Why is high androgenic activity especially in the early stages of puberty bad for final height regardless of estradiol levels

[Inosebreathonly]

First of all let's see how growth plates expand and then turn into bones which leads to height growth:

Chondrocytes first undergo a proliferative phase where they multiply in their number.

Then they get hypertrophied which leads to their expansion into 10-20x their previous size.

Then minerals start to accumulate and the ossification occurs which seals the growth plates and finishes growth window.

And unless proven otherwise, in humans this process goes in only one direction.

Obviously the timing and duration of these processes may differ from growth plate to growth plate and it could also be different in different chondrocytes that are in the same growth plate hence why we see height growth over a long period and not just at once..

For maximum height gains the best strategy is to prevent premature hypertrophy and ossification in the early puberty stages so you can maximize the proliferation of chondrocytes in their early proliferative stages.

When you are in later stages of puberty where majority of chondrocytes finished their proliferative phases and started getting into hypertrophic stages you want to maximize their hypertrophy.
And delaying chondrocyte ossification regardless of where you are at your puberty will lead to extension the growing window and higher final height.

This may differ from person to person but generally the primary driver of growth plate ossification is the activation of ER-α in bones and growth plates.

And more free testosterone means higher estradiol levels which leads to higher activation of ER-α, everybody knows that and this is why people use estradiol receptor antagonists like tamoxifen and aromatase inhibitors like aromasin, arimidex etc.

But even if we ignore estradiol one of the other main drivers of chondrocyte ossification is androgen receptor activation in bones and growth plates. (Regardless of estradiol)
Androgen receptor activation leads to increases in bone formation, mineralization and lateral growth of bones.
Excessive bone formation rates may also lead to mineralization and premature ossification of chondrocytes.

This is why adolescents with high androgen levels may experience earlier and more accelerated growth but also earlier closure of growth plates.

And earlier closure of growth plates will almost always lead to shorter final height.

This may also be the reason why countries with the highest testosterone levels like Mongolia, Uzbekistan, Ethiopia, Nigeria, Egypt, Azerbaijan etc. are also among the shortest


Androgenic hormone's are anabolic but not pro-proliferative like hgh and igf-1.


Androgen receptor activation in chondrocytes will mainly cause expansion/hypertrophy in chondrocytes. And this may be bad if you are in earlier stages of puberty because it may cause premature hypertrophy and this will lead to lower count of chondrocytes and lead to lower height growth potential in the later stages and overall shorter final height.
Also again too much hypertrophy stimuli from androgens may cause apoptosis or premature ossification of chondrocytes.

So what's the optimal strategy? How could we utilize androgenic hormones' anabolic and masculinization effects without limiting height growth potential?

I suggest keeping both estrogens and androgens and their receptor's activation low in earlier stages of puberty this could be done by taking low dose AI, estrogen receptor blockers, androgen receptor blockers, 5-AR blockers, high dose melatonin supplementation etc. while maximizing growth hormones and factors so you can reach your genetic potential of maximum chondrocyte proliferation.

And then once the majority of chondrocytes are out of their proliferative phase and are expanding/getting hypertrophied you can use SARMS, steroids etc. this will maximize the hypertrophy of chondrocytes and then with the ossification starting to occur your growth window will end but my maximizing both
chondrocyte proliferation and hypertrophy you will almost reach your maximum potential.

This will lead to a sudden grow/glow up both in height and dimorphism/striking features so you can surprise your crush at your school


Maybe there could be some strategies to still limit the ossification like using AI, using high dose vitamin K2 and magnesium to direct the calcium away from soft tissues to bones which will limit excess mineralization-induced ossification, upregulating WNT/B-catenin pathway etc. but once both proliferation and hypertrophy are maximized I don't think keeping growth plates open will lead to significantly more height growth..

Idk tell me your thoughts

 

[LLcel]

didnt have to read cause my anecdote matches. started puberty at 13 ended at 15. stayed 5,10 brutal

 

[Inosebreathonly]

didnt have to read cause my anecdote matches. started puberty at 13 ended at 15. stayed 5,10 brutal

I entered puberty at around 13 too and my testosterone was high (800-850 ng/dl) with average estradiol (23 pg/ml) when I was15-16 which led to both my wrist growth plates getting fully sealed at just 16.2 when the average is 17.5..
At least I took some precautions right after that, hopefully other growth plates are still open

 

[Inosebreathonly]

Bump

First of all let's see how growth plates expand and then turn into bones which leads to height growth:

Chondrocytes first undergo a proliferative phase where they multiply in their number.

