25 replies to this topic

[steampoweredgod]

CR= calorie restriction
BMR= basal metabolic rate
PI=peroxidation index
MLSP=maximum lifespan potential

These are several quotes from an article I found interesting, along with some comments

Many of the exceptions to the rate-of-living theory appear explicable when the particular membrane fatty acid composition is considered for each case. Here we review the links between metabolic rate and maximum life span of mammals and birds as well as the linking role of membrane fatty acid composition in determining the maximum life span. The more limited information for ectothermic animals and treatments that extend life span (e.g., caloric restriction) are also reviewed.

Laganiere and Yu (188) first showed CR altered the fatty acid composition of liver mitochondrial and microsomal membranes in rats such that they became less susceptible to peroxidative damage. Since this seminal observation, others have reported similar CR-induced changes for other tissues (53, 190, 201, 268, 270, 346) as well as for different classes of liver phospholipids (54, 168). All of these studies involved long-term CR in rats with the shortest period examined being 10-wk CR (54). A study of CR in mice (99) reports similar changes in the fatty acid composition of phospholipids from liver, heart, kidney, and brain, as well as liver and muscle mitochondria, with the changes in this study being manifest following 1 mo of CR (the earliest period sampled).

Naked mole rats are mouse sized and are the longest living rodents known, with a recorded MLSP exceeding 28 yr (44). Naked mole rats have a low BMR for their size (255), but the 30% reduction in BMR is not great enough to explain their fivefold extended maximum longevity. In a series of recent studies, several variables that are considered key tenets of the oxidative stress theory of aging have been compared between naked mole rats and similar-sized mice. Surprisingly, a large amount of the data obtained to date provide little support for a diminished level of oxidative damage in these long-living rodents. Although naked mole rats have low BMR, rates of hydrogen peroxide production are similar in heart mitochondria from both species (190a) and in vascular endothelial cells (187); no differences in overall antioxidant activities are evident (3), and levels of accrued oxidative damage to proteins, DNA, and lipids are greater in the longer-living species...

When membrane fatty acid composition was measured in tissues from naked mole rats, they were found to have very low levels of DHA in their tissue phospholipids for their body size. Although both mice and naked mole rats have similar levels of total unsaturated fatty acids in their tissue phospholipids, the low DHA levels in naked mole rats result in more peroxidation-resistant membranes. The PI values calculated for both skeletal muscle and liver mitochondria show that the peroxidation susceptibility of the membranes of naked mole rats is what one would predict for such a long-living rodent species

Humans also have low PI values, and iirc so do bats and long lived birds, the article elaborates more on this.

With regards to antioxidants, the article elaborates more(linked at the bottom), but in general it seems to suggest antioxidant defenses are at an adequate optimal level(though higher levels can protect from toxins, stresses, etc)

While maximum life span has been decreased in a number of studies following the complete removal of particular antioxidant defense (e.g., in homozygous knockouts), the overexpression of antioxidant defenses has essentially had no effect on maximum longevity. It is of interest that heterozygous knockouts (i.e., resulting in a 50% reduction in antioxidant levels) have often had no influence on maximum life span.

It seems the membrane composition can influence far longer lasting and likely more harmful byproducts...

The hydroperoxides and endoperoxides, generated by lipid peroxidation, can undergo fragmentation to produce a broad range of reactive intermediates, such as alkanals, alkenals, hydroxyalkenals, glyoxal, and malondialdehyde (MDA; Ref. 95) (see Fig. 2). These carbonyl compounds (collectively described as "propagators" in Fig. 2) have unique properties contrasted with free radicals. For instance, compared with ROS or RNS, reactive aldehydes have a much longer half-life (i.e., minutes instead of the microseconds-nanoseconds characteristic of most free radicals). Furthermore, the noncharged structure of aldehydes allows them to migrate with relative ease through hydrophobic membranes and hydrophilic cytosolic media, thereby extending the migration distance far from the production site. On the basis of these features alone, these carbonyl compounds can be more destructive than free radicals and may have far-reaching damaging effects on target sites both within and outside membranes.

