MEASURE YOUR BALLS TO DETERMINE YOUR BONE AGE

[TheEndHasNoEnd]

The roman numerals on the left indicate the tanner stages, the numbers in the balls indicate testicular volume in ml, and the numbers on the lines indicate the length of your testes in cm. How does this relate to bone age? Well, testosterone mediates how fast your puberty goes through, and testicle size is probably the most reliable measure of it in the tanner stages since it's literally how much testosterone you produce. Body and pubic hair, dick size, voice, adams apple, etc. could all be also due to genetics but ball size is reliant on testosterone. You cannot be average-high t on the adult scale and also have a young bone age, it's impossible as it's what ends puberty. We also all know that once puberty ends, height growth ends. Testosterone converts to estrogen through aromatization which fuses the growth plates, and unless you have taken an AI in your teens, big balls most likely means enough test to convert to estrogen to close your growth plates.

 

[Entschuldigung]

This thread title made me laugh irl

 

[Dionysus]

Lifefuel because small balls

 

[JizzFarmer]

Caging at title

 

[Deleted member 1774]

i legit have number 1

 

[TheEndHasNoEnd]

i legit have number 1

FUCK YOU LOW T TALLFAG IM AT 5.8 BUT I CANT COPE WITH HIGH T STUNTING MY HEIGHT CUZ NORMIES PUT TOO MUCH IMPORTANCE ON HEIGHT AND ITS OVER FOR ME

 

[sandcelmuttcel]

not accurate lately i've been having small balls idk why

 

[deer]

V gang rise up

 

[TheEndHasNoEnd]

not accurate lately i've been having small balls idk why

thats just the feel of it not the size, happens when u coom too much

 

[HurtfulVanity]

Thankfully for me my balls are on the smaller side yet voice is deep, I can only grow a thin moustache and 1 chin hair life fuel for me still growing as I've grown half an inch past month and a half

 

[Deleted member 1774]

FUCK YOU LOW T TALLFAG IM AT 5.8 BUT I CANT COPE WITH HIGH T STUNTING MY HEIGHT CUZ NORMIES PUT TOO MUCH IMPORTANCE ON HEIGHT AND ITS OVER FOR ME

nice

 

[Deleted member 5349]

If you’re super high t and have huge balls like me, this test is useless

 

[HighIQcel]

Does alcohol and smoking affect your hormones?

 

[HighIQcel]

alcohol fucking annihilates your growth hormone. smoking nicotine I believe slightly reduces aromatase.

Fuuuuck, when I turned out 18 I started partying therefore drinking booze because figured that 18 was ok age to drink alcohol. I would drink 2-3times per month ( was wasted)

 

[TheEndHasNoEnd]

I do agree that early blooming does stunt you (obviously). I've posted on the topic here:

https://looksmax.org/threads/early-blooming-is-peak-genetics.99289/page-2#post-1692521

https://looksmax.org/threads/early-blooming-is-peak-genetics.99289/page-2#post-1692583

It's just a dilemma as to whether you were actually "stunted" in the sense that your genetics were meaning for things to turn out differently.

alcohol fucking annihilates your growth hormone. smoking nicotine I believe slightly reduces aromatase.

i started puberty at a normal age i believe, it just ended too fast i feel like. but for some reason shit like armpit hair only came in like last year, i dont know if its genetics, the high e inhibiting dht production, or if im actually a slow bloomer. ill get my bone age checked anyways once the clinics are open and if it shows theyre young (somehow) ill take an ai and gh or whichever height stack seems effective.

 

[Schizoidcel]

It's over if flaccid dick doesn't hang lower than the balls

 

[thecel]

I’ll be 16 in about 1.5 months, and I’m at Tanner stage 4.0 according to this calculator

Tanner Stage Calculator for Boys: Growing Up in the Lord: A Study for Teenage Boys by Jeffrey W. Hamilton

growingupboys.info

 

[Deleted member 7901]

my balls are huge (wide), is it suifuel or lifefuel, because huge balls are correlated with high testosterone but length wise they seem stage 4

 

[Deleted member 7901]

I’ll be 16 in about 1.5 months, and I’m at Tanner stage 4.0 according to this calculator

Tanner Stage Calculator for Boys: Growing Up in the Lord: A Study for Teenage Boys by Jeffrey W. Hamilton

growingupboys.info

I did this test 2 months ago and I got tanner stage 3.8, hopefully it's correct

 

[Copemaxxing]

How to measure this shit

 

[JustBeCurry]

my balls are huge (wide), is it suifuel or lifefuel, because huge balls are correlated with high testosterone but length wise they seem stage 4

Same tbh, big balls so no more growth for me

 

[AlwaysHaveQuestions]

thats just the feel of it not the size, happens when u coom too much

coomer exposed

 

[Deleted member 2756]

good thread but lacking crucial information. It's not as simple as "testosterone converts to estradiol" or "testicular size is reliant on testosterone". Testicular size is thoroughly dependent on LH and FSH signaling. Feedback loops play a role in inhibiting the secretion of GnRH and subsequently LH and FSH if steroid hormone receptors are being agonized, signaling the hypothalamus to cease production of GnRH because the body has enough circulating bioavailable steroids. For example, the reason your testicular mass atrophies on exogenous steroids is because GnRH production will cease due to the androgen mediated negative feedback loop on a hypothalamic/pituitary level, anything that agonizes or has a binding affinity to a steroidal receptor will cause an induction of GnRH cessation.

