200mg of deca x 8 weeks yielded 5lbs (study)

[Theworm]

Heh AGREE. What's driving the deca cardio-/neuro- toxicity hysteria is the fact that nandrolone is used as a model androgen in research. So guys find all these rodent and in vitro studies on the model AAS and assume it must be particularly harmful.

While minor modifications to the steroidal structure of T (i.e., removal of the C-19 methyl) can cause massively different actions in vivo, I doubt that deca is particularly harmful in its cardio- and neuro-toxicity as is perceived/claimed (by a particular subreddit especially!)

MENT's popularity now is a classic example of using the absence of evidence to prove the contrary. Since there is little data on MENT (shit, it doesn't even have a CAS# yet!) people view the absence of evidence of harm as a "GTG."

I view the absence of its evidence as something to be wary of.

Yes, others speculated that nandrolone was toxic as the vascular endothelial didn’t have estrogen present as would have occurred with testosterone

 

[Type-IIx]

Yes, others speculated that nandrolone was toxic as the vascular endothelial didn’t have estrogen present as would have occurred with testosterone

Do you or @RebornNez have a link for the comparative in vitro study you mentioned?

 

[Theworm]

Do you or @RebornNez have a link for the comparative in vitro study you mentioned?

Nandrolone Damages Blood Vessels 11x More Than Testosterone

Nandrolone, the parent hormone in the popular injectable steroids – Deca-Durabolin and NPP – has been found to be damaging to blood vessels.

www.steroidal.com

 

[Type-IIx]

Nandrolone Damages Blood Vessels 11x More Than Testosterone

Nandrolone, the parent hormone in the popular injectable steroids – Deca-Durabolin and NPP – has been found to be damaging to blood vessels.

www.steroidal.com

Look at the distorted(!) image he at least posted showing relative potencies.

And he's using the old-school reference notation
Toxicol Lett. 2007 Mar 8; 169(2):129-36.

to make it more difficult to find the reference. I'll find it, nonetheless, but that's a classic example of misrepresentation of data. He actually put effort into physically distoring the graph!

 

[Type-IIx]

And here's the deobfuscated data:


This is actually a great paper @Theworm - thank you. It indicates that nandrolone is NOT particularly harmful versus testosterone in human endothelial cells. The opposite conclusion can fairly be drawn from the author's contention. Obviously I've only briefly skimmed it given this short duration, but I'm going to read it now.

 

[Theworm]

And here's the deobfuscated data:
View attachment 156928

This is actually a great paper @Theworm - thank you. It indicates that nandrolone is NOT particularly harmful versus testosterone in human endothelial cells. The opposite conclusion can fairly be drawn from the author's contention. Obviously I've only briefly skimmed it given this short duration, but I'm going to read it now.

Please do. Guys at excelmale claim it’s safe and they don’t account for the low E2 which you see with nandrolone administration. Others argue an ARB mitigates the endothelial damage etc..

 

[Millard]

They point to really one study showing nandrolone was 11x more toxic to vascular endothelial in rats

And here's the deobfuscated data:
View attachment 156928

This is actually a great paper @Theworm - thank you. It indicates that nandrolone is NOT particularly harmful versus testosterone in human endothelial cells. The opposite conclusion can fairly be drawn from the author's contention. Obviously I've only briefly skimmed it given this short duration, but I'm going to read it now.

I've commented on this paper before. I've rarely seen a researcher including SO MANY qualifiers when reaching a conclusion!

You can't make such conclusive statements with in vitro and rat studies, and correlational studies.

Even the researchers don't go so far:

For example, correlation does not equal causation in brain changes studies. It's just speculation:

View attachment 144511And the nandrolone is 11x worse than testosterone... it's a big leap to go from in vitro to human conclusions. Notice the qualifiers from researchers:

View attachment 144513

The conclusions are overstated, often mere speculation, and have not been proven in humans for most of these studies. We need to be careful speaking beyond what the evidence actually says.

Source:

Bjørnebekk, A., Walhovd, K. B., Jørstad, M. L., Due-Tønnessen, P., Hullstein, I. R., & Fjell, A. M. (2017). Structural Brain Imaging of Long-Term Anabolic-Androgenic Steroid Users and Nonusing Weightlifters. Biological Psychiatry, 82(4), 294–302. Redirecting

D’Ascenzo, S., Millimaggi, D., Di Massimo, C., Saccani-Jotti, G., Botrè, F., Carta, G., Tozzi-Ciancarelli, M. G., Pavan, A., & Dolo, V. (2007). Detrimental effects of anabolic steroids on human endothelial cells. Toxicology Letters, 169(2), 129–136. Redirecting

 

[Type-IIx]

I've commented on this paper before. I've rarely seen a researcher including SO MANY qualifiers when reaching a conclusion!

View attachment 156929

Nicely done!

Yes, after reading it. 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]."

Big fucking deal.

IC50(concentration for inhibition of growth) was 11x greater for nand... OK, people don't use 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.

Conclusion: since apoptosis was only very slightly altered, vascular endothelium dysfunction may arise from very high deca AND test dosages, accelerating atherosclerosis.

