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All Pros Have High Free Test

Calculated free testosterone is generally over-estimated. I posted on Dante's FB page a few weeks back when he posted up his free T levels. He wasn't aware that the different times his labs we're drawn, two different methodologies (assay's) we're used. One was an equilibrium assay and the other was direct assay. The comparison is like comparing a water melon to a cantaloupe, they're both melon's, yet they're not alike. Nevertheless, it's a common misinterpretation.



Your Albumin is a bit on the lowish side of normal, in which could indicate several different things. Most commonly it's related to an infection or chronic inflammation. It may be worthwhile to keep an eye on it and/or track back through your previous blood work to see if this is a constant or acute in this particular case.



Your SHBG is way too low as well. Which is more than likely gear related rather than insulin resistance. Or you may be one of thee unfortunate individuals with a genetically low SHBG?



I thought low SHBG = higher free test and thus a good thing ??

So nothing to do with Dante results - surely my free test here is a pretty high read isn’t it? In comparison to the range

and thus a very good thing for a bodybuilder wanting to utilise test to build muscle


Sent from my iPhone using Tapatalk
 
Sex Hormone Binding Globulin: New Science Questions Old Beliefs

The plasma Sex Hormone-Binding Globulin (SHBG) transports androgens and estradiol in the blood and regulates their bioavailable fraction and access to target cells. The recent advances in the knowledge of its structure and gene expression, and notabily the demonstration of a specific receptor (SHBG-R) located on membranes of sex steroid responsive cells, gave support to the thesis that SHBG has much more sophisticated functions at cell site. In particular, the receptor-mediated action of SHBG, which uses as a second messenger cAMP, has been linked to the effects of androgens and estradiol. It is conceivable that the SHBG/SHBG-R system works as an additional control mechanism which inhibits or amplifies the effects of DHT and estradiol in cells. In the prostate, it has been suggested that the estradiol-activated SHBG/SHBG-R complex cross-talks with the androgen receptor, and is able to activate AR even in the absence of DHT. Of great interest, for its potential clinical applications, is the observation that in estrogen-dependent breast cancer SHBG, through SHBG-R, cAMP and PKA, specifically inhibits the estradiol-induction of cell proliferation. This anti-proliferative, anti-estrogenic effect of human SHBG has not only increased and continues to increase our understanding of the molecular mechanisms involved in the biology of breast cancer, but could also be exploited as a future therapeutic strategy in the managing of estrogen-dependent tumours.
https://www.ncbi.nlm.nih.gov/pubmed/10219893

Who knows, SHBG may even increase androgen receptor signalling in muscle tissue?? Probably not, but things may not be as as simple as 'the lower SHBG the better'.
 
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There are so many variables with this. But sure it's common sense that most pro's should have great natural hormones (high free test) and a great response to gear. But common sense will show it's not always the case. Some of them are on huge doses all year so their response is almost irrelevant in many ways. Although it's also very true that everyone also has a different response to gear. I have seen very low responders to tren for example. Whereas others can take 300mg tren per week and eat an ok diet and transform in a matter of 2-3 weeks.

One of my mates regularly parties and won't train for long periods and will look a bit crap and he goes back on and trains for a few weeks and he transforms and looks better than many guys who have been abusing for years. Many pro's could look insane on 400mg test whereas others still look natural on triple that. This is a result of a lot more than just higher free test levels though and due to a combination of physical genetic gifts (or lack of).

This reminds me of when guys state pro's have a better mind muscle connection. Many have terrible form it's just the simple fact their bodies can build muscle so much easier so any form of weight training could have a big effect. The same can be said for any drug stack if you are a hyper responder to anabolics.
 
Jordan peters talked about this... He said that he doesn't feel he has great genetics .. He talked about how he has to take high doses to get the response that the genetic elite can take little of.. So some of the pros we feel are genetically superior in every way have to take large doses to get the effect we see on them.. So in essence , they may have great shape but for them to build musvle they are not in the elite class and have to take large amounts..
 
How to increase free testosterone? Take testosterone.. You're welcome:headbang:
 
How to increase free testosterone? Take testosterone.. You're welcome:headbang:
You all are cute. You do realize 100mg increase in test might lead to 6-10ng of free test for most.

We are talking about certain people who have total test at 600 and free at 200+...or total test at 1800 with free at 900.