The social insects have been suggested as particularly good model organisms to investigate the mechanisms of aging for two reasons: 1) "queens" can be extraordinarily long living, and 2) there is sometimes tremendous variation in life span between genetically identical "queens" and "workers" (171). In some ant species, queens can live up to 30 yr and frequently live 10 times longer than workers (144). Similarly, queen honeybees are reported to have a maximum longevity an order of magnitude greater than worker (i.e., nonreproductive female) honeybees (373). Enhanced antioxidant defenses in queens are not a likely explanation, as one study has shown queen ants have a reduced expression of Cu/Zn-SOD compared with shorter-living workers (282) while others have shown that queen honeybees generally have the same (or, in some cases, lower) levels of antioxidant defenses than worker honeybees (68, 370). The mass-specific metabolic rates of worker and queen honeybees are essentially the same (96). Recent measurements show that queen and worker honeybees have different membrane fatty acid composition and that the peroxidation index of phospholipids of from queen honeybees is 33% of that of workers (122). If the slope of the relationship between PI and MLSP is mathematically similar in honeybees to that described for mammals and birds (155, see Fig. 7), then this difference is capable of explaining the order of magnitude difference in longevity between queen and worker bees.

This is very interesting stuff, social insects can vary in lifespan in some cases by up two orders of magnitude despite being the same organisms from the same species with the same genome. An analysis of queens vs workers is in order, if we find that the main difference is membrane lipid composition even in cases of 100x lifespan increase, experimental intervention in mammals would be a must to see what kind of results can be obtained.

Some of these queens are hypothesized to exhibit negligible senescence, the naked mole rat appears to exhibit temporary negligible senescence for most of its lifespan, and it is also said that some birds appear to exhibit such in several tissues.

The details have to be investigated, but a cross species factor and intra species factor being found to have such a strong variation and correlation with lifespan is very intriguing.

Might it be that sufficiently lowering the production of these toxic substances with minute long half lifes, might be enough to allow existing maintenance mechanisms to exceed metabolic wear providing negligible senescence? After all if this turns out to be the primary intervention that provides two orders of magnitude increase in lifespan in some species, it would be extremely suggestive of being an extremely potent intervention in the aging process.

Rather, we suggest that the rate-of-living theory cannot alone explain all of the variation in longevity of animals. However, many of the exceptions that cannot be explained by the rate-of-living theory (and are summarized in sect. I) do appear capable of explanation by knowledge of membrane fatty acid composition in each particular case.

When the fact that fatty acids differ dramatically in their susceptibility to peroxidative damage is combined with species variation in membrane composition, the link between body size, metabolic rate, and longevity becomes more apparent.

In this contribution, we have discussed evidence that the fatty acid composition of membranes can potentially explain 1) the shorter longevity of small mammals compared with larger mammals, 2) the exceptional longevity of naked mole-rats compared with similar-sized mice, 3) the extended longevity of wild-derived lines of mice compared with laboratory mice, 4) the longer life spans of birds compared with similar-sized mammals, 5) the extended longevity of rodents caused by calorie restriction, 6) the longevity difference between workers and queens in honeybees, and 7) also suggested it may be an explanation for the exceptional longevity of our own species, Homo sapiens. Furthermore, we have also discussed the studies which show that membranes with fatty acid compositions prone to peroxidation are also associated with greater levels of lipoxidative damage to other cellular constituents. All these studies suggest that variation in membrane fatty acid composition may be an important missing piece of the jigsaw puzzle explaining aging and the mechanisms that determine the maximum life span specific for each species. It is a testable hypothesis that awaits further experiments.

Quote source link

Edited by steampoweredgod, 12 December 2011 - 09:00 PM.

[niner]

This is a great paper, and discusses one of the reasons that I prefer to keep my intake of multiply-unsaturated oils to a minimum. I just posted a paper that claims oxidized fish oil is safe, which is not exactly consistent with this paper. In order to seriously alter your membrane composition, you would need to not only reduce dietary PUFA, but also alter your lipid metabolism. We have enzymes that can desaturate a saturated fatty acid, so our membrane composition is likely to be fixed, at least to a degree. It just occurred to me that we discussed this issue here in the past, in this thread. There is some good discussion there, as well as some good links.

