Why do boys that are castrated before puberty have greater average height

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super302

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Can't figure this out, thanks for the help :confused:

Book says that Eunuchs, especially boys who were castrated before puberty, end up taller than non-eunuchs

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When a boy is castrated there will be a lower level of testosterone in the body. The presence of testosterone assists in the fusing of the epiphyseal plates in the long bones, therefore if a boy is castrated and lacks a normal level of testosterone his epiphyseal plates will take longer to fuse making him taller. A similar syndrome that this is seen in is Klinefelter's syndrome - XXY - the boys are taller with longer extremities due to testicular atrophy.
 
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Boys who are castrated become democratic senators later in life. True story.
 
When a boy is castrated there will be a lower level of testosterone in the body. The presence of testosterone assists in the fusing of the epiphyseal plates in the long bones, therefore if a boy is castrated and lacks a normal level of testosterone his epiphyseal plates will take longer to fuse making him taller.
This is what I came in here to say. I concur.
 
Can't figure this out, thanks for the help :confused:

Book says that Eunuchs, especially boys who were castrated before puberty, end up taller than non-eunuchs

Please do not use SDN for personal medical advice. :smuggrin:
 
The real answer: Gravity

I would have been like 7'6" if it weren't for these damn bowling balls weighing me down.
 
OK, now answer this one: Why isn't the average woman taller than the average man? (since women have low testosterone levels)

By the way KentW...that was a cheap shot (funny, though).
 
OK, now answer this one: Why isn't the average woman taller than the average man? (since women have low testosterone levels).

If I remember my endocrine phys correctly, its because estrogen closes the plates.
 
Now what good would your height be if you don't have the balls? Literally and figuretively LOL
 
When a boy is castrated there will be a lower level of testosterone in the body. The presence of testosterone assists in the fusing of the epiphyseal plates in the long bones, therefore if a boy is castrated and lacks a normal level of testosterone his epiphyseal plates will take longer to fuse making him taller. A similar syndrome that this is seen in is Klinefelter's syndrome - XXY - the boys are taller with longer extremities due to testicular atrophy.

wow, i learned something. thanks!
 
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Just to add one more thing, if you have early onset puberty (precocious puberty), where hormone levels are elevated early, you will get the opposite, the epiphyseal plates will close early, leading to a reduction in height.
 
If I remember my endocrine phys correctly, its because estrogen closes the plates.

True. Some girls, such as those who were considered "too tall" or (more recently) the pillow angel girl, have been given high dose estrogen to close their growth plates.
 
The above replies are correct. I guess I should have really answered that androgens assist in plate closings.

anymore brain busters? ;)
 
The above replies are correct. I guess I should have really answered that androgens assist in plate closings.

anymore brain busters? ;)

This is an oversimplified explanation and probably in reality is not so cut & dry. Adolescent males achieve a greater height following puberty than adolescent females...obviously androgens are responsible for long bone growth. What is likely responsible for epiphyseal plate closure is the rate of sex hormone production, the absolute androgen:estrogen ratio, and your genetic potential.

Classically, estrogens are consisdered responsible for epiphyseal plate closure, but if you look at female gymnasts (whose menstrual cycles are suppressed by the strenuous physical exertion and low body fat) they are shorter than the average female. With suppression of their menstrual cycles (lack of ovarian estrogen) and low fat mass (lack of androgen conversion) you would expect their low total estrogen to result in greater long bone growth.

The interplay b/w estrogens and androgens is much more complex b/c the E:A ratio is constantly balanced by production in the gonads/adrenal glands and peripheral conversion in fat cells.

Also interesting (and highly unlikely that you'll find a sound explanation) is the fact that the growth of the genitals has been found to correlate inversely with the growth of the extremities (arms, legs). According to this theory, androgens produced by rapidly growing [testes] cause the epiphyseal plates in the arms and legs to fuse early.
 
This is really interesting. I was under the impression that as children enter into puberty, their androgen and/or estrogen levels stimulate bone growth. And then at certain threshold levels of the hormones (e.g. later puberty), these high hormone levels stimulate epiphyseal plate closure. I was also under the impression that men are generally taller than women because they start puberty later; that women's high estrogen levels at an earlier age cause epiphyseal plate closure sooner. Will you please elaborate on the E:A ratio bit? Thanks!
 
Wait...so I'm not super tall because I didn't have delayed testerone during puberty? DAMMIT!!!

Presumably getting testerone later would still allow you to develop all your secondary (and primary I guess) sex characteristics, so does this mean that if you block testosterone for a few extra years you'd be super tall and be able to get a sweet NBA contract?

Heh.
 
Wait...so I'm not super tall because I didn't have delayed testerone during puberty? DAMMIT!!!

Presumably getting testerone later would still allow you to develop all your secondary (and primary I guess) sex characteristics, so does this mean that if you block testosterone for a few extra years you'd be super tall and be able to get a sweet NBA contract?

Heh.

Perhaps. But it would probably make for some awkwardness in the lockeroom.
 
Book says that Eunuchs, especially boys who were castrated before puberty, end up taller than non-eunuchs

xinsrc_392070327133951503478.jpg

"Aww crap."
 
This is really interesting. I was under the impression that as children enter into puberty, their androgen and/or estrogen levels stimulate bone growth. And then at certain threshold levels of the hormones (e.g. later puberty), these high hormone levels stimulate epiphyseal plate closure. I was also under the impression that men are generally taller than women because they start puberty later; that women's high estrogen levels at an earlier age cause epiphyseal plate closure sooner. Will you please elaborate on the E:A ratio bit? Thanks!

