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              Advocacy & Research for Unlimited Lifespans


Data on the Aging of Stem Cells From Supercentenarian Blood

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#31 xEva

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Posted 02 December 2014 - 07:05 AM

Sorry Brett for not replying earlier. At the time, the news of Odessa massacre totally threw me out of all this..

So, back to de Gray and SENS. They should alter their stance on the following issues:

  • Damaged mitochondria: they are not doomed to remain damaged (as was discussed above). They do get recycled when a cell is starving.
  • Telomeres: while most people are still undecided whether elongation of telomeres may be conducive to cancer development, it is already certain that short telomeres will definitely lead to cancer. So SENS proposal to disable/remove telomerase as an anti-cancer strategy needs revision.
  • SENS idea to remove T-cells that specialize in 'harmless' herpes viruses is also in need of revision (discussed here).
  • ..-? the list is not complete. These 3 things came to mind, 'cause they were discussed recently. I'm sure there is more. I'll update when I come across them.

Regarding this study:

The largest age-related cause of death has origins in molecular damage/events that are already visible in early childhood, just as SENS suggests:

1. Am J Clin Nutr. 2000 Nov;72(5 Suppl):1307S-1315S.

Origin of atherosclerosis in childhood and adolescence.


In my unlearned opinion, the cause of atherosclerosis are chronic infections that often originate in the mouth. Inflammation and patching up of the damaged vessel walls with cholesterol plaques, are the proper immune responses. IOW, what they found is the snapshot of a diseased state. When these children recover, the damage will be repaired.

Besides, they themselves express reservation in their study:

  • The ecologic, epidemiologic, and topographic analyses that showed little or no relation between aortic fatty streaks and the clinically important lesions of atherosclerosis are largely responsible for the skepticism about the significance of the fatty streaks.
  • However, although women have about the same extent of or more coronary artery fatty streaks than do men, they have only half the extent of raised lesions at older ages.

If fatty streaks in childhood were the precursors of plaques in adulthood, then women should age faster then men or be more susceptible to CVD, yet the opposite is true. Then they say:


About one-third of children under 9 y of age had simple intimal fatty streaks composed exclusively of macrophage foam cells. By the age of puberty, more than one-half of the children had larger accumulations of macrophage foam cells, extracellular lipid, and lipid in smooth muscle cells. A small percentage of these children had large accumulations of extracellular lipid. By the late 20s, about one-third of the young adults had well-developed raised lesions with large extracellular lipid cores and thick fibromuscular caps.


If this damage is part of normal aging, as defined by SENS,and not due to a disease, then all children should have these fatty streaks, not just one-third or a half. The fact that not all have these things speaks of a condition affecting those individuals, not something inherent in growing up (can't call this aging, sorry).

Edited by xEva, 02 December 2014 - 07:11 AM.

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