Serious Situation is still pretty fucked (33 Viewers)

[atrophicpyra]

https://looksmax.gg/threads/proof-that-dht-grows-bone.28528/

My response to your retarded ASS take:

The studies were performed on mice in vitro cells, specifically MC3T3-E1 cells (Which are non transformed pre osteoblast cells derived from C57BL/6 in mouse newborns skull.

studies showed that it increased proliferation, differentiation and mineralization markers.
also that it reduced resorption activity, TRAP / cathepsin B and direct androgen receptor signaling. which in simple terms, it showed that DHT shifts the bone turnover towards a more “bone-preserving” state.

Now the issue with claiming this will grow bone is as it follows

Study used rats with hormone deficiencies and osteoporosis.

Your logic is also flawed as your argument was "If bone formation increases and resorption decreases bones will grow larger", this is simply not true as it only displays that DHT works by mildly and locally aiding the maintenance of bone density not causing elongation or growth, bone balance control density, not growth, it's a homeostasis mechanism, now you will say, well, doesn't that mean that dut and fin will affect BMD? actually, quite the opposite, which ill address at the end.

Important to mention bone modeling and remodeling are far from the same, bone remodeling (which is osteoblast-osteoclast turnover) regulates the bone density, this doesn't mean it grows bones at all, whereas bone modeling is the real responsible for changes in bone size and shape.

To actually cause real bone enlargement and jaw growth or overall growth you need growth plates or active sutures, spatial remodeling signals, mechanical forces, coordinated tissue resorption and deposition in specific directions, the study you cited actually used none of this and only used isolated cell activity level.

The strongest argument you cited is that the studies found dht to have "anti resorptive properties", the issue with is that this means in a best case scenario that bone turnover slows, and bone is preserved, not that it enhances anabolism, actually scientific literature shows that androgens are mainly anti resorptive with very limited anabolic potential in vivo cells, which renders the theory useless.

The in vitro thing also has several problems, as the studies cited used mouse osteoblast cells in a dish and avian / isolated osteoclasts, this scenario and environment is highly unrealistic because it doesn't take into account real variables to consider such as that there was no endocrine system, no competing hormones and also no structural constraints, the fact cells behave a certain way doesn't mean it will grow localized projection the way you want it to.

Now let's talk about the point i made in the older threads about fin and dut having no effect whatsoever at BMD and actually increased circulating test levels and increased BMD, this is mainly because DHT itself play a tertiary role when it comes to regulating BMD and bone density overall, it's over run by test and E2 specifically as the most important hormone for preserving it, this mainly because estrogen is the primary inhibitor of osteoclasts, also not to mention DHT cannot aromatize unlike Testosterone which does convert to estrogen making it the main protective pathway and the reason why no BMD loss was shown, test and e2 go up when inhibiting test to DHT conversion cause it increases circulating test levels and it increases as well E2 (already explained the importance), this actually destroys the whole claim as the studies where performed not only in real humans (which they also were young healthy men) and also because the studies showed an increased of BMD, if DHT was a main factor for growth it would've shown a decrease of BMD and not the opposite which was shown, yet again if that theory of DHT growing bones and being “muh crucial” was true facial shrinkage would've been noticed clinically as well as BMD loss which wasn't noticed at all, if not the opposite ill quote the study “Circulating DHT does not appear to have a clinically significant role in modulating bone mass", this meaning the circulating test and e2 increase compensates for the loss of DHT and avoid the BMD loss and even go as far as to improve it, proving AGAIN how dht plays a tertiary role for bone density rather than a main role like E2 does.

anyways, point is If DHT were a important and crucial driver of bone growth, the long term suppression would result in measurable bone loss or craniofacial changes, which AGAIN neither of which are observed clinically.

studies: https://pmc.ncbi.nlm.nih.gov/articles/PMC2684818/

The study you cited again proves you wrong jfl, the study also used Beta DHT "beta-DHT (normally inactive) still affects osteoclasts" was mentioned in the studies, now what does this actually imply? ohhh, it implies that bone cells may respond through non standard pathways which makes the effect to be cell specific
and also non generalizable, this meaning that osteoclast responses may involve atypical or cell specific receptor interactions, limiting the extrapolation to systemic physiology in humans.

