Tag: Life Extension Advocacy Foundation

Cryonics – Article by Reason

Cryonics – Article by Reason

Comments 0 Comment

Reason

___________________________________________________________________________________________________

Photo Credit: pexels.com

_______________________________________________________________________________________________________

“Although no one can quantify the probability of cryonics working, I estimate it is at least 90% — and certainly nobody can say it is zero.” – Sir Arthur C. Clarke

Editor’s Note: In this article, the author writes that cryonics is the only present option offering a chance at a much longer life in the future that is open to older and seriously ill people, the many individuals who do not have the time to wait for the arrival of rejuvenation therapies. He went further to say that if you die tomorrow, then cryonics is the only chance you have at a longer life in the future. But there will always be a role for what we might term post-mortem critical care of the sort provided by the present cryonics industry. Now take a deep dive to read the author’s opinion. 

~ Urhefe Ogheneyoma Victor, Assistant to the  Director of Publication, United States Transhumanist Party, May 2022. 

      _________________________________________________________________

Cryonics is the only present option offering a chance at a much longer life in the future that is open to older and seriously ill people, the many individuals who do not have the time to wait for the arrival of rejuvenation therapies. Cryonics is a part of the broad field of low-temperature storage of biological materials, in this case the practice of placing humans and animals into that storage immediately following clinical death, thereby halting all biological processes and preserving tissues, especially the brain tissues that incorporate the fine structures presently thought to store the data of the mind. This is not mere freezing, which damages cells, but rather a process of vitrification that employs cryopreservant chemicals to prevent ice crystal formation and preserve the small-scale structure of tissues. This is known as cryosuspension within the industry.

Cryosuspension is undertaken with the expectation that advances in medical technology may eventually enable restoration of preserved individuals to life and health. For so long as the structure of tissue is preserved intact, it is possible that advanced technologies can one day work with it. Thus a small industry of cryonics providers offers cryosuspension services and a small number of patients take advantage of this in the hopes that future clinicians will have access to technologies for revival and repair, most likely based on applications of molecular nanotechnology.

Facing Up to an Unpleasant Reality

Death is not a topic that anyone likes to think about, and that is just as true of advocates for longevity science as anyone else. We have to recognize, however, that the future of greatly extended healthy lives, produced by technologies such as SENS therapies, regenerative medicine, and medical nanotechnology, will not arrive soon enough to benefit everyone. Many people are too old to wait for decades, or suffer from other conditions that will kill them before cures can be developed. This is an unpleasant reality and we must face up to it.

A billion people will die between now and the earliest possible plausible date for the first package of rough and ready but working rejuvenation therapies, at least twenty years in the future. That date will only be hit if fundraising and other matters proceed very well over the next few years. Another few decades will pass after that point in order for the technologies of rejuvenation to work their way out to global availability at low cost, and the toll of deaths caused by aging will continue in less fortunate regions while this happens. Do we just write these people off and forge ahead regardless? Of course not. Instead, we can turn to the science and business of cryonics: an industry presently small, but which in a better world would be large enough to help everyone.

The practice of cryonics is an ongoing medical experiment with an unknown chance of success, though the odds improve as progress continues towards reversible vitrification of organs, and evidence for maintenance of memory through vitrification and thawing is obtained from experiments in lower animals. Responsible cryonicists understand that cryonic suspension is an educated gamble. The chances are certainly better than zero, however, and as one wag noted, “the control group in this experiment isn’t doing so well.” By this, he was referring to the vast number of people who are cremated, buried, or otherwise interred. The chance of any plausible future science restoring them to life is zero.

Still the Only Viable Backup Plan

Front and center, the primary plan for longevity for people in middle age and younger today is to help push through enough of the right medical research focused on rejuvenation. Our bodies are aging, accumulating damage, but methods of repairing that damage are slowly edging their way towards clinical application. Once in the clinic they will slowly become better. At some point the improvement in repair methodologies will add healthy life expectancy for older people faster than a year with every passing chronological year. Everyone with access to the latest stable medical technology at that point will have beaten the curve: they will no longer suffer and die due to aging. The question for each of us is where that point occurs in the life span, or indeed whether it occurs at all – and that is where activism and funding comes in. We can’t make ourselves younger (yet), but you can help to speed up the development process.

That is the primary plan, and for every primary plan there must be a backup plan. Never bet on just one horse. The backup plan for evading the end that comes with death by aging is cryonics: low-temperature preservation of the fine structure of the brain on clinical death. Cryonics organizations will maintain the data of your mind in its physical form for the decades it will take for restoration to active life to become a viable possibility. That will, at minimum, require near complete control over cellular biochemistry and regeneration, as well as a mature molecular nanotechnology industry capable of repairing broken cell structures, removing cryoprotectant from tissues, and similar tasks. None of these goals are impossible or unforeseen, it is just that the necessary technologies don’t exist today. Preserved individuals have all the time in the world to wait, of course.

A backup plan is never as good as the primary plan. That is why it is the backup plan. In order to be cryopreserved you have to undergo a very unpleasant set of experiences; you have to age and you have to die, and do so naturally with little help, since our backwards legal systems don’t allow for assisted euthanasia in a constructive way that can mesh with cryonics protocols and organizational procedures. Further, in comparison to remaining alive and healthy thanks to the development of working rejuvenation treatments, cryonics will for a long time to come be a leap into the dark with an unknown chance at ultimate success. It is still infinitely better than any of the other possible choices open to the billions who will die too soon to benefit from near future rejuvenation therapies.

Where to Learn More

The cryonics community is friendly and supportive and has been around for decades. The community and the industry it supports have been ever-so-slowly growing since the early 1970s. To find out more about cryonics and its history of development, you might want to peruse the following pages:

In addition, an excellent article on the philosophy and practice of cryonics can be found here at Fight Aging!:

A Future that Includes Post-Mortem Critical Care

If you die tomorrow, then cryonics is the only chance you have at a longer life in the future. But there will always be a role for what we might term post-mortem critical care of the sort provided by the present cryonics industry. This is a shorthand for the collection of technologies and services assembled to preserve the fine structure of the brain (and thus the mind it contains) following death, and keep that tissue preserved until such time as the patient can be restored to life. At present cryonics is the only available post-mortem critical care option, and we have a fair few years to wait before medical technologies to advance to the point at which restoration is safe and feasible. Hence the chance of eventual restoration for any one preserved individual is unknown but greater than zero.

In a future in which the technology to restore a preserved person exists, cryonics and other preservation technologies such as plastination will occupy a more dynamic position in the medical toolkit, and patients might expect to wait in a preserved state only for transport to the nearest major population center. Even after aging and disease is completely conquered by means of advanced biotechnology, there will be an ongoing toll of death due to accidents. Death isn’t going away completely, no matter how well we do in the field of medicine in the foreseeable future: medicine can’t wave away falling rocks. But first things first. There is a way to go yet before that better world arrives.

How to Sign Up For Cryosuspension

You can sign up for cryosuspension fairly easily both inside and outside the US through one of the established cryonics providers or supporting organizations. You can learn more at the websites for the companies. Alcor is the largest of the providers, has the most comprehensive online information. If you have questions, just ask. Company staff will be happy to help.

More recently other providers and initiatives to start new providers have started to emerge outside the US, the most advanced of which is KrioRus in Russia. Cryosuspension is expensive, on a par with major surgery, but can be paid for in a cost-effective manner through life insurance. You purchase a policy that pays out to the provider on your death and they take it from there: if you set this up well in advance, the monthly cost of a life insurance policy is low. This is far and away the most common payment method and the majority of people suspended or signed up are of modest means.

Reason is the founder and writer of Fight Aging!, a leading voice in the rejuvenation biotechnology and patient advocacy communities for more than fifteen years. He is also co-founder and CEO of Repair Biotechnologies, a biotech startup working towards the reversal of atherosclerosis, and has presented at numerous industry conferences, including Undoing Aging and Ending Age-Related Diseases.

Why I Hope to Be Alive at 75 – Article by Steve Hill

Why I Hope to Be Alive at 75 – Article by Steve Hill

Comments 1 comment

U.S. Transhumanist Party Logo

Steve Hill

Editor’s Note: In this article, originally published on November 13, 2020, by our allies at the Life Extension Advocacy Foundation (LEAF), Steve Hill explains why the attitude of Joe Biden’s new advisor on COVID-19 strategy, Ezekiel Emanuel, is supremely counterproductive. Emanuel infamously wrote in 2014 that he hopes to die at age 75. Given that COVID-19 is a disease whose toll is greatly amplified by biological aging, Emanuel’s statements render him uniquely ill-suited  to remedy the ravages of the ongoing pandemic. Moreover, his pessimism toward what life is like at age 75 is no longer justified, in light of emerging medical advances that could enable rejuvenation and biological youthfulness for those who are in late middle age today. Perhaps, if he sees these advances become a reality in the not-too-distant future, Emanuel might change his mind regarding the desirability of longer lifespans.

~ Gennady Stolyarov II, Chairman, United States Transhumanist Party, November 17, 2020

2020 has been a strange year for a variety of reasons, but the societal changes that the COVID-19 pandemic has created are probably the strangest. However, it is perhaps even stranger that Dr. Ezekiel Emanuel has been appointed to advise Joe Biden on COVID strategy.

Emanuel is best known for writing a controversial article in the October 2014 edition of The Atlantic, headlined “Why I Hope to Die at 75”, in which he strongly rejects the desire to live beyond the age of 75 and expresses his opinion that continuing to live after such an age is meaningless.

Living too long is also a loss. It renders many of us, if not disabled, then faltering and declining, a state that may not be worse than death but is nonetheless deprived.

Needless to say, I strongly disagree with this baffling point of view and am somewhat concerned that someone who thinks this way of his own life, and presumably the lives of others, may be appointed to a position of influence for a disease whose primary risk group is the elderly. This seems almost as foolhardy as spending a vacation weekend in a caravan with Hannibal Lecter.

Emanuel listed quite a few methods by which people extend their lives and stated that they were a “valiant effort to cheat death and prolong life as long as possible,” but his response to them was, “I reject this aspiration. I think this manic desperation to endlessly extend life is misguided and potentially destructive.”

Age is the #1 risk factor for COVID

The scientific evidence clearly shows that the primary risk factor for contracting and dying from COVID-19 is age, with people over the age of 75 at particularly high risk. This is due to the decline of the immune system, which becomes increasingly weak and dysfunctional with age in a process known as immunosenescence.

Globally, the strategy has been to try to shield these vulnerable people as best as possible due to their weakened immune systems and limit their exposure to the disease while vaccines are developed.

Needless to say, I find Biden’s nomination of him to address a disease that mostly affects seniors ironic in itself, given that he thinks the lives of most people beyond 75 are pointless and that they don’t live meaningful lives and would be better off embracing death rather than desperately trying to extend them. Therefore, I hope for the sake of the older people in our society that he has rethought his priorities.

Why I hope to be alive at 75

Predictably, there is already a storm raging on social media around his appointment, so there is no purpose to adding more fuel to that fire. Instead, I am going to talk about why the future of aging could be very different to the grim picture that Emanuel paints.

At age 63, he is getting closer to the age at which he thinks life is pointless, and I believe that a large reason why he is so pessimistic about life beyond 75, whether he realizes it or not, is based on the current state of medicine. This line of reasoning does not take into account how medicine, and in particular how we treat aging could change in the next decade or two.

Current medicine does a great job at keeping people alive for longer, but they often have to live with one or more chronic diseases. Given that, I am not surprised that Emanuel is not enamored with living a long life, especially as that could entail being disabled, bed-bound, or otherwise suffering a poor quality of life as the result of debilitating age-related diseases.

Thankfully, the world healthcare strategy is slowly starting to shift to one of prevention over cure, but right now, the typical approach is to play whack-a-mole with diseases. As one pops up, it is treated, then the next, and the next, and so on. This strategy works great for infectious diseases, but it is an exercise in futility and diminishing returns when applied to the chronic diseases of aging.

However, things could be different in the not so distant future, and being 75 could see the majority of people far more fit, healthy, and vibrant than ever before in human history thanks to advances in aging research. Therapies that directly target aging could potentially make people biologically younger (in particular their immune systems) and much more able to withstand COVID-19 and other diseases.

As explained on LEAF’s What is Aging? page, aging consists of multiple processes (“hallmarks”) that gradually cause damage to organs and tissues and lead to age-related diseases. Rejuvenation biotechnology is advanced medical technology that directly addresses any of the various aging processes in order to restore tissue and organ function to a more youthful state, thereby ameliorating, delaying, or preventing age-related diseases. Let’s take a brief look at some of the promising near-future research that could bear fruit by the time Emanuel reaches 75 and perhaps change his mind.

Rejuvenating the immune system

The decline of the immune system is a key reason why the elderly are most susceptible to infectious diseases such as COVID, and there has been considerable interest in the rejuvenation of the immune system in recent years.

Dr. Greg Fahy from intervene immune has had some early success with thymus rejuvenation in a small human pilot study and demonstrated that it is possible to cause the thymus, which shrinks and loses its capacity to produce immune T cells during aging, to regrow and resume production of those cells. Dr. Fahy is now moving forward into a larger-scale study, and if the results continue to be positive, it is not hard to imagine that thymus regrowth could become a staple of helping the elderly stay healthy.

Another example of immune rejuvenation is currently being developed by Samumed, a biotechnology company that is developing drugs that target the Wnt pathway to restore it to youthful function. The Wnt pathway is a key pathway that regulates the function of our stem cells and ensures that they supply our tissues and organs with new cells to replace losses from injury, disease, and wear and tear.

If successful, this approach would allow the body to resume efficient repair of tissues, and it would replenish aged and failing tissues and organs with fresh, healthy cells supplied by the rejuvenated stem cells.

Therapeutic plasma exchange

Researchers Irina and Mike Conboy at UC Berkeley have been researching blood factors and their role in aging for over two decades. During that time, they have identified a number of factors present in aged blood that appear to regulate aging.

These factors are also present in younger people, but in typically far lower amounts, and tend to serve useful functions. However, during aging, the levels of these proteins become deregulated, and they often rise to detrimental levels and cause damage to the body, which typically involves preventing stem cells from working and tissue from regenerating.

Decades’ worth of research from the Conboy lab has shown that, in mice at least, it is possible to filter out these harmful pro-aging blood factors and bring them back down to a level similar to younger animals. When this happens, the result is rejuvenation of tissues and the reversal of some of the aspects of aging, making the mice more youthful.

This approach uses an already approved technique known as therapeutic plasma exchange to filter and calibrate these key factors and could be readily modified for human use. Should the results seen in animals translate to humans using this approach, it would have a profound effect on our health as we age and potentially delay, prevent, or even reverse some age-related diseases.

Conclusion

These are only some of the examples of why healthy life expectancy could rise significantly in the near future, and there are plenty of reasons to remain future positive. This is the future direction of medicine and healthcare that we support at Lifespan.io, a world where being 75 does not mean you are thrown on the scrap heap and where people like Emanuel will no longer feel that life has no meaning. I am confident that in such a world, being 75 would not be the burden he thinks it will be, and this is why I hope to be alive at 75.

Steve Hill serves on the Life Extension Advocacy Foundation (LEAF) Board of Directors and is the Editor-in-Chief, coordinating the daily news articles and social media content of the organization. He is an active journalist in the aging research and biotechnology field and has to date written over 500 articles on the topic, interviewed over 100 of the leading researchers in the field, hosted livestream events focused on aging, along with attending various medical industry conferences. His work has been featured in H+ Magazine, Psychology Today, Singularity Weblog, Standpoint Magazine, Swiss Monthly, Keep Me Prime, and New Economy Magazine. Steve has a background in project management and administration, which has helped him to build a united team for effective fundraising and content creation, while his additional knowledge of biology and statistical data analysis allows him to carefully assess and coordinate the scientific groups involved in the project.

Citi Lists Anti-Aging Medicines in Top 10 Disruptive Technologies – Article by Steve Hill

Citi Lists Anti-Aging Medicines in Top 10 Disruptive Technologies – Article by Steve Hill

Comments 0 Comment

Steve Hill

Editor’s Note: The U.S. Transhumanist Party features this article by our guest Steve Hill, originally published by the Life Extension Advocacy Foundation (LEAF) on August 30th, 2018. In this article, Mr. Hill presents Citi’s latest disruptive innovation publication, in which anti-aging medicine is #2 on the list! This is one more example, out of the myriad of examples, of how big of an impact this field is making. One of the reasons Citi considers the development of anti-aging medicines to have a high impact is the fact that “U.S. health spending, which increases significantly with age in concordance with age-related diseases, is expected to exceed ~20% of U.S. gross domestic product (GDP) by 2025.” 

~Bobby Ridge, Assistant Editor, June 27, 2019

Citi has produced another of its Disruptive Innovations publications, which takes a look at what it considers to be the top ten disruptive technologies. It is a sign of the changing times that anti-aging medicines are number 2 in its list.

1. All-Solid-State Batteries
2. Anti-Aging Medicines
3. Autonomous Vehicle Networks
4. Big Data & Healthcare
5. Dynamic Spectrum Access
6. eSports
7. 5G Technology
8. Floating Offshore Wind Farms
9. Real Estate Market Disruptors
10. Smart Voice-Activated Assistants

What was considered fringe science a decade ago is now rapidly becoming a mainstream industry. Our understanding of aging has advanced quickly in the last 10 years, and the tools and innovations seem to come more quickly with each passing year. A variety of therapies that target different aging processes are in development, and some are at fairly advanced stages; if you are interested in their progress, check out the Rejuvenation Roadmap.

Advancing Health by Turning Back Time

The legend of the restorative powers of the Fountain of Youth has fascinated human civilization throughout the generations, dating all the way back to the Greeks (e.g., Herodotus). Other hypothetical conduits for a return to a state of youthfulness (e.g. the Philosopher’s Stone) have featured prominently throughout human civilization as alluring, but equally elusive. Fast forward to 2018, and very recent cutting-edge scientific breakthroughs may, at long last, fundamentally explain why we age. This rapid scientific progress could spawn FDA-approved therapeutics potentially in the next decade, with the primary goal of keeping us younger and alive for longer.

Today, the anti-aging market, while huge (~$200 billion globally), is largely restricted to non-therapeutics (cosmetic products and procedures). At the same time, U.S. health spending, which increases significantly with age in concordance with age-related diseases (see Figure 8), is expected to exceed ~20% of U.S. gross domestic product (GDP) by 2025. Thus, with scientific breakthroughs emerging this decade on the cellular origins of why the tissues in our body’s age, novel anti-aging medicines may become one of the next big disruptions in the healthcare market.

Senolytics are the main focus here, which is logical given that, of all the therapies being developed to combat aging, they are the farthest along in the pipeline. These analysts suggest that we could see senolytics arrive by 2023; while these drugs are only part of the full suite of therapies required to bring aging under medical control, it is likely that we will see senolytics and, perhaps, a few other therapies arrive at that time.

First Senolytic Therapy Could Be Approved by 2023

The first senolytic therapy in clinical trials is a compound by Unity, UBX0101, which is a small-molecule drug that functions by inducing apoptosis (i.e., programmed cell death), specifically in senescent cells. The company is first testing UBX0101 locally in patients with moderate osteoarthritis of the knee, which is a substantially large market (~17 million patients). Initial proof-of-concept data from the Phase 1 trial are expected in the first quarter of 2019. If successful in later clinical development through Phase 3, UBX0101 could become commercially available by 2023.

