Random thoughts/questions regarding Test and AAS...

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BillyJ03z

Active Member
Like many of my brothers on this forum I/we have been struggling to get dialed in on TRT..... and the thought process has usual been to try to replicate the normal levels/diurnal rhythm of the body to maintain peak homeostasis, however, even with seemingly normal Total/Free T, E levels, etc.. we are still not feeling good... Is it possible that we may actually still be underdosed by limiting ourselves to these common lab ranges? for example, maybe some of us need to be in the 2000 and over range instead of the normal top lab ranges of 1000-1100, etc... Remember the T we are injecting even though labeled "Bio-identical" it is still basically "Synthetic-Plant derived". I've heard the guy "more plates more dates" talking about other versions of bio-identical testosterone that is actually synthesized from animal cholesterol but it is not mainstream due to cost. Maybe the body doesn't respond to the current version of plant based Test we currently use over long periods of time on TRT and/or need quite a bit more. Any thoughts???

Also, can anyone explain why seemingly other AAS compounds always seem to pack more punch than standard test even when they are fundamentally "EVEN" based on the Androgen/Anabolic ratio/ratings. Ex. I've used 40mg Tbol for a cycle (by itself) and I got insanely strong and pumped more than I ever have using 200 - 300mg's of Test. Anavar at small doses was even better than test. Thoughts?
 
Defy Medical TRT clinic doctor
i'm one of those who need more. on 200mg Cyp a week and my labs are still low. 600 total/20 free or around that.
i just don't feel right below 150mg. no idea why. my shbg is 11.
i recently started trying daily T propionate and it was a huge boost in how I feel. i started also having a higher libido and frequent erections on prop. i think a higher peak and quicker drop-off mimics a natural cycle and i just feel better on it.
 
i'm one of those who need more. on 200mg Cyp a week and my labs are still low. 600 total/20 free or around that.
i just don't feel right below 150mg. no idea why. my shbg is 11.
i recently started trying daily T propionate and it was a huge boost in how I feel. i started also having a higher libido and frequent erections on prop. i think a higher peak and quicker drop-off mimics a natural cycle and i just feel better on it.
Are you on UGL or doctor prescribed?

As you know, I am currently on Prop (15mg ED/SQ) I peak at 1300 and trough at 600 (would seem perfect of paper), however, recently I had a set back... Out of the blue last week I was getting insanely tired during the day, like literally almost falling asleep (my head felt like it was in a fish bowl).... It was most likely due to the Preg/DHEA I was dosing daily for the past 3 months which seemed to be working good as I noticed some days I was getting my verbal fluency/mental cognition back, but out of nowhere I just got extremely tired. Maybe the Preg (30mg) was converting to a lot of progesterone or something. My DHEA which has always been below range since starting trt was actually mid-range with only 20mg dhea sublingually ED. Since I have stopped Preg and started taking DHEA before bed, and in a few weeks I will add Preg back in at 12.5mg and see what happens.
 
Are you on UGL or doctor prescribed?

As you know, I am currently on Prop (15mg ED/SQ) I peak at 1300 and trough at 600 (would seem perfect of paper), however, recently I had a set back... Out of the blue last week I was getting insanely tired during the day, like literally almost falling asleep (my head felt like it was in a fish bowl).... It was most likely due to the Preg/DHEA I was dosing daily for the past 3 months which seemed to be working good as I noticed some days I was getting my verbal fluency/mental cognition back, but out of nowhere I just got extremely tired. Maybe the Preg (30mg) was converting to a lot of progesterone or something. My DHEA which has always been below range since starting trt was actually mid-range with only 20mg dhea sublingually ED. Since I have stopped Preg and started taking DHEA before bed, and in a few weeks I will add Preg back in at 12.5mg and see what happens.
right now UGL but will ask for real RX during next visit. I am taking 100mg preg+25mg dhea no ill effects. the UGL is mct while rx is grape-seed. i am not sure if the oil at those doses would make a difference, but the seed oils are quite toxic unfortunately. I assume you checked your Thyroid levels as well and overall blood work?
the way I found my sweet spot for Tprop is by doing daily injections starting at 20mg(0.2cc for prop) and going up to 50. at 50 i start feel too energized and a bit anxious. 30-35mg is really a sweet spot for me. at 20 or so i feel ok but slightly lethargic.
maybe your problem is not related to T directly. I would expand your search field and look at other things diet, exercise etc.
 
