Information loss doesn't happen in parallel at the same rate in all molecules.
I'm not suggesting that it does. On the contrary, my point was to illustrate that biomolecules have a tendency
not to fall to pieces in the same fashion that other structures do. Hayflick, for example, often will use the metaphor of a car and how it inevitably falls to pieces - but this is a fundamentally innapropriate analogy since biomolecules appear to prefer higher order structures.
DNA does not have a reference to compare to if it is mutated, thus it is in a fundamentally different situation than the other biological molecules.
It does have a reference so long as the damage is only on one strand. If it is on both then it is a matter of the effectiveness of innate repair systems of the cell. D. radiodurans has remarkable repair abilities and is an example of just how much repair is possible. There is also the possibility that at least a portion of the genome always exists in RNA form as evidenced by some very recent findings in arabidopsis genetics hence providing another reference point. More importantly, however, is that loss of genomic integrity does not appear to manifest in humans until after puberty and this is of paramount significance suggesting that endogenous genomic maintenance until this time is sufficient to overcome any attrition.
The rate of corruption is effected by evolution. Its inevitability, given our design (uni-directional flow of information), is not.
I'm not following what you mean here particularly in the second sentence.
It is not possible to obviate mutations through repair mechanisms.
If by obviation you mean to prevent and if by mutation you mean a molecular lesion in DNA that can lead to a base change then I cannot follow your reasoning. DNA lesions are occuring all the time in the cell, in some cases as many as a few hundred thousand per 24 hours. They are constantly repaired. If you are referring to damage that has escaped repair mechanisms and has become integrated in the genome and is able to propagate with cell division, then repair mechanisms no longer are relevant.
Is it possible to slow DNA mutations in the somatic body by orders of magnitude? Maybe. How far are we from being able to do that? I don't know. Would it cure aging? No.
We observe tremendous variation in nature in the ability of cells to deal with repairing DNA damage - by orders of magnitude. I'm uncomfortable with a scholar making an absolutist statement such as: "Would it cure aging? No". I think you meant unlikely. Otherwise you must be privy to knowledge that is outside of public domain to be so convinced that DNA mutations have no relevance to aging!
We've been over this before though. If you have a mechanistic explanation for how DNA could maintain its information content with 100% fidelity without a higher level reference, then please explain it in detail.
A detailed explanation I cannot offer but the general theory is eminently straight forward: it is a two pronged strategy that would involve upregulation of the "accurate" DNA repair mechanisms to deal with repair as soon as damage has occured and upregulation of antioxidant scavengers and organelle turnover signaling pathways to minimize the production of DNA damaging molecules. This methodology would, of course, not ensure 100% fidelity but would increase it sufficiently to induce measurable changes in cell lifespan and robustness. If genomic instability is related to aging, and I am convinced that it is, then one should observe a change in the lifespan of an organism that has had such genetic modifications.
The question that I have Prometheus, and which I have not seen a satisfactory answer for, is why the germ line must be coupled with the somatic line? This is the basic challenge that was brought up by Aubrey in one of the SENS threads. I think we all agree that evolution is a very creative and resourceful bio-engineer. Why then, didn't it just figure out a way to separate the germ line from the somatic line, and allow the germ line to maintain a higher degree of mutability?
We observe a great deal of conservation in many genetic mechanisms not merely across cell types within a single organism - such as between stem and somatic cells - but across species as diverse as single celled to multicelled organisms. It stands to reason that fundamental genomic DNA repair and other genomic stability mechanisms across eukaryotes are similarly conserved - and this is precisely what we observe. We also observe that cells carry on their processes in a fashion that expends the least amount of energy, hence it is unlikely that a cell will devise a novel mechanism for something that, for example, it can already do by way of altering regulation. These are the two pillars - conservation and economy - on which this hypothesis is based. In time, and with the aid of transcription studies where we can measure the difference in which genes are active between stem and somatic cells in the context of genomic stability I am confident that this theory will receive more experimental support. In the interim I must avail myself to deductive reasoning and the differences in gene expression as we presently understand between stem and somatic cells. We see that somatic cells have a great many genes switched off that are associated with growth and repair, thus it is in fact less likely for a stem cell to undergo damage (or be subject to mutation) than it is for a somatic cell.