While speculative given the novelty of the senolytic therapeutic strategy, a successful therapeutic that could resolve osteoarthritic knees and return knee tissue to a more youthful state could have a negative impact on the knee-replacement surgery market (currently projected to grow to >3 million knee replacements per year by 2030). Because other senolytics are being developed for multiple
ophthalmologic (wet AMD, glaucoma, diabetic retinopathy) and pulmonary (COPD, idiopathic pulmonary disease) indications, within the next ~10–20 years patients with a range of age-related diseases may experience a decreased need for therapies now considered standard of care.

UNITY, Siwa, and Oisin are all mentioned in the report. and it is worth having a read, as the section about aging is fairly large and detailed and takes a look at past and present attempts to combat age-related diseases by targeting the aging processes directly.

Conclusion

It is beyond question that progress and interest in the field is growing quickly, and with some therapies now entering human trials, we could be close to a societal tipping point at which more people start to take notice of the potential of new medical approaches. There is a long way to go before we can end age-related diseases, but the tide has turned.

Steve Hill serves on the LEAF Board of Directors and is the Editor in Chief, coordinating the daily news articles and social media content of the organization. He is an active journalist in the aging research and biotechnology field and has to date written over 500 articles on the topic as well as attending various medical industry conferences. In 2019 he was listed in the top 100 journalists covering biomedicine and longevity research in the industry report – Top-100 Journalists covering advanced biomedicine and longevity, created by the Aging Analytics Agency. His work has been featured in H+ Magazine, Psychology Today, Singularity Weblog, Standpoint Magazine, Keep Me Prime, and New Economy Magazine. Steve has a background in project management and administration which has helped him to build a united team for effective fundraising and content creation, while his additional knowledge of biology and statistical data analysis allows him to carefully assess and coordinate the scientific groups involved in the project. In 2015 he led the Major Mouse Testing Program (MMTP) for the International Longevity Alliance and in 2016 helped the team of the SENS Research Foundation to reach their goal for the OncoSENS campaign for cancer research.

 

A Poor Diet May Lead to Dysbiosis and Age-Related Diseases – Article by Steve Hill

A Poor Diet May Lead to Dysbiosis and Age-Related Diseases – Article by Steve Hill

Comments 0 Comment

Steve Hill

Editor’s Note: The U.S. Transhumanist Party features this article by our guest Steve Hill, originally published by the Life Extension Advocacy Foundation (LEAF) on May 27, 2019. This article reminds us of the strong connection between our gut microbiome and ageing, along with a review of a study that provides greater insight into the mechanism of how a poor diet can contribute to age-related diseases.

~ Bobby Ridge, Assistant Editor, June 21, 2019

The role that the gut microbiome plays in aging is increasingly being appreciated in the research world as more evidence arrives to support it. A new publication reviews the various supporting evidence and takes a look at the gut microbiome in the context of poor diets and how they may facilitate the progression of dysbiosis and disease [1].

What is the microbiome?

The microbiome is the varied community of bacteria, archaea, eukarya, and viruses that inhabit our guts. The four bacterial phyla of Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria comprise 98% of the intestinal microbiome.

The microbiome is a complex ecosystem whose activity regulates multiple functions of the gut and also interacts and helps to regulate our immune systems and energy metabolisms. The beneficial bacteria in our guts also help to prevent the growth of harmful bacteria, protect us from invasive microorganisms, and help to maintain the integrity of the intestinal barrier.

As we age, the diversity and numbers of beneficial bacteria tend to decline. There is a strong correlation between decreased microbiome diversity and declining health, and microbiome health has been associated with a number of metabolic conditions, such as type 2 diabetes and obesity. On the other hand, older people who maintain a more healthy gut microbiome tend to live longer and in better health.

We have talked about the role that dysbiosis, the age-related changes to the gut microbiome, plays in the loss of intestinal barrier integrity, which allows bacteria to infiltrate deeper into the body. This is likely to contribute to inflammaging, the chronic, age-related inflammation that drives disease progression and harms tissue regeneration.

Age-related gut dysbiosis is a microbial imbalance in the gut that favors a shift towards proinflammatory microbes and a decline of beneficial microbes, such as those responsible for creating butyrate (and other beneficial short-chain fatty acids), a compound vital for creating the energy that colonocytes and other gut wall cells feed on. These changes lead to chronic inflammation and impair the intestinal barrier, causing it to leak, hence the common name for the condition being “leaky gut” [2].

Abstract

Inflammatory diseases, such as inflammatory bowel diseases, are dramatically increasing worldwide, but an understanding of the underlying factors is lacking. We here present an ecoevolutionary perspective on the emergence of inflammatory diseases. We propose that adaptation has led to fine-tuned host-microbe interactions, which are maintained by secreted host metabolites nourishing the associated microbes. A constant elevation of nutrients in the gut environment leads to an increased activity and changed functionality of the microbiota, thus severely disturbing host-microbe interactions and leading to dysbiosis and disease development. In the past, starvation and pathogen infections, causing diarrhea, were common incidences that reset the gut bacterial community to its “human-specific-baseline.” However, these natural clearing mechanisms have been virtually eradicated in developed countries, allowing a constant uncontrolled growth of bacteria. This leads to an increase of bacterial products that stimulate the immune system and ultimately might initiate inflammatory reactions.

Easily digestible, energy-dense, low-fiber-content foods harm the microbiome

It is known that a diet with easily digestible, energy-dense, low-fiber-content is harmful to health and leads to the formation of visceral fat, the type of fat tissue that is stored deeper than normal belly fat and that forms around your major organs, including the liver, pancreas, and kidneys. Visceral fat also contributes to chronic inflammation and hence to inflammaging, helping to speed up aging and disease progression.

It also appears to influence the gut microbiome and cause changes to the bacterial populations in the gut. The strength of this influence remains to be seen, but its effect on health via changes to the microbiome may be considerable and equally as important as physical activity for health and aging.

Conclusion

This adds yet more fuel to the fire, making it increasingly clear that microbiome health and exercise are the foundations of longer, healthier lives and that we should do all we can now to ensure we achieve both things as part of a personal longevity strategy.

Science is progressing rapidly, especially in the aging field, but this is no reason to be complacent. Science, especially medicine, is, by its nature, complex and can be unpredictable. We all hope that rejuvenation therapies will arrive sooner rather than later, but it is hard to predict when they will be available; this could be in a decade, or it could be longer than we think. For that reason, we should do all we can now to increase our odds of making the cut.

Exercise and balanced diets are relatively low-tech and low-cost approaches to healthy longevity, and everyone in the community should be engaging in these practices if they are serious about living long enough to benefit from the arrival of more robust rejuvenation therapies.

Literature

[1] Lachnit, T., Bosch, T. C., & Deines, P. (2019). Exposure of the Host-Associated Microbiome to Nutrient-Rich Conditions May Lead to Dysbiosis and Disease Development—an Evolutionary Perspective. mBio, 10(3), e00355-19.

[2] Cullender TC, Chassaing B, Janzon A, et al. Innate and adaptiveimmunity interact to quench microbiome flagellar motility in the gut. Cell Host Microbe 2013; 14: 571–81.

Steve Hill serves on the LEAF Board of Directors and is the Editor in Chief, coordinating the daily news articles and social media content of the organization. He is an active journalist in the aging research and biotechnology field and has to date written over 500 articles on the topic as well as attending various medical industry conferences. In 2019 he was listed in the top 100 journalists covering biomedicine and longevity research in the industry report – Top-100 Journalists covering advanced biomedicine and longevity created by the Aging Analytics Agency. His work has been featured in H+ Magazine, Psychology Today, Singularity Weblog, Standpoint Magazine,  Keep Me Prime, and New Economy Magazine. Steve has a background in project management and administration which has helped him to build a united team for effective fundraising and content creation, while his additional knowledge of biology and statistical data analysis allows him to carefully assess and coordinate the scientific groups involved in the project. In 2015 he led the Major Mouse Testing Program (MMTP) for the International Longevity Alliance and in 2016 helped the team of the SENS Research Foundation to reach their goal for the OncoSENS campaign for cancer research.

Study Shows Telomerase Gene Therapy Does Not Increase Cancer Risk – Article by Steve Hill

Study Shows Telomerase Gene Therapy Does Not Increase Cancer Risk – Article by Steve Hill

Comments 0 Comment

Steve Hill

Editor’s Note: The U.S. Transhumanist Party features this article by our guest Steve Hill, originally published by the Life Extension Advocacy Foundation (LEAF) on August 27, 2018. This article takes another step forward toward clearing up a common misconception that many scientists and laypeople hold, i.e., the notion that extending telomeres causes cancer. Mr. Hill cited a recent article published in the journal PLOS Genetics, in which researchers found there to be no increase in cancer, even when telomeres were extended in mice from cancer-prone mouse strains. Hopefully this article will help researchers reevaluate this misconception so this very important age-reversal research will be advanced much faster.

~ Bobby Ridge, Assistant Editor, June 20, 2019

Researchers have demonstrated that telomerase gene therapy does not increase the risk of cancer, even in strains of mice that are particularly susceptible to cancer [1].

A tale of telomeres

Short telomeres trigger cellular senescence and are thought to be one of the primary hallmarks of aging, which has led to various researchers seeking ways to restore the telomeres in order to prevent cells from dying and to encourage division and tissue regeneration. We won’t go over the basics of telomeres and how they influence aging  here, but if you would like to learn more, check out our telomeres article, which explains it all.

Ever since Dr. Maria Blasco and her team at the Spanish National Cancer Research Centre (CNIO) first used telomerase gene therapy in mice back in 2012, a debate has raged about the potential of telomerase for regenerating tissue and reversing some aspects of aging versus the risk of it causing cancer.

Despite the concerns, it has proved effective against infarction by spurring regeneration of cardiac tissue and in treating aplastic anaemia and idiopathic pulmonary fibrosis in mice; all of these conditions are associated with critically short telomeres.

The CNIO’s Telomeres and Telomerase Group, which conducted the new study, has been investigating the potential of using telomerase therapy to treat age-related diseases for many years. Its 2012 publication featured a specially developed gene therapy that used an adeno-associated virus (AAV) to deliver a payload to cells that reactivated the telomerase gene, which can restore lost telomeres by creating the telomerase enzyme, and it appeared to delay and reverse certain aspects of aging [2].

Its AAV therapy is special in that the vectors do not integrate into the genomes of the target cells. Therefore, the telomerase activation only lasts for a few cell cycles before its effects cease. This transient activation of telomerase makes for a safety net, as unlimited cell division is only a step away from cancer.

Abstract

Short and dysfunctional telomeres are sufficient to induce a persistent DNA damage response at chromosome ends, which leads to the induction of senescence and/or apoptosis and to various age-related conditions, including a group of diseases known as “telomere syndromes”, which are provoked by extremely short telomeres owing to germline mutations in telomere genes. This opens the possibility of using telomerase activation as a potential therapeutic strategy to rescue short telomeres both in telomere syndromes and in age-related diseases, in this manner maintaining tissue homeostasis and ameliorating these diseases. In the past, we generated adeno-associated viral vectors carrying the telomerase gene (AAV9-Tert) and shown their therapeutic efficacy in mouse models of cardiac infarct, aplastic anemia, and pulmonary fibrosis. Although we did not observe increased cancer incidence as a consequence of Tert overexpression in any of those models, here we set to test the safety of AAV9-mediated Tert overexpression in the context of a cancer prone mouse model, owing to expression of oncogenic K-ras. As control, we also treated mice with AAV9 vectors carrying a catalytically inactive form of Tert, known to inhibit endogenous telomerase activity. We found that overexpression of Tert does not accelerate the onset or progression of lung carcinomas, even when in the setting of a p53-null background. These findings indicate that telomerase activation by using AAV9-mediated Tert gene therapy has no detectable cancer-prone effects in the context of oncogene-induced mouse tumors.

More support for telomerase gene therapy

Despite this safety measure, the medical use of telomerase therapy has been held back due to concerns of cancer risk, so the researchers at CNIO set out to see if this concern is justified.

To do this, they used this gene therapy in a mouse model that is at high risk of lung cancer. Their results showed that activating the telomerase gene via their gene therapy does not increase the risk of developing cancer, not even in this cancer-prone mouse strain.

These findings suggest that this gene therapy appears to be safe even in a pro-cancer environment. The authors chose this cancer-prone mouse strain to create a “killer experiment”, which creates a worst-case scenario that tests a hypothesis to its limit; if the hypothesis holds true despite the extreme scenario, it shows that the hypothesis is good. Because this therapy did not increase cancer risk in this extremely vulnerable mouse population, it demonstrates that telomerase gene therapy is possibly safe enough to use in humans.

The road ahead

The safety and utility of telomerase therapy is becoming more apparent with each passing year. The purpose of this new study was to demonstrate the plausibility of using telomerase to safely treat many diseases that currently have no cure, such as pulmonary fibrosis, and to help speed up its progress into human clinical trials.

Conclusion

The potential of telomerase gene therapy has long been debated amid cancer concerns, but this experiment suggests that those concerns are unfounded. There is no doubt that telomerase can and does regenerate tissue when it is delivered via gene therapy and that it does reverse various aspects of aging in multiple models.

Can we safely use what some people describe as a double-edged sword and apply it the fight against aging? This experiment strongly suggests that yes, we can.

Literature

[1] Muñoz-Lorente, M. A., Martínez, P., Tejera, Á., Whittemore, K., Moisés-Silva, A. C., Bosch, F., & Blasco, M. A. (2018). AAV9-mediated telomerase activation does not accelerate tumorigenesis in the context of oncogenic K-Ras-induced lung cancer. PLoS genetics, 14(8), e1007562.

[2] de Jesus, B. B., Vera, E., Schneeberger, K., Tejera, A. M., Ayuso, E., Bosch, F., & Blasco, M. A. (2012). Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer. EMBO molecular medicine, 4(8), 691-704.

Steve Hill serves on the LEAF Board of Directors and is the Editor in Chief, coordinating the daily news articles and social media content of the organization. He is an active journalist in the aging research and biotechnology field and has to date written over 500 articles on the topic as well as attending various medical industry conferences. In 2019 he was listed in the top 100 journalists covering biomedicine and longevity research in the industry report – Top-100 Journalists covering advanced biomedicine and longevity created by the Aging Analytics Agency. His work has been featured in H+ magazine, Psychology Today, Singularity Weblog, Standpoint Magazine, and, Keep me Prime, and New Economy Magazine. Steve has a background in project management and administration which has helped him to build a united team for effective fundraising and content creation, while his additional knowledge of biology and statistical data analysis allows him to carefully assess and coordinate the scientific groups involved in the project. In 2015 he led the Major Mouse Testing Program (MMTP) for the International Longevity Alliance and in 2016 helped the team of the SENS Research Foundation to reach their goal for the OncoSENS campaign for cancer research.

Dr. Aubrey de Grey Accelerates His Estimates – Article by Steve Hill

Dr. Aubrey de Grey Accelerates His Estimates – Article by Steve Hill

Comments 0 Comment

Steve Hill

Editor’s Note: In this article, Mr. Steve Hill highlights a recent webinar where Dr. Aubrey de Grey, the Biogerontology Advisor of the U.S. Transhumanist Party / Transhuman Party, revised his projections for the arrival of rejuvenation treatments in a more optimistic direction. This article was originally published by the Life Extension Advocacy Foundation (LEAF).

~ Gennady Stolyarov II, Chairman, United States Transhumanist Party / Transhuman Party, April 16, 2019

On January 28, 2019, we held a webinar with the SENS Research Foundation as part of a new ongoing series of research webinars. During the webinar, we asked Dr. Aubrey de Grey how close we might be to achieving robust mouse rejuvenation (RMR) and robust human rejuvenation, and his answer was somewhat surprising.

RMR is defined as reproducibly trebling the remaining lifespan of naturally long-lived (~3 years average lifespan) mice with therapies begun when they are already two years old.

Dr. de Grey now suggests that there is a 50/50 chance of achieving robust mouse rejuvenation within 3 years from now; recent interviews and conversation reveal that he’d adjusted this figure down from 5-6 years. He has also moved his estimation of this to arrive from around 20 years to 18 years for humans.

So, what is the basis for this advance in schedule? Dr. de Grey is more optimistic about how soon we might see these technologies arrive, as the level of crosstalk between damages appears to be higher than he originally anticipated a decade ago. This means that robust mouse and human rejuvenation may be easier than he previously believed.

We also asked Dr. de Grey which of the seven damages of aging was the most challenging to address. Originally, he thought solving cancer through OncoSENS methods was the biggest challenge in ending age-related diseases. However, intriguingly, he speaks about his enthusiasm for immunotherapy and how it may potentially solve the cancer issue and negate the need for Whole-body Interdiction of Lengthening of Telomeres (WILT), which was always considered a last-resort approach to shutting down cancer.

There are two main components of the WILT approach. The first is to delete telomerase-producing genes from as many cells as possible, as human cancers lengthen telomeres through one of two available pathways, and the second is to avoid the harmful consequences of our cells no longer having telomerase by periodically transplanting fresh stem cells, which have also had their telomerase-associated genes knocked out, to replace losses.

This approach has always been considered extreme, and Dr. de Grey has always acknowledged that this was the case. However, over a decade ago when Dr. de Grey and Michael Rae originally proposed this in the book Ending Aging, immunotherapy was simply not on the radar. Now, there are alternatives to WILT that show true potential and less need for radical solutions, and it is reassuring to see that Dr. de Grey is so enthusiastic about them.

He now suggests that MitoSENS is probably the most challenging to tackle of the seven types of damage in the SENS model of aging. This is no surprise given that DNA and mtDNA damage are highly complex issues to fix.

On that note, we asked Dr. Amutha Boominathan from the MitoSENS team which mitochondrial gene was their next target after they had successfully created nuclear copies of the ATP-6 and ATP-8 genes.

MitoSENS will be launching a new fundraising campaign on Lifespan.io later this year with the aim of raising funds to progress to more of the mitochondrial genes. This time, the aim will be to move the approach to an animal model and demonstrate how it could be used to correct mitochondrial defects.

Finally, if you are interested in getting involved directly with these webinars and joining the live audience, check out the Lifespan Heroes page.

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 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.

Announcing the Longevity Book Club for Lifespan Heroes – Announcement by Javier Noris

Announcing the Longevity Book Club for Lifespan Heroes – Announcement by Javier Noris

Comments 0 Comment

Javier Noris

Editor’s Note: The U.S. Transhumanist Party features this announcement by our cohorts at the Life Extension Advocacy Foundation, originally published on their site on March 19, 2019.  The program helps bring attention to published works promoting the mission of ending age-related diseases, a mission the U.S. Transhumanist Party supports as part of our policy goals.

~ Brent Reitze, Applicant for Director of Publication, United States Transhumanist Party, April 2, 2019

As mentioned in some recent articles, we are increasing our efforts to reward our loyal and invaluable monthly patrons that support us as Lifespan Heroes. We previously mentioned a brand-new, exclusive webinar series for Lifespan Heroes, and we want to take this opportunity to also announce another brand-new initiative that will commence in April.

