Nandrolone Experiences

[DS3]

"By one unusual anecdote? I don't think so. Any ideas on why your numbers are so low compared to what's typical?"

Honestly, I could not tell you why my numbers are so low. I have also tried 'micro-dosing' Propionate at 50 mgs per day with 250 IU of HCG per day. Here are my results 10 hours post-shot. This 50 mgs per day amounts to 350 mgs per week of Propionate, yet my labs are normal for TRT. TT < 1200 ng/dL.

View attachment 9184

"Any chance of under-dosed propionate?"

Any dosage of T that I take is prescribed by my doctor, and I acquire 100% of my testosterone from Empower Pharmacy, so not likely.

NOTE: While taking Testosterone Cypionate (175 mgs per week), my blood levels peak at nearly 1300 ng/dL. This is nearly half the dosage of Cypionate required to get my TT past where I achieve with 262 mgs of Propionate per week. So there are certainly differences in how my body metabolizes long v. short esters of testosterone. Additionally, E2 is impossible for me to handle while taking 175 mgs of Cypionate (mono). I have virtually no E2 issues with 262 mgs of Prop per week with 500 IU of HCG EOD. (Obviously something is vastly different here).

 

[Jason Sypolt]

In his defense, the largest estimates for endogenous testosterone production are still under 10 mg per day, so call that 70 mg pure T per week. The referenced protocol has over 200 mg of pure androgens, so almost triple the highest known endogenous production.

Is there some evidence I'm unaware of showing that exogenous androgens are used less efficiently? Otherwise I wouldn't quibble with his characterization of this possible excess, even if it is lower than traditional cycles.

And yes, I am suggesting that a lot of supposed "TRT-level" doses are unnaturally high. Sure the trough serum levels may just make it into the reference ranges, but measuring the peaks would tell a different story. However, all this is not to dispute @Gman86's point that if you see benefits at these levels and lab work looks ok then have at it.

I am not aware of any evidence, or that it is known, and I doubt that this information is something that would justify the cost in obtaining it.

From a purely logical standpoint though, you would really have to conclude that there have to be substantial differences between endogenous and exogenous. It is a sort of truth problem. Either it is all exactly the same, or none of it is and thus there is a difference somewhere.

• It is not brought into the body by the same method or in the same place.
• It has to travel through different tissue, largely because of the first point.
• Although "bioidentical", that is simply the molecule. There are preservatives and esters and those are not identical to anything in the body, nor do they release androgens at the same rate.

And then anecdotally, I have seen very few people who do well on an equivalent of 7-10mg per day even accounting for the weight of the ester. Although there are far more men than not who are mostly looking at T for the problems and not much (or anything) else.

As far as safety, higher-dose androgens have been regularly given to people with HIV since the 90's, so there must be some data on medium-term use relative to safety. Prescribing responsibly goes a long way as well. Tracking symptoms, requiring more and more frequent labs, and staying in communication. There some maybe borderline conspiracy theories that we are being intentionally feminized and that even our grandparents had far higher hormone levels, does that make higher androgens safe? Maybe, but then again maybe not. All of the information that would have been needed to determine that was lost to time.

Personally (and this is a personal decision for everyone), I would rather take this stuff even if it meant a shorter life (which it doesn't, according to most current data) in order to have a better life.

I no longer have 400+ triglycerides, throw out my back moving a chair and have to shuffle my feel like an old man for a week in excruciating pain, no interest in anything, and a circulating insulin level that is 6 times what a safe amount should be - all while accepting that as normal. I look better, feel better, and I can operate at a high level through my insanely busy work day which has not only been rewarding to me, but it changes others' lives as well. I will choose that any day.

