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U.S. Transhumanist Party Chairman Gennady Stolyarov II Interviewed by Nikola Danaylov of Singularity.FM

U.S. Transhumanist Party Chairman Gennady Stolyarov II Interviewed by Nikola Danaylov of Singularity.FM

logo_bgGennady Stolyarov II
Nikola Danaylov


On March 31, 2018, Gennady Stolyarov II, Chairman of the U.S. Transhumanist Party, was interviewed by Nikola Danaylov, a.k.a. Socrates, of Singularity.FM. A synopsis, audio download, and embedded video of the interview can be found on Singularity.FM here. You can also watch the YouTube video recording of the interview here.

Apparently this interview, nearly three hours in length, broke the record for the length of Nikola Danaylov’s in-depth, wide-ranging conversations on philosophy, politics, and the future.  The interview covered both some of Mr. Stolyarov’s personal work and ideas, such as the illustrated children’s book Death is Wrong, as well as the efforts and aspirations of the U.S. Transhumanist Party. The conversation also delved into such subjects as the definition of transhumanism, intelligence and morality, the technological Singularity or Singularities, health and fitness, and even cats. Everyone will find something of interest in this wide-ranging discussion.

The U.S. Transhumanist Party would like to thank its Director of Admissions and Public Relations, Dinorah Delfin, for the outreach that enabled this interview to happen.

To help advance the goals of the U.S. Transhumanist Party, as described in Mr. Stolyarov’s comments during the interview, become a member for free, no matter where you reside. Click here to fill out a membership application.

Beginners’ Explanation of Transhumanism – Bobby Ridge and Gennady Stolyarov II

Beginners’ Explanation of Transhumanism – Bobby Ridge and Gennady Stolyarov II

logo_bg

Bobby Ridge
Gennady Stolyarov II


Bobby Ridge, Secretary-Treasurer of the U.S. Transhumanist Party, and Gennady Stolyarov II, Chairman of the U.S. Transhumanist Party, provide a broad “big-picture” overview of transhumanism and major ongoing and future developments in emerging technologies that present the potential to revolutionize the human condition and resolve the age-old perils and limitations that have plagued humankind.

This is a beginners’ overview of transhumanism – which means that it is for everyone, including those who are new to transhumanism and the life-extension movement, as well as those who have been involved in it for many years – since, when it comes to dramatically expanding human longevity and potential, we are all beginners at the beginning of what could be our species’ next great era.

Become a member of the U.S. Transhumanist Party for free, no matter where you reside.

See Mr. Stolyarov’s presentation, “The U.S. Transhumanist Party: Pursuing a Peaceful Political Revolution for Longevity“.

In the background of some of the video segments is a painting now owned by Mr. Stolyarov, from “The Singularity is Here” series by artist Leah Montalto.

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

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

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

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

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

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.

International Team Publishes Roadmap to Enhance Radioresistance for Space Colonization – Press Release by Biogerontology Research Foundation

International Team Publishes Roadmap to Enhance Radioresistance for Space Colonization – Press Release by Biogerontology Research Foundation

Biogerontology Research Foundation


 

IMAGE: These are ways to reduce health risks from space radiation during deep space travels. Multiple approaches from medical selection of radioresistant individuals to gene therapy may be proposed.

Editor’s Note: Below is a press release by the Biogerontology Research Foundation which features a roadmap to enhance radioresistance for space exploration and colonization, published by an international team of scientists from NASA, Health Canada, Canadian Nuclear Laboratories and many other organizations. This press release was originally published here.

~ Dinorah Delfin, Director of Admissions and Public Relations, U.S. Transhumanist Party, February 22, 2018

An international team of researchers from NASA Ames Research Center, Environmental and Radiation Health Sciences Directorate at Health Canada, Oxford University, Canadian Nuclear Laboratories, Belgian Nuclear Research Centre, Insilico Medicine, the Biogerontology Research Center, Boston University, Johns Hopkins University, University of Lethbridge, Ghent University, Center for Healthy Aging, and many others have published a roadmap toward enhancing human radioresistance for space exploration and colonization in the peer-reviewed journal Oncotarget.