Introducing the Longevity Book Club for Lifespan Heroes

As special thanks to our Lifespan Hero patrons, we are pleased to announce the launch of our new Longevity Book Club, where you can join other longevity enthusiasts in reading the most interesting works that relate to our mission of ending age-related diseases. You will also get the opportunity to listen to discussion panels and take part in Q&A sessions that are focused on books that touch on these important scientific, philosophical, moral and futuristic longevity topics. This is the ideal place to meet like-minded longevity enthusiasts who are working on building their knowledge on longevity and all of the implications that come with ending age-related diseases.

Our first book circle will be reading Homo Deus: A Brief History of Tomorrow by Yuval Noah Harari, a New York Times best-selling author.

Here is a brief synopsis of the book:

Yuval Noah Harari, author of the critically-acclaimed New York Times bestseller and international phenomenon Sapiens, returns with an equally original, compelling, and provocative book, turning his focus toward humanity’s future, and our quest to upgrade humans into gods.

Over the past century, humankind has managed to do the impossible and rein in famine, plague, and war. This may seem hard to accept, but, as Harari explains in his trademark style—thorough, yet riveting—famine, plague and war have been transformed from incomprehensible and uncontrollable forces of nature into manageable challenges. For the first time ever, more people die from eating too much than from eating too little; more people die from old age than from infectious diseases; and more people commit suicide than are killed by soldiers, terrorists and criminals put together. The average American is a thousand times more likely to die from binging at McDonalds than from being blown up by Al Qaeda.

What then will replace famine, plague, and war at the top of the human agenda? As the self-made gods of planet earth, what destinies will we set ourselves, and which quests will we undertake? Homo Deus explores the projects, dreams and nightmares that will shape the twenty-first century—from overcoming death to creating artificial life. It asks the fundamental questions: Where do we go from here? And how will we protect this fragile world from our own destructive powers? This is the next stage of evolution. This is Homo Deus.

With the same insight and clarity that made Sapiens an international hit and a New York Times bestseller, Harari maps out our future.

We feel this is a good book to get started with, as it’s written in a user-friendly style that can appeal to a broad audience and touches on many topics that are directly or indirectly related to our mission of ending age-related disease. As we progress as a group, we will shift into different categories, including philosophy, genetics, biochemistry, ethics, and many more topics that are of interest to our mission and book club members.

As a Hero, you will have the opportunity to join us for the first of many book discussions and have the opportunity to learn about the fascinating knowledge that these authors have to share with us as well as the deconstructed meanings behind the books as seen by our book club members. We’ll email the connection instructions to our Heroes soon, so please check your inbox for our announcement.

Calling all the Heroes

This year, our plan is to reach out to an even wider audience and engage with them about the need to end age-related diseases. We aim to hire another team member so that we can cover more news stories, buy new equipment, produce more films with popular Youtube channels, launch a two-day conference in NYC, and do more online shows, including this new webinar series.

However, to do this, we need your help.

We are very grateful for the support of our monthly patrons, the Lifespan Heroes, and we are asking you to consider joining them today in order to help us achieve our ambitious goals for 2019.

By becoming a Lifespan Hero, you become a monthly patron and can change or halt your contributions at any time. In return for your support, you get access to the Heroes’ private Discord channel, enjoy discounts on our event tickets, get early access to conference videos and live access to webinars, and receive regular reports on our progress and future plans.

Please consider becoming a Lifespan Hero today. We look forward to seeing you at the MitoSENS webinar and our Longevity Book Club meetings.

A Biohacker’s Letter to Santa – Article by Elena Milova

A Biohacker’s Letter to Santa – Article by Elena Milova

Comments 1 comment

Elena Milova

Editor’s Note: Happy Holidays! If Santa Claus were real, life extension would be the greatest gift that he could possibly give. Elena Milova convincingly illustrates why in this letter, originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Gennady Stolyarov II, Chairman, U.S. Transhumanist Party, December 21, 2018

Dear Santa,
My name is Elena Milova, and I am from Moscow, Russia. I am a science popularizer, biohacker, and public health advocate in the field of aging and longevity. I am 39, single, and without children, but if you think that I am reaching out to you to ask for a CRISPR-designed baby, I am not. I believe that this type of wish is rather in the pile of letters from China. I am not asking you for a particular health improvement, as one could not wish for a better HOMA-IR (mine is 0.40, because I greatly reduced fast carbs) or total cholesterol level (below 4 mmol/L). I am fine without a new smartphone, too.

The thing that I am going to ask you for is much more tricky to get. I want everyone on Earth to realize that biological aging is amenable to medical intervention and that treatments targeting various mechanisms of aging are already in human clinical trials. 7.6 billion minds, one idea. That is my only wish.

Why this is so important to me

You have probably noticed yourself that your clientele is changing over time. There are more and more people over 60 in the world, and I assume that the number of wishes for recovery from this or that age-related disease are spiking higher every year. This must be a problem for you, as for many diseases of old age, there is still no effective treatment that would actually help to cure people. It must be frustrating to not be able to fulfill a sincere wish of a good person, especially when a child asks for her grandparents to recover so that they can walk and throw snowballs together.

Source: United Nations, Department of Economic and Social Affairs, Population Division (2017). World Population Prospects 2017 – Data Booklet (ST/ESA/SER.A/401)

By 2050, the elderly will be a quarter of the global population, and these people will likely be suffering from several chronic diseases at once, gradually losing their health, independence and dignity. For so many people, being a burden on their families because of their deteriorating health is unacceptable, which is why the number of suicides in this age group is so high.

Is aging an invisible problem?

The numbers of these voluntary deaths are very upsetting, but what is even more upsetting is that diseases of old age are the major cause of death worldwide and aging kills around 100,000 people every day. This is the population of a small city. Imagine what would happen if everyone in a city like Cambridge, Massachusetts were to die in one day. I bet that there would be a lot of media attention and that thousands of experts would be on television discussing the potential causes of death and ways of preventing this tragedy in the future. Let’s say that the next day, another city becomes deadly peaceful. Take the Russian city of Domodedovo, which has its own airport. Everyone dead. People in neighboring cities would probably be frightened, and some charismatic politicians would be trying to calm down the public and promising to do something about all these deaths. The next day, this happens to yet another city, maybe in India. Then another one in Australia. It would not take long before G20 would set up an urgent conference call to set up an international commission and allocate money and scientists to investigate and solve the problem.

                                                                                                                                              Source: WHO website

Guess what? This type of thing never happens in relation to aging, because people dying from it are spread around the globe, so the disaster does not make the headlines. The public only notices the problem when an actor, scientist, or other significant public figure dies from an age-related disease – most often heart disease, stroke, or cancer. Do you want an example? “Santa Claus, age 90, dies from a heart attack: a critical blow to the industry of giftmaking.”

Sorry, sorry. I didn’t mean to scare you, but you get the point, right? From looking at your pictures, I could suspect that you might have some minor problems with glucose metabolism, but your extensive physical activity during gift delivery should be compensating for that, so you should be fine. For other people aged 60 and older, aging is an ever-increasing problem. Here, we come to the other important issue.

What is aging? How it can be addressed?

You see, aging is the accumulation of damage that happens due to normal bodily functions. This damage builds up over time, normal cell functions erode, and, at some point, this leads to the manifestation of age-related diseases. Normal operations, damage accumulation, disease, more damage, aggravation of disease, death. Simple.

It turns out that at the beginning of this century, British scientist Aubrey de Grey published an article in which he described several types of damage done by aging. He suggested the heretical idea of targeting these damages with medical interventions instead of trying to cure the symptoms of each age-related disease. He argued that age-related diseases are only a consequence of damage accumulation and that it would be much more effective to address the root causes.

The seed that Dr. de Grey dropped into the fertile soil of scholarship produced nice fruit in 2013, which is when a group of famous researchers of aging published The Hallmarks of Aging, a paper in which they described nine types of damage that accumulate with age and could be made into new therapeutic targets.

Comparison of a mouse treated with senolytics (at right) and a same-age mouse of the control group (at left). Source: Baker, D. J., Childs, B. G., Durik, M., Wijers, M. E., Sieben, C. J., Zhong, J., … & Khazaie, K. (2016). Naturally occurring p16Ink4a-positive cells shorten healthy lifespan. Nature, 530(7589), 184.

There were other fruits as well: animal studies have definitively proven that even only addressing one type of damage can extend the healthy period of life, postpone age-related diseases, keep animals more active, and, as a positive side effect, extend lifespan. It is worms that hold the best record so far, as tweaking some of their longevity-related genes has allowed them to live 10 times longer. The results in mice are also impressive – the researchers can extend both their healthy period of life and lifespan by 30-35%. Honestly, I find myself jealous of these mice, sometimes. I would not mind adding another 30% of youthful and healthy years to my life, even if I would have to take some pills or get some regular injections.

Can we control aging in humans?

You see, Santa, where I am going with this. I am sure that you sometimes leave gifts under the trees of people who work for the FDA. Accumulating a critical mass of knowledge about interventions against murine aging made it possible to develop the same type of interventions for people. Now, drugs and therapies addressing some of the root mechanisms of aging are in official human clinical trials. At some point, some of these trials will be successful, and drugs and therapies targeting aging itself will come to market.

If you don’t believe me, here is the short list of people whose chimneys’ stacks are the best source of additional information on the topic: George Church, Anthony Atala, Judy Campisi, Vadim Gladyshev, Maria Blasco, Michael West, Vera Gorbunova, Irina Conboy, Kelsey Moody, Brian Kennedy, Linda Partridge, Alexey Moskalev, Cynthia Kenyon, Claudio Franceschi, Alex Zhavoronkov, Nir Barzilai, and, of course, Aubrey de Grey. He wears a great beard, so you have more in common with gerontologists than you would think.

Listen to these people tell their families about their research, and you will get my point. We are on the edge of a revolution in rejuvenation biotechnology. Yet, most people don’t know about it and don’t realize what kind of potential benefit this advancement holds for them and for our aging society as a whole. Most importantly, as they know nothing, they have no say in decision making. How can people possibly speed up the pace of aging research if they don’t realize that aging is amenable to intervention? How can they foster technology transfer and local production of the cures for aging, such as senolytics, in their countries? How can they control prices and make future distribution and access equal? How can they ensure that old people in their families, who need these new treatments the most, would get them sooner?

Knowledge is power. We hear this in almost every interview, and you should be hearing it every Christmas from the researchers of aging, too. They have golden brains; the only thing they need is an appropriate amount of funding to solve the problem of aging more quickly. A strong public movement for aging research could be a game changer and could act as leverage to allocate government funding towards researching and developing treatments that target the underlying mechanisms of aging.

Ending aging and age-related diseases is possible

It is obvious that you are a kind person, Santa. You are perceptive and generous; you know what people want, and you try to give them what they want. However, if you don’t help me with my information campaign, in a couple of decades from now, you will be delivering billions of adult diapers and wheelchairs all over the globe. Wouldn’t it be nicer if you were to pile these up in your warehouse to be covered in dust while you give people therapies and drugs that prevent aging and wipe age-related diseases out of human lives? Just imagine how much happier people would be if they could remain healthy and independent, enjoy full and productive lives, achieve more, and stay with their families and friends for longer.

I was a good girl the whole year, attending scientific conferences, interviewing researchers, speaking at public events, and supporting our partners and colleagues in every way I could, even if that much socializing makes me suffer from an introvert’s hangover. I was eating healthy food and promoting evidence-based means to slow down aging among my relatives and friends. I deserve a nice Christmas gift.

All you have to do is to let everyone on the planet know that aging is amenable to intervention and that treatments addressing the root causes of aging are currently being created. For real. That would make me the happiest creature on the planet. Thank you in advance!

Sincerely, Elena

Instead of a conclusion

I am 39 years old, and I am an agnostic. There is not much evidence that Santa Claus exists. However, I do believe that miracles happen: the miracles that we create with our own hands. You who are reading these words (thanks for getting this far, by the way!) possess this special power, too. Use it! Let people around you know that science is close to bringing aging under medical control, and let’s build a world where healthy longevity for everyone is a reality.

As a devoted advocate of rejuvenation technologies since 2013, Elena Milova is providing the community with a systemic vision how aging is affecting our society. Her research interests include global and local policies on aging, demographic changes, public perception of the application of rejuvenation technologies to prevent age-related diseases and extend life, and related public concerns. Elena is a co-author of the book Aging prevention for all (in Russian, 2015) and the organizer of multiple educational events helping the general public adopt the idea of eventually bringing aging under medical control.

Aubrey de Grey – Clinical Trials in Five Years – Interview by Laura Sanz Olacia

Aubrey de Grey – Clinical Trials in Five Years – Interview by Laura Sanz Olacia

Comments 0 Comment

logo_bgLaura Sanz Olacia
Aubrey de Grey

Editor’s Note: In this interview originally published by our allies at the Life Extension Advocacy Foundation (LEAF), Laura Sanz Olacia discusses with Dr. Aubrey de Grey his anticipation that treatments aimed at reversing biological aging may enter clinical trials within five years. The U.S. Transhumanist Party is pleased to feature these insights from Dr. de Grey. 

~ Gennady Stolyarov II, Chairman, United States Transhumanist Party, December 18, 2018

 

In November, Dr. Aubrey de Grey, a graduate of the University of Cambridge, was in Spain to attend the Longevity World Forum in the city of Valencia, and he gave a press conference organized by his friend, MIT engineer José Luis Cordeiro.

Dr. Aubrey de Grey is the scientific director (CSO) and founder of the SENS Research Foundation. In Madrid and Valencia, Dr. de Grey reaffirmed for Tendencias21 one of his most striking statements of 2018: “In the future, there will be many different medicines to reverse aging. In five years, we will have many of them working in early clinical trials.”

The Longevity World Forum is a congress on longevity and genomics in Europe. It is heir to the first congress in Spain, the International Longevity and Cryopreservation Summit, which was held at the CSIC headquarters in Madrid in May 2017, and Dr. de Grey also participated in that event. In Valencia, his presentation was recieved with interest, and Dr. de Grey explained to this select audience that aging will be treated as a medical problem in the near future. Rather than treating its symptoms using the infectious disease model, the root causes of aging will themselves be treated.

It was published recently on longevityworldforum.com that a therapy to reverse aging will be a reality within five years. What will be its mechanism of action, roughly?

There will not be just one medicine; there will be a lot of different medicines, and they will all have different mechanisms of action. For example, some of them will be stem cells, where we put cells back into the body in order to replace cells that the body is not replacing on its own. Sometimes, they will be drugs that kill cells that we don’t want. Sometimes, they will be gene therapy treatments that give cells new capabilities to break down waste products, for example. Sometimes, they will be vaccines or other immune therapies to stimulate the immune system to eliminate certain substances. Many different things. In five years from now, we will probably have most of that working. I do not think that we will really have it perfect by then; probably, we will still be at the early stages of clinical trials in some of these things. Then, we will need to combine them, one by one, to make sure that they do not affect each other negatively. So, there will still be some way to go. But, yes, I think it’s quite likely that in five years from now, we will have everything, or almost everything, in clinical trials.

Then clinical trials for seven years until it’s perfected. Don’t clinical trials usually take a long time?

It depends. For example, in aging, because there is this progressive accumulation of damage, you could have therapies that slow down the rate at which damage accumulates, or you could have therapies that repair the damage that has already happened. The second type of therapy is what we think is going to be most effective and is going to be easiest to do, and you can see results from that very quickly, like in one or two years. Now, of course, you still want to know what happens later on, but the first thing is to determine whether this is working at all, and as soon as it starts to work, then you can start to make it available. Clinical trials are changing in that way. Historically, clinical trials had to be completed before anybody could get these drugs, but now we are getting new policies; there is a thing called adaptive licensing, which is becoming popular in the US and elsewhere, where the therapy becomes approved at an earlier stage, and then it’s monitored after that.

Beyond the humanitarian perspective of avoiding the pain and suffering that comes with old age, if increasing the years of healthy life in people will significantly reduce health care spending by governments, why don’t they promote research in this area?

You’re absolutely right. It’s quite strange that governments are so short-sighted. But, of course, the real problem is psychological: it’s not just governments that are short-sighted. Almost everybody in the world is short-sighted about this. The reason I believe why that’s true is people still can’t quite convince themselves that it’s going to happen. Since the beginning of civilization, we have known that there is this terrible thing called aging, and we have been desperate to do something about it, to get rid of it. And people have been coming along, ever since the beginning of civilization, saying, “Yes, here’s the solution, here’s the fountain of youth!” And they’ve always been wrong. So, when the next person comes along and says they think they know how to do it, of course, there is going to be some skepticism until they have really shown that it’s true. Of course, if you don’t think it’s going to work, then you’re not going to support the effort financially. It’s very short-sighted, but it’s understandable.

Why do you think that the pharmaceutical industry does not devote its research and development efforts to this area, which causes the death of 100,000 people every day?

Today, the pharmaceutical industry is geared toward keeping old people alive when they are sick. It makes its money that way. It’s not just the pharmaceutical industry, it’s the whole of the medical industry. And so, most people say that they are worried that maybe the pharmaceutical industry will be against these therapies when they do come along. I don’t think that’s true at all. I think they will be in favor because people will be in favor, but people are not really in favor yet. People don’t really trust preventive medicine. They think “Okay if I am not yet sick…” They don’t trust medicine in general; they know that this is experimental. So, when they are not yet sick, they think “Well, I’ll wait until I am sick,” but we can change that. Eventually, people will understand that it’s going to be much more effective to treat yourself before you get sick, and then the whole medical industry will just respond to that; they will make the medicines that people want to pay for.

So you don’t think that they will be against these therapies?

No. They will follow.

But now, they are not focusing their research into this field.

That’s right because they don’t need to. The big pharmaceutical companies don’t really do much of their own research in the first place. They just wait to see what happens, and then they buy small companies.

In the car analogy that you use, you say that a car is built to last 10 or 15 years, but with proper maintenance, it can last up to 100 years. Isn’t this expressing the idea that aging is programmed and that the life of a car is also programmed?

No, it’s not. All of you know that, a long time ago, Henry Ford invented a concept called planned obsolescence, which was a way of building a car so that you could predict pretty accurately how long it would last. But, of course, the only reason that the prediction works is because people are lazy, and they don’t mind replacing their cars, so they only do the minimum amount of maintenance that the law tells them to. The reason that some cars last 100 years is not because those cars were built differently, it’s because there are a few people out there who fall in love with their cars and they don’t want them to get old. So, it really is exactly the same. In the human body, we have aging, because there are certain types of damage that are not automatically repaired when they happen. Of course, many types of damage in the human body are repaired automatically when they happen, so we don’t need medicine for that, but some of them are not. So, if we can develop medicines that do fix those things, it’s exactly the same as with a car.

If aging is not programmed, why do different species have different lifespans?

Because they have different qualities of built-in repair machinery. When I talk about all these types of damage, they are the types of damage that accumulate in the body, and they accumulate because the body does not have ways to repair them. There are massive amounts of other types of damage that I don’t call damage, and the reason I don’t call them damage is because they don’t accumulate. The reason that they don’t accumulate is because we already have built-in machinery to repair them when they happen. So, long-lived species have more comprehensive automatic repair machinery built into them.

Do you think that first we can focus on just replacing organs and restoring their function, and eventually we can eliminate the root causes of aging? Once we reach longevity escape velocity, maybe we can focus on just eliminating it?

We will never be able to stop the body from creating this damage. The body is going to do that because it is intrinsic to metabolism, but the better we get at repairing the damage, the fewer problems we have.

What healthy habits do you follow now?