Then they get hypertrophied which leads to their expansion into 10-20x their previous size.

Then minerals start to accumulate and the ossification occurs which seals the growth plates and finishes growth window.

And unless proven otherwise, in humans this process goes in only one direction.

Obviously the timing and duration of these processes may differ from growth plate to growth plate and it could also be different in different chondrocytes that are in the same growth plate hence why we see height growth over a long period and not just at once..

For maximum height gains the best strategy is to prevent premature hypertrophy and ossification in the early puberty stages so you can maximize the proliferation of chondrocytes in their early proliferative stages.

When you are in later stages of puberty where majority of chondrocytes finished their proliferative phases and started getting into hypertrophic stages you want to maximize their hypertrophy.
And delaying chondrocyte ossification regardless of where you are at your puberty will lead to extension the growing window and higher final height.

This may differ from person to person but generally the primary driver of growth plate ossification is the activation of ER-α in bones and growth plates.

And more free testosterone means higher estradiol levels which leads to higher activation of ER-α, everybody knows that and this is why people use estradiol receptor antagonists like tamoxifen and aromatase inhibitors like aromasin, arimidex etc.

But even if we ignore estradiol one of the other main drivers of chondrocyte ossification is androgen receptor activation in bones and growth plates. (Regardless of estradiol)
Androgen receptor activation leads to increases in bone formation, mineralization and lateral growth of bones.
Excessive bone formation rates may also lead to mineralization and premature ossification of chondrocytes.

This is why adolescents with high androgen levels may experience earlier and more accelerated growth but also earlier closure of growth plates.

And earlier closure of growth plates will almost always lead to shorter final height.

This may also be the reason why countries with the highest testosterone levels like Mongolia, Uzbekistan, Ethiopia, Nigeria, Egypt, Azerbaijan etc. are also among the shortest


Androgenic hormone's are anabolic but not pro-proliferative like hgh and igf-1.


Androgen receptor activation in chondrocytes will mainly cause expansion/hypertrophy in chondrocytes. And this may be bad if you are in earlier stages of puberty because it may cause premature hypertrophy and this will lead to lower count of chondrocytes and lead to lower height growth potential in the later stages and overall shorter final height.
Also again too much hypertrophy stimuli from androgens may cause apoptosis or premature ossification of chondrocytes.

So what's the optimal strategy? How could we utilize androgenic hormones' anabolic and masculinization effects without limiting height growth potential?

I suggest keeping both estrogens and androgens and their receptor's activation low in earlier stages of puberty this could be done by taking low dose AI, estrogen receptor blockers, androgen receptor blockers, 5-AR blockers, high dose melatonin supplementation etc. while maximizing growth hormones and factors so you can reach your genetic potential of maximum chondrocyte proliferation.

And then once the majority of chondrocytes are out of their proliferative phase and are expanding/getting hypertrophied you can use SARMS, steroids etc. this will maximize the hypertrophy of chondrocytes and then with the ossification starting to occur your growth window will end but my maximizing both
chondrocyte proliferation and hypertrophy you will almost reach your maximum potential.

This will lead to a sudden grow/glow up both in height and dimorphism/striking features so you can surprise your crush at your school


Maybe there could be some strategies to still limit the ossification like using AI, using high dose vitamin K2 and magnesium to direct the calcium away from soft tissues to bones which will limit excess mineralization-induced ossification, upregulating WNT/B-catenin pathway etc. but once both proliferation and hypertrophy are maximized I don't think keeping growth plates open will lead to significantly more height growth..

Idk tell me your thoughts

Bump

 

[Inosebreathonly]

Imma delete the thread if nobody else replies in 30 mins

 

[halloweed]

Water

 

[Inosebreathonly]

Water

What

 

[James47Max]

First of all let's see how growth plates expand and then turn into bones which leads to height growth:

Chondrocytes first undergo a proliferative phase where they multiply in their number.

Then they get hypertrophied which leads to their expansion into 10-20x their previous size.

Then minerals start to accumulate and the ossification occurs which seals the growth plates and finishes growth window.

And unless proven otherwise, in humans this process goes in only one direction.

Obviously the timing and duration of these processes may differ from growth plate to growth plate and it could also be different in different chondrocytes that are in the same growth plate hence why we see height growth over a long period and not just at once..

