Driada Education

[Driada Medical]

Greetings friends!

We invite you to the Driada Education thread. Here we will consider everything that can help us in improving any physical qualities we require, improving health indicators and overall well-being. Fortunately, nowadays nature and modern science give us wide opportunities and we will definitely tell you how to use them.

The Driada Education project invites you to increase your knowledge. Here we will share information that will help you improve the quality of your life and speed up the path to your sporting achievements. This project is aimed at your informative expansion. If you crave to receive something new, then here is the very place where you should hold your attention.

We have tried to collect constructive and actual information for you that will be applicable in your daily life. At the moment, among the huge amount of information on the Internet, it is really getting more and more sophisticated to find information that is supported by real scientific data. Finding and analyzing every piece of knowledge that you are looking for now requires a considerable amount of time.

If our fathers had a tiny amount of information available in the media, now our world is saturated with it and this is also becoming a big issue. Therefore, we want to give you a summary of the data that is believed to be true and already verified by specialists.

Enjoy reading.
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https://t.me/driadaeducation

 

[Driada Medical]

WHAT IS DECA DICK AND HOW WE CAN COUNTER IT? (PART 1)​

It’s not a secret that in nowadays era of chemical warfare nandrolone is the second most popular steroid in the world which is only topped with everyone's beloved testosterone.

Considering nandrolone’s popularity there is a lot of information on the internet and due to this fact, unfortunately, a ton of myths and misunderstandings about this steroid also occur. I would like to clear most of these confusions and make sure that by the time you will end reading this article, you will understand a lot more about the nature of this compound.

What do we actually know about nandrolone? Nandrolone, also known as 19-nortestosterone, is an androgenic and anabolic steroid which is actually one of the most well-studied steroids for today. It’s usually produced in two esters: nandrolone decanoate and nandrolone phenylpropionate(they do have their slight differences but it is mostly about the half-life of the ester).

Nandrolone is estimated by many as one of the best anabolic steroids which has many profound effects on human physiology and it has to do with the nandrolones affinity to androgen, estrogen, mineralocorticoid, and even progesterone receptors(the latest is believed to be its flaw but nandrolone has a much lower affinity to progesterone receptors than progesterone itself and this is why it’s not really an issue).

However today we are not discussing this steroid’s bright side. We are doing quite the opposite indeed. Let’s get started.

One of the most popular and notorious facts about this steroid is a rather unpleasant side effect which is known as “Deca Dick”(DD).

DD is a form of erectile dysfunction(ED) caused by different changes in hormonal balance and imbalances in neurotransmitters.

It is often thought that the main reason why people get DD is a raise in prolactin commonly seen amongst nandrolone. Although nandrolone has the potential of raising prolactin(testosterone is also capable of producing high prolactin but higher dosages are usually required, combining the two of them at high dosages usually leads to the worst outcomes), and high prolactin at the same time has the potential to crush someone’s libido and strongly delay ejaculation time, it doesn’t mean that prolactin is the villain behind the DD phenomenon.

If prolactin was to blame then the introduction of dopaminergic agents/D2 receptor agonists would have always been the ideal solution. However many people take bromocriptine and cabergoline and yet they safe somewhat vulnerable to DD. Please keep in mind that 0.25-0.5mg of cabergoline a week is enough for most people to hit the bottom of the reference range for prolactin. Still, it doesn’t always fix DD(if it does you were probably lucky and your weak erection was simply due to high prolactin).

Well, maybe then another feminine hormone is to blame? What about estrogen? It is also known to decrease libido when there is too much of it, maybe the problem could be solved with a simple aromatize inhibitor(AI)?

Let’s make sure we don’t forget about the fact that nandrolone indeed itself has its estrogenic properties(sensitizes estrogen receptors which are vice when dealing with estrogen related side effects) and is also prone to aromatization but the content of estrogen it provides is different than what we get from testosterone.

