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How Does Growth Hormone Function?
Question: Hello , I have a general query about growth hormone.
I understand its present throughout life even while we are still in uterus, and after being born. So in the rapid growth of baby after being born, does GH contribute to growth in first 6 months after being born?
I understand its present throughout life even while we are still in uterus, and after being born. So in the rapid growth of baby after being born, does GH contribute to growth in first 6 months after being born?
Brief Answer:
Growth phases and role of GH
Detailed Answer:
Hello,
Good day.
Since i have been answering most of your questions, i didnt attempt to answer your new question in the morning. But decided to answer it now as i found your question unanswered until now.
Growth is a beautiful process pre programed by our genes which is orchestrated by GH with contributions from other hormones.
Growth has 3 phases
1) Infancy phase: which starts at mid pregnancy and rapidly decelerating until 4 years of age,
2) Childhood phase: Slowly decelerating growth during early adolescence.
3) Puberty phase; contributes to adolescent growth spurt.
Before birth the average growth is around 1 to 1.5 cm per week and then at mid pregnancy, it reaches up to 2.5 cm per week and falls to 0.5 cm per week just before birth.
An average 15 cm per year is the growth during first 2 years of life. Then it slows down to 5- 6 cm per year during childhood until puberty.
The growth during all these phases and in puberty is mainly mediated by growth hormone with significant contributions from Thyroid hormones, sex hormones, parathyroid hormones etc.
So to answer your question, yes GH contribute to growth in first 6 months after birth and beyond
Regards
Binu
Growth phases and role of GH
Detailed Answer:
Hello,
Good day.
Since i have been answering most of your questions, i didnt attempt to answer your new question in the morning. But decided to answer it now as i found your question unanswered until now.
Growth is a beautiful process pre programed by our genes which is orchestrated by GH with contributions from other hormones.
Growth has 3 phases
1) Infancy phase: which starts at mid pregnancy and rapidly decelerating until 4 years of age,
2) Childhood phase: Slowly decelerating growth during early adolescence.
3) Puberty phase; contributes to adolescent growth spurt.
Before birth the average growth is around 1 to 1.5 cm per week and then at mid pregnancy, it reaches up to 2.5 cm per week and falls to 0.5 cm per week just before birth.
An average 15 cm per year is the growth during first 2 years of life. Then it slows down to 5- 6 cm per year during childhood until puberty.
The growth during all these phases and in puberty is mainly mediated by growth hormone with significant contributions from Thyroid hormones, sex hormones, parathyroid hormones etc.
So to answer your question, yes GH contribute to growth in first 6 months after birth and beyond
Regards
Binu
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Thank you Dr XXXXXXX for answering. I want to continue on theme of development, especially testosterone effects on genital and other development.
Do androgens in 'mini puberty' affect other non-genitalia tissue in the male baby? for example voice tissue, hair follicle tissue also always contain androgen receptors?
Best Regards
XXXX
Do androgens in 'mini puberty' affect other non-genitalia tissue in the male baby? for example voice tissue, hair follicle tissue also always contain androgen receptors?
Best Regards
XXXX
Brief Answer:
Hi
Detailed Answer:
Hi,
The main purpose of XXXXXXX puberty is for proliferation of sertoli cells which will form the bulk of testes later in life. The sertoli cells and germ cells proliferate and under go division and then they remain sort of arrested phase until the Puberty.
Adult level Testosterone concentration can be seen in XXXXXXX puberty and this cause genital development and some lengthening of penis. But voice change, vocal cord enlargement and actions on hair follicles doesn't happen until puberty. Androgen exposure during intrauterine life and in XXXXXXX puberty also plays a role in masculinization and gender identity of the growing child.
Regards
Binu
Hi
Detailed Answer:
Hi,
The main purpose of XXXXXXX puberty is for proliferation of sertoli cells which will form the bulk of testes later in life. The sertoli cells and germ cells proliferate and under go division and then they remain sort of arrested phase until the Puberty.
Adult level Testosterone concentration can be seen in XXXXXXX puberty and this cause genital development and some lengthening of penis. But voice change, vocal cord enlargement and actions on hair follicles doesn't happen until puberty. Androgen exposure during intrauterine life and in XXXXXXX puberty also plays a role in masculinization and gender identity of the growing child.
Regards
Binu
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Yes but androgen receptors are always present in vocal tissue and hair follicle tissue....so too in the baby. So does the high androgens in 'mini puberty' still bind to these receptors or not in the baby?
Maybe yes and then strong feedback mechanism stops further binding perhaps? Can you advise if this is correct?