 

[Cataceous]

NOTE: While taking Testosterone Cypionate (175 mgs per week), my blood levels peak at nearly 1300 ng/dL. This is nearly half the dosage of Cypionate required to get my TT past where I achieve with 262 mgs of Propionate per week. So there are certainly differences in how my body metabolizes long v. short esters of testosterone. Additionally, E2 is impossible for me to handle while taking 175 mgs of Cypionate (mono). I have virtually no E2 issues with 262 mgs of Prop per week with 500 IU of HCG EOD. (Obviously something is vastly different here).

What numbers did you get for two hours post-injection? This is closest to when the peak occurs, at least with propionate.

It's well established in the scientific literature that the area under the response curve is proportional to the dose. You don't have nearly enough data points to firmly establish a contradiction. Unfortunately it's not really practical for an individual to get enough data to figure out what's really happening in a case like this.

I've seen no credible scientific evidence for big differences in how different esters are metabolized. They all end up in the blood where the esters are quickly cleaved from the testosterone. The only differences are in the speed of release from injected depots. This is again well established, and the extraordinary claim that it's wrong requires more support than a few isolated measurements.

 

[slicktop]

NOTE: While taking Testosterone Cypionate (175 mgs per week), my blood levels peak at nearly 1300 ng/dL. This is nearly half the dosage of Cypionate required to get my TT past where I achieve with 262 mgs of Propionate per week. So there are certainly differences in how my body metabolizes long v. short esters of testosterone. Additionally, E2 is impossible for me to handle while taking 175 mgs of Cypionate (mono). I have virtually no E2 issues with 262 mgs of Prop per week with 500 IU of HCG EOD. (Obviously something is vastly different here).

I had an interesting reaction switching from cypionate to enanthate. I'm not sure what, if any, difference there is in my blood levels, but my cardio endurance is significantly reduced while on cypionate, and returned within two or three weeks after switching to enanthate. I can't point to any scientific evidence and frankly couldn't care less- if it's psychosomatic, that's fine, too. I feel significantly better.

 

[DS3]

I had an interesting reaction switching from cypionate to enanthate. I'm not sure what, if any, difference there is in my blood levels, but my cardio endurance is significantly reduced while on cypionate, and returned within two or three weeks after switching to enanthate. I can't point to any scientific evidence and frankly couldn't care less- if it's psychosomatic, that's fine, too. I feel significantly better.

I feel like I've read a post from you before where you have discussed this. Very interesting.

 

[Cataceous]

...
From a purely logical standpoint though, you would really have to conclude that there have to be substantial differences between endogenous and exogenous. It is a sort of truth problem. Either it is all exactly the same, or none of it is and thus there is a difference somewhere.
...

I think it's speculation more than logic.

It is not brought into the body by the same method or in the same place.​

It all ends up in the bloodstream for systemic use. Your body can't tell whether it came from your testicles or from an injection. One can argue that the diurnal variation is something that's hard to emulate well, though propionate sort of does it. The better argument is that exogenous testosterone is not under HPTA control, though the specific problems with that are still speculative.

It has to travel through different tissue, largely because of the first point.​

And this means what? Is this speculation that something important happens after Leydig cells secrete testosterone and before it hits general circulation?

Although "bioidentical", that is simply the molecule. There are preservatives and esters and those are not identical to anything in the body, nor do they release androgens at the same rate.​

Is this speculation that preservatives and esters mysteriously affect things? How? Is there evidence?

 

[DS3]

What numbers did you get for two hours post-injection? This is closest to when the peak occurs, at least with propionate.

It's well established in the scientific literature that the area under the response curve is proportional to the dose. You don't have nearly enough data points to firmly establish a contradiction. Unfortunately it's not really practical for an individual to get enough data to figure out what's really happening in a case like this.

I've seen no credible scientific evidence for big differences in how different esters are metabolized. They all end up in the blood where the esters are quickly cleaved from the testosterone. The only differences are in the speed of release from injected depots. This is again well established, and the extraordinary claim that it's wrong requires more support than a few isolated measurements.

"What numbers did you get for two hours post-injection? This is closest to when the peak occurs, at least with propionate."