There are free molecular forms of estrogen: estrone(E1), estradiol(E2) and estriol(E3). The one which is the most biologically active and is responsible for estrogenic side effects is E2. Nandrolone doesn’t convert to E2, but part of it(about 20-25%) aromatizes to E1(not an issue most of the time). However, if you stack testosterone with nandrolone your E1 can now be converted to E2 via the 17β-HSD metabolic pathway. And now you are sitting with a double “estrogen sandwich” which will affect your mood and libido 9/10 times.

Is it reversible? 100%. You can just take an aromatize inhibitor and “calm down” your aromatize enzyme. But… was it the mighty DD itself? Still no. Has nothing to do with it.

Most people don’t understand that DD is not about estrogen or prolactin, it’s not even about dopamine. Surprisingly enough it’s about 5α-reductase.

Yes, this one specific enzyme is responsible for testosterone conversion to dihydrotestosterone(DHT). Keep in mind that DHT is also responsible for the production of many neurosteroids that have a positive impact on anxiety and depression. Nandrolone however can’t give you DHT because it is turned into dihydro nandrolone(DHN) after interacting with 5α-reductase.

DHN is somewhat similar to DHT and most people state that it’s a good metabolite since DHT wreaks havoc on someone’s follicles and is mostly viewed as the number one reason of male pattern baldness(which is by the way only partly true but that’s a topic for another article). It might be tempting to see one molecule as evil and try to canonize the other, so let’s just say that both of them have their own good and bad properties. Well, when it comes to neurotoxicity DHN is actually the villain.

The penis tissue needs androgenic stimulation to function properly and if it lacks DHT then you can experience the symptoms of ED. Yes, and the excessive amounts of DHN can easily substitute DHT in androgen-dependent tissues and there we have, congratulations, it’s a Deca Dick.

So as you see DD is not caused by progesterone, estrogen, or prolactin. It doesn’t have anything to do with the fact that it’s a 19-nor. It has everything to do with 5α-reductase, DHN, and DHN/DHT ratio.

What is there to do about it? The most obvious answer would be to do simply raise the dose of DHT and thereby counter the effects of DHN. It probably would sound okay but there are definitely better ways to do it. I would try to break that down in the second part of the article. See you soon. Take care.

 

[All Nats McGee]

I think this is sticky worthy because this question comes up so often. Ive always advised people to run mast with deca, it’s like peanut butter and jelly. Great write up!

 

[Driada Medical]

WHAT IS DECA DICK AND HOW WE CAN COUNTER IT? (PART 2)​

As for today we already know that Deca Dick(DD) is a bad thing(unless it’s something that happened to your enemy) a pretty logical question pops up: how it can be countered and what exactly shall we do to get the maximum benefits of nandrolone and avoid any trouble.

If you have read the first part of the article(link) you probably know that I pointed out that simply raising the sheer amount of dihydrotestosterone(DHT) in your system isn’t your best option. However you can still do so.

Countering dihydronandrolone(DHN) with DHT might seem like a good idea and most people do it this way with unknowingly, but I still believe it is optional and to say the least not the only way to handle nandrolone side effects.

What I want to tell you further might sound like total obscurity and some people might even consider it trolling. Here is the thing: you don’t need to run testosterone with nandrolone simultaneously. Yes, it’s true. It’s been done this way many times in the past and a lot of old school bodybuilders managed to get great results with nandrolone only cycles.

I mentioned earlier that stacking testosterone(T) with nandrolone(N) gives you a more estrogenic outcome due to the fact that T encourages estrone(E1) conversion to estradiol(E2). For some people this additional E2 really messes up their cosmetic look because of all the water retention(keep in mind N is a pretty wet steroid by all means).

Please, try not to forget that N is indeed stronger than T when it comes to gaining strength and building muscle. This was its original purpose: to be better than T milligram to milligram in order to provide people prone to muscle wasting with a better nitrogen balance at the same dose with less amount of side effects.

Shall we then completely get rid of T? Not at all. You still want to keep some of it in your system since overall homeostasis requires it(people with low scores of T get several types of cancer a lot more often than individuals who prefer a double TRT dose) and it’s not all about the E2. The reasons are far more complicated(once again let’s not change the topic).