Anomalies.

You smartassess thinking you can just take more test and make a significant dent and alter the ratio of free test being activated aren't getting it.

Sent from my SM-N900V using Tapatalk
 
Good to hear. Although there may be more variables like time of days etc-I really don't know:) I'm just thankful ive got what I have.

My last labs in November was two days after a 75 mgs trt shot.

Total test 830 free test 255
 
You all are cute. You do realize 100mg increase in test might lead to 6-10ng of free test for most.

We are talking about certain people who have total test at 600 and free at 200+...or total test at 1800 with free at 900.

Anomalies.

You smartassess thinking you can just take more test and make a significant dent and alter the ratio of free test being activated aren't getting it.

Sent from my SM-N900V using Tapatalk



This is what I wanted to no cheers bud.

I’ve never seen any one post free test results so had no idea what was good to bad.

Especially as here in uk we use different ranges to you guys.

Cheers againb


Sent from my iPhone using Tapatalk
 
This is what I wanted to no cheers bud.

I’ve never seen any one post free test results so had no idea what was good to bad.

Especially as here in uk we use different ranges to you guys.

Cheers againb


Sent from my iPhone using Tapatalk

No problem man..
Don't get me wrong...if your free test goes from 36 to 48...technically, your free test is 25% higher than it was. But the specific anomalies we are talking about are the labs in which Meadows posted a few yrs ago where his total test was like 600 and his free was over 200.
I just talked to Matt Porter earlier today and he mentioned total test at 1800 and free at 980.

Dante hypotesized this is what many pro bodybuilders may have some degree of.
I'll go more into it with specific bloodwork. Personally, I always had pretty good response to gear..better than many..but not near what some are capable of. (Admittedly I haven't met many in real life who ive personally seen have some crazy response to aas so it isn't common.)


My test total baseline a few yrs back was 278. My free test was 7.4.
I've had seven subsequent tests where you will see my total:free test below.
1018/28.5 175mg e5d ugl
>1500/>50 800mg/wk
891/26.2 ?
>1500/48.1 400mg/wk +proviron
1379/35.6 300/wk
1174/28.9 300/wk(ugl)
1379/39.8 300/wk (differences is switched to aromasin and added Boron @ 9mg AM and 9mg PM and had 25mg mk-677 in the mix)

[SHBG is usually 25-30 and the one time I used Proviron, it dropped to 21. Assuming my total test was around 1800, 48.1 is still only about 2.6%...so the Proviron may have lowered my shbg, but didn't seem to help the rate at which my free test converted.]

All of you who just read this...did you notice that my free test was always converting at about 2.5-2.9% of total? Well, it was. I couldn't count the tests where total was over 1500. The first time it wasn't close and the second time it was probably slightly over 1800.

TWICE, I tested at 1379 on 300mg prescription test per week. The second time, I was using Boron which seems might have accounted for 4.2 point increase. Assume 36 to 40, so that is over 11% increase and converted at a 0.3%higher rate. Was it the Boron? Perhaps. Was it really worth anything? I don't think so. (Funny thing is while on Boron...I was totally expecting my free test to be high when I tested it because I seemed to be hornier with more output during orgasm--similar to proviron, BUT the tests didn't show anything significant.) Just like Citrus Bergamot didn't seem to do anything significant for my lipids when I used it.

Either way, I don't think ANYTHING is going to make my free test 200, 500 or 900. EVER. Meanwhile MPA, Meadows and several others are just anomalies.
 
Last edited:
BTW, typical guidelines that hormone doctors follow are:Free Testosterone greater than or equal to 2% of total T. So all that bloodwork I showed and discussed above lines up to me converting at 2.4-2.9% as I stated.

But someone converting at 33-50% is fucking crazy to me, but that's basically JM and MPA.
 
Last edited:
I was about 3 weeks off a cycle taking 200mg test and 50mg anadrol. Bloods came back 1300 total and 450 free while remaining only on 200mg test.


Sent from my iPhone using Tapatalk
 
You all are cute. You do realize 100mg increase in test might lead to 6-10ng of free test for most.

We are talking about certain people who have total test at 600 and free at 200+...or total test at 1800 with free at 900.

Anomalies.

