The Sane cycle : safe and effective use of steroids

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 (eventhough liver toxicity is a tad exaggerated, but then that just allows us more leeway with the winny).

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 proferred as a therapeutic means to treat BPH.

As we mentioned already, testosterone is a substrate for the aromatase enzyme and converts to E2. A female hormone. Here too demonisation 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). Eventhough 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), resorbing 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 ?).

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 relativate 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 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.

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.

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, eventhough 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 eph as described.

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.

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 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 triacylglycerides). 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.

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 profer 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-adrenrgic 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.

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.

Guggul sterones

Guggul sterones 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.

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 supraphysiological 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.

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 cholesterole 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, eventhough 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, ********) 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 !!!!

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 :

Supression 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

https://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):410-21.

wow... I'm copying this to my computer!

Looks pretty good, but i dont think Tren is very supressive, at least for me. What about what stanazol does to ones HDL? It is horrible on your chloresterol. Ill have to dig up those studies, but it was one of the worst steroids for your chloresterol.

Quote:

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Originally posted by prolangtum
Looks pretty good, but i dont think Tren is very supressive, at least for me. What about what stanazol does to ones HDL? It is horrible on your chloresterol. Ill have to dig up those studies, but it was one of the worst steroids for your chloresterol.

---

Stana lower HDL cholesterol because it has no aromatization properties. The addition of testosterone and boldenone more than compensates for this, as does the Clomiphene/tamoxifen post-cycle combo, so this is not even an issue.

On top of that all steroids lower total cholesterol, which makes the HDL/LDL ratio less important.

You've outdone yourself :)

Long but good read...:colgate::colgate:

I personally liek the Test and EQ, but i try to stary away from 17aa, plus winny kills my joints and my hairline, but some love it, so to each theri own.

Yeah this is a defenite copy to hard drive article. Thanks

nice informative post

I like it, good info