RE: [DIYbio] Prospects of anti-aging research

[Reason]

> -----Original Message-----
> From: diy...@googlegroups.com [mailto:diy...@googlegroups.com] On
> Behalf Of Jace
> Sent: Saturday, August 04, 2012 5:09 PM
> To: diy...@googlegroups.com
> Subject: [DIYbio] Prospects of anti-aging research
>
> Something I myself am looking
> into is the prospect of greatly extending human lifespan and in
> essence, dramatically slowing and possibly ending biological aging.
> Though it is largely considered fringe science, there are promising
> frontiers being forged on the matter, led by British scientist Aubrey
> de Grey. I have seen others comment on this scarcely on the forums
> here, and am wondering if any of you are actively pursuing this area,
> whether it is by the gathering of information on the subject or any
> experiments you may have carried out? I realize how large a project
> this is, but as I stated above, this is just the type of group that
> through a communal effort, can make massive strides forward that most
> researchers have not even considered.

I've put this idea forward in the past (e.g. some of the blurb at
http://www.opencures.org); a fair amount of work that falls under the SENS
banner that could be done well by distributed groups of volunteers. E.g.
bacterial discovery for bioremediation, finding novel soil bacteria species
that can break down the components of lipofuscin and other harmful metabolic
byproducts.

I would note that intervening in the aging process is far from fringe
science nowadays. It's a core concern for many research groups, and well
accepted as a goal in the research community - though most of those involved
in such work are focused on what I see as comparatively ineffective lines of
research involving metabolic and epigenetic manipulation to slow
accumulation of cellular and molecular damage. These research programs will
produce far more knowledge than actual benefit to patients, as measured in
years of health and life, and the end results of their work will prove
largely ineffective for old people.

The focus on repair of damage by de Grey and others is the way to go.

The DIYbio community is not at the present time involved in work on aging in
any meaningful way so far as I can tell, and some folk are actively hostile
to the idea - which mirrors the community at large in that respect, sadly.
One might argue that it's still way too early for the community to be doing
much other than tech demos, building incubators like Biocurious, and working
on lower cost basic device implementations needed for the next stage (e.g.
openpcr.org or any one a thousand other lines of development that fall into
the Kickstarter range of funding, all of which lower the barrier to entry
for the hobbyists who will later grow to become more than hobbyists). But
the future of medicine and medical development clearly involves a breakdown
of the priesthood and involvement of a far broader networked community of
varying levels of skill and for-profit inclinations, akin to wide
distribution presently in place for fields as varied as astronomy and
software development. Some people don't like that and don't want to see a
world of medicine that falls outside the heavy regulation that characterizes
today's field, but it is what it is. The way in which DIYbio finds its place
in that scheme of things is for people to come and do the work, talk about
it, and attract other folk to the fold.

Reason

[Mega]

Well,

>Some people don't like that and don't want to see a
world of medicine that falls outside the heavy regulation that characterizes
today's field, but it is what it is.

I think, anyhow, when somebody wants to have a tatoo, and is above 18, he can do it.

Everybody should be free to engineer his body the way he likes. If one wants to be a na'vi, why not?  xD

On the other hand,one's children shouldn't be affected, so no gametic cell engineering without the urge (genetic diseases).



I've heard of A. de Grey, and I love his words: "Aging is the most wide-spread disease ever. It kills people. We spend much money on fighting illnesses such as Aids, Alzheimers, etc.  But 90% [idk that number anymore] of the industrialized world's people die of aging. This way, it is obvious that we should put large sums into fighting it too!! "

It's very pitty that we don't throw in large money, because if we did, I'm sure that *we* could live at least 150 years. As he explained, when a medicine is invented that makes you live 10 years longer, in this time another medicine is invented that gives you another 15 years and so on!! (so in this case, the first medicine gave you 25 years longer, and because of exponential growth of technology, within this frame of time, another medicine will bee invented)

[Jace]

I'm glad to see that at least the two of you are open and enthusiastic about the prospects of anti-aging research.  As Reason mentioned, certain parts of de Grey's plan, like screening for microbial enzymes to degrade lipofuscin, is just the sort of thing I had in mind that would be much easier and quicker as a communal effort.  It's a shame that many people outright reject de Greys approach to the matter, including a lot of funding sources and the FDA which does not outright fund somethign labeled "anti-aging research."  Are either of you currently involved in any sort of aging research?  de Grey (among others) lays out a good foundation of where to start in several key areas, but as I'm sure you know, getting the people or the resources to tackle these problems is easier said than done. 

[Bryan Bishop]

On Sun, Aug 5, 2012 at 8:42 AM, Jace <jkry...@yahoo.com> wrote:
> s a shame that most of the DIYbio group is combative to this area of
> research, but it's something I expected given that a lot of academic and
> industry researchers are like this as well.

Well, I suggest you start reading:
http://diyhpl.us/~bryan/papers2/longevity/
(and contributions are appreciated...)

- Bryan
http://heybryan.org/
1 512 203 0507

[Bryan Bishop]

On Sat, Aug 4, 2012 at 8:25 PM, Reason <rea...@fightaging.org> wrote:
> The DIYbio community is not at the present time involved in work on aging in
> any meaningful way so far as I can tell, and some folk are actively hostile
> to the idea -

Sorry, I think you are sort of full of it. There has always been a
significant influence on DIYbio from the longevity and transhumanist
groups, starting all the way back in 2008. I agree though that people
working on aging projects have not been entirely public about their
work.

http://diyhpl.us/~bryan/irc/aubrey.jpg
(I kid, I kid..)

[Bryan Bishop]

On Sun, Aug 5, 2012 at 12:31 PM, Jace <jkry...@yahoo.com> wrote:
> Thanks a lot for the link. Were all these resources compiled by you? There

That's my file server, but obviously I did not write those papers?

> spring with a BS in biotechnology and minor in biochem, but my real
> interested are in aging research. Is that something you focus on in your
> work? I know in your videos you say you work on transhumanism in general,

No, I am not presently doing things that could be construed as
research, much less aging research. I do like to pretend I have some
hardware projects in the works, but most of my time is spent making
software.

> but was wondering if you could fill me in more specifically on what you are
> researching if you don't mind? I know you, as well as previous posters in
> this thread have said most people don't like sharing their research in this
> area openly on the forums, so if you don't I understand. You also mentioned

Well, in this case, it's because I have nothing to tell you, not
because I am not sharing. I am at least generally interested in
keeping up with longevity papers.

> something about a hackerspace, which I'm guessing are areas that the DIYbio
> community can go to do some hands on work in these areas? Is finding a

http://hackerspaces.org/wiki/List_of_Hacker_Spaces
http://diyhpl.us/wiki/diybio/groups
http://diybio.org/local

> hackerspace locally just as simple as looking for nearby biohackers on the
> forum?

[Matthias Bock]

Well, I suggest you start reading:
http://diyhpl.us/~bryan/papers2/longevity/
(and contributions are appreciated...)

It's a bit inconvenient to read all the separate files ;-)

Could you not maybe make a blog out of it or sth ?

[Matthias Bock]

What most disappoints me about the “established” scientific community is the seemingly sluggish trend of trying to push these same boundaries.

How come you think so ? Most scientists I know are quite eager to push boundaries.

One could criticize though, that most of them hold back their knowledge until it's published in press.

A big point is also, that publications, representing already gained knowledge,

are often not accessible by the public (that's the publishing companies fault, they often charge for papers, even online).

 

 What I would consider cutting edge research is constantly being shot down in media by so called science “experts.”

I don't understand. What do you mean ? Example maybe ?

 

Something I myself am looking into is the prospect of greatly extending human lifespan

Many people look into this, immortality is an old "dream of mankind" ;-)

It's not that easy though, since statements like "aging is a disease 90% of mankind die of"

are just populistic. Aging is not a disease, it's genetically programmed (with purpose), at least partly.