You smartassess thinking you can just take more test and make a significant dent and alter the ratio of free test being activated aren't getting it.

Sent from my SM-N900V using Tapatalk

I would like to see the methodology used in these individuals. As mentioned earlier, the validation of calculated and direct measurements of free testosterone can be highly inaccurate, more so the calculated methodologies have been cited to be generally grossly overestimated. (Sartorius G, et al. Ann Clin Biochem. 2009.)--(Ly LP, et al. Clin Endocrinol (Oxf). 2010). This is in contrast to the gold standard of measuring free testosterone through the methodologies of equilibrium dialysis, this is considered highly accurate. (Kacker R, et al. Aging Male. 2013)

So I'm not misunderstood, I'm not stating that these individuals don't have higher than normal levels of free testosterone versus the general population. I would just like to see the assay that was used.
 
Last edited:
No problem man..
Don't get me wrong...if your free test goes from 36 to 48...technically, your free test is 25% higher than it was. But the specific anomalies we are talking about are the labs in which Meadows posted a few yrs ago where his total test was like 600 and his free was over 200.
I just talked to Matt Porter earlier today and he mentioned total test at 1800 and free at 980.

Dante hypotesized this is what many pro bodybuilders may have some degree of.
I'll go more into it with specific bloodwork. Personally, I always had pretty good response to gear..better than many..but not near what some are capable of. (Admittedly I haven't met many in real life who ive personally seen have some crazy response to aas so it isn't common.)


My test total baseline a few yrs back was 278. My free test was 7.4.
I've had seven subsequent tests where you will see my total:free test below.
1018/28.5 175mg e5d ugl
>1500/>50 800mg/wk
891/26.2 ?
>1500/48.1 400mg/wk +proviron
1379/35.6 300/wk
1174/28.9 300/wk(ugl)
1379/39.8 300/wk (differences is switched to aromasin and added Boron @ 9mg AM and 9mg PM and had 25mg mk-677 in the mix)

[SHBG is usually 25-30 and the one time I used Proviron, it dropped to 21. Assuming my total test was around 1800, 48.1 is still only about 2.6%...so the Proviron may have lowered my shbg, but didn't seem to help the rate at which my free test converted.]

All of you who just read this...did you notice that my free test was always converting at about 2.5-2.9% of total? Well, it was. I couldn't count the tests where total was over 1500. The first time it wasn't close and the second time it was probably slightly over 1800.

TWICE, I tested at 1379 on 300mg prescription test per week. The second time, I was using Boron which seems might have accounted for 4.2 point increase. Assume 36 to 40, so that is over 11% increase and converted at a 0.3%higher rate. Was it the Boron? Perhaps. Was it really worth anything? I don't think so. (Funny thing is while on Boron...I was totally expecting my free test to be high when I tested it because I seemed to be hornier with more output during orgasm--similar to proviron, BUT the tests didn't show anything significant.) Just like Citrus Bergamot didn't seem to do anything significant for my lipids when I used it.

Either way, I don't think ANYTHING is going to make my free test 200, 500 or 900. EVER. Meanwhile MPA, Meadows and several others are just anomalies.


Ahh so my numbers are actually

1154 total test and 173 free test

Now I’ve converted them to your American measurement

On
500mg test
400mg mast
400mg NPP.




Sent from my iPhone using Tapatalk
 
..interesting thread

It's not that low within physiological, or slightly below ranges are bad per se. His is too low, which is an open door for higher free estradiol levels. Then there's the few tagged pathophysiological conditions that are associated with low SHBG, if it's genetic, such as non alcoholic fatty liver disease, endothelial cells mediated hypertension and hypertriglyceridemia.

In his case, I'm suspecting it's not genetic due to anabolics and GH.

great point and true, but this b'comes a bit of a catch-22

while it is true that ESTRADIOL binds to SHBG ..and it is true that lower SHBG would equal more FREE ESTROGEN
..the "catch" is the affinity that these sex hormones have for binding to SHBG
^^^ESTRADIOL has the weakest affinity for SHBG (..with ESTRONE n' ESTRIOL being even weaker)

DHT however, binds SHBG with 5x the affinity that TEST does ..and 20x the affinity that ESTRADIOL does

the binding affinity of sex hormones for SHBG goes as follows:
DHT>>>TEST>>>ESTRADIOL
(..from greatest affinity to poorest affinity)
 
Last edited:
Ahh so my numbers are actually

1154 total test and 173 free test

Now I’ve converted them to your American measurement

On
500mg test
400mg mast
400mg NPP.