"It's well established in the scientific literature that the area under the response curve is proportional to the dose. You don't have nearly enough data points to firmly establish a contradiction. Unfortunately it's not really practical for an individual to get enough data to figure out what's really happening in a case like this."

Think of it like this. If at 50 mgs of Prop per day I spike at 1400 ng/dL (speculative) and after 10 hours drop to 1178 ng/dL (previously shown), likely dropping somewhere at or below 800 ng/dL at 24 hours, then it can be logically inferred that 14/24 hours of the day (58.3% of the time) I am within range of TT levels that TRT patients aim to achieve. And if I were to drop my dosage, my spike and trough would be lower, which would not be desirable.

"I've seen no credible scientific evidence for big differences in how different esters are metabolized. They all end up in the blood where the esters are quickly cleaved from the testosterone. The only differences are in the speed of release from injected depots. This is again well established, and the extraordinary claim that it's wrong requires more support than a few isolated measurements.[/QUOTE]"

@Cataceous You seem to be laboring under the delusion that I am seeking validation in my claim that my body metabolizes long-acting esters differently than short-acting esters. After a decade of taking testosterone, I have tried just about every protocol you could think of. With long-acting esters, I experience higher TT and E2, gastrointestinal pain (only experienced with long-acting esters, regardless of dietary intake). With short-acting esters, I can run higher doses without experiencing E2 issues and a quantifiable difference in TT levels (lower) than with long-acting esters (of lower doses). These claims are all quantifiable from my end.

Don't labor my friend.

 

[DS3]

I think it's speculation more than logic.

It is not brought into the body by the same method or in the same place.​

It all ends up in the bloodstream for systemic use. Your body can't tell whether it came from your testicles or from an injection. One can argue that the diurnal variation is something that's hard to emulate well, though propionate sort of does it. The better argument is that exogenous testosterone is not under HPTA control, though the specific problems with that are still speculative.

It has to travel through different tissue, largely because of the first point.​

And this means what? Is this speculation that something important happens after Leydig cells secrete testosterone and before it hits general circulation?

Although "bioidentical", that is simply the molecule. There are preservatives and esters and those are not identical to anything in the body, nor do they release androgens at the same rate.​

Is this speculation that preservatives and esters mysteriously affect things? How? Is there evidence?

"I've seen no credible scientific evidence for big differences in how different esters are metabolized."

You've also failed to present scientific evidence that states esters are metabolized in the same manner. So until you do, this is no more consequential than mere SPECULATION.

(Don't post some theoretical mathematical model derived from theoretical pharmacokinetics of varying testosterone esters. Find a series of studies that demonstrate no substantial difference in patients receiving equal doses of testosterone from varying esters over a long enough time period with enough data points to determine whether or not there is a difference.)

"Your body can't tell whether it came from your testicles or from an injection."

You seem to be using INTUITION on this one, chief.

"Is this speculation that preservatives and esters mysteriously affect things? How? Is there evidence?"

Do you have evidence to support the notion that preservatives and esters don't affect things?

 

[Appassionato]

"What numbers did you get for two hours post-injection? This is closest to when the peak occurs, at least with propionate."

"It's well established in the scientific literature that the area under the response curve is proportional to the dose. You don't have nearly enough data points to firmly establish a contradiction. Unfortunately it's not really practical for an individual to get enough data to figure out what's really happening in a case like this."

Think of it like this. If at 50 mgs of Prop per day I spike at 1400 ng/dL (speculative) and after 10 hours drop to 1178 ng/dL (previously shown), likely dropping somewhere at or below 800 ng/dL at 24 hours, then it can be logically inferred that 14/24 hours of the day (58.3% of the time) I am within range of TT levels that TRT patients aim to achieve. And if I were to drop my dosage, my spike and trough would be lower, which would not be desirable.

"I've seen no credible scientific evidence for big differences in how different esters are metabolized. They all end up in the blood where the esters are quickly cleaved from the testosterone. The only differences are in the speed of release from injected depots. This is again well established, and the extraordinary claim that it's wrong requires more support than a few isolated measurementz.