For maximum height gains the best strategy is to prevent premature hypertrophy and ossification in the early puberty stages so you can maximize the proliferation of chondrocytes in their early proliferative stages.

When you are in later stages of puberty where majority of chondrocytes finished their proliferative phases and started getting into hypertrophic stages you want to maximize their hypertrophy.
And delaying chondrocyte ossification regardless of where you are at your puberty will lead to extension the growing window and higher final height.

This may differ from person to person but generally the primary driver of growth plate ossification is the activation of ER-α in bones and growth plates.

And more free testosterone means higher estradiol levels which leads to higher activation of ER-α, everybody knows that and this is why people use estradiol receptor antagonists like tamoxifen and aromatase inhibitors like aromasin, arimidex etc.

But even if we ignore estradiol one of the other main drivers of chondrocyte ossification is androgen receptor activation in bones and growth plates. (Regardless of estradiol)
Androgen receptor activation leads to increases in bone formation, mineralization and lateral growth of bones.
Excessive bone formation rates may also lead to mineralization and premature ossification of chondrocytes.

This is why adolescents with high androgen levels may experience earlier and more accelerated growth but also earlier closure of growth plates.

And earlier closure of growth plates will almost always lead to shorter final height.

This may also be the reason why countries with the highest testosterone levels like Mongolia, Uzbekistan, Ethiopia, Nigeria, Egypt, Azerbaijan etc. are also among the shortest


Androgenic hormone's are anabolic but not pro-proliferative like hgh and igf-1.


Androgen receptor activation in chondrocytes will mainly cause expansion/hypertrophy in chondrocytes. And this may be bad if you are in earlier stages of puberty because it may cause premature hypertrophy and this will lead to lower count of chondrocytes and lead to lower height growth potential in the later stages and overall shorter final height.
Also again too much hypertrophy stimuli from androgens may cause apoptosis or premature ossification of chondrocytes.

So what's the optimal strategy? How could we utilize androgenic hormones' anabolic and masculinization effects without limiting height growth potential?

I suggest keeping both estrogens and androgens and their receptor's activation low in earlier stages of puberty this could be done by taking low dose AI, estrogen receptor blockers, androgen receptor blockers, 5-AR blockers, high dose melatonin supplementation etc. while maximizing growth hormones and factors so you can reach your genetic potential of maximum chondrocyte proliferation.

And then once the majority of chondrocytes are out of their proliferative phase and are expanding/getting hypertrophied you can use SARMS, steroids etc. this will maximize the hypertrophy of chondrocytes and then with the ossification starting to occur your growth window will end but my maximizing both
chondrocyte proliferation and hypertrophy you will almost reach your maximum potential.

This will lead to a sudden grow/glow up both in height and dimorphism/striking features so you can surprise your crush at your school


Maybe there could be some strategies to still limit the ossification like using AI, using high dose vitamin K2 and magnesium to direct the calcium away from soft tissues to bones which will limit excess mineralization-induced ossification, upregulating WNT/B-catenin pathway etc. but once both proliferation and hypertrophy are maximized I don't think keeping growth plates open will lead to significantly more height growth..

Idk tell me your thoughts

I'm 16 ⅔ what should I do?

 

[idkwhattoputhere]

bump + true, had a friend who was 5’8 with a 6 inch dick at 12. hasn’t grown at all i was 4’11 with a 2 incher while i was in his grade now im 6’0 and 6.5 with open plates. early bloomer is good for slaying in grades 7-10 and after that you’re fucked

 

[DR. NICKGA]

You solution is too dumb and risky

 

[MK.abuser]

Do you have studies supporthing this? I have found some saying that DHT can have protecive effects on cartlidge

 

[Inosebreathonly]

You solution is too dumb and risky

Risky in what sense?

 

[Inosebreathonly]

I'm 16 ⅔ what should I do?

I feel like that's the last bit of your growth
But to make sure did you check your bone age and/or growth plates?
If no you can calculate your tanner stage

And how much did you grow in the past year?

