Of course, I mentioned that genetically speaking, it has gone downhill. The DNA message with the acumulation of mutation, loses its meaning and so eventually becomes 'incomprehensible' for the cells as we get older.
Genetically speaking, this is not a subjective statement.
I think you are wrong. Not in that mutations can accumulate but in the idea that as people get older their DNA becomes incomprehensible to their cells. In such an instance the cell would simply die in many cases. Alternatively such mutations could give rise to cancer, which certainly can cause death but doesn't sound quite like what you were saying.
The link between cellular senescence, when cells stop replicating due to telomere shortening or severe genetic damage, and aging is not well understood. The fact that a lack of telomerase, an enzyme that maintains telomere length, is associated with progeria is highly suggestive, but points more towards a failure in the stem cells specifically rather than a general cellular degradation. Telomeres are also not 'DNA message' in the way you describe. So one of the clearest genetic links to aging is not to any problem through mutation scrambling the message in DNA but rather an inbuilt limitation of cellular replication.
As I say this can be a result of genetic damage as well, but of major things like double strand breaks, not a slow accumulation of small mutations.
To reiterate, I don't disagree that the genome of individual cells in an organism will diverge over time as it ages from its original zygotic genome. What I disagree with is the assumption that this is a major mechanism involved in aging. For individual cells it might work this way and such cells would then apoptose, but the subsequent aging and degeneration of a tissue would be due to a failure to replace these cells, a breakdown in the stem cells. You might make a case that the failure of stem cells was due to accumulated mutations causing them to senesce.
So I think your model of aging is highly flawed.
TTFN,
WK
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