Sent from my iPhone using Tapatalk

..if your conversion is correct, then you'r FREE TEST represents 14.99% of your TOTAL TEST
^^^well above normal

I was about 3 weeks off a cycle taking 200mg test and 50mg anadrol. Bloods came back 1300 total and 450 free while remaining only on 200mg test.


Sent from my iPhone using Tapatalk

450 FREE TEST represents 34.61% of 1300 TOTAL TEST
^^^i think this is the type of ratio that knight9 was talkin' about
 
..if your conversion is correct, then you'r FREE TEST represents 14.99% of your TOTAL TEST

^^^well above normal







450 FREE TEST represents 34.61% of 1300 TOTAL TEST

^^^i think this is the type of ratio that knight9 was talkin' about



I had another test done 6 weeks after running mast E, that 6 weeks was only trt 200mg test and came out at 1250 total and 375 free. More recently my last test was on 150mg test per week and came up with 945 total and 160 free. Had ended a NPP run about 6 weeks prior.



Sent from my iPhone using Tapatalk
 
great point and true, but this b'comes a bit of a catch-22

while it is true that ESTRADIOL binds to SHBG ..and it is true that lower SHBG would equal more FREE ESTROGEN
..the "catch" is the affinity that these sex hormones have for binding to SHBG
^^^ESTRADIOL has the weakest affinity for SHBG (..with ESTRONE n' ESTRIOL being even weaker)

DHT however, binds SHBG with 5x the affinity that TEST does ..and 20x the affinity that ESTRADIOL does

the binding affinity of sex hormones for SHBG goes as follows:
DHT>>>TEST>>>ESTRADIOL
(..from greatest affinity to poorest affinity)

Thee 'free hormone hypothesis' has been of belief that bound hormones to SHBG are inactive. Tho, there's the belief that megalin interacts with SHBG allowing internalization of ligands to initiate conformation to it's target receptor.

What to believe, what to believe?

Given that, free hormones are considered bioavailable, loosely bound to carrier proteins. So the hypothesis is that the lower one's SHBG is, the more active estradiol is.

Then we have those that respond better to andogens is under belief is related to individualized CAG repeats lenght, shorter being the king $hit.
 
I'll just through this out here, in case folks aren't paying attention to Stewie... and Danieltx...

I've talked about the megalin receptor and free hormone hypothesis on Jay Campbell's Testosterone Optimization Therapy (TOT) podcast, and Superhuman radio, and talked about various factors that contribute to responsiveness to AAS on the podcast on John's site, as well as in my Be Your Own Bodybuilding Coach Book.

So, the CAG Repeats, as Stewie notes, affect androgen binding and presumably transactivation (which explains prostate cancer risk, for instance). There are also factors like variations in glucoronidation and hepatic PDE7B (enzyme cleaving esterified fatty acid from injectable AAS) Polymorphisms which can vary the bioavailability of injectables by like 60% on average.

Differences in SHBG could affect things, too, of course, not to mention variation in aromatase and 5-alpha reductase.

-S
 
I'll just through this out here, in case folks aren't paying attention to Stewie... and Danieltx...

I've talked about the megalin receptor and free hormone hypothesis on Jay Campbell's Testosterone Optimization Therapy (TOT) podcast, and Superhuman radio, and talked about various factors that contribute to responsiveness to AAS on the podcast on John's site, as well as in my Be Your Own Bodybuilding Coach Book.

So, the CAG Repeats, as Stewie notes, affect androgen binding and presumably transactivation (which explains prostate cancer risk, for instance). There are also factors like variations in glucoronidation and hepatic PDE7B (enzyme cleaving esterified fatty acid from injectable AAS) Polymorphisms which can vary the bioavailability of injectables by like 60% on average.

Differences in SHBG could affect things, too, of course, not to mention variation in aromatase and 5-alpha reductase.

