David Pescovitz at 10:27 am Fri, Mar 8, 2013
The latest episode by ASAP Science from biologists Mitchell Moffit and Gregory Brown explains why we age.
David Pescovitz is Boing Boing's co-editor/managing partner. He's also a research director at Institute for the Future. On Instagram, he's @pesco.
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Why do we age? Because lazy wolves get hungry too.
hey so if telomere length is inherited, does this mean that children who have older fathers at conception get shorter life-expectancy (due to older father’s shorter telomere) relative to younger fathers?
I’m thinking no.
Nope. Telomere length of the parents at the time of conception doesn’t appear to impact the initial telomere length of the offspring, BUT the parents’ initial telomere lengths appear to be significantly hereditary. This, however, doesn’t mean that the lifespan of offspring will be directly comparable to the lifespan of the parents because even if they all begin with the same telomere length, individual RATES of telomere shortening vary (based on an array of factors including genetics, epigenetics, environments [including diet, exercise, lifestyle, vitamins/supplements] and experience [including stress, exposures, infections, medications...] and probably lots of other stuff as well.[2, 3, 4, 5]
And many more: http://www.telome.com/telomeres.php
Your flimsy facts are nothing compared to my bastion of denial. In the immortal words of Gary Johnston: “I will never die”.
The telomere hypothesis is just one of many theories of aging. Most of the cells in our bodies are post-mitotic, so they don’t divide after development is over, and therefore don’t suffer from shortened telomeres. And yet these non-dividing tissues (like the brain) show various signs of aging long after the cells have stopped dividing. Several single-gene mutations in model organisms (flies, nematodes) can extend lifespan by a factor of two or more without telomere effects. In nematodes, all of the cells in the adult are post-mitotic (they don’t even have stem cells), so telomere effects can’t explain mutations that alter adult lifespan.The fact is we have no idea why nearly all organisms have limited lifespans. Many hypotheses exist, few of which rise to the level of theories. This would have been a great video on the telomere hypothesis if it didn’t go on to imply that this is the known underlying mechanism. Its not even one of the most prevalent hypotheses.
The relationship between telomere length and senescence is fairly well-established [1, 2, 3], and there’s growing evidence suggesting relationships between telomere length and degenerating health, even in organisms in relatively early to mid development [4, 5].
[1: http://www.ncbi.nlm.nih.gov/pubmed/23454763][2: http://www.ncbi.nlm.nih.gov/pubmed/23387887]
And lots more: http://www.telome.com/telomeres.php