Nandrolone Data (including joint pain relief mechanisms [by Type-IIx])

[Scorpyd]

I like TypeIIx posts , I just have to read it more than once , sometimes 3 x, but, at the end of the day I get it to the best that my factory worker brain can comprehend.

 

[xpoc]

I do mention the duality of RAS activation (vascoconstriction, cardiac hypertrophy, and fibrosis, despite water and electrolyte balance, connective tissue cell growth, and the connective tissue metabolism & tissue repair): it's a double-edged sword. But if you can share some study showing this "10x more damaging to the heart than straight testosterone?" Is it this study by chance? D’Ascenzo, S., Millimaggi, D., Di Massimo, C., Saccani-Jotti, G., Botrè, F., Carta, G., … Dolo, V. (2007). Detrimental effects of anabolic steroids on human endothelial cells. Toxicology Letters, 169(2), 129–136. doi:10.1016/j.toxlet.2006.12.008

With respect to erectile issues and "deca dick," consider testosterone as it is the anabolic agent you'd want to use for preserving (and augmenting) sexual function.

This is where I read it: https://www.steroidal.com/steroids-news/nandrolone-damages-blood-vessels-11x-testosterone/

 

[Bio]

I do mention the duality of RAS activation (vascoconstriction, cardiac hypertrophy, and fibrosis, despite water and electrolyte balance, connective tissue cell growth, and the connective tissue metabolism & tissue repair): it's a double-edged sword. But if you can share some study showing this "10x more damaging to the heart than straight testosterone?" Is it this study by chance? D’Ascenzo, S., Millimaggi, D., Di Massimo, C., Saccani-Jotti, G., Botrè, F., Carta, G., … Dolo, V. (2007). Detrimental effects of anabolic steroids on human endothelial cells. Toxicology Letters, 169(2), 129–136. doi:10.1016/j.toxlet.2006.12.008

With respect to erectile issues and "deca dick," consider testosterone as it is the anabolic agent you'd want to use for preserving (and augmenting) sexual function.

Yes, that is the study that is being referenced. Ergo-log.com referenced it in 2008 which brought it to light.

https://www.ergo-log.com/nandrotest.html

The actual study

https://pubmed.ncbi.nlm.nih.gov/17267145/

 

[Bio]

Brother I appreciate your posts, you are an intelligent guy, and you are trying to be helpful, but the mark of intelligence is making a complex subject simple, and the way you are currently approaching sharing information is the opposite of that, and really works against your ability to be of any help. It would be better if you wrote out your posts with more explanations, quotation marks, etc

Yeah, OTH is working with me on a more important quasi-article with a simplified section. Honestly, to me, this is rather simplified (as much as I believe it can be reduced without losing granularity). Sorry if it's incomprehensible, perhaps if there's enough demand (I didn't think this as much more than just a dump from my notes on Nandrolone) a guy like OuchThatHurts can put out a simplified version that preserves important detail.

Take Astrophysicist Neil deGrasse Tyson. He's quite the intellectual but he has the ability to take extremely complex subject matter and relay it to the average layperson in basic, understandable language.

 

[TeaMan]

So if im understand it correctly, nandrolone can couse a heart damage by increase fibrosis?

 

[johnjuanb1]

I don’t buy into the nandrolone heart damage thing. I’ll stick to the study on rats that were given nandrolone lived 10% longer on average than natty rats. Studies can be skewed many ways. Search hard enough and you’ll find a contradictory study for pretty much everything.
I love my nandrolone, and I’ll justify its use until I drop from heart damage.

 

[juggy38]

Yeah, OTH is working with me on a more important quasi-article with a simplified section. Honestly, to me, this is rather simplified (as much as I believe it can be reduced without losing granularity). Sorry if it's incomprehensible, perhaps if there's enough demand (I didn't think this as much more than just a dump from my notes on Nandrolone) a guy like OuchThatHurts can put out a simplified version that preserves important detail.

Don’t remove the molecular biology aspect of your posts! I love these.

But I can see how people not in fields of work that see literature like this ….this looks like Japanese calculus.

Hell I have to go dig through my textbooks and google on some
Of the info.

But we all appreciate the massive effort!

 

[Mufasa123]

Don’t remove the molecular biology aspect of your posts! I love these.

But I can see how people not in fields of work that see literature like this ….this looks like Japanese calculus.

Hell I have to go dig through my textbooks and google on some
Of the info.

But we all appreciate the massive effort!

Agree with this. Don't delete anything, this is what allows people to check/follow up etc. This is real understanding and credibility to thought. If you wanted to add some "layman takeaway bullets" at the end that might be accretive. Don't dumb it down though, that's how we end up with bro science quoted bullshit.