The best way to get some T and at the same time not to overdose it is to run human chorionic gonadotropin(HCG alongside with N. This will make sure that your intercellular immune function is not going to be hindered and as a nice bonus you will have a boost in your libido(HCG makes us utilize our cholesterol to produce pregnenolone/allopregnenolone which are believed to be really beneficial when it comes to treating several types of psychological disorders). The optimal dosage in an N solo cycle would be around 1500-3000IUs per week divided in several injections.

However this is not the only thing you will have to do because there is still DHN that requires to be taken care of. The answer here lays on the surface and is obviously about blocking the 5α-reductase enzyme.

Some folks state that the best way to do it is to simply introduce the notorious anti-hair loss drug: finasteride. It will work but in my humble opinion the anti-androgenic effect it provides is just to much for our goals. If you interested in what are more concerns in details you might google such thing as post finasteride syndrome(PFS). PFS happened to some of my friends and I want to assure you that DD is a total joke compared to this.

The name of the substance which we are going to use is spironlactone/aldactone. Most people have only heard of it because of its diuretic properties(relatively weak and adaptive btw) but it’s also a pretty popular medication among trichologists. At the same time a lot milder than finasteride.

There is a rumour, that it only takes 12.5mgs of spironlactone to mitigate most side effects you can get from the amount of DHN you get from 500mgs of N per week. Some people need more, others need less, but still general rule of the thumb indicates these proportions.

Running N without T while using HCG and spironlactone is a pretty advanced way of your performance enchantment and not everyone is ready to embrace it.

 

[Canknucklehead]

@Driada Medical
Great post!

 

[klokke23]

The best way to get some T and at the same time not to overdose it is to run human chorionic gonadotropin

Could you elaborate? Dosing test is already pretty accurate and straightforward. But the T that is produced as a result from hcg dosing is unpredictable.

 

[Driada Medical]

Could you elaborate? Dosing test is already pretty accurate and straightforward. But the T that is produced as a result from hcg dosing is unpredictable.

Hello, sir!

You are undoubtedly right, but I disagree with your conclusions and here's why...

The fact is that the average person produces up to 70 mg of pure testosterone per week. Of course, there are deviations - walking testosterone pumps, as well as people with hypogonadism.

Regarding HCG injections, existing protocols have calculated the appropriate dosage for most of average people, both: to maintain testicular function and to produce sufficient testosterone levels.

Of course, a reasonable approach would be to try the drug on yourself to see if there is a "special" sensitivity to it and make a personal dose correction.

 

[klokke23]

Hello, sir!

You are undoubtedly right, but I disagree with your conclusions and here's why...

The fact is that the average person produces up to 70 mg of pure testosterone per week. Of course, there are deviations - walking testosterone pumps, as well as people with hypogonadism.

Regarding HCG injections, existing protocols have calculated the appropriate dosage for most of average people, both: to maintain testicular function and to produce sufficient testosterone levels.

Of course, a reasonable approach would be to try the drug on yourself to see if there is a "special" sensitivity to it and make a personal dose correction.

I may have misinterpreted those studies then. Every time I've looked at the graphs of T serum in hcg studies, it seems to be all over the place.

 

[SwitchBlade]

Instead of using spironlactone/aldactone, why not introduce a DHT derivative such as mast, primo or even proviron? That's what I have done on my previous deca cycles and never experienced the deca dick syndrome. I must say that I always keep a trt dosage in the background and therefore the DHT derivative helps with the estrogen control and DNT issue at same time.

 

[Driada Medical]

Instead of using spironlactone/aldactone, why not introduce a DHT derivative such as mast, primo or even proviron? That's what I have done on my previous deca cycles and never experienced the deca dick syndrome. I must say that I always keep a trt dosage in the background and therefore the DHT derivative helps with the estrogen control and DNT issue at same time.

Hello, sir!

Yes, there are people who never met deca dick even on 1g of nandrolone per week with DHT derivative or without, but.... there is always "but"....

