you think about adding 12.5mcg or 25mcg/day of T3 to help with protein synthesis as well?

I'm not talking about a massive T3 pyramid cycle, but just running the 12.5mcg/day for the entire cycle. Do you think this would work against anything?

I see no use for T3 since T3 should be in a high normal range by itself throughout the cycle and the guggul should be adequate to cover the lower T3/T4 ratio which will ensue. The difficulty with exogenous T3 is that you don't know how much to take to get around those high normal numbers. Too little and you are shooting yourself in the foot, too much and you will suffer rebound due to TSH supression.

[SlateDrake]

Originally posted by Big Cat
Too little and you are shooting yourself in the foot.

Good call bro, I'll let the E/C/Y and For/Gugg do their stuff.

Thanks<

[CrAvEnCLiCK666]

Can i mix any of the injections? is this a good first cycle? also this is gonna put an extreme hole in my wallet?

[Big Cat]

All these products are on the cheap end of the list, If you are recommending a sane cycle, it has to be sane financially as well. This is VERY affordable. And yes, testosterone enth/cyp will mix well boldenone undecylenate. if you decide to shoot prop (preferred) then I wouldn't really mix them.

[SlateDrake]

Hey BC,

I know this is the SANE cycle, so you probably wouldn't recommend the use of 'slin in any way, but that being said....


Do you see anyway to utilize 'slin post-workout WITHOUT causing a large degree of adipose storage. My thoughts are that the beta-adrenergic stack that I would be using throughout the day while on cycle would allow too much fatty acid in the bloodstream to not put on additional fat if slin was used.

This seems to be logical, but I was wondering if there is anyway around this, perhaps not using the BA stack within four hours previous and prior to slin use would accomplish this, but then you're sabotaging the whole low-carb post-workout drink effect.

Any thoughts bro?

Perhaps it's simply "not this cycle" period...

Thanks,

[priapis]

assuming 50 mg oral a day as you reccommend in your writeups, is it ok to take whole thing at once, or spread over the day to take into account short half life?

[incognito]

Originally posted by priapis
assuming 50 mg oral a day as you reccommend in your writeups, is it ok to take whole thing at once, or spread over the day to take into account short half life?

spread it out.... like 2-4 doses

[spfb]

Product Per dose
Ephedrine Hcl 12.5 mg
Caffeine 100 mg
Yohimbine Hcl 3 mg
Forskolin 20-30 mg
Acetyl-L-Carnitine 200 mg
GuggulSterones 30 mg

You can opt to take 1 dose 6 times per day, roughly every 2.5 hours, or 2 doses 3 times per day, roughly every 5 hours.



Am i understanding this right? u want someone to take 75 mg ephedrine 600mg caffeine 18mg yohimbine 120-180mg forskoin etc....a day?

[ChallyRT]

I have the same question as spfb. Are you suggesting to use 75 milligrams of ephedrine, 600 milligrams of caffeine, 1200 milligrams of ALC, and 120-180 milligrams of forskolin a day for twelve weeks straight? Also, for the last six weeks, are you suggesting 180 milligrams of guggul and 18 milligrams of yohimbine a day?

[Big Cat]

yes.

And while I'm here, to answer slatedrake's question, no that would not work. To inhibit fat gain off slin, you need to lower insulin sensistivity, which seems to be what you are trying to achieve. Except you seem to forget that for anabolism to occur via slin, you need that very same receptor.

Additionally several modes of inhibition may occur downstream of the receptor and inhibit muscle building effects, while maintaining fat gaining effects. Glucose disposal can be mediated by PKC and PKB, but only PKB has anabolic effects.

[raybravo]

Originally posted by Big Cat

Additionally several modes of inhibition may occur downstream of the receptor and inhibit muscle building effects, while maintaining fat gaining effects. Glucose disposal can be mediated by PKC and PKB, but only PKB has anabolic effects.
didnt understand this part bro . several modes of inhibition from what ? and the part on glucose disposal . would appreciate it if u would expand on that .

[Big Cat]

Originally posted by raybravo
didnt understand this part bro . several modes of inhibition from what ? and the part on glucose disposal . would appreciate it if u would expand on that .

If downregulation of insulin's action occured at the receptor, then it would lead to equal downregulation of its effects on glucose disposal and fat gain, as well as on its muscle building effects.

However downregulation can occur downstream of the receptor, since the receptor has multiple pathways. One of the targets is PI3K, which activates both PKB and PKC. Both of these will stimulate glucose disposal and fat gain. But PKB also activates mammalian target of rapamycin, which leads to protein synthesis. If PKB or mTOR were inhibited, then glucose disposal and fat gain would continue through PKC, but protein synthesis would be blunted to a large degree.