studies used
(Osteoblast proliferation, differentiation and mineralization on (MC3T3-E1))
studies: https://pubmed.ncbi.nlm.nih.gov/7819831/
https://pubmed.ncbi.nlm.nih.gov/15694414/

(Explanation of the need for cofactors and synergy)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5294959/

(Dut and finasteride study)
https://pmc.ncbi.nlm.nih.gov/articles/PMC2684818/

https://pubmed.ncbi.nlm.nih.gov/9892663/ (study cited by you)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5651475/ ( yes the studies you cited debunk your own claim)

Still all theoretical btw

19x affinity binding halo could or could not grow ur bones u never know

once again, more bindning affinity does not equal more potency stupid nigger, i never claimed it would decrease BMD, but its not gonna do ANYTHING for your face.

literally show me one study proving it could or couldn’t and I’ll shut up but u can’t so we will forever not know whether or not it will have an impact

Btw it’s OBVIOUSLY potent

 

[atrophicpyra]

once again, more bindning affinity does not equal more potency stupid nigger, i never claimed it would decrease BMD, but its not gonna do ANYTHING for your face.

Also let’s not steer away from u guys saying enclo doesn’t work as a test base on sarms

 

[Syna]

Still all theoretical btw

19x affinity binding halo could or could not grow ur bones u never know

Holy shit you are way more fucking retarded than Doorhandle5, that shit was about DHT derivatives halotestin is not a fucking DHT derivative.

 

[atrophicpyra]

Holy shit you are way more fucking retarded than Doorhandle5, that shit was about DHT derivatives halotestin is not a fucking DHT derivative.

Halo has all characteristics and molecule shape of dht deriv

“but Saar its a test deriv”

 

[Syna]

Halo has all characteristics and molecule shape of dht deriv

“but Saar its a test deriv”

it's both similar to test and dht, so whats your point?

 

[Syna]

Also let’s not steer away from u guys saying enclo doesn’t work as a test base on sarms

not even gonna adress such a retarded take.

 

[atrophicpyra]

Holy shit you are way more fucking retarded than Doorhandle5, that shit was about DHT derivatives halotestin is not a fucking DHT derivative.

What happened to u guys thinking enclo doesn’t work as a test base on sarms? Or how rad140 is the grim reaper of ur liver?

 

[Syna]

What happened to u guys thinking enclo doesn’t work as a test base on sarms? Or how rad140 is the grim reaper of ur liver?

 

[atrophicpyra]

View attachment 50093

Buddy don’t even make me pull up all the deaths caused by low dose tren trust me there is more than u think

 

[Syna]

https://looksmax.gg/threads/proof-that-dht-grows-bone.28528/
read the fucking thread, there are 2 different studies on 5ARI siblings that showed the only difference was penile development and hair and skin quality, not a single fucking thing regarding less bonemass.

 

[atrophicpyra]

https://looksmax.gg/threads/proof-that-dht-grows-bone.28528/
read the fucking thread, there are 2 different studies on 5ARI siblings that showed the only difference was penile development and hair and skin quality, not a single fucking thing regarding less bonemass.

Dht vs halotestin

That’s not my point, literally you never know what could happen to Adolesent on halo for years, who knows maybe they look like an ogre

u cant confirm that ur bold statement says even if something had a million receptor binding but was a dht derivative it would never grow bones?

 

[Syna]

Still all theoretical btw

19x affinity binding halo could or could not grow ur bones u never know


literally show me one study proving it could or couldn’t and I’ll shut up but u can’t so we will forever not know whether or not it will have an impact

Btw it’s OBVIOUSLY potent

binding affinity measures how strongly a molecule binds to a receptor, potency refers to the amount of that molecule required to produce a specific biological output, more binding affinity never equals more potency cause they are two separate aspects.