Because nandrolone is really good at passing brain\blood barrier and if you have nandrolone vs other drug comparison, DHN will be more potent to disactivate androgen receptor in brain.

 

[PeterBond]

At the moment, among the huge amount of information on the Internet, it is really getting more and more sophisticated to find information that is supported by real scientific data.

And then you proceed without any inline references to the scientific literature?

 

[PeterBond]

Hello, sir!

Yes, there are people who never met deca dick even on 1g of nandrolone per week with DHT derivative or without, but.... there is always "but"....

Because nandrolone is really good at passing brain\blood barrier and if you have nandrolone vs other drug comparison, DHN will be more potent to disactivate androgen receptor in brain.

Why would nandrolone be better or worse at passing the blood-brain barrier than other AAS, and how is DHN supposed to disactivate the AR in the brain?

 

[PeterBond]

Hello, sir!

You are undoubtedly right, but I disagree with your conclusions and here's why...

The fact is that the average person produces up to 70 mg of pure testosterone per week. Of course, there are deviations - walking testosterone pumps, as well as people with hypogonadism.

Regarding HCG injections, existing protocols have calculated the appropriate dosage for most of average people, both: to maintain testicular function and to produce sufficient testosterone levels.

Of course, a reasonable approach would be to try the drug on yourself to see if there is a "special" sensitivity to it and make a personal dose correction.

How did you arrive at the number of 70 mg pure testosterone weekly, i.e. 10 mg daily? The estimates I know from the literature vary from 3.7 to 9.1 mg daily, i.e. 25.9 to 63.7 mg weekly. There's considerable interindividual variation among the eugonadal population, too.

And how do protocols calculate anything? And what protocols are you refering to, from which guidelines/organization?

Honestly, I see a lot of claims made in the texts you posted too that I'm pretty confident of that the scientific literature either contradicts or doesn't support.

 

[Driada Medical]

Why would nandrolone be better or worse at passing the blood-brain barrier than other AAS

Hello, sir

Most scientific research has been done on rats and this is the reality we are dealing with when we talk about the non-therapeutic effects of steroids.

At the same time, we understand that this is not the best source of information, but the only one available, that allows us to build our hypotheses and understanding.

People who block 5a reductase when taking nandrolone alone, report good libido and mood, people who don't block 5a reductase have to deal with "The Issue of deca dick".

Threads like this can be found all over the place: Meso, Reddit...dozens.

Also, judging by the experience of athletes, even megadoses of testosterone or another highly androgenic drug have little effect on deca dick when it occurs, while simple blocking 5a reductase treats deca dick.

Drugbank predicts(Predicted ADMET Features) the same BBB passing rate for most steroids- approx. 0,97. studies made on rats gave us different data.

Why would nandrolone be better or worse at passing the blood-brain barrier than other AAS, and how is DHN supposed to disactivate the AR in the brain?

Speaking strictly, "Deactivation" of the receptor is an artistic metaphor. When the weak androgen dihydronandrolone reliably blocks the androgen receptor, preventing more powerful androgens to activate it, I can say that it is "deactivated" or "blocked" or "not available for activation by a stronger androgen unit". Didn't expect to have to explain it, but probably this metaphor is not my best.

Next, please...

How did you arrive at the number of 70 mg pure testosterone weekly, i.e. 10 mg daily? The estimates I know from the literature vary from 3.7 to 9.1 mg daily, i.e. 25.9 to 63.7 mg weekly. There's considerable interindividual variation among the eugonadal population, too.

The fact is that the average person produces up to 70 mg of pure testosterone per week. Of course, there are deviations - walking testosterone pumps, as well as people with hypogonadism.

If I remember the math correctly, of course, I may be wrong, but 25.9 - 63.7 is included in "up to 70" term, so I cannot understand how your data contradicts mine.

And how do protocols calculate anything? And what protocols are you refering to, from which guidelines/organization?

