theartofwar
Bluelighter
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.
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 ?).
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.
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.
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 ?).
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.
(like you aren't already 
