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Whatever Future Comes, Life Extension Will Improve It – Article by Nicola Bagalà

Whatever Future Comes, Life Extension Will Improve It – Article by Nicola Bagalà

Nicola Bagalà


Editor’s Note: In this article originally published by our allies at the Life Extension Advocacy Foundation (LEAF),  Mr.Nicola Bagalà makes a persuasive case for optimism regarding the role of technology in the future. While the future will certainly have problems as well, technological progress – including progress in greatly increasing human health and longevity – can only contribute to solutions and improved quality of life. It is time to reject defeatism and build the future we wish to inhabit.

~ Gennady Stolyarov II, Chairman, United States Transhumanist Party, August 12, 2018


Right now, as I write this article, I’m sitting in a machine that, about 120 years ago, was laughed at as a pipe dream. The machine is a plane, by the way. The onboard wi-fi leaves much to be desired, but if you had told people living in the early 1900s that you could type an article on a paperless portable device while flying in a huge metal cabin at an altitude of 10.3 kilometers and a ground speed of 904 kilometers an hour (that’s what the huge metal cabin is magically telling my portable device through thin air), they’d have had you in a straitjacket before you could finish your sentence.

Talking about computers and planes in these terms today often feels cringeworthy, because we’re all familiar with this technology. We’re used to having all these cool devices and machines doing stuff for us; it isn’t surprising or awe-inducing in the least anymore. However, it’s not a bad idea to remind ourselves how what we now nearly shrug at wasn’t even conceivable not too long ago. Examples include a 27-kilometer ring buried underneath Geneva where ridiculously tiny particles are smashed together at near-lightspeed to unravel the inner workings of the universe and tools that allow us to modify the basic building blocks of your cells with unprecedented precision—neither of which would’ve made you come across as particularly sane, had you conjectured them in a conversation, say, 200 years ago.

This is not to say that people in the past lacked imagination; scientists and visionaries did try to predict what the future might look like—sometimes getting quite close to the mark and other times ending up embarrassingly far from it—but the average joes who had to tend their crops the whole day or work at some kind of drudgery 70 hours a week probably weren’t too optimistic about a future with sophisticated machines of all sorts that make your life much easier and open unthinkable possibilities. They were too used to the standards of the age in which they lived. In a similar way, people of today sometimes tend to look at the future as something that isn’t going to be much different from the present, as if most of what our species could realistically achieve—not only in terms of science and technology but also as a society—was already achieved, and all you could look forward to in the future was just more of the same, except perhaps with slightly fancier tools.

It’s easy to think that way when your days are taken up by a job you’re not crazy about, when you’ve got bills to pay, or when you don’t find world news too encouraging. It’s easy to fall into the trap of thinking that being alive 100 years from now wouldn’t be worth the trouble and just start looking forward to retirement and bowing out instead, but that’s all it is—a mind trap. A good chunk of the 1900s was a rather messy time to be alive, and people who witnessed not one but two World Wars had all the reasons to think that humanity was going south on them and that getting old and checking out was preferable to seeing whatever catastrophe the future might have in store. However, the world has been getting better and better since then as well as since the beginning of recorded history; if you’re not convinced of that, I recommend checking out Our World In Data and Gapminder, two excellent resources that demonstrate how our pessimism comes mostly from a tendency to focus on the negatives and disqualify the positives.

This is my answer to anyone who argues that longer lives would mean more time spent in an increasingly worsening world: The data simply don’t support this claim. At this point, a convinced pessimist would start throwing news items at me: world politics, climate issues, the refugee crisis, etc. I’m not denying the existence of these problems, nor that they may well have the potential to cause serious trouble if left unchecked; but their existence doesn’t mean that the world is getting worse. It only means that it is not getting better all at once; the state of human affairs isn’t improving at a uniform rate, but if you look at the general trend, you’ll see that it’s going up, with crests and troughs. Extrapolating from this general trend, it’s sensible to believe that things are likely to continue improving, but we cannot take for granted that things will get better of their own accord. That would be just as wrong as focusing only on the troughs in the graph and conclude that they signify that things are inevitably going to go downhill.

Now is a good moment to remind ourselves that life extension means, first and foremost, preserving our youthful health irrespective of our chronological age; any longevity benefits deriving from it would only be more than welcome side effects. Given this fact, even assuming that living on Earth will eventually be so intolerable that death would be preferable, it really makes no sense to wait for it to happen because of aging and go through about twenty years of declining health, thus adding insult to injury. To put it bluntly, people who really have had enough of life generally seek to terminate it quickly and painlessly; not too many choose pneumonia or ebola as a way out. Wanting to die of aging because you think the world won’t be worth living in beyond your “natural” lifespan is no different from wanting to die of pneumonia because you think that the world won’t be worth living in six months from now.

Eliminating the diseases of aging can only make life better, and it’s a different matter if it’lll be good enough to be worth living—that’s a personal choice that has nothing to do with whether life extension should be developed or not. To be completely honest, if you lived your entire life in a country torn by war, or fighting over food, then I would understand if you were pessimistic about the benefits of a longer life; however, when I hear people living reasonably comfortable lives in industrialized countries claiming “Living longer? Good God, that would be awful!” just because they don’t like their jobs or some other silly pretext like that, I can’t help thinking that they’re just having a bad case of first world problems.

Besides, what is a defeatist attitude going to accomplish? Assuming that life extension isn’t worth bothering with because the future won’t be worth it makes two more assumptions. The first is that the world is going to be too horrible to live in within the handful of decades of a currently normal lifespan, and the second is that it won’t really improve significantly after that point, so pulling through the bad times in the hopes of seeing better ones would be a waste of effort. If it really were that way, then we might as well throw in the towel, stop worrying about making the world a better place, stop having children, who could only expect to live in a world worse than we did, and just let everything collapse.

If we did this, the defeatist attitude would become a self-fulfilling prophecy, but thankfully, we don’t really do anything like that. We might be tempted to think like that when we feel discouraged, but throughout our history, we’ve always picked ourselves up and continued, not matter how dire the times, and always managed to make the world a little better than it was before. The right attitude is neither “the future will certainly be great” nor “the future will certainly be horrible”; the right attitude is “we don’t know for sure what the future will be like, but we are capable of making it better”. The data’s with us on that one.

About Nicola Bagalà

Nicola Bagalà  is a bit of a jack of all trades—a holder of an M.Sc. degree in mathematics; an amateur programmer; a hobbyist at novel writing, piano, and art; and, of course, a passionate life-extensionist. After his interest in the science of undoing aging arose in 2011, he gradually shifted from quiet supporter to active advocate in 2015, first launching his advocacy blog Rejuvenaction before eventually joining LEAF. These years in the field sparked an interest in molecular biology, which he actively studies. Other subjects he loves to discuss to no end are cosmology, artificial intelligence, and many others—far too many for a currently normal lifespan, which is one of the reasons he’s into life extension.

Choose Your Own Story – by Nicola Bagalà

Choose Your Own Story – by Nicola Bagalà

Nicola Bagalà


Editor’s Note: In this set of short stories originally published by our allies at the Life Extension Advocacy Foundation (LEAF), Nicola Bagalà illustrates  through convincing scenarios of possible futures why we should take seriously research and activism into rejuvenation biotechnology. It may make the difference between our own survival and flourishing into the indefinite future, or the painful suffering and demise that currently accompany old age.

~ Gennady Stolyarov II, Chairman, United States Transhumanist Party, July 30, 2018


Today, I would like to tell you two short stories describing what your far future might look like, depending on the choices that you—though not only you—will make in the near future. Feel free to leave a comment to let others know which one you’d rather have as your real future.

Story 1: A day in 2140

The blinds in your bedroom slowly whirr open, as a gentle melody gradually fills the environment. Ferdinand—your AI assistant, to whom you decided to give a far less extravagant name than most other people do—informs you that it’s 7:30, your bath is ready, and so will be your usual breakfast once you’re done in the bathroom. Getting up that early is never too easy, but your morning walk in the park is always worth it, because it puts you in a good mood.

As you enter the bathroom, you step into the health scanner, and, after a few seconds, a couple of charts and several biomarkers show up on the display—the final report says that you’re a perfectly healthy 137-year-old whose biological age is about 26. It’d be enough by itself, but you think the charts and the data look cool; Ferdinand knows that.

You’ve got one of those awesome bathrooms with HyperReal WallScreens—well, nearly everyone does anyway—so today you’re taking your bath in the rainforest. As you enjoy your hydromassage, you’re listening to the latest news; your heart almost skips a beat when you hear that the Stephen Hawking Deep Space Telescope, the one that NASA and the African Space Agency sent pretty much to the edge of the solar system, has finally confirmed earlier observations: JSS “Jessie” 431 c, an exoplanet 95 light-years away, harbors multicellular life. They’d been chasing “Jessie” for a while, and now the chase is over; it’s an unprecedented discovery, and while it took surprisingly long to finally get this data, this is a world-changing breakthrough, and it leaves you yelling and splashing around in joy embarrassingly loudly. As you quickly get out of the tub, you imagine that all the geeks at work won’t be talking about anything else.

Your breakfast, freshly out of your molecular assembler, is as delicious and tailored to your specific nutritional needs as Ferdinand got you used to, but you’re too hyped today to spend too much time eating. Ferdinand casts a virtual, disapproving glance at you as you quickly gobble your food up and leave the flat. Your usual walk is cancelled as well, you think as you get into the elevator, because you’re too eager to discuss the news at work. As Ferdinand leaves room for Alice—the building’s AI janitor—you look through the glass walls of the cabin, gaining inspiration from the several other elegant skyscrapers towering over your beautiful city. After a quick descent from the 87th floor, you’re finally on the ground and ready for the commute to work—a quick trip of about 400 kilometers, which, when you were in your 20s for real, would’ve been anything but quick.

At the time, the world was so very different, you think to yourself. Take work, for example: your life depended on it, in pretty much the literal sense of the word. Nowadays, although the word “work” stuck, it is just something you really enjoy doing and you’re good at, and people look back at the whole “having to earn a living” idea in pretty much the same way as they looked at hunter-gatherer tribes when you were a child. It’s unnerving to think that you could’ve missed all of this by a hair’s breadth; when you were in your early 20s, the social movement for the development of rejuvenation biotechnologies really started to pick up, and therapies eventually followed suit. If it hadn’t—and that might well have been—right now you’d be six feet under, just like your poor grandma. She’d have loved the world today, your father always says.

Anyway, there’s no time to get melancholic now; another great day awaits you.

Story 2: A day in 2078

If this story had the same year as the previous one, it’d be very short: you’re dead, and you’ve long been such. The end. However, that’s not how it’s titled, so it is going to be a little longer than that. Whether that’s better or not, I’ll leave up to you to decide.