right now UGL but will ask for real RX during next visit. I am taking 100mg preg+25mg dhea no ill effects. the UGL is mct while rx is grape-seed. i am not sure if the oil at those doses would make a difference, but the seed oils are quite toxic unfortunately. I assume you checked your Thyroid levels as well and overall blood work?
the way I found my sweet spot for Tprop is by doing daily injections starting at 20mg(0.2cc for prop) and going up to 50. at 50 i start feel too energized and a bit anxious. 30-35mg is really a sweet spot for me. at 20 or so i feel ok but slightly lethargic.
maybe your problem is not related to T directly. I would expand your search field and look at other things diet, exercise etc.
1.5 grains of Armour Thyroid put my Tsh at 1.56 (ideal between 1.0 and 2.0).. also, another benefit to Armour (NDT) is that it greatly helps my lipid profile and raises my SHBG. Only other issue I could possibly think my issue is adrenal exhaustion... I did have sleep study and I do have Sleep Apnea which started after I got on TRT. ( I tried Cpap and can't do it).... so just spinning my wheels that this point. I have been on TRT for 12 years now and if I'm not dialed in by the new year 2024 then I'm gonna start transitioning off. But..... even though things are not ideal for me I do feel better using Prop than Cyp.
 
I'll offer two thoughts. There are a number of people here who finally found their "sweet spot" by going to lower doses rather than higher, and as someone who does better on lower doses myself, I think there are a lot of people who start at too high a dose and then only move up from there, looking for improvement in the wrong direction. That said there are likely people who also do better at higher doses.

Regarding the anabolic/androgenic ratio, there is a well-respected member on another forum ( I think he occasionally comments here as well) who thinks that ratio is not close to reliable. Further, different compounds have different mechanisms of action that seem like they would be "outside" of that metric such as the potential for EPO stimulation, so I think the answer to your question is to not rely on that ratio for much of anything.
 
Is it possible that we may actually still be underdosed by limiting ourselves to these common lab ranges? for example, maybe some of us need to be in the 2000 and over range instead of the normal top lab ranges of 1000-1100, etc...
I recently watched a YT video of doctors talking about studies of men between 1500-3000 ng/dL, no noticeable muscle gain or fat loss, however there was negative side effects running 3000 versus 1500 ng/dL.

Dr Keith, Nicolas who is far from conservative, in his dosing of men on TRT doesn’t have any of his patients anywhere near 2000 ng/dL.
 
I recently watched a YT video of doctors talking about studies of men between 1500-3000 ng/dL, no noticeable muscle gain or fat loss, however there was negative side effects running 3000 versus 1500 ng/dL.

Dr Keith, Nicolas who is far from conservative, in his dosing of men on TRT doesn’t have any of his patients anywhere near 2000 ng/dL.
Yeah, I would be afraid to try being that high for even just a week or two....
 
Like many of my brothers on this forum I/we have been struggling to get dialed in on TRT..... and the thought process has usual been to try to replicate the normal levels/diurnal rhythm of the body to maintain peak homeostasis, however, even with seemingly normal Total/Free T, E levels, etc.. we are still not feeling good... Is it possible that we may actually still be underdosed by limiting ourselves to these common lab ranges? for example, maybe some of us need to be in the 2000 and over range instead of the normal top lab ranges of 1000-1100, etc... Remember the T we are injecting even though labeled "Bio-identical" it is still basically "Synthetic-Plant derived". I've heard the guy "more plates more dates" talking about other versions of bio-identical testosterone that is actually synthesized from animal cholesterol but it is not mainstream due to cost. Maybe the body doesn't respond to the current version of plant based Test we currently use over long periods of time on TRT and/or need quite a bit more. Any thoughts???

