There seems to be a 4 year old that is displaying adult musculature, or at least muscle mass that is well above normal. It turns out that he has a mutation in the gene for myostatin, a protein that shuts off muscle growth. The article can be found here
This message has been edited by Loudmouth, 06-25-2004 03:47 PM
Yeah, this article looked pretty interesting, but I wonder how much media-hype is involved here?
Two parts of the article I found interesting:
quote:In the mother, one copy of the gene is mutated and the other is normal; the boy has two mutated copies. One almost definitely came from his father, but no information about him has been disclosed. The mutation is very rare in people.
The boy is healthy now, but doctors worry he could eventually suffer heart or other health problems.
I suppose only time will tell if this mutations has no ill effects, but if it doesn't, how will this affect that old creationist argument? The one that goes: "We have never witnessed a mutation that was beneficial to the organism..."
I also wonder if he is really the first person to have this mutation. From the article it appears his mother and father both have a copy of the mutated gene; he has two copies. It's possible he's not unique (which goes back to my media hype question), even the article refers to the mutation as 'rare,' not unique.
quote:I also wonder if he is really the first person to have this mutation. From the article it appears his mother and father both have a copy of the mutated gene; he has two copies. It's possible he's not unique (which goes back to my media hype question), even the article refers to the mutation as 'rare,' not unique.
The article claims that this is the first DOCUMENTED case. There very well could have been other people with this disease. It would make an interesting population study if the family is from an area that tends to marry within the community. Being that both the mother and father carry the mutation seems to point in that direction. Either that, or the mutation is widespread by very rare, hence the first time there has been a homozygous mutant (ick, couldn't think of a better way to phrase it, go X-Men).
What is also curious is that you only need one copy of the myostatin protein to prevent the condition. Also, I didn't mean to propose that this could be a beneficial mutation, only that one mutation can make quite drastic changes to body morphology, although arguably a developmental change in this case.
Right. I read the 'documented' part and it still didn't register. Duh.
Population study would be very interesting. I wonder if the mutation is dominant?
True, the mutation may not end up being beneficial, but it appears that this kid's uncles are uncommonly strong as well - of course who knows if that is just an unqualified observation by the journalist - so maybe one copy of the mutation would be beneficial on its own.
If, ultimately, this does turn out not to have any negative side effects (like Marfan's Syndrome say), then how long do you think it will be before we see genetic tinkering for prospective athletes? Why mess with HGH when you can change the genes themselves.
For me, one of the more interesting things is that this is a recognizable mutaion. Whether or not it is evolution will depend on whether it expands through a population and whether or not that segment of the population survives better.
quote:Interesting. Do you know if this would work if an adult began taking this type of chemical? Or does it only work at a certain point in the organism's development?
I would think that adult muscle development and pre-adolescent muscle development are under the control of myostatin. That is, you can add muscle mass throughout your life barring illness. So yes, I think something like this would probably work. However, I haven't researched myostatin very closely but I do believe that it is a protein which would make it difficult to create a protease that selectively destroyed myostatin but left the rest of the proteins in the human body unaltered. The best bet would be a small biomolecule that bound the active site of myostatin or to its receptor without triggering conformational changes in the receptor.
quote:In the old days, this kid would probably have mate with every woman in town and have no competition at all, since he could beat the living crap out of all his competitors.
But he would be at a disadvantage if he was unable to run fast enough or far enough to kill game. Even though he could "beat up the competition" he still wouldn't be able to feed his family. Although, he could start stealing . . . many strategies exist. However, there seems to be cardiac problems in connection with larger muscle mass which might end up putting this mutation in the detrimental column.