You wake up in your hospital bed to the beeping coming from multiple monitors and sensors, which by now have become your most consistent companions. It’s not even morning: you fell asleep in the middle of the afternoon, and now that you think about it, some of your family was there with you. Probably, as you fell asleep, they decided it was best to let you rest.

Not that you’re that much awake, anyway. You feel barely conscious, and most of what you can feel is either pain or tiredness. Up until a month or two ago, you could still sort of manage with some difficulty, although with the help of your caregiver or your children, but then everything changed. You’ve been waking up in the same hospital bed ever since you passed out that day, and one of the first things you heard when you woke up right after they brought you in was that, at 92 years old, you’re lucky to be still alive.

You’d like to know what time it is, but you can’t quite make out the clock on the wall nor any of the screens around you. You could ask the computer in the room, if you had any breath left, but you don’t. If nothing else, it probably has alerted the doctors that you’re awake, and maybe someone will turn up soon. Spending energy to push the damn button doesn’t seem worth it, what’s the point, anyway, you wonder—today might well be your last day, and given the outlook, it’d be as good a day to go as any.

That’s too bad, though, you think, saddened. You’d really have wanted to see your great-grandkids grow up, and all in all, the world has surprised you, turning out much better than you expected. Not perfect, granted, but you’re genuinely curious to know how things will change in the coming decades, with all these advancements in technology and science—and the overall political situation looks okay, too. Well, looks like you’ll be taking your curiosity to the grave with you, because these advancements didn’t happen quite everywhere in science, nor did the bureaucrats do much to make them happen. Tough luck.

Bitterly, you think this was at least a little bit your fault too. You didn’t do much to make them happen either. When you were in your early thirties, there was a lot of talk about rejuvenation biotechnology, and the talk intensified somewhat by your late thirties, but the whole thing never really saw the light of day. Oh, you tell yourself, it’ll happen eventually, but not any time soon. It certainly didn’t happen in time to spare yourself what you’re going through right now—thankfully, it’s almost over.

Back in the day, you were in the “unsure” camp, tending to “best not to mess with nature.” In hindsight, you’re not so sure you actually agreed with that view; possibly, you only said so because so many other people said the same and you didn’t feel like being one of those fruitcakes who wanted to change everything, or something like that—what the heck, that was 60 years ago and the memories are foggy. You do remember, though, that when you saw your own parents go through an ordeal very similar to yours, some thirty years ago, the thought that you might have misjudged the “fruitcakes” crossed your mind, but it was already too late.

Unfortunately, by then, populist discourse appealing to the cycle of life, a bunch of other, supposedly more important issues, and “the future of our children” had won over the crowd, and rejuvenation research had taken a back seat, making way for better services for the elderly instead; they’re not bad, but maybe, if a choice was available between better machines to take you to the toilet and drugs that kept you able to walk there on your own, the latter might have been preferable.

The future for your great-grandchildren is similarly rosy, as they get to watch their own parents and grandparents turn into almost-vegetables and then die, not to mention the financial burden—not just on individual families, but the world as well. With so many old and dependent people, and fewer and fewer young people, the economy doesn’t look so okay. The way they’re going about this is by offering financial incentives for families with kids, which, coming from the very same people who opposed rejuvenation for fear of overpopulation among other things, is quite ironic.

Maybe, you tell yourself, you should’ve listened. Maybe you should have taken the whole issue more seriously and helped the early advocates somehow, rather than having dismissed the idea of rejuvenation. Maybe, if you had helped, and if others had too, it’ll have happened in time to save you, or at least your children—they’re in their sixties and seventies now, and if rejuvenation didn’t happen in the past sixty years, despite the initial wave of enthusiasm, you can bet that it isn’t going to happen in the next twenty years when nearly nobody cares.

You turn your head slightly towards the door. Nothing. No one’s coming, but then again, you’ve only been awake for ten minutes tops, and the doctors have got plenty of other geriatric patients in this wing. Your eyelids are becoming heavy again, and as you won’t accomplish much by staying awake anyway, you decide to let them go down. Who knows if they’ll open again.

Both of these stories are fictional, though the first one contains more fiction than the second, because it describes a future that might or might not come to be. The first story is perhaps overly optimistic and even a tad too Star Trek-ish for your taste, but it’s just my happy story—you are free to replace it with whatever positive future you’d like to see. It’s just a possible scenario, and for all we know, the future might be nothing like that and more like a dystopia. It’s hard to tell for a fact.

However, the second story contains much more reality than the first, because it’s pretty much what it means to be in your 90s these days; depending on a number of factors, even being in your 70s and 80s can be not much better, even if you’re not bedridden. Unless we do something about it today, a story similar to this will be our story—your story—too, just like stories of infectious diseases killing millions would’ve still been very much current even today if we hadn’t done anything to change those stories before they could unfold.

I’ve already chosen my favorite version of the story a long time ago. The question is, which one is yours?

About Nicola Bagalà

Nicola Bagalà has been an enthusiastic supporter and advocate of rejuvenation science since 2011. Although his preferred approach to treating age related diseases is Aubrey de Grey’s suggested SENS platform, he is very interested in any other potential approach as well. In 2015, he launched the blog Rejuvenaction to advocate for rejuvenation and to answer common concerns that generally come with the prospect of vastly extended healthy lifespans. Originally a mathematician graduated from Helsinki University, his scientific interests range from cosmology to AI, from drawing and writing to music, and he always complains he doesn’t have enough time to dedicate to all of them which is one of the reasons he’s into life extension. He’s also a computer programmer and web developer. All the years spent learning about the science of rejuvenation have sparked his interest in biology, in which he’s planning to get a university degree.

Could Filtering Our Aged Blood Keep us Young? – Article by Steve Hill and Nicola Bagalà

Could Filtering Our Aged Blood Keep us Young? – Article by Steve Hill and Nicola Bagalà

Steve Hill

Nicola Bagalà


Editor’s Note: In this article, Mr. Nicola Bagalà and Steve Hill present the interview they conducted with Dr. Irina Conboy of Berkeley University and Dr. Michael Conboy of Havard University on the topic of youthful blood.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, February 17, 2018

Due to a recently published study on the effects of young plasma on aged mice, we got in touch with Dr. Irina Conboy of Berkeley University. Dr. Conboy is an Associate Professor at the Department of Bioengineering and an expert in stem cell niche engineering, tissue repair, stem cell aging and rejuvenation. Before we dive into the main topic, let’s familiarize ourselves a little with Dr. Conboy and her work.

Dr. Conboy got her Ph.D. at Stanford University, focusing on autoimmunity. She met her partner in science—and in life—Dr. Michael Conboy at Harvard and they got married before embarking on graduate studies; they celebrated their Silver Anniversary a few years ago. During her postdoctoral studies, she began focusing on muscle stem cells, trying to figure out what directs them to make new healthy tissue and what causes them to lose their ability to regenerate the tissues they reside in as we age [1].

Together with her husband Michael, she eventually discovered that old stem cells could be reactivated and made to behave like young ones if appropriately stimulated. The Conboys’ parabiosis experiments—which consisted in hooking up the circulatory systems of aged and young mice—showed that old age is not set in stone and can be reversed in a matter of weeks [2].

The follow-up work by the Conboys uncovered that age-accumulated proteins, such as TGF-β1, inhibited stem cells’ ability to repair tissues even in young mice, and when TGF-β1 signaling is normalized to its young levels, old mice (equivalent to 80-year old people) have youthful muscle regeneration and better neurogenesis in the hippocampus (the area of the brain that is responsible for memory and learning) [3].

While young blood did appear to be beneficial to old stem cells, their evidence suggested that the real culprit of the broad loss of tissue repair with age was the negative influence of age-accumulated inhibitory proteins in aged tissues and circulation, also called the stem cell niche [4].

This conclusion is certainly compatible with the view of aging as a damage accumulation process [5]. As Irina herself pointed out in this interview, in the parabiosis experiments, the old mice had access to the more efficient young organs: lungs, liver, kidneys and immune system of the younger mice, which likely accounted for many of the benefits observed in the elderly parabiosed mice. With respect to the rejuvenation of the brain, the old mice experienced environmental enrichment by being sutured to young, more active parabionts, and this is known to improve the formation of new brain cells, learning, and memory.

An aged niche blocks the action of old and young stem cells alike very quickly; therefore, as Dr. Conboy observed in an article in the Journal of Cell Biology, we can’t treat the diseases of aging by simply transplanting more stem cells, because they will just stop working. Their niche needs to be appropriately engineered as well. Fortunately, there are potential solutions to this problem; such as the use of artificial gel niches and defined pharmacology that are designed to protect transplanted or endogenous stem cells from the deleterious environment of the old body.

This research holds the potential to significantly postpone the onset of age-related diseases and possibly reverse them one day, including frailty, muscle wasting, cognitive decline, liver adiposity and metabolic failure, but Dr. Conboy remains cautious about the possibilities until more data is in. However, she does think that longer and healthier productive lives could improve people’s attitudes towards the environment and treating each other with compassion and respect—a view that we definitely share.

We managed to catch up with Irina and Michael Conboy and talk to them about their work.

For the sake of those new to the topic, what is it in young blood and aged blood that affects aging?

Irina: Numerous changes in the levels of proteins that together regulate cell and tissue metabolism throughout the body.

Mike: We wondered why almost every tissue and organ in the body age together and at a similar rate, and from the parabiosis and blood exchange work now think that young blood has several positive factors, and old blood accumulates several negative, “pro-aging” factors.

A lot of media attention and funding is currently being directed to youthful blood transfusions; how can we move beyond this to potentially more promising approaches, such as filtering and calibration of aged blood?

Irina: People need to understand not just the titles, abstracts and popular highlights of research papers, but the results and whether they support (or not) the promise of rejuvenation by young blood. In contrast to vampire stories, we have no strong experimental evidence that this is true, and there is a lot of evidence that infusing your body with someone else’s blood has severe side effects (even if it is cell-free).

Mike: Translational research!

Some evidence suggests dilution is the most likely reason that young blood has some beneficial effects; what are your thoughts on this recent study [6] in rats that shows improved hepatic function partially via the restoration of autophagy?

Irina: There are certainly “young” blood factors that are beneficial, not just a dilution of the old blood, and this benefit differs from organ to organ. We have published on improved liver regeneration, reduced fibrosis and adiposity by transfusion of old mice with young blood, but these are genetically matched animals, and in people, we do not have our own identical but much younger twins [7].

If dilution is also playing a role here, then can we expect similar or better results from calibrating aged blood?

Irina: Yes, and our work in progress supports the idea.