Also, can anyone explain why seemingly other AAS compounds always seem to pack more punch than standard test even when they are fundamentally "EVEN" based on the Androgen/Anabolic ratio/ratings. Ex. I've used 40mg Tbol for a cycle (by itself) and I got insanely strong and pumped more than I ever have using 200 - 300mg's of Test. Anavar at small doses was even better than test. Thoughts?

Pure nonsense!

You were already running high-end/high FT from the get-go and constantly struggling.

You have numerous threads on here over the years and unfortunately, you are still chasing your tail.








As you very well know dysfunctional thyroid/adrenals, mental health disorders, quality of sleep, poor diet/lack of exercise can all have a negative impact on one's overall well-being.

Much more going on than just having healthy FT levels.

From your reply in post #5

*Only other issue I could possibly think my issue is adrenal exhaustion... I did have sleep study and I do have Sleep Apnea which started after I got on TRT. ( I tried Cpap and can't do it).... so just spinning my wheels that this point.


How many natty healthy young males hitting a peak TT 600-800 ng/dL let alone any outliers hitting 1000+ ng/dL even going back as far as the 70s when the first immunoassay to measure T was developed were running around with low SHBG?

Top it off that the peak is short-lived!




History of androgens and androgen action (2022)
David J. Handelsman

Invention

*This Golden Age also encompassed a third major but failed quest, that to invent a pure anabolic steroid, a synthetic androgen having purely anabolic effects but so devoid of any virilizing effects it could be used safely in women and children. Despite massive, invested effort, this failed quest left behind a legacy of thousands of synthetic androgens recorded in the expired patent literature, almost none ever tested in humans

*The comprehensive failure of this quest was ultimately due to its limited understanding of androgen physiology. These limitations included the subsequent discovery of a singular androgen receptor (AR), a final common pathway of androgen action that differs from other steroid receptors (estrogen progestin, glucocorticoid/mineralocorticoid) that feature complex dual receptor isoform control mechanisms

*More grievously, screening of steroid analogs was based on a misguided simplistic modification of the whole animal androgen bioassay. This purported to separate anabolic (represented by the levator ani muscle) from androgenic (represented by the ventral prostate) effects, an ad hoc refinement which made a false distinction where there was no difference


*This flawed approach is ultimately inconsistent with modern androgen physiology, findings rediscovered in more recent pharmaceutical research showing that the apparent differences between androgenic and anabolic endpoints in whole animal androgen bioassays reflected (a) whether the bioassay used maintenance or recovery of androgen effects and (b) differences in the speed of recovery from castration of androgen effects making the results depend on the timing of the endpoint [102]. Nevertheless, the term “anabolic” (or “androgenic-anabolic”) steroid persists in the common lexicon, serving largely as a journalistic pinata, long after it was known to be making a tautological distinction where there was no real difference e in reality, all androgens are anabolic, and all anabolic steroids are androgens [103]

*The next invention was that of the first non-steroidal androgen by Dalton et al. [111] in 1998, six decades after the first non-steroidal estrogen [112].
This creates a new class of non-steroidal synthetic androgen, often termed Specific Androgen Receptor Modulators (SARM), a misleading marketing term rather than an accurate pharmacological description [113,114], usurping a speculative but unsound analogy with Specific Estrogen Receptor Modulators (SERM). Non-steroidal androgens were developed by a rational drug design using computer-based structural modeling, an iterative approach exploiting a library of chemical substituents to optimize physicochemical interactions with the therapeutic target, in this case the androgen receptor using non-steroidal anti-androgens as lead compounds