The point I was trying to make is that the science is complex and our understanding is incomplete. All of the factors mentioned so far come into play. But, do not forget the critical role of hGH (growth hormone) and IGF-1 in long bone growth.


The most effective way to increase linear growth is by using hGH prior to epiphyseal plate closure. As I stated previously, testosterone is not the primary cause of epiphyseal closure...rather, it is the interplay between all hormones and growth factors. The hormonal milieu is in a constant state of flux and small differences in carrier proteins (which effect free hormone concentrations), receptors (polymorphisms), 2nd messengers, and subsequent gene expression play a big role in the final height of an individual.

You could give 2 prepubescent individuals equal concentrations of hormones (androgens, estrogens, hGH) at identical points in growth and development, and you'd still see striking differences in final adult height between the 2 individuals.

Cirrus83 said:
so does this mean that if you block testosterone for a few extra years you'd be super tall and be able to get a sweet NBA contract?

:rolleyes:No. But, google "androgen receptor insensitivity." These "women" are XY but fail to express male primary and secondary sex characteristics due to mutations in the androgen receptor causing it to be nonfunctional. They have no ovaries, uterus, or cervix(b/c they ain't girls) and have a blind vagina (not Ray Charles blind:cool:, but blind in the "dead end" sense of the word). But during pubesence (they still have testes due to the Y chromosome) they develop large, perky breasts (seriously) and grow tall and lean (most look like runway models) because much of the unused testosterone is converted to estrogen and causes female secondary sex characteristics.

Rumor mill says that Jamie Lee Curtis (HIPPA whaaaa?) has this condition and had "corrective surgery" at my medical center.
 
Will you please elaborate on the E:A ratio bit? Thanks!

No...only b/c it's written in textbooks much more clearly and authoritatively than I could.

Search in a physiology book or endocrinology book. "Aromatase" will lead you in the right direction. Now go amaze your friends with your new found knowledge:thumbup:
 
of course there are multiple factors involved in determining how tall an individual will be, i think when you are dealing with any question in science, medicine etc, there will be a highly complex and invovled answer. However, to the OP, castrated boys WILL typically be taller, due to the lack of testosterone. Other hormones, genetic factors, etc., will still play a role, but the factor associated with plate closure in a castrated boy will be the absence of testosterone; the E:A ratio will be altered b/c of the loss of testosterone. Although in a normal individual it is not the main factor in plate closer, it will play a large role in someone lacking the hormone (or receptor for the hormone).

how did we get from castrated boys height to Jamie Lee Curtis?...freakin hormones
 
castrated boys WILL typically be taller, due to the lack of testosterone.

I still disagree with this summation.

With this logic, women would be taller than the average male b/c they have less testosterone. Continuing with this logic, individuals with androgen insensitivity would be much taller than the average male (The NBA would be dominated by 7 foot models with large perky breasts:laugh:). The whole reason I brought up the Jamie Lee Curtis point was to discredit this line of reasoning.

You also don't seem to realize (or recall) that testosterone 1)derived from adrenal androgen, 2)derived from peripheral conversion of estrogen is still present in eunuchs. So they don't lack testosterone, rather their E:A ratio is shifted higher. The ratio is increased further b/c estrogen stimulates the production of steroid binding globulin (SBG) which further diminishes available testosterone.

Testosterone is a big reason men are taller than women . The right amount of testosterone in puberty triggering long bone growth while at the same time having less available estrogen to trigger epiphyseal plate closure.

Finally, to be completely correct...we should really be referring to dihydrotestosterone (DHT) which is the active form of the hormone responsible for all the positive (penile development, bone growth, facial hair) and negative (male pattern baldness, prostatic hyperplasia, back hair) effects.

Testosterone ---> DHT (by 5-alpha reductase)
Testosterone ---> Estrogen (aromatase)
Estrogen ---> Testosterone (aromatase)
 
the factor associated with plate closure in a castrated boy will be the absence of testosterone; the E:A ratio will be altered b/c of the loss of testosterone.

This is completely wrong. Sorry...not trying to be mean Buster, but I'm gonna use this to clarify further for those still interested.

The absence of gonadal sex steroids (testosterone, estrogen) is not of major importance in prepubertal growth...meaning, even without testosterone they will be roughly the same height as their (prepubertal) peers. The pubertal rise in gonadal and adrenal steroids is responsible for the sharp increase in growth rate. Much of the skeletal growth caused by estrogen (even in males) is mediated through the stimulation of hGH and IGF1.

BusterDO said:
A similar syndrome that this is seen in is Klinefelter's syndrome - XXY - the boys are taller...

This again is wrong:rolleyes: You were correct in stating they have longer extremities...but they are NOT generally taller. As I stated in an earlier post, gonadal development is inversely related to upper and lower extremity growth and this is the protypical example...small balls and long legs. To be absolutely correct (and shine on rounds) arm span greater than height is what we are really talking about when referring to eunuchoid proportions. Again, the clinical manifestations of klinefelter syndrome and androgen deficiency vary considerably from patient to patient.

The pathogenesis of abnormal growth in Klinefelter syndrome is presently unclear. It is well known that androgen deficiency is responsible for the "arm span > height" growth pattern, however, patients with Klinefelter syndrome have increased growth of the lower extremities > trunk and upper extremities and do not always have eunuchoid proportions.

Source:Basic and Clinical Endocrinology (Lange 2007)


Caribstudent07and DrBubbles you guys are correct:thumbup: Don't let misinformation confuse you...and always take what you read on here with a grain of salt and consult a text.
 
Thanks BlackNDecker...didn't feel picked on. I appreciate the clarification and even made corrections in some of my class lecture notes.:thumbup:
 
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