 

[Inosebreathonly]

bump + true, had a friend who was 5’8 with a 6 inch dick at 12. hasn’t grown at all i was 4’11 with a 2 incher while i was in his grade now im 6’0 and 6.5 with open plates. early bloomer is good for slaying in grades 7-10 and after that you’re fucked

Yes the more delay in puberty you get the taller you r likely gonna be. Some can even utilize things like AR-inhibitors, ER-αinhibitors, AI, high dose melatonin, nout touching their weiner etc. to delay puberty
I've talked about this in my last thread

 

[idkwhattoputhere]

Yes the more delay in puberty you get the taller you r likely gonna be. Some can even utilize things like AR-inhibitors, ER-αinhibitors, AI, high dose melatonin, nout touching their weiner etc. to delay puberty
I've talked about this in my last thread

fr, still tanner 3.5 so i should have a lot left in the tank

 

[Ashikai]

First of all let's see how growth plates expand and then turn into bones which leads to height growth:

Chondrocytes first undergo a proliferative phase where they multiply in their number.

Then they get hypertrophied which leads to their expansion into 10-20x their previous size.

Then minerals start to accumulate and the ossification occurs which seals the growth plates and finishes growth window.

And unless proven otherwise, in humans this process goes in only one direction.

Obviously the timing and duration of these processes may differ from growth plate to growth plate and it could also be different in different chondrocytes that are in the same growth plate hence why we see height growth over a long period and not just at once..

For maximum height gains the best strategy is to prevent premature hypertrophy and ossification in the early puberty stages so you can maximize the proliferation of chondrocytes in their early proliferative stages.

When you are in later stages of puberty where majority of chondrocytes finished their proliferative phases and started getting into hypertrophic stages you want to maximize their hypertrophy.
And delaying chondrocyte ossification regardless of where you are at your puberty will lead to extension the growing window and higher final height.

This may differ from person to person but generally the primary driver of growth plate ossification is the activation of ER-α in bones and growth plates.

And more free testosterone means higher estradiol levels which leads to higher activation of ER-α, everybody knows that and this is why people use estradiol receptor antagonists like tamoxifen and aromatase inhibitors like aromasin, arimidex etc.

But even if we ignore estradiol one of the other main drivers of chondrocyte ossification is androgen receptor activation in bones and growth plates. (Regardless of estradiol)
Androgen receptor activation leads to increases in bone formation, mineralization and lateral growth of bones.
Excessive bone formation rates may also lead to mineralization and premature ossification of chondrocytes.

This is why adolescents with high androgen levels may experience earlier and more accelerated growth but also earlier closure of growth plates.

And earlier closure of growth plates will almost always lead to shorter final height.

This may also be the reason why countries with the highest testosterone levels like Mongolia, Uzbekistan, Ethiopia, Nigeria, Egypt, Azerbaijan etc. are also among the shortest


Androgenic hormone's are anabolic but not pro-proliferative like hgh and igf-1.


Androgen receptor activation in chondrocytes will mainly cause expansion/hypertrophy in chondrocytes. And this may be bad if you are in earlier stages of puberty because it may cause premature hypertrophy and this will lead to lower count of chondrocytes and lead to lower height growth potential in the later stages and overall shorter final height.
Also again too much hypertrophy stimuli from androgens may cause apoptosis or premature ossification of chondrocytes.

So what's the optimal strategy? How could we utilize androgenic hormones' anabolic and masculinization effects without limiting height growth potential?

I suggest keeping both estrogens and androgens and their receptor's activation low in earlier stages of puberty this could be done by taking low dose AI, estrogen receptor blockers, androgen receptor blockers, 5-AR blockers, high dose melatonin supplementation etc. while maximizing growth hormones and factors so you can reach your genetic potential of maximum chondrocyte proliferation.

And then once the majority of chondrocytes are out of their proliferative phase and are expanding/getting hypertrophied you can use SARMS, steroids etc. this will maximize the hypertrophy of chondrocytes and then with the ossification starting to occur your growth window will end but my maximizing both
chondrocyte proliferation and hypertrophy you will almost reach your maximum potential.

This will lead to a sudden grow/glow up both in height and dimorphism/striking features so you can surprise your crush at your school


Maybe there could be some strategies to still limit the ossification like using AI, using high dose vitamin K2 and magnesium to direct the calcium away from soft tissues to bones which will limit excess mineralization-induced ossification, upregulating WNT/B-catenin pathway etc. but once both proliferation and hypertrophy are maximized I don't think keeping growth plates open will lead to significantly more height growth..

Idk tell me your thoughts

should i use ai + androgenic compounds at later stages of puberty or just androgens

 

[OxyFanNigga]

I just want you to know that meth is extremely important

 

[Bewusst]

Early puberty can result in short stature. For maximum height, you'll want to start and finish puberty as late as possible. Heck, puberty isn't even required to grow tall. Just look at Kinefelter's or eunuch singers.