*Nonsteroidal androgens are pharmacologically distinct from testosterone in being obligatorily pure androgens as they inherently lack testosterone's wider spectrum of activity. Pure (including nonsteroidal) androgens lack testosterone's capacity for amplification of androgenic potency by tissue-based 5a reduction to DHT as well as diversification by aromatization to estradiol to act upon estrogen receptors. Hence, while non-steroidal androgens may have potential roles in pharmacological androgen therapy, subject to rigorous efficacy, safety, and cost-effectiveness criteria, they could not replace testosterone for replacement therapy in men with pathologic hypogonadism due to their lack of testosterone's full spectrum of effects

*Nevertheless, although intended for pharmacological androgen therapy in indications such as prevention and treatment of muscle wasting in cancer [115], none of the non-steroidal androgens under development [116,117] are marketed by 2021. Yet hope springs eternal for this new attempt to separate anabolic from androgenic properties of androgens to facilitate marketing for muscle wasting and other selective effects of testosterone





Androgen pharmacology

*In replacement therapy, testosterone displays its full spectrum of effects including not just direct action via the androgen receptor, but also indirect effects via amplification by 5a reductase in some target tissues (prostate, skin, liver) as well as diversification of its effects via aromatization to estradiol to act on estrogen receptors in other target tissues (brain, bone). These effects are dose limited to replicate physiological androgen exposure intended to replicate the lifetime efficacy and safety of eugonadal men

*By contrast, synthetic androgens are exclusively pure androgens acting directly (or via metabolites) solely on the androgen receptor and are not suitable substitutes for testosterone in replacement therapy. However pharmacological androgen therapy uses synthetic androgens for their potent effects on muscle, liver, and other androgen target tissues aiming to modify the natural history of non-gonadal diseases [179]. In these applications, the dose and type of synthetic androgen are limited only by efficacy, safety, and cost-effectiveness of the androgen in placebo-controlled clinical trials

*Many such applications have been developed for synthetic androgens which remain cost-effective second-line alternatives even when more specific, purpose-designed therapeutics become available. For example, an oral alkylated androgens (stanozolol, danazol) can increase C1-inhibitor levels and reduce frequency of angioedema attacks; however, for prophylaxis, recombinant C1-inhibitor is more effective but costly [180]. Similarly, synthetic androgens are cost-effective at increasing hemoglobin in anemias due to renal or marrow failure [181] although recombinant erythropoietin or erythropoietin stimulating analogs are equally effective but higher cost









Androgen Physiology, Pharmacology, and Abuse (2020)

David J. Handelsman

Screenshot (24702).png



*Testosterone is used clinically at physiologic doses for androgen replacement therapy, and, at typically higher doses, testosterone, or more usually synthetic androgens based on its structure, is also used for pharmacologic androgen therapy.

*The principal goal of androgen replacement therapy is to restore a physiologic pattern of androgen exposure to all the body’s tissues. Such treatment is usually restricted to the major natural androgen, testosterone, aiming to replicate physiologic circulating testosterone levels and the full spectrum (including prereceptor androgen activation) of endogenous androgen effects on tissues and recapitulating the natural history of efficacy and safety.5

*By contrast, pharmacologic androgen therapy exploits the anabolic or other effects of androgens on muscle, bone, and other tissues as hormonal drugs, which are judged on their efficacy, safety, and relative cost-effectiveness similar to any other therapeutic agents. Insight into the physiology of testosterone is a prerequisite for understanding and making the most effective use of androgen pharmacology.6,7