While I'm in a completely different field far too many people take published research as gospel. Guys are "paid" to publish (call it integral to job), journals are paid to sell with memberships. I've seen major journal published conclusions that anyone on this board could fire a cannon through ie "We proved NOT A which means our long time published pet theory B is correct." Hell, no they didn't. A and B are not mutually exclusive in anyone's mind nor in world, and in no way if I submitted something like that would I not be tossed immediately upon the most cursory of first reads (but big names...apparently show up and check your brain at the door).

 

[Type-IIx]

Yes, that is the study that is being referenced. Ergo-log.com referenced it in 2008 which brought it to light.

https://www.ergo-log.com/nandrotest.html

The actual study

https://pubmed.ncbi.nlm.nih.gov/17267145/

@xpoc OK, with respect to this study, to start it should be noted that Steroidal obfuscated the data - perhaps intentionally. The actual graph from that study:



A major methodological weakness was the absurd concentrations used. Peter Bond pointed out the following:
They tested this range of concentrations:

The drugs were tested at the indicated range: testosterone, 10–200 μM; androstenedione, 50–400 μM; nandrolone, 5–100 μM; norandrostenedione, 125–750 μM; and norandrostenediol, 50–6000 μM.
5 μM = 5000 nM (= nmol/L).

Add to this that the cells were cultured in 10% heat-inactivated fetal calf serum, and 20% fetal calf serum. So you end up with a 45 * 0.3 = 13.5 g/L albumin concentration (SHBG is completely irrelevant at these concentrations). You'll end up with free nandrolone concentrations well in excess of 100 Nm, likely in the 1000 nM range. These are insanely high concentrations that no human on earth will ever reach. With such high concentrations you can get off-target effects with receptors with very low affinity that you'd otherwise never have.

Also, noteworthy from Discussion:
"Here, we provide evidence that nandrolone, testosterone, and norandrostenedione are able to induce increased Ca²⁺ that seems to be independent of incubation time and compound identity...
"the increase in Ca²⁺ observed in our system appears to be insufficient to induce a massive modification of the level of intracellular Ca²⁺ but it may be considered an early activation predisposing to subsequent [atherosclerosis]."

IC50(concentration for inhibition of growth) was 11x greater for nand... OK, people don't use these massive doses of deca, and inhibition of growth was not strongly associated with apoptosis (programmed cell death) @ IC50 concentrations T (31%) >> nand (18%)... sort of balancing things out.

Increases in actual intracellular Ca²⁺ were greater for test at 72 hr (149.8 v. 140.4), acute effects on intracellular Ca²⁺ showed T > nand > control.

So T has some particular harms vs. nandrolone at these absurd concentrations as well. But in conclusion, these concentrations will never be reached, so it's all truly moot. None of this spillover into harms to endothelial cells will occur at even 5 g weekly total AAS.

 

[NEMSZ]

@xpoc OK, with respect to this study, to start it should be noted that Steroidal obfuscated the data - perhaps intentionally. The actual graph from that study:

View attachment 156035

A major methodological weakness was the absurd concentrations used. Peter Bond pointed out the following:
They tested this range of concentrations:



Also, noteworthy from Discussion:
"Here, we provide evidence that nandrolone, testosterone, and norandrostenedione are able to induce increased Ca²⁺ that seems to be independent of incubation time and compound identity...
"the increase in Ca²⁺ observed in our system appears to be insufficient to induce a massive modification of the level of intracellular Ca²⁺ but it may be considered an early activation predisposing to subsequent [atherosclerosis]."

IC50(concentration for inhibition of growth) was 11x greater for nand... OK, people don't use these massive doses of deca, and inhibition of growth was not strongly associated with apoptosis (programmed cell death) @ IC50 concentrations T (31%) >> nand (18%)... sort of balancing things out.

Increases in actual intracellular Ca²⁺ were greater for test at 72 hr (149.8 v. 140.4), acute effects on intracellular Ca²⁺ showed T > nand > control.

So T has some particular harms vs. nandrolone at these absurd concentrations as well. But in conclusion, these concentrations will never be reached, so it's all truly moot. None of this spillover into harms to endothelial cells will occur at even 5 g weekly total AAS.

I totally agree with the fact that I love the info you give;

But also agree to please simplify the data… lol

I have no idea what 90% of this post means..

You can post the data then put at the bottom a little cliff note like if you were having a convo with one of us in the locker room, not a laboratory

 

[Type-IIx]

Thanks for the feedback everyone. I think that I must doing something right (at least on the right path) given the responses to my posts generally. I'm no Neil deGrasse Tyson certainly, that is a rather high bar to set. I'm also not sure my objective here needs to be to dilute my material for being massively clickworthy, but rather to give decent information. I'll certainly put more effort into a succinct conclusion and summary, but won't deviate from providing solid material and in my own style.

 

[Type-IIx]

I totally agree with the fact that I love the info you give;

But also agree to please simplify the data… lol

I have no idea what 90% of this post means..

You can post the data then put at the bottom a little cliff note like if you were having a convo with one of us in the locker room, not a laboratory

I appreciate this, will do better on providing a brief summary.