In any case, life is adapted to being subject to aging, so it will take more effort than just introducing

a gene into man, which confers some "toxic component degrading enzyme".

You may have to rewrite larger parts of the genome, so to say.

We lack both the understanding as well as the technology

(one could also add - a solid philosophical basis in our society -)

to do such stuff at the moment.

am wondering if any of you are actively pursuing this area

Not directly, but I'm researching mitochondrial metabolism and reactive oxygen species.

(knockout can increase life span in yeasts up to the 10-fold).

 

this is just the type of group that through a communal effort, can make massive strides forward that most researchers have not even considered.

Nicely formulated. Reminds me of "The cathedral and the bazaar" ...

There seems to be no reason, why scientific work shouldn't happen more "distributed".

But there are problems, DIYbio needs to solve:

* Laws: The sophisticated stuff usually requires genetic manipulation, which is restricted in many countries. But also without, it already starts when you want to order some pure chemicals ...

* Know-How: sophisticated stuff is ... sophisticated, I mean, often difficult to carry out, you need to have some pre-education

* Philosophy: What can we do, what shouldn't we ? Also from the communal safety point-of-view, stuff, that has far-reaching consequences to an ecosystem ...

* Publication and Reviewing: If you found sth, you need to match scientific standards for publication. You need to "announce" your finding (currently via scientific journal publication) and also need to provide others with the ability to try to reproduce your results and critically review your publication etc. ...

Cheers, Matthias

[jlund256]

I did research on aging for many years.  There scores of labs working aspects of the problem.  It is not fringe, but it is underfunded compared to the potential and likely payoffs.

 

I don't know of any DIY biology work on aging.  At this time, I don't see any point in trying treatments on people.  First, I don't think there are treatments with a good chance of working (except for caloric restriction).  And second, I don't see how it would be science.  There is no way to measure if a treatment is working.

 

However, there are quite inexpensive but very interesting aging experiments that can be done using model organisms--yeast, C. elegans (worms), fruit flies, and the high end of cost and time--mice.  There are interesting experiments studying existing extended lifespan strains.  There are interesting drug treatment experiments, interesting environmental manipulation experiments, gene knockout experiments.  There are hundreds of treatments or genetic manipulations known to extend lifespan, and nearly all of them have only been run through one or two experiments (sometimes only the lifespan test). 

 

Many of the papers are freely available--search on PubMed, or one of the aging blogs that links to research.

 

A DIY biology enthusiast can, for a few hundred bucks, get started doing novel and interesting (publishable, if that is your goal) experiments that only take a few weeks each.

 

[Mega]

>Aging is not a disease, it's genetically programmed (with purpose), at least partly.

Alzheimers is the same then. Deposition and deterioration. But it is considered an illness, so I consider aging an illness too.

Purpose of aging? I don't think so.



You know why mammals age? Because there is no selective pressure on aging. The ancestors of mammals were to be eaten at the dinosaure age. They had to propagate very quickly, longevity didn't help because they would be eaten anyway! As quick as possible as many children as possible, that was the best survival change of ancient mammals. In former times, at the age of 20 or 30 years you had children. And thus, evolution of you simply ends. You've passed your genes.  Whether you become 40 or 100 (or 500) has absolutely no effects on the genome of your descendants.

>Are either of you currently involved in any sort of aging research?

I'm not, at least until now :D

I sometimes read articles, and hear of some new approaches etc.

You probably heard of spermidine?

Extracting the synthesis gene(s) from  grapefruite and insert it (in yeast and after verification) into  mice cells / a common food plant (crop?) to make a daily vaccine against aging.

[Reason]

> -----Original Message-----
> From: diy...@googlegroups.com [mailto:diy...@googlegroups.com] On

> Behalf Of Matthias Bock
> Sent: Tuesday, August 07, 2012 12:19 AM
> To: diy...@googlegroups.com
> Subject: [DIYbio] Re: Prospects of anti-aging research
>
> It's not that easy though, since statements like "aging is a disease
> 90% of mankind die of"
> are just populistic. Aging is not a disease, it's genetically
> programmed (with purpose), at least partly.
> In any case, life is adapted to being subject to aging, so it will take
> more effort than just introducing a gene into man, which confers
> some "toxic component degrading enzyme".
> You may have to rewrite larger parts of the genome, so to say.
> We lack both the understanding as well as the technology (one could
> also add - a solid philosophical basis in our society -) to do such
> stuff at the moment.

This is far from being a good summary of the possible lines of research. The
present work on interventions into aging fall into two broad camps:

1) Metabolic, genetic, and epigenetic manipulations to slow aging

Researchers working on calorie restriction and exercise mimetic drugs fall
into this category, and form the majority of that small part of the aging
research community that does work on interventions. They are following the
traditional drug discovery process in search of targets that shift
metabolism into a state where aging proceeds more slowly. The obvious paths
here are things like boosting the operation of autophagy or trying to
recapitulate some of the epigenetic changes caused by calorie restriction in
the hopes of capturing some of its effects. The challenge here is that the
biochemistry of these states is exceedingly complex.

Evidently this is going slowly - a billion dollars have been sunk into work
on sirtuins alone, for example, with very little to show for it.

Structurally and strategically this is evidently an expensive path to a poor
end result. It is being taken because it is an easy evolution of the
existing drug development methodology, and therefore something that can be
shoehorned into the straightjacket regulatory process and sold to funding
sources. But it will take another few decades and a great deal of time and
money to obtain even a moderately good CR or exercise mimetic drug, or
something that works along similar lines, by following the present
regulatory path to approval. That drug will do next to nothing for people
already old, as slowing further damage has limited utility at that point,
and will in any case not be approved for use for anything other than
treating end stage diseases of aging.

(Absent regulatory changes, the FDA will not approve treatments for aging
and there is no present path short of revolution in that area of government
to declare aging a disease in the regulatory sense - this essentially
ensures that any commercial development must happen overseas, and that any
work in the US will be diverted to developer not-so-useful applications such
as incrementally better diabetes therapies or the like).

This is the path to wasting a great deal of time in generating nothing but
knowledge. If this path dominates over the next twenty years, we will let
the opportunity to extend human life slip through our fingers.

2) Repair the damage that forms aging

Aging is the accumulation of cellular and molecular damage, and evolved
reactions to that damage, some of which are the flailing of systems that
cause more issues in the old and damaged - because natural selection favored
front-loaded effectiveness in the young at the expense of later operation.
The immune system is a great example; at the most fundamental levels its
structure leads it to be both highly effective in the young and cause harm
in the old. Another is the way in which stem cells shut down in the old due
to changes in signaling in their niche tissues, reactions to rising levels
of cellular damage and dysfunction, most likely to damp the risk of cancer.

But at root it is damage that drives aging: mitochondrial mutations,
accumulated byproducts of metabolism that cannot be broken down (like
lipofuscin), cross-linked proteins, and so forth. These all happen as a
consequence of the operation of metabolism, build up, and kill you in the
end. It's like complicated rust - a metal structure left out in the rain can
fail in a thousand ways, but it's all down to the one root cause.

So it's possible to develop biotechnologies that can repair these forms of
damage. This is considerably better envisaged than attempts to slow aging -
there's a list and a roadmap. It shouldn't be any more expensive. It's hard
to imagine it to be any more expensive - that billion dollars spent on
sirtuins and a decade of time could give an even chance shot at repairing
all of the known fundamental forms of damage that drive aging in mice.

At the end of this road lies a package of therapies that will be of great
utility to the old, because they directly attempt to reverse the damage they
have suffered - not just slow down the final spiral, but reverse its course.
Yet as yet only a tiny - but growing! - minority of the research community
are working on this sort of thing, and as yet there is no regulatory path to
making the logical end result of once-a-decade preventative repair therapies
for the healthy easily available in the US or Europe.

