Tuesday, March 4, 2014
"Contrast that with the SENS hypothesis that aging is molecular and cellular damage that the body cannot repair at any reasonable cost."
If that were the case, we should see SENS like approaches being implemented by nature in negligible Senescence species. If all they've is mostly the same genes and differing expression patterns, then existing mechanisms are sufficient if ramped up. We have over 98% genetic similarity with our closest relative yet over twice the lifespan.
What approach doubled species lifespan?
If we were bonobos with 40year lifespans and we asked SENS proponents. They'd say most of the [easy] longevity changes were already implemented by nature in achieving this lifespan and they'd propose the SENS solutions as a way to lengthen lifespan.
If like me you believed existing mechanisms are mostly sufficient for vast lifespan increase, then you'd suggest mostly gene expression changes with high conservation of the genome. What did nature do? AFAIK, it simply mostly tweaked gene expression and presto triple lifespan.
If you ask me, it is likely that similar tweaks could very likely carry us all the way up to negligible senescence.
Let's see what we find from the genetic sequences of negligible senescence organisms.
"Indeed; it's not like there aren't plenty of species whose telomeres don't shorten with age, in fact there's a species of bird whose telomeres get -longer- with increasing age, and it ages quite normally."
I've not looked into it deeply, but according to Dr. Bill Andrews, it is only a few species who have significant aging contribution from short telomeres.
"The same thing should happen if you were to repair all the cellular and molecular damage of aging that suppresses stem cell activity."
And it also as mentioned seems to slightly begin to occur with lifestyle changes that increase telomeres.-Darian S in Fightaging
Monday, March 3, 2014
Thursday, February 27, 2014
New Victorian research reveals that running long-distance runs can slow the ageing process by protecting the part of the body that stops the genes from fraying.
Runners in The Federation University Australia study had an average age of 43, but their biological age was just 27.
Though previously in this blog we saw that benefits peaked at sub8mph 10miles per week and that exceeding 8mph or 20-25 miles per week could possibly damage the heart neutralizing some of the benefits. Yet it is said that low intensity exercise does not have such a cap on adding benefits(more research is needed.), which suggest walking for most of ultramarathon distances would be optimal. That is 10-15 miles per week with 2-3 days of resting per week at no more than 8mph and several hours of walking to achieve the ultramarathon distance.
The findings, to be presented at the Australian Society for Medical Research National Conference, found ultra-marathon runners clocking up 40-100 km a week had 11 per cent longer telomeres.-link
Yet lifestyle changes
Ten of the patients embarked on lifestyle changes that included: a plant-based diet (high in fruits, vegetables and unrefined grains, and low in fat and refined carbohydrates); moderate exercise (walking 30 minutes a day, six days a week); stress reduction (gentle yoga-based stretching, breathing, meditation). They also participated in weekly group support. -link
might allow similar benefit with much less exercise
The group that made the lifestyle changes experienced a “significant” increase in telomere length of approximately 10 percent. -link
But might not both interventions be combined and yield greater results?