Thanks and Best Regards
XXXX
Maybe yes and then strong feedback mechanism stops further binding perhaps? Can you advise if this is correct?
Thanks and Best Regards
XXXX
Brief Answer:
Hi
Detailed Answer:
You are right. Androgen receptors are present in many tissues in body including bones. As i said earlier, many functions in our body are preprogrammed by genes. The timing of puberty and its sequences are also pre programmed. Androgen receptors are internalized to the tissues and come to the surface of the cell only when the "time comes". Until then androgens can not bind to its receptors in these organs.
Vocal cord and hair follicle changes occur only at puberty, not at minipuberty
Binu
Hi
Detailed Answer:
You are right. Androgen receptors are present in many tissues in body including bones. As i said earlier, many functions in our body are preprogrammed by genes. The timing of puberty and its sequences are also pre programmed. Androgen receptors are internalized to the tissues and come to the surface of the cell only when the "time comes". Until then androgens can not bind to its receptors in these organs.
Vocal cord and hair follicle changes occur only at puberty, not at minipuberty
Binu
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
so how so there has been cases of newborn babies born with a single strand of thick hair in pubic region. This was a result from maternal androgens...and suggests receptors do exist then also!
I just want proof that i had gonadal steroids, and these reacted/binded, even to a small degree, with my receptors .
I just want proof that i had gonadal steroids, and these reacted/binded, even to a small degree, with my receptors .
Brief Answer:
Hi
Detailed Answer:
Hello,
Good day.
Noted your point. You said it. There has been "cases" of new born babies born with few thick pubic hairs. Which means that is not normal. These are exceptional cases.
Androgen receptors are pesent at all times. But they can not bind to androgens because these receptors are not on the surface of the tissues. Androgen receptors coome to the surface of the tissues at appropriate age and then it binds to androgens so that changes happen in corresponding tissues.
What brings the receptors to the surface of tissues is nit clear, But it has been hypothesized that high circulating androgen levels itself cause the translocation of receptors to the tissue surface.
If you havent had responsive androgen receptors, then the androgen effect wouldnt have taken place in your body. If you have facial/chest/pubic/axillary hair and male type voice, good libido, and well formed male genitals, means that you had responsive androgen receptors. The androgen receptors in certain tissues are responsive to androgens in intrauterine life itself. Eg: Genitals. Penis and scrotal formation happen during intrauterine life.
If there is absence of androgen receptors and if there is insenstiviy of androgen receptors to androgens, male babies will be born with ambiguous genitalia. If you have a normal looking genital with no hypospadias, this means your gonads made enough androgens in intrauterine life and it binded with receptors.
There is a conditon called androgen insensitivity syndrome. In this, androgen receptors can not bind to androgens. So they have many female features than male features ( even though they are genetically males) and will be born with ambiguous genitalia
Regards
Binu
Hi
Detailed Answer:
Hello,
Good day.
Noted your point. You said it. There has been "cases" of new born babies born with few thick pubic hairs. Which means that is not normal. These are exceptional cases.
Androgen receptors are pesent at all times. But they can not bind to androgens because these receptors are not on the surface of the tissues. Androgen receptors coome to the surface of the tissues at appropriate age and then it binds to androgens so that changes happen in corresponding tissues.
What brings the receptors to the surface of tissues is nit clear, But it has been hypothesized that high circulating androgen levels itself cause the translocation of receptors to the tissue surface.
If you havent had responsive androgen receptors, then the androgen effect wouldnt have taken place in your body. If you have facial/chest/pubic/axillary hair and male type voice, good libido, and well formed male genitals, means that you had responsive androgen receptors. The androgen receptors in certain tissues are responsive to androgens in intrauterine life itself. Eg: Genitals. Penis and scrotal formation happen during intrauterine life.
If there is absence of androgen receptors and if there is insenstiviy of androgen receptors to androgens, male babies will be born with ambiguous genitalia. If you have a normal looking genital with no hypospadias, this means your gonads made enough androgens in intrauterine life and it binded with receptors.
There is a conditon called androgen insensitivity syndrome. In this, androgen receptors can not bind to androgens. So they have many female features than male features ( even though they are genetically males) and will be born with ambiguous genitalia
Regards
Binu
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Thank you Dr XXXXXXX for indepth valued advice.
What i meant was i want proof that the 'first time' my gonadal steroids reacted/binded with my receptors THROUGH MY DOING ONLY and not through oxandrolone causing increased gonadal steroids.
