|trade names||Testoviron Depot®, Primoteston®|
|estrogen formation||yes (estradiol)|
|molecular weight||288.41 g / mol|
|melting point||155 ° C|
|Chemical formula (with ester)||C26H40O3|
|Molecular weight (ester)||112.17 g / mol (enanthate)|
|Melting point (ester)||34 - 39 ° C|
|Carbon atoms (esters)||7 (enanthate)|
The testosterone molecule
Structure of the enantate ester
When it comes to testosterone , it has to do with a very far-reaching topic. In front of me on the desk is just a stack of testosterone studies spread, which covers about 200 pages. And the book I was just browsing in, dealing exclusively with the topic of testosterone, is about 500 pages thick.
Since we want to use this text to provide a steroid profile to testosterone enanthate , and also do not want to take the risk of boring the inclined reader, we must set some emphasis. They will look like this:
If you take it exactly, then the exogenous intake of testosterone has a very long history. For it is about 4000 years ago when an Indian named Sushruta described in his Ayurvedic writings the administration of extracts from animal testicles for the treatment of impotence.
If you look into the more recent past, you come across the name of Charles Eduard Brown-Sequard. At the beginning of June 1889, the 72-year-old professor of medicine announced to an astonished Paris public that he had discovered a kind of fountain of youth and had already tried it on himself. The "fountain of youth" consisted of a liquid extract of dog and guinea pig testicles, which he had injected repeatedly. He felt that he was physically stronger and mentally fresher ever since. Quite uninhibited, he said he could even urinate again in a high arc ...
Whether the extracts really did him any good, is doubtful, but at least he is considered the father of modern endocrinology. Because he was the first to discover that organs can produce messengers, which in turn affect other organs.
Until testosterone could actually be isolated and synthesized, it should take a while. The first androgenic substance to be isolated was androsterone (a testosterone metabolite). That was in 1931, and the German researcher Butenandt and his team were able to gain just 15 mg of androsterone from 15,000 liters of urine.
It took another 4 years to isolate testosterone itself. The succeeded David et al. 1935 - 5 mg from a ton of beef testes ...
At the time, several groups of scientists were working on the study of sex hormones, and also in 1935, the Butenandt and Ruzicka teams succeeded in deciphering the chemical structure of testosterone at about the same time. The synthesis followed shortly thereafter. For their discoveries Butenandt and Ruzicka 1939 received the Nobel Prize.
Incidentally, it is rumored today that the German athletes already appreciated the benefits of testosterone at the 1936 Olympics ...
Once you were able to produce testosterone artificially, the development continued very quickly. The patents for testosterone propionate and testosterone cypionate were filed in 1941. Methyltestosterone followed in 1945. Until the testosterone enanthate it should take a while - it was patented in 1958.
Later followed by oral testosterone undecanoate (Andriol) in 1975 and testosterone buciclate in 1987.
Evidence for the muscle-building effect of testosterone was found early in the 1950s (Leonard 1952, Meyer and Hershberger 1957, Loring et al 1961). And that was also the time when testosterone began its triumphant advance in sport.
The ban on anabolic steroids by the International Olympic Committee came in 1964. What did not bother the athletes at the time - doping controls were only introduced in 1976.
Interestingly, the muscle-building effect of supraphysiological testosterone doses in eugonadal men (ie those with a normal testosterone self-production) in the community of physicians for a very long time controversial. This was because most of the medical studies conducted with eugonadal men used only low doses of testosterone (100 mg / week, etc.). And sometimes there was a result and sometimes not.
Only the study by Bhasin et al. from 1996 created clarity with 600 mg of testosterone enanthate / week. And now the anabolic effect is undisputed. This study will be discussed in more detail shortly.
As indicated in the last few sections, bodybuilders, weightlifters, and other athletes for over 50 years predicted physicians to know that a healthy, normal man builds muscle as he delivers enough testosterone.
In the '40s and' 50s, when compared to today, the scientists were still rather squeamish about trying out the effects of drugs on the living human subject. And so it was soon discovered that testosterone in pre-pubertal boys (!), Women (!), Hypogonadal men (ie those with testosterone underproduction) and castrates significantly increased fat-free muscle mass.
With the same dosages, which showed a clear effect in these groups, however, could not be "tear" in normal men much. This was also fast.
