
What Is Aging? Most Scientists Still Get It Wrong - sjcsjc
http://joshmitteldorf.scienceblog.com/2015/01/05/what-is-aging-most-scientists-still-get-it-wrong/
======
Htsthbjig
It is important to note that the fact "Starvation is also a way to live
longer." is probably wrong as some scientist have noticed.

The problem is that animals in laboratories are "coach potatoes". They don't
do the exercise they naturally do in their habitat searching for food.

They live overcrowded in small cages and overstressed. Most lab animals are
already ill from their artificial habitat, they have diabetes and other
disorders.

Strong social animals are isolated so they don't create problems like fighting
each other(what are thy going to do if not?).

Imagine you were forced to live in a sofa, or in your bed, all your life, with
no sunlight but LED lighting.

Most of those animals are overeating for their activity, so making them starve
is better than not doing it. But this tells us nothing about real animals in
the real world.

[http://www.vivisectioninformation.com/index.php?p=1_27_Unrep...](http://www.vivisectioninformation.com/index.php?p=1_27_Unreproducable-
results-from-the-animal-lab)

~~~
reasonattlm
You mischaracterize calorie restriction with optimal nutrition by calling it
starvation, and you mischaracterize the current research situation.

The evidence for it to extend healthy, mean, and maximum life span in a wide
range of species is very extensive: mice, flies, nematodes, etc, etc, etc. The
primate evidence for life span extension is mixed at this time, partially
because the two decades-long studies were poorly designed in hindsight, and
the expectation is that it doesn't extend life greatly in humans. Nonetheless,
it has enormously impressive short term health effects in we primates [1]. If
calorie restriction was a pill rather than a lifestyle, you'd beat a path to
the manufacturer's door, as it has far greater positive effects on health for
basically healthy people than any presently available medical technology.

It is true that there is some concern in the research community over the
degree to which laboratory mice are not good reflections of what is being
studied. This is not unknown, and it is not unacknowledged. A range of
rigorous testing programs aim to do something about past less rigorous results
- see for example the NIA Interventions Testing Program [2].

Interestingly it is worthy of note that many past research programs were
tainted by inadvertent calorie restriction - the things they tested led to led
to lab animals eating less. The effects of calorie restriction on health and
life span are many times larger than those produced by most other things under
testing.

To address your subtext of animal abuse, the only thing worse than running
animal studies to advance medicine and life science knowledge is to not run
those studies. Even the path to the future in which near all studies are
carried out in tissue engineered flesh or simulation, causing no harm to
creatures capable of suffering, requires present animal studies. Researchers
want that future as it is better on all counts. Further, studies of calorie
restriction and longevity are about the most benign of animal studies: these
animals are healthier and longer-lived as a result of the restriction. If you
want to do something about animal suffering, farming is the place to start,
not research, as it accounts for 99.9% of the harms you dislike.

[1]:
[http://impactaging.com/papers/v5/n7/full/100581.html](http://impactaging.com/papers/v5/n7/full/100581.html)

[2]: [http://www.nia.nih.gov/research/dab/interventions-testing-
pr...](http://www.nia.nih.gov/research/dab/interventions-testing-program-itp)

~~~
dschiptsov
Is it OK to try to establish a correlation between calorie intake and lifespan
without taking into account variety in calorie spending, or a "life style"?

It seems that excess of calories have a big negative effect for an "idle/aged"
lifestyle, and almost no effect for "hyper-active/young" lifestyle.

It seems also related to urban vs. rural populations.

------
gabriel34
The best explanation I found was on the book The Value of Tomorrow by Eduardo
Giannetti, Brazilian philosopher and economist (in this chapter he had several
consultants): If there is a trade-off between longer lifespan and reproductive
capacity at a young age, there will also be a point of equilibrium.

Suppose there was no senescence, we all lived perfectly healthy and at peak
capacity for the duration of our lives. We would still have limited lifespan
in nature, because of diseases, natural predators, etc. There would be a life
expectancy, since people would not live forever. Now suppose a mutation occurs
that grants the individual a boost in body functions at a young age with a
caveat: a gradual decline in body functions after a certain age. If this
certain age is way past the life expectancy of the population, this mutation
would give competitive advantage to its bearers, with no real downside, since
nobody lives way past the life expectancy anyway. This mutation would spread
throughout the entire population and aging would establish itself in this
population.