Some reading material on the difference between these two opposed strategies
can be found here:

http://www.fightaging.org/archives/2012/02/enthusiasm-for-the-slow-road.php

http://www.fightaging.org/archives/2008/09/the-scientific-debate-that-will-d
etermine-how-long-we-all-live.php

And for more in-depth coverage of the biology and present work, you might
look at the SENS Foundation's research report for 2011:

http://sens.org/files/pdf/2011_Research_Report.pdf

Reason

[Alessandro Siletto]

2012/8/7 Mega <masters...@gmail.com>

Purpose of aging? I don't think so.

You know why mammals age? Because there is no selective pressure on aging. The ancestors of mammals were to be eaten at the dinosaure age. They had to propagate very quickly, longevity didn't help because they would be eaten anyway! As quick as possible as many children as possible, that was the best survival change of ancient mammals. In former times, at the age of 20 or 30 years you had children. And thus, evolution of you simply ends. You've passed your genes.  Whether you become 40 or 100 (or 500) has absolutely no effects on the genome of your descendants. 

I think it could be something related to adaptation and natural selection. an animal that live only 50 years is more adaptable to changes compared to one that live 500 years. and generally the resources are limited and a population composed of younger (and reproductive) animals may be more competitive.

--
Alessandro Siletto
TC-Web - Technology Consulting
Via Venaria 37/C
10148 Torino
Tel. 011 2295193

[Reason]

> -----Original Message-----
> From: diy...@googlegroups.com [mailto:diy...@googlegroups.com] On

> Behalf Of Alessandro Siletto
> Sent: Tuesday, August 07, 2012 8:36 AM
> To: diy...@googlegroups.com
> Subject: Re: [DIYbio] Re: Prospects of anti-aging research
>
> 2012/8/7 Mega <masters...@gmail.com>
>
> Purpose of aging? I don't think so.

Aging has no purpose, just as any evolved feature has no purpose. It has
simply been a more effective adaptation than not aging in most evolutionary
niches. See:

http://www.fightaging.org/archives/2011/03/we-age-because-the-world-changes.
php

"When conditions change, a senescent species can drive immortal competitors
to extinction. This counter-intuitive result arises from the pruning caused
by the death of elder individuals. When there is change and mutation, each
generation is slightly better adapted to the new conditions, but some older
individuals survive by random chance. Senescence can eliminate those from
the genetic pool. Even though individual selection forces always win over
group selection ones, it is not exactly the individual that is selected, but
its lineage. While senescence damages the individuals and has an
evolutionary cost, it has a benefit of its own. It allows each lineage to
adapt faster to changing conditions."

This of course has no bearing on whether we should do something about it.
Biotechnology is one more tool that better allows us to steer our own course
rather than being limited by what an uncaring world thrusts upon us.

Reason

[Jeswin]

On Tue, Aug 7, 2012 at 11:43 AM, Reason <rea...@fightaging.org> wrote:
>
> Aging has no purpose, just as any evolved feature has no purpose. It has
> simply been a more effective adaptation than not aging in most evolutionary
> niches. See:
>

Sorry in advance if I steer this conversation in the wrong direction.

Have you all considered the thermodynamic law of entropy and its
effect on systems such any living organism? I haven't looked into it
so I am just posing a question that came to mind as I was reading this
thread.

This article was found as I was searching "law of entropy and aging":
"Entropy Explains Aging, Genetic Determinism Explains Longevity, and
Undefined Terminology Explains Misunderstanding Both"
http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.0030220

[Jace]

>How come you think so ? Most scientists I know are quite eager to push boundaries

 

I know that, in essence, all research is trying to discover new things and "push the boundaries," but I feel like the scientific community at large does this more gradually rather than taking large jumps past the current "boundaries" when it comes to aging and rejuvenation biotechnology research.  Its understandable, especially since this area of research is largely underfunded as you pointed out, meaning at the moment its a high risk, low reward scenario in terms of funding.     

 

>don't understand. What do you mean ? Example maybe ?

 

This is just my opinion, but in general it seems that any time there are stories in the news about some new research in a medical field, its either overhyped or sort of brushed off as science fiction. This is likely because these reports are coming from news anchors/magazines instead of someone who is familiar with the science, but either way, this can often lead to news about aging research being misconstrued.

 

>It's not that easy though, since statements like "aging is a disease 90% of mankind die of"

>are just populistic. Aging is not a disease, it's genetically programmed (with purpose), at least partly.

 

I think it all depends on how you define "aging."  The way I see it, aging is just an accumulation of of wear and tear in combination with the build up of cellular "junk" and natural DNA damge.  In that regard, I wouldn't suggest trying to rewrite the genome , but rather attack the problems at the source.  Most of my knowledge in the area comes from the SENS way of thinking, where the goal is to clean up intracellular and extracellular junk and tackle other key areas that, putting it simply, need a tune-up after years of natural biological use. 

 

>But there are problems, DIYbio needs to solve:

>* Laws: The sophisticated stuff usually requires genetic manipulation, which is restricted in many countries. But also without, it already starts when you want to order some pure chemicals ...

>* Know-How: sophisticated stuff is ... sophisticated, I mean, often difficult to carry out, you need to have some pre-education

>* Philosophy: What can we do, what shouldn't we ? Also from the communal safety point-of-view, stuff, that has far-reaching consequences to an ecosystem ...

>* Publication and Reviewing: If you found sth, you need to match scientific standards for publication. You need to "announce" your finding (currently via scientific journal publication) and also need to provide >others with the ability to try to reproduce your results and critically review your publication etc. ...

 

I completely agree with you on this.  There are no doubt hurdles outside just doing the research.  Things like "what ramifications will this have?" and issues of safety and legal procedures in acquiring componented needed are always an issue. 

 

One of the reasons I started this topic was to have conversations exactly like this, and get the word out there, so to speak.  I agree that this is sophisitcated science and not something one can just jump into, but simply having open discussion about it on the DIYbio forums is a step in the right direction.  Even if it gets a few people to look more into the science behind aging and rejuventation biotech research, it is a few more people than were knowledgeable about it compared to before. 

 

Thank you for the input,

 

Jason   

 

 

 

 

 

 

 

[Jace]

>Are either of you currently involved in any sort of aging research?
I'm not, at least until now :D

 

 

Glad you came across this topic and are interested in working on it. Always glad to find someone who shares my interest in aging research and rejuvenation biotechnology :).

Jason  

  

[Reason]

I notice that Longecity is soliciting submissions for the next round of
small grants on longevity science projects:

http://www.longecity.org/forum/page/index.html/_/science/projects/research-f
unding-2012-expression-of-interest-s-r14

LongeCity continues its proud tradition to support small-scale, high-impact
life extension research in 2012.
(For a review from 2011 see here:
http://www.longecity.org/forum/page/index.html/_/articles/longecity/longecit
y-science-initiatives-autumn-2011-review-r19
)

Projects should:

- aim to make a scientific contribution to the extension of the human
lifespan
- be applied research or basic research with some potential for applied
development
- present short updates for LongeCity Members with interim data, photos from
the facility etc at agreed intervals
- be led or overseen by a person with a postgraduate qualification in the
relevant field or by a person with demonstrable equivalent experience
- have a flexible project structure that can be adjusted according to the
amount of money raised
- be small in scale - one or two key workers
- be short in duration - approx 6 months maximum
- not be confidential. LongeCity will expect open and public presentation
and discussion of research results. However, confidentiality will be
accepted where a manuscript or patent is in preparation.

LongeCity will be able to support a project with a minimum of $2000 and up
to $8000, subject to matching by other donors. LongeCity will launch a call
for matching donations and every donation generated in that call will go
towards the project budget (Thus projects can have a total budget of $4000-
$16,000).

Interested parties should send
- a project outline of no more than 800 words written in lay language (can
be supported by up to 10 literature references)
- a curriculum vitae of the project leader to rese...@longecity.org

Initial Deadline: August 31st 2012!

