
An anti-aging strategy that works in mice is about to be tested in humans - molecule
https://www.scientificamerican.com/article/to-stay-young-kill-zombie-cells/
======
codingdave
There are quite a few comments skeptical about whether this would actually
prolong life, but that result is not the only possible benefit. Even keeping
our same lifespan, but not picking up age-related diseases, aches and pains,
and blindness would be a huge benefit to older folk. (And I mean those of us
in our 40s and 50s, who already curtail activities due to aging, not just
people over 80.)

Seriously, having been though some health problems, and seeing how much your
quality of life can suffer, I think some people would willingly take a
slightly shorter lifespan for increased quality of life as we age.

Are these drugs the answer? I have no clue. But the direction of the research
is encouraging, no matter how long we all live.

~~~
zild3d
Health span over life span

------
JPLeRouzic
In general in biology there is a simple criteria about the interest of an
article:

\- If it is tested in vitro, not only those results do not translate to human
health issues (it is not in a living tissue which is a complex milieu, not
simply the juxtaposition of cells), but commercial cell lines are not
representative of normal cells, as they reproduce indefinitively.

\- If it is tested on a mammalian animal model, it better but obviously
mammalian species are different from each other at the organe level (for
example the tail is used for thermoregulation in mouses).

\- The best thing for evaluating any human impact, is a phase III of a
clinical study.

------
reasonattlm
This is largely a promo for Unity Biotechnology and the associated labs. It
fails to mention, e.g. SIWA Therapeutics and their work on antibodies, Oisin
Biotechnologies and their gene therapy DNA constructs for destroying cells
based on internal chemistry, the company that David Sinclair is starting for
senolytics, that Betterhumans has beaten Unity to the punch and is currently
running phase 0 human pilots of dasatinib and quercetin on a non-profit basis.
Also that senescent cell clearance didn't magically spring into being in 2011,
but appears clearly in Aubrey de Grey's position paper on human rejuvenation
in 2002, and the Methuselah Foundation, SENS Research Foundation, and others
have been advocating hard for more work in this direction in the face of a
research community that rejected it for a decade.

But hey, if you beat the competitors to be the first to raise 9-figure sums of
venture capital, then you too can engineer attention to shine on you only, and
rewrite history more or less as you like for a while.

So far all ways to address aging in mice have slowed aging by tinkering with
metabolism, but slowing down the damage accumulation. They all produce much
larger effects in short-lived species, probably because long-lived species
have evolved to have many of these metabolic items turned on already. Calorie
restriction extends life by 40% in mice, and I can assure you that while it is
pretty beneficial in humans, you are not going to add more than a couple of
extra years. Senescent cell clearance is the first way to address aging that
involves repair of damage rather than slowing it down: we have no idea how the
size of benefit in mice will translate to humans. So 25% gains in mice can be
exciting here, whereas for any slowing-aging-only approach it would be a yawn.

------
dawhizkid
Isn't this yet another case for keto/intermittent fasting? It is well known
that in a fasting state you trigger cell autophagy -> essentially force
healthy cells to eat dead or diseased cells for energy...

~~~
dawhizkid
And btw...fasting is free, safe when done properly, and something anyone can
do today

I would much rather fast than ingest a drug pushed by big pharma...even if it
did work and triggered the same response

------
gojomo
The longevity benefits of fasting/caloric-restriction also appear to work
through the clearing of some cells ('autophagy'); see for example:

[https://en.wikipedia.org/wiki/Autophagy#Caloric_restriction](https://en.wikipedia.org/wiki/Autophagy#Caloric_restriction)

~~~
andai
<Conjecture> if you were a hungry body, which cells would you cannibalize
first, healthy cells or old malfunctioning troublemakers?

~~~
copperx
You just made a mind boggling amount of assumptions in one sentence.

~~~
andai
Fasting is also an effective remedy for a boggled mind.

------
lettergram
Took me a while to find, but this method apparently only increases the life
span of mice by 25%. Given how mice are prey animals - i.e. they aren't meant
to live long - I don't anticipate the same results with Humans. Although, it
may help reduce risks of diseases.

It'll be interesting to see results.

~~~
BurningFrog
I'll take an "only" 20 year life span increase.

~~~
SubiculumCode
Hell I'd take the normal span with my health and my mind intact. I've seen old
brains. It scares me.

~~~
andai
Yeah, I wonder if senolytics have a positive effect on the brain.

~~~
mcbits
We already have a potential treatment for age-related cognitive decline:
vampirism (kinda). [https://www.scientificamerican.com/article/fountain-of-
youth...](https://www.scientificamerican.com/article/fountain-of-youth-young-
blood-infusions-ldquo-rejuvenate-rdquo-old-mice/)

------
reasonattlm
Some papers showing direct connections between senescent cells and specific
aspects of aging, in many cases turning back that aspect by removing the
senescent cells.

Osteoporosis:
[https://doi.org/10.1038/nm.4385](https://doi.org/10.1038/nm.4385)

Fatty liver disease:
[https://doi.org/10.1038/ncomms15691](https://doi.org/10.1038/ncomms15691)

Disruption of platelet formation:
[https://doi.org/10.3389/fonc.2017.00188](https://doi.org/10.3389/fonc.2017.00188)

Osteoarthritis:
[https://dx.doi.org/10.1038/nm.4324](https://dx.doi.org/10.1038/nm.4324)

Disruption of regeneration:
[https://doi.org/10.3389/fcell.2017.00049](https://doi.org/10.3389/fcell.2017.00049)

Lung fibrosis:
[https://doi.org/10.1183/13993003.02367-2016](https://doi.org/10.1183/13993003.02367-2016)

Pulmonary function in general, including tissue elasticity:
[https://doi.org/10.1172/jci.insight.87732](https://doi.org/10.1172/jci.insight.87732)

Atherosclerosis:
[http://dx.doi.org/10.1126/science.aaf6659](http://dx.doi.org/10.1126/science.aaf6659)

Vascular calcification:
[http://dx.doi.org/10.18632/aging.101191](http://dx.doi.org/10.18632/aging.101191)

Chronic kidney disease:
[https://doi.org/10.18632/oncotarget.17327](https://doi.org/10.18632/oncotarget.17327)

Cardiac hypertrophy:
[https://doi.org/10.1371/journal.pone.0182668](https://doi.org/10.1371/journal.pone.0182668)

Cardiac fibrosis and function in general:
[https://doi.org/10.1093/eurheartj/ehx454](https://doi.org/10.1093/eurheartj/ehx454)

------
amelius
I would be surprised if people weren't already testing this, e.g. in China
where there is less regulation.

I think that could be a trend: US/European researcher publishes hypothesis,
and Asian researcher secretly tests it on humans, and if it works, publishes
it and/or becomes first to market.