-S

Glad to hear someone was giving attention :p

Here's to a sip of some red wine with you, Scott 🍷:)

...quercitin what's in your circulation :)

http://www.professionalmuscle.com/f...-dictating-what-compounds-you-should-run.html


I'm sure there would be some interplay of blood type. I dunno if one particular blood types may have pronounced effect of proteins and enzymes that augment AAS. Very doubtful it's significant. Again, I dunno?

There are hundreds of different things that regulate the anabolic response to AAS. Why everyone focuses just on one thing is quite bafflingly. There's gene expression such as PDE7B gene expression along with copressors, cofactors, receptor binding, translocation, these are just a few things that are involved in many, many steps.

In my opinion, blood type would be way down on the list.


Bioavailability of testosterone enanthate dependent on genetic variation in the phosphodiesterase 7B but not on the uridine 5'-diphospho-glucuronos... - PubMed - NCBI Bioavailability of testosterone enanthate dependent on genetic variation in the phosphodiesterase 7B but not on the uridine 5'-diphospho-glucuronosyltransferase (UGT2B17) gene. Ekström L1, Schulze JJ, Guillemette C, Belanger A, Rane A. Author information Abstract OBJECTIVE: To study the disposition of serum testosterone and seven of its metabolites before and after 2 days of an intramuscular dose (500 mg) of testosterone enanthate in relation to the phosphodiesterase (PDE7B) and the uridine 5'-diphospho-glucuronosyltransferase (UGT2B17) genotypes. METHODS: Patients were genotyped for UGT2B17 deletion polymorphism and single nucleotide polymorphisms in the PDE7B gene. The involvement of PDE7B in hydrolysis of enanthate was assessed in human liver homogenates. RESULTS: Genetic variation in the PDE7B gene was found to be associated with the serum level of testosterone. Individuals homozygous for PDE7B rs7774640 G allele had a smaller increase (2.5-fold) in the serum testosterone levels compared with carriers of the A allele (3.9-fold, P=0.0006). In addition, genetic variation in the PDE7B gene significantly influences the testosterone/epitestosterone ratio, a biomarker of testosterone doping. Our in-vitro incubation studies confirmed that PDE7B serves as a catalyst of the hydrolysis of testosterone enanthate. The UGT2B17 deletion polymorphism did not show any significant association with serum testosterone levels or the other androgen metabolites investigated. CONCLUSION: We have shown that PDE7B is involved in the hydrolysis of testosterone enanthate and that genetic variation in the PDE7B gene is a determinant of the systemic levels of testosterone after administration of testosterone enanthate. It is reasonable to believe that the genetic variation in testosterone bioavailability may be correlated to varying effects of this androgen, whether it is used for replacement therapy or abused in doping. Thus our results may be important to consider in doping test programmes and in therapeutics with androgens and other esterified drugs. And PDE7B is involved in nandrolone decanoate hydrolysis in liver cytosol and its transcription is up-regulated by androgens in HepG2 PDE7B is involved in nandrolone decanoate hydrolysis in liver cytosol and its transcription is up-regulated by androgens in HepG2 Emmanuel Strahm, Anders Rane, and Lena Ekström* Author information ► Article notes ► Copyright and License information ► Go to: Abstract Most androgenic drugs are available as esters for a prolonged depot action. However, the enzymes involved in the hydrolysis of the esters have not been identified. There is one study indicating that PDE7B may be involved in the activation of testosterone enanthate. The aims are to identify the cellular compartments where the hydrolysis of testosterone enanthate and nandrolone decanoate occurs, and to investigate the involvement of PDE7B in the activation. We also determined if testosterone and nandrolone affect the expression of the PDE7B gene. The hydrolysis studies were performed in isolated human liver cytosolic and microsomal preparations with and without specific PDE7B inhibitor. The gene expression was studied in human hepatoma cells (HepG2) exposed to testosterone and nandrolone. We show that PDE7B serves as a catalyst of the hydrolysis of testosterone enanthate and nandrolone decanoate in liver cytosol. The gene expression of PDE7B was significantly induced 3- and 5- fold after 2 h exposure to 1 μM testosterone enanthate and nandrolone decanoate, respectively. These results show that PDE7B is involved in the activation of esterified nandrolone and testosterone and that the gene expression of PDE7B is induced by supra-physiological concentrations of androgenic drugs.
 
Last edited:
If you get a chance, Scott. I'd like to take a listen to those podcasts if you may have a link to them?

Thanks :)
 

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