---------------------

Some of their past funding has gone towards laser ablation of lipofuscin in
nematode worms (the sort of work that is very amenable to DIYbio equipment
and levels of funding) and transplant of young microglia into old mice to
see whether it can impact neurodegeneration (less amenable, and conducted in
an academic lab).

Reason

[Lee Nelson]

There have been advances in life span with fruit flies.

http://www.google.com/search?q=fruit+fly+aging

[Mega]

We should put all our scientists and money into fighting aging.

Because then we would live 500 years, thus giving us 400 years more to do other science!! ;)

[Andreas Sturm]

I just read your link and it's amazing...

http://newsroom.ucla.edu/portal/ucla/ucla-biologists-slow-the-aging-218517.aspx

50% more life in fruit flies. A gene that makes mitochondria more active in ingestive cells was activated.

[Andreas Sturm]

Found sth about aging, yet haven't read them fully...


http://books.google.at/books?id=_ctHCoJgF3AC&pg=PA17&lpg=PA17&dq=nptl+gene&source=bl&ots=i9reFqJW8H&sig=tfY9gEMgOUtTlCf0deD9CXRc4YY&hl=de&sa=X&ei=L0EtUO-eBszAswaZ1oGACA&ved=0CDsQ6AEwAQ#v=onepage&q=nptl%20gene&f=false

http://books.google.at/books?id=2DOLBh7RGbkC&pg=PA203&lpg=PA203&dq=nptl+gene&source=bl&ots=2LzcQwaQNk&sig=JCQlkfAJgaPHiNG5_LE-qSVfMzg&hl=de&sa=X&ei=L0EtUO-eBszAswaZ1oGACA&ved=0CD4Q6AEwAg#v=onepage&q=nptl%20gene&f=false

[Jonathan Cline]

On Tuesday, August 7, 2012 8:35:55 AM UTC-7, Reason wrote:

 

The
present work on interventions into aging fall into two broad camps: 

...

Added to FAQ !

http://openwetware.org/wiki/DIYbio/FAQ/Projects#Longevity

Now, anyone present who isn't currently on a low fat vegan diet, please exit to the rear.

## Jonathan Cline
## jcl...@ieee.org
## Mobile: +1-805-617-0223

########################

[Andreas Sturm]

About the stomache-mitochondria thing that gives you +50% more lifetime...

Has anyone an idea how to do this in a DIY manner? ;D

2012/8/24 Jonathan Cline <jnc...@gmail.com>

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[Cathal Garvey]

I don't know about that particular research, but there are cellular
methods of "recycling" old or defective mitochondria that can be
upregulated by a few methods.

It's a subset of an overall process called "autophagy", which is
implicated in ageing, cancer, and some infections if memory serves. The
general autophagy process describes ways that the cell digests its own
components, either due to starvation or (more often) as a way of
cleaning up damaged components.

In the specific case of mitochondria, according to wikipedia
mitochondrial autophagy is downregulated after a meal, and upregulated
by the opposite; hunger, starvation or simply low blood sugar I suppose.

This would probably encompass some of the effects of caloric restriction
on mammalian lifespans, and if you were to upregulate the same system by
other means, perhaps you could avoid having to maintain caloric
restriction to see a protective effect.

When it comes to autophagy overall, I used to work with someone studying
its role in cancer, where it can be protective in some forms of cancer
resistant to chemotherapy. This clever person was contemplating methods
of kicking it into overdrive instead of fighting it, causing these cells
(which had lost their autophagy regulatory ability, unlike normal cells)
to eat themselves away.

If memory serves, and this should be published by now somewhere, Lithium
salts were among the inducers of autophagy. Of course, Lithium is also a
powerful psychoactive drug and can affect metabolism of other salts, so
it's not to be taken lightly. There were others, but I forget them..

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[Jonathan Cline]

Relevant summary article; open access.

http://rstb.royalsocietypublishing.org/content/365/1537/147.full

The new biology of ageing

Linda Partridge*

Institute of Healthy Ageing and GEE, UCL,

Darwin Building, Gower Street, London WC1E 6BT, UK  l.par...@ucl.ac.uk

doi: 10.1098/rstb.2009.0222 Phil. Trans. R. Soc. B 12 January 2010 vol. 365 no. 1537 147-154

Excerpt ( I suggest  reading the entire article ):

"""

Perhaps the single most important advance in ageing research in recent years has been discovery of mutations in single genes that extend the lifespan of laboratory animals. They first came to light as a result of a systematic chemical mutagenesis screen for lifespan-extending mutations in C. elegans (Klass 1983). Subsequent work with these mutations (Friedman & Johnson 1988), and further screening (Kenyon et al. 1993), revealed that it was possible to double the lifespan of the worm with a mutation in a single gene. Furthermore, rather than solely prolonging the moribund period at the end of the life, the mutations caused the worms to remain healthy and youthful for longer (Kenyon et al. 1993). The mutated genes were discovered to encode components of an invertebrate insulin/insulin-like growth-factor-like signalling (IIS) pathway (Kimura et al. 1997; Lin et al. 1997; Ogg et al. 1997). These findings came as a considerable surprise, because a signalling pathway previously associated with control of growth and metabolism in mammals now turned out to play a role in determination of lifespan in a distantly related invertebrate.

Mutations with similar effects on lifespan were soon discovered in other model organisms. For instance, a similar screening effort in yeast led to the discovery that over-expression of a protein deacetylase, SIR2, extended replicative lifespan (Sinclair & Guarente 1997; Kaeberlein et al. 1999), while mutations in methuselah in Drosophila increased fly lifespan (Lin Seroude & Benzer 1998). Likewise, in the mouse, mutations in genes encoding transcription factors involved in the development of the pituitary gland resulted in long-lived dwarf mice (Brown-Borg et al. 1996). By the late 1990s, it was firmly established that lifespan of these model organisms could indeed be extended by mutations in single genes.

It had also been known since the 1930s that an environmental intervention, dietary restriction (DR), could produce substantial increases in lifespan in laboratory rodents (McCay et al. 1935). Although the exact mechanisms at work still await full elucidation, detailed study of DR rodents has demonstrated a broad-spectrum improvement in health and a delay in or amelioration of the impact of a wide range of ageing-related diseases (Masoro 2005, 2006). For instance, the animals are protected against cancer, cataract, diabetes, motor decline, osteoporosis and nephropathy (Weindruch & Walford 1988). These findings suggested that, in principle, multiple aspects of the ageing phenotype could be simultaneously ameliorated by a single intervention, albeit, in the case of DR, a complex one.

[Mega]

Good news, everyone!!

http://news.nationalgeographic.com/news/2012/01/120106-aging-mice-stem-cells-old-young-science-health/

A special mouse strain, which age very quickly and live only <30 days was treated with stem cells in their end of their lives.
"To Huard's astonishment, the treated mice lived an average of 71 days—50 more than expected, and the equivalent of an 80-year-old human living to be 200, he said.

Not only did the animals live longer, they also seemed healthier, the scientists found"

[dale]

Thanks for posting what may be a link to the holy grail of anti aging research. It is my favorite article of the year. My son sent me that same link last week and it seems like one of those "TOO GOOD TO BE TRUE" articles. I mean, if it is true and accurate, why doesn't the entire world just stop what it is doing and take notice? Why isn't this on every national news channel?
 
My favorite DIY project is monitoring anti aging work in progress and last week I printed copy of this article for further review. I perceived credibility because it is a "National Geographic" article and the work was apparently done at the Institute for Regenerative Medicine in Pittsburgh which is part of the UPMC, (Pennsylvania's largest employer).