In your 2015 paper, you identified that TGF-β1 can be either pro-youthful or pro-aging in nature, depending on its level [8]. In the study, you periodically used an Alk-5 inhibitor to reduce TGF-β1 levels and promote regeneration in various tissues. In the study, you showed that TGF-β1 was important in myogenesis and neurogenesis; is there reason to believe that this mechanism might be ubiquitous in all tissues?

Irina: Yes, because TGF-β1 receptors are present in most cells and tissues.

Also, TGF-β1 is only one of a number of factors that need to be carefully balanced in order to create a pro-youthful signalling environment. How many factors do you believe we will need to calibrate?

Irina: There will be a certain benefit from calibrating just TGF-beta 1, but also additional benefits from more than one or just TGF-beta.

How do you propose to balance this cocktail of factors in aged blood to promote a youthful tissue environment?

Irina: We are working on the NextGen blood apheresis devices to accomplish this.

So, you are adapting the plasmapheresis process to effectively “scrub” aged blood clean and then return it to the patient. This would remove the need to transfuse blood from young people, as your own blood could be filtered and returned to you, and no immune reaction either, right?

Irina: Accurate.

This plasmapheresis technique is already approved by the FDA, we believe, so this should help you to develop your project faster, right?

Irina: Exactly.

Do you think a small molecule approach is a viable and, more importantly, a logistically practical approach to calibrate all these factors compared to filtering aged blood?

Irina: Yes, it is a very feasible alternative to the NextGen apheresis that we are working and publishing on.

It is thought that altered signaling is caused by other aging hallmarks higher up in the chain of events; even if we can “scrub” aged blood clean, is it likely to have a long-lasting effect, or would the factors reach pro-aging levels fairly quickly again if nothing is done about the other hallmarks antagonizing them?

Irina: That needs to be established experimentally, but due to the many feedback loops at the levels of proteins, genes and epigenetics, the acquired youthful state might persist.

Ultimately, could a wearable or an implanted device that constantly filters the blood be the solution to these quickly accumulating factors?

Irina: Maybe, but the first step of a day at a NextGen apheresis clinic once every few months might be more realistic.

Filtering seems to be a far more practical solution, so how are you progressing on the road to clinical trials?

Irina: We are collaborating with Dr. Dobri Kiprov, who is a practicing blood apheresis physician with 35 years of experience, and he is interested in repositioning this treatment for alleviating age-related illnesses.

Senolytics and removing senescent cells and the resulting inflammation they cause during the aging process has become a hot topic in the last year or so. What are your thoughts on senolytics as a potential co-therapy with a blood filtering approach?

Irina: Might be good, but we should be careful, as p16 is a normal, good gene that is needed for many productive activities by many cells.

What do you think it will take for the government to fully support the push to develop rejuvenation biotechnology?

Irina: Clear understanding of the current progress and separating the real science from snake oil is very important for guiding funding toward realistic clinical translation and away from the myth and hype.

The field is making amazing progress, but, sadly, it is plagued by snake oil. As much as an “anti-aging free market” encourages innovation, it also encourages hucksters. How can a member of the public tell the difference between credible science and snake oil?

Irina: I was thinking for some time about starting a popularized journal club webpage where ordinary people can see what we typically critically point out in the lab setting about published papers and clinical trials.

How can our readers learn more about your work and support your research?

Irina: The new Conboy lab website is coming up; meanwhile, contact me and Dr. Mike at iconboy@berkeley.edu and conboymj@berkeley.edu

Conclusion

We would like to thank Irina and Michael for taking the time to answer our questions and for providing the readers with a fascinating insight into their work.

Literature

[1] Conboy, I. M., Conboy, M. J., Smythe, G. M., & Rando, T. A. (2003). Notch-mediated restoration of regenerative potential to aged muscle. Science, 302(5650), 1575-1577.

[2] Conboy, I. M., Conboy, M. J., Wagers, A. J., Girma, E. R., Weissman, I. L., & Rando, T. A. (2005). Rejuvenation of aged progenitor cells by exposure to a young systemic environment. Nature, 433(7027), 760-764.

[3] Yousef, H., Conboy, M. J., Morgenthaler, A., Schlesinger, C., Bugaj, L., Paliwal, P., … & Schaffer, D. (2015). Systemic attenuation of the TGF-β pathway by a single drug simultaneously rejuvenates hippocampal neurogenesis and myogenesis in the same old mammal. Oncotarget, 6(14), 11959.

[4] Rebo, J., Mehdipour, M., Gathwala, R., Causey, K., Liu, Y., Conboy, M. J., & Conboy, I. M. (2016). A single heterochronic blood exchange reveals rapid inhibition of multiple tissues by old blood. Nature communications, 7.

[5] López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. Cell, 153(6), 1194-1217.

[6] Liu, A., Guo, E., Yang, J., Yang, Y., Liu, S., Jiang, X., … & Gewirtz, D. A. (2017). Young plasma reverses age‐dependent alterations in hepatic function through the restoration of autophagy. Aging cell.

[7] Rebo, J., Mehdipour, M., Gathwala, R., Causey, K., Liu, Y., Conboy, M. J., & Conboy, I. M. (2016). A single heterochronic blood exchange reveals rapid inhibition of multiple tissues by old blood. Nature communications, 7.

[8] Yousef, H., Conboy, M. J., Morgenthaler, A., Schlesinger, C., Bugaj, L., Paliwal, P., … & Schaffer, D. (2015). Systemic attenuation of the TGF-β pathway by a single drug simultaneously rejuvenates hippocampal neurogenesis and myogenesis in the same old mammal. Oncotarget, 6(14), 11959.

 

About Steve Hill

As a scientific writer and a devoted advocate of healthy longevity technologies Steve has provided the community with multiple educational articles, interviews and podcasts, helping the general public to better understand aging and the means to modify its dynamics. His materials can be found at H+ Magazine, Longevity reporter, Psychology Today and Singularity Weblog. He is a co-author of the book “Aging Prevention for All” – a guide for the general public exploring evidence-based means to extend healthy life (in press).

About Nicola Bagalà

Nicola Bagalà has been an enthusiastic supporter and advocate of rejuvenation science since 2011. Although his preferred approach to treating age related diseases is Aubrey de Grey’s suggested SENS platform, he is very interested in any other potential approach as well. In 2015, he launched the blog Rejuvenaction to advocate for rejuvenation and to answer common concerns that generally come with the prospect of vastly extended healthy lifespans. Originally a mathematician graduated from Helsinki University, his scientific interests range from cosmology to AI, from drawing and writing to music, and he always complains he doesn’t have enough time to dedicate to all of them which is one of the reasons he’s into life extension. He’s also a computer programmer and web developer. All the years spent learning about the science of rejuvenation have sparked his interest in biology, in which he’s planning to get a university degree.

About LIFE EXTENSION ADVOCACY FOUNDATION (LEAF)

In 2014, the Life Extension Advocacy Foundation was established as a 501(c)(3) non-profit organization dedicated to promoting increased healthy human lifespan through fiscally sponsoring longevity research projects and raising awareness regarding the societal benefits of life extension. In 2015 they launched Lifespan.io, the first nonprofit crowdfunding platform focused on the biomedical research of aging.

They believe that this will enable the general public to influence the pace of research directly. To date they have successfully supported four research projects aimed at investigating different processes of aging and developing therapies to treat age-related diseases.

The LEAF team organizes educational events, takes part in different public and scientific conferences, and actively engages with the public on social media in order to help disseminate this crucial information. They initiate public dialogue aimed at regulatory improvement in the fields related to rejuvenation biotechnology.

The Abolition of Aging – A Book Review – Article by Nicola Bagalà

The Abolition of Aging – A Book Review – Article by Nicola Bagalà

Nicola Bagalà


Editor’s Note: In this article, Mr. Nicola Bagalà provides a book review of the book The Abolition of Aging by David Wood, a book which explains in great detail the benefits that would derive from a successful implementation of the “rejuveneering project”.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, February 13, 2018

As you might recall, in my review of Ending Aging, I said that the book could have benefited from a more in-depth discussion of the benefits of rejuvenation as well as the concerns and objections often raised against it. Anyone else sharing the same feeling will find what they’re looking for in The Abolition of Aging, by Chair of London Futurists David Wood.

Written in an elegant, clear style, The Abolition of Aging brilliantly accomplishes the difficult task of guiding the reader through all the turns and twists of the topic, explaining in great detail the benefits that would derive from a successful implementation of the “rejuveneering project”—as Wood calls it—presenting all the typical objections and related counterarguments, and—in the words of 3G Doctor Director David Doherty—providing innumerable “stunning references and observations”.

Just like there’s no time to waste if we want to defeat aging in time for currently living people to benefit, Wood wastes no time with lengthy preambles; the very first line of the foreword comes directly to the point, bluntly stating what readers unfamiliar with the topic may find shocking: the possibility of eliminating biological aging is now within striking distance.

Possibly preventing the reader’s reaction, the author immediately gives a preliminary discussion of the traditional responses to his claim: “it’s not possible” and “it’s not desirable”, which Wood ascribes—correctly, in my opinion—in no small part to a great desire to avoid an unpleasant discussion that would force us to reconsider many assumptions on the inevitable finitude of human existence, with which most of us have already made our peace.

To succeed in his task of getting us to snap out of a multi-millenary Stockholm syndrome that pushes humanity to praise the tyranny of old age, Wood resorts to every weapon in his arsenal, making a very convincing case that rejuvenation is very much desirable as well as possible.

Skeptics who assume that the technology necessary to rejuvenate people is centuries away will be surprised to learn about how advanced the field actually is and how much faster it is likely to grow than conventional wisdom would have it. The word of senior scientists who claim that the reversal of aging is nothing but a pipe dream, as Wood warns us, should be taken with a grain of salt: The Abolition of Aging provides plenty of examples of luminaries and eminent experts of the past summarily dismissing scientific theories and technologies that today are well-established and taken for granted by everyone. (Among many such examples, one I really cannot abstain from mentioning is the hilariously wrong 1903 prediction by the New York Times that human flight, if at all possible, would take one to ten million years to come true. Less than 70 years later, not only was human flight commonplace, but human beings had landed on the Moon.)

Nonetheless, Wood’s optimism should not be mistaken for complacency. He makes no mystery that the success of the rejuveneering project is a mere possibility, however likely, and not at all a certainty. Many are the unknowns—scientific, political, societal, financial, and more—that could well thwart our efforts in this direction if we’re not careful. Wood offers advice on how to deal with these issues standing in the way of an aging-free world as well as those that might lurk beyond. After all, the functioning of society as we know it hinges on the existence of aging; our lives, our policies, and our customs are built around it. Eliminating aging would require a serious rethinking of much of society’s inner workings, and this operation is not free of risks, as Wood rightfully concedes. Great changes for the better often come with potential downsides, but we should not let this deter us; rather, we should appreciate how the fruits to be reaped are well worth the potential risks involved and act now to prevent or mitigate any unwanted consequences. A world without aging would need to be managed in a different way, but that is not a problem.

