[Biomaxx]

My mother having hightened androgen sensitivity throught genetic desease and my father using AAS throughout his life. Theoretically through epigenetics and androgen sens I should be a hyperresponder.

What other factors can I bring in ?
Much love bhais
9Dino dexter Ogre_cel

 

[9Dino]

Mirin hard yours muscles will also look full and not bloated and you won't need over 500mg to get huge

Also other factors like things you can do outside of genetics?

 

[Dexter]

You're right bro. But it's slightly more complex actually.

Epigenetically, IU androgen exposure (from maternal hyperandrogenism) can kinda change AR promoter methylation and downstream 5 alpha reductase expression which MIGHT (correct me if im wrong) prime enhanced androgenic signaling post natally. Then ob as you mentioned , there is paternal AAS exposure, so there’s potential for germline epigenetic remodeling also. (like an ex to understand better: altered DNA methylation and histone acetylation patterns in sperm affecting AR coregulator gene expression in child)

But if youre a hyperresponder depends on AR CAG repeat lengthh, polymorphisms in SRD5A2, SHBG, and CYP19A1 genes (bcz they regulate local DHT availability and aromatase balance), some androgen linked methylation signatures dont always stick around across generations yk and baseline endocrine milieu (LH, FSH, and insulin signaling modulate receptor density) also matters

basically yes you could have like a hyperresponder profile if your AR gene, co regulator networks and methylation architecture are aligned in ur favour but it's moreover based on your endocrine environment, receptor polymorphisms and epigenetic persistence

 

[Idec]

based lamarkians in this thread

 

[Biomaxx]

Mirin hard yours muscles will also look full and not bloated and you won't need over 500mg to get huge

View attachment 3742
Also other factors like things you can do outside of genetics?

Like other things the couldve made me a hyperresponder. Also where'd u get that pic of me from

 

[Biomaxx]

You're right bro. But it's slightly more complex actually.

Epigenetically, IU androgen exposure (from maternal hyperandrogenism) can kinda change AR promoter methylation and downstream 5 alpha reductase expression which MIGHT (correct me if im wrong) prime enhanced androgenic signaling post natally. Then ob as you mentioned , there is paternal AAS exposure, so there’s potential for germline epigenetic remodeling also. (like an ex to understand better: altered DNA methylation and histone acetylation patterns in sperm affecting AR coregulator gene expression in child)

But if youre a hyperresponder depends on AR CAG repeat lengthh, polymorphisms in SRD5A2, SHBG, and CYP19A1 genes (bcz they regulate local DHT availability and aromatase balance), some androgen linked methylation signatures dont always stick around across generations yk and baseline endocrine milieu (LH, FSH, and insulin signaling modulate receptor density) also matters

basically yes you could have like a hyperresponder profile if your AR gene, co regulator networks and methylation architecture are aligned in ur favour but it's moreover based on your endocrine environment, receptor polymorphisms and epigenetic persistence

High iq. Obv not garrunteed to js insta and hyper respond but the likely hood through sensitivity is almost garunteed as it was passed to my siblings. Gonna ask my dad some questions next time is see him and ilm keep yal updated. Appreciate the reply and mirin the intellect bhai

 

[Gigel]

You're right bro. But it's slightly more complex actually.

Epigenetically, IU androgen exposure (from maternal hyperandrogenism) can kinda change AR promoter methylation and downstream 5 alpha reductase expression which MIGHT (correct me if im wrong) prime enhanced androgenic signaling post natally. Then ob as you mentioned , there is paternal AAS exposure, so there’s potential for germline epigenetic remodeling also. (like an ex to understand better: altered DNA methylation and histone acetylation patterns in sperm affecting AR coregulator gene expression in child)

But if youre a hyperresponder depends on AR CAG repeat lengthh, polymorphisms in SRD5A2, SHBG, and CYP19A1 genes (bcz they regulate local DHT availability and aromatase balance), some androgen linked methylation signatures dont always stick around across generations yk and baseline endocrine milieu (LH, FSH, and insulin signaling modulate receptor density) also matters

basically yes you could have like a hyperresponder profile if your AR gene, co regulator networks and methylation architecture are aligned in ur favour but it's moreover based on your endocrine environment, receptor polymorphisms and epigenetic persistence

holy world salad

 

[Ogre_cel]

Epigenetically, IU androgen exposure (from maternal hyperandrogenism) can kinda change AR promoter methylation and downstream 5 alpha reductase expression which MIGHT (correct me if im wrong) prime enhanced androgenic signaling post natally. Then ob as you mentioned , there is paternal AAS exposure, so there’s potential for germline epigenetic remodeling also. (like an ex to understand better: altered DNA methylation and histone acetylation patterns in sperm affecting AR coregulator gene expression in child)

But if youre a hyperresponder depends on AR CAG repeat lengthh, polymorphisms in SRD5A2, SHBG, and CYP19A1 genes (bcz they regulate local DHT availability and aromatase balance), some androgen linked methylation signatures dont always stick around across generations yk and baseline endocrine milieu (LH, FSH, and insulin signaling modulate receptor density) also matters

basically yes you could have like a hyperresponder profile if your AR gene, co regulator networks and methylation architecture are aligned in ur favour but it's moreover based on your endocrine environment, receptor polymorphisms and epigenetic persistence

But tbh after fertilization the embryo does a massive epigenetic reset most sperm dna methylation and histone modifications are erased i doubt the father AAS usage would contribute to anything positive or negative cuz most children will be completely normal the embryo is very good at resetting sperm epigenetics the maternal hyperandrogenism has way more effect than the fathers AAS usage

 

[Biomaxx]

But tbh after fertilization the embryo does a massive epigenetic reset most sperm dna methylation and histone modifications are erased i doubt the father AAS usage would contribute to anything positive or negative cuz most children will be completely normal the embryo is very good at resetting sperm epigenetics the maternal hyperandrogenism has way more effect than the fathers AAS usage

Ur way to smart man get outta here