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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Deca (nandrolone) added to trt and wow!!
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<blockquote data-quote="madman" data-source="post: 164726" data-attributes="member: 13851"><p><span style="color: rgb(184, 49, 47)"><strong>when you state that there’s no such thing as someone’s SHBG binding more or less to testosterone,</strong></span> <span style="color: rgb(184, 49, 47)"><strong>even at the same level,</strong></span></p><p></p><p></p><p>After testicular secretion, a small proportion of testosterone undergoes activation to two bioactive metabolites, estradiol and DHT.</p><p></p><p>The amplification pathway converts roughly 5-10% of T--->DHT and roughly (~0.2-0.3%) of T--->estradiol.</p><p></p><p>Keep in mind that the amplification pathway converts ~4% of circulating testosterone to the more potent, pure androgen, DHT and DHT circulates at ~10% of blood testosterone concentrations, due to spillover from the prostate and nonprostatic sources.</p><p></p><p>Regarding RBA (relative binding affinity) of steroids to SHBG.....dihydrotestosterone (DHT)>testosterone>androstenediol>estradiol.</p><p></p><p>DHT binds to SHBG with about 5 times the affinity of testosterone and about 20 times the affinity of estradiol.</p><p></p><p>The RBA of DHT let alone testosterone and even estradiol to SHBG would trump the majority of various AAS (anabolic androgenic steroids) let alone nandrolone.</p><p></p><p>If anything the only steroid which would have a stronger RBA to SHBG than DHT, testosterone or even estradiol would be mesterolone (Proviron).</p><p></p><p>So as I stated previously.....You are lost on this one when you stated..... <span style="color: rgb(184, 49, 47)">"Plus the fact that you don’t understand that all SHBG isn’t created equal" </span></p><p></p><p></p><p><strong>*<span style="color: rgb(184, 49, 47)">The current algorithm and the experimental data reported here were generated using wild type SHBG which is present in nearly 98% of Caucasians.</span></strong> <strong><span style="color: rgb(26, 188, 156)">Genome wide association studies have revealed several SHBG polymorphisms, two of which have been reported to affect testosterone binding to SHBG (28).</span></strong></p><p></p><p></p><p>So if anything regarding SHBG:T binding unless you fall into the 2% which may have an SHBG polymorphism.....and only 2 have been reported to affect T binding to SHBG or you are using mesterolone (Proviron) added to trt than it is highly unlikely that <span style="color: rgb(184, 49, 47)">someone’s SHBG binding more or less to testosterone,</span> <span style="color: rgb(184, 49, 47)">even at the same level would happen.....hence FT level would not be different with the same TT/SHBG/Albumin level.....let alone to any significant degree.</span></p><p></p><p>Also regarding the TruT algorithm it has been shown that:</p><p></p><p><span style="color: rgb(184, 49, 47)"><strong>Effects of</strong> <strong>Estradiol and Dihydrotestosterone (DHT).</strong></span> <span style="color: rgb(184, 49, 47)"><strong>Addition of estradiol 17β in concentrations ranging from 10 to 500 pg/mL had </strong></span><span style="color: rgb(26, 188, 156)"><strong>no significant effect on percent free testosterone.</strong></span> <span style="color: rgb(44, 130, 201)">Similarly, free testosterone concentrations in men treated with graded doses of testosterone enanthate plus placebo whose DHT concentrations extended from <strong>physiologic to supraphysiologic range</strong> did not differ from those treated with testosterone enanthate plus dutasteride whose DHT concentrations were very low (Bhasin et al 2012), <strong>indicating that DHT over the range of concentrations relevant in male and female physiology has </strong></span><span style="color: rgb(26, 188, 156)"><strong>little effect on percent free testosterone. </strong></span></p><p></p><p></p><p><span style="color: rgb(184, 49, 47)">The new dynamic model leads to the reconsideration of several dogmas related to testosterone's binding to SHBG and has important physiologic and clinical implications. <strong>First, the fraction of circulating testosterone which is free is substantially greater (2.9±0.4%) than has been generally assumed (% cFTV 1.5±0.4%).</strong></span><span style="color: rgb(44, 130, 201)"><strong> Second, </strong></span><span style="color: rgb(26, 188, 156)"><strong>percent FT is not significantly </strong></span><span style="color: rgb(44, 130, 201)"><strong>related to total testosterone over a wide range of total testosterone concentrations.