The point of equilibrium in these trade-offs would be different for each
population, since the environments and species are different, hence why
hummingbirds, dogs, humans and turtles have wildly varying life expectancies.

Trying to stop aging would involve stopping or mitigating these mechanisms,
which are deeply ingrained in our systems. The consequences of doing so are
far from straightforward, both to the individual (if we could not stop side
effects to have the cake and eat it too) and to the population as a whole.

~~~
UhUhUhUh
Yup. And the trade off between reproduction and aging is extremely well
documented in biology. In short, reproduction prioritizes the set over the
element. Kinda Borg-ish but that's what we have so far.

~~~
mitteldorf
The tradeoff between reproduction and aging is sometimes present and sometimes
absent. The successes are over-reported and the failures under-reported, so
you might get the impression of "extremely well documented" with a cursory
reading. Here is an example from Cynthia Kenyon's lab, "Healthy Animals with
Extreme Longevity"
[http://www.sciencemag.org/content/302/5645/611.full](http://www.sciencemag.org/content/302/5645/611.full)

------
teekert
Oh how nice a couple of references to some peer reviewed articles would have
been. Quotes like "This is my own perspective, shared by a handful of world-
class aging scientists, but it is not yet mainstream." make all my scientific
alarms go off.

It is an interesting way of looking at it though.

~~~
hnnewguy
> _all my scientific alarms go off_

Is it required on HN that every article be terse list of peer-reviewed facts?

~~~
jacquesm
No, but when you make claims like those in the title then those peer-reviewed
facts make all the difference.

There's a ton of pseudo science and outright bs in the anti-aging scene so
some references would definitely help in this case.

Articles that don't make grandiose claims don't need to put their evidence up
front. For 'most scientists' in the title read 'most scientists that hold a
view contrary to that of the author'.

------
ekianjo
This article gets so many things wrong I dont know where to start. The
argument that "our bodies are useless after reproduction therefore aging makes
us die when we are done" is so flawed in itself. If that was even remotely
true, women would die much earlier than men since their bodies' reproductive
age stops way earlier. So what is in nature's interest to have women live in
their 80s versus men die in their 70s ? There is just no good "purpose" to
justify those difference which are anyway way beyond the best times for
reproductive ages for both genders.

~~~
reasonattlm
In answer to your questions:

The grandmother hypothesis:

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

Evolution of sexually dimorphic longevity in humans:

[http://www.impactaging.com/papers/v6/n2/full/100640.html](http://www.impactaging.com/papers/v6/n2/full/100640.html)

~~~
ealloc
I like another theory I read recently: That it's because women's mitochondria
are more fine-tuned to their nuclear genome:

"The inheritance of mitochondria is asymmetric: you only get them from your
mother, and your father makes no mitochondrial contribution at all. Your
father’s mitochondrial contribution dies with him and is not passed on. What
does that mean? It means that there can be no selection to fine tune
mitochondria to the male nuclear genome."

Mitochondria are extrmely important to the cell and have been linked to many
effects of aging. The reasoning above suggests that mitochondria work more
poorly in males. And indeed, the paper (linked below) explains that in fruit
flies, mitochondrial genes in males are expressed with much higher variability
than females.

Your two links depend on human biology, but early male death is a much more
general phenomenon. Males die earlier in the vast majority of animals (with
gender). This idea could explain it.

[http://scienceblogs.com/pharyngula/2013/02/06/mothers-
curse/](http://scienceblogs.com/pharyngula/2013/02/06/mothers-curse/)

[http://www.ncbi.nlm.nih.gov/pubmed/23281153](http://www.ncbi.nlm.nih.gov/pubmed/23281153)

------
danieltillett
Ageing like everything in biology is incredibly complex. About the only thing
we know for sure is that everyone with a simple theory to explain ageing is
wrong.

Ageing is at least as complex as cancer, but has received 1000th the study. If
we assume understanding of a field correlates with resources committed then
ageing research is in the 1920s. If you read the scientific literature from
1920s on cancer you will find everyone had a theory and everyone was wrong.

------
jamesfisher
> It is the body shutting itself down, putting itself out of the way after it
> has done its job, finished reproduction.

Males' reproductive abilities continue into much later life. Wouldn't this
theory then suggest that males would live longer? The opposite is in fact the
case.