A particular obstacle on the way to a world without aging is represented by adverse psychology, to which Wood dedicates an entire chapter. Ever since we had the ability to reflect upon ourselves and the human condition, as the author explains, we’ve had to face our own mortality and fear of death. Fear of death is a very useful adaptation to increase the chance that an individual will live long enough to reproduce, but in the case of a highly self-aware species like us, it’s a double-edged sword. Our deep desire to express ourselves, to learn, create, grow, to live, inevitably clashes against the knowledge of our apparently inescapable demise.

If left unresolved, this inner conflict could strike terror so paralyzing that living our lives would be impossible. With no hope of defeating an apparently all-powerful enemy such as death, the young human race had to devise other ways out of this conundrum—psychological expedients to sugar the pill or even make it appear better than the alternative; for some, having children, creating art, changing the world through their work and so on may all offer the comforting thought of their legacy, and thus part of themselves, carrying on at least to some extent; believers have faith that their immortal souls will continue existing even after their bodies will have perished; others assume a world without death would, for one reason or another, be so unbearable that oblivion would be preferable.

These mental devices have existed for so long that they’ve shaped our society and our morals; accepting death has become a sign of wisdom while trying to avoid or delay it when “the right time” has come is seen as a sign of immaturity and selfishness. These views are so entrenched in most people that any attempt to question their validity is likely to trigger aggressive defensive reactions or, sometimes, contempt and ridicule. For these reasons, life extension is not an easy idea to sell. In his detailed discussion, though, Wood provides valuable advice to ease the advocates’ task, listing the dos and don’ts of how to present the subject.

Rejuvenation is not all the book deals with. Wood’s futurist soul fully reveals itself in his vision of the futures of humanity, faith, and death, which are discussed in the chapter “Towards Humanity+” as well as in the possibilities outlined in chapter 12, “Radical alternatives”, such as cryonics, head transplants, and mind uploading. While these ideas are often plagued by abundant hype and unjustified premature enthusiasm, I find that Wood simply presented relevant facts as they are, with an appropriate dose of healthy skepticism where needed but without any undue disbelief. Cryonics in particular, which is usually unjustly regarded as a scam to part rich fools from their money, is presented as a valid backup plan for those who don’t expect to live long enough to see the dawn of rejuvenation; just like cryonics companies themselves, Wood makes no mystery that it is uncertain if bringing back to life cryopreserved patients will ever be possible, despite encouraging successes with transplantation of cryopreserved animal organs. Then again, I would add that if the chances of coming back to life from cryopreservation are uncertain, there’s no chance whatsoever of coming back after being buried or cremated.

Summing up, I believe that The Abolition of Aging is a must-read for experienced advocates and newcomers alike. People who haven’t made up their minds about supporting rejuvenation will be fully equipped to make an informed decision after reading this book, or, at the very least, will be able to research the topic further; advocates will have plenty of references and useful information for their advocacy efforts. Together with Ending Aging, this book answers pretty much all the whats, whens, hows, and whys to the best of our current understanding.

About Nicola Bagalà

Nicola Bagalà has been an enthusiastic supporter and advocate of rejuvenation science since 2011. Although his preferred approach to treating age related diseases is Aubrey de Grey’s suggested SENS platform, he is very interested in any other potential approach as well. In 2015, he launched the blog Rejuvenaction to advocate for rejuvenation and to answer common concerns that generally come with the prospect of vastly extended healthy lifespans. Originally a mathematician graduated from Helsinki University, his scientific interests range from cosmology to AI, from drawing and writing to music, and he always complains he doesn’t have enough time to dedicate to all of them which is one of the reasons he’s into life extension. He’s also a computer programmer and web developer. All the years spent learning about the science of rejuvenation have sparked his interest in biology, in which he’s planning to get a university degree.

About LIFE EXTENSION ADVOCACY FOUNDATION (LEAF)

In 2014, the Life Extension Advocacy Foundation was established as a 501(c)(3) non-profit organization dedicated to promoting increased healthy human lifespan through fiscally sponsoring longevity research projects and raising awareness regarding the societal benefits of life extension. In 2015 they launched Lifespan.io, the first nonprofit crowdfunding platform focused on the biomedical research of aging.

They believe that this will enable the general public to influence the pace of research directly. To date they have successfully supported four research projects aimed at investigating different processes of aging and developing therapies to treat age-related diseases.

The LEAF team organizes educational events, takes part in different public and scientific conferences, and actively engages with the public on social media in order to help disseminate this crucial information. They initiate public dialogue aimed at regulatory improvement in the fields related to rejuvenation biotechnology.

Zeb2-NAT Molecule May Reverse Cellular Aging – Article by Nicola Bagalà

Zeb2-NAT Molecule May Reverse Cellular Aging – Article by Nicola Bagalà

Nicola Bagalà


Editor’s Note: In this article, Mr. Nicola Bagalà explains a study that shows aged cells that usually resist reprogramming can be regenerated by reducing the level of Zeb2-NAT without harming the cells’ developmental potency.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, January 28, 2018

Researchers have found that by manipulating a single RNA molecule, they can reverse some aspects of cellular aging and regenerate aged cells.

Old cells resist regeneration

As we grow older, our cells gradually age, leading to the development of various diseases. Therefore, inducing cellular regeneration is one of the approaches that researchers are using to combat the age-related diseases associated with cellular aging. Unfortunately, aged cells are often highly resistant to therapies aimed at inducing regeneration.

Ribonucleic acid (RNA) is responsible for the creation of cellular proteins. However, a special type of molecule called non-coding RNA is never made into protein. In fact, when they mapped the human genome in 2001, they discovered that only around 2% of RNA is actually made into proteins.

Now, researchers have found a way to bypass the resistance of aged cells to being regenerated and becoming functionally more youthful.

What the study found out

In a recent Nature Communications paper, a team led by Dr. Bruno Bernardes de Jesus of the Instituto de Medicina Molecular (iMM) João Lobo Antunes in Lisboa discusses a technique that allowed the team to achieve easier cellular reprogramming of old fibroblasts into pluripotent cells [1].

Fibroblasts are connective tissue cells in animals that synthesize both the extracellular matrix, which is a “scaffolding” made up of extracellular molecules that provides structural and biochemical support to cells, and collagen, which is the main structural protein of connective tissues in animal bodies.

The study showed that the fibroblasts of old mice express higher levels of the transcription factor Zeb2. A transcription factor is a protein that regulates the DNA-to-messenger-RNA transcription rate, and Zeb2, in particular, induces epithelial cells to transition to mesenchymal cells. Epithelial cells are one of the four basic tissue types of animal cells, whereas mesenchymal cells are multipotent stem cells that give rise to fibroblasts, among others.

The synthesis of Zeb2 is controlled by the ribonucleic acid Zeb2-NAT (NAT stands for “natural antisense transcript”). What the scientists demonstrated in this paper is that by knocking down Zeb2-NAT in old mouse fibroblasts, Zeb2 can be downregulated significantly, which, in turn, leads to an enhanced fibroblast ability to turn into pluripotent cells rather than mesenchymal cells. The difference is that while mesenchymal cells can turn into only a certain range of related cells, pluripotent stem cells can turn into nearly all types of cells.

The way the researchers silenced Zeb2-NAT was by transfecting the fibroblasts with certain ribonucleic acid sequences—in other words, they introduced these sequences into the fibroblasts’ nuclei to modify their behavior.

Essentially, what they demonstrated is that aged cells that usually resist reprogramming can be regenerated by reducing the level of Zeb2-NAT without harming the cells’ developmental potency.

Conclusion

This study results spotlight the role of non-coding RNA in the fine-tuning and expression of protein-coding genes involved in pluripotency, differentiation, and reprogramming.

This opens the door for the regeneration of aged cells and tissues in an effort to prevent or reverse age-related diseases caused by cellular aging.

Literature

[1] Bernardes de Jesus, B., Pires Marinho, S., Barros, S., Sousa-Franco A., Alves-Vale, C., Carvalho, T., Carmo-Fonseca, M. (2018). Silencing of the lncRNA Zeb2-NAT facilitates reprogramming of aged fibroblasts and safeguards stem cell pluripotency. Nature Communications.

About Nicola Bagalà

Nicola Bagalà has been an enthusiastic supporter and advocate of rejuvenation science since 2011. Although his preferred approach to treating age related diseases is Aubrey de Grey’s suggested SENS platform, he is very interested in any other potential approach as well. In 2015, he launched the blog Rejuvenaction to advocate for rejuvenation and to answer common concerns that generally come with the prospect of vastly extended healthy lifespans. Originally a mathematician graduated from Helsinki University, his scientific interests range from cosmology to AI, from drawing and writing to music, and he always complains he doesn’t have enough time to dedicate to all of them which is one of the reasons he’s into life extension. He’s also a computer programmer and web developer. All the years spent learning about the science of rejuvenation have sparked his interest in biology, in which he’s planning to get a university degree.

About LIFE EXTENSION ADVOCACY FOUNDATION (LEAF)

In 2014, the Life Extension Advocacy Foundation was established as a 501(c)(3) non-profit organization dedicated to promoting increased healthy human lifespan through fiscally sponsoring longevity research projects and raising awareness regarding the societal benefits of life extension. In 2015 they launched Lifespan.io, the first nonprofit crowdfunding platform focused on the biomedical research of aging.

They believe that this will enable the general public to influence the pace of research directly. To date they have successfully supported four research projects aimed at investigating different processes of aging and developing therapies to treat age-related diseases.

The LEAF team organizes educational events, takes part in different public and scientific conferences, and actively engages with the public on social media in order to help disseminate this crucial information. They initiate public dialogue aimed at regulatory improvement in the fields related to rejuvenation biotechnology.

Looking Back at 2017: A Year in Rejuvenation Biotechnology – Article by Nicola Bagalà

Looking Back at 2017: A Year in Rejuvenation Biotechnology – Article by Nicola Bagalà

Nicola Bagalà


 

Editor’s Note: In this article, Mr. Nicola Bagalà highlights various events of rejuvenation biotechnology in the year 2017.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, January 11, 2018

Winter kick-off

This year has been pretty intense, with a lot going on both at LEAF and in the rest of the community. January saw the launch of the LEAF website, shortly followed by both the Lifeboat Foundation and Trust me – I’m a biologist partnering with us. Given that it’s been only a year, we’re amazed at how enthusiastic and supportive the community has been—and how fast it has grown, with nearly 30,000 Facebook followers late in December! We’re also very grateful to our friends at Fight Aging! for their encouragement, support, and appreciation for our work, including honoring us by featuring it on their website!