</strong> <strong>However, the percent FT declines as SHBG concentrations increase, although it does not decline as precipitously as predicted by the Vermeulen's model. Due to the allostery between the two binding sites, </strong></span><span style="color: rgb(26, 188, 156)"><strong>SHBG is able to regulate FT levels in much larger dynamic range. </strong></span></p><p></p><p></p><p>Let me state this again:</p><p></p><p><span style="color: rgb(44, 130, 201)"><strong>Second, </strong></span><span style="color: rgb(26, 188, 156)"><strong>percent FT is not significantly </strong></span><span style="color: rgb(44, 130, 201)"><strong>related to total testosterone over a wide range of total testosterone concentrations.</strong> <strong>However, the percent FT declines as SHBG concentrations increase, although it does not decline as precipitously as predicted by the Vermeulen's model. Due to the allostery between the two binding sites, </strong></span><span style="color: rgb(26, 188, 156)"><strong>SHBG is able to regulate FT levels in much larger dynamic range. </strong></span></p><p></p><p></p><p>Key point being....."<span style="color: rgb(44, 130, 201)"><strong>Due to the allostery between the two binding sites, </strong></span><span style="color: rgb(184, 49, 47)"><strong>SHBG is able to regulate FT levels in much larger dynamic range"</strong></span></p><p></p><p>Again let's top it off with the fact that this is what you are truly not understanding when it comes to SHBG:T binding.</p><p></p><p><strong><span style="color: rgb(44, 130, 201)">Relation between Percent FT with Total Testosterone and SHBG. Intra-dimer complex allostery suggests that </span><span style="color: rgb(251, 160, 38)">SHBG can regulate FT fraction over a wide range of total testosterone concentrations without getting saturated.</span></strong><span style="color: rgb(44, 130, 201)"> <strong>Indeed, it was found that percent FT calculated using the new model changed very modestly over a wide range of total testosterone concentrations.</strong> </span><strong><span style="color: rgb(26, 188, 156)">In contrast, the Vermeulen's equation suggests a negative relation between percent FT and total testosterone. </span><span style="color: rgb(44, 130, 201)">Furthermore, as SHBG concentrations increase, percent FT calculated using our new model shows only a modest decline</span></strong> <strong><span style="color: rgb(26, 188, 156)">in contrast to the marked decline in percent FT calculated using Vermeulen's equation.</span></strong></p><p></p><p></p><p>Too make it clearer to you of the significance here:</p><p></p><p><strong>* <span style="color: rgb(251, 160, 38)">SHBG can regulate FT fraction over a wide range of total testosterone concentrations without getting saturated.</span></strong></p></blockquote><p></p>
[QUOTE="madman, post: 164726, member: 13851"] [COLOR=rgb(184, 49, 47)][B]when you state that there’s no such thing as someone’s SHBG binding more or less to testosterone,[/B][/COLOR] [COLOR=rgb(184, 49, 47)][B]even at the same level,[/B][/COLOR] After testicular secretion, a small proportion of testosterone undergoes activation to two bioactive metabolites, estradiol and DHT. The amplification pathway converts roughly 5-10% of T--->DHT and roughly (~0.2-0.3%) of T--->estradiol. Keep in mind that the amplification pathway converts ~4% of circulating testosterone to the more potent, pure androgen, DHT and DHT circulates at ~10% of blood testosterone concentrations, due to spillover from the prostate and nonprostatic sources. Regarding RBA (relative binding affinity) of steroids to SHBG.....dihydrotestosterone (DHT)>testosterone>androstenediol>estradiol. DHT binds to SHBG with about 5 times the affinity of testosterone and about 20 times the affinity of estradiol. The RBA of DHT let alone testosterone and even estradiol to SHBG would trump the majority of various AAS (anabolic androgenic steroids) let alone nandrolone. If anything the only steroid which would have a stronger RBA to SHBG than DHT, testosterone or even estradiol would be mesterolone (Proviron). So as I stated previously.....You are lost on this one when you stated..... [COLOR=rgb(184, 49, 47)]"Plus the fact that you don’t understand that all SHBG isn’t created equal" [/COLOR] [B]*[COLOR=rgb(184, 49, 47)]The current algorithm and the experimental data reported here were generated using wild type SHBG which is present in nearly 98% of Caucasians.[/COLOR][/B] [B][COLOR=rgb(26, 188, 156)]Genome wide association studies have revealed several SHBG polymorphisms, two of which have been reported to affect testosterone binding to SHBG (28).