And while the bodybuilders found that an increase in the testosterone dose of 1 gram / week to 2 grams / week again means a pretty increase in muscle and strength, sat the doctors in their ivory tower and controversially discussed the effect of testosterone doses such as 100 mg / week (American College of Sports Medicine 1988, Bardin 1996, Casaburi et al 1996, Elashoff et al 1991, Haupt and Rovere 1984, Strauss and Yesalis 1991, Wilson 1988).
This condition continued until Bhasin et al. In 1996, the study <! - -> "The Effects of Supraphysiologic Doses of Testosterone" <! - -> published. For that was very different from anything that had happened before:
The following chart shows the most important results of the study. Namely, the average change in lean body mass and the change in power output in bench press. Each shown separately for the four groups.
Considering the increase in lean body mass, placebo always performs worse than testosterone enanthate, with or without training.
Let's take a look at the strength gains in bench press:
Undoubtedly interesting results. Because it is not only clear that testosterone enanthate at 600 mg / week in combination with training has a significant effect on the muscles. It turns out that testosterone enanthate at this dosage has a clear effect even when administered without training.
Of course it works a lot better in combination with training. And then it becomes apparent that optimal results in terms of musculature can probably be achieved by combining both. If you think you can do "natural" the same way you do with anabolic steroids, you're probably wrong. But obviously, those who believe that optimal results are due only to the administration of anabolic steroids are also wrong.
According to this study, the muscle-building effect of testosterone enanthate has been proven in healthy men. And even with the doctors began a rethinking.
However, what has not been studied here has been the effect of varying high doses of testosterone enanthate. So the answer to the question of how much testosterone brings what effect. But that was also considered. Let's take a look at another study.
We have already published an article about Testosterone - Dose and Effect a while ago, in which the design and results are explained in detail. At this point only the quintessence is shown.
The main aim of the study was to derive formulas by applying statistical methods that can be used to calculate the anabolic effect depending on the dose of testosterone:
The following graph shows the change in lean body mass for each individual subject.
The vertical axis indicates the increase in fat-free in kg. The axis starts at -6 (which would correspond to a decrease of 6 kg) and ends at 16 (increase by 16 kg).
The horizontal axis shows the weekly administered amount of testosterone enanthate in mg. It starts at 0 and ends at 700. Measurement results are only at 25, 50, 125, 300 and 600 mg, because these were the doses used.
Each point in the graph represents the increase in lean body mass in one study participant.
Let's take a closer look at the results.
If one compares the results with each other, it also becomes clear that the reactions can be individually quite different.
The authors of the study then apply a few statistical methods and finally derive the link between testosterone dose and increase in lean body mass. The result is shown in the following table.
|scheme||T-dose [mg / week]||Increase FFM [kg]|
|250 mg / 12 days||146||2.73|
|250 mg / 10 days||175||3.15|
|250 mg / 7 days||250||4.23|
|250 mg / 6 days||292||4.83|
|250 mg / 5 days||350||5.68|
|250 mg / 4 days||438||6.94|
|500 mg / 7 days||500||7.84|
|250 mg / 3 days||583||9.04|
|500 mg / 5 days||700||10.73|
|750 mg / 7 days||750||11,45|
Thus, the values in this table are the scientific answer to the question of weight gain from testosterone and therefore probably the essential part of this study. Note that the numbers refer to the administration of testosterone enanthate over a period of 20 weeks.
The study also makes a few more statements. It appears that body size, weight, body composition, muscle volume and BMI play virtually no role in the increase in lean body mass. Thus, weight gain from testosterone in a 60 kg man with an ectomorphic body is no different than that in a 90 kg man.
The dosages used in the studies just described cover what is so common in the hobby field. 500 mg / week is often used, and some people may go one step higher with 750 mg or 1 gram.
But what are the people who really want to know? The set again a neat on it. 2 grams / week is not uncommon and there are also people who think that it must be 4 grams. Now the question arises, whether such high doses can bring even a plus in musculature?
As it stands, yes. The connection between dose and effect is then no longer linear as in the table above, but rather corresponds to what the mathematicians call "logarithmic". In German: If you increase from 250 mg to 500 mg, then this will give a better boost than increasing the dose from 2000 mg to 2250 mg.
But everything indicates that more still brings a bit more. Also in the range of very high dosages.
The biochemical mechanisms by which testosterone causes an increase in protein synthesis and thus the development of muscle, are still largely unclear. But there are some explanations that I would like to deal with briefly.