I don’t do healthy habits. I’m lucky, I don’t need to do anything; I can drink whatever I like and nothing happens. I don’t even do much exercise, and also I don’t get nearly enough sleep, which is probably shortening my life, but it is worth it because I am hastening the defeat of aging, so it is a net positive.

Which generation will live to be a thousand years old? Do you think it is born already?

I think it is very probably born already, yes. But, of course, we cannot know until we get the medicines.

Which country do you think is more aware, or the people is more aware that this is a problem that we need to fix?

I would say Russia.

Russia?

Yeah. Surprising, isn’t it? But when I go to Russia and I talk about all of this, it’s so wonderful; I don’t get any of the uninformed questions, and everyone seems to understand it.

They don’t ask you ethical questions?

That’s right, yeah. They understand that this is a medical problem, it needs to be fixed, and it can be fixed.

Kriorus [the first and only cryonics company in Eurasia] is there right?

Yeah, I know Kriorus, I know the people very well.

Alcor [the world leader in cryonics located in Arizona] is the most expensive.

It gives the best service. I mean, it makes sense to have a very expensive, high-quality service and also less expensive and lower quality service. That is normal.

Where are you currently living?

I live in the United States, but I go everywhere when I am invited to speak and so on.

Laura Sanz Olacia, has a degree in Pharmacy from the Complutense University of Madrid (2015). Between 2016 and 2017 she worked for nine months in different pharmacies in London. She also worked in a pharmacy laboratory compounding medicines and cosmetics in Madrid. More recently she worked in IQVIA as Data Management Analyst. She is very interested in research and, in particular, in the area of ​aging. During her stay in London, she participated in the organization of the Antiaging Conference London 2016, and back in Madrid, she collaborated closely with the organizing committee of the International Longevity and Cryopreservation Summit 2017. She wants to devote her career to doing research in this field.

Andrés Grases Interviews U.S. Transhumanist Party Chairman Gennady Stolyarov II on Transhumanism and the Transition to the Next Technological Era

Andrés Grases Interviews U.S. Transhumanist Party Chairman Gennady Stolyarov II on Transhumanism and the Transition to the Next Technological Era

Comments 0 Comment

logo_bgGennady Stolyarov II
Andrés Grases

Andrés Grases, the publisher of the Transhuman Plus website (http://transhumanplus.com/) interviews U.S. Transhumanist Party Chairman Gennady Stolyarov II at RAAD Fest 2018 in San Diego, CA, on September 23, 2018. During the course of this conversation, both the contemporary state of transhumanist politics and future directions are covered – along with the challenges to reforming the educational system, the need to create open access to academic works, the manner in which the transition toward the next era of technologies will occur, the meaning of transhumanism and its applications in the proximate future – including promising advances that we can expect to see during the next several years.

Watch the video here.

Become a member of the U.S. Transhumanist Party for free, no matter where you reside. Apply online here in less than a minute.

Choose Your Own Story – by Nicola Bagalà

Choose Your Own Story – by Nicola Bagalà

Comments 0 Comment

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.

Katrin Brunier Art Gallery Opens, Featuring Transhumanist-Oriented Art in Support of Medical Research

Katrin Brunier Art Gallery Opens, Featuring Transhumanist-Oriented Art in Support of Medical Research

Comments 0 Comment

logo_bg

There is a new venue for transhumanist art, whose purchasers and collectors can simultaneously aid in supporting medical research. The Katrin Brunier gallery, an ethical investment-grade art gallery for the Neo-Renaissance Era, was launched on May 18, 2018, by U.S. Transhumanist Party member Dr. Laura-Katrin Brunier (Laura Katrin Weston). You can view some of the available artworks here and here.

Proceeds from sales will support Lifespan.io / Life Extension Advocacy Foundation and Turtlesoup Films conservation.

Statement from Katrin Brunier:

“At katrinbrunier we believe that Art should play its part in shaping a better world for future generations. Our clients share these ideals, which is why we wanted to create an ethical option for investors, collectors, clients and gallery owners alike. Proceeds from sales support conservation charities and fund medical research. All materials are ethically sourced or Fairtrade where possible.

Our artworks are all from notable up and coming players in abstraction, and focus on themes of human advancements in pioneering knowledge, trans-humanism, unconditionality, our place in the universe, sensory perception and the neo-renaissance.”

Dr. Laura Katrin Weston took part in the U.S. Transhumanist Party’s Discussion Panel on Art and Transhumanism on November 18, 2017. To find out more about her ideas and work as an artist, watch her conversation with other artists and life-extension advocates here.

Boosting Bone Healing Using a Key Protein – Article by Steve Hill

Boosting Bone Healing Using a Key Protein – Article by Steve Hill

Comments 0 Comment

Steve Hill

Editor’s Note: In this article, Mr. Steve Hill highlights research on selective bone regeneration using a protein called Jagged-1. This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, March 7, 2018

Today, we would like to highlight a recent study in which researchers show a way to selectively accelerate bone regeneration. They have achieved this by delivering Jagged-1 to injuries instead of the bone morphogenetic proteins (BMPs) that have been traditionally used.

What is Jagged-1?

Jagged-1 is an osteoinductive protein that activates the Notch signaling pathway, which regulates bone healing at the site of injury. Osteoinduction is the process by which osteogenesis is induced.

Osteoinduction involves recruiting immature cells and stimulating them to change into preosteoblasts. In a bone healing situation, such as during a fracture, the majority of bone healing depends on osteoinduction.

The new technique avoids the issues of inappropriate or excessive bone growth because, unlike BMPs, it targets osteoinductive mechanisms that are more directly associated with the regenerative process.

Testing their hypothesis

The researchers led by Kurt Hankenson, D.V.M., Ph.D., a professor of orthopedic surgery at Michigan Medicine, hypothesized for some years that by binding Jagged-1 to a biomaterial structure and delivering it to the site of injury, it could improve healing of the bone.

The published study results confirm this to be the case [1]. Mice and rats that were given Jagged-1, applied using a wet collagen sponge, saw improvements to both femoral and skull injuries. In contrast, the rodents treated with BMPs benefited but also experienced problematic bone hypertrophy, which is also observed in humans using BMPs.

The findings of this study suggest that the use of Jagged-1 for location-specific bone injury could potentially be developed into a therapy to help people recover from fractures and broken bones.

Conclusion

The use of signal molecules rather than drugs to encourage tissue regeneration is likely to increase in popularity in the coming years as the process becomes increasingly refined. This study is yet another example of how researchers are exploring the use of signalling molecules produced naturally in the body as an alternative to drug approaches, which can often have unwanted side effects. It should prove interesting to see how this approach develops in the next few years.

Literature

[1] Youngstrom, D. W., Senos, R., Zondervan, R. L., Brodeur, J. D., Lints, A. R., Young, D. R., … & Loomes, K. M. (2017). Intraoperative delivery of the Notch ligand Jagged-1 regenerates appendicular and craniofacial bone defects. NPJ Regenerative medicine, 2(1), 32.

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 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.

Dentists May Soon Regenerate Teeth Using GSK3 Antagonists – Article by Steve Hill

Dentists May Soon Regenerate Teeth Using GSK3 Antagonists – Article by Steve Hill

Comments 0 Comment

Steve Hill

Editor’s Note: In this article, Mr. Steve Hill explains a teeth-regeneration technique that works by activating the stem cells that reside in the dental pulp of teeth. The technique has the potential to translate to other tissues to help encourage regeneration. This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, March 6, 2018

What if I told you that we could regenerate our teeth? Well, that may soon be a possibility thanks to new research showing that teeth can be encouraged to regrow. Rather than drilling holes into teeth and plugging them with artificial fillers, dentists in the near future may be able to rebuild your teeth with a new technique.

Stimulating stem cells

Professor Paul Sharpe, a scientist based at King’s College in London, and his team have found a way to do just this in mice. They published a study last year that described this new approach [1].

The researchers wanted to increase the natural ability of teeth to repair themselves by activating the stem cells that reside in the dental pulp of teeth. They knew that previous research showed that the wnt signaling pathway is a key pathway for stem cell activity in many parts of the body, and they wanted to see if it works the same way in teeth.

The researchers believed by that using drugs to stimulate the wnt pathway, they could increase stem cell activity in teeth and boost their regenerative potential significantly. Normally, this level of regeneration is only seen in animals like starfish and salamanders, but the researchers wanted to see if we can benefit from the same regenerative capacity.

To see if this would work, the team drilled holes into the molar teeth of mice to simulate dental cavities. Next, they exposed collagen sponges (the same protein found in the dentin in teeth) to a variety of drugs known to stimulate the wnt pathway. Then, they placed these sponges into the cavities and sealed them in for between 4 to 6 weeks.

After this time, the researchers saw that the teeth exposed to these sponges had created a lot more dentin than the control mice and mice given typical dental fillers. The researchers observed that this was essentially a full repair and, in most cases, the teeth of the mice were as good as new.

The next step towards clinical trials

Since then, the researchers have tested the technique on rats, which have considerably larger teeth than mice, making them the logical next step. The research team report that the therapy worked equally well on the rats as it did in the mice in the original study; however, the data is yet to be published.

The researchers are now screening their drug candidates to identify the most effective of the wnt-stimulating drugs. They are also adapting the technique to work with modern dental practices by injecting a gel containing the drug into a dental cavity and hardening it using a UV light to seal it in. This is similar to how dentists currently seal and repair teeth, so this technique would be easy to incorporate into dental practice.

Literature

It will be several years before this enters human clinical trials, but the results so far are promising, and the process may be quicker than normal because a number of the candidate drugs are already approved for human use. The arrival of this technique will revolutionize dentistry and is a great step forward for regenerative medicine in general.

Such techniques have the potential to translate to other tissues to help encourage regeneration, so it is also relevant to aging research. We look forward to more developments from this team in the future.

References

[1] Neves, V. C., Babb, R., Chandrasekaran, D., & Sharpe, P. T. (2017). Promotion of natural tooth repair by small molecule GSK3 antagonists. Scientific reports, 7, 39654.

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 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.

Exosome Therapy Repairs Stroke-Damaged Brain Tissue – Article by Steve Hill

Exosome Therapy Repairs Stroke-Damaged Brain Tissue – Article by Steve Hill

Comments 1 comment

Steve Hill

Editor’s Note: In this article, Mr. Steve Hill explains a new therapy that uses exosomes to repair damaged brain cells. The human trials are intended to begin in the year 2019. This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, March 5, 2018

Today, we wanted to highlight more progress in a rapidly advancing area of medicine and talk about a new study that uses an exosomes-based approach for stroke treatment that repairs brain tissue.

A stem cell-based approach to treating stroke

Professor Steven Stice from the University of Georgia (UGA) and Nasrul Hoda of Augusta University led the team that developed AB126, a treatment that uses a type of extracellular vesicle known as an exosome [1]. Exosomes are small fluid-filled structures that are created by stem cells and, in the case of AB126, are produced by human neural stem cells.

Essentially, the researchers are isolating the beneficial signals given out by stem cells and using them rather than the stem cells as a therapy. This makes sense, as other cells react to these signals and change their behavior accordingly. We have talked about the therapeutic potential of extracellular vesicles, particularly exosomes, in a previous article.

An exosome can remain hidden in the bloodstream, carry multiple doses, and store and administer treatment, and its small size allows it to cross barriers that cells cannot. This is ideal for delivering therapies to the brain, as it crosses the blood-brain barrier and other checkpoints in the body.

After the administration of AB126,  the researchers used MRI scans to assess brain atrophy rates in an animal model of stroke. The scans showed around 35 percent decrease in the size of injury and a 50 percent reduction in brain tissue loss. These results were also replicated by Franklin West, associate professor of animal and dairy science at UGA, in a pig model of stroke.

Within days, the researchers observed improved mobility, better balance, and measurable behavioral benefits in treated animal models of stroke.

Based on the successful results of these preclinical tests, the next step is to take this therapy to human clinical trials by 2019 via ArunA Biomedical, a UGA startup company. The company plans to expand its scope beyond stroke, and preclinical studies in epilepsy, traumatic brain, and spinal cord injuries begin later this year.

Conclusion

This is another example of the recent interest in using extracellular vesicles, such as exosomes, as therapies rather than stem cells themselves. Multiple research groups are now developing these therapies to treat various age-related diseases, so we can almost certainly expect to hear more in the near future.

The use of extracellular vesicles also holds the promise of being more cost-effective from the point of view of storage, logistics, manufacture, and delivery. With the first clinical trials now in the cards for the near future, it will be interesting to see how this develops in the next few years.

References

[1] Webb, R. L., Kaiser, E. E., Scoville, S. L., Thompson, T. A., Fatima, S., Pandya, C., … & Baban, B. (2017). Human Neural Stem Cell Extracellular Vesicles Improve Tissue and Functional Recovery in the Murine Thromboembolic Stroke Model. Translational stroke research, 1-10.

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 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.

Gene Cocktail Helps Hearts to Regenerate – Article by Steve Hill

Gene Cocktail Helps Hearts to Regenerate – Article by Steve Hill

Comments 0 Comment

Steve Hill

Editor’s Note: In this article, Steve Hill explains a technique that enables significant human tissue regeneration, so that it becomes possible to repair damaged human hearts. This technique can also be potentially applied to other body organs.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, March 4, 2018

The human heart is an organ whose cells rarely divide, making tissue repair and regeneration a huge problem following a heart attack. Many animals, such as zebrafish and salamanders, are different; they can regenerate damaged hearts easily.

As humans, we also once had the same regenerative capacity during our early development, but after we were born, we lost this ability. This is also true for many other organs, including the brain, spinal cord, and pancreas. The cells in these tissues divide very rarely if at all, and this is a big problem. But, what if we could get that regenerative ability back and repair damage to our hearts the way these amazing animals do?

Researchers have been trying for decades to find out how we can enjoy the same tissue regeneration, but they have met with limited success—until now.

Unlocking cell division in cardiomyocytes

A research team led by Dr. Deepak Srivastava, president of the Gladstone Institutes, has finally achieved this long sought-after goal in a study published in the journal Cell [1]. The researchers have developed an efficient and reliable way of making non-dividing adult cardiomyocytes divide so that they can repair damaged hearts.

They identified four genes that regulate cell division in adult cardiomyocytes. When all four of them are combined together, they cause the cardiomyocytes to re-enter the cell cycle and start dividing quickly. They also demonstrated that following heart failure, these combined genes improve cardiac function significantly.

The researchers tested the technique in animal models using cardiomyocytes derived from human stem cells. They stained newly divided cells with a special dye in order to track them; they found that between 15 to 20 percent of the cells divided and remained alive thanks to the four-gene combo. This is a vast improvement on previous studies, which have only managed around 1 percent cell division in adult cardiomyocytes.

The team also made the technique simpler by identifying drugs that could replace two of the four genes involved in the combination. This still produced the same result as using all four genes and is significantly easier, logistically speaking.

Could be used in multiple tissues

As mentioned, the heart is not the only tissue that has cells that either do not divide or do so very slowly. The researchers believe that their technique could also potentially be applied to encourage other tissues and organs to regenerate. This is because the four genes are not unique to the heart and are found in other cells around the body.

If science can unlock the same regeneration in nerve cells, pancreatic cells, and retinal cells, this could be the basis of therapies for heart failure, brain damage, diabetes, blindness, and many other conditions. The good news is these four genes encourage cell division the same way in mice, rats, and human cells.

Conclusion

Manipulating non-dividing cells and returning them to the cell cycle to boost regeneration in organs and tissues holds great potential. Scientists have been working for decades to achieve this in the heart, and now it has been achieved. The next big step is to translate this approach to humans, and we wish them the very best in their future research.

Literature

[1] Mohamed, T. M., Ang, Y. S., Radzinsky, E., Zhou, P., Huang, Y., Elfenbein, A., … & Srivastava, D. (2017). Regulation of Cell Cycle to Stimulate Adult Cardiomyocyte Proliferation and Cardiac Regeneration.

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 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.

New FDA Regenerative Medicine Framework is Win-Win for Gene Therapies – Article by Keith Comito and Elena Milova

New FDA Regenerative Medicine Framework is Win-Win for Gene Therapies – Article by Keith Comito and Elena Milova

Comments 0 Comment

Elena Milova
Keith Comito

Editor’s Note: In this article, Keith Comito and Elena Milova positively discuss new a FDA regulatory framework on RMAT (regenerative medicine advanced therapies) and on how it benefits the healthy-life-extension community. This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, March 3, 2018

Back in November 2017, the FDA announced a comprehensive policy framework for the development and oversight of regenerative medicine products, including novel cellular therapies. Both draft guidance documents had 90-day comment periods, and we at LEAF joined forces with the Niskanen Center to submit comments to the FDA to ensure that the voice of the community for healthy life extension was heard. These new regulations could have considerable implications for the therapies and technologies being developed as part of the biomedical gerontology field.

The first draft guidance addresses how the FDA intends to optimize its regulatory requirements for devices used in the recovery, isolation, and delivery of RMATs (regenerative medicine advanced therapies), including combination products.

The second document explains what expedited programs may be available to sponsors of regenerative medicine therapies and describes what therapies may be eligible for RMAT designation.

According to new FDA regulations, a drug is eligible for designation as an RMAT if:

  • The drug is a regenerative medicine therapy, which is defined as a cell therapy, therapeutic tissue engineering product, human cell and tissue product, or any combination product using such therapies or products, except for those regulated solely under Section 361 of the Public Health Service Act and part 1271 of Title 21, Code of Federal Regulations;
  • The drug is intended to treat, modify, reverse, or cure a serious or life-threatening disease or condition; and
  • Preliminary clinical evidence indicates that the drug has the potential to address unmet medical needs for such disease or condition

We hope that this joint project will support the improvement of US regulations that concern these innovative treatments and will make the overall regulatory landscape more friendly. Below, we cite the most important notes from our resulting paper.

Last week, the Niskanen Center joined with the Life Extension Advocacy Foundation in filing comments to the Food and Drug Administration (FDA), offering our support for the agency’s new regenerative medicine advanced therapy (RMAT) designation draft guidance for industry.

Although there are opportunities for marginal improvements to the guidance, and FDA approval processes more generally, we are happy to see that the agency chose to include gene therapies in its interpretation of what qualifies as a regenerative medicine therapy.

Under section 3033 of the 21st Century Cures Act, the FDA was tasked with developing an accelerated approval process for regenerative advanced therapies. Such therapies would qualify for expedited review and approval so long as the drug (a) met the definition of a regenerative medicine therapy, (b) was “intended to treat, modify, reverse, or cure a serious condition,” and (c) “has the potential to address unmet medical needs” for a serious disease or condition. Unfortunately, the bill’s definition of a regenerative medicine advanced therapy was unclear on whether gene therapies, in particular, would qualify. Luckily, the FDA clarified this point. As the RMAT guidance document notes:

gene therapies, including genetically modified cells, that lead to a durable modification of cells or tissues may meet the definition of a regenerative medicine therapy. Additionally, a combination product (biologic-device, biologic-drug, or biologic-device-drug) can be eligible for RMAT designation when the biological product component provides the greatest contribution to the overall intended therapeutic effects of the combination product.

This is an excellent development and one that portends immense benefits for future gene therapy applications submitted for FDA approval. According to the guidance, the new RMAT designation, unlike other fast-track approval and review processes, “does not require evidence to indicate that the drug may offer a substantial improvement over available therapies.” Liberalizing the threshold standards of evidence for RMAT designation ensures that future gene therapies will encounter fewer unnecessary roadblocks in delivering more effective and innovative treatments for individuals suffering from debilitating diseases.