My own diy work in this field has been limited to enjoying articles on the work of others due to personal time constraints of running my own small (unrelated) business and 4 children. Years ago I built www.antiagingtech.info (antiagingtech.info) to help me easily monitor current anti aging work in progress. Now that my last child has gone off to college I plan to have much more time available next year. I am building a RepRap 3d printer I hope to finish and want to build a way improved AntiAgingTech website/DASHBOARD for myself and any other anti aging diy enthusiasts that care to use it.

[Andreas Sturm]

Yeah, you're welcome... ;)

I mean, if it is true and accurate, why doesn't the entire world just stop what it is doing and take notice? Why isn't this on every national news channel?

Because the new hairstyle of Paris Hilton is a billion times more important to the public than anything science could ever achieve... Very unfortunately, but it's the world we live in.

You know how much dollar was spent for the olympic games? I read about 12 bio (billion) Dollars. If (that is true and) we spent that money into anti-aging science like this, our generation would live at least 150 years, very conservatively estimated (because if you live 10 years longer, new treatments are invented which in turn expand your lifespan even furter...)


I hope this experiment is very soon done again  with normal mice, cats, .... and humans!

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[jlund256]

The model mice used have a mutation that kills fast dividing cells off.  Stem cells are cells that divide fast and often, so this kills off stem cells, and this produces (through poorly understood mechanisms) premature aging and early death. 

So it is not super surprising that a stem cell treatment would partially correct that.  The interesting part is that the stem cells provided in the treatment could find their way to the stem cell niches in the mice, and then take on the local stem cell type and contribute to local tissues.

What does this mean for normal aging?  Can stem cells partially reverse it?  I'm not up to date on the literature, but certainly injecting stems has been tried and failed in experiments in many labs.  So while it is interesting that there are positive results in this paper, simply repeating it in old mice is unlikely to work. 

The interesting bit is that is had some effect in this very artificial model, and if the result holds up, it can be used to investigate why it works in progeria model mice but not in old mice.  Was it the type or stem cells, or how they were delivered, or are the progeria model mice receptive in a way that old normal mice are not?

Jim Lund

[Reason]

Stem cells and aging: the current thinking is that the dominant effect of
reduced stem cell activity and failing tissue maintenance is due to changes
in the niches that support and control stem cell activity. They become
damaged or otherwise change their behavior in response to rising levels of
cellular and molecular damage. Stem cells themselves do also become damaged,
but that seems to be a small effect in comparison to the niches, as you can
get stem cells from old individuals to behave the same as stem cells from
young individuals by changing the environment they find themselves in.

See:

http://www.fightaging.org/archives/2012/03/an-introduction-to-the-stem-cell-
niche-what-is-it-really.php

http://www.fightaging.org/archives/2010/01/another-run-at-making-old-stem-ce
lls-act-as-though-young.php

The explanation for this behavior is that is an evolved response to reduce
risk of death by cancer (due to that damage in the stem cells) at the cost
of failing tissue maintenance, a part of the parcel of mechanisms that make
us longer lived than other mammals of our size.

So if you want to fix stem cells you need to fix aging in general (such as
through SENS or similar, see http://sens.org/sens-research/research-themes )
so as to restore the youthful niche behavior by removing the damage that
they react to - or at least figure out how to reprogram or override the
chemical signals from the niches, of which there are numerous different
varieties, poorly understood still. But that second approach would just be
patching over the problem, and likely no more effective than any other
modern medicine that follows that line of attack.

Replacing damaged stem cells with pristine stem cells is almost the easiest
part of the problem: it's pretty clear to see how to get to that point from
where we are, and it's been done already for some stem cell types. So it's
just a long slog to get to be able to do it for all of them, given the
number of different types of stem cell there are.

Reason

[Cathal Garvey]

The punchline that they lived 150% longer seems to be based on the shortened lifespan of the mouse strain used, too. If so, it's pretty unimpressive; they are correcting for a genetic defect that leads to early death by complementing with new stem cells. Very useful data for person suffering similar conditions, but I don't see that it has any relevance to normal ageing, I'm sorry to say.

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[Andreas Sturm]

Yeah, perhaps. But if the genetic defect just makes the decay appear earlier but same mechanism, it may still be useful??

[Mega]

http://www.ncbi.nlm.nih.gov/pubmed/10506576

I heard about  Glutathione today at university, that it affects lifespan. It prevents proteins (e.g. from the skin, but also from the cytoskeleton, etc.) from being attacked by free radicals.


Here is an article that states, in fruit flies there's enough glutathione so that more does not keep you alive longer under normal conditions. However, the rate of oxygen consumption, however, was slightly decreased.


It may still be useful for divers, so they can stay under water for some seconds longer ;)
Or also, if one has a heart attack. every second (every molecule of oxygen in his brain) counts. 
 

[Cathal Garvey]

Glutathione is great, but it's worth pointing out to the uninitiated that there is next to no value in simply eating glutathione, as it's not absorbed from supplements. There are, however, plenty of ways of encouraging your body to make glutathione. Check wikipedia as a nice initial source of info.

 

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[Jonathan Cline]

Telomerase Is Required for Zebrafish Lifespan

http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1003214

"telomerase function is truly limiting for zebrafish lifespan and tissue homeostasis, closely mimicking the human scenario."
 
Henriques CM, Carneiro MC, Tenente IM, Jacinto A, Ferreira MG (2013) Telomerase Is Required for Zebrafish Lifespan. PLoS Genet 9(1): e1003214. doi:10.1371/journal.pgen.1003214

[Andreas Sturm]

I thought overexpression of telomerase makes cancer??

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[Andreas Sturm]

Maybe getting 30 to 50% more telomerase enzyme would be desirable for humans in each case ;) 

[Matthias Bock]

I also read, that telomerase is upregulated in cancer cells.

The fact that telomerase is required for wild-type lifespan control,
doesn't immediately mean that more telomerase is more desirable
or can extend a human's lifespan.
If it was that easy, I suppose evolution would have done it.

Telomerase AFAIK extends chromose ends which are continuously
cut off by other enzymes. So there is a mechanism of regulation
present.

[Andreas Sturm]

If it was that easy, I suppose evolution would have done it.

Well, that not, too. 

Evolution just cares that you can be healthy for 25-30 years. By that age humans had already children. So their genes were passed ahead, and  aging had no influence on evolution, so it was not counter-selected...  

[Reason]

Humans are comparatively long-lived for their size as mammals, requiring
something like the grandmother hypothesis to explain how selection continued
to operate at older ages to create that state of affairs - such as by
selecting for mechanisms of stem cell decline to balance increasing cancer
risk.

The "it's a simple change, so evolution should have done it" view fails for
all species we can easily gene engineer. Mice, flies, and worms all have
numerous single-gene changes that can extend life by 10% or more. In worms
and flies there are single gene changes that extend life more greatly than
calorie restriction. None of these changes have been selected for by
evolutionary processes.

In humans, should we expect there to be analogous single gene changes?
Probably not by current thinking.

http://www.fightaging.org/archives/2009/06/significant-single-gene-longevity
-mutations-in-humans-what-are-the-odds.php

The changing nature of the environment operates on timescales that are long
in comparison to the lifespans of lower animals, but short in comparison to
a human life span. So there are good evolutionary reasons to expect lower
animals to have more plastic lifespans in their present genome (e.g. larger
calorie restriction effects to better survive famines) and the potential for
more plastic lifespans through genomic alterations. But that cuts both ways
- shorter can be better from the point of view of natural selection.

Reason

[Cathal Garvey]

-----BEGIN PGP SIGNED MESSAGE-----
Hash: SHA256

Indeed, there's lots more than just reproduction to human genetics.
For example, humans would have evolved with a community that is far
more extended-family-based than most modern western societies;
childrearing and labour were shared extensively among family members,
meaning that the survival of a person's genetic line could be affected
by their ability to provide for their close relatives even late in life.

