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BioViva

liz parrish bioviva

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#181 Rocket

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Posted 07 May 2016 - 02:56 AM

"Better yet, explain why a lab mouse and a naked mole-rat have such vastly different lifespans. According to you, due to their very similar ratty "chemical constitutions" they should have the same levels of AGEs and ROS in the same timeframe."

Better yet, how about I didn't claim that AGE accumulation and ROS generation explain the varying lifespans of mammals. Where
the funk did you see me say that? Huh? I only said that the programmed theory of aging does not take them into account.

Prove to me that mice and naked mole rats don't accumulate ages and ROS at the same rates accounting for weight differences.

Logically you assume they don't because of their varying lifespan, per your argument. Bullshit! Nonsense!

You jumped to the conclusion that they don't accumulate AGE and generate ROS at the same rate.... You just claimed to solve the riddle of the varying lifespan. So now be a grown up scientist and back up your claim about ROS generation and AGE accumulation is different between the two animals.

And oh my god, the albatros lives to be 40. Wow, an immortal species!? What's your jaw dropping point? There are other birds with equally long lifespans. Are you saying they generate ROS and accumulate AGEs slower than sparrows? What is your point about the albatros? Be a grown up and explain to the dummies here.

And now you bring up long lived whales? Oh yeah, whales and humans are biological equivalents. Why didn't you mention sharks for that matter? Or what about.... Clams?

Before I brought up AGEs and ROS none of your prior posts even mention these. Now you're focused on them.

Care to enlighten us next on lipofuscin accumulation in humans and whales?

Edited by Rocket, 07 May 2016 - 03:09 AM.

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#182 xEva

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Posted 09 May 2016 - 03:29 AM

Better yet, how about I didn't claim that AGE accumulation and ROS generation explain the varying lifespans of mammals. Where
the funk did you see me say that? Huh? I only said that the programmed theory of aging does not take them into account.

Prove to me that mice and naked mole rats don't accumulate ages and ROS at the same rates accounting for weight differences.

Logically you assume they don't because of their varying lifespan, per your argument. Bullshit! Nonsense!

You jumped to the conclusion that they don't accumulate AGE and generate ROS at the same rate.... You just claimed to solve the riddle of the varying lifespan. So now be a grown up scientist and back up your claim about ROS generation and AGE accumulation is different between the two animals.

And oh my god, the albatros lives to be 40. Wow, an immortal species!? What's your jaw dropping point? There are other birds with equally long lifespans. Are you saying they generate ROS and accumulate AGEs slower than sparrows? What is your point about the albatros? Be a grown up and explain to the dummies here.

And now you bring up long lived whales? Oh yeah, whales and humans are biological equivalents. Why didn't you mention sharks for that matter? Or what about.... Clams?

Before I brought up AGEs and ROS none of your prior posts even mention these. Now you're focused on them.

Care to enlighten us next on lipofuscin accumulation in humans and whales?

 
 
Gee Rocket, why getting worked up? 
 
Re albatross,

"Studies of grey-headed albatrosses have not yet continued for long enough to document close to maximum longevity records; the oldest known-age individuals are now 46 years old, but it is quite likely that some individuals live considerably longer."

http://www.ncbi.nlm....les/PMC1634918/

 

But 46 y. is not the point. The point about the animals with negligible senescence is that they remain fit, iow young, until the very end of their rather long lives -- long in comparison to similar species.  
 
Re ROS and AGEs, you were the one who brought them up, in a context of a stupid question. You asked, how they are programmed. They are not. No damage is programmed. What's programmed is the attenuation of repairs, which, with time, allows the damage to start accumulating. This is an interesting concept. Think about it.
 

We should split this thread and move the off-topic posts to a new thread in the aging theories section, where we can have fun debating these issues. Mods can do it :)

 

 
This discussion, especially posts by Logjam and re-reading the Principles of Alt. Gerontology, made me realize that fixing molecular damage must be the very basic  program that sits at the bottom of all other programs in a cell. If it were not, life would not be possible. This is very encouraging, don't you think?

 

So, fixing molecular damage must be the default. The aging programs, whatever they are, must sit on top of it, somehow messing up with it. And the studies on heterochronic parabiosis confirm this.  Otherwise, why would an old cell start behaving young again, when placed in a young environment? This alone should bring doubt in the hearts of the believers in simplistic accumulation of damage theories of aging. 