Protocols usually go already calculated. Calculation methods differ depending on the author's approach.
I didn't recommend specific protocols, but would you argue that protocols exist or that they can be found?
so I cannot understand how your data contradicts mine #2


But I would thank you for your interest and activity, sir!
Have a nice evening!

 

[PeterBond]

Hello, sir

Most scientific research has been done on rats and this is the reality we are dealing with when we talk about the non-therapeutic effects of steroids.

At the same time, we understand that this is not the best source of information, but the only one available, that allows us to build our hypotheses and understanding.

People who block 5a reductase when taking nandrolone alone, report good libido and mood, people who don't block 5a reductase report deca dick.

Threads like this can be found all over the place: Meso, Reddit...dozens.

Also, judging by the experience of athletes, even megadoses of testosterone or another highly androgenic drug have little effect on deca dick when it occurs, while simple blocking 5a reductase treats deca dick.

Drugbank predicts the same BBB passing rate for most steroids- approx. 0,97. studies made on rats gave us different data.

So you have no data to support your claim and extrapolate subjective anecdotes to BBB passage rate? Or are you trying to explain subjective anecdotes by supporting them with unsupported claims?

Speaking strictly, "Deactivation" of the receptor is an artistic metaphor. When the weak androgen dihydronandrolone reliably blocks the androgen receptor, preventing more powerful androgens to activate it, I can say that it is "deactivated" or "blocked" or "not available for activation by a stronger androgen unit". Didn't expect to have to explain it, but probably this metaphor is not my best.

Next, please...

No, it's a wrong term. It doesn't deactivate the androgen receptor. Deactivation has a specific meaning. You're now suggesting the presence of DHN can lower the biological effect mediated by binding of other androgens to the androgen receptor through competitive binding. Or in other words, you're suggesting it acts as a competitive inhibitor (which would be the correct term). As such, it needs to function as a partial agonist or antagonist. Do you have something to support this? I'm only aware of DHN having a lower binding affinity for the AR. I'm not aware of any data that suggests that it's a partial agonist or antagonist for the AR. A full agonist with lower binding affinity cannot act as a competitive inhibitor. (And a partial agonist or antagonist with low binding affinity makes for a lousy competitive inhibitor )

If I remember the math correctly, of course, I may be wrong, but 25.9 - 63.7 is included in "up to 70" term, so I cannot understand how your data contradicts mine.

It's also included in "up to 10000". It's a meaningless range as there's an infinite-fold difference between the lower bound (0 mg) and upper bound (70 mg) of the range you provide. Which average man produces 0 mg of testosterone? Also curious for the paper that goes beyond the range that I provided.

But regardless, you gave this as an argument to support that hCG dosing gives predictable T responses. How does such a wide range (0-70 mg weekly) support this? It does the contrary: if there's a wide interindividual range in the production of a hormone, how would a set amount of injecting a hormone that induces its production yield a predictable response? Accurate dosing requires titration based on blood measurements.

Protocols usually go already calculated. Calculation methods differ depending on the author's approach.
I didn't recommend specific protocols, but would you argue that protocols exist or that they can be found?
so I cannot understand how your data contradicts mine #2


But I would thank you for your interest and activity, sir!
Have a nice evening!

I know of no hCG protocols for "intercellular immune function". For males, there are protocols for delayed puberty, cryptorchidism, and reduced sperm count.

 

[Driada Medical]

I know of no hCG protocols for "intercellular immune function". For males, there are protocols for delayed puberty, cryptorchidism, and reduced sperm count.

I don't know protocols for "intercellular immune function" too.
And what about other protocols, cool, I never had a client with delayed puberty.

You know about delayed puberty and intercellular immune function- you just showed us this, even if it's out of topic. Wow.

But is this the thing you wanted? need some social proof?

So you have no data to support your claim and extrapolate subjective anecdotes to BBB passage rate? Or are you trying to explain subjective anecdotes by supporting them with unsupported claims?