[Mind]

Another good thread about PUFA and lipid metabolism.

[steampoweredgod]

Posted the following in the alzheimer's thread

Now, a study by researchers in the University of Georgia College of Pharmacy has shown that an antioxidant can delay the onset of all the indicators of Alzheimer's disease, including cognitive decline. The researchers administered an antioxidant compound called MitoQ to mice genetically engineered to develop Alzheimer's. The results of their study were published in the Nov. 2 issue of the Journal of Neuroscience.

"MitoQ selectively accumulates in the mitochondria,"


In their study, mice engineered to carry three genes associated with familial Alzheimer's were tested for cognitive impairment using the Morris Water Maze, a common test for memory retention. The mice that had received MitoQ in their drinking water performed significantly better than those that didn't. Additionally, the treated mice tested negative for the oxidative stress, amyloid burden, neural death and synaptic loss associated with Alzheimer's.-sciencedaily

MitoQ appears to be a lipophilic antioxidant that accumulates in the mitochondria and protects its membrane. In other species membrane composition changes to resist oxidation have been one of the factors behind an order of magnitude increase in lifespan.

MitoQ^® is targeted to mitochondria by covalent attachment to a lipophilic triphenylphosphonium cation.

Because of the large mitochondria membrane potential, the cations accumulate within cellular mitochondria up to 1,000 fold, compared to non-targeted antioxidants such as Coenzyme Q or its analogues. This accumulation enables the antioxidant moiety to block lipid peroxidation, and maintain the integrity of the mitochondria membrane by protecting it from oxidative damage.-link

It is very interesting that altering membrane PI would protect against genetically induced Alzheimer's like disease.

[eighthman]

I don't understand how to sort out the apparent contradictions between this quoted material and the "Best Aging Theory" stuff that I posted separately. In my article, long life is associated with less mtDNA ROS production and less leakage. Longer lived species have less protein/DNA damage. They don't have an increase in endogenous antioxidant production because it is unnecessary.

Any ideas here?

[steampoweredgod]

I don't understand how to sort out the apparent contradictions between this quoted material and the "Best Aging Theory" stuff that I posted separately. In my article, long life is associated with less mtDNA ROS production and less leakage. Longer lived species have less protein/DNA damage. They don't have an increase in endogenous antioxidant production because it is unnecessary.

Any ideas here?

oxygen and many radical species are several times more soluble in lipid membrane bilayers than in the aqueous solution-link

The idea is that primary ros interacts with membrane lipids generating potent secondary ROS. These appear to be important, and by altering the membrane composition the generation of these can be reduced substantially.

It emphasises that a large number of powerful lipid-based ROS are secondarily produced by the action of primary ROS (superoxide, hydrogen peroxide, hydroxyl radicals) on membrane lipids...

We conclude from this comparison that some, but not all components of the “oxidative stress” theory support the notion that the relatively long life of pigeons compared to rats is associated with a lower level of oxidative stress in pigeon tissues. Our results suggest that differences in the production of primary ROS (superoxide and hydrogen peroxide) may not be as important as production of secondary ROS (especially lipid-based ROS)...

The importance of membrane lipid composition lies in the fact that if we compare two membranes that differ in their fatty acid composition and PI (and consequently their susceptibility to peroxidative damage) under conditions of identical challenge from primary ROS, it is the more susceptible membrane (the one with the higher PI) that will produce a greater degree of oxidative stress. In other words, it is the level of total ROS production (primary ROS + secondary ROS) that is responsible for determining the level of oxidative stress and not solely superoxide production. Thus the lack of a difference in mitochondrial superoxide production does not necessarily mean a lack of a difference in the level of oxidative stress and conversely, differences in the level of oxidative stress do not necessarily require differences in mitochondrial superoxide production.-link

The potential importance of membrane fatty acid composition in the determination of longevity is supported by other recent reports on membrane composition in other exceptionally long-living mammals (e.g. naked mole-rats and echidnas) . It is also supported by two other recent genetic studies. One of these examining C.elegans mutants encompassing a 10-fold longevity difference showed that modulation of lipid biosynthesis and membrane composition contributed to stress resistance and longevity of these worms. They showed a similar relationship between membrane PUFA content (and peroxidation index) and maximum lifespan in C.elegans to that previously reported for birds and mammals.The other genetic study examined the evolutionary selection of candidate genes for longevity in mammals and identified those involved with lipid composition to be one of two genes strongly conserved among mammals with high MLSP-link

The lipid ros can autocatalize further secondary ros, thus amplifying ros generation, and some of the products generated can travel vast distances and start reactions elsewhere.