------
quonn
"These compromises have been made up ad hoc to avoid the inference that aging
evolved to benefit the community, not the individual."

Isn't this just group selection again? Has this view become more accepted
nowadays among biologists? There are very compelling arguments against it.

Maybe a better way to phrase it would be to say that aging has evolved to
benefit the offspring, which traditionally happened to make up a significant
part of the community?

~~~
facepalm
What arguments are there against it? I had assumed that evolution applies on
all levels (and not only to organisms). and what about ants - their evolution
would always be to benefit the community, I suppose?

~~~
Nevermark
Ants are often siblings of each other due to the high number of ants produced
by a single queen, so "group selection" for ants is really just "offspring
selection".

Most cases where group/community selection appears to take place have been
explained by individual selection. Similarly, most (if not all) cases of
symbiotic and cooperative behavior between species have been explained by an
evolution of selfish survival behavior of each species.

In both cases cooperation is not being directly selected for, but occurs as a
special case of individual/selfish selection.

~~~
facepalm
You mean groups are selected for because the group benefits the individual?
Sure - but that seems to me to just be a point of view, not a refutation of
group selection.

For example (to clarify), would you say religions are subject to evolution?

------
aetherson
Does anyone here have the background to address this author's claims about
telomeres? It seems like if telomeres were really a silver bullet to stop
cellular aging, we'd have huge scientific consensus about it right now. My
impression was that it was a promising line of investigation 20 years ago that
didn't have the dramatic results that were hoped for.

But I'm not in biology or medicine, and I may be wildly off base. I'm
naturally cynical about the presence of a silver bullet for aging, though.

~~~
xaa
The most convincing piece of evidence that telomeres are important in aging is
that lack of telomerase (the protein that extends telomeres) or otherwise
shortened telomeres causes progeroid (premature aging) disorders.

But there are problems. First, telomerase is activated in many cancers to
allow cancer cells to divide indefinitely, so there is a fear that adding
telomerase as an anti-aging treatment would increase cancer risk. It is
assumed that the finite length and existence of telomeres is an anti-cancer
mechanism by cells.

Secondly and even more problematic, aging occurs in tissues, and aging-like
gene expression signatures in cells, which still have ample telomeres. There
is a lot of evidence that other things like inflammation and metabolism, which
have no direct connection to telomeres, are critical to aging.

So telomerase/telomere lengthening is exceedingly unlikely to be a "silver
bullet" for aging. Experiments show that it can extend lifespan in mice
modestly. Conversely, though, upregulating or downregulating many other
proteins which have nothing to do with telomeres can also increase lifespan.

It is possible that telomeres are important in stem cell maintenance, since
stem cells have to last a long time and replicate repeatedly (stem cells
themselves are a very hot topic in aging right now).

------
jrh555
One idea that I'm surprised I've never seen mentioned is the possibility that
life ages in the same way that companies do. New high growth companies often
have lots of money to hire new people, buy new equipment, build new office
buildings, etc. When revenue eventually levels off or drops, often there are
no longer enough resources to support everything that was built up in the
growth phase. In older companies you might see a lot of old worn out equipment
and infrastructure that is not getting repaired due to lack of resources. This
effect can be seen on a larger scale in cities or even nations that experience
a slowdown in growth.

What if aging is simply a side effect of the fact that we stop growing at a
certain age? It could be that certain key resources needed to fully repair the
body are reduced or shut off once growth stops. Aging might even be a kind of
negative growth.

It's interesting that the effects of aging don't start showing up until after
we stop growing. Also, the rate at which different forms of life age seems to
be related to the growth rate. Some types of turtle can live to be over 200
years old but take 50 years to grow to full size.