 

[atrophicpyra]

binding affinity measures how strongly a molecule binds to a receptor, potency refers to the amount of that molecule required to produce a specific biological output, more binding affinity never equals more potency cause they are two separate aspects.

Halo is obviously potent, that’s why I’m not fixated by it but rather the receptor affinity binding

 

[Syna]

Dht vs halotestin

That’s not my point, literally you never know what could happen to Adolesent on halo for years, who knows maybe they look like an ogre

u cant confirm that ur bold statement says even if something had a million receptor binding but was a dht derivative it would never grow bones?

DHT is not even a main regulator of BMD, all the 5 ARI and 5ar blockers show us that, it doesn't even affect BMD, and take into account BMD doesn't fucking affect the outer shape of the bones.

 

[Syna]

What happened to u guys thinking enclo doesn’t work as a test base on sarms? Or how rad140 is the grim reaper of ur liver?

Nardicus

ISTG im dying laughing rn

 

[atrophicpyra]

binding affinity measures how strongly a molecule binds to a receptor, potency refers to the amount of that molecule required to produce a specific biological output, more binding affinity never equals more potency cause they are two separate aspects.

Also idk why u keep talking abt the dht deriv argument its not gonna go anywhere ur wrong and I’m wrong because nobody will truly know what dht derivs at a higher receptor affinity than test derivs during pubertal years will do

Either way its all theoretical stop being so confident in claims that have no evidence backed up by it

 

[Syna]

Also idk why u keep talking abt the dht deriv argument its not gonna go anywhere ur wrong and I’m wrong because nobody will truly know what dht derivs at a higher receptor affinity than test derivs during pubertal years will do

Either way its all theoretical stop being so confident in claims that have no evidence backed up by it

how about we use the studies you cited on this thread? https://looksmax.gg/threads/proof-that-dht-grows-bone.28528/


The studies were performed on mice in vitro cells, specifically MC3T3-E1 cells (Which are non transformed pre osteoblast cells derived from C57BL/6 in mouse newborns skull.

studies showed that it increased proliferation, differentiation and mineralization markers.
also that it reduced resorption activity, TRAP / cathepsin B and direct androgen receptor signaling. which in simple terms, it showed that DHT shifts the bone turnover towards a more “bone-preserving” state.

Now the issue with claiming this will grow bone is as it follows

Study used rats with hormone deficiencies and osteoporosis.

Your logic is also flawed as your argument was "If bone formation increases and resorption decreases bones will grow larger", this is simply not true as it only displays that DHT works by mildly and locally aiding the maintenance of bone density not causing elongation or growth, bone balance control density, not growth, it's a homeostasis mechanism, now you will say, well, doesn't that mean that dut and fin will affect BMD? actually, quite the opposite, which ill address at the end.

Important to mention bone modeling and remodeling are far from the same, bone remodeling (which is osteoblast-osteoclast turnover) regulates the bone density, this doesn't mean it grows bones at all, whereas bone modeling is the real responsible for changes in bone size and shape.

To actually cause real bone enlargement and jaw growth or overall growth you need growth plates or active sutures, spatial remodeling signals, mechanical forces, coordinated tissue resorption and deposition in specific directions, the study you cited actually used none of this and only used isolated cell activity level.

The strongest argument you cited is that the studies found dht to have "anti resorptive properties", the issue with is that this means in a best case scenario that bone turnover slows, and bone is preserved, not that it enhances anabolism, actually scientific literature shows that androgens are mainly anti resorptive with very limited anabolic potential in vivo cells, which renders the theory useless.

The in vitro thing also has several problems, as the studies cited used mouse osteoblast cells in a dish and avian / isolated osteoclasts, this scenario and environment is highly unrealistic because it doesn't take into account real variables to consider such as that there was no endocrine system, no competing hormones and also no structural constraints, the fact cells behave a certain way doesn't mean it will grow localized projection the way you want it to.