[steampoweredgod]

From one of the referenced articles in the previous comment

We show that genes involved in lipid composition and (collagen associated) vitamin C binding have collectively undergone increased selective pressure in long-lived species, whereas genes involved in DNA replication/repair or antioxidation have not. Most of the candidate genes experimentally associated with aging (e.g., PolG, Sod, Foxo) have played no detectable role in the evolution of longevity in mammals...

A large body of current medical research aims at discovering how to increase longevity in human. In this study, we uncovered the way natural selection has completed this task during mammalian evolution. Cellular membrane and extracellular collagen composition, not genome integrity, have apparently been the optimized features. -link

The peroxidation of lipids by ROS produces reactive carbonyl species, which, being more stable than ROS, can diffuse and oxidize other cellular or extracellular components. Fatty acids are also known to stimulate uncoupling proteins, thereby reducing ROS generation, particularly in calorie-restricted organisms. Such a link implicates fatty acid biosynthesis, not only in the reduction of peroxidative damage (via increased saturation) but also in the control of mitochondrial ROS production through reduced membrane potential and efficient uncoupling of the electron transport chain.-link

advanced lipoxidation end-products =ALEs

Compared to reactive oxygen and nitrogen species, lipid-derived RCS are stable and can diffuse within or even escape from the cell and attack targets far from the site of formation. Therefore, these soluble reactive intermediates, precursors of ALEs, are not only cytotoxic per se, but they also behave as mediators and propagators of oxidative stress and cellular and tissue damage. The consequent loss-of-function and structural integrity of modified biomolecules can have a wide range of downstream functional consequences and may be the cause of subsequent cellular dysfunctions and tissue damage. The causal role of ALEs in aging and longevity is inferred from the findings that follow: a) its accumulation with aging in several tissues and species; b) physiological interventions (dietary restriction) that increase longevity, decrease ALEs content; c) the longer the longevity of a species, the lower is the lipoxidation-derived molecular damage; and finally d) exacerbated levels of ALEs are associated with pathological states.-link

[GhostBuster]

So all this also shows how the mitochondrial decline theory of aging and the membrane hypothesis of aging are interrelated?

http://www.amazon.co...y/dp/0849367387

[eighthman]

OK, I've read over the above material and tried to fully absorb it. There may be several correlations between extreme life spans or negligible senescence and various factors. Perhaps the factors I've read about on ageless animals are better correlated with hypoxia and selection for strong protein management as their environment requires it.I'm surprized by the report that DNA repair is no better but still skeptical until I can find membrane related material to these special animals because they really 'hit the ball out of the park', way beyond mole rats (some whales, clams, rockfish, lobsters).

Now, what about autophagy within this membrane theory? Could part of the longevity be related to an ability of cells to expel damaged material - or digest it within? Perhaps autophagy can be integrated into this.

[steampoweredgod]

OK, I've read over the above material and tried to fully absorb it. There may be several correlations between extreme life spans or negligible senescence and various factors. Perhaps the factors I've read about on ageless animals are better correlated with hypoxia and selection for strong protein management as their environment requires it.I'm surprized by the report that DNA repair is no better but still skeptical until I can find membrane related material to these special animals because they really 'hit the ball out of the park', way beyond mole rats (some whales, clams, rockfish, lobsters).

Now, what about autophagy within this membrane theory? Could part of the longevity be related to an ability of cells to expel damaged material - or digest it within? Perhaps autophagy can be integrated into this.

By reducing the damage produced, it would seem autophagy processes would have an easier time clearing it out. It may be that if damage is reduced sufficiently, maintenance mechanisms(autophagy, dna repair, etc) would be able to substantially reduce damage accumulation thanks to the easier load, given the right level of reduction in damage and the right rate of maintenance some types of damage might not even accumulate at all through time.

