Anonymous at Sun, 7 Jul 2024 14:25:24 UTC No. 16271508

>prevents runaway cell division
Don't thank me. Just doing my job.

Anonymous at Sun, 7 Jul 2024 14:58:34 UTC No. 16271534

>>16271504
It's loss of telomeres that makes you die of old age idiot.

Anonymous at Sun, 7 Jul 2024 15:00:10 UTC No. 16271535

>>16271504
>>16271534
AKSHUALLY telomere length is a very poor predictor of remaining lifespan. This theory is considered an incomplete picture at best. The idea was proposed by a physicist originally.

Anonymous at Sun, 7 Jul 2024 15:10:05 UTC No. 16271542

>>16271504
this crappy research has been debunked so many time before.

Anonymous at Sun, 7 Jul 2024 15:41:18 UTC No. 16271564

>>16271542
got a source for that sweaty?

Anonymous at Sun, 7 Jul 2024 16:52:28 UTC No. 16271627

>>16271504
90%+ of tumors have active telomerase, i.e. infinitely regenerating telomeres

Anonymous at Sun, 7 Jul 2024 20:43:59 UTC No. 16271915

>>16271535
Can physicists go five minutes without embarrassing themselves?

Anonymous at Sun, 7 Jul 2024 20:45:47 UTC No. 16271920

>>16271627
telomerase would be dissolving telomeres. -ace is for enzymes

Anonymous at Sun, 7 Jul 2024 21:47:03 UTC No. 16272003

>>16271504
Cell senescence prevents cancer. Immune system does imperfect job of removing senescent cells hence aging.

Anonymous at Mon, 8 Jul 2024 04:18:55 UTC No. 16272444

>>16271535
>telomerase activating drugs and gene therapies extend lifespan and healthspan in mice
>telomeres are a poor predictor of lifespan
pick one

Anonymous at Mon, 8 Jul 2024 05:06:01 UTC No. 16272476

>>16272444
>in mice
meanwhile in humans we measured telomere length and found it was one of the weakest predictors of lifespan
cool story about the mice though

Anonymous at Mon, 8 Jul 2024 05:12:21 UTC No. 16272483

>>16272476
my favorite story about mice is the secret of nimh

Anonymous at Mon, 8 Jul 2024 05:14:58 UTC No. 16272485

>>16271504
Stupid question, can I just take Telomerase supplements and live forever? Why has no one thought of this?

Anonymous at Mon, 8 Jul 2024 05:15:45 UTC No. 16272486

>>16272476
My impression is that the story about the mice is also bullshit. They probably created a very specific breed of lab mice where their health condition correlate strongly with telomere length. If it were really telomere lengthening can increase mice lifespan they would've been able to keep doing that shit forever and it would've been huge. Immortal mices. Instead the mices died off, probably because they reached their maximum natural lifespan and the lifespan lengthening effects they claimed probably are just from the other mices dying off earlier than their maximum lifespan due to maltreatments.

Anonymous at Mon, 8 Jul 2024 05:22:56 UTC No. 16272493

>>16272486
or maybe telomere length is merely one factor amongst many in aging and lengthening the telomeres provided a noticeable benefit but not an infinite one

Anonymous at Mon, 8 Jul 2024 05:24:25 UTC No. 16272494

>>16272493
the other big factor would be gradual oxidative stress from the collection of unstable free radicals over time

Anonymous at Mon, 8 Jul 2024 05:27:32 UTC No. 16272496

>>16272476
>muh in mice
You can't conduct experimental studies on humans without isolating them for a lifetime nor conduct vivisection not post mortem dissection. Mice studies are extremely useful you stupid fucking retard midwit. You can put mice in ideal conditions and ensure they have enriched excellent lives for the duration. You can't do that for humans. Pay hundreds of participants $175k a year to have a stress free existence and comply with a telamorase inhibitor or placebo in exchange for dissecting them at the end from birth until death. Otherwise a similar study cannot be conducted.

Anonymous at Mon, 8 Jul 2024 06:21:16 UTC No. 16272537

>>16272496
Except we did do a longitudinal study on how telomere length and death by old age were related. It showed it wasn't a good predictor of death by old age.

Anonymous at Tue, 9 Jul 2024 19:47:57 UTC No. 16274849

>>16272494
the oxidative stress model hasn't held up super well either - it's always struggled to find direct evidence in vertebrates, and especially so in mammals. studies directly, provably reducing oxidative stress in mammals have rather consistently had no impact on longevity.

one popular current model is related to general stresses and damage, including oxidative/free radical, but isn't from cumulative damage directly - rather, what is presumed to accumulate are barriers to the self-repair and cell replacement processes already present (i.e. accumulating senescent cells, decline in healthy/regenerative cell proportions, increase in proportion of cells with accumulated genetic damage).

if correct, this is extremely good news from a longevity standpoint - the hardest part of reversing and preventing the effects of aging already has an extant, natural solution. those self-repair mechanisms do some work in maintaining themselves, and the existence of multiple failure modes means the effects of multiple different efforts to prevent each failure mode compounds on each other. this means that not only does reducing one help reduce and counteract others, but simultaneously reducing multiple modes of failure (or sources of those modes) flat out causes better health outcomes across the board (which is currently being seen in studies), which means any direction of progress assists the viability of all other treatments - it's difficult to overstate how rare in medicine a relationship between differing treatments like that is, especially with how broad the benefits of a given treatment appear to be.

only funding specific problem-related solutions until very recently is arguably a (justified) result of just how uncommon systems like that are, and the "walled garden" mindset that has prevailed in aging-related disease research until very recently.