Now let's talk about the point i made in the older threads about fin and dut having no effect whatsoever at BMD and actually increased circulating test levels and increased BMD, this is mainly because DHT itself play a tertiary role when it comes to regulating BMD and bone density overall, it's over run by test and E2 specifically as the most important hormone for preserving it, this mainly because estrogen is the primary inhibitor of osteoclasts, also not to mention DHT cannot aromatize unlike Testosterone which does convert to estrogen making it the main protective pathway and the reason why no BMD loss was shown, test and e2 go up when inhibiting test to DHT conversion cause it increases circulating test levels and it increases as well E2 (already explained the importance), this actually destroys the whole claim as the studies where performed not only in real humans (which they also were young healthy men) and also because the studies showed an increased of BMD, if DHT was a main factor for growth it would've shown a decrease of BMD and not the opposite which was shown, yet again if that theory of DHT growing bones and being “muh crucial” was true facial shrinkage would've been noticed clinically as well as BMD loss which wasn't noticed at all, if not the opposite ill quote the study “Circulating DHT does not appear to have a clinically significant role in modulating bone mass", this meaning the circulating test and e2 increase compensates for the loss of DHT and avoid the BMD loss and even go as far as to improve it, proving AGAIN how dht plays a tertiary role for bone density rather than a main role like E2 does.

anyways, point is If DHT were a important and crucial driver of bone growth, the long term suppression would result in measurable bone loss or craniofacial changes, which AGAIN neither of which are observed clinically.

studies: https://pmc.ncbi.nlm.nih.gov/articles/PMC2684818/

The study you cited again proves you wrong jfl, the study also used Beta DHT "beta-DHT (normally inactive) still affects osteoclasts" was mentioned in the studies, now what does this actually imply? ohhh, it implies that bone cells may respond through non standard pathways which makes the effect to be cell specific
and also non generalizable, this meaning that osteoclast responses may involve atypical or cell specific receptor interactions, limiting the extrapolation to systemic physiology in humans.

studies used
(Osteoblast proliferation, differentiation and mineralization on (MC3T3-E1))
studies: https://pubmed.ncbi.nlm.nih.gov/7819831/
https://pubmed.ncbi.nlm.nih.gov/15694414/

(Explanation of the need for cofactors and synergy)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5294959/

(Dut and finasteride study)
https://pmc.ncbi.nlm.nih.gov/articles/PMC2684818/

https://pubmed.ncbi.nlm.nih.gov/9892663/ (study cited by you)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5651475/ ( yes the studies you cited debunk your own claim)

 

[atrophicpyra]

Nardicus

ISTG im dying laughing rn

Enclo base works not bec it make sense but bec I have seen ppl do it and it works


Search up enclo base rad140 on Reddit there is a whole community based off of ppl using 6.25mg enclo as a test base with a sarm

 

[Syna]

how about we use the studies you cited on this thread? https://looksmax.gg/threads/proof-that-dht-grows-bone.28528/


The studies were performed on mice in vitro cells, specifically MC3T3-E1 cells (Which are non transformed pre osteoblast cells derived from C57BL/6 in mouse newborns skull.

studies showed that it increased proliferation, differentiation and mineralization markers.
also that it reduced resorption activity, TRAP / cathepsin B and direct androgen receptor signaling. which in simple terms, it showed that DHT shifts the bone turnover towards a more “bone-preserving” state.

Now the issue with claiming this will grow bone is as it follows

Study used rats with hormone deficiencies and osteoporosis.

Your logic is also flawed as your argument was "If bone formation increases and resorption decreases bones will grow larger", this is simply not true as it only displays that DHT works by mildly and locally aiding the maintenance of bone density not causing elongation or growth, bone balance control density, not growth, it's a homeostasis mechanism, now you will say, well, doesn't that mean that dut and fin will affect BMD? actually, quite the opposite, which ill address at the end.

Important to mention bone modeling and remodeling are far from the same, bone remodeling (which is osteoblast-osteoclast turnover) regulates the bone density, this doesn't mean it grows bones at all, whereas bone modeling is the real responsible for changes in bone size and shape.

To actually cause real bone enlargement and jaw growth or overall growth you need growth plates or active sutures, spatial remodeling signals, mechanical forces, coordinated tissue resorption and deposition in specific directions, the study you cited actually used none of this and only used isolated cell activity level.