Practical Goals of Androgen Replacement Therapy


The goal of androgen replacement therapy is to replicate the physiologic actions of endogenous testosterone, usually for the remainder of life, as the pathological basis of hypogonadism usually involves irreversible disorders of the hypothalamus, pituitary, or testis. This requires rectifying the deficit and maintaining androgenic/anabolic effects on bone,132,482 muscle,357 blood-forming marrow,360,483 sexual function,484,485, and other androgen-responsive tissues. The ideal product for long-term androgen replacement therapy should be a safe, effective, convenient, and inexpensive form of testosterone with long-acting depot properties providing steady-state blood testosterone levels as a result of reproducible, zero-order release kinetics. Following the aim to maintain physiologic testosterone levels and resulting tissue androgen effects, androgen replacement therapy usually uses testosterone rather than synthetic androgens for reasons of safety, full-spectrum efficacy, and ease of monitoring. Synthetic steroidal and nonsteroidal androgens are likely to lack the full spectrum of testosterone tissue effects because of local amplification by 5α reductase to DHT and/or diversification to act on ERα by aromatization to estradiol.5,124 The practical goal of androgen replacement therapy is therefore to maintain stable, physiologic testosterone levels for prolonged periods using convenient depot testosterone formulations that facilitate compliance and avoid either supranormal or excessive fluctuation of androgen levels.
 

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i'm one of those who need more. on 200mg Cyp a week and my labs are still low. 600 total/20 free or around that.
i just don't feel right below 150mg. no idea why. my shbg is 11.
i recently started trying daily T propionate and it was a huge boost in how I feel. i started also having a higher libido and frequent erections on prop. i think a higher peak and quicker drop-off mimics a natural cycle and i just feel better on it.

Seriously!

You are hitting a robust TT 600 ng/dL with a low SHBG of 11 nmol/L.

Where do you think a FT 20 ng/dL stands using the cFTV?

LMFAO.

Screenshot (24704).png
 
Pure nonsense!

You were already running high-end/high FT from the get-go and constantly struggling.

You have numerous threads on here over the years and unfortunately, you are still chasing your tail.








As you very well know dysfunctional thyroid/adrenals, mental health disorders, quality of sleep, poor diet/lack of exercise can all have a negative impact on one's overall well-being.

Much more going on than just having healthy FT levels.

From your reply in post #5

*Only other issue I could possibly think my issue is adrenal exhaustion... I did have sleep study and I do have Sleep Apnea which started after I got on TRT. ( I tried Cpap and can't do it).... so just spinning my wheels that this point.


How many natty healthy young males hitting a peak TT 600-800 ng/dL let alone any outliers hitting 1000+ ng/dL even going back as far as the 70s when the first immunoassay to measure T was developed were running around with low SHBG?

Top it off that the peak is short-lived!




History of androgens and androgen action (2022)
David J. Handelsman

Invention

*This Golden Age also encompassed a third major but failed quest, that to invent a pure anabolic steroid, a synthetic androgen having purely anabolic effects but so devoid of any virilizing effects it could be used safely in women and children. Despite massive, invested effort, this failed quest left behind a legacy of thousands of synthetic androgens recorded in the expired patent literature, almost none ever tested in humans

*The comprehensive failure of this quest was ultimately due to its limited understanding of androgen physiology. These limitations included the subsequent discovery of a singular androgen receptor (AR), a final common pathway of androgen action that differs from other steroid receptors (estrogen progestin, glucocorticoid/mineralocorticoid) that feature complex dual receptor isoform control mechanisms

*More grievously, screening of steroid analogs was based on a misguided simplistic modification of the whole animal androgen bioassay. This purported to separate anabolic (represented by the levator ani muscle) from androgenic (represented by the ventral prostate) effects, an ad hoc refinement which made a false distinction where there was no difference


*This flawed approach is ultimately inconsistent with modern androgen physiology, findings rediscovered in more recent pharmaceutical research showing that the apparent differences between androgenic and anabolic endpoints in whole animal androgen bioassays reflected (a) whether the bioassay used maintenance or recovery of androgen effects and (b) differences in the speed of recovery from castration of androgen effects making the results depend on the timing of the endpoint [102]. Nevertheless, the term “anabolic” (or “androgenic-anabolic”) steroid persists in the common lexicon, serving largely as a journalistic pinata, long after it was known to be making a tautological distinction where there was no real difference e in reality, all androgens are anabolic, and all anabolic steroids are androgens [103]