[biketuna]

Week 1-12 : Testosterone enanthate / cypionate 400-500 mg/week
Or : Testosterone propionate 150 mg every other day

Week 1-2 : Boldenone Undecylenate 600-800 mg/week
Week 3-12 : Boldenone Undecylenate 300-400 mg/week
Week 6-13 : Stanozolol 50-100 mg/day
Week 12-14 : HCG 3000/3000/1500/1500 IU / 5days
Week 12-17 : Tamoxifen Citrate 20 mg/day
Week 14-15 : Clomiphene Citrate 100 mg/day
Week 16-17 : Clomiphene Citrate 50 mg/day
Week 14-15 : (Spironolactone) 50 mg/day

Week 7-18 : Beta-adrenergic mix with eph as described.



I thought PCT started 2 weeks after last Test E shot.
Is this going to hurt gains at the end ????

[biketuna]

bump

[peregrine]

i was considering to stack these and then i read this article. wow. i'm stoked. thumbs up on this stack from the big cat, thats cool.


this is subjective with many variables, BUT how much could one reasonably gain on this stack? and how much could one retain?
12-13wk on cycle?
i am thinking 8-12lb gain post cycle? is that reasonable? i am sure more could be gained and less if diet / training / rest is not adequate but 8-12lbs kept sounds reasonable? for a first cycle.

[jdailey6969]

Sorry for the tangent but:

Big Cat said,
"Many people regard DHT as the enemy, because among these androgen-specific tissues are the scalp (aggravating a genetic tendency to hair loss) and the skin (causing outbreaks of acne). But in fact DHT is more than that to us. Since it is the prime androgen in nerve tissue, it will be imperative to have ample DHT levels for optimal neuromuscular response. This is why many people taking the 5-alpha-reductase inhibitor finasteride (Proscar) find that their strength does not increase, or even decreases."

Was wondering if I could get a little further explanation.

As I've mentioned before, I've got this disorder called Chronic Inflamatory Demylinating Polyneuropothy (CIDP), basically, my immune system thinks the mylein sheath that insulates my nerves is a virus and attacks them, its similar to multiple schlerosis, only its the peripheral nerves, not the central nerves. Anyway, I've noticed that when on PH's (M1-t...etc, haven't tried AS's yet), my CIDP symptoms are drastically reduced. I normally go in for a 4 hour IV drip to keep myself from being paralized once a month, but when on a PH cycle, this treatment isn't needed for 3 or 4 months, a HUGE gain, and I can now predictably increase or shorten the time needed between treatments based on my use of PH's.

Perhaps what you've stated in your article could be one of the reasons. I've hypothesized that androgens increase the rate at which the mylein sheath repairs itself, though that's only guess. I do know that SOMETHING beneficial is going on. Any ideas BigCat?

[Big Cat]

I'm not a neurologist of course, but certainly evidence does point that way. Testosterone, DHT and 5AA, through interactions with the GABA(A) and androgen receptors do seem to have an effect on peripheral nerves that stimulates synthesis of proteins involved in myelin formation (1). Might be worth getting a copy of the whole study and giving it a read.

1) Magnaghi V, Cavarretta I, Galbiati M, Martini L, Melcangi RC.
Neuroactive steroids and peripheral myelin proteins.Brain Res Brain Res Rev. 2001 Nov;37(1-3):360-71.

[Blacksmith]

Great thread BC.
How about modifying this cycle for the older (35+) bodybuilder.

There's a lot of us out here who play sports as well as hit the gym 5 days a week, who would benefit from this cycle.
I feel however that the dosages may be to large.

Honestly I'm more concerned about co-workers impressions, because the mass gains will be dramatic with this cycle.
I'm already 235 lb after a much milder cycle.
So I'd appreciate any feedback.

[The.Giant]

This is probably what my first cycle is gonna look like, but without the EQ.

Just prop @ 150 mg EOD and Winny.

I was considering using dbol and enanth, but i figured by switching to prop i could drop the dbol (which i was gonna use as a quick boost) and add the winny to solidify the gains.

1 year to go :P

[juiceman1001]

"A combination of trenbolone, a much stronger androgen, and oxymetholone (which has direct estrogenic action, without requiring aromatisation) only yields roughly the same amount of mass as equipotent or even lesser doses of testosterone."

Is this true?