Increasing autophagy could very well prove to be synergistic with reduced damage production

Edited by steampoweredgod, 10 January 2012 - 06:10 PM.

[treonsverdery]

There is an easy way to tell if "Membrane composition variation key to exponential maximum lifespan increase" just swap out the membrane lipid composition genes from naked mole rats with other rodents. If the naked mole rats with ordinary rat lipid membrane construction continue with hyperlongevity then the naked mole rats superlongevity comes from a different source.

There is a wonderful lipid resource at http://www.cyberlipi...ip/home0001.htm

Notably it provides references to current things like gene therapy to optimize human lipid composition

Edited by treonsverdery, 10 January 2012 - 08:35 PM.

[eighthman]

This is interesting stuff. Thank you for posting it.

That said, I'm not sure if it has any strong meaning or directive power for anti aging research. You have a lot of results derived from animals that have relatively better lifespans than their 'peers' - and maybe a few results derived from humans, who live about 'three score and ten'. Do these results tell us anything that would lead us to a dramatic life span extension for people? For that, we would have to guess and extrapolate that further improving human cell membranes do the trick.

I think the curent state of aging research is pointing to mtROS damage being done and accumulated. The mystery is: What damage is critical as to dramatic lifespan extension?

[steampoweredgod]

This is interesting stuff. Thank you for posting it.

That said, I'm not sure if it has any strong meaning or directive power for anti aging research. You have a lot of results derived from animals that have relatively better lifespans than their 'peers' - and maybe a few results derived from humans, who live about 'three score and ten'. Do these results tell us anything that would lead us to a dramatic life span extension for people? For that, we would have to guess and extrapolate that further improving human cell membranes do the trick.

I think the curent state of aging research is pointing to mtROS damage being done and accumulated. The mystery is: What damage is critical as to dramatic lifespan extension?

There's an interesting suggestion in one of the links indicating that humans may've adaptations causing mitochondrial lipids to be even more resistant than other cellular lipids, if true this would suggest that such is important enough to merit such adaptation.

With regards to applicability as indicated membrane alterations can alter uncoupling rates reducing mtROS, and also by reducing lipid peroxidation reduce the negative effects of such.

many radical species are several times more soluble in lipid membrane bilayers than in the aqueous solution

lipid ros can autocatalize further secondary ros, thus amplifying ros generation

We've also seen the results of the seventh day adventist studies wherein frequent nut consumption provided lifespan benefits greater than exercise or vegetarianism. One could hypothesize that the complex lipophilic antioxidant mixture might be behind such benefit.

The exact impact of healthy living on life span is not known, but several studies have provided some fairly accurate estimates. For example, let's assume that you decide to eat nuts five times a week. Would that affect how long you live? A review of all studies on this topic show that, on average, you would gain almost three years of life compared to those who rarely eat nuts.-The culprit and the cure by Steven Aldana

When Loma Linda University researchers tracked the lifestyle habits of 34,000 Seventh-Day Adventists—a population famous for its longevity—they discovered that those who munched nuts 5 days a week, earned an extra 2.9 years on the planet.-Men's health

The key is not merely comparison of causes of differing animal lifespans, but a factor that with uncoupling may be behind the exceptions to the connection between metabolic rate and aging rate. By clarifying factors involved in such exceptions, it helps elucidate the nature of the problem, such that the exceptions rather than confound provide insight. And it being one of the factors behind exponential lifespan differences between genetically identical organisms(bee vs queen bee), if this holds for some of the even longer lived queens from other species(some ant and termite species) which some say exhibit negligible senescence, and if they too have genetically identical short lived peers, it would be highly suggestive especially if no other major difference is found to be behind such.

The key question is how nature achieves negligible senescence. If it is true that High metabolic rate organisms have attained such, it would bode well for organisms with lower metabolic rates such as humans.

[eighthman]

Agreed, negligible senescence is the goal and it be great if some more convenient creatures (like insects) happened to have achieved it. Eating nuts and such is all well and good but I'm lookin' for more than a few years of life here.