In February, the CellAge campaign launched in late 2016 concluded successfully, also thanks to the matching fund put together by Longecity. That’s also when LEAF President Keith Comito met Mikhail Batin to discuss the Russian initiative Open Longevity and when Series A funding was announced for LYSOCLEAR, a LysoSENS-based approach to treating macular degeneration.

An eventful spring

The Lifespan Heroes campaign was launched in the spring, and thus far, it has greatly helped us carry out our activities, especially in terms of web development—so thank you to all our generous donors!

In the spring, we also started our advocacy projects with global policymakers. During April 10-15, LEAF Board Director Elena Milova attended a training program conducted by the International Institute on Ageing (INIA) in Saint Petersburg, where she met and interviewed INIA director Dr. Marvin Formosa and former Head of the UN Programs on Ageing Dr. Alexandre Sidorenko.

Later in April, the SENS Research Foundation announced a collaboration on a cellular senescence project with the Buck Institute for Research on Aging.

The month of May was busy with conferences and networking; at the International Longevity and Cryopreservation Summit in Madrid, Elena Milova had the opportunity to interview life extension advocate Didier Coeurnelle, London Futurists Chair David Wood, Dr. Jose Luis Cordeiro, Senior Scientist at CONICET Dr. Rodolfo Goya (we hope to support his studies related to Yamanaka factors in 2018 via crowdfunding at Lifespan.io), and SRF’s Chief Science Officer Dr. Aubrey de Grey. Elena herself gave a talk about effective life extension advocacy methodologies; LEAF board member Paul Spiegel also gave a talk about the need for society to adapt to longer lives. In Paris, the International Cell Senescence Association (ICSA) held a conference discussing senescence triggers, physiological functions of senescence, and pathologies and therapies. We announced the event here.

Our Journal Club series was also launched at the end of May, for a total of eight Journal Club episodes this year, which you can watch here. The Journal Club is a monthly science show on which Dr. Oliver Medvedik hosts guests, and this show is supported by our patrons, the Lifespan Heroes. We broadcast this show live to our Facebook Page every month, where we invite the audience to ask questions and join in with the discussion.

Summer news

In the summer, LEAF and MMTP co-hosted a panel featuring Dr. Alexandra Stolzing, Dr. Aubrey de Grey, and Dr. Oliver Medvedik. This live broadcast included discussions about funding, research progress, and advocacy, providing some interesting insights into the field. They were joined by Alen Akhabaev, one of the project donors who supported the MMTP project on Lifespan.io, as well as Steve Hill and Elena Milova from the MMTP and LEAF.

The AgeMeter campaign was launched on Lifespan.io by Elliott Small in July, and in August, we celebrated the first birthday of our crowdfunding platform—you could say Lifespan.io’s birthday present was the MouseAge campaign launched shortly thereafter. The campaign was successful, and the MouseAge app is now ready and expected to be launched shortly. The use of AI is trending more and more in the field of aging research, so this app is certainly only one of many that will be employed in the future.

A great autumn

The autumn has been, without doubt, the busiest time of the year. The Undoing Aging conference was announced by the Forever Healthy Foundation in September, as was a series of small-scale human senolytic pilot studies by Betterhumans. Almost at the same time as the AgeMeter campaign reached 100% of its goal, Dr. Aubrey de Grey joined our SAB (Scientific Advisory Board), shortly followed by Dr. Robert Shmookler Reis. At this time, SRF and the Spiegel Lab launched a collaboration on developing monoclonal antibodies against glucosepane.

September also saw the Basel Life 2017 conference held in Basel, Switzerland, where Dr. Alex Zhavoronkov chaired the Artificial intelligence and block chain in healthcare and the Aging & drug discovery forums. Insilico Medicine’s Young.AI aging-rate tracking app was officially announced at this conference.

Juvenescence by Jim Mellon and Al Chalabi—a thorough, investor-focused introduction to the science of aging and the world of rejuvenation biotech—was published on September 25. LEAF has published two reviews of the book, which you can read here and here.

Open Longevity ICO, a Russian project focused on conducting clinical trials of geroprotective therapies and introducing diagnoses of aging into clinical practice, was launched in September. It is currently entering the second phase of pre-ICO, and we wish Anastasia Egorova’s team good luck.

In October (which is traditionally considered the Longevity Month) we launched the #IAmTheLifespan campaign, inviting all our supporters to make videos describing what brought them to join our cause, and you can watch some of them here. To help out MouseAge, and for Inktober 2017, our volunteer Laura Weston launched a fundraiser offering her beautiful artwork as a reward for donors.

The Pathways to Healthy Longevity 2017 conference was organized on October 15th by Dr. Ilia Stambler, a famous longevity activist, in Bar Ilan University (Israel), with Prof. Nir Barzilai and Prof. Haim Cohen as key speakers.

In late October and early November, the popular YouTube channel Kurzgesagt published End Aging? and Cure Aging?, which were both created with help from the Lifespan.io team. We saw overwhelming support from old and new members of the community, showing that healthy life extension is much more popular with the public than one might think.

As MouseAge reached and surpassed its goal, news started to spread that WHO was planning to leave healthy aging out of the general programme of work 2019-2023; thanks to the advocacy efforts of the community, though, WHO has received plenty of feedback on the issue and may hopefully reconsider.

During November 8-10th, the TransVision conference was held in Brussels. It was organised by Didier Coeurnelle, the head of HEALES, the Healthy Life Extension Society. Among its other objectives, the Technoprogressive declaration presented at the conference mentions the defeat of aging; it’s good to see that this objective is now considered to be of primary importance by a growing number of organisations.

During December, LEAF took part in Project4Awesome; many amazing videos were made to support us, and we’re really grateful to the community for that. It was a truly beautiful display of generosity, and not the only one; thanks to many fantastic donors, including the mysterious Pineapple Fund creator, the SENS Research Foundation has smashed its funding goals for the year. You can read more about the December highlights here.

Coming up in 2018

In 2018, we will be working towards creating more major media collaborations with awesome content creators to spread further awareness about the problem of aging and the upcoming advent of rejuvenation biotechnologies.

Our web development team will be, and in fact already is, working on improving the overall user experience of our followers and scaling our systems up to meet the needs of a larger user base; we experienced a significant growth in this sense after our collaboration videos with Kurzgesagt were published, and we’re most definitely looking forward to this happening again!

Our Journal Club will, of course, continue discussing and providing commentary on the latest aging research news in the company of special guests from the biogerontology world. More livestream events are in the cards too, so keep an eye on our Facebook page, and subscribe if you haven’t already!

As the community grows larger, so does the need to establish and develop regional presences; our next objective will be starting the Russian chapter of LEAF to engage with a wider audience. Aging is a global problem, so the more communities and audiences we can get involved in the fight against age-related diseases, the better.

LEAF will naturally take part in as many events in the healthy longevity world as possible to keep our readers in the loop. A big must is definitely the March 15-17 Undoing Aging conference in Berlin, Germany, as is the April 22-26 Interventions to Extend Healthspan and Lifespan conference in Kazan, Russia. There will certainly be much exciting news to share, so stay tuned!

The Eurosymposium on Healthy Ageing—a scientific conference organized by the European aging research advocacy group HEALES—will be held in Brussels on November 8-10. It is likely that at least a few of the LEAF team will be at the event, and it is sure to be an interesting one.

Finally, of course, more exciting crowdfunding projects are in the works!

About Nicola Bagalà

Nicola Bagalà has been an enthusiastic supporter and advocate of rejuvenation science since 2011. Although his preferred approach to treating age related diseases is Aubrey de Grey’s suggested SENS platform, he is very interested in any other potential approach as well. In 2015, he launched the blog Rejuvenaction to advocate for rejuvenation and to answer common concerns that generally come with the prospect of vastly extended healthy lifespans. Originally a mathematician graduated from Helsinki University, his scientific interests range from cosmology to AI, from drawing and writing to music, and he always complains he doesn’t have enough time to dedicate to all of them which is one of the reasons he’s into life extension. He’s also a computer programmer and web developer. All the years spent learning about the science of rejuvenation have sparked his interest in biology, in which he’s planning to get a university degree.

About LIFE EXTENSION ADVOCACY FOUNDATION (LEAF)

In 2014, the Life Extension Advocacy Foundation was established as a 501(c)(3) non-profit organization dedicated to promoting increased healthy human lifespan through fiscally sponsoring longevity research projects and raising awareness regarding the societal benefits of life extension. In 2015 they launched Lifespan.io, the first nonprofit crowdfunding platform focused on the biomedical research of aging.

They believe that this will enable the general public to influence the pace of research directly. To date they have successfully supported four research projects aimed at investigating different processes of aging and developing therapies to treat age-related diseases.

The LEAF team organizes educational events, takes part in different public and scientific conferences, and actively engages with the public on social media in order to help disseminate this crucial information. They initiate public dialogue aimed at regulatory improvement in the fields related to rejuvenation biotechnology.

For the Last Time: Rejuvenation is Not Immortality – Article by Nicola Bagalà

For the Last Time: Rejuvenation is Not Immortality – Article by Nicola Bagalà

Nicola Bagalà


Editor’s Note: In this article, Mr. Nicola Bagalà explains to us the terms “rejuvenation”  and “immortality” and how they should not be construed to mean one and the same.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, January 10, 2018

When doing science, it is crucially important to have clear, unambiguous definitions. These definitions must be firmly established to avoid confusion and misunderstandings and possibly to prevent people from going around telling everyone that you’re working on something that you’re actually not.

The I-word

It’s not uncommon, especially for outsiders of a given field, to use an inappropriate word to indicate a more complex concept than the word itself conveys—maybe because they think that the two are close enough or possibly because they just don’t see the difference.

For this reason, it’s likely that each field has its own unspeakably profane word; in the field of rejuvenation, that word is the dreaded I-word: immortality.

Before I explain why it is a dreaded word, it’s important to define what the heck it even means. Now, of course definitions are entirely arbitrary, and the same word could mean a different thing to a different person; but if we go with the most intuitive, commonly accepted meaning of “immortality” when nothing else is specified, then we can safely say it describes the quality of someone who cannot die. In other words, it refers to an immortal being could not be killed or die in any way, even if it wanted to. Just like people today who would like to live for an indefinitely long time (like me) are forced to eventually die by aging and are thus stuck without a choice (at least until we figure rejuvenation out), a hypothetical immortal being would be in a similar situation, with no choice to terminate its life because its immortality would force it to live forever. This brief article explains the issue very nicely and concisely.