If I were have a convo with you in the locker room about nandrolone I'd definitely mention, if asked about cardiovascular harms, that there is a double-edged sword inherent to the benefits Deca gives for joint pain but by the same mechanism also can cause fibrotic tissue to accrue in the heart, liver, etc. And also, I'd say that these claims that Deca is >10x more potent than Test in causing (endothelial cell) harms are massively overblown because the absurd concentrations they used to study these things don't apply to the real world: we'd never take high enough doses for these harms to occur.

 

[NEMSZ]

I appreciate this, will do better on providing a brief summary.

If I were have a convo with you in the locker room about nandrolone I'd definitely mention, if asked about cardiovascular harms, that there is a double-edged sword inherent to the benefits Deca gives for joint pain but by the same mechanism also can cause fibrotic tissue to accrue in the heart, liver, etc. And also, I'd say that these claims that Deca is >10x more potent than Test in causing (endothelial cell) harms are massively overblown because the absurd concentrations they used to study these things don't apply to the real world: we'd never take high enough doses for these harms to occur.

THATS WHAT IM TALKING ABOUT!! lol

Thank you for that bro, I really do enjoy your posts, as well as a lot of other people, as you can see…

At what dosage and duration would you “recommend” is safe to run nandrolone to keep away the damages you speak of?

 

[Type-IIx]

THATS WHAT IM TALKING ABOUT!! lol

Thank you for that bro, I really do enjoy your posts, as well as a lot of other people, as you can see…

At what dosage and duration would you “recommend” is safe to run nandrolone to keep away the damages you speak of?

If you stick to 25 mg/kg (body weight) total androgens and don't run Deca only at that concentration (in line with all the sane stuff I've seen) you basically just need to worry about the standard cardiovascular harms arising out of androgen use:

Reversible increased left-ventricular hypertrophy (substantial increase in mass even at <1 g weekly) & impaired diastolic function, necessitating a 1 on/3 off (time on/time off) scheme for reversal to base-line values. Don't become mesmerized by bloodwork values returning to base-line as they don't reflect morphological and functional changes.

 

[Swifto]

Great post, well done, this must of taken some time.

 

[Scorpyd]

Thank you Type-IIx. Have a blessed Easter.
The way I see it , things (information) are getting better here all the time.

 

[Type-IIx]

Thanks for the research, TypeII!

Uneducated question: Would Telmisartan be useful in mitigating the effect nandrolone has on the RAS?

Just saw this. So, Telmisartan is highly beneficial for high blood pressure, but should not be viewed as a prophylactic (a preventive cure-all). Some guidelines:

Telmisartan use can be initiated if and only if blood pressure is > 140/90 mmHg (doctor's office) and > 135/85 (home). Start with 1/2 the manufacturer's maximal dose. Cessation of AAS, lifestyle factors preferred. Immediate drug treatment is indicated for 160/100 mmHg.

Have bloodwork performed prior to initiating and 1 month after starting (or after an increase in dose), and if everything comes back normal, every half a year. Include creatinine, eGFR and electrolytes. It takes about 4 to 6 weeks for the full effect of treatment. Ideally you reach a blood pressure below or equal to 130/80 mmHg (but above 120 mmHg).

Concerns with the use of ARBs and Telmisartan include hypotension (low blood pressure), hyperkalemia (high potassium) and renal (kidney) dysfunction.

 

[luki7788]

Just saw this. So, Telmisartan is highly beneficial for high blood pressure, but should not be viewed as a prophylactic (a preventive cure-all). Some guidelines:

Telmisartan use can be initiated if and only if blood pressure is > 140/90 mmHg (doctor's office) and > 135/85 (home). Start with 1/2 the manufacturer's maximal dose. Cessation of AAS, lifestyle factors preferred. Immediate drug treatment is indicated for 160/100 mmHg.

Have bloodwork performed prior to initiating and 1 month after starting (or after an increase in dose), and if everything comes back normal, every half a year. Include creatinine, eGFR and electrolytes. It takes about 4 to 6 weeks for the full effect of treatment. Ideally you reach a blood pressure below or equal to 130/80 mmHg (but above 120 mmHg).

Concerns with the use of ARBs and Telmisartan include hypotension (low blood pressure), hyperkalemia (high potassium) and renal (kidney) dysfunction.

What about boldenone and its effect on joints and collagen synthesis? in theory, it has a much greater impact on collagen synthesis than nandrolone, but in practice I never felt it

 

[jaxino]

What about boldenone and its effect on joints and collagen synthesis? in theory, it has a much greater impact on collagen synthesis than nandrolone, but in practice I never felt it

Yes exactly.... What about EQ?

 

[LATS]

The study referring to nandrolone being 10x worse for cardiac etc is WAY overblown and very flawed.. Scott Stevenson addressed this a couple times on how the study was flawed and why.. so we can calm down a bit about the " deadly" deca.. im not saying its benign.. but don't go by that study.