http://www.grg.org/r...yflickChapt.htm
People here may not agree with Hayflicks opinions about life extension but is this a good article to use when reading about aging?
Posted 27 June 2008 - 09:31 PM
Posted 27 June 2008 - 09:46 PM
Posted 30 June 2008 - 12:57 AM
Posted 30 June 2008 - 02:59 PM
...the approximate 25-year increase in life expectancy that occurred in the United States from [1900 - 2000] will be impossible to achieve in the 21st Century, if ever.
The only known way that the aging process can be circumvented in inanimate objects is by the replacement of old parts with new. Although parts replacement is possible in organisms including humans, the only certainty is that replacing old organs with young organs increases life expectancy. This result is no different from the many other medical, hygienic, and safety procedures that have been implemented to avoid or postpone death. None treat the fundamental process of aging.
Posted 30 June 2008 - 03:21 PM
Posted 30 June 2008 - 05:23 PM
LH's discovery of cell division limits looks more and more ordinary when you read some of the inane stuff that he writes like:
"Aging is not a programmed process governed directly or entirely by genes. It is mostly those who work with invertebrates who have interpreted their findings to involve genes in the aging process. They have failed to appreciate that the genes that they have identified are involved in longevity determination and not in aging."
Conboy et al and their work on heterochronic parabiosis (in mammals) have pretty much blown that one out of the water.
Posted 30 June 2008 - 08:36 PM
Posted 30 June 2008 - 08:42 PM
Posted 30 June 2008 - 09:13 PM
Posted 30 June 2008 - 11:34 PM
Posted 01 July 2008 - 02:18 AM
Edited by HYP86, 01 July 2008 - 02:20 AM.
Posted 01 July 2008 - 10:19 AM
LH's discovery of cell division limits looks more and more ordinary when you read some of the inane stuff that he writes like:
"Aging is not a programmed process governed directly or entirely by genes. It is mostly those who work with invertebrates who have interpreted their findings to involve genes in the aging process. They have failed to appreciate that the genes that they have identified are involved in longevity determination and not in aging."
Conboy et al and their work on heterochronic parabiosis (in mammals) have pretty much blown that one out of the water.
But aging isn't caused by "death genes" in humans? It is not evolutionary intent but evolutionary neglect........
Posted 01 July 2008 - 04:29 PM
LH's discovery of cell division limits looks more and more ordinary when you read some of the inane stuff that he writes like:
"Aging is not a programmed process governed directly or entirely by genes. It is mostly those who work with invertebrates who have interpreted their findings to involve genes in the aging process. They have failed to appreciate that the genes that they have identified are involved in longevity determination and not in aging."
Conboy et al and their work on heterochronic parabiosis (in mammals) have pretty much blown that one out of the water.
But aging isn't caused by "death genes" in humans? It is not evolutionary intent but evolutionary neglect........
Evolutionary neglect should see a stochastic disruption of physiological processes. Evolutionary intent, on the other hand, would proceed along a well defined trajectory (development and aging).
There are many death genes in humans and all life forms. The most obvious ones are those that cause apoptosis. A process that occurs with great frequency during development.
Apoptosis is a finely orchestrated event, i.e, it is programmed to respond according to a specific range of stimuli. Consider the phenomenon first described by the author of the paper being discussed (the Hayflick limit). With each cell division there is the ticking of a molecular clock. When the clock reaches a certain time, apoptosis is triggered. It is not hard to see the evolutionary intent on a single cell level. But what about an entire organism?
Aging, is also finely orchestrated. It is brought about by a systematic dampening down of stem niches that result in a reduction of regenerative potential permitting metabolic byproduct accumulation to reach toxic concentrations which eventually overwhelm tissues and organs. Conboy et al have shown that this dampening down effect is reversible. This would not be possible unless the dampening process was controlled - there are specific steps that stem cell niches follow as part of their aging subroutine.
Posted 01 July 2008 - 04:47 PM
LH's discovery of cell division limits looks more and more ordinary when you read some of the inane stuff that he writes like:
"Aging is not a programmed process governed directly or entirely by genes. It is mostly those who work with invertebrates who have interpreted their findings to involve genes in the aging process. They have failed to appreciate that the genes that they have identified are involved in longevity determination and not in aging."
Conboy et al and their work on heterochronic parabiosis (in mammals) have pretty much blown that one out of the water.
But aging isn't caused by "death genes" in humans? It is not evolutionary intent but evolutionary neglect........
Evolutionary neglect should see a stochastic disruption of physiological processes. Evolutionary intent, on the other hand, would proceed along a well defined trajectory (development and aging).
There are many death genes in humans and all life forms. The most obvious ones are those that cause apoptosis. A process that occurs with great frequency during development.