Now, the way I approach life, immortality wouldn’t be all that bad, because I am skeptical that I’d ever have a reason to want to die. Still, I appreciate that I might be wrong, so if I could choose and wanted to play it really safe, I’d opt for an “immortality switch”; as long as it is on, you’re immortal; if and when you get tired of life, you flip it off and you become mortal again, free to get rid of your own life however you see fit.

Unfortunately, an immortality switch is just as improbable as immortality itself. Think about it: to be immortal, your chance of ever dying of any cause at all should be exactly zero. There’d be no gun, no disease, no poison, no amount of air taken out of your lungs, no stellar explosion capable of terminating your existence. The inner workings—biological or not—keeping you alive should be indestructible, able to withstand forces of any magnitude and keep going under any possible circumstance (including running out of energy). Even without dragging the fabled heat death of the universe into the mix, it’s difficult to imagine how any of this could ever be possible—let alone a switch turning this unlikely ability on and off.

What’s the difference?

I’m not going to go as far as to say that the above is completely impossible; I was trained to make such bold claims only when I can prove them, so I’ll just say that, to the best of my knowledge, this sort of immortality appears to be exceedingly unlikely.

Now, whether immortality is possible or not is an intriguing question, but it is decidedly off-topic in the field of rejuvenation, because rejuvenation is not immortality. If a universal antiviral drug able to wipe the floor with every conceivable virus existed, you wouldn’t call it an immortality drug, because right after leaving the doctor’s office where you got your miracle shot, a grand piano might happen to crush you after a 50-story free fall, and the antiviral drug wouldn’t be especially effective against that particular cause of death. Similarly, rejuvenation would save you from death by age-related diseases, but not by falling grand pianos, sadly.

Yet, both people and the media keep talking about “curing death” and “immortality pills” when the actual topic is rejuvenation biotechnology; this is a cause of particular annoyance to Dr. Aubrey de Grey, whose pioneering work is constantly called an “immortality quest” and similar things. Since immortality reasonably seems a pipe dream and is laden with all sorts of ethical issues and concerns, whether justified or not, this results in a gross misrepresentation of the entire field and a lot of unwarranted bashing of completely legitimate medical research whose only fault is that it aims to prevent the diseases of aging rather than just coping with them.

The same story is true of negligible senescence. If a successful rejuvenation platform were implemented, people would still age biologically, but we would have therapies capable of undoing such aging. Through periodic reapplication of these therapies, the hallmarks of aging would always be kept well below the pathology threshold. In other words, we would still senesce (that is, age), but our level of senescence would stay negligible—that’s where the term comes from. Yet, many people keep calling negligible senescence immortality just like they do rejuvenation biotechnology, whether deliberately or by genuine mistake, thereby providing an excellent strawman for needy critics to beat. This is why the I-word is dreaded in this field, by the way.

Negligible senescence is the expected result of truly comprehensive rejuvenation biotechnologies, and yes, if we got there, our healthspan would be vastly increased, and consequently, so would our lifespan; if you were in perfect health for longer than, say, 100 years, it is a disarmingly trivial consequence that you would live for longer than 100 years. However, whether a negligibly senescent person then lives on forever or not, or ten thousand years from now, someone beats the odds and comes up with a fancy immortality switch, is an entirely different matter that is beyond the scope of the field of rejuvenation biotechnology. Speaking of which, let me reiterate once more what its actual scope is: to eradicate age-related diseases. All the rest, whether consequential effects or downright made-up rubbish, is just unnecessary embroidery.

About Nicola Bagalà

Nicola Bagalà has been an enthusiastic supporter and advocate of rejuvenation science since 2011. Although his preferred approach to treating age related diseases is Aubrey de Grey’s suggested SENS platform, he is very interested in any other potential approach as well. In 2015, he launched the blog Rejuvenaction to advocate for rejuvenation and to answer common concerns that generally come with the prospect of vastly extended healthy lifespans. Originally a mathematician graduated from Helsinki University, his scientific interests range from cosmology to AI, from drawing and writing to music, and he always complains he doesn’t have enough time to dedicate to all of them which is one of the reasons he’s into life extension. He’s also a computer programmer and web developer. All the years spent learning about the science of rejuvenation have sparked his interest in biology, in which he’s planning to get a university degree.

About LIFE EXTENSION ADVOCACY FOUNDATION (LEAF)

In 2014, the Life Extension Advocacy Foundation was established as a 501(c)(3) non-profit organization dedicated to promoting increased healthy human lifespan through fiscally sponsoring longevity research projects and raising awareness regarding the societal benefits of life extension. In 2015 they launched Lifespan.io, the first nonprofit crowdfunding platform focused on the biomedical research of aging.

They believe that this will enable the general public to influence the pace of research directly. To date they have successfully supported four research projects aimed at investigating different processes of aging and developing therapies to treat age-related diseases.

The LEAF team organizes educational events, takes part in different public and scientific conferences, and actively engages with the public on social media in order to help disseminate this crucial information. They initiate public dialogue aimed at regulatory improvement in the fields related to rejuvenation biotechnology.

SENS: Progress in the Fight Against Age-Related Diseases – Article by Nicola Bagalà and Steve Hill

SENS: Progress in the Fight Against Age-Related Diseases – Article by Nicola Bagalà and Steve Hill

Nicola Bagalà

Steve Hill


Editor’s Note: In this article, Mr. Nicola Bagalà and Steve Hill discuss the progress that the SENS Research Foundation has made in tackling the aging processes. Below is a brief summary of some of the highlights of their research efforts.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, December 8, 2017

 

 

Today, there are many drugs and therapies that we take for granted. However, we should not forget that what is common and easily accessible today didn’t just magically appear out of thin air; rather, at some point, it used to be an unclear subject of study on which “more research was needed”, and even earlier, it was just a conjecture in some researcher’s head.

Hopefully, one day not too far into the future, rejuvenation biotechnologies will be as normal and widespread as aspirin is today, but right now, we’re in the R&D phase, so we should be patient and remind ourselves that the fact that we can’t rejuvenate people today doesn’t mean that nothing is being done or has been achieved to that end. On the contrary, we are witnessing exciting progress in basic research—the fundamental building blocks without which rejuvenation, or any new technology at all, would stay a conjecture.

In particular, SENS Research Foundation (SRF), a pioneering organization of the field, is sometimes unjustly accused by skeptics for failing to produce results. But produce results it has, and many at that. Skeptics either decide to ignore them or do not have access to reliable sources. For the benefit of the latter, we’ll discuss below what has been achieved by SRF over the past few years, in relation to the infamous “seven deadly things”, the seven categories of damage that aging causes as described in the SENS repair approach.

Mitochondrial mutations

In a nutshell, a mitochondrion is a cell component that is in charge of converting food nutrients into ATP (adenosine triphosphate), a chemical that powers cellular function. Your DNA is contained within the nucleus of each of your cells, but this isn’t the only DNA in your body; mitochondria have their own DNA (known as mtDNA), likely because, at the dawn of life, they were independent organisms that eventually entered a symbiotic relationship with eukaryotic cells, such as those found in our bodies.

Unfortunately, as mitochondria produce ATP, they also produce so-called free radicals as a byproduct—atoms with unpaired electrons that seek to “pair up” with other electrons, and to do so, they’ll gladly snatch them from other molecules nearby, damaging them. As free radicals are created by mitochondria, they’re very close to mtDNA, which is thus very susceptible to being damaged and undergoing mutations.

Mitochondria with damaged DNA may become unable to produce ATP or even produce large amounts of waste that cells cannot get rid of. To add insult to injury, mutant mitochondria have a tendency to outlive normal ones and take over the cells in which they reside, turning them into waste production facilities that increase oxidative stress—one of the driving factors of aging.

MitoSENS: How to solve this problem, and how far we’ve got

Cell nuclei are far less exposed to free-radical bombardment than mitochondria, which makes nuclear DNA less susceptible to mutations. For this reason, the cell nucleus would be a much better place for mitochondrial genes, and in fact, evolution has driven around 1000 of them there. Through a technique called allotopic expression, we could migrate the remaining genes to the nucleus and solve the problem of mitochondrial mutations.

Human-made allotopic expression was a mere theory until late 2016, when, thanks to the successful MitoSENS crowdfunding campaign on Lifespan.io, a proof of concept was finally completed. Dr. Matthew O’Connor and his team managed to achieve stable allotopic expression of two mitochondrial genes in cell culture, as reported in the open-access paper[1] they published in the journal Nucleic Acids Research. As Aubrey de Grey himself explains in this video, of the 13 genes SRF is focusing on, it’s now managed to migrate almost four. This had never been done before and is a huge step towards addressing this aspect of aging in humans. In the past few months, the MitoSENS team has presented its results around the world and worked on some problems encountered in the project.

A list of SRF-funded papers on the topic of mitochondrial mutations can be found here. A more detailed description of its intramural MitoSENS research can be found here.

Lysosomal dysfunction

Lysosomes are digestive organelles within cells that dispose of intracellular garbage—harmful byproducts that would otherwise harm cells. Enzymes within lysosomes can dispose of most of the waste that normally accumulates within cells, but some types of waste, collectively known as lipofuscin, turn out to be impossible to break down. As a result, this waste accumulates within the lysosomes, eventually making it harder for them to degrade even other types of waste; in a worst-case scenario, overloaded lysosomes can burst open and spread their toxic contents around.

This eventuality is especially problematic for cells that replicate little or not at all, such as heart and nerve cells—they’ve got all the time in the world to become swamped in waste, which eventually leads to age-related pathologies, such as heart disease and age-related macular degeneration.

LysoSENS: How to solve this problem, and how far we’ve got

As normal lysosomal enzymes cannot break down lipofuscin, a possible therapy could equip lysosomes with better enzymes that can do the job. The approach suggested by SRF originates with ERT—enzyme replacement therapy—for lysosomal storage diseases. This involves identifying enzymes capable of breaking down different types of intracellular junk, identifying genes that encode for these enzymes, and finally delivering the enzymes in different ways, depending on the tissues and cell types involved.

SRF funded a preliminary research project on lipofuscin clearance therapeutics at Rice University[2] and another project relating to atherosclerosis and the clearance of 7-ketocholesterol[3] (a lipofuscin subtype), which eventually spun into Human Rejuvenation Biotechnologies, an early-stage private startup funded by Jason Hope.

A LysoSENS-based approach is currently being pursued by Dr. Kelsey Moody, who used to work at SRF. Dr. Moody has been working on an ERT treatment for age-related macular degeneration. The treatment consists in providing cells of the macula (a region of the eye’s retina) with an enzyme capable of breaking down a type of intracellular waste known as A2E. The treatment, called LYSOCLEAR, is being worked on by Moody’s company Ichor Therapeutics, which earlier this year has announced a series A offering to start Phase I clinical trials of its product.