 

[Inosebreathonly]

should i use ai + androgenic compounds at later stages of puberty or just androgens

You don't want EXCESS estradiol..
So androgens+LOW dose AI or tamoxifen would be the safer choice (I'd say don't use letrozole or even anastrozole bcz they are too strong, also tamoxifen is really tricky to use when aiming for height growth.
Tamoxifen can induce apoptosis (cell death) of chondrocytes and crashing your estrogen will also lead to same thing, inhibit chondrocyte proliferation and igf-1's activity/expression+plethora of other side effects both in general and height growth wise

So around 3-6.25 mg aromasin or 0.5-2.5 mg tamoxifen ED or EOD would in the safe range
Or maybe you can even use natural aromatase inhibitors and/or ER-alpha antagonists which can produce similar results with low dose of those drugs

 

[unknownslayer--]

i wish i knew this at 13 but the time your body start producing androgens is genetic, blocking both androgens and estrogen sounds risky and probably would lead to problems in the future because you are literally fucking up the natural time your body hits puberty

 

[Inosebreathonly]

i wish i knew this at 13 but the time your body start producing androgens is genetic, blocking both androgens and estrogen sounds risky and probably would lead to problems in the future because you are literally fucking up the natural time your body hits puberty

I talked about this a little in my other thread "My thoughts on sugar theory"
So one of the best ways to do that would be by maximizing serum melatonin levels which inhibits the production of GnRH (gonadotropin releasing hormone
Which stimulates the production of LH thus other sex hormones

So there is a threshold of melatonin in the blood (around 500 pmol/L). And if it exceeds that level the GnRH pulse get deactivated, inhibiting the GnRH axis.
So when you are a pre-puberty kid melatonin levels are above these levels almost every single night.
But at some point your total body mass increases to a point that the melatonin levels go below the threshold and the amount of melatonin in your blood is not enough to fully inhibit the GnRH axis.
So basically GnRH axis gets re-activated, stimulating LH levels which leads to accelerated sex hormone production and you basically hit puberty...

So what you want to do to delay puberty is constantly keeping that melatonin levels above that threshold range during the whole night.
And you can take melatonin supplements for that, spend time in dim environment during the evening and fully dark at night..
And there are some more ways to naturally/synthetically increase melatonin levels I can explain if anyone's interested

 

[Inosebreathonly]

First of all let's see how growth plates expand and then turn into bones which leads to height growth:

Chondrocytes first undergo a proliferative phase where they multiply in their number.

Then they get hypertrophied which leads to their expansion into 10-20x their previous size.

Then minerals start to accumulate and the ossification occurs which seals the growth plates and finishes growth window.

And unless proven otherwise, in humans this process goes in only one direction.

Obviously the timing and duration of these processes may differ from growth plate to growth plate and it could also be different in different chondrocytes that are in the same growth plate hence why we see height growth over a long period and not just at once..

For maximum height gains the best strategy is to prevent premature hypertrophy and ossification in the early puberty stages so you can maximize the proliferation of chondrocytes in their early proliferative stages.

When you are in later stages of puberty where majority of chondrocytes finished their proliferative phases and started getting into hypertrophic stages you want to maximize their hypertrophy.
And delaying chondrocyte ossification regardless of where you are at your puberty will lead to extension the growing window and higher final height.

This may differ from person to person but generally the primary driver of growth plate ossification is the activation of ER-α in bones and growth plates.

And more free testosterone means higher estradiol levels which leads to higher activation of ER-α, everybody knows that and this is why people use estradiol receptor antagonists like tamoxifen and aromatase inhibitors like aromasin, arimidex etc.

But even if we ignore estradiol one of the other main drivers of chondrocyte ossification is androgen receptor activation in bones and growth plates. (Regardless of estradiol)
Androgen receptor activation leads to increases in bone formation, mineralization and lateral growth of bones.
Excessive bone formation rates may also lead to mineralization and premature ossification of chondrocytes.

This is why adolescents with high androgen levels may experience earlier and more accelerated growth but also earlier closure of growth plates.

And earlier closure of growth plates will almost always lead to shorter final height.

This may also be the reason why countries with the highest testosterone levels like Mongolia, Uzbekistan, Ethiopia, Nigeria, Egypt, Azerbaijan etc. are also among the shortest


Androgenic hormone's are anabolic but not pro-proliferative like hgh and igf-1.