You seem to be laboring under the delusion that I am seeking validation in my claim that my body metabolizes long-acting esters differently than short-acting esters. After a decade of taking testosterone, I have tried just about every protocol you could think of. With long-acting esters, I experience higher TT and E2, gastrointestinal pain (only experienced with long-acting esters, regardless of dietary intake). With short-acting esters, I can run higher doses without experiencing E2 issues and a quantifiable difference in TT levels (lower) than with long-acting esters (of lower doses). These claims are all quantifiable from my end.

Don't labor my friend.

Do you have E2 numbers with both protocols?
I'm trying the same way, switched to ED propionate and then EOD propionate (due to insomnia kicking in again) from enanthate, but it's been a failure so far. I don't have labs with a propionate protocol yet though.

But I'm exactly the opposite than you. I need tiny doses to get good levels of T, otherwise it just all converts to E2 and DHT.
We are kind of rare examples, but the general TRT trend is evolving dangerously towards mild androgens cycle, as pointed by another user.

The argument "if you feel well, don't worry about it" is plain ridiculous. Body builders on steroids will tell you they feel great.
Same goes with women body builders doing cocaine before jumping on stage to stay ripped.

This is a must read for everyone:

Why I Quit Using Steroids | T Nation

As a word of warning, nandrolone has a strong effect on neurotransmitters and not in a good way. The topic has been discussed several times on forums. Google is your friend.
I've taken it roughly 10 years ago and I wouldn't advise it to anyone, unless you have unbearable joints pain.

 

[DS3]

Do you have E2 numbers with both protocols?
I'm trying the same way, switched to ED propionate and then EOD propionate (due to insomnia kicking in again) from enanthate, but it's been a failure so far. I don't have labs with a propionate protocol yet though.

But I'm exactly the opposite than you. I need tiny doses to get good levels of T, otherwise it just all converts to E2 and DHT.
We are kind of rare examples, but the general TRT trend is evolving dangerously towards mild androgens cycle, as pointed by another user.

The argument "if you feel well, don't worry about it" is plain ridiculous. Body builders on steroids will tell you they feel great.
Same goes with women body builders doing cocaine before jumping on stage to stay ripped.

This is a must read for everyone:

Why I Quit Using Steroids | T Nation

As a word of warning, nandrolone has a strong effect on neurotransmitters and not in a good way. The topic has been discussed several times on forums. Google is your friend.
I've taken it roughly 10 years ago and I wouldn't advise it to anyone, unless you have unbearable joints pain.

"Do you have E2 numbers with both protocols?"

E2 on both ED and EOD prop were both in the range of 40-50 pg/mL. (I feel best in this range. The lower range of 20-30 does not work for me). I can tell you that I definitely feel better on EOD injections of Prop as opposed to ED injections. My energy suffered with ED injections.

"The argument "if you feel well, don't worry about it" is plain ridiculous. Body builders on steroids will tell you they feel great.
Same goes with women body builders doing cocaine before jumping on stage to stay ripped."

From my past experience as a bodybuilder and being involved in that world, I can tell you that most do not feel good on true steroid cycle dosages. (Even if individuals report that they do).

"As a word of warning, nandrolone has a strong effect on neurotransmitters and not in a good way."

I agree with this wholeheartedly.

 

[Appassionato]

"Do you have E2 numbers with both protocols?"

E2 on both ED and EOD prop were both in the range of 40-50 pg/mL. (I feel best in this range. The lower range of 20-30 does not work for me). I can tell you that I definitely feel better on EOD injections of Prop as opposed to ED injections. My energy suffered with ED injections.

"The argument "if you feel well, don't worry about it" is plain ridiculous. Body builders on steroids will tell you they feel great.
Same goes with women body builders doing cocaine before jumping on stage to stay ripped."