Basically i want the first reaction/binding of my gonadal steroids with its receptors to have happened BEFORE the oxandrolone treatment. Did this happen? To give you idea about my pubertal status before starting treatment, i was considered to be in 'very early puberty' , i had adrenarche maybe two years before starting the treatment. I was examined and said to be in XXXXXXX stage 2/3.
Please advise.
Best Regards
XXXX
What i meant was i want proof that the 'first time' my gonadal steroids reacted/binded with my receptors THROUGH MY DOING ONLY and not through oxandrolone causing increased gonadal steroids.
Basically i want the first reaction/binding of my gonadal steroids with its receptors to have happened BEFORE the oxandrolone treatment. Did this happen? To give you idea about my pubertal status before starting treatment, i was considered to be in 'very early puberty' , i had adrenarche maybe two years before starting the treatment. I was examined and said to be in XXXXXXX stage 2/3.
Please advise.
Best Regards
XXXX
Brief Answer:
Hello
Detailed Answer:
Hi XXXX
Good day and sorry for the delay.
I presume that you never had ambiguous genitalia at birth. If you have had normal appearing genitalia at birth ( normal appearing penis with opening at the tip and a well formed scrotum), then it means that your androgens made in intrauterine life have sucessfully bound to the androgen receptors. Thats why you had a normal apperaring genitalia at birth.
So the answer is YES. If you have a normal appearing genitalia at birth, your androgens have bound to its receptors.
You had adrenarche and the adrenal androgens have coupled with the androgen receptors. That is why your puberty progressed to stage 3. Please remember that adrenal androgens can not push puberty beyond stage 3 and then, testicular androgen production is required to progress further.
So you have had a normal genital formation and normal adrenarche even before oxandrolone treatment. This means that your androgens did the job and your receptors happily accepted those androgens.
Regards
Binu
Hello
Detailed Answer:
Hi XXXX
Good day and sorry for the delay.
I presume that you never had ambiguous genitalia at birth. If you have had normal appearing genitalia at birth ( normal appearing penis with opening at the tip and a well formed scrotum), then it means that your androgens made in intrauterine life have sucessfully bound to the androgen receptors. Thats why you had a normal apperaring genitalia at birth.
So the answer is YES. If you have a normal appearing genitalia at birth, your androgens have bound to its receptors.
You had adrenarche and the adrenal androgens have coupled with the androgen receptors. That is why your puberty progressed to stage 3. Please remember that adrenal androgens can not push puberty beyond stage 3 and then, testicular androgen production is required to progress further.
So you have had a normal genital formation and normal adrenarche even before oxandrolone treatment. This means that your androgens did the job and your receptors happily accepted those androgens.
Regards
Binu
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Dear Dr XXXXXXX thank you for your time in reading my question...and for the valued advice.
Earlier we discussed how hormone treatments induce puberty. The problem i have is the first testicular androgen production was caused by the hormone treatment. And these treatment-induced testicular androgens went on to act on various sites for the 'first time'.
This is what bugs me. The first time my gonadal androgens were coupled with receptors was due to external influence(hormone treatment)
Hope you can give valued advice.
Best Regards,
A very sad XXXX
Earlier we discussed how hormone treatments induce puberty. The problem i have is the first testicular androgen production was caused by the hormone treatment. And these treatment-induced testicular androgens went on to act on various sites for the 'first time'.
This is what bugs me. The first time my gonadal androgens were coupled with receptors was due to external influence(hormone treatment)
Hope you can give valued advice.
Best Regards,
A very sad XXXX
Brief Answer:
Hi
Detailed Answer:
Hi.
Good day.
As i mentioned earlier, your first testicular androgen production would have started in intrauterine life iteself under the influence of your own LH(produced by pituitary) and the placental hCG. Thats why you had a normal genitalia at birth followed by a XXXXXXX puberty. ( this XXXXXXX puberty led to increase in sertoli cells in testes. If u have a normal sperm count and testicular volume, your minipuberty also was normal)
Later in puberty, your hypothalamic gNRH neurons were bit lazy which was stimulated by oxadrolone.
Regards
Binu
Hi
Detailed Answer:
Hi.
Good day.
As i mentioned earlier, your first testicular androgen production would have started in intrauterine life iteself under the influence of your own LH(produced by pituitary) and the placental hCG. Thats why you had a normal genitalia at birth followed by a XXXXXXX puberty. ( this XXXXXXX puberty led to increase in sertoli cells in testes. If u have a normal sperm count and testicular volume, your minipuberty also was normal)
Later in puberty, your hypothalamic gNRH neurons were bit lazy which was stimulated by oxadrolone.