*The next invention was that of the first non-steroidal androgen by Dalton et al. [111] in 1998, six decades after the first non-steroidal estrogen [112].
This creates a new class of non-steroidal synthetic androgen, often termed Specific Androgen Receptor Modulators (SARM), a misleading marketing term rather than an accurate pharmacological description [113,114], usurping a speculative but unsound analogy with Specific Estrogen Receptor Modulators (SERM). Non-steroidal androgens were developed by a rational drug design using computer-based structural modeling, an iterative approach exploiting a library of chemical substituents to optimize physicochemical interactions with the therapeutic target, in this case the androgen receptor using non-steroidal anti-androgens as lead compounds

*Nonsteroidal androgens are pharmacologically distinct from testosterone in being obligatorily pure androgens as they inherently lack testosterone's wider spectrum of activity. Pure (including nonsteroidal) androgens lack testosterone's capacity for amplification of androgenic potency by tissue-based 5a reduction to DHT as well as diversification by aromatization to estradiol to act upon estrogen receptors. Hence, while non-steroidal androgens may have potential roles in pharmacological androgen therapy, subject to rigorous efficacy, safety, and cost-effectiveness criteria, they could not replace testosterone for replacement therapy in men with pathologic hypogonadism due to their lack of testosterone's full spectrum of effects

*Nevertheless, although intended for pharmacological androgen therapy in indications such as prevention and treatment of muscle wasting in cancer [115], none of the non-steroidal androgens under development [116,117] are marketed by 2021. Yet hope springs eternal for this new attempt to separate anabolic from androgenic properties of androgens to facilitate marketing for muscle wasting and other selective effects of testosterone





Androgen pharmacology

*In replacement therapy, testosterone displays its full spectrum of effects including not just direct action via the androgen receptor, but also indirect effects via amplification by 5a reductase in some target tissues (prostate, skin, liver) as well as diversification of its effects via aromatization to estradiol to act on estrogen receptors in other target tissues (brain, bone). These effects are dose limited to replicate physiological androgen exposure intended to replicate the lifetime efficacy and safety of eugonadal men

*By contrast, synthetic androgens are exclusively pure androgens acting directly (or via metabolites) solely on the androgen receptor and are not suitable substitutes for testosterone in replacement therapy. However pharmacological androgen therapy uses synthetic androgens for their potent effects on muscle, liver, and other androgen target tissues aiming to modify the natural history of non-gonadal diseases [179]. In these applications, the dose and type of synthetic androgen are limited only by efficacy, safety, and cost-effectiveness of the androgen in placebo-controlled clinical trials

*Many such applications have been developed for synthetic androgens which remain cost-effective second-line alternatives even when more specific, purpose-designed therapeutics become available. For example, an oral alkylated androgens (stanozolol, danazol) can increase C1-inhibitor levels and reduce frequency of angioedema attacks; however, for prophylaxis, recombinant C1-inhibitor is more effective but costly [180]. Similarly, synthetic androgens are cost-effective at increasing hemoglobin in anemias due to renal or marrow failure [181] although recombinant erythropoietin or erythropoietin stimulating analogs are equally effective but higher cost









Androgen Physiology, Pharmacology, and Abuse (2020)

David J. Handelsman

View attachment 33073



*Testosterone is used clinically at physiologic doses for androgen replacement therapy, and, at typically higher doses, testosterone, or more usually synthetic androgens based on its structure, is also used for pharmacologic androgen therapy.