Androgen receptor activation in chondrocytes will mainly cause expansion/hypertrophy in chondrocytes. And this may be bad if you are in earlier stages of puberty because it may cause premature hypertrophy and this will lead to lower count of chondrocytes and lead to lower height growth potential in the later stages and overall shorter final height.
Also again too much hypertrophy stimuli from androgens may cause apoptosis or premature ossification of chondrocytes.

So what's the optimal strategy? How could we utilize androgenic hormones' anabolic and masculinization effects without limiting height growth potential?

I suggest keeping both estrogens and androgens and their receptor's activation low in earlier stages of puberty this could be done by taking low dose AI, estrogen receptor blockers, androgen receptor blockers, 5-AR blockers, high dose melatonin supplementation etc. while maximizing growth hormones and factors so you can reach your genetic potential of maximum chondrocyte proliferation.

And then once the majority of chondrocytes are out of their proliferative phase and are expanding/getting hypertrophied you can use SARMS, steroids etc. this will maximize the hypertrophy of chondrocytes and then with the ossification starting to occur your growth window will end but my maximizing both
chondrocyte proliferation and hypertrophy you will almost reach your maximum potential.

This will lead to a sudden grow/glow up both in height and dimorphism/striking features so you can surprise your crush at your school


Maybe there could be some strategies to still limit the ossification like using AI, using high dose vitamin K2 and magnesium to direct the calcium away from soft tissues to bones which will limit excess mineralization-induced ossification, upregulating WNT/B-catenin pathway etc. but once both proliferation and hypertrophy are maximized I don't think keeping growth plates open will lead to significantly more height growth..

Idk tell me your thoughts

Btw it is especially DHT that increases chondrocyte maturation and pushes them to ossification so I say DHT is really bad for height growth during puberty
So idk what to tell to my "DHTmaxxing" fellas

 

[ll_3O]

You don't want EXCESS estradiol..
So androgens+LOW dose AI or tamoxifen would be the safer choice (I'd say don't use letrozole or even anastrozole bcz they are too strong, also tamoxifen is really tricky to use when aiming for height growth.
Tamoxifen can induce apoptosis (cell death) of chondrocytes and crashing your estrogen will also lead to same thing, inhibit chondrocyte proliferation and igf-1's activity/expression+plethora of other side effects both in general and height growth wise

So around 3-6.25 mg aromasin or 0.5-2.5 mg tamoxifen ED or EOD would in the safe range
Or maybe you can even use natural aromatase inhibitors and/or ER-alpha antagonists which can produce similar results with low dose of those drugs

Wait so would a low dose aromasin at like 17 1/4 work for just a little bit more of height? And would there be much sides?

 

[Inosebreathonly]

Wait so would a low dose aromasin at like 17 1/4 work for just a little bit more of height? And would there be much sides?

Depends on the state of your growth plates but no harm in trying
Supplement with vit. D to avoid bone mineral density loss and aromasin doesn't have much severe side effects

 

[unknownslayer--]

I talked about this a little in my other thread "My thoughts on sugar theory"
So one of the best ways to do that would be by maximizing serum melatonin levels which inhibits the production of GnRH (gonadotropin releasing hormone
Which stimulates the production of LH thus other sex hormones

So there is a threshold of melatonin in the blood (around 500 pmol/L). And if it exceeds that level the GnRH pulse get deactivated, inhibiting the GnRH axis.
So when you are a pre-puberty kid melatonin levels are above these levels almost every single night.
But at some point your total body mass increases to a point that the melatonin levels go below the threshold and the amount of melatonin in your blood is not enough to fully inhibit the GnRH axis.
So basically GnRH axis gets re-activated, stimulating LH levels which leads to accelerated sex hormone production and you basically hit puberty...

So what you want to do to delay puberty is constantly keeping that melatonin levels above that threshold range during the whole night.
And you can take melatonin supplements for that, spend time in dim environment during the evening and fully dark at night..
And there are some more ways to naturally/synthetically increase melatonin levels I can explain if anyone's interested

at 13 i hitted puberty growthspurt from 5'2 to 5'7 and my test and dht was trough the roof
now am stunted at 5'11 at 17 and norwood 2, my dad hitted puberty at 15 and hes 6'3, my uncle at 17 and hes 6'6, some people are just unlucky asf