If it would be an honest question of an interested person, I would spend my time to find it for you, but ...
If you trying to catch me on 63.7mg test is so different from 70, while, you didn't even bother to quote the entire sentence. Damn, I bet if other things are equal, no one will feel the difference between 63 and 70 mg of testosterone.
I do NOT analyze a specific example of a specific person with his blood tests. why do I need the details? what for? To impress you?
How will my text be affected if I replace the erroneous "up to 70" with the absolutely correct "from 23 to 63" (but you ask me to find an evidence paper lol)?
Why these quibbles?
you just want to draw attention to yourself - ok. you get two big messages.

https://gupea.ub.gu.se/bitstream/handle/2077/68/gupea_2077_68_1.pdf;jsessionid=AA2825D751F74C8EA686C8BBD0D081FF?sequence=1

here you can find the research I mentioned, hope you are smart enough to find your answers, cos I'm demotivated.

It's also included in "up to 10000".

If you think that up to 70 in this context is equal to up to 100000 I have a piece of bad news for your math. It is included but makes no sense here, as all you attempt to catch on the details, missing the big picture, using school demagogic techniques.
And even with this, I would try to support the discussion...but...

Also curious for the paper that goes beyond the range that I provided.

Do you want me to search for a piece of evidence for the range YOU provided? Really?

Is it possible to take seriously the guy who cannot use internet search even for his own statements?

next time try to make your claims make sense.

have a good evening,sir!

 

[PeterBond]

I don't know protocols for "intercellular immune function" too.
And what about other protocols, cool, I never had a client with delayed puberty.

Then why start about intercellular immune function in your hCG piece?

You know about delayed puberty and intercellular immune function- you just showed us this, even if it's out of topic. Wow.

I just listed known protocols for it, since you're suggesting there is one for "intercellular immune function" as per your own writing.

But is this the thing you wanted? need some social proof?

Want what?

If it would be an honest question of an interested person, I would spend my time to find it for you, but ...
If you trying to catch me on 63.7mg test is so different from 70, while, you didn't even bother to quote the entire sentence. Damn, I bet if other things are equal, no one will feel the difference between 63 and 70 mg of testosterone.

You're completely missing the point of my post. Please reread:
It's also included in "up to 10000". It's a meaningless range as there's an infinite-fold difference between the lower bound (0 mg) and upper bound (70 mg) of the range you provide. Which average man produces 0 mg of testosterone? Also curious for the paper that goes beyond the range that I provided.

But regardless, you gave this as an argument to support that hCG dosing gives predictable T responses. How does such a wide range (0-70 mg weekly) support this? It does the contrary: if there's a wide interindividual range in the production of a hormone, how would a set amount of injecting a hormone that induces its production yield a predictable response? Accurate dosing requires titration based on blood measurements.

I do NOT analyze a specific example of a specific person with his blood tests. why do I need the details? what for? To impress you?

I don't eat fries in the morning. Why should I?
What does this have to do with any of this?

How will my text be affected if I replace the erroneous "up to 70" with the absolutely correct "from 23 to 63" (but you ask me to find an evidence paper lol)?
Why these quibbles?

Please reread the 2 paragraphs further above.

you just want to draw attention to yourself - ok. you get two big messages.

https://gupea.ub.gu.se/bitstream/handle/2077/68/gupea_2077_68_1.pdf;jsessionid=AA2825D751F74C8EA686C8BBD0D081FF?sequence=1

here you can find the research I mentioned, hope you are smart enough to find your answers, cos I'm demotivated.

Did you accidentally place the wrong link here? Nowhere does this dissertation mention the blood-brain barrier or the rate at which nandrolone passes it relative to other anabolic steroids. Thus, again:

So you have no data to support your claim and extrapolate subjective anecdotes to BBB passage rate? Or are you trying to explain subjective anecdotes by supporting them with unsupported claims?

If you think that up to 70 in this context is equal to up to 100000 I have a piece of bad news for your math. It is included but makes no sense here, as all you attempt to catch on the details, missing the big picture, using school demagogic techniques.
And even with this, I would try to support the discussion...but...


Do you want me to search for a piece of evidence for the range YOU provided? Really?