The strongest argument you cited is that the studies found dht to have "anti resorptive properties", the issue with is that this means in a best case scenario that bone turnover slows, and bone is preserved, not that it enhances anabolism, actually scientific literature shows that androgens are mainly anti resorptive with very limited anabolic potential in vivo cells, which renders the theory useless.

The in vitro thing also has several problems, as the studies cited used mouse osteoblast cells in a dish and avian / isolated osteoclasts, this scenario and environment is highly unrealistic because it doesn't take into account real variables to consider such as that there was no endocrine system, no competing hormones and also no structural constraints, the fact cells behave a certain way doesn't mean it will grow localized projection the way you want it to.

Now let's talk about the point i made in the older threads about fin and dut having no effect whatsoever at BMD and actually increased circulating test levels and increased BMD, this is mainly because DHT itself play a tertiary role when it comes to regulating BMD and bone density overall, it's over run by test and E2 specifically as the most important hormone for preserving it, this mainly because estrogen is the primary inhibitor of osteoclasts, also not to mention DHT cannot aromatize unlike Testosterone which does convert to estrogen making it the main protective pathway and the reason why no BMD loss was shown, test and e2 go up when inhibiting test to DHT conversion cause it increases circulating test levels and it increases as well E2 (already explained the importance), this actually destroys the whole claim as the studies where performed not only in real humans (which they also were young healthy men) and also because the studies showed an increased of BMD, if DHT was a main factor for growth it would've shown a decrease of BMD and not the opposite which was shown, yet again if that theory of DHT growing bones and being “muh crucial” was true facial shrinkage would've been noticed clinically as well as BMD loss which wasn't noticed at all, if not the opposite ill quote the study “Circulating DHT does not appear to have a clinically significant role in modulating bone mass", this meaning the circulating test and e2 increase compensates for the loss of DHT and avoid the BMD loss and even go as far as to improve it, proving AGAIN how dht plays a tertiary role for bone density rather than a main role like E2 does.

anyways, point is If DHT were a important and crucial driver of bone growth, the long term suppression would result in measurable bone loss or craniofacial changes, which AGAIN neither of which are observed clinically.

studies: https://pmc.ncbi.nlm.nih.gov/articles/PMC2684818/

The study you cited again proves you wrong jfl, the study also used Beta DHT "beta-DHT (normally inactive) still affects osteoclasts" was mentioned in the studies, now what does this actually imply? ohhh, it implies that bone cells may respond through non standard pathways which makes the effect to be cell specific
and also non generalizable, this meaning that osteoclast responses may involve atypical or cell specific receptor interactions, limiting the extrapolation to systemic physiology in humans.

studies used
(Osteoblast proliferation, differentiation and mineralization on (MC3T3-E1))
studies: https://pubmed.ncbi.nlm.nih.gov/7819831/
https://pubmed.ncbi.nlm.nih.gov/15694414/

(Explanation of the need for cofactors and synergy)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5294959/

(Dut and finasteride study)
https://pmc.ncbi.nlm.nih.gov/articles/PMC2684818/

https://pubmed.ncbi.nlm.nih.gov/9892663/ (study cited by you)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5651475/ ( yes the studies you cited debunk your own claim)

 

[XvideosDemon]

Dragon FoidSlayer

 

[atrophicpyra]

how about we use the studies you cited on this thread? https://looksmax.gg/threads/proof-that-dht-grows-bone.28528/


The studies were performed on mice in vitro cells, specifically MC3T3-E1 cells (Which are non transformed pre osteoblast cells derived from C57BL/6 in mouse newborns skull.

studies showed that it increased proliferation, differentiation and mineralization markers.
also that it reduced resorption activity, TRAP / cathepsin B and direct androgen receptor signaling. which in simple terms, it showed that DHT shifts the bone turnover towards a more “bone-preserving” state.

Now the issue with claiming this will grow bone is as it follows

Study used rats with hormone deficiencies and osteoporosis.