As we note in our concluding remarks:

Overall, we consider the RMAT guidance to be a stellar improvement over other expedited programs, especially in its qualifying criteria. However, greater clarity is needed in order to capture the benefits of more advanced cell therapies that can help contribute to the healthy aging and well-being of American citizens. As FDA Commissioner Scott Gottlieb recently noted: “The benefits of [gene therapy] science—and the products that become available—are likely to accelerate. How we define the modern framework for safely advancing these opportunities will determine whether we’re able to fully realize the benefits that these new technologies can offer.”

We agree wholeheartedly. Developing a regulatory framework that accommodates safety and innovation will be a key determinant of how quickly the benefits of regenerative medicine, gene therapy, and anti-aging research revolutionize the lives of Americans. This guidance is an important and promising step in the right direction. With the right modifications, it can help usher in a new age of healthcare improvement for individuals from all walks of life.

Read the full comments submitted to the FDA here.

Source: Niskanen Center

About Elena Milova

As a devoted advocate of rejuvenation technologies since 2013, Elena is providing the community with a systemic vision how aging is affecting our society. Her research interests include global and local policies on aging, demographic changes, public perception of the application of rejuvenation technologies to prevent age-related diseases and extend life, and related public concerns. Elena is a co-author of the book “Aging prevention for all” (in Russian, 2015) and the organizer of multiple educational events helping the general public adopt the idea of eventually bringing aging under medical control.

About Keith Comito

Keith Comito is President of LEAF / Lifespan.io and a long-time advocate of longevity research. He is also a computer programmer, mathematician, musician, lover of life and perhaps a man with too many hobbies. He earned a B.S. in Mathematics, B.S. in Computer science, and M.S. in Applied Mathematics at Hofstra University, where his work included analysis of the LMNA protein.

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.

Google’s Calico Labs Announces Discovery of a “Non-Aging Mammal” – Article by Brady Hartman

Google’s Calico Labs Announces Discovery of a “Non-Aging Mammal” – Article by Brady Hartman

Comments 0 Comment

Brady Hartman

Editor’s Note: In this article, Mr. Brady Hartman explains a study that shows the naked mole-rats have an extremely low rate of aging.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, February 19, 2018

Completely bald and with wrinkly skin, the naked mole rat is one of the ugliest creatures around but lives an exceptionally long life for a small mammal. It rarely develops the chronic diseases of aging, such as cancer, and lives 10 times longer than regular rats.

The First Non-Aging Mammal

In the first significant announcement from Calico Labs since it was formed in 2013, researchers Rochelle Buffenstein, Megan Smith, and J. Graham Ruby have announced that the naked mole rat is a “non-aging mammal.”

The researchers followed the naked mole rats – housed at the Buck Institute – over a three-decade-long study period. They found that these creatures show hardly any signs of aging, such as problems with their metabolism, heart, or bones. Females do not go through menopause and continue to reproduce into their 30s, which is an amazing feat for an animal that lives at least 30 years of age in captivity. Even the cells in their bodies have a remarkable resistance to oxidative damage caused by free radicals. Small rodents the size of the naked mole rat live for no more than six years.

Senior Principal Investigator Rochelle (Shelley) Buffenstein, Ph.D. spent the early part of her career at the Medical School of the University of Witwatersrand, South Africa, where she studied the naked mole rat for ten years. Principal Investigator J. Graham Ruby, Ph.D. received his doctorate in biology from MIT and performs biometric, biostatistical, bioinformatic, and quantitative genetic analyses of diverse data to decipher the aging process in humans and model organisms. The researchers published their results on Jan 24th in the open access journal eLife [1].

How the Non-Aging Mammal Was Discovered

To judge the rate of aging, the Calico team used a mathematical model called the Gompertz-Makeham law of mortality. This statistically validated law states that the risk of death for every mammal increases exponentially with increasing age. The Calico researchers used this model to analyze an existing data set of more than 3000 naked mole rats over a 30-year timespan and found that the small mammals did not conform to the Gompertz-Makeham law. Unlike every other mammal, the mole rats do not face an increased hazard of death with each birthday; as the Calico authors said, “This absence of hazard increase with age, in defiance of Gompertz’s law, uniquely identifies the naked mole-rat as a non-aging mammal.”

Estimated probability of a US person dying at each age (2003.) Credit: Uscitizenjason CC BY SA 3.0

This is astonishing given that all other mammals, including humans, face an increased rate of death with each passing birthday. Consider this hazard chart for US citizens in 2003, in which the mortality rates increase exponentially with age after the age of 30.  In contrast, the equivalent chart for the naked mole rat is almost flat.

Caleb E. Finch and Hiram Beltrán-Sánchez, a pair of scientists from the University of Southern California (USC) in Los Angeles, analyzed and commented on the study. Caleb E. Finch, Ph.D. is a molecular biologist in the Leonard Davis School of Gerontology and Dornsife College. Hiram Beltrán-Sánchez is from the Department of Community Health Sciences and the California Center for Population Research.

Commenting on the remarkable results of the study in a companion piece [2], Finch and Beltrán-Sánchez said that the naked mole rat defied the Gompertz-Makeham law, remarking, “their risk of death does not increase as they get older” and “this is unprecedented for mammals.”

Finch and Beltrán-Sánchez said that previous studies of the non-aging mammal suggest that aging creeps in, nevertheless. Naked mole rats can accumulate oxidative damage in their cells and experience muscle wasting. There is also some evidence for small amounts of cancer. But, after reviewing the evidence, the USC authors said, “This would suggest that unlike any other mammal, the naked mole rats have an extremely low rate of aging.”

Finch and Beltrán-Sánchez said that the minimal age-related problems of the mole rat combined with its long lifespan allow it to achieve ‘negligible senescence,’ a phenomenon in which an animal reaches an advanced age without increased mortality or disability.

Other scientists believe that the longevity of naked mole rats is due to the limited oxygen of their subterranean habitat. Because of this environment, their metabolic rates are abnormally slow, and an abundance of repair mechanisms keeps their cells astonishingly youthful.

About Longevityfacts

LEAF has teamed up with its friends at LongevityFacts and will be publishing some of their articles as part of an agreed syndication deal. This article originally appeared here at LongevityFacts.

References

[1] J Graham Ruby, Megan Smith, Rochelle Buffenstein, Calico Life Sciences LLC. “Naked mole-rat mortality rates defy Gompertzian laws by not increasing with age.” eLife 2018;7:e31157 DOI: 10.7554/eLife.31157, Jan 24, 2018.

[2] Hiram Beltrán-Sánchez, Caleb Finch. “Life Expectancy: Age is just a number.” eLife 2018;7:e34427 DOI: 10.7554/eLife.34427 Jan 24, 2018.

 

About Brady Hartman

Brady is the editor of the longevity focused blog LongevityFacts.com and is an active advocate for rejuvenation biotechnology and geroscience.

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.

Is Aging Natural, a Disease That We Can Treat, or Both? – Article by Steve Hill

Is Aging Natural, a Disease That We Can Treat, or Both? – Article by Steve Hill

Comments 2 comments

Steve Hill

Editor’s Note: In this article, Mr. Steve Hill explains that aging can be described as both natural and pathological without contradiction. This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, February 16, 2018

Aging is something that we all share, rich or poor; it is something that happens to us all, and we are taught from a young age that it is inevitable. However, some scientists believe that aging is amenable to medical intervention and that such interventions could be the solution to preventing or reversing age-related diseases.

Academics are currently debating whether aging is natural or a pathological disease that we can treat.

In fact, there is now pressure from many academics to classify aging itself as a disease; indeed, doing so could potentially improve funding for aging research and help to speed up progress in finding solutions to age-related diseases. [1] The debate continues, but does it really matter if aging is classified as a disease, or is it largely a matter of semantics?

Fighting a losing battle

Current medical practice sees us trying to treat age-related diseases in the same way we do other diseases; this is the “infectious disease model”, and when it comes to treating age-related diseases, it is a losing battle.

The current approach works like this: as soon as a disease appears, the doctor attacks the disease using everything in the medical armory, and the patient can then continue with life until the next disease happens; this process is repeated until failure. This is an excellent way to deal with infectious diseases, and it has helped to increase life expectancy greatly in the last century; however, there are signs are that this approach is starting to run out of steam. [2-4]

Unfortunately, this “whack-a-mole” approach is a poor choice when it comes to treating the chronic diseases of old age. This is because the damage that the aging processes cause still continues to take its toll; therefore, treating the symptoms will ultimately achieve very little and certainly not cure the disease.

So, given that the aging processes lead to the diseases of aging, it is understandable that scientists are starting to consider aging itself to be a disease. While we do not yet fully understand all the intricacies of aging, we already know a great deal about the individual processes.[5] Certainly, we now know enough about aging to begin developing and testing interventions that directly target the underlying processes in order to prevent or treat pathology.

Treating the underlying processes and repairing their damage, which leads to the familiar diseases of old age, is the basis for the medical approach known as rejuvenation biotechnology, a multidisciplinary field that aims to prevent and treat age-related diseases by targeting the aging processes directly.

Aging is the foundation of age-related diseases

Even if aging is not a disease itself, the individual processes do lead to pathology and age-related diseases, such as cancer, heart disease, Parkinson’s, and Alzheimer’s. So, knowing that these processes create the conditions for diseases to develop, it makes sense to target the processes themselves in order to potentially prevent or treat a slew of age-related diseases at once.

The changes that aging brings vary from one person to another, but the common processes of aging are at work in all of us, albeit with some small variances between individuals. For example, we all suffer wear and tear in our joints due to the loss of cartilage, and we all experience the loss of skin elasticity due to the degradation of elastin and the failure of connective tissues. We all encounter other age-related changes, such as the accumulation of non-dividing senescent cells that cause chronic inflammation and disrupt tissue repair, and we also suffer from the accumulation of metabolic waste products that collect in our bodies over time.

As these changes progress, they eventually lead to the familiar diseases of aging. For example, lipids are critical for the function of our metabolism and are essential as part of our diet; however, over time, these processed lipids begin to accumulate in the blood vessel walls. Macrophages arrive to clear the toxic fatty waste away, but they become immobilized and die. This causes inflammation, attracting more macrophages and continuing the cycle. Ultimately, this debris forms plaques that harden the blood vessels and cause them to narrow; this causes blood pressure to rise and can eventually result in a heart attack or stroke.

This demonstrates that the normal metabolic processes that keep us alive ultimately lead to disease. Importantly, in this case, the early age-related changes that set the scene for disease progression, such as high cholesterol, have no symptoms. Nevertheless, such changes are the precursors of deadly diseases and are considered suitable targets for treatment. The same can be said for the other, more subtle, changes and damages that the aging processes cause.

Age-related conditions, such as arthritis, diabetes, osteoporosis, Alzheimer’s, Parkinson’s and many cancers, all follow this dynamic. Simply put, given the sufficient passage of time, the aging processes will cause us to suffer from multiple diseases. Therefore, we should consider these diseases to be the clinical manifestation of these age-related changes. In fact, medicine has been fighting against age-related changes for a long time, even if it was not obvious. For example, a doctor recommending that his patient should reduce his fat and carbohydrate intake to delay heart disease is already fighting those age-related changes. The diabetic who modifies her diet to better manage blood sugar levels is also doing the same thing.

Some people might contest this point of view, stating that the aging process is “natural” and therefore cannot be a disease. The argument that natural things are always good, the appeal to nature, is a logical fallacy. Such people may see natural and pathological as being mutually exclusive. Thus, what is natural must always be good, and what is pathological is bad, and so it cannot also be natural. This is, of course, false when you consider the meaning of each word. Natural simply means something that follows the normal, established course of events, and pathological means something that is harmful.

Conclusion

So, is aging natural or pathological? Well, by the dictionary definitions, aging can be described as both natural and pathological without contradiction.

Additionally, as it is currently classified, aging could be considered a syndrome, specifically a co-morbid syndrome. This really does describe aging perfectly; it is a group of symptoms that consistently occur together and a condition characterized by a set of associated symptoms. Ultimately, aging is an umbrella term describing a range of pathological changes; it may struggle to be accepted as a disease, but it already qualifies as a syndrome.

However, the question of aging being a disease or not is essentially semantic in nature. What rejuvenation biotechnology seeks to achieve is nothing more than preventing age-related diseases by treating the early stages of pathology, which are considered a natural process. While these early age-related changes have not been given a disease name, they are instrumental in the development of diseases, and surely, when it comes to medical treatment, that is all that matters.

References

[1] Bulterijs, S., Hull, R. S., Björk, V. C., & Roy, A. G. (2015). It is time to classify biological aging as a disease. Frontiers in genetics, 6.

[2] Crimmins, E. M. (2015). Lifespan and healthspan: Past, present, and promise. The Gerontologist, 55(6), 901-911.

[3] Olshansky, S. J., Passaro, D. J., Hershow, R. C., Layden, J., Carnes, B. A., Brody, J., … & Ludwig, D. S. (2005). A potential decline in life expectancy in the United States in the 21st century. New England Journal of Medicine, 352(11), 1138-1145.

[4] Reither, E. N., Olshansky, S. J., & Yang, Y. (2011). New forecasting methodology indicates more disease and earlier mortality ahead for today’s younger Americans. Health Affairs, 10-1377.

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

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 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.

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

Comments 0 Comment

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

Comments 0 Comment

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

Comments 0 Comment

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.

World Health Organization Puts the Elderly Back in the Picture – Article by Elena Milova

World Health Organization Puts the Elderly Back in the Picture – Article by Elena Milova

Comments 0 Comment

Elena Milova

Editor’s Note: In this article, Miss Elena Milova explains the success the anti-aging community has had in influencing policy makers at the WHO in including several provisions related to aging, in their global strategy and action plans of the next decade. This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, January 27, 2018

Not long ago, we wrote about some complications involving the WHO 13th programme of work. In the initial version of this document, developed by the WHO working group in November 2017, the problems of the elderly were nearly completely overlooked. The joint effort of our community helped to bring this critical flaw to public attention.

During the meeting of the working group, it was announced that 90% of the comments received by WHO (out of 400) pointed out the need to set healthy aging as one of the priorities of the new programme of work. However, we didn’t know if our demand to focus on the implementation of the global strategy and action plan on aging and health would be fulfilled.

The good news is that the new draft programme published on the WHO site on November 5th includes several provisions related to aging. Our community managed to persuade these global policymakers to implement all activities listed in the global strategy to help society prepare for the Decade of Healthy Aging (2020-2030). Let’s have a closer look at these provisions.

15. The foundation of WHO’s work is SDG 3: ensuring healthy lives and promoting well-being for all at all ages. WHO is an organization focused principally on promoting health rather than merely fighting disease, and especially on improving health among vulnerable populations and reducing inequities. Leaving no-one behind, the Organization aims to give women and men, girls and boys, in all social groups, the opportunity to live not just long but also healthy lives. WHO will explore measuring this foundation of its work using healthy life expectancy, which could serve as one overarching measure aligned with SDG 3, complemented by the triple billion goal, which leads to three more specific priorities, each with overlapping one-billion people goals.

Healthy life expectancy (HALE) is an assessment of the period of time a person can live in full health. HALE is usually lower than total life expectancy, and the difference between HALE and total life expectancy is regarded as years of life lost to disease.

As the goal of our community is to prolong the healthy period of life by addressing the root mechanisms of aging and postponing age-related disease, the introduction of HALE as a way to measure WHO activities is a very good outcome. It is very hard to preserve health in older ages without addressing the underlying mechanisms of aging and implementing an extensive program that involves educating the public about healthy lifestyles. This choice of indicator means that WHO will strengthen its efforts to keep people healthy for as long as possible, which will ease the introduction of rejuvenation interventions once they are available, as it will likely be a cost-effective way to achieve a more favorable HALE.

16. Life expectancy at birth has consistently increased since the 19th century, largely due to socioeconomic developments and public health measures such as vaccination, nutrition and
sanitation. Today, socioeconomic, political, cultural, environmental and economic forces continue to drive changes in the burden of disease. However, efforts are needed to ensure that their impact is positive. Poor health literacy coupled with weak health-promoting policies make it difficult for people to make healthy choices for themselves and their families. Investment in health promotion and disease prevention allows countries to address economic concerns about the rising costs of the health system and enables potential savings if disease can be avoided.

The WHO draft programme of work refers here to the increasing burden of chronic, non-communicable diseases due to the increasing proportion of people age 60 and over. Indeed, it would be really hard to double or even triple healthcare and pension expenditures for many countries, especially taking into account the ongoing economic crisis. However, this is what aging societies will have to do, if HALE does not grow faster.

This is why WHO is only promoting evidence-based interventions that represent the “best buy” scenarios: the most realistic and cost-effective. When it comes to age-related diseases, which can last 20-30 years or longer, prevention could be much cheaper, and it is more humane, as this scenario would reduce unnecessary human suffering. Therefore, we could consider this provision of the new draft programme as supporting our efforts to introduce longevity lifestyles and even “soft” (careful and evidence-based) biohacking.

17. Healthy life expectancy has not increased at the same pace as life expectancy, and increasing age often brings increasing morbidity and reduced functioning, making healthy ageing an important focus. Most disability-adjusted life years in older age are attributable to chronic conditions and the accumulated impact of such conditions can lead to significant loss in function and care dependence in older age. At the same time, there is emerging evidence that healthy ageing depends on early childhood development and is epigenetically determined. Ensuring healthy ageing is an urgent challenge in all countries.

This provision once again underlines how important it is to focus on prevention. I would like to point out that if childhood is perceived as the foundation of healthy lifestyles, longevity advocates receive carte blanche for working with the younger generation. Activists could think of developing corresponding education programs for schools and universities, and this very provision can be a strong argument when offering such a program to educational authorities.

37. Ensuring healthy ageing is central to universal health coverage, just as it is to the other priorities of GPW 13. The number of people over the age of 60 is expected to double by 2050 and this unprecedented demographic transition will require a radical societal response. The Secretariat will support Member States to promote healthy ageing through the actions defined by the Global strategy and action plan on ageing and health (2016), as well as through the Decade of Healthy Ageing that is planned for the period 2020−2030. These actions include aligning health systems to the needs of older populations, with a special focus on enhancing the functioning of older persons and the management of chronic disease; improving access to medicines; developing systems of longterm care including community-based services; promoting palliative care, creating age-friendly environments; and improving measurement, monitoring and understanding of healthy ageing.

This provision is exactly what we were aiming for when calling the members of our community to take part in the Open Consultation or the Draft. As you remember, all mentions of the WHO documents related to aging were absent; this provision clearly shows that we achieved our goal! Even though the global strategy and action plan on aging and health may not be ideal in terms of rejuvenation research promotion, it helps member states navigate the field with more confidence. This global strategy, which we wanted so much to be the foundation of the draft programme provisions related to aging, contains a very important paragraph that every activist should know about:

105. Finally, better clinical research is urgently needed on the etiology of, and treatments for, the key health conditions of older age, including musculoskeletal and sensory impairments, cardiovascular disease and risk factors such as hypertension and diabetes, mental disorders, dementia and cognitive declines, cancer, and geriatric syndromes such as frailty. This must include much better consideration of the specific physiological differences of older men and women and the high likelihood that they will be experiencing mutimorbidities. This could also be extended to include possible interventions to modify the underlying physiological and psychological changes associated with ageing.

