18 replies to this topic

[APBT]

Popular press article:  http://gizmodo.com/w...campaign=buffer

 

 

 

http://www.nature.co...ature19793.html

 

Driven by technological progress, human life expectancy has increased greatly since the nineteenth century. Demographic evidence has revealed an ongoing reduction in old-age mortality and a rise of the maximum age at death, which may gradually extend human longevity^1, 2. Together with observations that lifespan in various animal species is flexible and can be increased by genetic or pharmaceutical intervention, these results have led to suggestions that longevity may not be subject to strict, species-specific genetic constraints. Here, by analysing global demographic data, we show that improvements in survival with age tend to decline after age 100, and that the age at death of the world’s oldest person has not increased since the 1990s. Our results strongly suggest that the maximum lifespan of humans is fixed and subject to natural constraints.

 

 

[niner]

Sure, max lifespan is fixed if you don't do anything to lengthen it.  So far, none of the interventions that have extended the lifespan of younger people were rejuvenative; they were just compensatory.  That was the case with 100% of their subjects, so what else would they expect?  When we start employing therapies that repair damage rather than paper it over, then their "hardwired" max lifespan will change.

[sthira]

Sure, max lifespan is fixed if you don't do anything to lengthen it. So far, none of the interventions that have extended the lifespan of younger people were rejuvenative; they were just compensatory. That was the case with 100% of their subjects, so what else would they expect? When we start employing therapies that repair damage rather than paper it over, then their "hardwired" max lifespan will change.

Welcome back, niner! I've missed your optimism. You cheer me up when I get dark about the sloooow pace of this science.

[elfanjo]

Lifespan as we know it = aging at full speed = maximum damage before body breaks i.e. death.
Slowing aging = same amounth of damage before dying, only later.
Efforts to slow aging until recently = close to 0.
Value of the study = 0.
And I am not even talking about repairing like niner did !

[Bloomfield]

I would have argued that this was already assumed when we discovered the Second Law of Thermodynamics. The only way any sentient being with immortal life that I can conceive of is a Boltzmann Brane, or something that lives in close equilibrium with the Entropy of the Universe.

[niner]

I would have argued that this was already assumed when we discovered the Second Law of Thermodynamics. The only way any sentient being with immortal life that I can conceive of is a Boltzmann Brane, or something that lives in close equilibrium with the Entropy of the Universe.

 

The second law doesn't apply here because humans aren't closed systems.  Biological cells have systems that do work to overcome entropy.  They "take out the garbage" (autophagy), for example.  These processes continue from conception until death.

[Rocket]

The limit is because there is a lack of regenerative medicine.  You get arthritis, take this pill. You get sick more easily with age because your immune system weakens, take these pills to ward off infection. You Alzheimer's, take these pills to slow it down a little.  Medicine (today) does nothing to treat the reasons for which people die of old age... They treat the symptoms of, and not the cause of the things that kill us.  There are no treatments out there for shortening telomeres, lipofuscin accumulation, AGE accumulation, senescent cell removal, ROS, sarcopenia, nothing for thymus regeneration, and nothing for all the other hallmarks of aging.

 

 

[corb]

Vijg has been becoming increasing pessimistic in the last 2 or 3 years. A stark contrast to when he was giving talks at SENS conferences.

I suppose it has to do with his field of genetics expanding as it has, the more you know the more you know you don't know kind of thing.

[Skyguy2005]

The limit is because there is a lack of regenerative medicine.  You get arthritis, take this pill. You get sick more easily with age because your immune system weakens, take these pills to ward off infection. You Alzheimer's, take these pills to slow it down a little.  Medicine (today) does nothing to treat the reasons for which people die of old age... They treat the symptoms of, and not the cause of the things that kill us.  There are no treatments out there for shortening telomeres, lipofuscin accumulation, AGE accumulation, senescent cell removal, ROS, sarcopenia, nothing for thymus regeneration, and nothing for all the other hallmarks of aging.

