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Jordan Peters to TRT

An example .. the armed services did a study comparing testosterone to nandrolone.. ( forgive me I am going by memory here).. what they found was in the lower doses ( 200 to 300 mgs) they were very comparable in terms of muscle gained.. protein accrete.. now when raising the dosage they found test started to outshine deca a bit.. why ?
Well again we can go to its secondary characteristics. When they raised test they also got a rise in dht and estrogen.. we know the importance of estrogen in muscle growth.. now deca also converts but at roughly 20 percent of testosterone and its dht is not worth mentioning.
So what's the takeaway?
Test is great up to a point then we need A aromatase inhibitor to combat too much estro.. not ideal.. studies show bone lose using aromatase inhibitors that is not related to the loss of estrogen but the elimination of certain minerals.. plus it sometimes can be negative on lipids etc..
Now another study shows that primobolan actually adds a decent amount of tissue in subjects at only 200mgs.. now primo does not convert to estro but its abilities with protein are very good..
So my point is if they do decent at protein accrete.. and we can avoid certain secondary characteristics that might be negative to what we want then why woukdnt we use test ( up to a point where the negatives outweigh the positive) then throw a compound in that can help us add tissue with adding to conversions we don't want.. like primo.. like mast.. again they add tissue with out bloat.. we are getting ample estro from the test..
So once we understand the characteristics of all the compounds it opens up alot more options.. instead of throwing one aromatase nightmare after another..
 
An example .. the armed services did a study comparing testosterone to nandrolone.. ( forgive me I am going by memory here).. what they found was in the lower doses ( 200 to 300 mgs) they were very comparable in terms of muscle gained.. protein accrete.. now when raising the dosage they found test started to outshine deca a bit.. why ?
Well again we can go to its secondary characteristics. When they raised test they also got a rise in dht and estrogen.. we know the importance of estrogen in muscle growth.. now deca also converts but at roughly 20 percent of testosterone and its dht is not worth mentioning.
So what's the takeaway?
Test is great up to a point then we need A aromatase inhibitor to combat too much estro.. not ideal.. studies show bone lose using aromatase inhibitors that is not related to the loss of estrogen but the elimination of certain minerals.. plus it sometimes can be negative on lipids etc..
Now another study shows that primobolan actually adds a decent amount of tissue in subjects at only 200mgs.. now primo does not convert to estro but its abilities with protein are very good..
So my point is if they do decent at protein accrete.. and we can avoid certain secondary characteristics that might be negative to what we want then why woukdnt we use test ( up to a point where the negatives outweigh the positive) then throw a compound in that can help us add tissue with adding to conversions we don't want.. like primo.. like mast.. again they add tissue with out bloat.. we are getting ample estro from the test..
So once we understand the characteristics of all the compounds it opens up alot more options.. instead of throwing one aromatase nightmare after another..
Protein accretion (protein synthesis) is not a metric that's commonly used in humans with AAS. I found a study from 1989 measuring protein accretion in man... just so people understand what's involved for this, a primed continuous infusion of radioactive leucine must be administered to determine leucine incorporation in muscle samples taken by needle biopsy (they must remove muscle tissue at various time points for measurement to determine the uptake into muscle of the radiolabeled leucine). This is completely impracticable and hence it is only typically done in rodents! It's not even an ACCURATE measure because it's looking at protein synthesis while AAS are anabolic in muscle through other mechanisms not the least of which is reduction of protein catabolism... Leucine incorporation misses all of this.

Those studies sound fascinating LATS brother, I just cannot believe I haven't read them.
 
An example .. the armed services did a study comparing testosterone to nandrolone.. ( forgive me I am going by memory here).. what they found was in the lower doses ( 200 to 300 mgs) they were very comparable in terms of muscle gained.. protein accrete.. now when raising the dosage they found test started to outshine deca a bit.. why ?
Well again we can go to its secondary characteristics. When they raised test they also got a rise in dht and estrogen.. we know the importance of estrogen in muscle growth.. now deca also converts but at roughly 20 percent of testosterone and its dht is not worth mentioning.
So what's the takeaway?
Test is great up to a point then we need A aromatase inhibitor to combat too much estro.. not ideal.. studies show bone lose using aromatase inhibitors that is not related to the loss of estrogen but the elimination of certain minerals.. plus it sometimes can be negative on lipids etc..
Now another study shows that primobolan actually adds a decent amount of tissue in subjects at only 200mgs.. now primo does not convert to estro but its abilities with protein are very good..
So my point is if they do decent at protein accrete.. and we can avoid certain secondary characteristics that might be negative to what we want then why woukdnt we use test ( up to a point where the negatives outweigh the positive) then throw a compound in that can help us add tissue with adding to conversions we don't want.. like primo.. like mast.. again they add tissue with out bloat.. we are getting ample estro from the test..
So once we understand the characteristics of all the compounds it opens up alot more options.. instead of throwing one aromatase nightmare after another..
Here's the results of the study you referenced.
 