This concept has been used to explain why humans undergo menopause, a
nearly unique event in the animal kingdom; why would an animal cease
being able to reproduce while still alive and healthy?
A) Because the risks of an unhealthy child are far higher, distracting
them from healthier offspring and relatives.
B) Because they *will* continue to have sex, because it's so important
to human pair bonding and family cohesion.

The real reason (probably) why nature doesn't bother selecting for
longevity is that beyond a certain level, it's no longer beneficial
simply because natural organisms tend to die of other things. Death by
aging and cancer would have been pretty uncommon if not for
antibiotics, hygeine and vaccines, the "big three" of human health
that have eradicated some of the most common forms of death in prior
centuries.

So, we're weird, and unusually long-lived already, but until recently
we'd hit our upper limit in terms of "required longevity to be
successful".

As to Telomerase and Cancer, Telomerase expression alone will not
cause cancer, however it allows other mutations to lead to cancers.
The absence of Telomerase activity in somatic cells is what creates
the "Hayflick Limit", where normal cells can only divide a finite
number of times before running out of Telomeres and losing critical
genetic information. This limit helps prevent mutations that lead to
uncontrolled growth and division from leading to malignant tumours and
other cancers. Providing telomerase to these cells removes the
hayflick limit, allowing cells to resume growth.

- -mutations-in-humans-what-are-the-odds.php

>
> The changing nature of the environment operates on timescales that
> are long in comparison to the lifespans of lower animals, but short
> in comparison to a human life span. So there are good evolutionary
> reasons to expect lower animals to have more plastic lifespans in
> their present genome (e.g. larger calorie restriction effects to
> better survive famines) and the potential for more plastic
> lifespans through genomic alterations. But that cuts both ways -
> shorter can be better from the point of view of natural selection.
>
> Reason
>

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[jacob edward]

Hi,
You are what you eat.  80% of our skin health depends on what we eat and the rest 20% on what we use topically. So if you are using expensive serums and treatments and still eating junk food you are not doing the right thing. Eat well and it will show up on your skin.

[Andreas Sturm]

>You are what you eat.  80% of our skin health depends on what we eat and the rest 20% on what we use topically.

And how much is determined genetically? 0% ? :D

On Tue, Sep 17, 2013 at 11:27 AM, jacob edward <jacobe...@gmail.com> wrote:

Hi,
You are what you eat.  80% of our skin health depends on what we eat and the rest 20% on what we use topically. So if you are using expensive serums and treatments and still eating junk food you are not doing the right thing. Eat well and it will show up on your skin.

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[Mega [Andreas Stuermer]]

Here's something some may find interesting... Although, she is speaking a bit slow... And, I don't think entirely new research is shown, but it's job is to spread the message of anti-ageing...

http://www.tedmed.com/talks/show?id=47035 (Laura Deming on fighting ageing) 

[Mega [Andreas Stuermer]]

http://www.theguardian.com/science/2012/oct/17/young-blood-reverse-effects-ageing

Fascinating! Injecting young blood into old mice rejuvinated them to some degree. And, what surprised me the most - it was blood plasm (cell free). That means no external stemm cells applied. Just young growth factors that made the old stem cells speed up.

[Reason]

On 04/06/2014 04:08 AM, Mega [Andreas Stuermer] wrote:
> http://www.theguardian.com/science/2012/oct/17/young-blood-reverse-effects-ageing
>
> Fascinating! Injecting young blood into old mice rejuvinated them to some degree. And, what surprised me the most - it was blood plasm (cell free). That means no external stemm cells applied. Just young growth factors that made the old stem cells speed up.
>

There has been a growing amount of work on heterochronic parabiosis in
mice. As I understand it, the current thinking is that the factors
involved are short-lived which is why you actually need the physical
connection to see effects (in absence of a list of those factors to be
delivered as drugs). Another expectation is that achieving the same
result in old humans would greatly raise the risk of cancer - which may
be an acceptable cost during the years ahead in which cancer treatment
is highly effective but researchers have not yet found safe ways to
restore stem cell populations to youthful levels of activity.

http://www.deepdyve.com/lp/wiley/heterochronic-parabiosis-historical-perspective-and-methodological-iQgxME31z2

Some reports on the leading edge of investigations as to the mechanisms
by which heterochronic parabiosis works:

https://www.fightaging.org/archives/2013/09/the-prospects-for-therapies-based-on-heterochronic-plasma-exchange.php

https://www.fightaging.org/archives/2014/03/digging-into-the-details-of-why-a-young-environment-restores-the-activity-of-old-cells.php

https://www.fightaging.org/archives/2013/05/parabiosis-points-to-gdf-11-as-a-means-to-reverse-age-related-cardiac-hypertrophy.php

Reason

[htert2020]

Hello Jason,

I have the same bio-tech goals as you do (e.g. de Grey). I live in Old Bridge, NJ. If you're open to the possibility of working together, let's discuss. htert2020_gmail_com

htert2020

[Katherine Gordon]

Can you please express your goals for anti aging? I am of the opinion that DIY technology is going to provide useful answers quite soon. I would love to be part of your research.

I am 54 and studied Chemistry and Biology and Nutrition in College, I currently work as a coordinator at a childrens museum.

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[Andreas Stuermer]

If you want to genetically engineer human sperm to make the baby immortal, why not :D

 

We gotta do this somewhere where there are no laws though xD And test it in mice bfore

 

xD

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[Mega [Andreas Stuermer]]

http://www.the-scientist.com/?articles.view/articleNo/40436/title/Mutations-Pervade-Mitochondrial-DNA/

Mitochondrial defects (with low frequencies) are common in healthy humans. A healthy cell has thousands of mtDNA copies and tolerates it well. But once it gets high frequencies, disease occurs.


Btw, learnt an interesting hypothesis: During egg cell production you have a bottleneck. Thus the new organism can only bring a few mitos. That may ensure most of the mitos the child gets are healthy (else the fetus dies off).

[Matthew Harbowy]

I have quite a few problems with this article. In short, they can't tell the difference between a mistake and the truth.

http://www.pnas.org/content/early/2014/07/02/1403521111.abstract (paywalled, but... https://drive.google.com/file/d/0B23vC9DUdmT9ODZpNHk5emxQcjg/edit?usp=sharing)

First, this study is retrospective, using 1000 Genomes data. It was not collected using some kind of protocol that separated individual cells, let alone mitochondria, then sequenced those to high coverage.

1000 Genomes was (some? mostly?) exome data. So in addition to sequencing errors, you might have errors introduced by the exome concentration process. And no sequencing process is going to be perfect. But directly to the point- this is not confirmation of numbers or incidence of mutation- this is just a selection of sequenced fragments. 

These sequences were (presumably) taken from the B-lymphocytes stored at Coriell or from some other patient blood source, e.g.

http://ccr.coriell.org/Sections/Search/Search.aspx?PgId=165&q=NA12045

B-lymphocytes (a white blood cell, http://en.wikipedia.org/wiki/B_cell) live for about 3-4 days in the bloodstream, which out of all environments is probably the most oxidizing and free-radical generating of all. But somatic mutations of mitochondria in this environment are at best an estimate of the mutation rate of longer-lived cells and cells in general, so it seems hasty to generalize this to causation of disease.