 

"There are a number of natural therapies that can be used to reduce the accumulation of lipofuscin.  The following natural substances have been studied for their ability to reduce lipofuscin accumulation:

• Acetyl-L-Carnitine  1
• Centrophenoxine  2
• Creatine  3
• DMAE  4
• Ginkgo Biloba  5
• Piracetam  6" http://biofoundations.org/?p=3354

[corb]

 

The limit is because there is a lack of regenerative medicine.  You get arthritis, take this pill. You get sick more easily with age because your immune system weakens, take these pills to ward off infection. You Alzheimer's, take these pills to slow it down a little.  Medicine (today) does nothing to treat the reasons for which people die of old age... They treat the symptoms of, and not the cause of the things that kill us.  There are no treatments out there for shortening telomeres, lipofuscin accumulation, AGE accumulation, senescent cell removal, ROS, sarcopenia, nothing for thymus regeneration, and nothing for all the other hallmarks of aging.

 

"There are a number of natural therapies that can be used to reduce the accumulation of lipofuscin.  The following natural substances have been studied for their ability to reduce lipofuscin accumulation:

• Acetyl-L-Carnitine  1
• Centrophenoxine  2
• Creatine  3
• DMAE  4
• Ginkgo Biloba  5
• Piracetam  6" http://biofoundations.org/?p=3354

 

 

A lot of these were studied in humans and failed to produce a good outcome.

I remember very clearly when DMAE failed the trial, I was just getting into life extension.

There's more to lysosomal storage diseases of aging than simply moving a protein or lipid from one place to another or metabolizing it to something else. The way we study these reactions is incomplete and very rarely accurate as even the literature admits. And a lot of these compounds were studied a good time ago that the research can easily be questioned.

What we do know is - oxysterols and lipofuscin accumulate in the cells and in the extra cellular matrix during aging - and we know they are the closest we've come to a root cause to a good chunk of the chronic diseases of old age.

 

Beta cyclodextrin is more interesting than any of these compounds in the wiki because it can supposeldy clear out both oxysterols and lipofuscin. Unfortunately it does have a nasty side effect. But it's quite possibly a good starting point for a safe prophylactic drug that actually works and is already used in humans with some measure of success.

[Danail Bulgaria]

Some basics of the regenerative medicine are already here. For example you may grow new hairs on your head with stem cells. 

 

You may see more in my topic about the stem cells used in people 

http://www.longecity...used-on-people/

 

With some more luck after lets say 20-30 years people may have strong enough regenrative medicine for us to break the limit. 

[to age or not to age]

I'm fairly optimistic and intrigued by the idea of combining treatments to influence several major aging pathways at once

which have been identified.

 

mtor - down regulated with rapamycin and its analogues - recent papers indicate that it may in fact reset the immune system to an earlier age. And, intermittent treatment has proven to be even more effective. 

 

NAD - NR and NMN precursors may give way to beta lapachone, which appears to over lap the gene activity of CR, while impacting the warburg effect - keeping the mitochondria more intact. Sirt1 activity goes hand in hand with NAD, and several sirloins reside in the mitochondria   

 

senescent cells removal - getting rid the bad players that outlive their usefulness and accumulate with age.  Compounds are being discovered

which do this.

 

stem cell environment - Irina Convoy, bioengineer at Berkeley, believes that with only two interventions, stem cells can be made to act young again, producing younger tissues. I interviewed her on video, and she said something like 'if the various organs themselves become younger -

heart, liver etc. - will there be an additional systemic effect.'

 

My instinctive question is: if the body does a number of things younger across different realms, will it start to solve many of the problems on its own, which, when today's medicine tries to do it, seems so piecemeal.

 

My two cents. 

 

[alc]

 

 

My instinctive question is: if the body does a number of things younger across different realms, will it start to solve many of the problems on its own, which, when today's medicine tries to do it, seems so piecemeal.

 

 

 

Most likely that is why parabiosis works.

When we were young most of the scars went away easily.

 

Do you have a recent interview with Irina Conboy? if yes, is it posted somewhere?

 

Question is: why there are no funds for her group?

 

I suggested to lifespan.io to have her work supported, but seems like lifespan.io is interested mostly in sens's work, which is ok up to a point, but not too

exciting with their approach missing many critical things in aging.

[to age or not to age]

I have a recent taped interview with Irina Conboy and her partner Michael Conboy  but I haven't posted it.  I'm using pieces of it

for an aging series I'm filming and editing.  Irina expounded on the funding process's inefficiencies and catch 22's.  For instance,

she feels 10 years have been wasted with regard to this research, needlessly.  At this point, she believes it is now a matter of dosing

and method of administration; and she anticipates human clinical trials within a year or two; again funding is the key.

