
Blood of world’s oldest woman hints at limits of life - rottyguy
https://www.newscientist.com/article/dn25458-blood-of-worlds-oldest-woman-hints-at-limits-of-life
======
adevine
Thanks for posting this, I thought it was fascinating research. This sentence
in particular was a surprise to me:

It’s estimated that we’re born with around 20,000 blood stem cells, and at any
one time, around 1000 are simultaneously active to replenish blood.

I was surprised the number was so low. Interesting to think this relatively
small number of little factories has to sustain us throughout life.

~~~
jrapdx3
That is a low number, but not the only example of limited resources in our
systems.

Dopamine neurons in the brain are essential for normal functioning.
Parkinson's develops when dopamine neurons die off with age or due to other
injury (toxins, trauma, etc.). It takes only a 15% loss of these irreplaceable
cells for the condition to begin to show up.

In contrast to the cortex of the brain with its 100's of millions of neurons,
we are born with only 250K dopamine cells which are never regenerated.

That's a narrow margin to rely on, we skate on very thin ice throughout our
lives. Nature is the staunchest conservative and doesn't throw away the things
that work. Our bodies still retain the archaic mechanisms of the earliest
multicellular organisms in our brains and bodies.

Looks like blood forming tissues are similarly following Nature's way.

~~~
btilly
Good evolution and good engineering principles are at odds.

In engineering an idea that has been found to work in one place gets adapted
in another. Also you often build reliability through adding layers of
redundancy.

Evolution has no straightforward way for good ideas to be identified and
reapplied to another system. It has to evolve again. Also if you have two
fully redundant systems, there is nothing to stop deleterious mutations from
disrupting one of them. The end result is that one of the redundant systems
will become unreliable, and then the other one gets maintained by selection
pressure. (This is also why creatures that live in a cave eventually become
blind, and parasites lose their ability to use now unnecessary body parts.
There is no engineering reason why this would happen, but is a natural result
of selection pressures being eliminated.)

~~~
antisthenes
"Good evolution" is essentially devoting the maximum amount of (usually very
limited) resources towards successful procreation and rearing offspring.

Hence the "features" or "redundancy" which would otherwise consume resources
and not significantly affect procreation chances (like your cave example)
eventually get selected against and disappear.

"Good Engineering" on the other hand usually devotes additional resources to
redundancy, fault-tolerances, which do not necessarily offer a competitive
advantage in procreation.

~~~
datenwolf
> "Good evolution" is essentially devoting the maximum amount of (usually very
> limited) resources towards successful procreation and rearing offspring.

It's not that simple. If producing the maximum amount of offspring were the
goal, populations of a species would quickly collapse. It's also a poor
principle to explain social behavior and organisms living in hives or strictly
hierarchically procreating groups.

A much better model principle would be, that evolution optimizes for maximum
probability of the _offspring_ to successfully procreate. By adding this layer
of indirection a lot more of what we can observe in biology can be explained
with less presumptions (Occam's Razor).

~~~
antisthenes
That does sound like a better way to explain it.

My post was just layman speculation, as I'm not a biologist/ecologist.

------
raverbashing
Now the real question is: when are the telomeres rebuilt?

Because every individual started with one single cell, from a father and
mother cells that also underwent cell division

Hence at some point in time these telomeres get rebuilt/replenished.

~~~
tathougies
Telomeres are lengthened in women when their eggs are made, while still in
their mother's wombs. Men are constantly lengthening telomeres in the cells
that form sperm. This is one reason why children of older men tend to live
longer. Of course, this benefit only really comes from fathers in their late
twenties, because otherwise other paterrnal-age-related pathologies can
outweigh the benefits.

~~~
echelon
I wasn't aware of a higher paternal age ever being a good thing. Are there
papers or articles on this? What's the "sweet spot" before genetic mutations
in the germ line become a problem?

~~~
themartorana
I'm hoping it's some time after 36 for no particular reason...

------
reasonattlm
It helps to think about the basics when talking about telomere length and cell
behavior.

1) Telomeres shorten with each cell division in ordinary somatic cells. When
they get too short, cells self-destruct or stop dividing. So average telomere
length in tissue is a function of cell division rates.

2) Stem cells support their associated tissue type by providing new cells with
long telomeres. Thus average telomere length is also a function of cell
replacement rates.

3) Average telomere length is at present usually measured in white blood
cells. The rates of division and replacement here are tied in to many factors,
including general health, autoimmunity, infection, state of the thymus, and so
on and so forth. It would probably be better to use another tissue, such as
skin, but that isn't the way things worked out in practice.