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Here's the results of the study you referenced.
Nice find! Well, of course the results are similar between test and deca when there are 8 or 9 subjects per group and the method used to determine changes in body composition (not protein accretion) is... calipers.
 
An example .. the armed services did a study comparing testosterone to nandrolone.. ( forgive me I am going by memory here).. what they found was in the lower doses ( 200 to 300 mgs) they were very comparable in terms of muscle gained.. protein accrete.. now when raising the dosage they found test started to outshine deca a bit.. why ?
Well again we can go to its secondary characteristics. When they raised test they also got a rise in dht and estrogen.. we know the importance of estrogen in muscle growth.. now deca also converts but at roughly 20 percent of testosterone and its dht is not worth mentioning.
So what's the takeaway?
Test is great up to a point then we need A aromatase inhibitor to combat too much estro.. not ideal.. studies show bone lose using aromatase inhibitors that is not related to the loss of estrogen but the elimination of certain minerals.. plus it sometimes can be negative on lipids etc..
Now another study shows that primobolan actually adds a decent amount of tissue in subjects at only 200mgs.. now primo does not convert to estro but its abilities with protein are very good..
So my point is if they do decent at protein accrete.. and we can avoid certain secondary characteristics that might be negative to what we want then why woukdnt we use test ( up to a point where the negatives outweigh the positive) then throw a compound in that can help us add tissue with adding to conversions we don't want.. like primo.. like mast.. again they add tissue with out bloat.. we are getting ample estro from the test..
So once we understand the characteristics of all the compounds it opens up alot more options.. instead of throwing one aromatase nightmare after another..
Good stuff here Lats. I have only been a TRT guy at 200mg per week. I went to the dark side and added 400mg of primo and started getting very fatigued with terrible joint pain so I dropped it to 300mg and eventually 200mg. My gains were minimal at best. Prior to the primo I had a great lipid profile. Afterward my HDL tanked from 60+ to the 20's and my estro was undetectable. Zero. I was not taking anything else and no AI. If I had a "do over" I wish I would have just doubled up on the test to 400 per week for 10 weeks or so and called that my "blast."
 
Nice find! Well, of course the results are similar between test and deca when there are 8 or 9 subjects per group and the method used to determine changes in body composition (not protein accretion) is... calipers.
They'd have to run some statistics on that and see if it's significant or not. The P value. With a sample that small its hard to get a good value.
 
Good stuff here Lats. I have only been a TRT guy at 200mg per week. I went to the dark side and added 400mg of primo and started getting very fatigued with terrible joint pain so I dropped it to 300mg and eventually 200mg. My gains were minimal at best. Prior to the primo I had a great lipid profile. Afterward my HDL tanked from 60+ to the 20's and my estro was undetectable. Zero. I was not taking anything else and no AI. If I had a "do over" I wish I would have just doubled up on the test to 400 per week for 10 weeks or so and called that my "blast."
It's amazing that just a few years ago no one believed that primo or mast effected blood levels of estro. They assumed it was a " blocker" .. but more and more we see these compounds thrashing estro levels in lower test usage.. I loved running low test high primo.. did it forever. Now I get achey joints in just a week..
 
They'd have to run some statistics on that and see if it's significant or not. The P value. With a sample that small its hard to get a good value.
That, in addition to the fact that skinfold calipers introduce tremendous variability between administrators (the person doing the skinfold measurement) and samples if the administrator doesn't have a solid technique. They're also just not a sensitive measure for the sort of changes that occur in body composition over 6 weeks at 300mg weekly of test vs. 300mg weekly of deca.

I had something typed up in response to the studies but nobody really cares that much and I'm not changing anyone's mind on this.
 
I had something typed up in response to the studies but nobody really cares that much and I'm not changing anyone's mind on this.
I'm interested. I have no dog in this fight. I haven't gone through this literature myself yet.
 