If LYSOCLEAR proves successful, it could pave the way for future LysoSENS-based therapies to treat lysosomal dysfunction in different tissues.

A list of SRF-funded papers on the topic can be found here.

Cellular senescence

As cells divide, their telomeres—the end-parts of chromosomes protecting them from damage—shorten. Once a critical length has been reached, cells stop dividing altogether and enter a state known as senescence. Senescent cells are known to secrete a cocktail of chemicals called SASP (Senescence Associated Secretory Phenotype), which promotes inflammation and is associated with several age-related conditions.

However, senescent cells are a bit of a double-edged sword; as explained by Professor Judy Campisi during RB2016, as long as they’re not too numerous, senescent cells carry out an anti-cancer function and may promote wound healing; however, too many of them have the opposite effect, and on top of that, they induce neighboring cells to undergo senescence themselves, starting a dangerous spiral.

Normally, senescent cells destroy themselves via programmed cell death, known as apoptosis, and are then disposed of by the immune system, but some of them manage to escape destruction, and as the immune system declines with age, this gets worse.

The result is that late in life, senescent cells have accumulated to unhealthy amounts and significantly contribute to the development of age-related diseases. Osteoarthritis, cardiovascular diseases, cancer, metabolic disorders such as diabetes, and obesity are all linked to the chronic age-related inflammation to which senescent cells contribute.

ApoptoSENS: How to solve this problem, and how far we’ve got

The proposed SENS solution is straightforward: if senescent cells become too numerous, then they need to be purged. Since they are useful in small amounts, the optimal solution would be periodically removing excess senescent cells without eradicating them entirely—and more importantly, leaving other cells unharmed.

This could potentially be achieved by either senolytic drugs or gene therapies that selectively target senescent cells and trigger programmed cell death. Indeed, a great deal of recent focus by researchers have been on finding ways to remove senescent cells using senolytic therapies.

Another approach that could complement senolytics is to address why the immune system stops clearing senescent cells effectively in the first place. This approach focuses on macrophages and other immune cells involved in clearing senescent cells, aiming to reduce inflammation so that these cells begin to function properly again. The irony is that as inflammation rises with age, the immune system that is supposed to clear senescent cells and keep inflammation levels down actually starts to create more inflammation and becomes part of the problem by not doing its job properly.

SRF has funded a number of studies on the subject of cellular senescence, and it’s recently begun working on a project in collaboration with the Buck Institute for Research on Aging, which is focusing on the immune system and its role in clearing senescent cells. Another extramural project, again with the Buck Institute, is focussed on SASP inhibition.

Senescent cell clearance has been all the rage for the past two years or so; Lifespan.io has hosted the MMTP project, which focused on testing senolytics in mice, and this was later followed by CellAge’s project to design synthetic biology-based senolytics.

There are other companies that have joined the race to add senescent cell clearance to the standard toolkit of doctors, such as Unity Biotechnology and Oisin Biotechnologies.

Unity’s approach uses a drug-based approach to senolytics and is scheduled to enter human clinical trials in 2018. A number of other research teams are also developing drug-based approaches to removing senescent cells, and the competition looks set to be fierce in this area in the coming years.

Oisin’s approach, which we discussed here, makes use of suicide genes and hopefully will be tested in clinical trials not too far into the future, thanks to venture funding presently being collected. If this system can be made to work, it will allow very selective targeting of senescent cells by destroying only those giving off a target gene or genes. Thus, if a unique gene expression profile for senescent cells is determined, it would mean only those cells were destroyed, with less risk of off-target effects.

Oisin owes its existence to the SENS Research Foundation and the Methuselah Foundation, which provided the necessary seed funding. Kizoo Technology Ventures has also invested in Oisin.

Extracellular crosslinks

The so-called extracellular matrix is a collection of proteins that act as scaffolding for the cells in our body. This scaffolding is rarely if ever replaced, and a really bad consequence of this is that its parts eventually end up being improperly linked to each other through a process called glycation—the reaction of (mainly) blood sugar with the proteins that make up the extracellular matrix itself.

The resulting cross-links impair the function and movement of the linked proteins, ultimately stiffening the extracellular matrix, which makes organs and blood vessels more rigid. Eventually, this leads to hypertension, high blood pressure, loss of skin elasticity, and organ damage, among other problems.

While there are different types of cross-links—known as AGEs, short for advanced glycation end-products—glucosepane is arguably the worst, being the most common and long-lasting of all, and the body is very ill-equipped to break it down.

GlycoSENS: How to solve this problem, and how far we’ve got

In order to eliminate unwanted cross-links, the SENS approach proposes to develop AGE-breaking molecules that may indeed sever the linkages and return tissues to their original flexibility. Of course, in order to do so, crosslink molecules need to be available for research to attempt to combat them with drugs, and especially in the case of glucosepane, this has been a problem for years.

Glucosepane is a very complex molecule, and very little of it can be extracted from human bodies, and not even in its pure form. This has been greatly hampering the progress of research against glucosepane, but thankfully, this problem is now solved thanks to a collaboration between the Spiegel Lab at Yale University and the SENS Research Foundation, which financially supported the study. It is now possible to fully synthesize glucosepane, allowing for researchers to create it on demand and at a cost-effective price.

The Spiegel Lab’s scientists are now developing anti-glucosepane monoclonal antibodies to cleave unwanted cross-links. The collaboration between the Spiegel Lab and SRF dates all the way back to 2011, but it was in 2015 that the Lab announced its success and published a related paper [4] in the journal Science.

Further information on glucosepane cross-link breakers can be found in this interview with Dr. David Spiegel from Yale University on Fight Aging!; a list of studies on the subject funded or otherwise supported by the SRF is available here.

SRF also worked with the Babraham Institute on a cross-link quantification project.

Let’s help SRF move forward

Readers who wish to donate to SRF to help the organization in its crusade against the ill health of old age can do so by contributing to its winter fundraiser or even becoming SRF patrons. Have a look at SRF’s donation page to find out more.

NB: Dr. Aubrey de Grey (Chief Science Officer and Co-founder of SENS Research Foundation) himself held an AMA (“ask me anything”) on Reddit on December 7, at 14:00 PST (22:00 UTC, 17:00 EST). The questions and Dr. de Grey’s responses can be found here.

Literature

[1] Boominathan, A., Vanhoozer, S., Basisty, N., Powers, K., Crampton, A. L., Wang, X., … & O’Connor, M. S. (2016). Stable nuclear expression of ATP8 and ATP6 genes rescues a mtDNA Complex V null mutant. Nucleic acids research, 44(19), 9342-9357.

[2] Gaspar, J., Mathieu, J., & Alvarez, P. (2016). A rapid platform to generate lipofuscin and screen therapeutic drugs for efficacy in lipofuscin removal. Materials, Methods and Technologies, 10, 1-9.

[3] Mathieu, J. M., Wang, F., Segatori, L., & Alvarez, P. J. (2012). Increased resistance to oxysterol cytotoxicity in fibroblasts transfected with a lysosomally targeted Chromobacterium oxidase. Biotechnology and bioengineering, 109(9), 2409-2415.

[4] Draghici, C., Wang, T., & Spiegel, D. A. (2015). Concise total synthesis of glucosepane. Science, 350(6258), 294-298.

 

About Steve Hill

As a scientific writer and a devoted advocate of healthy longevity technologies, Steve has provided the community with multiple educational articles, interviews, and podcasts, helping the general public to better understand aging and the means to modify its dynamics. His materials can be found at H+ Magazine, Longevity Reporter, Psychology Today, and Singularity Weblog. He is a co-author of the book Aging Prevention for All – a guide for the general public exploring evidence-based means to extend healthy life (in press).

About Nicola Bagalà

Nicola Bagalà has been an enthusiastic supporter and advocate of rejuvenation science since 2011. Although his preferred approach to treating age related diseases is Aubrey de Grey’s suggested SENS platform, he is very interested in any other potential approach as well. In 2015, he launched the blog Rejuvenaction to advocate for rejuvenation and to answer common concerns that generally come with the prospect of vastly extended healthy lifespans. Originally a mathematician graduated from Helsinki University, his scientific interests range from cosmology to AI, from drawing and writing to music, and he always complains he doesn’t have enough time to dedicate to all of them which is one of the reasons he’s into life extension. He’s also a computer programmer and web developer. All the years spent learning about the science of rejuvenation have sparked his interest in biology, in which he’s planning to get a university degree.

About LIFE EXTENSION ADVOCACY FOUNDATION (LEAF)

In 2014, the Life Extension Advocacy Foundation was established as a 501(c)(3) non-profit organization dedicated to promoting increased healthy human lifespan through fiscally sponsoring longevity research projects and raising awareness regarding the societal benefits of life extension. In 2015 they launched Lifespan.io, the first nonprofit crowdfunding platform focused on the biomedical research of aging.

They believe that this will enable the general public to influence the pace of research directly. To date they have successfully supported four research projects aimed at investigating different processes of aging and developing therapies to treat age-related diseases.

The LEAF team organizes educational events, takes part in different public and scientific conferences, and actively engages with the public on social media in order to help disseminate this crucial information. They initiate public dialogue aimed at regulatory improvement in the fields related to rejuvenation biotechnology.

Why Rejuvenation Biotechnology Could Benefit You – Article by Nicola Bagalà

Why Rejuvenation Biotechnology Could Benefit You – Article by Nicola Bagalà

Nicola Bagalà


Editor’s Note: In this article, Mr. Nicola Bagalà discusses the benefits of Rejuvenation Biotechnology (age-reversing technology).  This article was originally published by the Life Extension Advocacy Foundation (LEAF) .

~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, October 25, 2017

The benefits are many; some are obvious, and some are less so. The ones I’ll discuss in this article are the ones I see as obvious, tangible, immediate benefits for the people undergoing rejuvenation.

Health

We’ve kind of made a rather big deal of this one, haven’t we? Rejuvenation, we have said time and again, is pretty much all about health. The causal link between biological aging and pathologies is well established, and even when we account for the few elderly who are exceptionally healthy for their age, we’re left with the obvious fact that the older you are, the sicker you are, and even the aforementioned exceptions aren’t in the best of shape.

To the best of my knowledge, the number of people who actively wish to be sick at some point tends to be fairly small; so, when you think that a truly comprehensive rejuvenation platform would allow people to maintain youthful health irrespective of their age, the health benefits of rejuvenation become crystal clear. To be honest, this benefit alone would be enough for me, and I wouldn’t even need to look into the other ones.