Edited by xEva, 09 May 2016 - 03:45 AM.

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#183 niner

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Posted 09 May 2016 - 03:50 AM

This discussion, especially posts by Logjam and re-reading the Principles of Alt. Gerontology, made me realize that fixing molecular damage must be the very basic  program that sits at the bottom of all other programs in a cell. If it were not, life would not be possible. This is very encouraging, don't you think?

 

So, fixing molecular damage must be the default. The aging programs, whatever they are, must sit on top of it, somehow messing up with it. And the studies on heterochronic parabiosis confirm this.  Otherwise, why would an old cell start behaving young again, when placed in a young environment? This alone should bring doubt in the hearts of believers into simplistic accumulation of damage theories of aging. 

 

The Alt. Gerontology paper was good.  Thanks for that.  One mechanism for fixing (or hiding) damage is diluting it with new tissue.  From conception to the end of development around two decades later, we add fresh new tissue as we grow.  After that, it isn't long before we start showing our age.  This suggests that there are not other good mechanisms for repairing some of the more problematic forms of damage like glucosepane crosslinks or lipofuscin.  If there are mechanisms that do this, then I guess they haven't been discovered.  This is not to say that paracrine signaling resulting in cells acting older doesn't happen.  It clearly does happen.  There is more to aging than crosslinks and lipofuscin, but I don't think that means we can ignore molecular damage.  It will still need to be fixed, and there's no evidence that I'm aware of for repair mechanisms that could somehow be restarted if only we knew the right input.


Edited by niner, 09 May 2016 - 03:57 AM.


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#184 Logjam

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Posted 09 May 2016 - 05:25 AM

The problem with evolution is that if nothing ever dies nothing ever improves—there's no reason beyond a point.  We're pretty advanced, though.  And that did evolve somehow.  Why?  Predators that eat you help with the dying part, but sexual reproduction and programmed dying helps even more.  They go together, mostly.  And they may accelerate the evolution algorithm a whole lot.

 

We needed to evolve the ability to decay and die before we actually progress faster, right?  Why wait until something kills you?  And yes, I suppose it would be a bolt on program because evolution itself evolved.  Or God created it.  Whichever you prefer.  I'm mostly a believer, which is unpopular these days.  Don't shoot!

 

A bunch of assumption and conjecture, but it makes complete sense (to me).  The reason we're here is because we die.  If we didn't, I doubt we're be on an internet connected by billions of wires all talking about cheating death.  We'd still be gray goop.


Edited by Logjam, 09 May 2016 - 05:40 AM.

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#185 xEva

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Posted 09 May 2016 - 08:39 AM

One mechanism for fixing (or hiding) damage is diluting it with new tissue.  From conception to the end of development around two decades later, we add fresh new tissue as we grow.  After that, it isn't long before we start showing our age.  This suggests that there are not other good mechanisms for repairing some of the more problematic forms of damage like glucosepane crosslinks or lipofuscin.  If there are mechanisms that do this, then I guess they haven't been discovered.  This is not to say that paracrine signaling resulting in cells acting older doesn't happen.  It clearly does happen.  There is more to aging than crosslinks and lipofuscin, but I don't think that means we can ignore molecular damage.  It will still need to be fixed, and there's no evidence that I'm aware of for repair mechanisms that could somehow be restarted if only we knew the right input.

 
 
Why do you say "restarted"? They never stop. Wounds heal, skin peals, hair and nails grow, intestinal epithelium changes every 3-5 days. Lotsa stuff goes on in a cell itself, invisible to the naked eye. The problem is, these repair programs become sluggish with age, and the more sluggish they become, the quicker damage accumulates.

 

Dilution of damage via cell division must be very old strategy, but not as old as fixing the molecular damage. This is basic and it happens every time when a new life starts -- does not matter how old the parents were! And then, lots of it goes on daily. Our cells are continuously repairing themselves. When you elicit hormetic response, you actually stimulate molecular repair mechanisms. You sorta upregulate them. When you workout, you create lotsa damage to be fixed later on. The idea that we have no molecular repair mechanisms worth talking about is patently wrong. 