Your logic is also flawed as your argument was "If bone formation increases and resorption decreases bones will grow larger", this is simply not true as it only displays that DHT works by mildly and locally aiding the maintenance of bone density not causing elongation or growth, bone balance control density, not growth, it's a homeostasis mechanism, now you will say, well, doesn't that mean that dut and fin will affect BMD? actually, quite the opposite, which ill address at the end.

Important to mention bone modeling and remodeling are far from the same, bone remodeling (which is osteoblast-osteoclast turnover) regulates the bone density, this doesn't mean it grows bones at all, whereas bone modeling is the real responsible for changes in bone size and shape.

To actually cause real bone enlargement and jaw growth or overall growth you need growth plates or active sutures, spatial remodeling signals, mechanical forces, coordinated tissue resorption and deposition in specific directions, the study you cited actually used none of this and only used isolated cell activity level.

The strongest argument you cited is that the studies found dht to have "anti resorptive properties", the issue with is that this means in a best case scenario that bone turnover slows, and bone is preserved, not that it enhances anabolism, actually scientific literature shows that androgens are mainly anti resorptive with very limited anabolic potential in vivo cells, which renders the theory useless.

The in vitro thing also has several problems, as the studies cited used mouse osteoblast cells in a dish and avian / isolated osteoclasts, this scenario and environment is highly unrealistic because it doesn't take into account real variables to consider such as that there was no endocrine system, no competing hormones and also no structural constraints, the fact cells behave a certain way doesn't mean it will grow localized projection the way you want it to.

Now let's talk about the point i made in the older threads about fin and dut having no effect whatsoever at BMD and actually increased circulating test levels and increased BMD, this is mainly because DHT itself play a tertiary role when it comes to regulating BMD and bone density overall, it's over run by test and E2 specifically as the most important hormone for preserving it, this mainly because estrogen is the primary inhibitor of osteoclasts, also not to mention DHT cannot aromatize unlike Testosterone which does convert to estrogen making it the main protective pathway and the reason why no BMD loss was shown, test and e2 go up when inhibiting test to DHT conversion cause it increases circulating test levels and it increases as well E2 (already explained the importance), this actually destroys the whole claim as the studies where performed not only in real humans (which they also were young healthy men) and also because the studies showed an increased of BMD, if DHT was a main factor for growth it would've shown a decrease of BMD and not the opposite which was shown, yet again if that theory of DHT growing bones and being “muh crucial” was true facial shrinkage would've been noticed clinically as well as BMD loss which wasn't noticed at all, if not the opposite ill quote the study “Circulating DHT does not appear to have a clinically significant role in modulating bone mass", this meaning the circulating test and e2 increase compensates for the loss of DHT and avoid the BMD loss and even go as far as to improve it, proving AGAIN how dht plays a tertiary role for bone density rather than a main role like E2 does.

anyways, point is If DHT were a important and crucial driver of bone growth, the long term suppression would result in measurable bone loss or craniofacial changes, which AGAIN neither of which are observed clinically.

studies: https://pmc.ncbi.nlm.nih.gov/articles/PMC2684818/

The study you cited again proves you wrong jfl, the study also used Beta DHT "beta-DHT (normally inactive) still affects osteoclasts" was mentioned in the studies, now what does this actually imply? ohhh, it implies that bone cells may respond through non standard pathways which makes the effect to be cell specific
and also non generalizable, this meaning that osteoclast responses may involve atypical or cell specific receptor interactions, limiting the extrapolation to systemic physiology in humans.

studies used
(Osteoblast proliferation, differentiation and mineralization on (MC3T3-E1))
studies: https://pubmed.ncbi.nlm.nih.gov/7819831/
https://pubmed.ncbi.nlm.nih.gov/15694414/

(Explanation of the need for cofactors and synergy)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5294959/

(Dut and finasteride study)
https://pmc.ncbi.nlm.nih.gov/articles/PMC2684818/

https://pubmed.ncbi.nlm.nih.gov/9892663/ (study cited by you)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5651475/ ( yes the studies you cited debunk your own claim)

??? Bro ngl I can prob pull up retarded posts u posted as well when u were newer to forums if u want

But either way im trying to be more mature and logical and actually tell u the truth that everything there r all theoretical zero studies on dht derivs megadosed in teens

 

[Syna]

How do you know show me 1 anecdote of somebody blasting halo whilst facial sutures r nowhere near fusing and let’s see how much male dimo they get

It does nothing for bmd sure but who knows what can be achieved with 19x receptor affinity binding dht deriv compound

Ok show me a study where halo decreased bmd due to cortisol rise

except halotestin fucking increases your bone age a fuck ton.

