h a l f b a k e r yThis ain't rocket surgery.
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I thouight of a way to velocitize longevity research. Many drugs and chemicals have been measured at a few studies as causing greater longevity. Follow up stuidies, as well as new studies could use this protocol
Creating a group of 40 cohorts (groups) of 11 mice each, where each cohort is a different
month of age quantifies longevization effects of new molecules more rapidly
thus there are
11 mice at 39 months of age
11 mice at 38 month of age
11 mice at 37 months of age
continuing to
11 mice at one month of age
at the beginning
Giving each of these cohorts a longevity molecule then noting the p value of any longevity effect at a group of 11 causes rapid data gathering as to effectiveness
I may have read that 8 mammals are sufficient to generate a p value at .05
thus 11 mice have higher validity
Trending such as when month 28 to month 37 all show a trend to greater longevity improves the p Value further, while bringing the welcome extra data that the molecule might work on the already mature.
Different, yet valid metaanlyses are available from each entire multi cohort is also producible
One of the advantages is that you might be able to test new longevity molecules in months rather than years, because of the small cohorts of elderly mice.
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Note that this differs from something similar to "we got a lot of middle aged mice, then gave them a molecule, made a graph, and determined a p value." |
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One of the advantages is that you might be able to test new longevity molecules in months rather than years, because of the small cohorts of elderly mice. |
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Also it is a commercial product! There are places that maintain mouse breeds as well as genetics. These could improve the quantification math described here then create Ready to research mouse multipaks (multiage distributions) as an list item |
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Yes, this is brilliant, because obviously scientists in present don't use any sort of statistical analysis. If only they had your insight. [+]. |
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I do not know [mb] wouldn't it be great to screen say, all 1450 FDA drugs on last six months of lifespan mice to find p <.05 at that group. Just a few months to find a lot of immediately prescribable longevity drugs. |
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No, it wouldn't. At p<0.05 you would just find several hundred flukes. |
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Researchers who want to use vertebrates in any kind of research already have to do a rigorous assessment of the statistical power available from a given number of animals. So this is either WIBNI, let's all, or WKTEBPWAKWTTA. |
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" I may have read that 8 mammals are sufficient to generate a p value " |
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All mammals can generate pee. |
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the problem with this idea starts with the fact that all the
mice have already been cured |
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So, four legions of mice. Two mouse proconsuls in command. It has a certain something. |
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Well, 1/20th of 1450 is just 73 false leads. at p<.01 it is just 15 false leads. follow up studies that go amiss on just 15 molecules is not so terrible. Think of 5% of the earths population (365 million) on longevity drugs that cause 30% greater longevity. That represents about 100 million additional human lifetimes of existence. That is about twice as many lives saved than all the casualties of WWII (or three Stalins!) I strongly support this research. |
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Currently deprenyl has been measured at three mammal species at about 20% greater longevity, N acetyl cysteine is near 30%. Metformin varies between 5% and 37%. Highly unusual rapamycin is 60% (!) |
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Once the FDA pharmacopoeia was analyzed for longevity effects, new drugs for other conditions might be formed around longevity effects so they could compete with the generics. |
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//N acetyl cystein is near 30%// I'll bet cash money that
NAC does jack diddly bugger all in human longevity. I can
take the cash now if you like because there's trials, more
trials and meta reviews of trials showing antioxdants
(that word needs to go away) don't do anything. Mucus
and paracetamol overdose are the only uses of any
antioxidant anywhere in medicine. Grr. If you have an
oxidation problem, I'm happy to sell Oxygen depleted air..
anyhow, why mop up oxidants with a disposable molecule
like NAC when you can reduce the source with a little
DNP? It would make a fine treat for the elderly and stop
all that complaining about the winter fuel allowance. |
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Anyhow, we have a lot of people on all the approved
drugs, they're all out there doing the experiment in
humans right now. I'm sure a couple of compounds will
start to shake out in the stats. In the mean time, there's
no need to start getting a massive animal bill. Mice are
sucky metabolism and ageing models. So are worms and
all that. If you want to get old mice faster, well, there's
ageing model mice, with mutations to speed that up. |
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Here's a thought, why don't we do it the other way
around? Look for compounds that speed up ageing.
Success shortens the experiment! Then work out how it
works and do the opposite! Simples. |
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// reduce the source with a little DNP?// Yes, but the question is, how little? In [sucky] mouse models, the DNP dose for extended lifespan was quite low, if I recall - much lower than is used for weight loss. |
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they went with 1mg/litre. That level will still bioaccumulate
a little. Maybe 10uM? More than enough for shaving the
peaks off any membrane potential spikes, maybe tipping
slightly sick mitochondria over the edge to degradation? A
bigger dose would still do that, but would also mimic caloric
restriction to an extent. |
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Ah yes - if I remember (can't be arsed to re-find the paper), that was in drinking water? Anyone know how much a mouse drinks? |
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Divide a few hundred RESEARCHERS into age groups,
then calculate p values from each group, showing
trend as well as different-age efficacy ? |
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Throw a party for the last ten surviving mice er ahh
researchers. |
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