Nothing new here. Unless you thought deca was particularly harmful!

 

[GuerillaPete]

Deca is underrated ! Some people dont get side on it at all using a reasonable dosage.

 

[Theworm]

Nicely done!

Yes, after reading it. 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]."

Big fucking deal.

IC50(concentration for inhibition of growth) was 11x greater for nand... OK, people don't use 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.

Conclusion: since apoptosis was only very slightly altered, vascular endothelium dysfunction may arise from very high deca AND test dosages, accelerating atherosclerosis.

Nothing new here. Unless you thought deca was particularly harmful!

Nicely done by you and @Millard
So basically it’s most likely that since it’s the most studies anabolic behind test, you see some evidence like this. Also in vitro etc...
so as I suspect, it’s much safer than that study claimed.
Also I think once blast for 16 weeks at 3-400 mg once a year prob not going to cut decades off your life. Agree @Type-IIx ?

 

[Type-IIx]

Nicely done by you and @Millard
So basically it’s most likely that since it’s the most studies anabolic behind test, you see some evidence like this. Also in vitro etc...
so as I suspect, it’s much safer than that study claimed.
Also I think once blast for 16 weeks at 3-400 mg once a year prob not going to cut decades off your life. Agree @Type-IIx ?

Agreed!

 

[RebornNez]

Plus in rat studies heart enlargement was prevented by using blood pressure medication

 

[PeterBond]

Look at the distorted(!) image he at least posted showing relative potencies.

And he's using the old-school reference notation
Toxicol Lett. 2007 Mar 8; 169(2):129-36.

to make it more difficult to find the reference. I'll find it, nonetheless, but that's a classic example of misrepresentation of data. He actually put effort into physically distoring the graph!

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.

With in vitro research per se already translating very poorly to clinical meaningful stuff, these concentrations have just made it completely irrelevant across the board.

 

[PeterBond]

Please do. Guys at excelmale claim it’s safe and they don’t account for the low E2 which you see with nandrolone administration. Others argue an ARB mitigates the endothelial damage etc..

This kind of research has no capability of determining whether or not a compound is safe or unsafe, at all.

 

[Type-IIx]

They tested this range of concentrations:


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.

With in vitro research per se already translating very poorly to clinical meaningful stuff, these concentrations have just made it completely irrelevant across the board.

Great analysis, straight to the point. A question: the 45 value, does that represent basal albumin g/L (i.e., with supraphysiological dosing of androgens, are we safe to always use 45 g/L as a static human albumin? Is this an extrapolation from Vermeulen's finding that "in the adult man free testosterone represents 2%, albumin bound testosterone 40%, and TeBG (SHBG) bound testosterone 58%?"

Thank you, @PeterBond

 

[PeterBond]

Great analysis, straight to the point. A question: the 45 value, does that represent basal albumin g/L (i.e., with supraphysiological dosing of androgens, are we safe to always use 45 g/L as a static human albumin? Is this an extrapolation from Vermeulen's finding that "in the adult man free testosterone represents 2%, albumin bound testosterone 40%, and TeBG (SHBG) bound testosterone 58%?"

Thank you, @PeterBond

I've assumed the concentration of albumin found in fetal calf serum, which is 45 g/L. It's roughly the same in human adults. Albumin levels are not affected by AAS—thank god. (And, of course, they are also unaffected by it when its used to culture cells.)

You can use the Vermeulen equation to get a (very) rough estimate of the free hormone concentration, assuming the binding affinity for calf albumin is similar to that in humans. Although, admittedly, the equation has a good chance of being way off because it's not intended to be used for such absurd concentrations of neither hormones nor binding proteins.

Either way, the takeaway here is that the concentrations are just ridiculous.

 

[Type-IIx]

I've assumed the concentration of albumin found in fetal calf serum, which is 45 g/L. It's roughly the same in human adults. Albumin levels are not affected by AAS—thank god. (And, of course, they are also unaffected by it when its used to culture cells.)

You can use the Vermeulen equation to get a (very) rough estimate of the free hormone concentration, assuming the binding affinity for calf albumin is similar to that in humans. Although, admittedly, the equation has a good chance of being way off because it's not intended to be used for such absurd concentrations of neither hormones nor binding proteins.

Either way, the takeaway here is that the concentrations are just ridiculous.

If you ever write an uber-nerd post devoted to the weaknesses of AAS research methods, like discussing BSA/HSA differences, assays, translating data from different species (oh that reminds me, have you researched LR3-IGF-I at all? so many different behaviors across ruminants/rodent/sheep), throw in some weaknesses of relying on bloodwork for health monitoring, I would be so, so happy.

 

[Theworm]

Great insight guys!

 

[BachmanityInsanity]

Anyone get calcium score angiograms before and after a cycle?That's the highest resolution look at plaque is that right? I will be getting one done in the next 3-4 months while off any steroids except test replacement and have not used higher doses for quite a while. Is the radiation risk of two of these within 20 weeks too much. What in vitro tests on ourselves can we do to get the very best idea of what harm is going on?