Testosterone has been shown to increase IGF-1 levels by increasing growth hormone secretion. This mechanism has recently been highlighted in the various bodybuilding forums.
On the other hand, men who had to undergo hypophysectomy also build muscle tissue with testosterone. "Hypophysectomy" means removal of the pituitary gland. This may be necessary, for example, for a tumor on the pituitary gland. But now it is so that the body without pituitary can produce any growth hormone at all. Therefore, it seems unlikely that growth hormone-enhanced IGF-1 levels are the major mechanism when it comes to the muscle building effect of testosterone.
However, it can be objected that testosterone can also increase IGF-1 production directly in the muscle. For more information, see> MGF - The Muscle IGF-1 <
The androgenic receptor has long been the explanatory model for the effects of testosterone and other anabolic steroids. However, it is also unclear here whether the effects of supraphysiological testosterone dosages can really be mediated via the androgenic receptor.
The stupid thing is that the androgenic receptors in skeletal muscle are actually already saturated at a testosterone level in the physiological range. At least this could be shown in animal experiments (Bartsch et al., 1980).
Glucocorticoids (eg cortisone, dexamethasone) have anti-inflammatory and anti-allergic effects, but also catabolic effects. It has been shown that testosterone and other androgens can reduce the binding ability of dexamethasone to the glucocorticoid receptor in skeletal muscle.
On the other hand, it can again be argued that androgens do not possess such high binding affinity to the glucocorticoid receptor. At least not nearly as high as that of glucocorticoid antagonists. And in the latter, the muscle-building effect of testosterone can not be determined.
It is also not entirely clear whether DHT is necessary for testosterone to mediate its anabolic effects. Several observations suggest that this is not the case.
For example, in men who received the DHT inhibitor finasteride because of a benign prostate enlargement, no degradation of the muscles was observed.
And then there are people with a congenital 5-alpha reductase deficiency, a deficiency in the enzyme that makes DHT out of testosterone. Genetically speaking, a human being is a man, but it usually becomes a kind of hermaphrodite. The genitals are often inadequately developed or have a more feminine appearance (or anything in between). The muscles, on the other hand, are those of a normal man.
There are also a number of other mechanisms that occasionally appear in the discussion. For example, the influence of testosterone on the neuromuscular signal transmission, or on other growth factors, such as differentiation factor-8 or cytokines. The connections here are still very vague and largely unexplored.
When in the 40s, 50s and early 60s the now known anabolic steroids were developed, the researchers especially had the relation of anabolic to andogenic effects in the eye. Reference substance was always testosterone with a ratio of 1. And except some exotics, such as mestanolone (17-alpha-alkylated DHT) actually all anabolic steroids have a better ratio than testosterone, that is a ratio> 1. This also applies to anabolic steroids, which one likes to say a very high androgenic effect, such as oxymetholone (better known as anapolone).
The following figure (Hickson et al., 1989) shows a table showing the values for some anabolic steroids.
Thus, for example, Oxymetholone has only 45% of the androgenic effect of testosterone, but is 3.2 times as anabolic. The other anabolic steroids are similar. Does that mean testosterone enanthate is always androgenic than anything left?
I would not just sign that, because in order to interpret the numbers, one must also know how they came about:
However, these figures are not entirely to be dismissed. Testosterone is a natural substance that is subject to natural metabolism. Therefore, it is in the tissues in which the 5-alpha reductase enzyme occurs increasingly occurs (eg skin, hair cells and prostate) from the body converted into dihydrotestosterone, which displays a much stronger activity. And that can lead to the well-known androgenic side effects like acne, hair loss or increase in body hair.
Incidentally, testosterone and methyltestosterone appear to be the only representatives of the class of anabolic steroids where this effect occurs to a significant extent.
Finasteride (Proscar, Propecia) has been available on the market for several years, and more recently, the even more efficient dutasteride (Avodart). Thus, the conversion of testosterone to DHT can be significantly reduced. Lt. Finasteride provides a reduction of DHT levels by 70%, dutasteride by 85-90%.
Some bodybuilders use these reductase inhibitors during a testosterone enanthate regimen to keep the androgenic side effects at bay.
I do not like the stuff myself - one of the nice effects of testosterone is the so-called "testo pump". This refers to the power that sets in during training under testosterone. And that's exactly what I miss when using Reduktasehemmern.
However, it would undoubtedly be of great interest if a Hershberger assay were once carried out using these drugs.