I'd be curious to see if there is any research into aging along these lines.
If aging is related to growth, perhaps an anti-aging treatment could be as
simple as finding a way to restart growth for short periods of time to
generate the additional resources needed to repair damaged tissue. I have
heard of human growth hormone being used as an anti-aging treatment though
something tells me there would be more involved than just one hormone.

~~~
xaa
Well, if the problem were "not enough resources", then you would expect that
calories consumed would positively correlate with lifespan. But of course,
calorie restriction increases lifespan. This theory was rather popular before
1950 and part of why people found calorie restriction's success surprising.

A more modern and sophisticated version is called the "disposable soma" theory
of aging, which states that reproduction competes with maintenance activities
for the body's resources. But it too suffers from the same problem, and the
additional problem that some organisms do not appreciably age.

Yes, you are right that lifespan correlates with body mass/volume among
species quite nicely, with some exceptions. And it is indeed quite suspicious
that aging begins just about the same time growth stops. Growth hormone (GH)
levels drop with age and GH supplementation can slow some age-related
phenotypes. But, on the other hand, GH-deficient mice have increased lifespan,
and GH is induced by cancer and its supplementation may increase cancer risk.
There is a similar story for other growth hormones like IGF-1. Of course,
these hormones, especially IGF-1, are intimately connected with metabolism,
which is probably the set of pathways most heavily implicated in aging.

So I am not sure this "coincidence" of aging starting when growth stops has a
known explanation. It would however make an intriguing sci-fi novel if the
"cure" for aging involved always growing larger and larger in size.

~~~
jrh555
By resources I wasn't necessarily referring to calories consumed. I was
thinking of something like stem cells or some other resource useful for
repairing damaged tissues that might be deliberately restricted or "turned
off" by the body as part of the process of shutting down overall growth.

The rate of aging seems to be tied to the rate of growth with slower growing
organisms also aging more slowly so you might expect GH-deficient mice to live
longer if it resulted in a slower rate of growth.

Hopefully turning growth back on for a short period of time would not result
in the body actually growing larger in size. With luck, resources made
available by new growth would go to repair tissues damaged by aging before
initiating new growth.

------
dschiptsov
This "hard-wired cease of regeneration/renew" is a nice high-level theory,
while attempts to find a single cause (or a single gene) to stop or reverse
the process, is, probably, waste of time. There is no single process to be
stopped, leave alone reversed. Each major subsystem (if not each major cell
type) probably has its own "enough markers". That's why there are so many
different causes of "natural" death.

~~~
uniformlyrandom
Well, it is possible that every subsystem has its own self-destruction
procedures, but that would be such an inefficient way to design a system. And
nature is usually a very efficient designer.

~~~
dschiptsov
It is not self-destruction, I think, it is rather "never evolved/selected for
a long run". Everything "important" is supposed to happen in youth, at peak
and then "doesn't matter".

It is rather "stopping investing in repair" rather than "intentional self-
destruction". But I think there is no single "marker/indicator" for this.

So, they could keep regeneration of some specific kind of cells in a lab
animal, by manipulating some hormone, but it doesn't affect the other parallel
processes in different kinds of cells.

------
reasonattlm
Despite the fact that the principal, fundamental biochemical differences
distinguishing old tissue from young tissue are a largely settled and
defensible consensus these past twenty years [1], there are many theories of
aging [2]. From the point of view of development of treatments for aging, the
most important divide is between programmed aging theories (a loud minority)
and the view of aging as accumulated damage (the majority). A simplistic way
of looking at it is to say that in the programmed aging view epigenetic change
causes damage, while in the aging as damage view the damage is a side-effect
of the normal operation of metabolism and leads to epigenetic changes as a
reaction.

(This simplistic view obscures a lot of argument within programmed aging, just
as there is a lot of argument within the aging as damage view. The author of
this article has developed a novel evolutionary theory of programmed aging to
compare and contrast with a range of others, such as the hyperfunction theory
of aging).

At the present time we are entering an age of genetics. Whether the research
community thinks of aging as a program or not is very important from the point
of view of which treatments they try to chase. If aging is programmed, we'd
expect damage repair to be of limited utility. If aging is accumulated damage,
we'd expect attempts to change epigenetic patterns and gene expression levels
to be of limited utility.

Strangely, despite the fact that most researchers think of aging as damage
accumulation, the research community actually spends much more time on trying
to catalog and alter epigenetic and gene expression changes - the path that
clearly won't have any great impact on the underlying causes of aging in that
model. So if you do support programmed aging you should be pretty happy with
the way things are going. If you don't, you really shouldn't: the field is
heading in the wrong direction, for bad reasons. i.e. that it is easier to
raise funds for the study and alteration of epigenetics, or the Big Pharma
style development of drugs to do the same, which is the very hard exploration
of how to safely alter a massively complex system that is very poorly
understood, while it is much harder to raise funds to aim at rejuvenation
through repair of damage, as this latter is a comparatively new approach in
medicine.