 

But, other than lipofuscin and glucosepane, what molecular damage you;re talking about? (please don't start on mitochondria again : ))) they too can be fixed! ) 

 

As for lipofuscin, I imagine the vacuoles with it can be removed via exocytosis. IOW, the cell can sorta poop it out into the extracellular environment, to be picked up and carried away by macrophages. This seems like a perfectly  natural way of getting rid of unwanted stuff. In fact, I just googled "llipofuscin vacuoles exocytosis" and get "exocytosis of ceroid/lipofuscin" all over. 

 

There gotta be something for glucosepane as well. My point is, everything can be fixed. Everything IS fixed -- for a while at least. And then it sorta starts slowing down. But it never stops. 

 

 

 

 

We needed to evolve the ability to decay and die before we actually progress faster, right?  Why wait until something kills you?

 
-? not sure I understand you. Aging is good for group survival (limited resources and such). I noticed that most, if not all, animals with negligible senescence are not confined to particular habitats but are free to roam (the ocean, mostly). If it becomes crowded or resources get depleted in one area, they can move on to find another. 
 
In any rate, individual does not matter. It's the species, the group, that matters. And it looks like aging is advantageous for a group competing with others within confines of a specific habitat.  


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#186 corb

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Posted 09 May 2016 - 02:41 PM

Lipofuscin degradation and exocytosis HAS NOT BEEN OBSERVED in mammalian cells neither in vivo nor in vitro. Last time I checked was 2013 that might have changed in the last 2-3 years but I've not heard of it.

The many hits you get on lipofuscin exocytosis are from a talk given on a SENS conference and a couple of threads on this topic and from FightingAging.com - basically they're all talking about a proposed therapy not a biological reality.

 

Also diluting damage is not a "new" mechanism multicelularity has ushered in, It's the oldest one - asymmetric cell division.


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#187 alc

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Posted 16 May 2016 - 01:13 AM

In his recent blog post Michael Fossel addressed the discussion about lengthening the telomeres (vis-a-vis BioViva results):

 

Telomeres: Are They Worth Measuring?

 

http://www.michaelfo...com/blog/?p=182

 

Short and nice explanation.


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#188 niner

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Posted 16 May 2016 - 02:06 AM

That's an insightful article from Michael Fossel.    (Whoever rated that "Pointless", please reconsider.)   I don't agree that someone who looks old would have been a better patient zero.  There is no evidence that telomerase enhancement would change most of the things that make people look old, like photodamage, hair greying and hair loss, nor is there any reason to believe that it would.  A person who looked old both before and after the treatment would be like an advertisement telling the uninformed that it "didn't work".  At least with Liz, after the treatment she'll still look good, whether it "works" or not.


Edited by niner, 16 May 2016 - 02:08 AM.

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#189 corb

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Posted 16 May 2016 - 03:47 AM

Michael Fossel is asking the same question I asked for the Liz Parish interview. Blood cell telomere length is really not something you should be particularly worried about, lots of infants have shorter telomeres in their blood than 80 year olds and they don't drop dead.

 

Something I've been thinking about for a couple of days - the telomere therapy Liz took is "interesting" but what I've been more interested about recently is her "myostatin" therapy. She hasn't talked much about it but the papers I see posted on the Bioviva website talk about Folistatin. Now what's interesting about Folistatin is - indeed it binds and disables myostatin BUT it does the same for GDF11! It does it to most tgf beta proteins but in the case of GDF11 and GDF8 aka myostatin it should be doing it with about the same efficiency because they are homologous.

 

So Liz Parish has genetically modified herself to inhibit GDF11 function. And a scientist in her lab has had the same therapy for over 5 years? With no ill effects observed?
Definitely something to think about.


Edited by corb, 16 May 2016 - 04:14 AM.

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#190 marcobjj

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Posted 21 May 2016 - 10:19 PM

Does she look younger? Cheeks a bit plumper perhaps, hard to tell.



#191 xEva

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Posted 22 May 2016 - 12:12 AM

yes! 


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#192 ceridwen

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Posted 22 May 2016 - 01:25 AM

I think she looks and sounds a little disappointed y
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#193 reason

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Posted 23 May 2016 - 11:19 PM

At a recent conference, Bill Andrews of Sierra Sciences announced a forthcoming collaboration with BioViva, currently pushing regulatory boundaries to develop gene therapies as treatments for aging. A new company will be formed, BioViva Fiji, to offer gene therapies that can compensate for some of the aspects of degenerative aging via medical tourism in Fiji. The principle focus, given that this is Sierra Sciences we are talking about here, is telomerase gene therapy, but BioViva is also working on a follistatin gene therapy, and it is worth bearing in mind that in this age of CRISPR rolling out any single target gene therapy that has some background work in the research community isn't the huge technical undertaking it would have been in past years. All of the time and cost goes into a reasonable level of testing, and the only real hurdle left from a technical point of view is proving that a therapy can reliably introduce genes into a large enough number of cells to produce benefits. We're going to see a lot of work on gene therapies in the next few years - this is just the start and the tip of the iceberg.