From my past experience as a bodybuilder and being involved in that world, I can tell you that most do not feel good on true steroid cycle dosages. (Even if individuals report that they do).

"As a word of warning, nandrolone has a strong effect on neurotransmitters and not in a good way."

I agree with this wholeheartedly.

What were your E2 levels on your best enanthate/cypionate protocol?
I can't run E2 levels like yours, I get horrible anxiety and I feel warm all the time.

How is your sleep? Do you notice any difference between long esters vs short esters?

 

[DS3]

What were your E2 levels on your best enanthate/cypionate protocol?
I can't run E2 levels like yours, I get horrible anxiety and I feel warm all the time.

How is your sleep? Do you notice any difference between long esters vs short esters?

My test results would show approximately 40 pg/mL with Cypionte @175mgs/week, but that is because I had to stay on Adex 2x per week @ 0.25 mg to keep it at that level. Otherwise, my E2 would climb until the point that I had HORRIBLE migraines and head fog. (This level of symptoms has, for me, tested around 60-70 pg/mL years ago).

Long-ester v. Short-ester symptoms in me:

Long-Ester: NEGATIVE- Horrible GI pain, wild swings in mood, unstable libido, 'feminized' feeling, higher TT at lower dosages (compared to Prop), higher E2 with substantially increased need for Adex multiple times per week (which kills joints), head fog.
POSITIVE- More joint cushioning (perhaps because of higher conversion into E2), fuller muscles in the gym, need less MGs per week to maintain goal TT.

Short-Ester: NEGATIVE- Need to take a higher dosage to achieve goal TT, a little more joint pain.
POSITIVE- No GI pain, more stable mood, slightly better libido, less 'feminized' feeling, less E2 issues/symptoms, less head fog, much less Adex needed long-term (once every 10 days or so).

 

[Appassionato]

My test results would show approximately 40 pg/mL with Cypionte @175mgs/week, but that is because I had to stay on Adex 2x per week @ 0.25 mg to keep it at that level. Otherwise, my E2 would climb until the point that I had HORRIBLE migraines and head fog. (This level of symptoms has, for me, tested around 60-70 pg/mL years ago).

Long-ester v. Short-ester symptoms in me:

Long-Ester: NEGATIVE- Horrible GI pain, wild swings in mood, unstable libido, 'feminized' feeling, higher TT at lower dosages (compared to Prop), higher E2 with substantially increased need for Adex multiple times per week (which kills joints), head fog.
POSITIVE- More joint cushioning (perhaps because of higher conversion into E2), fuller muscles in the gym, need less MGs per week to maintain goal TT.

Short-Ester: NEGATIVE- Need to take a higher dosage to achieve goal TT, a little more joint pain.
POSITIVE- No GI pain, more stable mood, slightly better libido, less 'feminized' feeling, less E2 issues/symptoms, less head fog, much less Adex needed long-term (once every 10 days or so).

It seems you are the exact opposite of me, you are quite resistant to drugs.
That dose of anastrazole would have sent me to nearly 0 pg/mL.

So you are basically achieving a cut of roughly 10 pg/mL of E2, which is the same I can get cleaning my liver with TUDCA or sylimarine, but that resolve your symptoms, which is good.

What SHBG number are your running? It could be you can tolerate higher numbers of E2 because of higher SHBG levels.
I get migraines and brain fog exactly like you when my E2 goes above 30, with 40 being the worst. Also my gynecomastia gets worse, which is like a ring bell for me of higher levels of estrogens floating around.

 

[DS3]

It seems you are the exact opposite of me, you are quite resistant to drugs.
That dose of anastrazole would have sent me to nearly 0 pg/mL.

So you are basically achieving a cut of roughly 10 pg/mL of E2, which is the same I can get cleaning my liver with TUDCA or sylimarine, but that resolve your symptoms, which is good.

What SHBG number are your running? It could be you can tolerate higher numbers of E2 because of higher SHBG levels.
I get migraines and brain fog exactly like you when my E2 goes above 30, with 40 being the worst. Also my gynecomastia gets worse, which is like a ring bell for me of higher levels of estrogens floating around.

