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Uh, ackshully, that's approximately where the state-of-the-art on anti-aging is heading.
Sirtuins are involved in DNA repair, which allows cells to keep replicating accurately, which is what keeps you alive and minimizes the effects of 'age' as we understand it.
There's currently a LOT of research into Sirtuin activators for this reason.
This might be a part of the book that gets borne out really well in the end.
My understanding is there is a large metabolic and structural component. Heart disease is still the #1 killer and this is almost entirely due to a break down in how the circulatory system functions. There is a genetic component but ti's not like fixing people's DNA will really help
Why does the heart/circulatory system break down, if not due to the failure of the cells to properly replicate over time, thanks to DNA damage?
Uhhh that is not the reason. You get build up of atherosclerotic plaque in the circulatory system for reasons we don't really understand fully yet, but has something to do with the activity of immune cells and levels of dietary fat. Over time the plaque blocks the vessel and you get a heart attack. No cell replication involved. I can point to a bunch of other diseases of aging (T2D for example) that have similar mechanisms of action that are metabolic, not replicator dependent. In the case of T2D for example, making the beta cells of the pancreas more robust won't fix the fact that your body doesn't respond to insulin any more. Of course there are things you can do to prevent these diseases (exercise and diet), but those only work up into a point.
There's also the theory of mitochondrial dysfunction causing aging. This one is a DNA-caused problem. Basically mitochondrial genomes accumulate mutations much more rapidly than cellular genomes. Since a large amount of the DNA for mitochondrial proteins is stored in the nucleus, not in the mitochondria, this eventually leads to some serious incompatibilities and dysfunctions in mitochondrial energy production. These eventually become so large that one by one the individual tissues in your body can no longer keep up and you die from multiple organ failure. This could theoretically be fixed by fixing mutated DNA in the mitochondria, but it's not clear to me yet how you could accomplish this, nor what template you would use for repair.
Is this considered an actual symptom of 'aging' wherein its inevitable as one gets older? I mean, do we see old people without much plaque as often as we see them with it (Yes yes, accounting for the survival of such persons to old age).
And likewise, if there was a mechanism for preventing the buildup of plaque in the body, wouldn't that also be impacted by failed cellular replication?
Since there are certainly other animals that have cardiovascular systems that nonetheless live an extremely long time.
We do see people without much plaque who have eaten diets relatively low in fat, especially saturated fat. But this usually means that one's diet is high in protein (which greatly increases cancer risk and kidney failure, although at least the former can be greatly mitigated through DNA-repair), or carbohydrates (which greatly increases the risk of insulin resistance). Now many traditional populations experience none of these three metabolic failure modes. Yet that is (as far as I understand it) usually a result of them being on the edge of starvation most of time, which increases risks for other things like malnutrition which would negatively impact cellular replication.
I certainly think it would help, but I'm not sure it would solve things completely. Kids can get T2D and athero, so merely having robust new cells wouldn't fix things completely.
Certainly, and I'm by no means arguing that enhanced DNA repair wouldn't help improve lifespans significantly. I just don't believe that this would be the magic bullet, as there are many other things going wrong as one ages. In addition to metabolism there's also the problem of the brain no longer producing new cells at all, which you point out in a comment thread below.
This does sound like a problem that can be solved via pharmacueticals, some chemical that breaks up the plaques (without hurting other cells), and removing the plaque from the blood would probably involve filtering (possibly via an external device?) and reintroducing it.
It sounds more like an oil change type problem, rather than an engine swap type problem.
Yea certainly! I've been very excited about nattokinase recently. This is a compound found in the Japanese fermented soybean dish Natto, that has been shown to reduce plaque by up to 36% in a single year. Been trying to get the parents on it with little success. I myself take it daily.
Based on family history i've adjusted diet but still anticipate a high risk of plaque buildup, so this is good to know! Any particular brand you trust for nattokinase as a supplement? My tolerance for funk isn't what it used to be; I don't have it in me to eat natto regularly.
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