Incidentally, with an entry-level regimen of 250 mg testosterone enanthate / week, androgenic side effects are unlikely. There are some Pill-for-the-Man studies that used 200 mg a week. And it only happened in isolated cases.
As a natural substance, testosterone undergoes another transformation that can sometimes make it problematic. This is because the aromatase enzyme turns it into estradiol, the dominant female hormone.
An idea of the extent of conversion of testosterone to estradiol is given in the following graph (from Anderson & Wu, 1996).
In the study from which the graph was taken, 33 men received 200 mg of testosterone enanthate / week for 20 weeks. The picture shows the oestradiol level after the 1st (left) and after the 16th injection (right). The dashed line is the upper limit of the normal range. This upper limit is given here as 200 pmol / L, which corresponds to approximately 55 pg / ml (conversion factor = 3.671). Elsewhere you will find other definitions - on the sheet with my own laboratory values, the normal range is only up to 38 pg / ml, which corresponds to about 140 pmol / L.
It can be seen that estradiol goes up well even at this moderate dosage. From below 100 pmol / L to approximately 250 pmol / L. At significantly higher dosages, the estradiol level will be a good deal higher, and then it can lead to estrogen-related side effects. This includes
In the latter case, it is a growth of the mammary glands, so in principle nothing else than the formation of a female breast in the man. Gynecomastia is actually the medical term for it, in bodybuilding one usually speaks more of a "gyno" or sometimes a little unattractive of "bitch tits". The photo on the left shows a bodybuilder who has a pretty perfect physique.
But as Arnold Schwarzenegger said - double biceps from the front is one of the toughest poses. And that puts the gyno here pretty well in the view of the viewer. Once a gynecomastia has properly trained, then only the surgeon's knife usually helps.
Against estrogen-related side effects in bodybuilding often the aromatase inhibitors Anastrazol (Arimidex), letrozole (Femara) and exemestane (Aromasin) are used. Under Aromatase you will find a detailed article.
The receptor blocker tamoxifen (Nolvadex) has a more specific effect on the breast tissue.
One should always keep in mind with these drugs, however, that are the remedy of cancer therapy, which also have their side effects.
Most synthetic anabolic steroids have been able to abolish the property of estradiol formation through structural modifications. Of the common anabolic steroids, only DBol, boldenone, and to some extent nandrolone, tend to form estradiol.
In so-called lipoproteins, a distinction is made between HDL (high density lipoprotein) and LDL (low density lipoprotein) cholesterol. HDL cholesterol is also called the "good" cholesterol, as it seems to protect the vessels from fatty deposits and thus atherosclerosis. LDL, on the other hand, is the "bad" cholesterol. It can form deposits on the inner layers of the blood vessels and is therefore considered a risk factor for arteriosclerosis.
Androgens in supraphysiological doses have a more or less strong influence on the cholesterol levels and unfortunately no good. For example, boldenone and trenbolone are known to be more potent. And most extreme is Winstrol (Stanozolol). Since then can ever come out an HDL value that can doubt the lab technician on his meter ...
Testosterone, on the other hand, is not a foreign substance and that is probably the reason why it scores here. If the dosage is not too high, its influence on cholesterol levels is very low.
An interesting study on this topic was published in 1989 by Thompson et al. titled "Contrasting Effects of Testosterone and Stanozolol on Serum Lipoprotein Levels". There, the effect of 200 mg testosterone enanthate / week was compared with that of 6 mg stanozolol / day. The duration of administration was 6 weeks each. The following chart shows what HDL cholesterol does.
Under testosterone enanthate, HDL (the "good" cholesterol) goes from 1.11 to 1.01 mmol / l, or 9%. In the case of stanozolol, however, the value drops from 1.16 to 0.7 mmol / l - a decrease of 33%. And here is the graphic for LDL.
Bad cholesterol decreases by 16% from 3.12 to 2.63 mmol / L on testosterone administration, while it increases by 29% from 2.87 to 3.7 mmol / L in stanozolol.
Well, those are probably values that speak for themselves. Especially when you consider that 6 mg / day is an extremely low stanozolol dosage. It is common practice to use 50 mg of eod (ie every other day), which is 4 times that used here. Should not get better with it ...
In the case of testosterone, on the other hand, one sees a slight decrease in HDL, but LDL also drops. So you can not speak of deterioration here. Incidentally, the LDL value for the reference range is all <4.0 mmol / l and for the HDL everything> 1.0 mmol / l.
