How do I SLOW DOWN AGING?
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Date: April 22nd, 2018 10:18 PM Author: rusted concupiscible mad cow disease state
Meditate, ginseng, green tea, not eating processed shit, eating fresh fruits/veggies raw, not eating meat (fish is great), not eating starchy shit, physical activity, sleeping enough/well, drinking 1.5-2 liters of water (more if lots of activity or in the heat), cutting back on alcohol/smoking.
The body is a machine. The more you abuse it the quicker it breaks down.
(http://www.autoadmit.com/thread.php?thread_id=3956869&forum_id=2#35897257) |
Date: April 22nd, 2018 10:48 PM Author: Heady geriatric garrison
calorie restriction retards aging in many species, including primates like rhesus monkeys and lemurs. the results on lemurs came out pretty recently and were fairly large (50% gain in lifespan), which is surprising considering they are long lived and the gains in rhesus monkeys were more like 10%. CR is unlikely to work that well in humans, but i would bet it works to some extent.
there are CR mimetic drugs too. rapamycin is one that probably works. metformin might as well, but it doesn't work nearly as consistently as rapamycin. there is some reason to believe that rapamycin might be synergistic with CR, so lifespan gains might be additive if you were willing to do both.
(http://www.autoadmit.com/thread.php?thread_id=3956869&forum_id=2#35897414) |
Date: April 22nd, 2018 11:13 PM Author: know-it-all sapphire school hissy fit
So, let's define aging as the accumulation of damage in the body.
How do we limit or slow the way we accrue this damage? This damage mainly occurs at the cellular (or smaller) level.
With 2018 technology, there aren't many ways to slow down aging but there are some things you can do. There are also technologies in development that could change the game in the coming decades and prevent or even reverse damage to keep the body in a youthful state, akin to getting a tune up on your car or certain parts replaced.
But for now, what's most important is:
1) do not smoke
2) do not do drugs
3) drink in moderation, if at all. Moderate drinking has been linked to beneficial effects.
4) SLEEP (7-8 hours) More or less than this, generally, is linked to negative outcomes.
5) Stress reduction (laugh, get a massage, take mental health days, meditate, yoga, see a show, do something that makes you happy)
6) Diet & exercise (the two most important by far) In terms of diet, vegetarian or Mediterranean are most associated with longevity gains. Contrary to popular belief, you can get all the protein you need quite easily eating a veg diet.
7) Do not go into the sun, use sunscreen on the beach always. The sun causes irreversible damage to skin as well as wrinkles.
8) Get regular check ups for markers of disease.
9) Floss and take care of your teeth
8) Eat foods high in antioxidants that scavenge free radicals in the body.
In the coming decades, treatments may become available that can "treat" aging on a cellular level. For more information on this, look at someone like Aubrey De Grey who has made that his life's work, along with the SENS foundation. It's pretty fascinating. He doesn't advocate immortality (not achievable) but we can slow or perhaps one day, entirely reverse "aging".
*cue Rod Stewart's Forever Young*
(http://www.autoadmit.com/thread.php?thread_id=3956869&forum_id=2#35897571) |
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Date: April 22nd, 2018 11:57 PM Author: Heady geriatric garrison
there are a number of different theories of aging. many of the common ones that researchers cling to are clearly deeply flawed (free radical theory of aging being the major one). until pretty recently i think it's been a reasonable debate, but over the last 10 years two things have happened:
1. Horvath's clock was created based on epigenetic changes. over time there are highly regular changes in cellular gene expression that can be used to reliably predict chronological age and (more importantly) mortality. this is a much more accurate predictor of mortality than other indicators of biological age (like telomere length). this suggests that epigenetic changes play an important role in the aging process.
https://en.wikipedia.org/wiki/Epigenetic_clock
2. induced pluripotent stem cells are stem cells that have been generated from adult cells. they basically take an old cell and expose it to different proteins, and the cell dedifferentiates (loses its cellular identity, so it becomes a pluripotent stem cell again). the interesting thing about this process is that the aged cells start looking very much like young ones, and the only real change happening is related to epigenetics.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3219229/
Direct reprogramming of somatic cells into induced pluripotent stem cells (iPSCs) provides a unique opportunity to derive patient-specific stem cells with potential applications in tissue replacement therapies and without the ethical concerns of human embryonic stem cells (hESCs). However, cellular senescence, which contributes to aging and restricted longevity, has been described as a barrier to the derivation of iPSCs. Here we demonstrate, using an optimized protocol, that cellular senescence is not a limit to reprogramming and that age-related cellular physiology is reversible. Thus, we show that our iPSCs generated from senescent and centenarian cells have reset telomere size, gene expression profiles, oxidative stress, and mitochondrial metabolism, and are indistinguishable from hESCs.
they have already done research on temporarily exposing mice cells to OSKM factors (the factors used to create IPSCs). it significantly lengthened their maximum lifespans. these were mice that had an accelerated aging disease, but i will be very surprised if the results don't carry over to normal mice and humans. the tricky thing will be figuring out optimal dosage schedules and delivery mechanisms - you don't want cells to completely dedifferentiate.