Conclusion

Dear friends, this is a victory! Our community managed to influence policymakers of the highest level: the World Health Organization. We managed to ensure that the new programme of work considers aging and age-related diseases to be an important issue, and the resulting global strategy and action plan on aging and health is an effective guide to helping our society adapt to population aging.

In terms of advocacy, this is a complete victory, which shows two important things. First, when we join forces, we can influence global health policy at the highest level. Our community became stronger, and our voice is being heard! Second, this victory shows that dialogue with the UN and its institutions, including decision-makers in these agencies, is possible, and it goes in the directions that we need: more focus on prevention and more focus on public health education related to aging.

I offer special thanks to Dr. Ilia Stambler for initially turning the attention of the community to this issue. I want to thank and congratulate all participants of the Open Consultation with this achievement. Of course, we are still at the beginning of our path to rejuvenation as a public health priority, but outcomes like this one make me believe that there are more victories to come. Let’s keep working, as the main reward is worth it: health, youth, and freedom from age-related diseases for all!

About Elena Milova

As a devoted advocate of rejuvenation technologies since 2013, Elena is providing the community with a systemic vision how aging is affecting our society. Her research interests include global and local policies on aging, demographic changes, public perception of the application of rejuvenation technologies to prevent age-related diseases and extend life, and related public concerns. Elena is a co-author of the book Aging Prevention for All (in Russian, 2015) and the organizer of multiple educational events helping the general public adopt the idea of eventually bringing aging under medical control.

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.

Alzheimer’s Drug Turns Back the Clock in Mitochondria – Article by Steve Hill

Alzheimer’s Drug Turns Back the Clock in Mitochondria – Article by Steve Hill

Comments 0 Comment

Steve Hill

Editor’s Note: In this article, Mr. Steve Hill discusses an experimental drug, J147, for treating Alzheimer’s disease and also how Alzheimer’s disease is closely linked to aging.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, January 26, 2018

J147 is an experimental drug that has been shown to treat Alzheimer’s disease, and it also appears to reverse some aspects of aging. It is also poised to enter human clinical trials in the near future, although how it works has been somewhat of a puzzle.

A new study  published in the journal Aging Cell has changed all that, and the results are quite intriguing [1]. Researchers at the Salk Institute have solved the mystery of how J147 works and why it makes old flies, mice, and cells more youthful.

Rejuvenating mitochondria

The drug apparently works because it binds to a protein found in mitochondria, the powerhouses of cells; this, in turn, causes cells to function in a more youthful manner. Mitochondrial dysfunction is one of the hallmarks of aging and is thought to be a key reason why we age and develop age-related diseases [2]. This drug appears, at least partially, to address some of that dysfunction.

Finding the target of J147 was the key to revealing the link between Alzheimer’s disease and the aging process. It was the critical information the researchers needed and was holding the drug back from clinical trials.

Dave Schubert, head of Salk’s Cellular Neurobiology Laboratory, and his team originally developed the J147 drug in 2011. The team screened numerous plant-sourced compounds with the potential to reverse the cellular and molecular signs of aging in the brain. The drug was developed as a modified version of a molecule found in the spice curcumin, a common ingredient in Asian foods such as curry.

Since then, the researchers have shown that J147 can reverse memory deficits, increases the production of brain cells, and slows the progression of Alzheimer’s in mice [3]. However, at that point, they did not understand how J147 worked.

Finding the target

During the new study lead by Dave Schubert and Salk Research Associate Josh Goldberg, the researchers used a number of approaches to find out how J147 worked. They eventually identified that the target of J147 was the mitochondrial protein known as ATP synthase, specifically ATP5A, a subunit of that protein. ATP synthase is involved in the mitochondrial generation of ATP, which cells use for energy.

The researchers demonstrated that by reducing the activity of ATP synthase, they were able to protect neuronal cells from a number of toxicities associated with the aging of the brain. One reason for this neuroprotective effect is thought to be the role of excitotoxicity in neuronal cell damage.

Excitotoxicity is the pathological process by which neurons are damaged and killed by the overactivation of receptors for the excitatory neurotransmitter glutamate. Think of it being a bit like a light switch being turned on and off so rapidly that it ends up causing the light bulb to blow.

Recently, the role of ATP synthase inhibition for neuroprotection against excitotoxic damage was demonstrated in a mouse study [4]. The second study showed that mouse models expressing the human form of mutant ATPase inhibitory factor 1 (hIF1), which causes a sustained inhibition of ATP synthase, were more resilient to neuronal death after excitotoxic damage. This data is consistent with this new J147 study, in which an increase in IF1 in the mice reduced the activity of ATP synthase (specifically ATP5A) and was neuroprotective.

ATP synthase is implicated in aging

ATP synthase has previously been shown to influence aging in C. elegans worms and flies. Given that aging is the greatest risk factor for developing Alzheimer’s disease, it is no surprise that the target of the drug is also involved in the aging process.

The team also revealed that by modulating the activity of ATP synthase, they could influence the levels of ATP and other molecules and were able to encourage healthier, more stable mitochondria during aging. Mice given the compound showed profound changes, appearing to look younger at a cellular and molecular level.

The researchers believe that these results are not only encouraging for the treatment of Alzheimer’s, they suggest that J147 may also be useful in treating other age-related diseases.

“People have always thought that you need separate drugs for Alzheimer’s, Parkinson’s and stroke,” said Dave Schubert. “But it may be that by targeting aging we can treat or slow down many pathological conditions that are old-age-associated.”

With J147 having just completed the FDA required toxicology testing in animals, the next step is phase 1 human clinical trials, and the road to approval begins.

Conclusion

It is very heartening to hear important researchers suggesting that in order to treat age-related diseases, one needs to treat the aging processes themselves. This is the exactly what Dr. Aubrey de Grey and others have been saying for many years. It is good to hear more voices joining the call to tackle age-related diseases at their root: the hallmarks and damages where they all begin.

The process of age-related disease begins long before the familiar signs and diagnoses are made; by targeting the early processes that are not given specific disease names, we might yet defeat horrific diseases, such as Alzheimer’s, which rob us of who we are.

Literature

[1] Joshua Goldberg et al. The mitochondrial ATP synthase is a shared drug target for aging and dementia. Aging Cell, 2018 DOI: 10.1111/acel.12715
[2] López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. Cell, 153(6), 1194-1217.
[3] Prior, M., Dargusch, R., Ehren, J. L., Chiruta, C., & Schubert, D. (2013). The neurotrophic compound J147 reverses cognitive impairment in aged Alzheimer’s disease mice. Alzheimer’s research & therapy, 5(3), 25.
[4] Formentini, L., Pereira, M. P., Sánchez‐Cenizo, L., Santacatterina, F., Lucas, J. J., Navarro, C., … & Cuezva, J. M. (2014). In vivo inhibition of the mitochondrial H+‐ATP synthase in neurons promotes metabolic preconditioning. The EMBO journal, 33(7), 762-778.

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 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.

Exercise is Currently the Best Way to Slow Down Aging – Article by Michael Falk

Exercise is Currently the Best Way to Slow Down Aging – Article by Michael Falk

Comments 0 Comment

Michael Falk

Editor’s Note: In this article, Mr. Michael Falk explains how exercising slows down aging. This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, January 25, 2018

We have all heard that exercise is good for our health. However, it can not only keep you healthy, it can also slow down some aspects of aging. Some researchers even think that it might be possible to use this knowledge to develop new therapies against aging. While waiting for that to happen, we need to exercise in order to slow down the effects of aging.

How important is it to keep fit?

So, how beneficial is exercising? Well, one of the best studies conducted on this subject showed that women will live 5.6 years longer and men 6.2 years longer if they exercise between 1 and 2.5 hours per week [1]. This makes exercise a better lifestyle choice than any other, at least as long as you’re not counting avoiding downright dangerous behavior, such as smoking.

The main benefits of physical activity may come from better health for the heart. Exercise lessens the risk for many types of heart disease [2]. It is even more beneficial for people who already suffered age-related conditions, including stroke and coronary heart disease, and it is more effective than any known drug in preventing repeated episodes [3].

The key improvements also include increased muscle strength, stronger bones, better weight control, and improved cognitive function. This means less risk of age-related diseases, such as Alzheimer’s disease, as well as lethal falls, which are a major risk for the elderly.

The conclusion is that exercise helps with a lot of different aspects of your health in several ways, and we can summarize its effects as improving quality of life and increasing healthspan.

How much exercise do you need?

More exercise does not always improve outcomes. Professional athletes exercise more than the rest of us, and they generally live longer than the average person [4]. However, correlation isn’t causation, and robust individuals are perhaps more likely to become athletes, instead of the other way around. There could even be negative effects from too much exercise, although that is far from certain.

Even moderate exercise leads to better health. Half an hour a day seems to be enough to see positive effects, and it is also a common recommendation for the minimum amount of exercise you should get. The biggest difference can be seen between people who hardly move around at all and people who get at least a little exercise a few times a week. Taking the stairs and walking short distances is clearly better than nothing. In fact, some studies show that even light activity, such as housework, can have an effect on mortality risk.

It should also be noted that there are different types of exercise and that these could have different benefits. Jogging increases your aerobic ability, which should, among other things, lead to better heart health. Lifting weights is an anaerobic exercise that improves strength and should bring other benefits, such as stronger bones. A lot of research about this has been done already, but so far, we don’t definitively know the optimal amount and type of training for each particular type of person.

Drugs to mimic exercise

Some of the positive effects have to do with the anti-inflammatory processes that occur when exercising [5]. Other mechanisms appear to be involved, although more research on these mechanisms is needed.

Since the advantages of exercise are clear, the idea has occurred to some researchers that it may be possible to mimic the effects of exercise without doing the hard work and getting sweaty. Research is now being conducted using drugs that target the same mechanisms to try to get the same benefits of exercise.

This typically involves adjusting a part of the human metabolism, which is not an easy matter. However, there have been at least some tentative breakthroughs already, and last year, a team found a drug that boosted the endurance of mice by roughly 70 percent [6]. Where this might lead in the future is not clear, but some positive effects may come from this research.

Will exercise lead to longevity?

Even though exercise is beneficial for your health, there is no guarantee it will keep you alive until you reach 100, although staying fit will almost certainly improve your chances. This is why if we want to remain in good health and live longer, we need to develop rejuvenation biotechnology and therapies that address the aging processes directly. That said, if you want to increase your chances of living long enough to see these therapies arrive, then exercise is the best option you have right now.

Literature

[1] Schnohr, P., Lange, P., Scharling, H., & Jensen, J. S. (2006). Long-term physical activity in leisure time and mortality from coronary heart disease, stroke, respiratory diseases, and cancer. The Copenhagen City Heart Study. European Journal of Cardiovascular Prevention & Rehabilitation, 13(2), 173-179.

[2] Jakovljevic, D. G. (2017). Physical activity and cardiovascular aging: Physiological and molecular insights. Experimental Gerontology.

[3] Naci, H., & Ioannidis, J. P. (2013). Comparative effectiveness of exercise and drug interventions on mortality outcomes: metaepidemiological study. Bmj, 347, f5577.

[4] Lemez, S., & Baker, J. (2015). Do elite athletes live longer? a systematic review of mortality and longevity in elite athletes. Sports medicine-open, 1(1), 16.

[5] Fan, W., Waizenegger, W., Lin, C. S., Sorrentino, V., He, M. X., Wall, C. E., … & Auwerx, J. (2017). PPARδ Promotes Running Endurance by Preserving Glucose. Cell Metabolism, 25(5), 1186-1193.

[6] Dimitrov, S., Hulteng, E., & Hong, S. (2017). Inflammation and exercise: Inhibition of monocytic intracellular TNF production by acute exercise via β 2-adrenergic activation. Brain, behavior, and immunity, 61, 60-68.

About Michael Falk

Michael Falk is a communication specialist with 15 years of experience writing about healthcare and technology. He has been an advocate of longevity research since 2013, when he started his longevity blog Unggamma (www.unggammal.se).

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

Comments 0 Comment

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

Comments 0 Comment

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.

A Review of Immunosenescence – Article by Steve Hill

A Review of Immunosenescence – Article by Steve Hill

Comments 0 Comment

Steve Hill

Editor’s Note: In this article, Steve Hill discusses some of the reasons for the decline of the immune system.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, January 9, 2018

Immunosenescence is the age-related decline of the immune system. The reason why our immune systems start to fail and weaken as we age is not fully understood, and, indeed, there are a variety of hypotheses as to why this happens.

Inflammaging

Inflammation certainly plays a role in this process, and it is well documented that inflammation has a considerable effect on immune cells such as macrophages, causing them to become dysfunctional and stop cleaning house. This is in line with the proposed concept of “inflammaging”, which describes an ever-increasing chronic background of inflammation from sources such as senescent cells, cell debris, and changes in the gut microbiota. This inflammaging then drives immune system dysfunction, which then creates more inflammation, continuing a downward spiral.

We recently learned that inflammation can cause problems with weight control by causing nerve-associated macrophages to stop signaling fat cells to release their stored energy[1]. We also know that macrophage dysfunction occurs in other tissues due to inflammation, and so it seems clear that inflammation plays at least a partial role in immune system decline.

Cellular Senescence

Some research suggests that the immune system declines due to its cells becoming senescent, just as other cell populations do. Over time, our cells reach their maximum number of divisions, or they are damaged and enter senescence and destroy themselves via apoptosis, a kind of programmed self-destruct sequence.

However, sometimes these cells resist apoptosis and cling on to life, but in doing so, they prevent fresh cells replacing them while generating inflammatory signals that cause nearby cells to become dysfunctional, too. It is proposed that the immune system experiences the same senescence as our other cells, leading to immune system failure.

Stem-cell depletion

Another player in immune system decline is stem-cell depletion; for example, the thymus begins to shrink from an early age and eventually stops producing new T cells to help defend us from invading pathogens. The production of T cells is facilitated by thymic stem cells, which are gradually depleted over our lifetime, and eventually, we have so few T cells that we cannot fight off diseases such as flu and pneumonia, which often kill the elderly. Some attempts are currently being made to rejuvenate the thymus and have enjoyed some success.

A review of immunosenescence

It is likely the case that immunosenescence is a combination of all of these proposed things and more, and each plays a role in the resulting decline of our immune systems as we age. When it comes to establishing the exact chain of events that leads to immunosenescence, it will take reversing each of those causes to see what happens.

Today, we wanted to bring your attention to an open-access paper that reviews the current knowledge of immunosenescence and provides a good introduction to the topic[2].

Conclusion

Developing the therapies that target the aging processes directly is likely the most expedient path to understanding immunosenescence, as these therapies will give us the tools with which to discover what drives the process. Approaches such as thymic rejuvenation or creating a replacement thymus, replacing lost stem-cell populations such as hematopoietic stem cells that create all immune cells, removing overspecialized immune cells, and removing senescent cells are all valid approaches towards discovering how immunosenescence works.

Our knowledge is growing rapidly by the passing month, and more and more is being understood about the aging processes and how we might directly target them to prevent or reverse age-related diseases. It is almost certain that medicine is going to change dramatically in the next decade or two as our understanding grows.

Literature

[1] Camell, C. D., Sander, J., Spadaro, O., Lee, A., Nguyen, K. Y., Wing, A., … & Rodeheffer, M. S. (2017). Inflammasome-driven catecholamine catabolism in macrophages blunts lipolysis during ageing. Nature, 550(7674), 119-123.

[2] Ventura, M. T., Casciaro, M., Gangemi, S., & Buquicchio, R. (2017). Immunosenescence in aging: between immune cells depletion and cytokines up-regulation. Clinical and Molecular Allergy, 15(1), 21.

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 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 Link Between Cellular Senescence and Cellular Reprogramming – Article by Steve Hill

The Link Between Cellular Senescence and Cellular Reprogramming – Article by Steve Hill

Comments 0 Comment

Steve Hill

Editor’s Note: In this article, Steve Hill discusses the link between Cellular Senescence and Cellular Reprogramming.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

            ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, January 8, 2018

The reprogramming of cells is a well-established technique in medicine and has been for over a decade now. It allows the en masse creation of patient-matched cells and is the basis for multiple current therapies.

Cellular Senescence and Cellular Reprogramming share mechanisms

Induced pluripotent stem cells (also known as iPS cells or iPSCs) can be created directly from adult cells. The iPSC technology was pioneered by Shinya Yamanaka, who demonstrated in 2006 that the introduction of four specific genes encoding transcription factors could convert adult cells into pluripotent stem cells[1]. These factors are Oct4, Sox2, Klf4, and c-Myc (OSKM), or as many call them, the Yamanaka factors.

Today, we have a new paper that discusses how induced pluripotency and cellular senescence, two of several possible cellular states, share similarities[2]. It is likely no surprise that the two states are closely related and that some of the mechanisms for one process are shared by the other. It appears that certain key signaling molecules are important in determining both cell fate and senescence.

Controlling cell behavior in living animals

As our understanding of guiding cell fate grows rapidly by the passing year, it has huge implications for therapies that seek to control cellular activities and encourage certain types of cells to be created. Research is now starting to move beyond the petri dish and to where cells are being programmed in situ in living animals.

In 2013, the Hallmarks of Aging proposed that epigenetic changes are a primary reason we age, but, at the time, the evidence in living animals was lacking[3]. All this changed in late 2015 when researchers induced pluripotency in living animals using the OSKM reprogramming factors, in much the same way as iPSC technology creates on-demand cell types outside the body. In this case, they only very briefly induced OSKM so that the aging markers in cells were reset but not long enough to cause the cells to revert to a developmental state.

The results of this first attempt to reprogram cells in living animals resulted in the cells of the mice becoming functionally younger in many ways and increased their healthy lifespan[4]. These results lend yet more support for the hypothesis that epigenetic alterations are one of the reasons we age and that reversing those changes is a path to maintaining health and tissue function as we age. A number of research teams are now exploring cellular reprogramming in living animals with a view to translating this to humans. We discussed the findings of this paper during our monthly Journal Club here.

Conclusion

This paper may be of interest to those wishing to delve deeper into the world of cell fate and understand the connection between cellular senescence and induced pluripotency. This builds on the knowledge we already have, and it is not difficult to imagine a time in the near future when we will have a very high level of control over our cells via reprogramming techniques.

If the hypothesis of epigenetic alterations being one of the causes of aging turns out to be correct, then that would be a real game changer. We are likely not too far off from determining if this is the case or not, and we may have the answer in the next few years, given the current pace of progress.

Literature

[1] Takahashi, K., & Yamanaka, S. (2006). Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. cell, 126(4), 663-676.

[2] Mosteiro, L., Pantoja, C., Martino, A., & Serrano, M. (2017). Senescence promotes in vivo reprogramming through p16INK4a and IL‐6. Aging cell.

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

[4] Ocampo, A., Reddy, P., Martinez-Redondo, P., Platero-Luengo, A., Hatanaka, F., Hishida, T., … & Araoka, T. (2016). In vivo amelioration of age-associated hallmarks by partial reprogramming. Cell, 167(7), 1719-1733.