SHBG sits around 20 nmol/L, so relatively low.

Trust me, man, I understand what you are saying. As my E2 creeps up too high, I have the same symptoms (head fog, nipple sensitivity, feeling feminized, migraine). I also hate Adex because it MURDERS my joints, which is why I opt for Prop because I experience less E2 symptoms.

I will tell you, though, that as soon as Jatenzo is on the market I will be making the switch without a question.

 

[Appassionato]

SHBG sits around 20 nmol/L, so relatively low.

Trust me, man, I understand what you are saying. As my E2 creeps up too high, I have the same symptoms (head fog, nipple sensitivity, feeling feminized, migraine). I also hate Adex because it MURDERS my joints, which is why I opt for Prop because I experience less E2 symptoms.

I will tell you, though, that as soon as Jatenzo is on the market I will be making the switch without a question.

Why switching to oral testo?

 

[DS3]

Why switching to oral testo?

My honest answer is that because as I changed from Cyp to Prop, my negative symptoms improved, but not eliminated. I have tried no-ester Test before (this was not prescribed), and while I can say that I would not want to shoot this 2x per day to keep steady blood levels, I am hopeful that Oral undecanoate will alleviate all or most all of my negative symptoms. (It will also make it much easier to not 'overdose' and end up with negative symptoms in the first place).

So, in short, the shorter the ester the better I tend to feel.

 

[Appassionato]

My honest answer is that because as I changed from Cyp to Prop, my negative symptoms improved, but not eliminated. I have tried no-ester Test before (this was not prescribed), and while I can say that I would not want to shoot this 2x per day to keep steady blood levels, I am hopeful that Oral undecanoate will alleviate all or most all of my negative symptoms. (It will also make it much easier to not 'overdose' and end up with negative symptoms in the first place).

So, in short, the shorter the ester the better I tend to feel.

What's the half life of Jatenzo?
What about liver toxicity though? The oral testo needs to go through the liver.

 

[DS3]

What's the half life of Jatenzo?
What about liver toxicity though? The oral testo needs to go through the liver.

"The concern in the past about pills is that previous formulations caused liver toxicity. This agent works differently. It is absorbed through the lymphatic system, rather than the bloodstream, and therefore bypasses metabolism by the liver, the so-called “first-pass effect.” -Abraham Morgentaler, MD

FDA approves oral testosterone capsule for men with hypogonadism

 

[DS3]

What's the half life of Jatenzo?
What about liver toxicity though? The oral testo needs to go through the liver.

As far as half-life, I am not exactly sure what the precise half-life is given that it isn't stated anywhere in the literature (that I can find). However, figure 2 represents the mean plasma TT profiles of particapints of the Jatenzo trials.

https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/206089s000lbl.pdf

 

[Jason Sypolt]

I think it's speculation more than logic.

It is not brought into the body by the same method or in the same place.​

It all ends up in the bloodstream for systemic use. Your body can't tell whether it came from your testicles or from an injection. One can argue that the diurnal variation is something that's hard to emulate well, though propionate sort of does it. The better argument is that exogenous testosterone is not under HPTA control, though the specific problems with that are still speculative.

It has to travel through different tissue, largely because of the first point.​

And this means what? Is this speculation that something important happens after Leydig cells secrete testosterone and before it hits general circulation?

Although "bioidentical", that is simply the molecule. There are preservatives and esters and those are not identical to anything in the body, nor do they release androgens at the same rate.​

Is this speculation that preservatives and esters mysteriously affect things? How? Is there evidence?

You missed my point. It is exactly that - speculation. None of that can be proved or disproved and unless it can be proven that there is no difference between natural production of androgens and replacement therapy, then we must treat it as speculation and not truth. We assume there is a difference because we can't prove there is not and we treat with different (higher) amounts of androgens