So despite the fact that the majority of the field thinks that aging is
damage, next to no groups work on damage repair. They are largely working on
building a catalog of the precise way in which damage interacts with
metabolism in great detail, a part of the ongoing process of producing a
complete map of metabolism, a process that has only just started in the grand
scheme of things: what we have today is just the sketch of an outline.

But that list of forms of damage that cause aging? That's good and defensible
and therapies could be built starting now, with a proposed ten year timeline
to get to working prototypes in mice given $100m/yr funding. The whole and
main point of the SENS strategies for aging is that we can skip over the need
for full understanding of the detailed operation of metabolism and just fix
the damage we know distinguishes old tissue from young tissue. This is the
logical way to go if aging is thought to be damage. And yet it has taken a
decade of advocacy to get even a small number of researchers in the field to
support this approach. [3]

Want to prove whether aging is programmed or not? Implement SENS therapies, a
clear and very detailed research program with a billion dollar price tag (much
less than has already been spent on investigating sirtuins and mTOR, efforts
that have produced nothing but knowledge of metabolism, and none of the
promised treatments to modestly slow aging in healthy individuals). If that
produces actual rejuvenation in mice, then aging is damage accumulation. If it
doesn't, then it is programmed. End of story, fastest way to the target, job
done.

[1]: [http://sens.org/research/introduction-to-sens-
research](http://sens.org/research/introduction-to-sens-research)

[2]:
[http://www.senescence.info/aging_theories.html](http://www.senescence.info/aging_theories.html)

[3]: [http://sens.org/about/leadership/research-advisory-
board](http://sens.org/about/leadership/research-advisory-board)

------
sorokod
Can't take seriously an article with this kind of anthropomorphic attitude to
biology

------
breck
I enjoyed the post. Have one thing to add.

IIRC the role of telomeres in aging has been known for twenty or thirty years.
I'm blanking on the name, but there was a biotech company that went public in
the 90's that had a drug in the works to lengthen or prevent the shortening of
telomeres. But two decades later they haven't made much progress.

------
Houshalter
I was extremely skeptical of the title, but he makes a good case. Still it's
very unlikely aging is evolved. An animal that lives longer would be able to
reproduce more, therefore there is selection pressure for longer
(reproductive) life spans.

It's far more likely there are other reasons. For example limited telomeres
prevent cells from multiplying out of control. And if aging was easy to
biologically prevent/reverse, we would expect to find a few people out of
billions that live far outside the normal life expectancy. Like someone with a
rare combination of genes that happens to have longer telomeres or younger
hormones etc. Instead everyone dies pretty consistently within 90 years, give
or take a decade.

~~~
rwissmann
"therefore there is selection pressure for longer (reproductive) life spans"

this is too simplistic. there is also selection pressure for shorter
generational cycles, leading to faster evolution. keeping older generations
around would consume extra resources.

~~~
Houshalter
You are anthropomorphising evolution. Natural selection only favors
individuals, not the species as a whole. Plus it's not clear if that would
actually be a benefit. An organism which has survived and reproduced for
hundreds of years probably has very fit genes.

------
jostmey
My favorite explanation of Againg comes from William Hamilton. He took
advantage of the Euler-Lotka equation to calculate the number of offspring
that would be alive at any given point in the future. Using this equation from
the field of demographics, he showed that senescence has only a marginal
effect on fitness. As such, selective pressure would not be strong enough to
filter out mutations that might result in aging. Finally, he was able to
derive various mortality curves that "seem" to match pretty well with real
living systems.

~~~
mitteldorf
Marginal effect on INDIVIDUAL fitness, but a huge effect on THE FITNESS OF
ECOSYSTEMS. Without aging, ecosystems would be unstable dynamic systems, and
would not last more than a single generation. Without aging, everyone would
die at once, in famines and natural disasters. Aging is necessary to spread
out the death rate, so that populations don't swing wildly up and down.

------
amelius
I wonder what are the currently best established DIY techniques to slow aging.
I know low food intake could help, but what else?

~~~
sanxiyn
There is nothing else. Basically, calorie restriction works, and nothing else
does. I recommend Fight Aging! if you are interested.