 

[FoidSlayer]

except halotestin fucking increases your bone age a fuck ton.

is he arguing for halo?

 

[Syna]

??? Bro ngl I can prob pull up retarded posts u posted as well when u were newer to forums if u want

But either way im trying to be more mature and logical and actually tell u the truth that everything there r all theoretical zero studies on dht derivs megadosed in teens

Maybe because scientist are not retarded????? and no, never made posts like this, at least not that were not obvious trolling.

 

[Syna]

is he arguing for halo?

he says that you can use RAD 140 with enclo as a test base and that megadose DHT derivatives grow bones

 

[atrophicpyra]

except halotestin fucking increases your bone age a fuck ton.

Bro you do know that for differentiation to occur u need prolfieration right? Further supporting my argument that dht derivs in extreme megadoses and high affinity bindings like halos similar dht structure can increase male dimo

 

[atrophicpyra]

is he arguing for halo?

no he’s just pulling up old threads of me saying dht grows bone when I was newer to forums, either way I’m not right and he’s not right because nobody actually knows if they do or not

 

[FoidSlayer]

he says DHT grows bone, that you can use RAD 140 with enclo as a test base and that megadose DHT derivatives grow bones

enclo as a test base

atrophicpyra HOW THE FUCK DOES DHT GROW BONES!!!!!!

 

[Syna]

is he arguing for halo?

Yes cause mega dose halo test will ascend me saarrrrrrr

 

[FoidSlayer]

no he’s just pulling up old threads of me saying dht grows bone when I was newer to forums, either way I’m not right and he’s not right because nobody actually knows if they do or not

dht doesnt grow bones

 

[Syna]

no he’s just pulling up old threads of me saying dht grows bone when I was newer to forums, either way I’m not right and he’s not right because nobody actually knows if they do or not

ive quoted and cited every single one of my claims.

 

[atrophicpyra]

Maybe because scientist are not retarded????? and no, never made posts like this, at least not that were not obvious trolling.

U def made a post when u started the forums abt cjc and ipa vs hgh

Even if i went to go look in ur profile to find those sorta posts to embarrass u it leads to no logical conclusion and it would be endless,

 

[Syna]

U def made a post when u started the forums abt cjc and ipa vs hgh

Even if i went to go look in ur profile to find those sorta posts to embarrass u it leads to no logical conclusion and it would be endless,

dont project yourself lol, im not a retard like you.

 

[FoidSlayer]

U def made a post when u started the forums abt cjc and ipa vs hgh

Even if i went to go look in ur profile to find those sorta posts to embarrass u it leads to no logical conclusion and it would be endless,

synap is not a retard bro

 

[Syna]

okay this is a fuck ton of nonsense, what are your claims and will debunk each and every single one of them, list them here rn.

 

[atrophicpyra]

dont project yourself lol, im not a retard like you.

oh nah this is some next level narcissism your telling me u don’t got one post where u said some dumb ass shit when u first started?

 

[Syna]

oh nah this is some next level narcissism your telling me u don’t got one post where u said some dumb ass shit when u first started?

not one that comes right through my mind, all the dumb posts i make are clear ragebait.

 

[FoidSlayer]

not one that comes right through my mind, all the dumb posts i make are clear ragebait.

DHT GROWS BONE THO

 

[atrophicpyra]

okay this is a fuck ton of nonsense, what are your claims and will debunk each and every single one of them, list them here rn.