the same biological function is expressed on the other side of the spectrum, the same mechanism, just the opposite outcome. Let's start with aromatase inhibitors, exemestane, for example, acts via binding to the aromatase enzyme and destroying it, the drug can be used medicinally to free up more testosterone and slightly lower estradiol, but it can also be used as a tool to inhibit the powerful estrogen-mediated negative feedback loop, through expelling estrogen from the body, the hypothalamic estradiol receptors are no longer going to be agonized, signaling the axis to upregulate LH to potentially counteract the deprivation of estradiol through heightened steroidogenesis. Higher LH equates to a higher demand of LH receptors, meaning the Leydig cells and the Sertoli cells in the testicular tissue need to biologically adapt to the influx of LH, the same sort of mechanism can be seen through exogenous testosterone administration, androgen receptors upregulate to adapt to the heightened levels of androgens. To put it simply, aromatase inhibitors deprive the body of estrogen, so in response, the counterpart enzymes, receptors, and steroidal inducers upregulate to counteract the lowered level of blood estrogen, thus leading to an increased of androgens, progestins, and corticoids.

Basically the point I'm trying to make is that the reason testicle size increases during puberty is because of the influx of LH and subsequently the increase in steroidogenic enzymes. If someone takes Clomifene, (which is acts both antagonistically and agonistically within the body, but primarily exerts its effects through blocking endogenous estradiol from binding to the hypothalamic receptors.) they're going to notice an increased overall testicular size. The same could be said about someone taking, for example, an anti-androgen, like cyproterone, which acts solely as an antagonist to the androgen receptors. That's my two cents on it all.

 

[Copemaxxing]

good thread but lacking crucial information. It's not as simple as "testosterone converts to estradiol" or "testicular size is reliant on testosterone". Testicular size is thoroughly dependent on LH and FSH signaling. Feedback loops play a role in inhibiting the secretion of GnRH and subsequently LH and FSH if steroid hormone receptors are being agonized, signaling the hypothalamus to cease production of GnRH because the body has enough circulating bioavailable steroids. For example, the reason your testicular mass atrophies on exogenous steroids is because GnRH production will cease due to the androgen mediated negative feedback loop on a hypothalamic/pituitary level, anything that agonizes or has a binding affinity to a steroidal receptor will cause an induction of GnRH cessation.

the same biological function is expressed on the other side of the spectrum, the same mechanism, just the opposite outcome. Let's start with aromatase inhibitors, exemestane, for example, acts via binding to the aromatase enzyme and destroying it, the drug can be used medicinally to free up more testosterone and slightly lower estradiol, but it can also be used as a tool to inhibit the powerful estrogen-mediated negative feedback loop, through expelling estrogen from the body, the hypothalamic estradiol receptors are no longer going to be agonized, signaling the axis to upregulate LH to potentially counteract the deprivation of estradiol through heightened steroidogenesis. Higher LH equates to a higher demand of LH receptors, meaning the Leydig cells and the Sertoli cells in the testicular tissue need to biologically adapt to the influx of LH, the same sort of mechanism can be seen through exogenous testosterone administration, androgen receptors upregulate to adapt to the heightened levels of androgens. To put it simply, aromatase inhibitors deprive the body of estrogen, so in response, the counterpart enzymes, receptors, and steroidal inducers upregulate to counteract the lowered level of blood estrogen, thus leading to an increased of androgens, progestins, and corticoids.

Basically the point I'm trying to make is that the reason testicle size increases during puberty is because of the influx of LH and subsequently the increase in steroidogenic enzymes. If someone takes Clomifene, (which is acts both antagonistically and agonistically within the body, but primarily exerts its effects through blocking endogenous estradiol from binding to the hypothalamic receptors.) they're going to notice an increased overall testicular size. The same could be said about someone taking, for example, an anti-androgen, like cyproterone, which acts solely as an antagonist to the androgen receptors. That's my two cents on it all.

Why you took time to write this

 

[Deleted member 2756]

Why you took time to write this

wrote it in under less than 8 minutes. Not much of a big deal.

 

[TheEndHasNoEnd]

If someone takes Clomifene, (which is acts both antagonistically and agonistically within the body, but primarily exerts its effects through blocking endogenous estradiol from binding to the hypothalamic receptors.) they're going to notice an increased overall testicular size

ooh shit ballsize maxxing

 

[Deleted member 2756]

ooh shit ballsize maxxing

Could do, but it also agonizes estrogen receptors in bone tissue, so very counterproductive, unless you're surmising that your plates are already closed.

 

[Deleted member 7901]

Same tbh, big balls so no more growth for me

the weird thing is that by some I past as older then I am (I was asked what job I have while I am 17)
but by some ask younger, and the tanner stage calculator said that I am tanner stage 3.8

 

[Tom2004]

wrote it in under less than 8 minutes. Not much of a big deal.

 

[Deleted member 2756]

View attachment 526502

5'6 and my little bitch, keep crying for me in discord.

 

[Tom2004]

5'6 and my little bitch, keep crying for me in discord.

 

[TheEndHasNoEnd]

Could do, but it also agonizes estrogen receptors in bone tissue, so very counterproductive, unless you're surmising that your plates are already closed.

Wouldnt any ai work as well?

 

[Deleted member 2756]

Wouldnt any ai work as well?

Estradiol receptor antagonists work better because they completely block the receptor sites and force absolutely trick the body into producing more LH. Aromatase inhibitors also work because technically you can clear your entire serum estradiol concentration and deprive the receptors of stimulation, thus the hypothalamus begins producing an excess of GnRH and subsequently LH.