Independence

Frailty, failing senses, weakness, and diseases aren’t good friends of independence, but they are good friends of old age. That’s why nursing homes exist in the first place to take care of elderly people who are no longer independent. Again, even the few exceptional cases who manage on their own until death don’t have it easy. Having people doing things for you can be nice in small doses, but having to have people doing things for you, not so much. Rejuvenation would eliminate the health issues that make the elderly dependent on others, which is a rather evident benefit.

Longevity

As odd as it may sound, longevity is really just a ‘side effect’ of health, because you can’t be healthy and dead. The longer you’re healthy enough to be alive, the longer you’ll live. Since rejuvenation would keep you in a state of youthful health, the obvious consequence is that you’d live longer. How much longer exactly is hard to say, but as long as you’re healthy enough to enjoy life, it’s safe to say that longevity would be a benefit; you’d have more time and energy to dedicate to what you love doing, and you could keep learning and growing as a person for an indefinitely long time.

You would not have to worry about the right age to change your job, get married, or start practicing a new sport, because your health wouldn’t depend on your age, and the time at your disposal would not have a definite upper limit. If the first few decades of your life weren’t as good as they could have been for one reason or another, you would still have time ahead and a chance of a better future, which sounds more appealing than ten years in a hospice with deteriorating health to me. (Let’s face it: If your life isn’t very good to begin with, a disease is hardly going to make it better.)

Additionally, a longer life would allow you to see what the future has in store for humanity. I wouldn’t be too quick to think the future will be all doom and gloom.

Today’s world is more peaceful and prosperous than it was in the past, and while there’s no certainty it will be at least this good in the future, there’s no certainty that it won’t be worth living in either. I would argue it’s best not to cross our bridges before we get there, and we shouldn’t opt out of life before we actually reach a point when we don’t care for it anymore, if ever.

I don’t think I will ever have a reason to give up on life or get bored with it, but I accept that somebody might think otherwise. Even so, I think being able to choose how long you want to live, and always living in the prime of health, is a much better deal than the current situation of having a more-or-less fixed lifespan with poor health near the end.

Choice

Ultimately, all of these perks can be summarised into one: choice. If we had fully working rejuvenation therapies available and were thus able to keep ourselves always perfectly healthy, regardless of our age, we could choose whether we wanted to use these therapies or not. Those who wish a longer, healthier life could avail themselves of the opportunity and escape aging for as long as they wanted; those who prefer to age and bow out the traditional way could just as easily not use the therapies.

Rejuvenation would give us an extra option we currently don’t have; everyone is forced to face the burden of aging and eventually die of it, for the moment. Being able to choose what we wish for ourselves is one of the most fundamental human rights and an obvious, unquestionable benefit.

About Nicola Bagalà

Nicola Bagalà has been an enthusiastic supporter and advocate of rejuvenation science since 2011. Although his preferred approach to treating age related diseases is Aubrey de Grey’s suggested SENS platform, he is very interested in any other potential approach as well. In 2015, he launched the blog Rejuvenaction to advocate for rejuvenation and to answer common concerns that generally come with the prospect of vastly extended healthy lifespans. Originally a mathematician graduated from Helsinki University, his scientific interests range from cosmology to AI, from drawing and writing to music, and he always complains he doesn’t have enough time to dedicate to all of them which is one of the reasons he’s into life extension. He’s also a computer programmer and web developer. All the years spent learning about the science of rejuvenation have sparked his interest in biology, in which he’s planning to get a university degree.

About LIFE EXTENSION ADVOCACY FOUNDATION (LEAF)

In 2014, the Life Extension Advocacy Foundation was established as a 501(c)(3) non-profit organization dedicated to promoting increased healthy human lifespan through fiscally sponsoring longevity research projects and raising awareness regarding the societal benefits of life extension. In 2015 they launched Lifespan.io, the first nonprofit crowdfunding platform focused on the biomedical research of aging.

They believe that this will enable the general public to influence the pace of research directly. To date they have successfully supported four research projects aimed at investigating different processes of aging and developing therapies to treat age-related diseases.

The LEAF team organizes educational events, takes part in different public and scientific conferences, and actively engages with the public on social media in order to help disseminate this crucial information. They initiate public dialogue aimed at regulatory improvement in the fields related to rejuvenation biotechnology.

The Good Sides of Aging? – Article by Nicola Bagalà

The Good Sides of Aging? – Article by Nicola Bagalà

Nicola Bagalà


Editor’s Note: Nicola Bagalà in this guest article elaborates upon aging as a topic distinguished in terms of Chronological Aging and Biological Aging. This article was originally published by the Life Extension Advocacy Foundation (LEAF).

~ Kenneth Alum, Director of Publication, U.S. Transhumanist Party, October 17, 2017

Sometimes, and especially in articles aimed at mitigating people’s fear of aging, it is said that aging doesn’t come just with downsides, such as frailty and diseases, but also with upsides — for example, wisdom and a long life experience.

It is often subtly implied that these two very different aspects are two sides of the same coin, that you can’t have one without the other, and perhaps even that the ill health of old age is a fair price to pay for the benefits that also come with it.

Nothing could be further from the truth.

Setting the record straight

There are plenty of good reasons to be afraid of aging, because the diseases and disabilities it causes are very real and far from being observed only in exceptional cases. It would be foolish not to fear cancer, for example, because it is an extremely serious and often fatal condition; in the same way, and for the same reasons, it is foolish not to fear aging; perhaps, an even stronger fear is justified, because aging can and does give rise to many diseases, including cancer itself.

There’s nothing wrong with fearing aging, because it may help us steer clear from its inherent dangers, just like the fear of any other harmful thing keeps us away from it. This is true so long as by ‘aging’ we mean biological aging, which is not at all the same as chronological aging. It is very important to draw a line between the two so that we don’t end up accepting the downsides of the former, which are neither necessary nor sufficient to enjoy the benefits of the latter.

What’s the difference?

Chronological aging is a rather fancy term to indicate a very mundane thing, namely the passing of time. For as long as time will keep passing, everything will age chronologically. This is obviously a good thing because if time did not pass, the universe would stand still and nothing at all, including ourselves, would ever happen.

However, it is easy to see how chronological and biological aging are not the same thing by means of a simple observation: Although time runs essentially uniformly everywhere on Earth, different life forms have different health- and lifespans. If time passes at the same rate for me and for a cat, and yet I’m (biologically) old at age 80 while a cat is (biologically) old already at age 15, clearly there must be something else than just the passing of time that accounts for this discrepancy.

This ‘something else’ is metabolism—the intricate set of chemical reactions the bodies of living creatures perform on a daily basis for the very purpose of staying alive. As we have discussed in other articles, what we call biological aging is really just a process of damage accumulation; this damage, which eventually leads to pathologies, is caused by metabolism itself, and therefore a faster metabolism means faster aging. Different species have different metabolic rates; as a rule of thumb, the smaller the species, the faster its metabolism and thus its aging, leading to shorter health- and lifespan. This is, in a nutshell, why a cat ages faster than I do.

As a confirmation of this fact, one may observe that species in a regimen of caloric restriction tend to live longer (sometimes much longer) than their normal lifespan, and the insurgence of age-related diseases is delayed accordingly: A lower caloric intake causes metabolism to slow down; consequently, the aging process follows suit.

Interestingly, some lucky species, the so-called negligibly senescent organisms, don’t show any signs of biological aging at all with the passing of time.

At this point, you don’t have to be clairvoyant to see that biological aging implies chronological aging, but not vice-versa. No chronological aging means no time passing, and no time passing means nothing takes place, metabolism included. However, since different creatures age differently (or not at all) despite time passing at the same rate for all of them, chronological aging doesn’t imply biological aging. Quite simply, they’re not the same thing.

Render unto Caesar the things which are Caesar’s

Having cleared the difference between chronological and biological aging, we must now correctly attribute the aforementioned pros and cons of old age to each of them.

From the very definition of biological aging above, it’s clear that it is the culprit responsible for the cons—the diseases of old age.

Speaking of the pros, all possible benefits of old age—life experience, wisdom, sense of accomplishment—certainly do not come from the damage that metabolism has wrecked throughout your body over the years. Clearly, they depend on the events of your life, and thus they’re not at all granted to happen, no matter how long you live. If you spent your life in isolation doing nothing, avoiding new experiences, and not learning anything new, your wisdom as an eighty-year-old would hardly compare to that of a well-traveled, seasoned scientist or philosopher of the same age, for example. Ultimately, the benefits traditionally attributed to old age obviously depend on the passing of time (i.e., chronological aging), and most of all on the use you made of your time. Just because you’re old, you’re not automatically wise, accomplished, or well-learned.

What’s more, the debilitation that comes with biological aging makes it harder for you to relish and expand the wisdom and experience you’ve accrued over the years. So, not only does biological aging bring no benefits; it is a hindrance as well.

In conclusion, the pros and cons of old age are due to different causes, and, as such, they aren’t interdependent. The diseases of old age are not a currency you can use to buy yourself the wisdom of the aged, and thanks to the emergence of rejuvenation biotechnologies, you might relatively soon be able to enjoy the pros of old age without having to pay any undue and unfair tolls.

 

About Nicola Bagalà

Nicola Bagalà has been an enthusiastic supporter and advocate of rejuvenation science since 2011. Although his preferred approach to treating age-related diseases is Aubrey de Grey’s suggested SENS platform, he is very interested in any other potential approach as well. In 2015, he launched the blog Rejuvenaction to advocate for rejuvenation and to answer common concerns that generally come with the prospect of vastly extended healthy lifespans. Originally a mathematician graduated from Helsinki University, his scientific interests range from cosmology to AI, from drawing and writing to music, and he always complains he doesn’t have enough time to dedicate to all of them—which is one of the reasons he’s into life extension. He’s also a computer programmer and web developer. All the years spent learning about the science of rejuvenation have sparked his interest in biology, in which he’s planning to get a university degree.

About LIFE EXTENSION ADVOCACY FOUNDATION (LEAF)

In 2014, the Life Extension Advocacy Foundation was established as a 501(c)(3) non-profit organization dedicated to promoting increased healthy human lifespan through fiscally sponsoring longevity research projects and raising awareness regarding the societal benefits of life extension. In 2015 they launched Lifespan.io, the first nonprofit crowdfunding platform focused on the biomedical research of aging.

They believe that this will enable the general public to influence the pace of research directly. To date they have successfully supported four research projects aimed at investigating different processes of aging and developing therapies to treat age-related diseases.

The LEAF team organizes educational events, takes part in different public and scientific conferences, and actively engages with the public on social media in order to help disseminate this crucial information. They initiate public dialogue aimed at regulatory improvement in the fields related to rejuvenation biotechnology.