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 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 Best of the SENS AMA – Article by Steve Hill and Aubrey de Grey

The Best of the SENS AMA – Article by Steve Hill and Aubrey de Grey

Comments 1 comment

Steve Hill

Dr. Aubrey de Grey

Editor’s Note: In this article, Steve Hill highlights the Ask Me Anything on Reddit held on December 7th by Dr. Aubrey de Grey.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, December 13, 2017

 

Dr. Aubrey de Grey from the SENS Research Foundation (SRF) did an Ask Me Anything on Reddit on December 7th, and there were many great questions and answers; we thought it would be a great time to summarize some of the best ones and offer a little commentary.

What do you think were the biggest wins of the last couple of years in SENS-relevant advocacy, research, and development? What has moved the needle?

There have been lots. On the research, I would highlight our paper in Science two years ago, which shows how to synthesize glucosepane, and our paper in Nucleic Acids Research one year ago, which shows simultaneous allotopic expression of two of the 13 mitochondrial genes. Both of those projects have been greatly accelerated in the meantime as a result of those key enabling breakthroughs; watch this space.

On advocacy, I think the main win has been the arrival of private capital; I would especially highlight Jim Mellon and his Juvenescence initiative because he is not only a successful, energetic and visionary investor, he is also a highly vocal giver of investment advice.

We are pleased to have been involved with the second project mentioned here, as we hosted the MitoSENS project at Lifespan.io, where it raised 153% of its initial fundraising goal. Less than a year later, after raising this money, it went on to publish the groundbreaking study showing that backup copies of mitochondrial genes could indeed be created in the nucleus. Dr. de Grey originally proposed the idea over a decade ago amid much scepticism; it is really good to see that years later he has been vindicated. This is the power of crowdfunding and how we as a community can make big changes in science by working together.

How do you feel about the impact of groups like LEAF advocating and reporting on rejuvenation biotech? Has the advocacy and reporting of these groups made your life any easier?

Massively! A huge thing that I say all the time is that advocacy absolutely relies upon the diversity of its messengers. Different people listen to different forms of words, different styles of messaging, etc. The more, the better.

It’s good to know that our work is appreciated and helping. Working together as a community is essential for progress, so it was nice to see this question and response from someone we respect a great deal.

We have said many times before effective advocacy efforts are just as important as the research itself. Professional advocacy has the potential to increase public support and funding, paving the way for the arrival of rejuvenation biotechnology. In the past decade or so, advocacy has mostly been left to volunteers and people such as Dr. de Grey.

Popular causes attract celebrities, public support, funding and investment; if we want a revolution in medicine and how we treat aging, then we must popularize the movement. There has been a serious shortage of full-time and organized advocacy; therefore, we decided to create LEAF to support groups like the SRF, advocate to popularize the cause, and help to raise much-needed funds for research efforts. We are only able to do this thanks to the support of the community, and we are extremely grateful to our Lifespan Heroes for helping us to do the work we do.

Aside from funding, what do you consider to be a burden or delay for your type of research?

Nothing. Seriously, nothing at all. We have the plan, and we have the people. It’s all about enabling those people by giving them the resources to get on with the job.

Indeed, funding for research is one of the four major bottlenecks slowing down the development of therapies that address the aging processes. The more funding the field gets, the more projects can be launched, the sooner breakthroughs can potentially happen, and the greater the benefits will likely be for all of us.

Is there anything new you are able to say about the breaking of cross-links in the extracellular matrix?

Absolutely. Short story, we now have a bunch of glucosepane-breaking enzymes, and we are within a few months of spinning the work out into a startup.

A suspected cause of degenerative aging is the accumulation of sugary metabolic wastes known as advanced glycation end-products (AGEs). These are wastes that are, in some cases, hard for our metabolism to break down fast enough or even at all. Some types, such as glucosepane, can form cross-links, gumming together important proteins such as those making up the supporting extracellular matrix scaffold.

The properties of elastic tissues (skin and the blood vessel walls) derive from the particular structure of the extracellular matrix, and cross-links degrade that structure, preventing it from functioning correctly. AGEs’ presence contributes to blood vessel stiffening with age, and it is implicated in hypertension and diabetes.

That SRF now has candidate enzymes is very significant because it means that there are now potential ways to remove these crosslinks from our tissues. There are many types of crosslinks, and we already know of compounds and drugs that can break other kind of crosslinks; the major problem is glucosepane, as it lasts a very long time, and, so far, nothing is known to remove it. Given that other types of crosslinks can be removed, Dr. de Grey rightly thought that there must be ways to remove (cleave) glucosepane from tissues; now, it seems that we are a step closer to that potentially becoming a reality.

If the SRF is successful in finding ways to break glucosepane crosslinks, this has huge implications for diabetes, hypertension and aging. It is great to hear that the organization is now reaching the point at which it is almost time to develop this as a therapy by creating a startup company.

It seems likely that artificial intelligence will be a necessary tool in order to reach longevity escape velocity. I was wondering how much of a role does artificial intelligence play in your research? Is this something you devote many resources to?

We don’t, but that is because other major players in this field (and good friends of mine), such as Alex Zhavoronkov and Kristen Fortney, are doing it so well already (with Insilico Med and BioAge, respectively). Check out the BioData West conference that will occur in SF a couple of days before our Undoing Aging conference in Berlin; I will be chairing a session on this.

We believe that the application of AI and, in particular, machine learning will prove to be a very valuable tool for research in the coming years. Such systems are ideally suited for high-throughput, laborious tasks that also require high attention to detail and would take humans a long time to do. Drug discovery, image analysis and many more tasks in the lab could potentially be automated, saving time and freeing up researchers to work on other critical tasks.

We are proud to have hosted the MouseAge project this year, which is an AI-based visual aging biomarker application that helps researchers determine the age of mice without the use of harmful tests. In a few months, researchers will be able to use the MouseAge application in the lab to help speed research progress up. This is just one example of how AI can be used in aging research and how the community helped to make it happen.

Given current funding, how far away from robust mouse rejuvenation do you think you are?

My estimate is 5-7 years, but that’s not quite “given current funding”. My overoptimism in saying “10 years” 13 years ago consisted entirely of overoptimism about funding – the science itself has not thrown up any nasty surprises whatsoever – but, nonetheless, I am quite optimistic as of now about funding, simply because the progress we have made has led to a whole new world of startups (including spinoffs from the SENS Research Foundation) and investors, so it’s not only philanthropy anymore. Plus, the increase in overall credibility of the approach is also helping to nurture the philanthropic side. We are still struggling, that’s for sure, but I’m feeling a lot surer that the funding drought’s days are numbered than I felt even two or three years ago.

Robust mouse rejuvenation (RMR) has long been a goal for the SENS Research Foundation, going back to when the SENS approach was initially proposed. RMR was originally outlined as being able to demonstrate and replicate SENS to double the remaining life expectancy of an already aged mouse. This would not mean the first RMR would be a total implementation of all the SENS approaches or that rejuvenation would need to be absolute; it would be a first pass to demonstrate the viability of multiple SENS approaches combined to produce robust results.

Being able to achieve a first-pass RMR could do much to convince academia that the repair approach to aging is plausible and attract more funding and interest in the approach. While RMR working in mice may not sound that exciting, it has huge implications for the field and potentially the rate of funding and progress.

How confident are you still in your previous prediction that humans will be able to control aging by 2029?

I think we’ve slipped a few years, entirely because of lack of funding. The tipping point will be when results in mice convince a critical mass of my curmudgeonly, reputation-protecting expert colleagues that rejuvenation will eventually work, such that they start to feel able to say so publicly. I think that’s on the order of five years away.

We think that the tipping point could well be if senolytics have the same result in humans as they have in mice. Enhanced tissue repair and regeneration in older people would be a very strong case for the repair approach to aging and almost certain to convince the academics sitting on the fence.

Certainly, if AGE breakers could be demonstrated to work in humans, this would also go a long way towards not only convincing academia but also grabbing public interest. Removing AGEs from the skin may potentially reverse wrinkles, for example, and restore skin elasticity, offering a very visual demonstration of repair being plausible.

There is almost certainly going to be a tipping point at which the bulk of academic and public support swings in favour of a repair approach to aging; the only question is when? Well, the sooner the basic science can be done and moved to translational research, the sooner we can all potentially benefit from these technologies. This makes supporting both the research and advocacy of rejuvenation biotechnology very important for progress.

 

About Dr. Aubrey de Grey

Dr. Aubrey de Grey is a biomedical gerontologist based in Cambridge, UK and Mountain View, California, USA, and is the Chief Science Officer of SENS Research Foundation, a California-based 501(c)(3) charity dedicated to combating the aging process. He is also Editor-in-Chief of Rejuvenation Research, the world’s highest-impact peer-reviewed journal focused on intervention in aging. He received his BA and Ph.D. from the University of Cambridge in 1985 and 2000 respectively. His original field was computer science, and he did research in the private sector for six years in the area of software verification before switching to biogerontology in the mid-1990s. His research interests encompass the characterisation of all the accumulating and eventually pathogenic molecular and cellular side-effects of metabolism (“damage”) that constitute mammalian aging and the design of interventions to repair and/or obviate that damage. He has developed a possibly comprehensive plan for such repair, termed Strategies for Engineered Negligible Senescence (SENS), which breaks aging down into seven major classes of damage and identifies detailed approaches to addressing each one. A key aspect of SENS is that it can potentially extend healthy lifespan without limit, even though these repair processes will probably never be perfect, as the repair only needs to approach perfection rapidly enough to keep the overall level of damage below pathogenic levels. Dr. de Grey has termed this required rate of improvement of repair therapies “longevity escape velocity”. Dr. de Grey is a Fellow of both the Gerontological Society of America and the American Aging Association, and sits on the editorial and scientific advisory boards of numerous journals and organisations.

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 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

Comments 1 comment

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 Bringing Aging Under Medical Control Probably Will Not Create a Gerontocracy – Article by Nicola Bagalà

Why Bringing Aging Under Medical Control Probably Will Not Create a Gerontocracy – Article by Nicola Bagalà

Comments 0 Comment

Nicola Bagalà

Editor’s Note: In this article, Mr. Nicola Bagalà discusses Gerontocracy and how it is becoming less likely due to factors such as increasing wide availability of knowledge and equal opportunities.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                      ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, December 05, 2017

 

As I discussed in another article, rejuvenation biotechnology would allow older adults to continue working and producing wealth for much longer than they can today, thus benefiting society in many ways.

However, some people are concerned that this might do more harm than good; imagine all those rejuvenated old farts holding onto their jobs forever, preventing the young from getting jobs themselves! Not to mention the risk of a gerontocratic world, where powerful older people get too attached to their chairs, never allowing younger people a chance!

New is not always better

If you’re more concerned that dictators could live for centuries, then you should have a look at this article; here, I’m going to deal with another scenario: old, rejuvenated people who hold on to positions of power—not necessarily as heads of countries—or their jobs for a really long time.

Quite frankly, what’s wrong with that?

Just because someone has been in charge of the same position for long, it doesn’t mean that it’s necessarily a bad thing. If you think otherwise, you might be making the assumption I rebutted here, namely that, rejuvenated or not, older people will always tend to do things in old ways, eventually making them a worse choice than younger people. On the contrary, their long experience might make them more fit than others, especially if we’re talking about chronologically older but open-minded people who keep up to date. Younger people aren’t necessarily the default better option. Think about all those times when a great person of our time died and you found yourself thinking that the world would have been better off if he or she had lived longer.

Personally, I think what matters is that people in certain positions, whether within government or a company, are the right people for the job. If they aren’t, old or young, they should be replaced by other people who are more fit, and, generally, there are more efficient and humane ways to do so than letting them get age-related diseases—for example, voting for someone else or hiring a different person. Granted, if the person to be kicked out is really powerful, this may well be easier said than done; however, when the holder of a position of such power dies of old age, his successor is rarely a nobody with no string-pulling abilities whatsoever. It’s not really a matter of longevity; rather, it’s that power attracts power, and I doubt that creating or not creating rejuvenation will make much of a difference in this respect.

Where does power come from?

It’s easy to hypothesize that a generation of rejuvenated 200-year-olds could end up becoming a gerontocratic elite that maintains power over younger people, but how would this be accomplished, exactly?

Maybe the older generation is rich and powerful, but unless we’re talking about a totalitarian world in which the masses are intentionally kept ignorant and poor, younger generations do have fair chances to make positions for themselves. Power and wealth come from knowledge, and, these days, knowledge is more freely and widely available than ever before.

Learning new professional skills and acquiring knowledge, in general, is possible for virtually everyone, thanks to the pervasiveness of educational media and the open availability of information on the Internet, including free (or reasonably affordable) online education projects, such as Coursera and Edx. The recent European initiative to ensure that all scientific papers are open access by 2020 represents another step towards a world that shares information rather than hides it.

Truth to be told, power and wealth don’t come only from knowledge; they also come from powerful and wealthy ancestors. If we didn’t develop rejuvenation, certainly all the Scrooge McDucks of the world would die sooner than they would otherwise, but their power and wealth would go to their heirs, and so on over the generations, which wouldn’t do much to prevent the creation of an elite. So, no, old age is not an easy way out of the problem of powerful elites ruling the world, and its absence wouldn’t make the problem any worse, really. The only possible way out is giving everyone equal access to knowledge and equal opportunities.

Inevitably, some will end up being more successful and thus more powerful than others anyway; however, if this allows them to become an oppressive force on the rest of us, I think this is a problem with our socio-economic system, not with the existence of lifesaving medical technology. I don’t know about you, but I’m not very keen on waiting until the “perfect” society or “perfect” economic system are built before we decide to cure the diseases of old age.

The fortune teller’s error

We shouldn’t make the mistake of predicting a negative outcome without considering the actual odds of it happening. I think fears of a society where rejuvenated elderly make younger people’s lives more difficult are misplaced in that they assume present-day scenarios will exist in the far future.

Take the concern about jobs, for example, rejuvenated old people would stick to their jobs forever and make it harder for young people to enter the workforce. It sounds bad, but there are a few assumptions behind it that we should question.

First, would rejuvenated old people actually stick to their jobs forever? Why? You hardly hear of a professional who was in the exact same job for forty years these days. More broadly, career change is a thing already. After all, after 40 years in the same line of work, it’s conceivable you might want to try something else, thus making room for others to take your place.

Will rejuvenated old people be allowed to stick to their jobs forever? Not everyone is a manager in charge of decisions, and your boss may well decide to lay you off, rejuvenated or not, and hire someone else.

Even if old rejuvenated people did stick to the same jobs forever, would they never take a break? Even if you’re in the prime of health, after a few decades, you may well wish to “retire” for a few years before going back to work, and your employer is probably not going to wait for you that long.

Will there be so many chronologically younger people in need of jobs in the future? The world population growth rate has been hopelessly corkscrew-diving for over 50 years now, and it is projected to keep going down as larger portions of the world transition from a developing to a developed economy. (In case you’re wondering, the population growth rate is going down not because more people die, but on the contrary, because fewer are born.)

Will people’s living depend on having a job in the future? We can’t expect indefinite life extension to happen very soon; before we can have 200-year-old people in the workforce, it’ll be at least a century. Is the economy going to be the same as today’s by then? Automation already seems on its way to cause the end of work as we know it.

I’d say it’s rather silly to oppose rejuvenation today for the reason that, in a century or two, it might cause an unemployment problem due to too many people being alive. It’s simply too long a time to make any even remotely accurate predictions on what the job market will be like or if there even will be any. In all honesty, I think it makes more sense to worry about a concrete problem that we already have today—the ill health of old age—than worry about a hypothetical one that might or might not happen in a hundred years’ time—massive unemployment. As time goes by, we’ll have a better picture of potential future problems lying ahead, and we’ll be in a better position than we are in today to do something about them.

Conclusion

I’ve said this many times over: the bottom line is always the same. Yes, life extension will most likely bring challenges along with benefits, but none of these challenges are certain, insurmountable, or not more than compensated for by the expected benefits. Let’s not deny ourselves and our descendants the chance for healthier, longer lives.

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.

We are the Lifespan – Video and Commentary by the Life Extension Advocacy Foundation

We are the Lifespan – Video and Commentary by the Life Extension Advocacy Foundation

Comments 0 Comment

logo_bg

Life Extension Advocacy Foundation

The U.S. Transhumanist Party is pleased to share this message and video from our allies at LEAF – the Life Extension Advocacy Foundation. The video includes a short clip of remarks from U.S. Transhumanist Party Chairman Gennady Stolyarov II, taken from his video for the “I am the Lifespan” campaign.

As you might remember, during the month of October (often called Longevity Month) we at LEAF were accepting videos to hear your reasons why defeating the diseases of aging is so important — and hear from you we did!

Dozens of videos poured in, and this #GivingTuesday we at LEAF are so proud to share with you all a video that shows how strong we can be when we join forces for longer, healthier lives — how together #WeAreTheLifespan.

Thank you so much for raising your voice with us in support of longevity research, and if you wish to continue to help us please feel free to join our Hero campaign or to participate in Facebook’s #GivingTuesday donation match by clicking any of the donate buttons on our Facebook page or posts. If you want to get creative, you can even make your own fundraisers easily on Facebook on posts or with a live video.

Finally, to illustrate the importance of speaking freely on what you care about, we are pleased to let you know of the developments related to the recent Open Consultation on the 13th draft programme of work of the WHO. As we wrote not long ago, the problems related to population aging and corresponding health and social issues were left out of the draft, and we invited the members of the community to step in and recommend an improvement.

90% of responses during the Open Consultation (out of around 400 responses) underlined the need to make healthy longevity one of the priorities for the 13th programme of work, and the WHO have recognized this. A joint effort of many pro-longevity organizations made that happen.

Each voice matters. Your voice matters. So please, keep being active and vocal, and let’s become the generation who can say: “I helped set all people free from age-related diseases. I helped defeat aging.”

Thank you, and happy #GivingTuesday!

Stem-Cell Clinical Trials Show Remarkable Results Against Age-Related Frailty – Article by Steve Hill

Stem-Cell Clinical Trials Show Remarkable Results Against Age-Related Frailty – Article by Steve Hill

Comments 1 comment

Steve Hill

Editor’s Note: In this article, Mr. Steve Hill discusses two very promising human clinical trials using stem cell therapy for age-related frailty. This article was originally published by the Life Extension Advocacy Foundation (LEAF) .

~ Kenneth Alum, Director of Publication, U.S. Transhumanist Party, October 29, 2017

The first results of two human clinical trials using stem cell therapy for age-related frailty have been published, and the results are very impressive indeed. The studies show that the approach used is effective in tackling multiple key age-related factors.

Aging research has made significant progress in the last few years, with senescent-cell-clearing therapies entering human trials this year, DNA repair in human trials, and a number of other exciting therapies nearing human testing. We are reaching the point where therapies that target aging processes are no longer a matter of speculation; they are now an undeniable matter of fact.

What are mesenchymal stem cells?

Mesenchymal stem cells (MSCs) are one of the most commonly used types of stem cells in therapy. MSCs are adult stem cells that can become other types of cells, depending on stimulus; this ability to become a variety of other cell types is known as multipotency. [1]

The cells into which MSCs can transform (differentiate) include osteoblasts (bone cells), chondrocytes (cartilage cells), myocytes (muscle cells), and adipocytes (fat cells). MSCs are of great interest to aging researchers and are arguably one of the most well studied and understood types of stem cells. [2]

MSCs are currently in various trials to treat conditions such as cancer, heart disease, and arthritis. [3] The potential of MSCs for treating neurodegenerative diseases, such as Alzheimer’s, are also being explored in preclinical testing. [4-5]

A therapy for age-related frailty

The focus of the MSC therapy in the case of these two clinical trials is to reduce the effects of age-related frailty on senior citizens. This also marks an important step for rejuvenation biotechnology, as this is the first stem-cell treatment that is close to final FDA approval for specifically targeting age-related frailty. Should this be approved, then it opens the door for other similar approaches and the potential treatment of many age-related diseases.