[/COLOR][/B] So if anything regarding SHBG:T binding unless you fall into the 2% which may have an SHBG polymorphism.....and only 2 have been reported to affect T binding to SHBG or you are using mesterolone (Proviron) added to trt than it is highly unlikely that [COLOR=rgb(184, 49, 47)]someone’s SHBG binding more or less to testosterone,[/COLOR] [COLOR=rgb(184, 49, 47)]even at the same level would happen.....hence FT level would not be different with the same TT/SHBG/Albumin level.....let alone to any significant degree.[/COLOR] Also regarding the TruT algorithm it has been shown that: [COLOR=rgb(184, 49, 47)][B]Effects of[/B] [B]Estradiol and Dihydrotestosterone (DHT).[/B][/COLOR] [COLOR=rgb(184, 49, 47)][B]Addition of estradiol 17β in concentrations ranging from 10 to 500 pg/mL had [/B][/COLOR][COLOR=rgb(26, 188, 156)][B]no significant effect on percent free testosterone.[/B][/COLOR] [COLOR=rgb(44, 130, 201)]Similarly, free testosterone concentrations in men treated with graded doses of testosterone enanthate plus placebo whose DHT concentrations extended from [B]physiologic to supraphysiologic range[/B] did not differ from those treated with testosterone enanthate plus dutasteride whose DHT concentrations were very low (Bhasin et al 2012), [B]indicating that DHT over the range of concentrations relevant in male and female physiology has [/B][/COLOR][COLOR=rgb(26, 188, 156)][B]little effect on percent free testosterone. [/B][/COLOR] [COLOR=rgb(184, 49, 47)]The new dynamic model leads to the reconsideration of several dogmas related to testosterone's binding to SHBG and has important physiologic and clinical implications. [B]First, the fraction of circulating testosterone which is free is substantially greater (2.9±0.4%) than has been generally assumed (% cFTV 1.5±0.4%).[/B][/COLOR][COLOR=rgb(44, 130, 201)][B] Second, [/B][/COLOR][COLOR=rgb(26, 188, 156)][B]percent FT is not significantly [/B][/COLOR][COLOR=rgb(44, 130, 201)][B]related to total testosterone over a wide range of total testosterone concentrations.[/B] [B]However, the percent FT declines as SHBG concentrations increase, although it does not decline as precipitously as predicted by the Vermeulen's model. Due to the allostery between the two binding sites, [/B][/COLOR][COLOR=rgb(26, 188, 156)][B]SHBG is able to regulate FT levels in much larger dynamic range. [/B][/COLOR] Let me state this again: [COLOR=rgb(44, 130, 201)][B]Second, [/B][/COLOR][COLOR=rgb(26, 188, 156)][B]percent FT is not significantly [/B][/COLOR][COLOR=rgb(44, 130, 201)][B]related to total testosterone over a wide range of total testosterone concentrations.[/B] [B]However, the percent FT declines as SHBG concentrations increase, although it does not decline as precipitously as predicted by the Vermeulen's model. Due to the allostery between the two binding sites, [/B][/COLOR][COLOR=rgb(26, 188, 156)][B]SHBG is able to regulate FT levels in much larger dynamic range. [/B][/COLOR] Key point being....."[COLOR=rgb(44, 130, 201)][B]Due to the allostery between the two binding sites, [/B][/COLOR][COLOR=rgb(184, 49, 47)][B]SHBG is able to regulate FT levels in much larger dynamic range"[/B][/COLOR] Again let's top it off with the fact that this is what you are truly not understanding when it comes to SHBG:T binding. [B][COLOR=rgb(44, 130, 201)]Relation between Percent FT with Total Testosterone and SHBG. Intra-dimer complex allostery suggests that [/COLOR][COLOR=rgb(251, 160, 38)]SHBG can regulate FT fraction over a wide range of total testosterone concentrations without getting saturated.[/COLOR][/B][COLOR=rgb(44, 130, 201)] [B]Indeed, it was found that percent FT calculated using the new model changed very modestly over a wide range of total testosterone concentrations.[/B] [/COLOR][B][COLOR=rgb(26, 188, 156)]In contrast, the Vermeulen's equation suggests a negative relation between percent FT and total testosterone. [/COLOR][COLOR=rgb(44, 130, 201)]Furthermore, as SHBG concentrations increase, percent FT calculated using our new model shows only a modest decline[/COLOR][/B] [B][COLOR=rgb(26, 188, 156)]in contrast to the marked decline in percent FT calculated using Vermeulen's equation.[/COLOR][/B] Too make it clearer to you of the significance here: [B]* [COLOR=rgb(251, 160, 38)]SHBG can regulate FT fraction over a wide range of total testosterone concentrations without getting saturated.[/COLOR][/B] [/QUOTE]
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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Deca (nandrolone) added to trt and wow!!
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