Nowhere did I claim the weekly testosterone production is upward to 70 mg weekly. That's your claim.

Is it possible to take seriously the guy who cannot use internet search even for his own statements?

Are you purposely dancing around my questions and quoting only part of my reply? You forgot this one:

No, it's a wrong term. It doesn't deactivate the androgen receptor. Deactivation has a specific meaning. You're now suggesting the presence of DHN can lower the biological effect mediated by binding of other androgens to the androgen receptor through competitive binding. Or in other words, you're suggesting it acts as a competitive inhibitor (which would be the correct term). As such, it needs to function as a partial agonist or antagonist. Do you have something to support this? I'm only aware of DHN having a lower binding affinity for the AR. I'm not aware of any data that suggests that it's a partial agonist or antagonist for the AR. A full agonist with lower binding affinity cannot act as a competitive inhibitor.

next time try to make your claims make sense.

have a good evening,sir!

Which claims of mine are you referring to?

As a final note: you come here posting, for the lack of a more accurate term, articles, with dubious content. Pretending to deliver, by your own words, information that is supported by real scientific data. Yet, you proceed without any inline references to the scientific literature and either accidentally posted a wrong link to a dissertation, or actually posted a link to a 79-page dissertation of which we need to guess what claim is supported by it?

 

[klokke23]

Hello sir

 

[Driada Medical]

I just listed known protocols for it, since you're suggesting there is one for "intercellular immune function" as per your own writing.

Where did you read about the special "intercellular immune function" HCG protocol?

Then why start about intercellular immune function in your hCG piece?

Low testosterone in blood plasma leads to testosterone
production by prostate cells, and cancer is a compensatory disease of the immune system, that's why.

here is another link, you may consider as random...if you will not read it, of course,

https://pubmed.ncbi.nlm.nih.gov/27068735/

You're completely missing the point of my post. Please reread:
It's also included in "up to 10000". It's a meaningless range as there's an infinite-fold difference between the lower bound (0 mg) and upper bound (70 mg) of the range you provide. Which average man produces 0 mg of testosterone? Also curious for the paper that goes beyond the range that I provided.

In fact, you missed the idea of the post. The point was not to deny people an individual approach but to point out the average majority.
and the ''T that is produced as a result from hcg dosing is unpredictable.'' - yes, this quote. it is unpredictable, but according to a normal distribution, in most cases, this unpredictability will be within very predictable limits.




Are you aware of your hypersensitivity? Look for a proper personal dose, but for most people with an average response, there are protocols that work.

and yes, this chart is not supported by scientific research, it just my paint sketch to explain you math

Shall we still practice demagogy?
Instead, you start to practice math. up to 10000, up to 63, not the 70 - very advanced.

Did you accidentally place the wrong link here? Nowhere does this dissertation mention the blood-brain barrier or the rate at which nandrolone passes it relative to other anabolic steroids.

that is - if the scientific work is not called "WHY NANDROLONE EXCELLENTLY PASSES THE BLOOD OF THE BRAIN BARRIER FOR THE DUMMIES" is this not proof? wow

this approach looks comedic even for youtube biohackers who are only trying to sell iherb supplements there

there is a lot of evidence of how nandrolone affects the neurons and brain, read it if you are really interested in it, because you making picky/captious claims, despite the context and the main idea, trying to find your epic correctness that 63 is not under 70.
so read the research.

Nowhere did I claim the weekly testosterone production is upward to 70 mg weekly.

yepp! lower than 70

How did you arrive at the number of 70 mg pure testosterone weekly, i.e. 10 mg daily? The estimates I know from the literature vary from 3.7 to 9.1 mg daily, i.e. 25.9 to 63.7 mg weekly.

Nowhere...

Deactivation has a specific meaning.

The mechanism was explained in the article, so the claim is meaningless. Unless you just need a reason to complain.

and as I get your point and the way you make your conclusions and questions, you just need a reason ... should I find scientific research to support it too?

 

[Barbarian]

My question is the following - if I use only 100 mg of nandrolone per week - can it also affect the libido level?