I'm interested. I have no dog in this fight. I haven't gone through this literature myself yet.
OK I'm online so I'll try to hash out in one last post (seriously) on this. What I see from the literature:

To date the only study that does what we're interested in in measuring hypertrophy on a per-dose basis is Bhasin's famous 2001 study. It's famous in fitness circles for a reason.

The 1991 study funded by the armed services referenced by Table above would be great if we ran it under modern conditions using DXA or MRI and strictly-controlled caloric balance with set protein comparing deca vs test over 20 weeks at incrementally higher dosages into the supra-physiological.

There is a recent study funded by the armed services looking at 200mg test enanthate (solo) under conditions of severe caloric restriction, set protein intake (strict dietary control) that yields interesting result (true muscle growth in the face of severe caloric restriction with 200mg TE)... it'd be great to see something more like that.

The study I thought was Victor's by Tang (there's a 2009 and an earlier 2008 paper published in J. Steroids) is actually a better model for our purposes than Victor's (but doesn't do between group comparisons for intact nandrolone vs. intact testosterone nor do we know the human equivalent dosages as they used proprietary pellets). But it's not the one he uses.

Looking at Victor's graphic, he's referring to rat levator ani weight which is just totally useless for extrapolation to humans. I'm not even inclined to look for the rat levator ani comparative study since it's not extrapolable for our purposes. (Does it not bother anyone that these graphical blurbs don't even cite the original study?)

The use of the Hershberger Assay (i.e., measuring anabolism by reference to rat organ weight) does not translate to humans not least of all because the rat levator ani is the dorsal bulbocavernous muscle, a male rat sex organ, and thus its measurement reflects both androgenic and anabolic growth. To put things in practical terms: if looking at the rat levator ani was useful for measuring anabolism, Proviron would be a great muscle tissue builder in humans... we know that it's not.

The study I reference in the Primo science/broscience: assessment of strengths and weaknesses... thread is a good middle ground. It looks at nitrogen balance IN HUMANS (AAS by definition are compounds that promote nitrogen retention). The human intramuscular compartment is composed principally of nitrogen and it is a good proxy for muscle anabolism in humans.

We'll never see as good a study comparing Primo to other AAS in terms of muscle anabolism again as it's not approved for medical use in wasting conditions anywhere in the world.
 
It is unfair for people to try to understand his statements and end up misrepresenting him (unintentional in this case) but it's an imperfect solution for people that don't want to leave their respective sites (him behind his paywall or on instagram, us here on ProM where he has an account).

To your point that the data is grabbed randomly and piecemealed together, it still paints an accurate picture as it's done under well-controlled conditions in the studies I cite and it's actually IN HUMANS.

I really want to read the comparative rodent study. I respect Victor's approach and the push for safe use, and he did a great job finding that Parenabol study.
The conditions MAY be well controlled within each respective study but they are NOT the same if they are not done within the same study. I was not posting in reference to anything you posted in particular just a general statement about how often I see his theories being absolutely bastardized when being explained lol. Was not thinking you at all really.
 
I'm still waiting to give away this 50.00
(Crickets chirp)
 
I'm still waiting to give away this 50.00
(Crickets chirp)

Its not going to happen.

Its like me saying I'll give you $50 if Lilleo187 posts his blood work.
 
That, in addition to the fact that skinfold calipers introduce tremendous variability between administrators (the person doing the skinfold measurement) and samples if the administrator doesn't have a solid technique. They're also just not a sensitive measure for the sort of changes that occur in body composition over 6 weeks at 300mg weekly of test vs. 300mg weekly of deca.

I had something typed up in response to the studies but nobody really cares that much and I'm not changing anyone's mind on this.
If they are administered by the same person repeated who knows what they are doing, they are extremely accurate. Dexa and hydrostatic both have a 2% margin of error, not saying they aren't better but for measuring changes over time, skinfold is very accurate.

This is all moot though because none of these studies translate well to what bodybuilders are doing.
 
I heard Jordan is back to blasting and being 300 lb again to try to get that card. Can anyone confirm?

Yes, its true.

He's going to start pre contest at the end of this year ready for a comp early next year.
 
I heard Jordan is back to blasting and being 300 lb again to try to get that card. Can anyone confirm?
Yep he’s back. He was at 270 a couple months ago and is back into the high 290s now.
 
I’m pretty heavy at the moment

Can’t imagine being 290+ at 5’5 or whatever height he is

Putting socks on in the morning is the hardest part of my day.. I guess that’s why he tends to wear slides
 
I'm guessing he'll get down to about 2-3 weeks out and then bail.
 

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