 

[alc]

I have a recent taped interview with Irina Conboy and her partner Michael Conboy  but I haven't posted it.  I'm using pieces of it

for an aging series I'm filming and editing.  Irina expounded on the funding process's inefficiencies and catch 22's.  For instance,

she feels 10 years have been wasted with regard to this research, needlessly.  At this point, she believes it is now a matter of dosing

and method of administration; and she anticipates human clinical trials within a year or two; again funding is the key.

 

Thanks for your reply.

 

Couple questions:

 

1. I saw few of your interviews, and I liked them.

 

If this one becomes available, please post an announcement  here. Thanks.

 

Do you raise funds to create your interviews?

 

I mean, if you publish a list with researchers that you want to interview and you create a donate

page, I'm sure people will donate small sums for such project.

 

2. Funding Irina & Michael Conboy's work: I believe there are several people here interested in creating a group

to setup a work frame to seek funds to consolidate/accelerate their work into human trials.

 

I'm also very interested to see others like

Izpisua, Rando, Church, Sinclair, etc.having their research accelerated.

 

We can brainstorm if you are interested. Send a pm if you like.

 

thanks.

[Aardvark202]

It's sad to see Vijg's name on a paper this useless.  They present no real mechanistic reasons why life extension should be impossible and use misleading figures for their demographic argument.  Figure 2a for example uses 2 seperate arbitrary timespans to calculate linear regressions, where the second timespan just happens to start at the point that Jeanne Calment and Sarah Knauss died (the two oldest verified people ever).  This in essence uses a few outliers to give the illusion of a peak whereas the regression over the entire timespan from 1970 to 2010 is still positive.

 

Anyways, by the logic of relying on current trends exclusively, someone in the year 1800 may have estimated that there would be only 1 billion people in the world today.

 

 

And yet doing the same thing with an n of 33 for lifespan over a 40 year period makes Nature Communications?!?!

 

Obviously technology can shake things up.

[Futuredoc]

I'm fairly optimistic and intrigued by the idea of combining treatments to influence several major aging pathways at once

which have been identified.

 

mtor - down regulated with rapamycin and its analogues - recent papers indicate that it may in fact reset the immune system to an earlier age. And, intermittent treatment has proven to be even more effective. 

 

NAD - NR and NMN precursors may give way to beta lapachone, which appears to over lap the gene activity of CR, while impacting the warburg effect - keeping the mitochondria more intact. Sirt1 activity goes hand in hand with NAD, and several sirloins reside in the mitochondria   

 

senescent cells removal - getting rid the bad players that outlive their usefulness and accumulate with age.  Compounds are being discovered

which do this.

 

stem cell environment - Irina Convoy, bioengineer at Berkeley, believes that with only two interventions, stem cells can be made to act young again, producing younger tissues. I interviewed her on video, and she said something like 'if the various organs themselves become younger -

heart, liver etc. - will there be an additional systemic effect.'

 

My instinctive question is: if the body does a number of things younger across different realms, will it start to solve many of the problems on its own, which, when today's medicine tries to do it, seems so piecemeal.

 

My two cents. 

 

I now it's been a few months, I'm hoping you end up seeing this.  Which technology do you think has the most potential uses?

 

[to age or not to age]

I'm quite taken with beta lapachone.  I have had two chemists I know synthesize pure beta lapachone.  Unfortunately it is expensive to make. The only cheaper alternative being

to get it from China, and that adds other complications. We successfully got our hands on rapamycin (sirolimus) and several of us are planning to combine beta lapachone and 

rapamycin therapy, while keeping tabs on the effects - I plan on filming the process. 

[shadowhawk]

Ultimately the proof is in the pudding.  Humans have long tried to find ways of living longer.  We have extended life for the middle ages but not for the oldest so far.  110 - 120 seems to be the upper limit for a very few.  Even if we doubled that something else will probably kill us unrelated to our biology.  240 years sounds great but in the grand scheme of things is but a moment.  We will keep trying but death seems to be in store for us unless the evidence changes.  This is not defeatist but seems to be realistic.  Don't get me wrong I am against death but it has something to teach us.