Regards
Binu
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Dear Dr XXXXXXX sorry for late reply. Thanks for all your time and valued advice.
Just a quick question.
You mentioned before higher test leads to binding to its receptors, and low test doesnt bind. But what is definition of high test? For example, during first nocturnal oncrease in LH and Testosterone, do these bind to receptors in the voice??
Secondly, during adrenarche i saw hair. Means i already had receptors in hair follicles......but during this same period, wouldve i had receptors in my voice also??
Just a quick question.
You mentioned before higher test leads to binding to its receptors, and low test doesnt bind. But what is definition of high test? For example, during first nocturnal oncrease in LH and Testosterone, do these bind to receptors in the voice??
Secondly, during adrenarche i saw hair. Means i already had receptors in hair follicles......but during this same period, wouldve i had receptors in my voice also??
Brief Answer:
Hi
Detailed Answer:
Hi XXXX
Welcome back.
Voice change typically occurs in puberty, say around 12-13 yrs. What i meant by" high" testosterone is the pubertal range testosterone. Yes, during the initial phase of puberty itelf some voice cracking occurs.. But the real change occur when testicular adrogen production starts. The androgen receptors in voice apparatus are dormant till then. Once the androgens attach to receptors in voice apparatus, it causes lenthening and thickening changing the pitch of voice.
Adrenarche is initiated by ACTH rather than LH/FSH. Adrenal tisue respond to ACTH rather than LH/FSH. During adrenarche, pubic and axillarry hair development starts. Bt as i said eaarlier, adrenal androgen concentration is not enough to push puberty beyond stage 3. Further thickening and progression of sexual hair need testosterone from testes itself. It is that time when the voice change occur too. Adrenal androgens are weaker compaared to testicular androgens.
I hope i have answered your question. I am on my annual vaccation from tomorrow. Internet may not be available continuously for few days. I am happy to answer more questions if you have any. Otherwise you may please close this query.
Regards
Binu
Hi
Detailed Answer:
Hi XXXX
Welcome back.
Voice change typically occurs in puberty, say around 12-13 yrs. What i meant by" high" testosterone is the pubertal range testosterone. Yes, during the initial phase of puberty itelf some voice cracking occurs.. But the real change occur when testicular adrogen production starts. The androgen receptors in voice apparatus are dormant till then. Once the androgens attach to receptors in voice apparatus, it causes lenthening and thickening changing the pitch of voice.
Adrenarche is initiated by ACTH rather than LH/FSH. Adrenal tisue respond to ACTH rather than LH/FSH. During adrenarche, pubic and axillarry hair development starts. Bt as i said eaarlier, adrenal androgen concentration is not enough to push puberty beyond stage 3. Further thickening and progression of sexual hair need testosterone from testes itself. It is that time when the voice change occur too. Adrenal androgens are weaker compaared to testicular androgens.
I hope i have answered your question. I am on my annual vaccation from tomorrow. Internet may not be available continuously for few days. I am happy to answer more questions if you have any. Otherwise you may please close this query.
Regards
Binu
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Dear Dr XXXXXXX
I still find it difficult to understand how steroids stimulate central puberty (at hypo level).
The gnrh is central nervous system controlled, so how can some mere weak steroids change this....it means our central nervous system dna and genes can be changed.
Secondly, i read some patients with congenital adrenal hyperlasia have central puberty very early on - but only in some of them. This is after prolonged exposure to high androgens....would weak steroids given at young age ie 7year old also lead to central puberty? I only ask as ive read steroids such as oxandrolone may induce puberty only in patients with testis volume of >4ml in other words speed up existing puberty.
My final question: are gonadotropins ALWAYS present in us throughout life in varying degrees, ie are extremely low levels still present even in juvenile phase?
Please could you advise on your return? Wishing you a nice vacation.
Regards,
XXXX
I still find it difficult to understand how steroids stimulate central puberty (at hypo level).
The gnrh is central nervous system controlled, so how can some mere weak steroids change this....it means our central nervous system dna and genes can be changed.
Secondly, i read some patients with congenital adrenal hyperlasia have central puberty very early on - but only in some of them. This is after prolonged exposure to high androgens....would weak steroids given at young age ie 7year old also lead to central puberty? I only ask as ive read steroids such as oxandrolone may induce puberty only in patients with testis volume of >4ml in other words speed up existing puberty.
My final question: are gonadotropins ALWAYS present in us throughout life in varying degrees, ie are extremely low levels still present even in juvenile phase?
Please could you advise on your return? Wishing you a nice vacation.
Regards,
XXXX
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