They identify this individual (NA12045) who was sequenced with both 454 and Illumina

IND	POS	Ref_allele	Alt_allele	Alt_fre_Illumina	Alt_fre_LS454		Individuals	position(rRCS)	ref_allele	other_allele	fre_of_ref_allele
NA12045	291	A	T	0.1185093647	0.3050027667		NA12045	291	A	T	0.881490635
NA12045	830	T	C	0.0645316644	0.0445306566		NA12045	830	T	C	0.935468336
NA12045	2454	G	A	0.0093588371	1.58E-06		NA12045	2454	G	A	0.990641163
NA12045	5442	T	C	0.0727707436	0.0591629249		NA12045	5442	T	C	0.927229256
NA12045	7695	T	C	0.1454196028	0.1345376616		NA12045	7695	T	C	0.854580397
NA12045	8152	G	A	0.0646419045	0.1162926433		NA12045	8152	G	A	0.935358096
NA12045	12868	G	A	0.0289551884	0.0160194434		NA12045	12868	G	A	0.971044812

I'm in the process of downloading the full genome data for this sample, so that I can get a better look at the aligned reads and determine exactly what they're seeing in this data. But these levels of "heteroplasmy" range from ~15-30% down to ~1%. Given that "heteroplasmy" is different for the two sequencing methods (454 vs illumina) by sometimes as much as 6-19%, any one of these single-data-point-from-a-person studies shouldn't be finding "heteroplasmy" in samples where there is anything less than ~5% occurence, though I haven't computed level of significance- that's just eyeballing it. 

Shit like this, though bothers me to no end:

IND	POS	Ref_allele	Alt_allele	Alt_fre_Illumina	Alt_fre_LS454
NA11918	575	C	T	0.982335903	0.9831326903
NA11918	8701	A	G	0.7944136904	0.9948053047
NA11918	12877	G	A	0.0615655364	0.0618067655

If they are saying that the alternate allele is 0.98... that seems to suggest for this person it appears at 98% which would not make it an alternate, no? It seems to be really poor curation of the supplemental material.

The repeated citation of the existence of extensive mutation in mitochondria (exaggerated to as much as 90% of population in this report) follows a chain of exaggeration. in fact, if you trace it back through the references in the paper to its evidence that "earlier reports suggest...", you find that many of the papers are reviews which speculate the point, and others don't study mDNA damage, and the most obnoxious I have found is 

http://www.ncbi.nlm.nih.gov/pubmed/18674747

This group studied a cluster of sequentially sampled neonatal cord blood in North Cumbria, England. In about ~3000 samples, they found 15 with some amount of mutated DNA. The mutations were clustered by haplogroup, indicating possible relations. About half of those were tested for inheritance from the mother, and half again inherited these (in part) from mom. The irony of this is that one of three are blue in the chart above, and two are black: so the known cases of INHERITED disease-causing mutations range from 0-100% HETEROPLASMY in the cord blood. So let's say that out of the 15, half have de-novo mutations from mom. 6/3000 is 0.2%

Chinnery et al in an earlier article (http://www.ncbi.nlm.nih.gov/pubmed/16437486) found no evidence of successful treatment of mitochondrial diseases among all the therapies reviewed. 

Furthermore, incidence of actual mitochondrial disease is estimated by Chinnery to be 14.5/100000, so the 0.2% number (200/100000) is an extremely unrepresentative sample, or cord blood is a really shitty place to get stem cells from. But look at his summary:

Table 2. Epidemiology of Mitochondrial Disease

Study Population	Mutation or Disease	Disease Prevalence/100,000 (95% C.I.) 1
Northern England; Point prevalence August 1997, Population size = 2,122,290 [Chinnery et al 2000]	All mtDNA deletions	1.33 2  (0.76-1.89)
	All mtDNA point mutations	5.24 2  (4.12-6.37)
	m.11778G>A, m.3460G>A (LHON)	3.29 2  (2.39-4.18)
	m.3243A>G	0.95 2  (0.47-1.43)
	m.8344A>G	0.25 2  (0.01-0.5)
	All mtDNA mutations	6.57 3  (5.30-7.83)
Northern Finland;  Adult point prevalence, Population size = 245,201  [Majamaa et al 1998]	m.3243A>G	5.71  (4.53-6.89)
Western Sweden;  Children age <16 = 385,616  [Darin et al 2001]	Childhood mitochondrial encephalomyopathies	4.7 4  (2.8-7.6)
Victoria, Australia; Birth prevalence: 1,710,000 births [Skladal et al 2003]	Childhood respiratory chain disease	4.7 5  (3.2-5.0)
Summary	Adults and children with mitochondrial disease	~11.5

  Somehow, among results that say mtdna disease incidence ranges from 4 to 7 in 100,000, he comes up with a summary number double that value. Basically, anything relying on Chinnery et al is immediately suspect in its statistical methods.

If anything like 0.2% of babies have some heteroplasmy of mtdna, and NA12045 has 7 heteroplasmies (and is a "paternal grandfather" of NA12035, '36, '37 ,38', '39, '40, '41 and '42, , and the three granddaughters and five grandsons have a maternal grandmother NA12046)

These Utah family lines should be useful in finding out if aging influences measured heteroplasmy in any meaningful way.

Individuals

position(rRCS)

ref_allele

other_allele

fre_of_ref_allele

NA12043	3608	G	A	0.81199869
NA12043	15498	G	A	0.980632597

NA12044	228	G	A	0.017276906
NA12044	295	C	T	0.015793661
NA12044	462	C	T	0.017800664
NA12044	489	T	C	0.015633723
NA12044	2706	A	G	0.989317886
NA12044	10398	A	G	0.022339194
NA12044	10544	C	T	0.988068716
NA12044	10792	A	G	0.985765747
NA12044	11251	A	G	0.019083767
NA12044	12612	A	G	0.012654926
NA12044	13934	C	T	0.019407354
NA12044	15452	C	A	0.012786066
NA12044	16069	C	T	0.017301814
NA12044	16126	T	C	0.015944685
NA12044	16172	T	C	0.014490257
NA12044	16192	C	T	0.991608201
NA12044	16222	C	T	0.024497749

NA12045	291	A	T	0.881490635
NA12045	830	T	C	0.935468336
NA12045	2454	G	A	0.990641163
NA12045	5442	T	C	0.927229256
NA12045	7695	T	C	0.854580397
NA12045	8152	G	A	0.935358096
NA12045	12868	G	A	0.971044812

 

NA12043 (♂Gf, 2 hp) NA12044 (♂Gm, 17 hp) and NA12045 (♀Gf, 7 hp) have heteroplasmy, but the maternal grandmother, and the children and grandkids who get ther mitochondria all have no detectable heteroplasmy by the methods of this paper. Yes, it could be good clean Mormon living, but really? Do Mormons have significant longevity advantages not shared by the general public? Why is '46 so "clean"? And why is it not detected in 11 of 14 of the samples correlated by family relation (and the fact that 14/1085 are closely related really calls into question the actual randomness of the data set). If Mom "inherits" stem cells and becomes slightly chimeric by stem cell transfer/leakage from her sons and daughters (http://www.scientificamerican.com/article/scientists-discover-childrens-cells-living-in-mothers-brain/), what implications does this have for heteroplasmy? I would assume little because children and moms typically share mtdna, but what about http://en.wikipedia.org/wiki/Paternal_mtDNA_transmission ?

TL;DR: FYNFW. This paper means nothing. It would seem that although heteroplasmies (point mutations) are "detected" in 90% of the population, if it were that common, then it is a surprise that http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0074636 only found them in 11/101 samples. As with this earlier paper, the possibility that amplification/PCR errors get introduced is glossed over, and the majority of defects found is stuttering or deletion, to be expected in PCR. If a consistent or trending heteroplasmy was detected in different somatic cells of a single experimental subject over time, this would be actual evidence in favor. Without a noticeable pedigree of mutation from stem cell to somatic cell (e.g. stem cell has 1 or 2, APS has a couple more or cause bunches of heteroplasmy, etc etc, these papers are not evidence.

-matt

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[Jonathan Cline]

Maca root


http://www.med.nyu.edu/content?ChunkIID=104590

Quote

Maca is a Peruvian root vegetable used both as food and medicine. It is sometimes called "Peruvian ginseng," not because the plants have any botanical relationship, but because their traditional uses are somewhat similar. Traditionally, maca has been said to increase energy and stamina, and enhance both fertility and sex drive in men and women.

*

What is Maca Used for Today?  

Maca is widely marketed for improving male sexual function , female sexual function , and both male fertility and female fertility . However, at present there is no reliable evidence that it actually provides any benefits at all.