[cappa12434]

I read your article in the forum on testosterone. Very good article. I was just wondering if you can help me out with a question. I did one cycle on test on 1cc of 200mg a week for 10 weeks. I didn't feel much. I did this while on Growth hitting 6iu's a day 5 days a week. Well, I've lowered my growth down to 2iu's a day, 5 days a week/2 days off, and now am on my second cycle of test, and am taking HCG on my cylce with taking one 25mg anastrozole every tuesday and thursday. Now I was wondering why I didn't feel nothing from my test last cycle, so my doctor increased it to 300mg/1cc a week. I just did my third shot today. I noticed I don't have much muscle where I inject in my ass. I don't have much muscle there at all. My question is, if I miss the muscle and just end up injecting test into my body and not the muscle, will the test still do its job or not. I was wondering if it was possible to inject the test maybe in different large muscle, like the hip or something... which part of the hip exactly. I mean, I get nervous when injecting in my asa because of that stupid nerve that freaks the hell out of my leg if I hit it. Also, does it take four weeks for test to kick in because the oil has to break down in the muscle, or because the more you inject, the more that adds up in your body, to where your levels increase with each injection. Please get back to me if you have a chance. Thanks, Chris

[Kroms_laugh]

I read your article in the forum on testosterone. Very good article. I was just wondering if you can help me out with a question. I did one cycle on test on 1cc of 200mg a week for 10 weeks. I didn't feel much. I did this while on Growth hitting 6iu's a day 5 days a week. Well, I've lowered my growth down to 2iu's a day, 5 days a week/2 days off, and now am on my second cycle of test, and am taking HCG on my cylce with taking one 25mg anastrozole every tuesday and thursday. Now I was wondering why I didn't feel nothing from my test last cycle, so my doctor increased it to 300mg/1cc a week. I just did my third shot today. I noticed I don't have much muscle where I inject in my ass. I don't have much muscle there at all. My question is, if I miss the muscle and just end up injecting test into my body and not the muscle, will the test still do its job or not. I was wondering if it was possible to inject the test maybe in different large muscle, like the hip or something... which part of the hip exactly. I mean, I get nervous when injecting in my asa because of that stupid nerve that freaks the hell out of my leg if I hit it. Also, does it take four weeks for test to kick in because the oil has to break down in the muscle, or because the more you inject, the more that adds up in your body, to where your levels increase with each injection. Please get back to me if you have a chance. Thanks, Chris


Your muscles are in your body, so even if you got it into your muscle it's still in your body. If you 'missed' your glute, which is hard to do... unless you're fat... you got it in the sub-q fat. It'll still work, but the absorption rate is much less when you inject a depo outside of a muscle with a compound that's intended for IM injection.

And I'm confused. If you're cycling testosterone, you're not on true testosterone replacement therapy. Hormone replacement is for life (unless you're post pubescent and have not started puberty, and THAT's what you're being treated for).

[cappa12434]

I'm actually not on TRT. I'm just on TT i guess. It's to help me with my osteoporosis among other symptoms. But okay, thanks. That helps. At least I know I'm not fully waisting this supplement. Also wondering if you can inject it anywhere else besides the glute. Like the hip which is also a big muscle. I just want to inject somewhere else to avoid that stupid nerve in my ass. I've hit it one too many times. It makes me nervous.

[Habeed]

This is an excellent post.

One question : if one were using the long test esters flavor of this cycle and also was using dianabol for improved gains, would proviron at 25-50mg/day likely be enough anti-estrogen? (just like in your B&B cycle posted on this website)

Second, what is your take on IGF-1. The hype about is that even used in a teensy dose (1000mcg total), it dramatically improves PCT; preventing any muscle loss and causing an improvement in body composition.

[Big Cat]

This is an excellent post.

One question : if one were using the long test esters flavor of this cycle and also was using dianabol for improved gains, would proviron at 25-50mg/day likely be enough anti-estrogen? (just like in your B&B cycle posted on this website)

Second, what is your take on IGF-1. The hype about is that even used in a teensy dose (1000mcg total), it dramatically improves PCT; preventing any muscle loss and causing an improvement in body composition.

Depends on your sensitivity to estrogen. Either way you need Nolva on hand for PCT, can't hurt to have a little extra around in any case where there is reason to assume estrogenic problems might arise.

On the second part, hell no. But IGF does help in recovery somewhat.

[Habeed]

I didn't mean alone, I meant in conjunction with a proper PCT it might be 'just anabolic enough' to prevent any loss of muscle. Same concept with PCT : the whole idea is to get our ~roughly 77mg of natural test production/week back online to prevent loss of the muscle we built by using the equivalent of 5 to 10 times that much test.

Does IGF-1 LR3 do that?

[Big Cat]

I meant in conjunction with PCT as well, or did you really think I would ever suggest any cycle without proper PCT ?

The IGF would be part of PCT then. And yes the point of PCT is to minimize muscle loss, eliminating however is until further notice rather wishful thinking.

[youngBuilder]

"One reason, with regards to safety, why I chose to include stanozolol and not a more potent bulk-up agent as the oral component of this cycle, is because of its effects on tendons.... Stanozolol however, has been found to increase collagen synthesis (16) where testosterone did not. Collagen is a key component in fibrous tissue such as cartilage and tendons, and may therefore offer us the bonus effect of maintaining tendon health or even repairing damage of microtrauma, and keep our cartilage healthy so we can resist the pressure on our joints."


