I was doing research for adipose derived stem cells when I read something from the Wikipedia article on Adipose Tissue which made me see that there might indeed be a connection between the issue of childhood obesity, an earlier onset of puberty, and possible effects of stunted growth leading to shorter final height.
It seems that adipose tissue, which is what our fat is greatest peripheral source of aromatase in both males and females.
Since we know that having a lot of aromatase means more conversion into estrogen, it would means that there are going to be higher levels of estrogen, which is something which we have always said for the developing child with open growth plates is a bad thing.
I remember reading years ago about the fact that “fatter” than average children would start puberty earlier in age than children who are not as overweight. The journalist who wrote the article would talk about how the over excess of food and eating behavior caused an increase in the amount fo hormones going through the body.
This idea seems to have some validation when we realize that adipose tissue is supposed to be the biggest source of aromatase in the bodies of females and males.
Aromatase would convert any type of hormones that can be converted into estrogen or estrogen like compounds which would cause the initial spark in physical development starting puberty. As we know from our research, an earlier onset of puberty usually means an earliest onset of complete endochondral ossification closure. It doesn’t always have to mean that earlier puberty means earlier growth plate closure, but there is a positive correlation.
This would then imply then that people who have more adipose tissue probably have a higher level of aromatase in their blood stream than a person of similar age with different tissue composition.
We know that females are supposed to have higher fat composition levels than males on average. This is supposed to be because the female reproductive organs and hormones require more fat than the male reproductive organs and hormones. If the fat percentage in the female body falls below a certain amount, their fertility rate would actually drop. This is often seen when female bodybuilders start to take supplements to make their body fat percentage to drop. They develop masculine and male physiques and traits, increased muscularity, muscle leanness, etc. In addition, their fertility also sees strange changes.
It could be that from the higher body percentage fat in females, that is one of the main reasons why they go through puberty as a an earlier age than men. This also leads to females being on average shorter than men.
So the correlation goes…
Overweight child or Obese Child —> Increased levels of fat to overall body composition —> The fat is composed of adipose tissue —> The adipose tissue is the main peripheral source of aromatase —> The increased aromatase causes more estrogen to be made from aromatization —-> The extra estrogen causes puberty to start earlier —> There is less years for natural growth —-> Earlier onset of bone maturity leading to a shorter final adult height
The correlation may be weak, but I would guess that the correlation is still positive.
From another source, the USMLE Forum, a post did ask about which places aromatase seem to come from, besides just the adipose tissue.
Other locations where the aromatase seems to originate are….
- Granulosa Cell –
- Sertoli Cells –
- Leydig Cell –
For the sertoli cell someone writes…
“…aromatase is present in sertoli cells ….here it converts testosterone to estradiol…one third of estradiol in men comes through this, remainder comes by aromatase in adipose tissue..
leydig cells make testosterone that is made from cholesterol. this testosterone is secreted and taken up by sertoli cells.”
For the leydig cell something states…
“…i just wanted to say that leydig cells are also capable of producing aromatase in klienfelters synd….but goljan book says hyperplasia of leydig cells and incresed aromatase there caused by increased FSH….so increase conversion of testosterone to estrogen…reason for increased estrogen in kleinfelters”
The discussion seems to reach a really interesting ending by the post by someone named JonBC
“Testicular production of estrogen is poorly understood. The Sertoli cells manufacture estrogens during fetal and neonatal life. However, beginning at puberty and continuing through adulthood the site of estrogen synthesis shifts to the Leydig cell. The Leydig cells express high mRNA and protein levels of the CYP19 (aromatase) enzyme. The mechanisms regulating the site of estrogen synthesis, and the shift of estrogen production between Sertoli and Leydig cells, are completely unknown.”
Analysis:
This may be a good breakthrough for the research because this is the first place where I finally realize that apparently the location of where estrogen is produced actually changes from when the human is in develop in the uterus and when the person is going through the stages of puberty.
This might explain why estrogen levels cause the onset of puberty. Let’s look at what the person says…
- Sertoli Cells – manufacture estrogen during fetal and neonatal life.
- Leydig Cell – site of estrogen synthesis during puberty and throughout adulthood.
It seems that the leydig cells express high mRNA and protein levels of the aromatase enzyme, which goes by the name CYP19.
So for the height increase seeker, does that mean that the spark in every person’s development, which causes them to go from Sertoli Cell to Leydig Cell production of estrogen is what causes this entire thing???
The person does state that the mechanism of how estrogen production is shifted from Sertoli Cell to Leydig Cell is not known at this time. This may be the very key that we should be looking for. This may be the key to everything. If we can somehow break the process of the shift, by preventing the Leydig Cells from ever given the chance to produce estrogens, since they are the cells that really have the high mRNA and protein production of the aromatase, then maybe we can completely hold off puberty until we want to.
This would be the one step in the entire growth process where we can manipulate and modulate slightly to control our growth rate and how long we would wish to grow. Remember, if we can control at which age we wish to start puberty, we can control the amount of time we have left to grow, which means that we can continue to grow as much as we want, at least theoretically.