Apoptosis is a finely orchestrated event, i.e, it is programmed to respond according to a specific range of stimuli. Consider the phenomenon first described by the author of the paper being discussed (the Hayflick limit). With each cell division there is the ticking of a molecular clock. When the clock reaches a certain time, apoptosis is triggered. It is not hard to see the evolutionary intent on a single cell level. But what about an entire organism?
Aging, is also finely orchestrated. It is brought about by a systematic dampening down of stem niches that result in a reduction of regenerative potential permitting metabolic byproduct accumulation to reach toxic concentrations which eventually overwhelm tissues and organs. Conboy et al have shown that this dampening down effect is reversible. This would not be possible unless the dampening process was controlled - there are specific steps that stem cell niches follow as part of their aging subroutine.
Posted 02 July 2008 - 02:17 AM
I've not heard about this
Any other studies than Conboy backing this up?
Posted 02 July 2008 - 02:23 AM
Posted 02 July 2008 - 09:09 AM
I've not heard about this
Any other studies than Conboy backing this up?
Posted 02 July 2008 - 09:28 AM
It is the conclusion implied by the authors of the Nature paper.mygene's assertion that there is a controlled aging subroutine is speculation on his part.
HSCs = hematopoietic stem cells - these reside in bone marrow. Conboy looked at satellite cells which is a muscle stem cell. Her work is associated with these types of cells. By effectiveness you are meaning she reversed their aging phenotype.The Conboy research shows that gene expression levels can be adjusted such that HSCs effectiveness can be improved by tinkering with particular pathways.
Is a program a sequence of instructions?It says nothing about an aging program that is being followed.
What Conboy did was reverse this.There are several recent papers that demonstrate that stem cells show signs of aging and loss in fidelity.
No doubt. However, it is difficult to conceive of many pathologies that would manifest in a sufficiently youthful cellular environment, i.e. an environment where stem cells did not exhibit aging.There is much more to aging than declining stem cell activity though.
Posted 02 July 2008 - 06:38 PM
Posted 03 July 2008 - 10:34 AM
Firstly, separate the term program from aging. It's important to appreciate that many of these aging processes, just like developmental ones, appear to follow a program. By program I mean changes that can be mapped as a distinct pattern able to be manipulated or reversed (subject to technical capacity and detailed knowledge of that pattern).By your criteria, every molecular change in an organism is programmed aging as they are all effectively just precursors to the ultimate changes that have deleterious changes.
If something appears to follow a program then from an evolutionary consideration it follows that such a program confers a selective advantage. If you read Dawkins' Selfish Gene it may spare you the hypothesizing. He explains it pretty well. Single sentence summary: fitness of the gene pool has a higher priority than the fitness of the organism.Programmed aging implies an intent to bring about an aging phenotype which is characterized as a lower chance of an organisms survival.
If so, there would be evidence of satellite cell transformation (tumorigenesis), which was not the case. Also helpful to consider was that satellite cells in young models were directed to an aging phenotype by a single growth factor and when this factor is inhibited in old cells it rejuvenates repair function.This particular gene expression change could have easily been for other functional goals, e.g. to suppress oncogenes or proto-oncogenes rather than to guide the organism towards one with a lower chance of survival in a stepwise fashion.
Posted 03 July 2008 - 07:44 PM
Firstly, separate the term program from aging. It's important to appreciate that many of these aging processes, just like developmental ones, appear to follow a program. By program I mean changes that can be mapped as a distinct pattern able to be manipulated or reversed (subject to technical capacity and detailed knowledge of that pattern).By your criteria, every molecular change in an organism is programmed aging as they are all effectively just precursors to the ultimate changes that have deleterious changes.
If something appears to follow a program then from an evolutionary consideration it follows that such a program confers a selective advantage. If you read Dawkins' Selfish Gene it may spare you the hypothesizing. He explains it pretty well. Single sentence summary: fitness of the gene pool has a higher priority than the fitness of the organism.Programmed aging implies an intent to bring about an aging phenotype which is characterized as a lower chance of an organisms survival.
If so, there would be evidence of satellite cell transformation (tumorigenesis), which was not the case. Also helpful to consider was that satellite cells in young models were directed to an aging phenotype by a single growth factor and when this factor is inhibited in old cells it rejuvenates repair function.This particular gene expression change could have easily been for other functional goals, e.g. to suppress oncogenes or proto-oncogenes rather than to guide the organism towards one with a lower chance of survival in a stepwise fashion.
Posted 04 July 2008 - 11:33 AM
So you mean aging is a natural developing process just like puberty?
Posted 07 July 2008 - 01:10 AM
From an evolutionary perspective it is energetically favorable to gradually shut down the regenerative capacity in an organism rather than sustain high levels of molecular activity to maintain stability.
After all, once the genes have been passed along and recombined there is no pressing need to keep the organism alive for much longer.
Edited by maestro949, 07 July 2008 - 01:40 AM.
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