Enclo test base works with a sarm for ex enclo with rad140, that’s my only claim

Idgaf abt dht derivs growing bone they probably don’t but I’m trying to calm ur narcissistic profile of being obnoxiously confident in things that have no genuine proof or studies behind, those studies of bmd being measured from those 2 twins don’t actually say anything bec the test increase from dht enzyme mutation could have compensated for the less bmd from dht inhibition.

 

[FoidSlayer]

Enclo test base works with a sarm for ex enclo with rad140, that’s my only claim

Idgaf abt dht derivs growing bone they probably don’t but I’m trying to calm ur narcissistic profile of being obnoxiously confident in things that have no genuine proof or studies behind, those studies of bmd being measured from those 2 twins don’t actually say anything bec the test increase from dht enzyme mutation could have compensated for the less bmd from dht.

DHT doesnt grow bones

also to my knowledge, SARMS are shit just pin.

 

[Syna]

Enclo test base works with a sarm for ex enclo with rad140, that’s my only claim

Idgaf abt dht derivs growing bone they probably don’t but I’m trying to calm ur narcissistic profile of being obnoxiously confident in things that have no genuine proof or studies behind, those studies of bmd being measured from those 2 twins don’t actually say anything bec the test increase from dht enzyme mutation could have compensated for the less bmd from dht.

Dude do you even know the kind of stuff you're saying? you literally proved your own point wrong


There a ton of studies about 5Ar blockers that even showed BMD improved, if dht played a key role it would've been noticed

 

[atrophicpyra]

Dude do you even know the kind of stuff you're saying? you literally proved your own point wrong


There a ton of studies about 5Ar blockers that even showed BMD improved, if dht played a key role it would've been noticed

View attachment 50099

jfl jfl jfl


Just proved my point that it could be overcompensation from the increase of test from inhibiting dht

 

[FoidSlayer]

Dude do you even know the kind of stuff you're saying? you literally proved your own point wrong


There a ton of studies about 5Ar blockers that even showed BMD improved, if dht played a key role it would've been noticed

View attachment 50099

this reminds me of a nigger in a tik tok comment section that tried to argue with me saying that blocking dht after 18 is bad because craniofacial development ensues until youre 25

 

[Syna]

jfl jfl jfl


Just proved my point that it could be overcompensation from the increase of test from inhibiting dht

THEN DHT IS NOT FUCKING RELEVANT, THATS WHAT I MEANS.

 

[looksmin]

Just skipped a workout half way because my back injury that has been trying to heal for weeks just flared and I can’t even fucking walk anymore jfl

Bye bye to all my gains bro I’m cooked

I got a horrible back muscle injury in my lower back and it won’t go away it’s literally stopping me from doing normal shit bro

I can’t run
I can’t lift my right leg
Now I can’t walk properly
I can’t bend over and pick shit
I can’t deadlift
I can’t do so much other things now I’m heavily fucking restricted



Pray for me boys

Time to BPC-157 maxx

 

[FoidSlayer]

THEN DHT IS NOT FUCKING RELEVANT, THATS WHAT I MEANS.

arguing about DHT causes a different type of rage

 

[atrophicpyra]

THEN DHT IS NOT FUCKING RELEVANT, THATS WHAT I MEANS.

It’s obviously relevant for dick size wtf

Either way u never know unless u get little Timmy on 50mg of halotestin for 3 months and measure his bmd before and after

 

[atrophicpyra]

arguing about DHT causes a different type of rage

I never even argued he just brought my thread up for no reason

 

[Syna]

It’s obviously relevant for dick size wtf

Either way u never know unless u get little Timmy on 50mg of halotestin for 3 months and measure his bmd before and after

you were talking about dht being relevant for bones and now u change to dick....olympic level of backpeddling

 

[FoidSlayer]

It’s obviously relevant for dick size wtf

Either way u never know unless u get little Timmy on 50mg of halotestin for 3 months and measure his bmd before and after

NIGGER OBVIOUSLY ITS RELEVANT FOR DICK

ive never seen synap deny that, infact he suggests you wait until your dick is done growing to take any sort of 5ARI so whats your point?

also fuck halo