The therapy itself uses MSCs taken from adult donor bone marrow and is infused into patients with an average age of 76 years old. The good news is that patients in both the phase 1 and phase 2 clinical trials have shown no adverse effects to treatment.

This is excellent news and now paves the way to move to phase 3 clinical trials, which are larger-scale tests to further determine the efficacy and compare it to the best currently available treatments, for which there are basically none beyond simple coping approaches, such as walking sticks and frames to compensate for frailty.

It is also important to note that at this at this point, the drug or therapy is accepted as having some effect. You can read more about the clinical trial process and what each phase means here.

In the first trial, 15 patients with age-related frailty were given a single transplant of MSCs from donors aged between 20 and 45. [6] Six months later, all patients in the trial showed an improved level of fitness, lower levels of inflammatory tumor necrosis factor (TNF), and improved quality of life in general. TNF is one of the regulators of inflammation and contributes to the chronic age-related inflammation known as “inflammaging”, which drives a number of age-related diseases. [7]

The second trial was a randomized, double-blind study including a placebo group. An improved physical performance level was observed in patients, and, again, the level of systemic TNF, and thus inflammation, was reduced. [8] Once again, there were no adverse effects observed in the patients, and the researchers wrote:

Treated groups had remarkable improvements in physical performance measures and inflammatory biomarkers, both of which characterize the frailty syndrome.

David G. Le Couter and colleagues have written about the clinical trials in a guest editorial in The Journals of Gerontology:

There are always caveats associated with interpreting efficacy in small numbers of subjects, yet it is remarkable that a single treatment seems to have generated improvement in key features of frailty that are sustained for many months.

The next step for the researchers here is to begin a phase 2b clinical trial with 120 patients in ten different locations. Following the conclusion of this, a large randomized phase 3 trial will be launched, and this will be the final barrier to public approval for the therapy.

Conclusion

With an ever-increasing number of aged people in our population, stem cells hold great potential for treating a number of age-related diseases and combating the disability and frailty that accompany the aging process. Developing therapies like these could potentially help older people to enjoy an improved level of physical performance and a better quality of life. Being able to remain mobile and independent as we grow older would be of huge benefit to not only the individual but also to families and society as a whole.

There are currently no FDA-approved treatments for age-related frailty, so this represents a huge unmet need that will only worsen with an increasingly aging population if those needs are not met by new medicines.

Seeing such tangible results in humans is a clear indication of the potential of rejuvenation biotechnology, and how we regard and treat aging will be changing in the near future.

Literature

[1] Nardi, N. B., & da Silva Meirelles, L. (2008). Mesenchymal stem cells: isolation, in vitro expansion and characterization. In Stem cells (pp. 249-282). Springer Berlin Heidelberg.

[2] Stolzing, A., Jones, E., McGonagle, D., & Scutt, A. (2008). Age-related changes in human bone marrow-derived mesenchymal stem cells: consequences for cell therapies. Mechanisms of ageing and development, 129(3), 163-173.

[3] Wang, S., Qu, X., & Zhao, R. C. (2012). Clinical applications of mesenchymal stem cells. Journal of hematology & oncology, 5(1), 19.

[4] Danielyan, L., Beer-Hammer, S., Stolzing, A., Schäfer, R., Siegel, G., Fabian, C., … & Novakovic, A. (2014). Intranasal delivery of bone marrow-derived mesenchymal stem cells, macrophages, and microglia to the brain in mouse models of Alzheimer’s and Parkinson’s disease. Cell transplantation, 23(1), S123-S139.

[5] Naaldijk, Y., Jaeger, C., Fabian, C., Leovsky, C., Blüher, A., Rudolph, L., … & Stolzing, A. (2017). Effect of systemic transplantation of bone marrow‐derived mesenchymal stem cells on neuropathology markers in APP/PS1 Alzheimer mice. Neuropathology and applied neurobiology, 43(4), 299-314.

[6] Golpanian, S., DiFede, D. L., Khan, A., Schulman, I. H., Landin, A. M., Tompkins, B. A., … & Levis-Dusseau, S. (2017). Allogeneic Human Mesenchymal Stem Cell Infusions for Aging Frailty. Journals of Gerontology Series A: Biomedical Sciences and Medical Sciences, glx056.

[7] Franceschi, C., Garagnani, P., Vitale, G., Capri, M., & Salvioli, S. (2017). Inflammaging and ‘Garb-aging’. Trends in Endocrinology & Metabolism, 28(3), 199-212.

[8] Tompkins, B. A., DiFede, D. L., Khan, A., Landin, A. M., Schulman, I. H., Pujol, M. V., … & Mushtaq, M. (2017). Allogeneic Mesenchymal Stem Cells Ameliorate Aging Frailty: A Phase II Randomized, Double-Blind, Placebo-Controlled Clinical Trial. Journals of Gerontology Series A: Biomedical Sciences and Medical Sciences, 72(11), 1513-1522.

 

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 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.

Hallmarks of Aging: Epigenetic Alterations – Article by Steve Hill

Hallmarks of Aging: Epigenetic Alterations – Article by Steve Hill

Comments 0 Comment

Steve Hill

Editor’s Note: In this article, Mr. Steve Hill discusses one of the hallmarks of aging – in this case, Epigenetic Alterations. It is part of a paper published in 2013. It divides aging into a number of distinct categories (“hallmarks”) of damage to explain how the aging process works and how it causes age-related diseases [1]. This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                        ~ Kenneth Alum, Director of Publication, U.S. Transhumanist Party, October 18, 2017

What are epigenetic alterations?

The DNA in every one of our cells is identical, with only small variations, so why do our various organs and tissues look so different, and how do cells know what to become?

DNA is modified by the addition of epigenetic information that changes the pattern of gene expression in a cell, suppressing or enhancing the expression of certain genes in a cell as the situation demands. This is how a cell in the liver knows that it needs to develop into a liver cell; the epigenetic instructions make sure that it is given the right orders to become the correct cell type.

At a basic level, these epigenetic instructions make sure that the genes needed to develop into a liver cell are turned on, while the instructions specific to other types of cells are turned off. Imagine if a heart cell was given the wrong instructions and became a bone cell!

How epigenetic alterations accumulate

The aging process can cause alterations to our epigenome, which can lead to alterations in gene expression that can potentially change and ultimately compromise cell function. As an example, epigenetic alterations of the immune system can harm activation and suppress immune cells, thus causing our immune system to fail and leaving us vulnerable to pathogens.

Inflammation is implicated in epigenetic alterations, and studies show that caloric restriction slows the rate of these epigenetic changes [2]. Metabolism and epigenetic alterations are closely linked with inflammation, facilitating a feedback loop leading to ever-worsening epigenetic alterations. Alterations to gene expression patterns are an important driver of the aging process. These alterations involve changes to DNA methylation patterns, histone modification, transcriptional alterations (variance in gene expression) and remodeling of chromatin (a DNA support structure that assists or impedes its transcription).

In the cell, gene expression is activated by hypomethylation (a loss of methylation) or silenced by hypermethylation (an increase of methylation) at a gene location. The aging process causes changes that reduce or increase methylation at different gene locations throughout the body. For example, some tumour suppressor genes become hypermethylated during aging, meaning that they cease functioning, which increases the risk of cancer [3]. Post-translational modifications of histones regulate gene expression by organizing the genome into active euchromatin regions, where DNA is accessible for transcription, or inactive heterochromatin regions, where DNA is compacted and less accessible for transcription. The aging process causes changes to these regions, which changes gene expression.

The aging process also causes an increase in transcriptional noise, which is the primary cause of variance in the gene expression happening between cells [4]. Researchers compared young and old tissues from several species and identified age-related transcriptional changes in the genes encoding key components of inflammatory, mitochondrial, and lysosomal degradation pathways [5].

 Finally, chromatin remodeling alters chromatin from a condensed state to a transcriptionally accessible state, allowing transcription factors and other DNA binding proteins to access DNA and control gene expression.

Conclusion

If we can find ways to reset age-related epigenetic alterations, we can potentially improve cell function, thus improving tissue and organ health.

One potential approach is the use of reprogramming factors, which reset cells to a developmental state, thus reverting epigenetic changes. We have been doing this for over a decade to create induced pluripotent stem cells, and recent work has seen a therapy based on that technique applied to living animals to reset their epigenetic alterations [6]. This reversed a number of age-related changes, and work is now proceeding with the goal of translating this to humans.

Epigenetic alterations might be considered like a program in a computer, but in this case, it is the cell, not a computer, being given instructions. Ultimately, damage causes changes that contribute to the cell moving from an efficient “program” of youth to a dysfunctional one of old age. If we can reset that program, we can potentially address this hallmark of aging, and a number of researchers are working on that right now.

 

Literature

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

[2] Maegawa, S., Lu, Y., Tahara, T., Lee, J. T., Madzo, J., Liang, S., … & Issa, J. P. J. (2017). Caloric restriction delays age-related methylation drift. Nature Communications, 8.
[3] Maegawa, S., Hinkal, G., Kim, H. S., Shen, L., Zhang, L., Zhang, J., … & Issa, J. P. J. (2010). Widespread and tissue specific age-related DNA methylation changes in mice. Genome research, 20(3), 332-340.

[4] Bahar, R., Hartmann, C. H., Rodriguez, K. A., Denny, A. D., Busuttil, R. A., Dollé, M. E., … & Vijg, J. (2006). Increased cell-to-cell variation in gene expression in ageing mouse heart. Nature, 441(7096), 1011-1014.

[5] De Magalhães, J. P., Curado, J., & Church, G. M. (2009). Meta-analysis of age-related gene expression profiles identifies common signatures of aging. Bioinformatics, 25(7), 875-881.

[6] Ocampo, A., Reddy, P., Martinez-Redondo, P., Platero-Luengo, A., Hatanaka, F., Hishida, T., … & Araoka, T. (2016). In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming. Cell, 167(7), 1719-1733.

 

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 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.

Hallmarks of Aging: Genomic Instability – Article by Steve Hill

Hallmarks of Aging: Genomic Instability – Article by Steve Hill

Comments 0 Comment

Steve Hill

Editor’s Note: In this article, Mr. Steve Hill discusses one of the hallmarks of aging – in this case, Genomic Instability. This article was originally published by the Life Extension Advocacy Foundation (LEAF).

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

What is genomic instability?

The cells of your body produce a constant flow of proteins and other materials; these are built according to the blueprints contained in our DNA and are vital to cell function and survival. A large amount of information contained in the DNA is ignored during this process, and this is thought to be junk DNA, remnants of our evolutionary past that are no longer used.

However, if a part of the DNA important to cell function mutates or is damaged, the cell can experience a loss of proteostasis, in which the cell produces misfolded proteins. These misfolded proteins can be very harmful, such as when neurons in the brain produce masses of the toxic amyloid beta protein, as seen in Alzheimer’s disease.

Now, the odd dysfunctional cell is not really a huge problem; however, as we get older, an increasing number of cells succumb to this damage and begin to accumulate in tissue over time. Eventually, the number of these damaged cells reaches a point where tissue or organ function is compromised. Normally, the body removes these problem cells via a self-destruct sequence known as apoptosis, a sort of kill switch that senses the damage and destroys the cell in conjunction with the immune system.

Unfortunately, some cells evade apoptosis, taking up space in the tissue and pumping out inflammatory signals that damage the local tissue. These cells are known as senescent cells, and we will be covering them in a later Hallmarks article.

Another possible outcome of damaged DNA is cells that mutate and do not become senescent cells or destroy themselves via apoptosis. These cells continue to replicate, becoming more mutated each time they divide, and if a mutation damages the systems that regulate cell division or switches off the safety mechanisms against tumor formation, this can lead to cancer. The unchecked and rampant cell growth of cancer is probably the most well-known result of genomic instability.

How DNA damage accumulates

There are many ways for DNA to become damaged. UV rays, radiation, chemicals, and tobacco are all examples of environmental stressors that can damage the genome. Even chemotherapy agents designed to kill cancer can also potentially cause DNA damage and senescent cells, leading to later relapse [2].

Finally, even if we avoided all the external threats to our DNA, the body still damages itself. Reactive oxygen and nitrogen species produced during the operation of normal metabolism can damage both DNA and mitochondrial DNA.

Thankfully, we have evolved a robust network of repair systems and mechanisms that can repair most of this damage. We have enzymes that can detect and repair broken strands of DNA or reverse alterations made to base pairs. This repair process is not perfect, and sometimes the DNA is not repaired. This can lead to the cell replication machinery misreading the information contained in the DNA, causing a mutation.

As mutations are passed to daughter cells, the cell tries to prevent this from happening by checking DNA integrity before and after replication. Unfortunately, some cells do manage to slip through the net.

The consequences of DNA damage

A large number of age-related diseases are linked to damaged DNA or faulty DNA repair systems. Alzheimer’s, Parkinson’s, Lou Gehrig’s disease (ALS), and cancer are all the result of genomic instability.

Another example are the progeric diseases. Progerias are congenital disorders that result in rapid aging-like symptoms and a dramatically shortened lifespan, with Hutchinson-Gilford progeria syndrome (HGPS) probably being the most well known. The disease is caused by a defect in Lamin A, a major component of a protein scaffold on the inner edge of the nucleus called the nuclear lamina. The lamina helps organize nuclear processes, such as RNA and DNA synthesis, and lamins are responsible for supporting key proteins in the DNA repair process.

This defect leads to HGPS sufferers only living until their early 20s and developing atherosclerosis, stiff joints, hair loss and wrinkles, and other accelerated aging-like characteristics.

Conclusion

Despite the various repair systems we have evolved, our body is constantly being assaulted from exposure to environmental stressors and even damaged through its own metabolic processes. Coupled with this, our repair systems also decline in effectiveness over time, meaning that DNA damage and mutations are inevitable.

There is some evidence to suggest that caloric restriction may help combat this, but as of now, no drugs or therapies are available yet that can prevent or repair DNA damage. The good news is human trials for DNA repair are launching this year at Harvard, and Dr. David Sinclair and other researchers are also working on their own solutions.

For the time being, the best we can do is to avoid risks, such as excessive sun exposure, industrial chemicals, smoking, and, of course, staying away from radioactive waste; there are no comic-book superpowers from these mutations!

Literature

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

[2] Demaria, M., O’Leary, M. N., Chang, J., Shao, L., Liu, S., Alimirah, F., … & Alston, S. (2017). Cellular senescence promotes adverse effects of chemotherapy and cancer relapse. Cancer discovery, 7(2), 165-176.

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 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

Comments 0 Comment

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.

I am the Lifespan – Video by Gennady Stolyarov II

I am the Lifespan – Video by Gennady Stolyarov II

Comments 1 comment

logo_bg

Gennady Stolyarov II

Gennady Stolyarov II, Chairman of the United States Transhumanist Party, discusses why longevity research is crucial, and how our generation stands on the threshold of finally dealing a decisive blow to the age-old enemies of aging and death, which have destroyed great human minds since the emergence of our species.

This video is part of the #IAmTheLifespan campaign, coordinated by Lifespan.io and the Life Extension Advocacy Foundation (LEAF) for Longevity Month, October 2017. Read more about this campaign here.

Become a member of the U.S. Transhumanist Party for free, no matter where you reside. Fill out our Membership Application Form here.

Become a Foreign Ambassador for the U.S. Transhumanist Party. Apply here.

LEAF Panel: How to Promote Longevity? ft. Drs. Aubrey de Grey, Alexandra Stolzing, Oliver Medvedik

LEAF Panel: How to Promote Longevity? ft. Drs. Aubrey de Grey, Alexandra Stolzing, Oliver Medvedik

Comments 0 Comment

logo_bg

Keith Comito
Oliver Medvedik
Steve Hill
Elena Milova
Aubrey de Grey
Alexandra Stolzing
Alen Akhabaev

The U.S. Transhumanist Party is pleased to feature this extensive discussion, hosted by our allies at LEAF – the Life Extension Advocacy Foundation.

Description by LEAF: Dr. Alexandra Stolzing, Dr. Aubrey de Grey, Dr. Oliver Medvedik and a number of other guests discuss longevity, advocacy and rejuvenation biotechnology in an exclusive panel hosted by the Life Extension Advocacy Foundation (LEAF). This panel, moderated by LEAF president Keith Comito, talks about the latest progress in rejuvenation biotechnology and about how to engage, educate and excite the public regarding cutting-edge medicine.

Panel: Dr. Alexandra Stolzing, Dr. Aubrey de Grey, Dr. Oliver Medvedik , Elena Milova, Keith Comito, Steve Hill and Alen Akhabaev.

Subscribe to LEAF’s video channel for more.

Support LEAF’s work by becoming a “Lifespan Hero”: http://lifespan.io/hero

A “Disease” Approach in Life-Extension Advocacy Can Facilitate Communication with the General Public – Infographic by Elena Milova and Keith Comito

A “Disease” Approach in Life-Extension Advocacy Can Facilitate Communication with the General Public – Infographic by Elena Milova and Keith Comito

Comments 0 Comment

logo_bg

Elena Milova and Keith Comito

The U.S. Transhumanist Party is pleased to share this infographic from our friends at the Life Extension Advocacy Foundation (LEAF), one of the Transhumanist Party’s most active Allied Organizations. Life-extension advocates Elena Milova and Keith Comito have compiled a set of tips for communicating ideas regarding the progress of medical science and technology, for the pursuit of healthy life extension, in such a manner as to enable many in the general public to understand and sympathize with our goals and the science behind them. We encourage you to distribute this infographic to any activists and advocates who you think would benefit from the advice therein.

LEAF Interview with Dr. Aubrey de Grey: Controlling the Main Aging Damages

LEAF Interview with Dr. Aubrey de Grey: Controlling the Main Aging Damages

Comments 1 comment

logo_bg

Aubrey de Grey and Life Extension Advocacy Foundation

The U.S. Transhumanist Party is pleased to feature this interview of Dr. Aubrey de Grey, the Transhumanist Party’s Anti-Aging Advisor, conducted by Elena Milova of the Life Extension Advocacy Foundation (LEAF), one of the Transhumanist Party’s most active Allied Organizations. You can also see this interview on YouTube here.

Description by LEAF: Please enjoy this interview with Dr. Aubrey de Grey, Chief Science Officer and Co-founder of SENS Research Foundation — one of the most successful advocacy and fundraising initiatives supporting breakthrough research on the main mechanisms of aging and age-related diseases.

In this video Dr. de Grey speaks about the progress in developing interventions to tackle age-related damages identified by SENS as the main ones.

Interviewer – LEAF/Lifespan.io Board member Elena Milova.

Dr. de Grey received his BA in Computer Science and Ph.D. in Biology from the University of Cambridge in 1985 and 2000, respectively. He is Editor-in-Chief of Rejuvenation Research , is a Fellow of both the Gerontological Society of America and the American Aging Association, and sits on the editorial and scientific advisory boards of numerous journals and organizations.

Subscribe to Lifespan.io’s YouTube channel for more.

This interview is presented by LEAF. Please support its work by becoming a “Lifespan Hero“.