Anonymous at Tue, 9 Jul 2024 20:53:09 UTC No. 16274987

>>16272537
Paper or didn't happen

Anonymous at Tue, 9 Jul 2024 21:48:44 UTC No. 16275073

>>16274849
wouldn't it be a trivial matter of injecting mice with antioxidants (real ones, not that blueberry crap) every day until they die?

Anonymous at Tue, 9 Jul 2024 22:04:52 UTC No. 16275103

>>16275073
this was (albeit in the form of upregulated/inserted antioxidant-producing genes rather than continuous injection) essentially what they did in the early 2000s. that's part of what i'm referring to when i say those studies consistently had no impact on longevity. the antioxidant mice also had increased cancer rates relative to the control.

that "blueberry crap" IS still real antioxidants. bioavailability and efficacy at those concentrations is highly dubious, though.

Anonymous at Tue, 9 Jul 2024 22:11:47 UTC No. 16275112

>>16275103
ok. but did they actively monitor ROS levels in the blood? I'm seeing an awful lack of papers here
>that "blueberry crap" IS still real antioxidants
yeah and bleach IS still a real antibiotic, so you should just drink that right

Anonymous at Tue, 9 Jul 2024 23:50:35 UTC No. 16275283

>>16272537
>we

Anonymous at Tue, 9 Jul 2024 23:54:32 UTC No. 16275295

>>16271504
>muh telomeres
Like everything else söyence has shat out in the last 25 years, this will turn out to be bullshit. We'll find out that telomeres do not reliably govern cell death, or that they are being greatly accelerated by toxic substances, or that they don't always perform the same function.
I'm old enough to have seen this far too many times.

Anonymous at Wed, 10 Jul 2024 00:00:19 UTC No. 16275305

>>16274987
https://www.thelancet.com/article/S2352-3964(15)30081-5/fulltext
Denial in 3...2...1...

Anonymous at Wed, 10 Jul 2024 00:16:13 UTC No. 16275331

Bio brainlet here, but I had a thought, why have Henrietta Lack's cells continued to reproduce without signs of aging? What do her telomeres look like today compared to 60 years ago?

Anonymous at Wed, 10 Jul 2024 00:31:17 UTC No. 16275352

>>16275112
>but did they actively monitor ROS levels in the blood
...yes. and prevalence of proteins damaged by free radicals. that's what i meant by "provably reducing oxidative stress"

Anonymous at Wed, 10 Jul 2024 00:49:08 UTC No. 16275376

>>16275331
>cultured in nutrient-rich environment at all times, in the body by blood and later on by nutrient-rich substrates to provide a steady supply of the cells for lab work
>cancer cells have their telomerase on; completely disregard the Hayflick limit as a basic prerequisite to being cancerous in the first place
>rapid mutation of cancer cells allows for the strong selection against forms of senescence that would lower reproductive fitness of daughter cells to arrive at and then propagate the relevant mutations to avoid cumulative senescence across cell generations; the cells failing this step generally aren't going to make it to "cancer" status, and can't unless some of their descendant cells manage to overcome the barrier
>individual cancer cells don't need to live long, they only need to divide and consume enough to divide again; their turnover rate is extremely high
>it's the line of cells that doesn't age as an aggregate, but with cancer it's more like a highly dependent colony organism with originally human DNA than a biologically immortal individual organism

all makes sense to me.

Anonymous at Wed, 10 Jul 2024 00:55:12 UTC No. 16275384

>>16275305
Lmao, a study on old japs that showed how many of them had long telomeres somehow disproves anything. The extremely old had long telomeres but within the extremely old group telomere length didn't correlate with age... Except that they already had long telomeres.

Anonymous at Wed, 10 Jul 2024 03:43:07 UTC No. 16275548

I'm so fucking tired of retards making endless longevity threads based out their own headcanon conjectures. they don't even know what rapamycin or what the latest updates from the robust mouse rejuvenation study are
I hate this husk of a forum
I'm gonna go shitpost with Aubrey on x

🗑️ Anonymous at Wed, 10 Jul 2024 12:13:56 UTC No. 16275902

>>16275548
>robust mouse rejuvenation study
explain

🗑️ Anonymous at Wed, 10 Jul 2024 12:17:11 UTC No. 16275904

>you can't know
wordcel cope