*The principal goal of androgen replacement therapy is to restore a physiologic pattern of androgen exposure to all the body’s tissues. Such treatment is usually restricted to the major natural androgen, testosterone, aiming to replicate physiologic circulating testosterone levels and the full spectrum (including prereceptor androgen activation) of endogenous androgen effects on tissues and recapitulating the natural history of efficacy and safety.5

*By contrast, pharmacologic androgen therapy exploits the anabolic or other effects of androgens on muscle, bone, and other tissues as hormonal drugs, which are judged on their efficacy, safety, and relative cost-effectiveness similar to any other therapeutic agents. Insight into the physiology of testosterone is a prerequisite for understanding and making the most effective use of androgen pharmacology.6,7





Practical Goals of Androgen Replacement Therapy


The goal of androgen replacement therapy is to replicate the physiologic actions of endogenous testosterone, usually for the remainder of life, as the pathological basis of hypogonadism usually involves irreversible disorders of the hypothalamus, pituitary, or testis. This requires rectifying the deficit and maintaining androgenic/anabolic effects on bone,132,482 muscle,357 blood-forming marrow,360,483 sexual function,484,485, and other androgen-responsive tissues. The ideal product for long-term androgen replacement therapy should be a safe, effective, convenient, and inexpensive form of testosterone with long-acting depot properties providing steady-state blood testosterone levels as a result of reproducible, zero-order release kinetics. Following the aim to maintain physiologic testosterone levels and resulting tissue androgen effects, androgen replacement therapy usually uses testosterone rather than synthetic androgens for reasons of safety, full-spectrum efficacy, and ease of monitoring. Synthetic steroidal and nonsteroidal androgens are likely to lack the full spectrum of testosterone tissue effects because of local amplification by 5α reductase to DHT and/or diversification to act on ERα by aromatization to estradiol.5,124 The practical goal of androgen replacement therapy is therefore to maintain stable, physiologic testosterone levels for prolonged periods using convenient depot testosterone formulations that facilitate compliance and avoid either supranormal or excessive fluctuation of androgen levels.
That's my entire point of chasing my tail... I've never ran anything supra-physiologic.... I've always ran doses that kept me within various ranges of the established labs and at times my FT ran higher due to the low SHBG. I've mostly ran low and moderate dosing throughout my entire time of TRT.. Oddly, I believe I never strayed over 150mg per week (only in the beginning when I first got on TRT I was placed on 200mg for about a half a year but quickly dropped down). Maybe for me there is no light at the end of the tunnel with TRT. Even now on a Prop protocol 15mg ED/SQ puts me at 1300 peak and 600 trough (don't remember my FT number but it was a little higher than peak labs and about half at trough).
 
That's my entire point of chasing my tail... I've never ran anything supra-physiologic.... I've always ran doses that kept me within various ranges of the established labs and at times my FT ran higher due to the low SHBG. I've mostly ran low and moderate dosing throughout my entire time of TRT.. Oddly, I believe I never strayed over 150mg per week (only in the beginning when I first got on TRT I was placed on 200mg for about a half a year but quickly dropped down). Maybe for me there is no light at the end of the tunnel with TRT. Even now on a Prop protocol 15mg ED/SQ puts me at 1300 peak and 600 trough (don't remember my FT number but it was a little higher than peak labs and about half at trough).

Peak TT 1300 ng/dL and low/lowish SHBG would have FT level through the roof and even then trough TT 600 ng/dL with low/lowish SHBG would have FT on the high end!

Even with normal SHBG (30-35 nmol/L) peak TT 1300ng/dL would have your FT very high.
 
Peak TT 1300 ng/dL and low/lowish SHBG would have FT level through the roof and even then trough TT 600 ng/dL with low/lowish SHBG would have FT on the high end!

Even with normal SHBG (30-35 nmol/L) peak TT 1300ng/dL would have your FT very high.
The last lab test (15mg Prop ed/sq) at 4hr peak TT 1312 (280-1100) & FT 321 (47-244) and 24 hr trough TT 624 & FT 172.....

When I run Cyp as opposed to Prop my FT doesn't spike as high at peak and drops 50% or more at trough .... not too mention I feel like crap running steady levels on Cyp than I do on Prop.
 
The last lab test (15mg Prop ed/sq) at 4hr peak TT 1312 (280-1100) & FT 321 (47-244) and 24 hr trough TT 624 & FT 172.....

When I run Cyp as opposed to Prop my FT doesn't spike as high at peak and drops 50% or more at trough .... not too mention I feel like crap running steady levels on Cyp than I do on Prop.