Off topic: I wonder if anyone has studied the idea that a big life extension would be possible for most people, if you just replaced their heart with a fully cloned model. I would think that would be more critical than anything else and first to fail.

[niner]

Off topic: I wonder if anyone has studied the idea that a big life extension would be possible for most people, if you just replaced their heart with a fully cloned model. I would think that would be more critical than anything else and first to fail.

Wouldn't help much. Everything else is in decline at the same time; just replacing one part would leave too much still defective. If you could rejuvenate the entire circulatory and immune systems, that would buy you some time, but there's still everything else.

[eighthman]

A fair point but not everything declines at the same rate. An Extremely Wrinkly Old Lady survived to be 122 even though she looked like might collapse at any moment.

The major problem with heart replacement would be the risk of hemorragic stroke, making it all futile.

[steampoweredgod]

The major problem with heart replacement would be the risk of hemorragic stroke, making it all futile.

IF human stem cells could be modified to gain more vigorous regenerative abilities and bypass scar tissue, they could rejuvenate the heart.

A fair point but not everything declines at the same rate. An Extremely Wrinkly Old Lady survived to be 122 even though she looked like might collapse at any moment.

The oldest supercentenarian in the world was reeported to've been a chocoholic(2 pounds per week), along with some other supercentenarian. Given the extreme odds of becoming a supercentenarian this factor may've had some influence.

Chocolate-loving Sarah Knauss is the second oldest person whose age has ever been authenticated. She was a youthful 99 years old in the picture above. She lived another 20 years. The only person ever proven to have lived longer than Sarah Knauss was fellow chocoholic Jeanne Calment - who lived to be 122.-link

Given that cacao is mostly fat, like nuts there are likely plenty of lipophilic antioxidants too. Some sources say Jeanne Calment was told to give up chocolate 3 years before her death(deeper biographical data needed to verify this).

With regards to supercentenarian deaths, it is said it is not the usual causes of cancer and normal heart disease that do them in, but something called Senile Cardiac TTR-Amyloidosis

The most likely cause of death of Supercentenarians is called Senile Cardiac TTR-Amyloidosis (Diagnosis by Autopsy [6 of 10 in all of history] and not by what is written on Death Certificates).-link

Edited by steampoweredgod, 19 January 2012 - 03:21 PM.

[eighthman]

Hey, Wait a minute! Consider this ! Take a look at recent lab mouse results in regard to removing senescent cells, sharing a young blood supply or improving telomere length. There appears to be some evidence that the context consisting of older cells may improve or even rejuvenate!

Is it possible that, if whole organs such as the heart, liver, etc were replaced with new cloned units, that the brain and blood vessels would be renewed? (Woo-Hoo!)

[niner]

Is it possible that, if whole organs such as the heart, liver, etc were replaced with new cloned units, that the brain and blood vessels would be renewed? (Woo-Hoo!)

Well, kinda, but probably not that much from a heart. Maybe more from a liver. However, when we get to the point of being able to create new immunogenically compatible organs, we will probably be able to do some other things that will rejuvenate all sorts of things. For example, removing sensecent cells and adding any needed stem cells, and lengthening short telomeres in existing somatic cells.

[Anthony_Loera]

Would D-Carnosine help?

"

Design, synthesis, and evaluation of carnosine derivatives as selective and efficient sequestering agents of cytotoxic reactive carbonyl species."

http://www.ncbi.nlm....pubmed/19301317

A

[steampoweredgod]

Would D-Carnosine help?

"

Design, synthesis, and evaluation of carnosine derivatives as selective and efficient sequestering agents of cytotoxic reactive carbonyl species."

http://www.ncbi.nlm....pubmed/19301317

A

It likely helps, but moderate Calorie Restriction is likely a more effective intervention working on multiple areas. Mtor activity interventions are also likely quite potent.