So telomere length is far removed from first causes in aging - it is largely a
marker, largely of stem cell function in most tissues, but in immune cells
with their varying rates of division according to circumstances, also a marker
of all sorts of other unrelated or partly related things.

If telomere length is globally extended, you have cells that can divide more
often without the need for stem cell support, and you also have more energetic
stem cells. But those cells dividing more often are more damaged on average.
This may or may not be important enough to do bad things such as raise cancer
risk significantly in our species: more data needed.

------
4bpp
Blood storage for autologous transfusion has apparently already been a thing
for a while[1] and has been indicated to be effective in animal
experiments[2], but as far as I can tell, no provider is willing to store it
for more than about 20 years (and what is stored may not in fact contain stem
cells, but rather only something that spurs the existing ones into activity).
My general impression is that the medical community's moral gut reaction is
unfavourable towards the idea.

[1]
[http://www.bloodbook.com/storage.html](http://www.bloodbook.com/storage.html)
[2] [https://www.newscientist.com/article/mg22329831-400-young-
bl...](https://www.newscientist.com/article/mg22329831-400-young-blood-to-be-
used-in-ultimate-rejuvenation-trial/)

~~~
elsewhen
i believe that foreverlabs[0] is a startup that aims to do what you are
suggesting

[0] [http://www.foreverlabs.co/](http://www.foreverlabs.co/)

~~~
4bpp
Looks interesting. Unfortunately, I'm not sure my prior probability that a
random startup would survive for sufficiently long to be of use to future me
is sufficiently high to justify whatever cost their services would come at...

~~~
cbhl
It never hurts to send them an email and ask them what the price of their
services is.

------
blackbagboys
IIRC there was a doctor posting in other threads about his bone-marrow stem
cell banking startup. My understanding was that these stem cells were stored
when young, and could be multiplied in a lab environment and then re-injected
therapeutically (to cure MS or arthritis or whatever). Would these kind of
banked stem cells (say, banked in one's early or late twenties) also
potentially assist with life extension?

~~~
codecamper
Or might you have problems because now you have fewer stem cells.

------
1dKFpcxn
Does this mean that people who give blood are losing valuable stem cells and
wont live as long?

~~~
maxerickson
There aren't really stem cells floating around in the blood. The donation
would likely still impose some cost on the stem cells though (I doubt anybody
has much of a handle on that cost).

There is some evidence that frequent blood donors live longer than occasional
donors. Being healthy is a selection criteria for blood donation, so it can be
hard to study the impact.

[http://sciencenordic.com/frequent-blood-donors-live-
longer](http://sciencenordic.com/frequent-blood-donors-live-longer)

~~~
1dKFpcxn
Interesting. I looks like there are Peripheral Blood Stem cells, as opposed to
those in your bone marrow.

[http://www.bloodjournal.org/content/bloodjournal/98/10/2900....](http://www.bloodjournal.org/content/bloodjournal/98/10/2900.full.pdf?sso-
checked=true)

------
zeristor
Hmmm.

From an engineering perspective what are the MTBFs for the various human
components; are a dearth of White blood cells a prime reason for aging and
death?

Great progress has been made in genetics surely one could read the DNA of a
few thousand cells and have an extremely strong confidence of what the
unmutated DNA for a person once was.

And from this you could make new white blood cells et voila.

This all seems rather Blade Runnery. Mind you there would be societal problems
with people who can live much older: slowing of cultural evolution, career
blocking, and monopolising property; we've got that now but it would get
worse.

I'm worried about the Brexiters kicking out the metric system;that and fascist
tyranny.

~~~
reasonattlm
From an engineering point of view, there has been some work on the application
of reliability theory to aging, though not to the point where your question
can be answered using this approach:

[https://en.wikipedia.org/wiki/Reliability_theory_of_aging_an...](https://en.wikipedia.org/wiki/Reliability_theory_of_aging_and_longevity)

[http://www.ncbi.nlm.nih.gov/pubmed/20469937](http://www.ncbi.nlm.nih.gov/pubmed/20469937)

Immune system aging is an important component of age-related frailty, and
probably also accounts for the rising number of senescent cells and higher
cancer risk. It isn't as simple as a dearth of cells, however. It is more of a
complex configuration/whole-system failure in which rate of cell replacement
is just one variable contributing to the bad state endpoint. See for example:

[https://www.fightaging.org/archives/2006/12/when-and-how-
doe...](https://www.fightaging.org/archives/2006/12/when-and-how-does-the-
decay-of-your-immune-system/)

[https://longevityandhealthspan.biomedcentral.com/articles/10...](https://longevityandhealthspan.biomedcentral.com/articles/10.1186/2046-2395-2-8)

~~~
ilaksh
From an engineering point of view, this article is an oversimplification.
Check out [http://www.sens.org](http://www.sens.org) for a more comprehensive
and sophisticated approach.