Much of the evidence for maca comes from animal studies. In one study in rats, use of maca enhanced male sexual function. ¹ Animal studies have had mixed results regarding male and female fertility. ^2-7

There are two published human trials on maca, performed by a single research group.

In one small 12-week, double-blind , placebo-controlled study, use of maca at 1,500 mg or 3,000 mg increased male libido. ⁸ While this was an interesting finding, the study did not report benefits in male sexual function, just desire. Since loss of sexual function (eg, impotence) is a more common problem in men than loss of sexual desire, these results do not justify the widespread claim that maca has been shown to act like a kind of herbal Viagra.

Another small study found that 4 months of maca use increased sperm count and sperm function. ⁹ Unfortunately, this study failed to use a control group, and for this reason its results are essentially meaningless. (For more information on why studies must use a control group, see Why Does This Database Rely on Double-blind Studies? )

There are no human trials on maca for female fertility or female sexual function.

Contrary to widespread reporting, maca does not appear to increase testosterone levels, or, in fact, affect any male hormones. ¹⁰

Other animal studies hint that maca might offer benefits for prostate enlargement , ^11,12stress , ¹³diabetes , ¹⁴ and high blood pressure . ¹⁵ However, this evidence is as yet too weak to justify any claims regarding maca and these conditions.

One human trial evaluated a combination of maca and cat’s claw for osteoarthritis, but because it failed to include a placebo group, its results mean little. ¹⁶

*

Dosage  

The usual dose of maca is 500 to 1,000 mg three times a day.

*

Safety Issues  

In the two reported human clinical trials, use of maca has not led to any serious adverse effects. However, this herb has not undergone comprehensive safety testing. Safety in young children, pregnant or nursing women, or people with severe liver or kidney disease has not been established.

References

* Cicero AF, Piacente S, Plaza A, et al. Hexanic Maca extract improves rat sexual performance more effectively than methanolic and chloroformic Maca extracts. Andrologia . 2002;34:177-179.

* Ruiz-Luna AC, Salazar S, Aspajo NJ, et al. Lepidium meyenii (Maca) increases litter size in normal adult female mice. Reprod Biol Endocrinol . 2005;3:16.

* Oshima M, Gu Y, Tsukada S, et al. Effects of Lepidium meyenii Walp and Jatropha macrantha on blood levels of estradiol-17 beta, progesterone, testosterone and the rate of embryo implantation in mice. J Vet Med Sci . 2003;65:1145-1146.

* Chung F, Rubio J, Gonzales C, et al. Dose-response effects of Lepidium meyenii (Maca) aqueous extract on testicular function and weight of different organs in adult rats. J Ethnopharmacol . 2005;98:143-147.

* Gonzales GF, Rubio J, Chung A, et al. Effect of alcoholic extract of Lepidium meyenii (Maca) on testicular function in male rats. Asian J Androl . 2003;5:349-352.

* Bustos-Obregon E, Yucra S, Gonzales GF, et al. Lepidium meyenii (Maca) reduces spermatogenic damage induced by a single dose of malathion in mice. Asian J Androl . 2005;7:71-76.

* Gonzales GF, Gasco M, Cordova A, et al. Effect of Lepidium meyenii (Maca) on spermatogenesis in male rats acutely exposed to high altitude (4340 m). J Endocrinol . 2004;180:87-95.

* Gonzales GF, Cordova A, Vega K, et al. Effect of Lepidium meyenii (Maca) on sexual desire and its absent relationship with serum testosterone levels in adult healthy men. Andrologia . 2002;34:367.

* Gonzales GF, Cordova A, Gonzales C, et al. Lepidium meyenii (Maca) improved semen parameters in adult men. Asian J Androl . 2002;3:301-303.

* Gonzales GF, Cordova A, Vega K, et al. Effect of Lepidium meyenii (Maca), a root with aphrodisiac and fertility-enhancing properties, on serum reproductive hormone levels in adult healthy men. J Endocrinol . 2003;176:163-168.

* Gonzales GF, Miranda S, Nieto J, et al. Red maca ( Lepidium meyenii ) reduced prostate size in rats. ReprodBiol Endocrinol . 2005;3:5.

* Martinez Caballero S, Carricajo Fernandez C, Perez-Fernandez R, et al. Effect of an integral suspension of Lepidium latifolium on prostate hyperplasia in rats. Fitoterapia . 2004;75:187-191.

* Lopez-Fando A, Gomez-Serranillos MP, Iglesias I, et al. Lepidium peruvianum chacon restores homeostasis impaired by restraint stress. Phytother Res . 2004;18:471-474.

* Eddouks M, Maghrani M, Zeggwagh NA, et al. Study of the hypoglycaemic activity of Lepidium sativum L. aqueous extract in normal and diabetic rats. J Ethnopharmacol . 2005;97:391-395.

* Maghrani M, Zeggwagh NA, Michel JB, et al. Antihypertensive effect of Lepidium sativum L. in spontaneously hypertensive rats. J Ethnopharmacol . 2005 Jun 11. [Epub ahead of print]

* Mehta K, Gala J, Bhasale S, et al. Comparison of glucosamine sulfate and a polyherbal supplement for the relief of osteoarthritis of the knee: a randomized controlled trial [ISRCTN25438351]. BMC Complement Altern Med. 2007 Oct 31. [Epub ahead of print]

Last reviewed August 2013 by EBSCO CAM Review Board

End Quote

[Mega [Andreas Stuermer]]

If Maca works boosting male fertility, it may increase testosterone levels. 

http://jap.physiology.org/content/106/1/333 

-> estrogen activates telomerase (in endothelial cells). 

Fun fact: aspirin does too

Is that a contradiction? 

[Cathal Garvey]

Maca's effects on human sexuality are less simple than "boosting"; it
appears to improve libido, but has no impact on impotence, for example
(given that this is the primary market for Maca, seems unfair). It is
possible it increases testosterone, but a quick look into Maca after J's
post didn't yield much on anti-aging potential.

There's no contradition between testosterone and oestrogen, contrary to
the popular view that they are in opposition they are important hormones
for both genders.

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[Andreas Stuermer]

Ah right, after testosterone therapy bodybuilders take beta-blockers, else the testosterone would be converted into estrogen and that would be bad for gaining muscles. Or wold the body just produce less testosterone and estrogen would prevail? Never read too deep into that.

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[Jonathan Cline]

Occam's razor: that which boosts mating also boots evolutionary
selection which equates to health and longevity. (?) Characterization
is a big unknown.


Figure 2: Score of health status from men and women residents of
Carhuamayo, Junin at 4100 m in the Peruvian Central Andes. Upper line:
population consuming extracts of maca. Bottom line: population not
consuming maca.
http://www.hindawi.com/journals/ecam/2012/193496.fig.002.jpg


Reference:
http://dx.doi.org/10.1155/2012/193496
Ethnobiology and Ethnopharmacology of Lepidium meyenii (Maca), a Plant
from the Peruvian Highlands (2011)

## Jonathan Cline
## jcl...@ieee.org
## Mobile: +1-805-617-0223
########################

[Andreas Stuermer]

>Occam's razor:  that which boosts mating also boots evolutionary selection which equates to health and longevity.   (?) Characterization is a big unknown. 

Disagree. 

Mating selects that you are attractive and in good health until the age of 20-30. By that age you have passed on your genes by making children. 

If you die immediately afterwards or live in bad health, evolution does not care for that too much. 

Of course in social animals it brings benefit to the species if you live another 15 years to help your children grow and surviive So after age 40-50 selection stops anyway.

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[Mega [Andreas Stuermer]]

http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1004860

http://www.geek.com/science/scientists-accidentally-stop-skin-aging-in-mice-1611888/ 

Anti-inflammatory often seems to mean life prolonging. Though that also means less ability to fight cancer?