(http://www.autoadmit.com/thread.php?thread_id=3956869&forum_id=2#35897918) |
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Date: April 23rd, 2018 12:21 AM Author: know-it-all sapphire school hissy fit
Suggestive yes, I would like to learn more about it though and the science of how/why it's "driving" the aging, that's the part that needs to be discovered. It's also possible it's a variety of factors.
FWIW, here's de Grey's take:
Feinerman: There is growing evidence that epigenetic changes are highly organized and may be one of the causes of ageing. What do you think? Maybe should we consider epigenetic changes as another type of damage in SENS model, calling EpiSENS?
de Grey: We need to be much more precise with definitions in order to answer your question. Epigenetic changes can be classified into two main classes: shift and noise. Shift means changes that occur in a coordinated manner among all cells of a given type and tissue, whereas noise means changes that occur in some such cells but not others, increasing the variability of that type of cell. Shifts are caused by some sort of program (genetic changes to the cell's environment), so yes, they can potentially be reversed by restoring the environment and putting the program into reverse. Noise, on the other hand, is not reversible. And we have for several years worked on determining whether it happens enough to matter in a currently normal lifetime. We have not got to a definitive answer, but it's looking though no, epigenetic noise accumulates too slowly to matter, other than maybe for cancer (which, of course, we are addressing in other ways).
(http://www.autoadmit.com/thread.php?thread_id=3956869&forum_id=2#35898068) |
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Date: April 22nd, 2018 11:41 PM Author: know-it-all sapphire school hissy fit
There is an epigenetic component of aging, there's no question some genes are linked to longer lifespans and others to shorter ones for a plethora of reasons based on what they do or do not do when expressed. Our genetic make up is a stochastic component as much as damage is, but regardless of certain genes, aging is defined primarily as the accumulation of damage in the body to the point where disease states emerge. How do you address that problem? SENS for example offers 7 problems to address appropriately to bring about "negligible senescence'
1)cell loss or atrophy (without replacement)
2)oncogenic nuclear mutations and epimutations
3)cell senescence (Death-resistant cells)
4)mitochondrial mutations
5)Intracellular junk or junk inside cells (lysosomal aggregates)
6)extracellular junk or junk outside cells (extracellular aggregates)
7)random extracellular cross-linking
DNA methylation can certainly be used to determine or estimate the biological age of a tissue but the global loss of methylation via aging is something that can be reduced or prevented under the umbrella of the problems identified above. It's more of a measure than something that is a primary means or cause of aging.
Edit: Another example is telomere length. Say we find a way to re-lengthen as they become shorter with age and shorter telomeres are a sign of aging. If we lengthen to a more "youthful" state you'd measure a younger biological age. It's both an indicator and effect of aging that can be reversed, but also useful as a measure.
(http://www.autoadmit.com/thread.php?thread_id=3956869&forum_id=2#35897778) |
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Date: April 23rd, 2018 12:06 AM Author: Heady geriatric garrison
i think most of those hallmarks are related to epigenetic dysfunction or aren't very important.
"DNA methylation can certainly be used to determine or estimate the biological age of a tissue but the global loss of methylation via aging is something that can be reduced or prevented under the umbrella of the problems identified above. It's more of a measure than something that is a primary means or cause of aging. "
there's little reason to believe that DNA methylation changes can be prevented or reversed through the SENS strategies.
the interpretation that epigenetic changes are simply an indicator of damage doesn't make much sense. if this was the case, we wouldn't expect to see dramatic reversal of the aged phenotype through cellular reprogramming.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3219229/
(http://www.autoadmit.com/thread.php?thread_id=3956869&forum_id=2#35897975)
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Date: April 23rd, 2018 12:39 AM Author: talented circlehead
8-9 hours of sleep every night
minimize stress
don't be fat
eat a diet that is actually rich in fresh vegetables, particularly cruciferous vegetables and other greens. you don't NEED to be a vegetarian unless you can't otherwise regulate your animal product intake to reasonable levels
don't be addicted to poison and nicotine
exercise and stay active
maintain a network of friends and family who you see regularly and enjoy spending time with
that's about as good as you're going to get. all the supplements and bizarre fads and minutia are easily overwhelmed by genetics and daily lifestyle factors you will never be aware of.
(http://www.autoadmit.com/thread.php?thread_id=3956869&forum_id=2#35898152) |
Date: April 23rd, 2018 1:29 AM Author: Obsidian Knife
Have frequent novel life experiences and meaningful relationships with a close social group.
Basically the opposite of living like a lawyer.
(http://www.autoadmit.com/thread.php?thread_id=3956869&forum_id=2#35898310) |
Date: April 23rd, 2018 1:34 AM Author: Marvelous rebellious persian corner
Eat less, maintain low BMI (like 18)
Sleep enough
Avoid the sun
Not be pure white
(http://www.autoadmit.com/thread.php?thread_id=3956869&forum_id=2#35898321) |
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