If one doses testosterone enanthate higher, then it makes itself however somewhat more strongly with the cholesterol values noticeable. The following figure is from a study (Bhasin et al., 2001) in which a total of 54 healthy men aged 18-35 years participated. They received either 25, 50, 125, 300 or 600 mg of testosterone enanthate (per week) for 20 weeks. In addition, a GnrH agonist was administered to paralyze the self-production and thus to exclude the influence of the body's own testosterone.
It can be seen that the HDL value decreases with increasing testosterone enanthate dose. Incidentally, one should not be confused here, if one compares these numbers with those above. The data are here in mg / dl, while they were up in mmol / l. For this unit, everything> 40 mg / dl is in the reference range.
When it comes to the liver, things are sometimes messed up. There are anabolic steroids that can definitely damage the liver. But these are only those anabolic steroids that have a very specific chemical modification, the so-called 17-alpha alkylation. This alteration of the chemical structure blocks the liver of one of the main pathways of degradation, namely the "oxidation of the 17-hydroxy group" to a 17-keto group.
Simply administering anabolic steroids orally would mean virtually nothing in the bloodstream because the liver classifies them as toxins and therefore almost completely metabolizes them.
The 17-alpha-alkylation has the advantage that the anabolic steroid becomes orally active and can be taken in tablet form. Disadvantage: The liver gets stressed. Illnesses, which occur again and again in the context, are cholestasis, peliosis hepatis and also liver tumors.
Incidentally, the damage to the liver is different from that caused by alcohol, for example. Toxic hepatitis is very rare in 17-alpha-alkylated steroids. The danger of tumors, however, is quite real and was mostly observed in Dianabol and Oxymetholone (Anapolon).
Testosterone enanthate is not chemically modified in this way, so there is no danger to the liver. Even at high dosages. This is also documented by studies (eg Gooren 1994).
As is known, the administration of anabolic steroids causes the body to reduce or even completely shut down the testosterone self-production. The process of the body's own testosterone production is also called the axis. And there are anabolic steroids that "flatten" these more than others.
Let's take a closer look at what happens to the axis under testosterone enanthate. The following graphic is from one of the studies on the pill for men (Anderson and Wu 1996). Thirty-three healthy men, ages 21 to 41, who received 200 mg of testosterone enanthate per week for 18 months, participated in this study.
Shown here are the blood levels of LH and FSH before starting testosterone administration and for the first 12 weeks of testosterone.
Shortly after the B2 measurement, the first syringe is given with 200 mg of testosterone enanthate. And then the LH value goes back quickly and clearly. After 4 days he has dropped from about 4 U / L to 1 U / L. So the axle is already buckling after a short time. After 4 weeks, the LH value has almost reached 0, after 12 weeks LH is no longer measurable.
Thus, even a moderate dose of 200 mg testosterone enanthate / week obviously leads to a rapid decline and finally to cessation of endogenous hormone production.
However, it should not be forgotten here that in the meantime some further studies have been carried out in this way with a far greater number of participants. And there was the general consensus that the axle has recovered from each participant within 6 months.
An anabolic steroid known to have little effect on the axis is oxandrolone. And there is a study on 32 older men (Schroeder et al 2002) who received oxandrolone at a dose of 20 mg / day for 12 weeks.
The LH value decreased within the 12 weeks from 8.3 U / L to 5.0 U / L. Quite obviously Oxandrolone unlike testosterone enanthate leads only to a decline, not to the cessation of self-production.
But there are also a few candidates among the anabolic steroids, the application of which just as quickly leads to a decline or cessation of endogenous hormone production. Only this effect is much more sustainable for those. These include Deca-Durabolin (Nandrolone) and Trenbolone. This is generally explained by their affinity to it. the progesterone receptor.
As far as the axis is concerned, testosterone enanthate obviously plays somewhere in the middle class.
Pharmacokinetics describes the changes in drug concentrations in the body, mostly as a function of time. Here terms such as absorption, distribution and elimination play a role.
Describing the pharmacokinetics of testosterone enanthate, for example, means expressing the testosterone blood concentration that results from a single injection or even an injection regimen as a function of time.
The following figure, taken from the Jenapharm testosterone depot summary, shows the empirically determined testosterone blood concentration over time following a single injection of 250 mg of testosterone enanthate. "Empirically ascertained" here means that a study was carried out on a total of 27 subjects who were regularly bled after an injection.