You would need to have your FT tested using Equilibrium Dialysis to know where it truly sits.
 
Like many of my brothers on this forum I/we have been struggling to get dialed in on TRT..... and the thought process has usual been to try to replicate the normal levels/diurnal rhythm of the body to maintain peak homeostasis, however, even with seemingly normal Total/Free T, E levels, etc.. we are still not feeling good... Is it possible that we may actually still be underdosed by limiting ourselves to these common lab ranges? for example, maybe some of us need to be in the 2000 and over range instead of the normal top lab ranges of 1000-1100, etc... Remember the T we are injecting even though labeled "Bio-identical" it is still basically "Synthetic-Plant derived". I've heard the guy "more plates more dates" talking about other versions of bio-identical testosterone that is actually synthesized from animal cholesterol but it is not mainstream due to cost. Maybe the body doesn't respond to the current version of plant based Test we currently use over long periods of time on TRT and/or need quite a bit more. Any thoughts???

Also, can anyone explain why seemingly other AAS compounds always seem to pack more punch than standard test even when they are fundamentally "EVEN" based on the Androgen/Anabolic ratio/ratings. Ex. I've used 40mg Tbol for a cycle (by itself) and I got insanely strong and pumped more than I ever have using 200 - 300mg's of Test. Anavar at small doses was even better than test. Thoughts?
I am wondering if this is also why many men do very well on the newer compounded topicals applied to the scrotum. the newer higher strength versions need less cream (less messy) and deliver lots of T. Higher DHT more libido, better mood, and because you apply them 2 times a day, (morning and 4 hours before bedtime is ideal, it can closely mimic you natural cycles. And trust me, your total t can get easily up into the 2,000 range if you take enough "clicks" of it. I was prescribed two clicks twice a day by my doc, who was willing to "optimize" me, and man it did have me charged up, but that isn't all a great thing. it drove Hemaglobin and Hematocrit up mostly, and put my libido into over drive. It's a wonder my head didn't snap off from turning it to look at every woman who came within eyesight. Constantly interested 24 - 7. The sex was great but it wore her out. So, I backed down, got my hematocrit and hemoglobin under control and still have damn good results. A word about sleep and thyroid. If either are not right, optimized T will still leave you feeling tired, and not in a great mood. I was there too. Armour is good stuff if you need it. I had long standing sleep apnea prior to starting T replacement, and after catching covid last year the apnea got dramatically worse. I ended up on a sleep study which lead to a cpap unit. A pain in the butt yes, but damn they do work. I feel so much better will use it as long as I need it, it really helps to sleep well.
 
Beyond Testosterone Book by Nelson Vergel
I am wondering if this is also why many men do very well on the newer compounded topicals applied to the scrotum. the newer higher strength versions need less cream (less messy) and deliver lots of T. Higher DHT more libido, better mood, and because you apply them 2 times a day, (morning and 4 hours before bedtime is ideal, it can closely mimic you natural cycles. And trust me, your total t can get easily up into the 2,000 range if you take enough "clicks" of it. I was prescribed two clicks twice a day by my doc, who was willing to "optimize" me, and man it did have me charged up, but that isn't all a great thing. it drove Hemaglobin and Hematocrit up mostly, and put my libido into over drive. It's a wonder my head didn't snap off from turning it to look at every woman who came within eyesight. Constantly interested 24 - 7. The sex was great but it wore her out. So, I backed down, got my hematocrit and hemoglobin under control and still have damn good results. A word about sleep and thyroid. If either are not right, optimized T will still leave you feeling tired, and not in a great mood. I was there too. Armour is good stuff if you need it. I had long standing sleep apnea prior to starting T replacement, and after catching covid last year the apnea got dramatically worse. I ended up on a sleep study which lead to a cpap unit. A pain in the butt yes, but damn they do work. I feel so much better will use it as long as I need it, it really helps to sleep well.

Need to rethink that one.


 
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