Reverse aging? Scientists find way to make old muscles young again

Originally posted by AfterInfinity
reply to post by daskakik

 

Slowing down the cells slows down the metabolism. Slowing down the metabolism means less energy.

Staying young = less energy.

Does anyone here think this is a worthwhile trade?

The tradeoff you encounter with this probably will mean reduced liver function. This is why I discontinued studying this. Maybe you will save the muscles but reducing liver function screws the organs. We can't be doing that, too much of that is being done with medications now. They are treating symptoms, not curing diseases. I have a slow metabolism and my life expectancy should be high. The problems with having a slow metabolism are also a pain in the butt. I had my share of metabolic problems throughout my life from eating things that others were eating with no ill effects.

Ya it's actually called "A dumbell" ..... who knew!!!!

I'm quite young.. approaching middle 30's (feel old sometimes, but that's just kids), but I have seen a several people get old and a couple die of old age (a few more of cancer, in fact dying of old age almost seems an achievement). After seeing aging in action, what I'm starting to suspect is that loneliness and activeness play equal parts.
It seems to me that those who stay active and stave off loneliness age later in life than anybody else. Then again, it could be that they are able to remain active and social due to not aging until later, but I don't suspect that.

To the point:

use it or lose it.

where there's a will there's a way


what is life....


as we are!

Originally posted by TDawgRex
reply to post by sonnny1

 

I have always believed that people allow pain to immobilize themselves thoughout life and it gets worst as we age.

Quite true, you don't stop doing things because you get older, you get older because you stop doing things.


Not sure about this new research though because it involves taking medicine and with that comes side effects.

reply to post by TDawgRex

I don't think it's any mystery that if you live a sedentary life your muscles will atrophy. Soreness from exercise or activity is your muscles healing/rebuilding and you should stretch to feel better not rest. I think most people don't realize that. If you don't use it, you lose it.

As all in the universe: Use it or loose it.

Life is movement if you go that way life will keep on showing. My old man used to be like a mummy, at 85 he started to lift weights, do stretch, walking around and basically he started to be in charge of himself instead of being pet and treated like a veggie.

Treat a man like a dumb and he will respond that way, Treat him like a god and he will respond the same way.

This makes me wonder in which way do government, media and TPTB treat humanity? We respond very well to that insinuation they make.

Many of you seem to be missing the point. It isn't about normal muscle maintenance it is about muscle loss in the elderly. Sure use it or lose it is part of it but the problem that they have identified is that even if they, the elderly, use it they don't regain it because their body doesn't have what it had available to it when they were in their 20s.

Actually I don't see big pharma getting behind this because it would probably gouge into sales down the line. This would be preventive medicine and that usually hurts the bottom line

There is a reason for our advancement in knowledge of science, medicine and space in this short span of human history compared to the civilisation since the dawn of mankind.

We are being prepared for evolution, into space.

Most planets we see are often inhospitable and remote. It will take Terraforming to create another Earth nearby. Our moon, mars and a few other planets would be possible. Terraforming takes time. It will need mankind to be able to live longer to see the fruits of his labour.

There is more to come, if we evolve in peace. If conflicts will not cease, then all would have been in vain, for none of us will be left alive.

Originally posted by daskakik

Originally posted by TDawgRex
I think that is the idea here.

Stay active.

That is not the idea that I got from the article. In fact, what it seems they are going to try to do is slow down the cells. So, it would seem to be as blackmarketeer said, if the cells have a finite number of divisions them having them divide more often should be bad.

edit on 28-9-2012 by daskakik because: (no reason given)

The cell end cap (telemere) gets smaller every time a cell divides. As an average, telemere length can be looked at for lifespan - the shorter the telemere, the closer to the end of the life. However, there are things which shorten them at more rapid rates, such as smoking, over-exercising, excess stress, cured meats, trans fats. There are also supplements which can be taken to help keep the length and even regrow to an extent. Read this guy's blog - he explains a lot even though you might have to dig through it to find what you are searching for and do a little research on your own.

www.anti-agingfirewalls.com...

reply to post by mjfromga


Thanks but that is not what this article is about. This article is about a protein which regulates the division itself, and how division tends to go unchecked in old age, not how that division affects telomeres.

If humanity survives itself it is inevitable one day science will come up with ways to control the bodily processes in such a way to extend the lifespan into thousands of years. Afterall everything is already there in the body from birth to grow the cells needed, it should only be a matter of stimulating certain parts so DNA will 'think' it needs to build the same cells again as it did while being a baby. Except the brain ofcourse or at least the memory cells which are irreplaceable but even memory can be recorded to allow for renewal. Although such a process if ever invented might raise the question whether the price for immortality is worth it, having the brain renewed but losing many memories and so experiences with only a basic character remaining.

reply to post by daskakik


But, both have to do with cell division and longevity. Since the one technology is not available for human benefit, people could look at ways which can benefit them. That is why I attached the blog. If you would like to search, you will see this is not a new topic but has been around a few years - Klotho, FGF(23) et.el. Cells divide. There is a finite amount of cell divisions. With each division, the telemeres shorten until they are considered old and finally die. When this happens, we die. From the article, it appears that in aging muscles, the "fixer" cells don't remain dormant but become activated unnecessarily and divide causing them to die at a faster rate. The cells have more of this protein. Why do they have more of this protein? That is the question. If we can keep our cells "young" as per telemere length, will that affect the protein level and keep it low? After all, if our bodies don't consider our cells old (even if we are more than a little long in the tooth, age-wise), wouldn't they also have less of this protein? Just a thought, but maybe I'm adding 2 + 2 and getting 5.

Originally posted by mjfromga
reply to post by daskakik

 

But, both have to do with cell division and longevity. Since the one technology is not available for human benefit, people could look at ways which can benefit them.

They both do have to do with cell division and longevity but at different parts of the process.

I think both technologies are not available.

The cells have more of this protein. Why do they have more of this protein? That is the question. If we can keep our cells "young" as per telemere length, will that affect the protein level and keep it low? After all, if our bodies don't consider our cells old (even if we are more than a little long in the tooth, age-wise), wouldn't they also have less of this protein? Just a thought, but maybe I'm adding 2 + 2 and getting 5.

I think you are looking at one way to attack the problem while the doctors in the article are looking at another way. One is to extend telomeres so that the protein is kept in check and the other is to administer SPRY2 to keep FGF2 in check. They would both be doing the same thing but I'm not sure which will be available first. The article states that administration of FGF suppressors is already available, although not administered like this, so that is probably going to be the first.

The blog you linked states that we are still a ways off from achieving the type of longevity that the blog discusses.