On the vertical axis the testosterone blood concentration is given in ng / ml, on the horizontal axis the time in hours. As can be seen from the curve, it takes about 1 to 3 days until the maximum blood concentration of 12 to 13 ng / ml has been reached. And after 2 - 3 weeks you are back at the starting level. For comparison, the physiological (ie the normal) blood concentration is somewhere between 3.5 and 8.6 ng / ml.
The curve is the result of a rather elaborate examination, because it finally takes 27 subjects, each of whom is given an injection and must take 20 blood samples.
In order to determine the course of testosterone blood levels easily and quickly in any scheme with testosterone enanthate, one can use mathematical models. Here at androgen-steroids we have provided a Roidrechner for download, in which such a mathematical model is shown.
For comparison, let's take a look at how the curve looks after a single 250 mg / testosterone enantate injection.
The curve here, of course, has a smooth, idealized course. But one compares them with the empirically determined curve. so it is very similar to this. It reaches the maximum after 3 days. The testosterone level is then between 11 and 12 ng / ml, which is slightly lower than in the Jenapharm curve. But this is simply because there is some endogenous testosterone left in the empirical graph. And it takes 2-3 weeks for the effect to dissipate.
With the Roidrechner can also show quite well how the testosterone blood levels at long and short injection intervals or behaves with and without frontload. First, consider a course of treatment in which 500 mg of testosterone enanthate are injected every 8 days.
It can be seen that the cure leads to relatively high fluctuations of the testosterone level. That is here namely between 20 and 36 ng / ml. Now let's see what happens if we change to 250 mg / 4 days instead of 500 mg / 8 days.
The testosterone level is in this scheme already a good deal evenly. For now he only moves between 26.5 and 31 ng / ml. However, it is striking that it takes a relatively long time until the cumulative maximum is reached, namely about 3 weeks. We therefore add a frontload. At the first injection, we use 500 mg instead of 250 mg.
Now the maximum level is reached noticeably faster - namely in the 2nd week, shortly after the third injection. And so the cure is pretty well optimized.
The Roidrechner is based on a so-called "biexponentielles model", known under the name "Bateman function". A distinction is made between a half-life for invasion and for evasion. One can imagine (simplified) that the invasion is the entry from the depot into the bloodstream, while the evasion represents the degradation in the body. Here, an invasion half-life of 1.19 days and an evasion half-life of 4.5 days is expected. The total half-life is 5.89 days.
There are even more complicated models, but they give only marginally better results (Wijnand et al., 1985).
On two points that many bodybuilders have a misconception in mind, I would like to comment on the pharmacokinetics of testosterone enanthate:
To understand why the first point is not correct, you have to let the story half-times melt on your tongue. You can imagine that, for example, as if you were married to a woman who always needs exactly 5.89 days to spend half of the money. If you pay up the common fund on a weekly basis with a constant amount of money, then the cash register will initially rise for several weeks. After a while, however, a cash balance is reached that does not increase any further. Because if more money is in the cash, she spends more. What is added per week, but is always only the same amount ...
The second point is easier to explain. The accumulation of testosterone enanthate takes place in the depot, ie in the muscles into which it has been injected. And it is not there yet. It will only be when it has left the muscle and entered the bloodstream. Once it is in the bloodstream and the ester is split off, there is no difference between testosterone enanthate and testosterone propionate, because then only testosterone is left.
No matter which testosterone ester you inject, it always has to pass the entire amount of testosterone through the body. And all the testosterone that goes through the body works to increase the testosterone blood concentration. So, if you inject 500 mg of testosterone propionate per week over a longer period of time, your blood levels will rise as well as 500 mg of testosterone enanthate. The only difference is that the blood level in testosterone propionate fluctuates more. And if you take it very carefully, the weight of the ester naturally also plays a role.
Testosterone Enanthate is an anabolic steroid whose effects are well documented and proven. It is a natural substance, from which advantages and disadvantages arise.
It is non-toxic and the body can handle it better than with its chemically modified relatives, such as the lesser impact on lipid levels. This is probably why it is the only anabolic steroid (apart from Deca) that can be used for a long time without putting your health at risk.
On the other hand, its application can lead to more pronounced estrogenic and androgenic side effects than most other anabolic steroids.
Effect and side effects are studied up to a dose of 600 mg / week over a period of 20 weeks. What happens when higher doses are used over a longer period of time is unclear. It is possible that damage to the cardiovascular system may occur, significantly shortening the lifespan.
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