Fiji, like many countries in the Asia-Pacific region, has been taking steps in recent years to make itself attractive as a destination for medical tourism, and thereby encourage the growth of high-end local industries that benefit from the wealth of larger and more prosperous countries. It makes a lot of sense as a long-term plan, and competition between regions for medical tourism will hopefully prevent these countries from falling into the overregulated repression of medical development found in the US and Europe, a state of affairs that slows development and that gave rise to medical tourism in the first place. Fiji is the destination for this particular effort, but it could equally have been any of a number of other choices.

"Sierra Sciences and BioViva - Liz Parrish - have now joined forces. We have started a new company, called BioViva Fiji, on Fiji island, and we are now building a large-scale production facility and a clinic to soon be able to provide a gene therapy approach towards curing aging."

Bill Andrews is, as many of you will recall, an enthusiast for telomerase and telomere length as a key to aging, and he is in full sales mode above. The goal of Sierra Sciences before the company floundered was to build a viable treatment along these lines, but they ran out of funding and then turned to selling herbal nonsense. That was a sad end for a group that was at the outset working on interesting science. Interesting, yes, but from where I stand age-related reduction in average telomere length is a marker of aging, not a cause of aging. Telomerase gene therapies most likely extend life in mice through increased stem cell activity, counteracting some of the decline in stem cell populations that occurs with advancing age. It was surprising to find that this doesn't raise the risk of cancer, as those stem cell populations become damaged by age, and their decline is generally through to be an evolved defense against cancer in later life. It may be that the general enhancement of cell activity extends to the immune system, and better immune surveillance and clearance of cancerous cells is enough to offset that raised risk due to pushing damaged cells back to work. This or any other thesis is far from proven at this point, and telomerase gene therapies in humans still seem overly risky on this count to my eyes.

I believe based on the evidence to date that telomerase gene therapy should be classed as a compensatory treatment. It is pushing a damaged engine to do more, and it may well be the case that in humans as well as mice the balance of factors brings a net improvement in the same way as do stem cell therapies, another field associated with a prospering medical tourism industry, but that is yet to be nailed down and proven. Follistatin or myostatin gene therapies are similarly compensatory. They do not address the damage that causes aging, but they compensate partially for one its effects, in this case by adding extra muscle tissue to offset that lost over time to the mechanisms of aging. Is this all useful? Yes - if you think that stem cell therapies are worth it, then you should also think that this sort of gene therapy is worth it. I'm pleased to see Bill Andrews working on something that doesn't make me sad for the waste of potential it signifies, as was the case for the end of Sierra Sciences as a legitimate scientific venture.

We should not forget, however, that telomerase therapies cannot cure aging. A lot of people would like to think that they do, but it simply isn't the case. They don't treat the causes of aging, they instead adjust a lot of factors to paper over those causes just a little bit better than the papering over that the present mainstream of medicine can achieve. Undergo a telomerase gene therapy and you may benefit in a very similar way to a stem cell treatment, but in both cases you are still aging and still damaged. You still have mitochondrial DNA damage, lipofusin in your long-lived cells, cross-links stiffening your arteries, and so on and so forth, and all those things are still killing you.


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#194 marcobjj

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Posted 07 June 2016 - 08:59 PM

Telomere shortening exerts influence in mitochondrial aging, free radicals do not:


Abstract
Age-associated cardiovascular diseases are at least partially ascribable to vascular cell senescence. Replicative senescence (RS) and stress-induced premature senescence (SIPS) are provoked respectively by endogenous (telomere erosion) and exogenous (H2O2, UV) stimuli resulting in cell cycle arrest in G1 and G2 phases. In both scenarios, mitochondria-derived ROS are important players in senescence initiation. We aimed to define whether a mtDNA-transcribed long-non-coding-RNA (lncRNA), ASncmtRNA-2, has a role in vascular aging and senescence. Aortas of old mice, characterized by increased senescence, showed an increment in ASncmtRNA-2 expression.