I have read numerous times that stanozolol increases tendon size, but the side effect of that is that the tendon is made more brital and more susceptable to rupture. I do agree with you that hightened levels of testosterone does severly slow down the collagen synthesis. It has been compared to the collagen synthesis of the elderly, which is almost nil.

[Habeed]

What can IGF-1 do for you if you just use 1000mcg (a small dose) as part of PCT? Of course everyone responds differently to any of the drugs we have mentioned, but what are fairly typical results? An anabolic agent that doesn't touch HPTA would seem to be very, very useful.

[Big Cat]

What can IGF-1 do for you if you just use 1000mcg (a small dose) as part of PCT? Of course everyone responds differently to any of the drugs we have mentioned, but what are fairly typical results? An anabolic agent that doesn't touch HPTA would seem to be very, very useful.

The anabolic effect of exogenously adminstered systemic IGF is limited even in higher doses, and it has no real anti-catabolic effect, but as I touched on briefly in my new findings on PCT thread, IGF does positively influence HPTA recovery. ANd that is why its not a bad idea to include some in PCT.

[Habeed]

What would you add to your PCT protocal, then? You wrote a thread on the subject but failed to mention specific products or dosages, just general research. Some sort of nitrous oxide product?

[G0Big0rGoHoMe]

Hi Big cat,

Whenever you find a minute, I would be very greatful if you could answer some questions:

1.Do you still reccomend the use of HCG in PCT as 3000iu/3000iu/1500iu/1500iu every 5 days?

2.You mention on your steroid profiles that Proviron increases the yield of whatever Testosterone you are using while limiting estrogen. Whats your opinion on stacking proviron 25mg/day everyday with say 500mg Testosterone Enanthate/week for 12 weeks?
Would this be a small enough dose to increase the yield of the test while keeping some estrogen to be able to work its positive effects aswell? or would a larger dose be required?

3. Injections: Do you reccomend injections of Test E 500mg once a week or bi-weekly at 250mg say every mon thursday to keep stable blood levels? Theres seems to be some debate on this.

4. In regards to frontloading Test E on a 500mg/week 12 week cycle.
Is one better to frontload at 1000mg for 2 weeks or just for the first?

When injecting in the case of frontloading should you inject 1000mg all at once or split it up into a bi-weekly injection at 500mg on the monday and the thursday of that week?

[Big Cat]

What would you add to your PCT protocal, then? You wrote a thread on the subject but failed to mention specific products or dosages, just general research. Some sort of nitrous oxide product?

Just plain old arginine will do, no need to go broke over the fancy stuff.

[bazooka_tooth]

I've just spent the past two days assimilating all of the information here and it has increased my still low level of knowledge ten fold. I'm interested in the answers to the questions in regards to Test E front-loading (1,000 bi-weekly) and so on...

A highly informative post. Thanks Big Cat.

[Big Cat]

1.Do you still reccomend the use of HCG in PCT as 3000iu/3000iu/1500iu/1500iu every 5 days?

Yes, but mostly for comforts sake. I have guided a few athletes with 250 IU a day, two days a week, throughout the cycle, and recovery according to bloodwork was not significantly different. I recommend the 3000/3000/1500/1500 mostly because its less pokes on less days. The alternative works just as well though.

2.You mention on your steroid profiles that Proviron increases the yield of whatever Testosterone you are using while limiting estrogen. Whats your opinion on stacking proviron 25mg/day everyday with say 500mg Testosterone Enanthate/week for 12 weeks?
Would this be a small enough dose to increase the yield of the test while keeping some estrogen to be able to work its positive effects aswell? or would a larger dose be required?

Actually more recent evidence I have already posted in a few threads seems to suggest that lowering SHBG has no effect on the level of free testosterone. So feel free to ignore the entire paragraph about provi and SHBG.

3. Injections: Do you reccomend injections of Test E 500mg once a week or bi-weekly at 250mg say every mon thursday to keep stable blood levels? Theres seems to be some debate on this.

Once a week. Objectively speaking strictly as a comfort measure, although I do get a very subjective impression the final yield is better as well. But purely objectively, either is fine. 1 poke is simply more comfortable than two, especially since most people using 21/22G needles often start building scar tissue even in a single cycle.

4. In regards to frontloading Test E on a 500mg/week 12 week cycle.
Is one better to frontload at 1000mg for 2 weeks or just for the first?

2 weeks, but I'd add 20 mg of nolva daily during those two weeks as well.

When injecting in the case of frontloading should you inject 1000mg all at once or split it up into a bi-weekly injection at 500mg on the monday and the thursday of that week?

I've seen injections up to 8 ml with no prob in the glute. However the rule of thumb is no more than 5 in the glute, or 3 in the quad at one time. Depending on site of injection you can decide which of the two would work better for you. The idea of frontloading is to get a fast highly elevated dose, so once a week would be better.