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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.
This is probably the single best piece of info I could have gotten.
NEAT.
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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.
I haven't done any testing myself (which I could because I have access to Western blotting materials), but this is the supplement that I take. You need to take triple the dose they say though: you need at least 10,000 FU to see what they saw in the study, which means 6 tablets not 2. Also more effective if taken with K2, which is unsurprisingly in natto itself.
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It's maybe a depressing take, but I'd bet that aging and age-driven mortality is hugely multivariate as the result of at least a dozen factors that have all been locally optimized under a "needs to work at least one lifetime" metric. One could imagine a poorly[1] engineered car hitting it's warranty limit and immediately having all the wheels and seats fall out at once, without a simple "one weird trick" existing to maintain it indefinitely. I'm more hopeful for a bunch of weird tricks, though.
There's a famous legend about Henry Ford trying to engineer cars this way - if the car you buy has ten parts that might wear out, but in practice only nine of them ever fail, doesn't that mean you probably paid too much for an over-engineered design on the tenth?
If the lifetime of your car (or your body) was actually strictly determined by a L=min_i(L_i) formula, in fact, evolution would have a really tough time improving that - once you get L_i = L_j for some i,j, you can't improve L by improving either component, but only with a change that improves both at once. I think evolution is helped here by the addition of uncertainty - even when something like "heart failure kills people before cancer can" was true at some point in some average sense, there'd still be individuals getting lucky with their heart or unlucky with cancer and so cancer-fighting mutations would still give non-zero fitness improvements.
Perhaps a more subtle problem is that evolution doesn't care about the longevity of your body, only the fitness of your genes. By the time your biological mortality is really catching up to you, you're supposed to have a few kids and a bunch of grandkids running around, and from the point of view of an allele's frequency your life is only worth approximately as much as two of the former or four of the latter. So if age has made your body a significantly less efficient carrier of the genes you share, then evolution would be happy to put you out on an ice floe (as in a somewhat less mythical metaphor) rather than let you drag them down with you. Not only do alleles that reduce mortality become less useful in the face of different causes of death, but also in the face of other causes of weakness!
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This fits what I have read and seen of the research as well. There was a poster at a meeting I went to this year in San Diego where they selected flies for long lifespans by only taking offspring after a certain date (usually around 40 days I think). The genes that they found to be modified were all over the genome and didn't point to a single nice answer about aging other than it's something that affects the whole organism through many different pathways.
Nick Lane (one of my favorite biologists these days) has a theory that aging is caused by accumulations of mitochondrial mutations that prevent optimal ATP production. Eventually you get to the point where tissues can't produce enough energy to sustain themselves and then you get multiple organ failure and die. I'm attracted to this model because it means that in order to combat aging you should do a lot of aerobic (easy) exercise and have kids with people who are physically fit. Over time the average human lifespan should increase.
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The thing is, the body has many built-in repair mechanisms, unlike your average engine, and in theory (i.e. we do observe this in nature) is able to keep repairing things 'indefinitely' if it is able to function at full capacity.
One of the major drivers of 'aging' appears to be the breakdown of the repair mechanisms. Including the repair mechanisms for DNA in the cells. But that, too, is downstream of damage to DNA. And eventually damage to the DNA accumulates and outpaces the ability of the repair mechanisms to repair.
Bolstering the natural repair mechanisms is likely to get us a lot of improvement on the longevity front.
There will almost certainly need to be other interventions for certain ailments, though. Big one would be accumulated damage to the brain, due to blunt force trauma or similar damage that is additive over time with no natural means of repair.
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