------
sharpercoder
Does this mean donating blood reduces your lifespan?

~~~
tr1ck5t3r
The opposite.

Having a blood transfusion from someone younger than you will increase
longevity.

[https://www.theguardian.com/science/2014/may/04/young-
blood-...](https://www.theguardian.com/science/2014/may/04/young-blood-
reverse-ageing-mice-studies)

So it pays to be a vampire!

~~~
kyriakos
how long before the rich start exploiting this?

~~~
tudorw
Or how long have they been...

~~~
Snowdax
I believe the term is vampires. That concept has been around for quite a long
long time...

------
codecamper
If stem cells are finite & small in number. And you have some removed to be
preserved for later life... Then maybe you will have problems due to having
fewer stem cells?

------
ilaksh
Stem cells are a part of it, but there is much more to it. For a realistic,
comprehensive, and much more informed approach to aging research, see
[http://www.sens.org](http://www.sens.org).

~~~
x2398dh1
They aren't engaged in general, "aging," research actually, DeGray has stated
he's interested in life-extension technology, to the extent that it might be
possible. Their goal, as stated on the website you just linked to, is as
follows:

> Our goal is to help build the industry that will cure the diseases of aging.

I'm not saying you're wrong...I just think there's some confusion online as to
what they really are trying to do. They don't research aging in general, which
would imply they are a University Body whose sole function is research for the
purpose of research...they are specifically attempting to create a kind of
science, which may or may not be valid, by funding certain types of research
done by recognized research institutions, with the hope that evidence will
support what they believe to be true...sort of like how the Koch brothers fund
all sorts of research hoping to poke all sorts of holes and nuances into the
accepted version of how climate change is understood. They may very well come
up with something interesting, informed, and comprehensive...but that does not
mean that they are being realistic. In research you don't get to choose
whether your hypothesis is realistic or not...you just sort of go out into the
woods and start picking things up and seeing whether what you think the laws
of nature are...really are true...but you could be completely wrong and you
might find nothing. You don't get to choose whether you catch a fish...you may
come back to shore with zero fish after fishing for 50 years...or 100
years...or an infinite number of years.

~~~
reasonattlm
SENS isn't new science. It is a synthesis of existing evidence for what causes
aging and age-related disease, pulled in from many branches of medical
research. The original contributions are the high level view of damage repair
as the guiding basis for treatment, plus specific plans for how to address
these causes.

I don't think you can say it's wrong in wholesale at this point, given where
things stand. The mainstream position in the aging research community is that
aging is caused by an accumulation of damage.

Senescent cell clearance has been on the SENS agenda since day one, with
plenty of evidence to back it as a cause of aging from the past decades of
research. Life extension has been demonstrated in mice through senescent cell
clearance. There are two funded startups moving senescent cell clearance
therapies to the clinic.

You'll also find it hard to argue against the proposition that amyloid causes
specific age-related conditions. E.g. amyloid beta in Alzheimer's disease,
transthyretin amyloid in heart disease. These are very mainstream concerns.

Similarly, there are few objections to the idea that declining stem cell
function is a cause of aging, and plenty of evidence to show that restoring
stem cell activity is beneficial.

And so on.

------
ape4
So luck is the key. If your mutations are good you live a long healthy life.

~~~
thaumasiotes
We knew that long before this study. It's true of everything, not just
longevity.

------
tr1ck5t3r
Vitamin D derived from sunshine notably UVB reduces the shrinkage of the
telomeres.

~~~
Lio
Does dietary vitamin D not have the same effect?

~~~
f00a99s
The source matters because there are two common types of vitamin D: D2 and D3.
Sunlight lets you produce D3, while supplements are typically D2.

In food that's been fortified, it will probably have D2, while food that has
natural vitamin D (like fatty fish) will probably have D3.

Although the two forms are metabolized through different mechanisms, the
difference is negligible for most people. However, for some people (depending
on genetics, diet, or lifestyle), supplemental Vitamin D2 will not be an
adequate replacement for Vitamin D3.

[0]
[http://ajcn.nutrition.org/content/84/4/694.full](http://ajcn.nutrition.org/content/84/4/694.full)

~~~
mrfusion
Vitamin d3 supplements seem widely available.