Regards a new article relating membrane lipoxidation resistance and longevity in mice

In the present study investigators sought to determine if extremely old aged mice had different cell membranes than the average middle aged mice. They reasoned that certain individual mice and humans may live very long because their cell membranes where somehow more resistant to oxidative damage.
They indeed found that the cell membranes in exceptionally old mice had the highest resistance to oxidative injury, as well as the lowest amount of oxidative damage.
They concluded that “low lipid oxidation susceptibility and maintenance of adult-like protein lipoxidative damage could be key mechanisms for longevity achievement.”-link

[eighthman]

OK, then. If dolichol is related to membrane changes and if membrane integrity is the Big Deal, then perhaps fasting and Acipimox are the answer .

http://morelife.org/...rs/15236765.pdf

Never heard if this (anti-) lipolytic stuff actually extended mice lifespan.

[Mind]

As to the theory of replacing the heart in order to gain extra years, from what we have learned from stem cell studies, this would probably not work too well. A young heart placed in a very old body might deteriorate rapidly. What has been found in stem cells is that when they are injected into an aged cell environment, they just take on the characteristics of the "environment". They don't work their rejuvenation magic.

Like niner mentioned earlier, what is likely to be more successful are cellular interventions that work on the body as a whole, of course when combined with new organs, you would probably get a bigger effect on life extension.

[steampoweredgod]

As to the theory of replacing the heart in order to gain extra years, from what we have learned from stem cell studies, this would probably not work too well. A young heart placed in a very old body might deteriorate rapidly. What has been found in stem cells is that when they are injected into an aged cell environment, they just take on the characteristics of the "environment". They don't work their rejuvenation magic.

Like niner mentioned earlier, what is likely to be more successful are cellular interventions that work on the body as a whole, of course when combined with new organs, you would probably get a bigger effect on life extension.

One'd have to work with immune system cells, for novel proteins introduced being accepted immunologically. But in principle a cell may be engineered with vast cancer resistance(say ala elephant with 12+ p53, etc genes, or even whale like genetic resistance providing millenia+ of cancer free function), good telomerase activity, and vast regenerative ability that ignores cellular environment signals and retain youthful gene expression profiles while regenerating all tissues with new young acting cells.

IT would take massive effort to engineer such a cell, but it would outcompete native cells and restore function, in theory it may also be engineered to hunt senescent cell and use immune signalling to cause them to commit apoptosis. It could even destroy scar tissue, and regenerate, if such is possible.

Edited by steampoweredgod, 24 March 2012 - 05:25 PM.

[steampoweredgod]

With regards to dna information, the possibility exist that information transfer or exchange may occur in multicellular lifeforms

In unicellular bacteria information exchange allows the resistance to antibiotics to accumulate generating super resistance to broad spectrum.

some stem cells have been shown fusing with other cells. If say glia can fuse and exchange information, multi copy error correction may hypothetically speaking be possible, and such would actually halt information decay or loss indefinitely.

Venter hinted that some sections of the genome are absolutely critical in his speech, so nature may have ways of completely protecting such from the ravages of time.



and a nice inspirational video

Edited by steampoweredgod, 26 March 2012 - 03:05 AM.

[steampoweredgod]

Continuing the preceding, the creation of a high speed low cost dna synthesizer molecular machine, what i call the molecular tape synthesizer may be possible by utilizing fiber optics, optic reactive protein molecules and rna-protein reverse-ribosozome like structure that works with dna, lots of supercomputer hours and protein folding fun I know, but once constructed, the cell lines could be used to synthesize in parallel multiple different chromosomes and bring closer the dream brought about in blade runner, of replicants and synthetic multicellular lifeforms. as well as ageless superhuman organs combining the best of diamondoid mechanosynthesis and biological machinery into a hybrid kind of synthetic molecular machinery.


Regards dna sharing p2p style repair and acquisition unicellular bacteria do it, and such acquire not just resistant but multiresistance and become superbugs immune to virtually all antibiotics. As mentioned stem cell fusion has been observed in multicellular lifeforms. It is possible the so called 10x1 glia to neuron ratio, may mean the glia population acts as redundant dna copy data backup and exchange is possible as in unicellular which may explain how some nondividing hypermetabolic motor neurons can last what seems like over 200 years(some bowhead whales, btw, as mentioned elsewhere some have commented such whales seem not only cancer proof but stroke proof).

Edited by steampoweredgod, 18 April 2012 - 11:49 PM.