~~~
cvsh
What do you think the solution would be, should this take off? Wrapping early
stage trials in a veil of secrecy?

~~~
ImSkeptical
I'd say we should encourage this, but just make sure our intellectual property
agreements are strong enough so that both parties benefit from their
contribution.

In my view, we need to be moving much faster on developing technologies,
drugs, and therapies. If some societies are able to help out, we should be
grateful and welcome that - so long as the subjects all consent.

~~~
amelius
So basically you would applaud weaker ethical rules in China?

~~~
ImSkeptical
Making a choice to protect people trying new treatments keeps those people
safer but the trade-off is that you develop new treatments slower, which means
more people suffer and die waiting for treatments.

Developing quickly versus safely are different decisions, but I don't think
one is purely stronger or weaker than the other.

------
maga
I wonder if exercising contributes to killing off these senescent cells. In
muscle building one is breaking down and rebuilding muscle cells, this might
as well prevent cell "aging" and going into senescence.

~~~
rsync
"I wonder if exercising contributes to killing off these senescent cells. In
muscle building one is breaking down and rebuilding muscle cells, this might
as well prevent cell "aging" and going into senescence."

I think this is already known and understood - at least with muscle and bone
cells. My understanding was that by putting energy production stresses on your
cells, you weed out the ones that perform poorly. Specifically, you weed out
those cells whose mitochondria are less efficient at producing energy.[1]

So there is a selection process that takes place, over time, in your own cell
population.

I find this very interesting but I have also grown very pessimistic about its
import ... people that don't like exercising will _do anything not to
exercise_ so it really doesn't matter.

We don't need any new findings that demonstrate the (clear, obvious, _nearly
immediate_ ) benefits of exercise. What we need are fewer cars and more
walking.

[1] I highly recommend Nick Lanes first two books - _Oxygen_ and _Power, Sex,
Suicide: Mitochondria and the Meaning of Life_.

------
tomohawk
Just thinking about the societal implications of this. For example, death is
one of the few things that causes turnover in the Senate.

It seems ironic that the mechanism here (killing off old cells) enables humans
to live longer, thereby possibly enabling these same humans to case society to
age.

~~~
api
Life extension will be horribly dystopian unless we can also find ways to
restore neuroplasticity and enable re-learning-- a kind of "second childhood."
Otherwise it'll be a bunch of immortal old curmudgeons sitting on top of
society saying "get off my lawn!"

Personally I'm not sure I'd even want too much life extension without
neuroplasticity restoration and quality of life extension. I'd rather be dead
than walking dead.

------
summer_steven
Not going to prevent aging as well as people think.

As cells age, the risk for mutations occuring when they divide increases. The
reason these cells stop dividing and become senescent is because dividing
elderly cells poses a high cancer risk.

I think this may buy the trappings of youth (plump skin, clear eyes, etc) at
the cost of a higher risk of cancer.

~~~
manmal
Yes, but the remaining non-senescent cells are obviously not damaged too much,
and thus CAN divide - perhaps they did not divide as often in their lifetime,
their ancestors were not as stressed, or their DNA was not compromised. If you
make room for those cells to divide, that should be a good thing.

------
batrat
Where do I sign up? (-:

------
trthomps
Where's the catch?

~~~
jlebrech
7 Billion humans

~~~
SubiculumCode
The universe is big. There is energy everywhere.

~~~
goatlover
Meanwhile, the Earth is not, and we still primarily use fossil fuels.

But maybe someday we'll have terraformed Venus and Mars, and found a way to
travel those light years. Probably not this century, though.

~~~
mcbits
Long-term survival could be the sort of problem that requires people to think
about it for 100-500 years beyond kindergarten. Moreover, societies here on
Earth could benefit from people caring more about the impact they will have
beyond their (currently) inevitable death in 0-100 years.

~~~
qw
It could actually be beneficial to the planet. If today's politicians knew
that climate changes, social inequalities and water shortages would actually
affect them in their lifetime, they might reconsider the short term benefits
of accepting donations from harmful lobbyists.

~~~
diggernet
In other words, it could redefine "short term".

------
ars
Summary: Kill cells that have stopped dividing, but that are still alive.
(Called: Senescent cells.)

Don't prevent them from entering this state (which could cause tumors), just
kill them if they do enter this state.

Hard part: Each organ/tissue has different types of cells, so each needs a
unique medication to kill those cells.

~~~
lsh
are you an auto-summary bot?

~~~
lsh
thankyou for the downvotes, it was a genuine question. I see a lot of this
bot-like behaviour on HN these days

~~~
grzm
A cursory review of their comment history would lead me to think that they're
not.