[https://www.fightaging.org/faq/](https://www.fightaging.org/faq/)

~~~
Madmallard
I'm not so sure those are the only two. I'm fairly certain high dietary intake
of various vegetables, fruits, and legumes over processed foods would probably
greatly add to the life expectancy of regular people. Don't have a lot of hard
evidence but I have relatives who outlived their brothers and sisters by 10-20
years because they just ate significantly healthier and moved around more.

~~~
sanxiyn
Healthy diet keeps you healthy, but it does not slow aging. It prevents death
from reasons other than aging.

To prove "slowing aging", you need to demonstrate increase in maximum
lifespan, not average lifespan. Exercise, diet, etc. increase average
lifespan. There is no evidence they increase maximum lifespan, none at all.

------
Widdershin
This is truly the most amazing time to be alive (so far). No matter what
repercussions the destruction of aging might have, it awes me that we talk of
dramatically extended life and the colonization of the stars not only as
something feasible, but even possible within the next century.

~~~
givan
Unfortunately it's just talking, there is no real progress in either space
exploration let alone colonization or aging, hygiene and antibiotics was and
it's still is the only thing that prolonged life in the last century, we still
have a long way in both directions.

~~~
sergiosgc
Not really. Life expectancy at birth has steadily climbed:

[https://en.wikipedia.org/wiki/Life_expectancy#mediaviewer/Fi...](https://en.wikipedia.org/wiki/Life_expectancy#mediaviewer/File:Life_Expectancy_at_Birth_by_Region_1950-2050.png)

The effect continued past the large effects of hygiene, antibiotics and child
vaccination. You may argue that the curve is clearly asymptotic, and that a
maximum age genetic barrier is clearly visible. You can't argue, however, that
there isn't real progress after antibiotics and hygiene.

This type of barrier is typical of technological evolution. We do strain a
technology until returns are minimal, and only then sidestep to the next level
of evolution. Steam machines were mechanical wonders before the combustion
engine. Valves were amazing right before the transistor made an entrance.
Current "corrective medicine" will reach its peak right before "manipulative
medicine" enters the fray.

~~~
ekianjo
> The effect continued past the large effects of hygiene, antibiotics and
> child vaccination. You may argue that the curve is clearly asymptotic, and
> that a maximum age genetic barrier is clearly visible. You can't argue,
> however, that there isn't real progress after antibiotics and hygiene.

we are seeing a resurgence of bacteria resistant to antibiotics, though, and
we have no new lines of antibiotics to fight them. These advances may only be
temporary.

~~~
venomsnake
> we are seeing a resurgence of bacteria resistant to antibiotics, though, and
> we have no new lines of antibiotics to fight them. These advances may only
> be temporary.

We don't develop such, due to the broken way our pharmacy research is done.

It makes no sense for pharma companies to develop antibiotics due to low ROI
and lifetime of the product. A better approach for this is government to fund
researchers for areas that private sector has abandoned.

~~~
ekianjo
> A better approach for this is government to fund researchers for areas that
> private sector has abandoned.

yeah, like Ebola research funding done by the government ? That was an
efficient model.

------
ExpiredLink
You need not be a scientist to understand aging.

------
netforay
To be Immortal, or not to be, that is the question for each cell. Here is
simple explanation of Aging(and probably cure)

[https://www.authorea.com/users/13335/articles/13690/_show_ar...](https://www.authorea.com/users/13335/articles/13690/_show_article)

This is a result of more than year of research by the Author.

------
givan
Aging is encoded in our DNA with a purpose, if we will be able to fully
understand how DNA works me might be able to partially disable it but will we
want to? maybe when we will reach that level of knowledge we will also have
the wisdom to understand the implications.

~~~
sanxiyn
Do you want to die?

Of course we will want to. I am sure there will be lots of side effects, but
almost anything beats dying.

~~~
nicky0
Do you want to live forever? In a world where everyone lives forever? I'm
pretty sure most people will have had enough after the first million or so
years.

Someone must have written sci-fi of this.

~~~
Intermernet
I'd like to be able to choose when I die.

~~~
ramanan
and what number would you choose ? waitbutwhy had an interesting discussion on
this a few weeks back: [http://waitbutwhy.com/table/how-long-would-you-live-
if-you-c...](http://waitbutwhy.com/table/how-long-would-you-live-if-you-could-
choose-any-number-of-years)

~~~
placebo
Thanks for the link. I think this is a fascinating question.