In vitro analysis of Endothelial Cells (EC) and Vascular Smooth Muscle Cells (VSMC) established that ASncmtRNA-2 is induced in EC, but not in VSMC, during RS. Surprisingly, ASncmtRNA-2 is not upregulated in two different EC SIPS scenarios, treated with H2O2 and UV. The p16 gene displayed similar ASncmtRNA-2 expression patterns, suggesting a possible co-regulation of the two genes. Interestingly, the expression of two miRNAs, hsa-miR-4485 and hsa-miR-1973, with perfect homology to the double strand region of ASncmtRNA-2 and originating at least in part from a mitochondrial transcript, was induced in RS, opening to the possibility that this lncRNA functions as a non-canonical precursor of these miRNAs.


Cell cycle analysis of EC transiently over-expressing ASncmtRNA-2 revealed an accumulation of EC in the G2/M phase, but not in the G1 phase. We propose that ASncmtRNA-2 in EC might be involved in the RS establishment by participating in the cell cycle arrest in G2/M phase, possibly through the production of hsa-miR-4485 and hsa-miR-1973. This article is part of a Special Issue entitled: Mitochondria.

http://www.ncbi.nlm....pubmed/25640160

#195 Steve H

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Posted 07 June 2016 - 09:10 PM

Telomere shortening exerts influence in mitochondrial aging, free radicals do not:

 

 

Yes via the PCG-1a - P53 Axis as shown by Dephino.


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#196 corb

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Posted 04 July 2016 - 06:24 PM

I've been hearing some worrisome things about Bioviva recently.
So instead of making a big fuss and making a new thread, let's start small.

Does someone more interested in this have some concrete information about the tests Liz Parish did and whether she did them with a reputable lab?

 

Man... I hope we're not headed towards yet another press fiasco painting our community as a bunch of looneys and quacks.


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#197 nevlugion

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Posted 05 July 2016 - 09:50 AM

I've been hearing some worrisome things about Bioviva recently.
So instead of making a big fuss and making a new thread, let's start small.

Does someone more interested in this have some concrete information about the tests Liz Parish did and whether she did them with a reputable lab?

 

Man... I hope we're not headed towards yet another press fiasco painting our community as a bunch of looneys and quacks.

 

I've also been reading quite allot of negative news about Bioviva (she being the only employee of the company, its official HQ just being a normal residence and several others) and I fear all of this is more of a marketing stunt too. It worries me too that some Longevity scientists/proponents (George Church / Aubrey) still support her, while I believe she is a fraud/quack trying to sell expensive "snake oil" (no offense intended).

 

"Bioviva fuji" also seems to work with Bill Andrews who has a dubious reputation due to his questionable supplements...


Edited by nevlugion, 05 July 2016 - 09:55 AM.

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#198 corb

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Posted 05 July 2016 - 10:26 AM

 It worries me too that some Longevity scientists/proponents (George Church / Aubrey) still support her

 

It's the only thing I'm worried about.
From all I'm seeing BioViva seems to just be a front for Precision StemCell, Jason Williams's company which is under scrutiny by the FDA - he's known for selling adipose stem cell therapies to rich athletes.

 

Stunts like this can only hurt longevity advocacy.


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#199 alc

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Posted 17 July 2016 - 01:10 PM

from their blog:

 

BioViva, Gene Therapy and BlockChain merges in Russia

 

 

http://bioviva-scien...rges-in-russia/



#200 reason

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Posted 30 November 2016 - 02:08 PM

Back in 2015, Elizabeth Parrish underwent telomerase and follistatin gene therapy as a part of forming the startup BioViva: a human safety trial of one person, made public as a way to push the bounds of the current debate over when we should get started on human testing of these technologies. Personally, I agree that there is too much talk, too much unnecessary caution and hand-wringing, and not enough action. Sooner rather than later is better, especially given the large amount of animal data showing safety. Parrish is to be congratulated for forging ahead.

