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  1. Here is something technical I've been wondering about for a while now. I'm hoping one of the resident experts on science of aging (Michael, James, Brian?) can help to clarify it for me. Back in the old days, about a decade ago, it seems from my recollection that there was a distinction between the concept of "Intrinsic Aging" (IA) and the diseases of aging. IA was an inexorable process that wasn't well understood, other than that it proceeded in the background, accelerated over time (maybe leveling off at some extreme age), and eventually and almost inevitably leads to one or more of the diseases of aging, which are almost always what kills a person. People almost never die of "old age" per se, but some specific cause resulting from the body's inability to indefinitely keep itself in good repair. Furthermore, under this model, certain interventions, like exercise or a healthy diet, were able to "square the mortality curve" and extend mean lifespan by preventing some of the damage associated with the diseases of aging, but they couldn't slow down the underlying IA process itself, and so couldn't extend "maximum lifespan" - which I understood to be something like the age an organism could reach if it wasn't killed off prematurely by a disease of aging. But there was one intervention that was known to be different - calorie restriction. CR, it was said, could slow the rate of IA, sometimes quantified as "mortality doubling time" and hence it was able to extend maximum lifespan, not just mean lifespan. Nothing else anyone had discovered was able to do this. Fast forward 10 years and it seems like the idea of IA isn't as popular or prevalent, at least as far as I can see. Instead, aging is described by experts like Aubrey as the accumulation of damage, which Aubrey and company have compartmentalized into the famous seven categories. As an example, one such category is the accumulation of intracellular junk, like when macrophages swallow toxic byproducts of cholesterol which they can't effectively break down, leading to their accumulation in the walls of arteries and eventually atherosclerosis, the plaques in our arteries that are responsible for heart disease. But the thing is, interventions like a healthy diet and exercise can impact the rate of accumulation of damage caused by at least some of these seven categories, including the accumulation of intracellular junk in the form of toxic cholesterol byproducts. So while exercise and a healthy diet were previously seen as completely ineffective at slowing intrinsic aging, now it seems they can positively influence at least one of (actually several of) the underlying causes of aging - the accumulation of damage from the seven categories. And so it would seem they are capable of slowing what amounts to the aging process. From this perspective, it would seem to me that exercise and a healthy diet would now have to be considered bona fide anti-aging interventions (albeit relatively narrow and therefore ultimately ineffectual ones), whereas they didn't used to be considered anti-aging interventions at all, at least by the formal definition used in the gerontology community. So am I understanding this correctly and there has been a shift in what scientists believe aging amounts to, or am I missing something? More specifically, is intrinsic aging now an outdated concept? And as a corollary, is calorie restriction just a better (although only modestly better if you ask Aubrey) anti-aging intervention than a good diet or exercise because it is more comprehensive i.e. it obviates a wider range of damage categories, a wider range of damage types within a category and the degree of damage of a given type it prevents? --Dean
  2. All, Mutations in mitochondrial DNA (as opposed to nuclear DNA), are thought to be an important driver of aging. Aubrey has had this perspective for many years, and SENS has been funding research to basically get mitochondrial genes copied to the nucleus, where they are less likely to get damaged by the free radicals generated in mitochondria. Once manufactured in the nucleus, the proteins expressed by these genes can then be imported into mitochondria where they are needed. It's proven to be a difficult challenge, to put it mildly. But two days ago Aubrey announced at the Rejuvenation Biotechnology Conference (RB2016), that the team SENS has been sponsoring succeeded getting a paper accepted to a journal (Nucleic Acid Research) documenting their recent success. Specifically, the team was able to get two (of the 13) mitochondrial genes simultaneously expressed in the nucleus and functioning properly. That's about all the details Aubrey gave in the short video below. Perhaps Michael knows more and can share with us an update?! Great to see progress! --Dean https://www.youtube.com/watch?v=-teTeyUPsJM