The latter of these two gene therapies is more interesting to me, as there is much more evidence in animal studies of the safety and effectiveness of either directly suppressing myostatin or enhancing follistatin to suppress myostatin. This has the effect of increasing muscle mass and reducing fat tissue, along the way tuning the operation of metabolism into a healthier mode of operation. It seems to me to be an enhancement that everyone should undergo, based on the evidence to date: a way to improve health and slow the age-related loss of muscle mass and strength. BioViva has now released some more data on the long term effects of the gene therapies, which show increased muscle mass, reduced fat, and improved aspects of metabolism. In a study of one, this should be taken as an anecdote, especially given that these items can all be changed over the longer term to some degree by lifestyle adjustments. The important thing is that safety has been proven, and that there appear to be benefits is just an added incentive to move to the next step of larger studies and availability of therapy via medical tourism. Hopefully the company will find the funding to achieve both of these goals.

In April 2016 BioViva stated that Elizabeth Parrish, CEO, had experienced telomere lengthening in her leukocytes, as a result of an injection of two experimental therapies. These consisted of a myostatin inhibitor to protect against loss of muscle mass with age, and a telomerase inducer to battle stem cell depletion responsible for diverse age-related diseases and infirmities. While the test was designed to establish the first human safety data regarding telomerase induction, in tests conducted by SpectraCell Laboratories, data indicated that her leukocyte telomeres had lengthened by approximately 20 years, from 6.71kb to 7.33kb. Further data will be released later this year. Upon further examination and testing, comparison of Parrish's data prior to the therapy and following the therapy has revealed additional positive changes. MRI scans taken before and after depict a slight increase in muscle size in conjunction with a noticeable reduction in muscle fat content. An over-accumulation of intramuscular fat, also known as 'marbling', is associated with increased insulin resistance, and as such an appropriate reduction may be linked to beneficial metabolic changes, in addition to the improved musculature. The aforementioned patient's total body weight has also not decreased during this period, and as such weight loss is not a confounding variable. The muscle growth achieved post-therapy corresponds with observed improvements in patients with Becker's Muscular Dystrophy, after receipt of myostatin inhibition gene therapy.

Researchers have noted that a significant reduction in fasting glucose was apparent in mice following telomerase gene therapy. The subject's fasting glucose has declined from previous measurements of 94 mg/dL and 86 mg/dL, to a fasting glucose level of 71 mg/dL by August 2016, as measured by Quest Diagnostics. Repeated testing will confirm the implied increase in insulin sensitivity. Previous research has also indicated that telomerase deficiency impairs glucose metabolism and insulin secretion in telomerase deficient mice, which may explain an apparent improvement in metabolic markers. In accordance with an improvement in metabolic health, triglyceride levels have also declined from 140 mg/dL in 2015 prior to the therapy, to 36 mg/dL in February 2016, subsequently rising to 80 and 84 mg/dL in August 2016. While there has been an increase in blood triglyceride content following the February reading, it is still measurably lower than before treatment. Both decreases in fasting glucose and triglycerides can be potentially explained by prior studies, of both telomerase and myostatin. Raised myostatin mRNA seen in type 2 diabetes patients is associated with impaired insulin sensitivity, raising triglyceride levels and low-grade chronic inflammation. Myostatin inhibition in mice has also been shown to reduce triglyceride levels and improve insulin sensitivity.

No negative effects have been reported, and there are no visible detrimental effects in blood analysis thus far; providing tentative evidence of safety in the first human test of BioViva's dual gene therapy strategy.

Link: http://bioviva-scien...cle-composition


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#201 johnross47

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Posted 30 November 2016 - 10:37 PM

So what are the chances of 70 year olds like me getting either of these treatments any time soon?



#202 DareDevil

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Posted 22 January 2017 - 12:37 PM

This seems interesting to eventually follow-up. However, there is the issue of a prohibitively high price for natural human Follistatin at $4800/mg versus the much lower price of its precursor peptide called Follistatin 344 which can be sourced for under $100/mg. 

 

Keep us updated on any news you hear of this as an anti-aging therapy.

 

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#203 Mind

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Posted 26 February 2018 - 07:44 PM

BioViva is partnering with Integrated health systems to offer treatments: https://www.integrat...ntact-1-section



#204 Believer

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Posted 29 June 2018 - 10:52 AM

What about the Fiji clinics?

It seems nothing has happened. I followed her almost daily expecting something big to happen



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#205 Mind

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Posted 12 December 2018 - 09:01 PM

BioViva is partnering with Rutgers University to explore virus-vector anti-aging treatments. https://www.eurekale...sKaOiDx1-VCXzYM

 

I wonder who is the angel-funder for this effort. University projects do not come cheap.







Also tagged with one or more of these keywords: liz parrish, bioviva

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