“Our recent manuscript provides a comprehensive review of radioresistance for space radiation. Currently there is minimal research being done for radioresistance against HZE irradiation. The importance of these types of studies will be to reduce the associated health risks for long-term space exploration and allow for the development of potential countermeasures against space radiation. In addition, the synergy between understanding aging with radioresistance will allow for further benefits for humans in long-term space missions and allow for reduced health risk. This review sets the stage for the potential research the scientific community can do to allow for safe long term space exploration” said Afshin Beheshti, an author of the paper and a Bioinformatician at NASA Ames Research Center.

The roadmap outlines future research directions toward the goal of enhancing human radioresistance, including upregulation of endogenous repair and radioprotective mechanisms, possible leeways into gene therapy in order to enhance radioresistance via the translation of exogenous and engineered DNA repair and radioprotective mechanisms, the substitution of organic molecules with fortified isoforms, the coordination of regenerative and ablative technologies, and methods of slowing metabolic activity while preserving cognitive function. The paper concludes by presenting the known associations between radioresistance and longevity, and articulating the position that enhancing human radioresistance is likely to extend the healthspan of human spacefarers as well.

“This paper explores the foreseeable means by which human radioresistance could be biomedically enhanced for the purposes of space exploration and colonization. It also aims to elucidate the links between aging, longevity and radioresistance, and the ways in which research into enhancing human radioresistance could synergistically enable human healthspan extension, ultimately highlighting how ongoing research into the very well-funded sphere of aerospace research could galvanize progress in biomedical gerontology, a massively under-funded area of research despite the grave economic burden posed by demographic aging” said Franco Cortese, an author of the paper and Deputy Director of the Biogerontology Research Foundation.

The publication of the paper in Oncotarget this week is timely, given the test launch of the Falcon Heavy, SpaceX’s largest rocket to date, just last week. Interest into space exploration and even colonisation has been mounting for a number of years. Less than one year ago Elon Musk, CEO of SpaceX, unveiled a roadmap toward colonizing Mars, outlining the ambitious goal of placing a million people on Mars within the next 40 to 100 years. If interest in space colonization continues apace, research into methods of enhancing radioresistance to protect against the various forms of space radiation that spacefarers would be subjected to needs to be accelerated accordingly.

“In linking ageing and radioresistance and tying together research into enhancing the radioresistance of astronauts with the extension of healthy longevity, we hope to have shown how aerospace research could be used to leapfrog the massive funding deficit surrounding the clinical translation of healthspan-extending interventions, in order to brave the storm of the oncoming Silver Tsunami and prevent the looming economic crisis posed by demographic aging” said Dmitry Kaminskiy, an author of the paper and Managing Trustee of the Biogerontology Research Foundation.

The roadmap highlights the need to converge and accelerate research in radiobiology, biogerontology and AI to enable spacefarers to address both the healthcare challenges that we are already aware of, as well as those that we are not.

“Sooner or later we’ll have to do it – leave Earth and wander into deep space. Such travel, taking one or more years outside the Earth’s magnetosphere, would take a high toll on astronauts’ health due to exposure to cosmic radiation. So it’s better to start thinking now about how we are going to cope with that challenge. Luckily, current knowledge from such fields as radiobiology, aging research and biotechnology in general, with the wealth of recent advances in gene editing and regenerative medicine, allow for the drafting of conceptual roadmaps to enhance human resistance to cosmic radiation. This is exactly what this work is all about. It was fun and a pleasure to partake in this theoretical project with such a diverse international team. We were just throwing ideas on the table, some being quite ambitious and futuristic, and then examining them carefully for feasibility and assessing their potential. The work laid out several interesting directions and concepts that can eventually pay off. Last but not least, I think it is also very important to attract widespread attention and interest to this topic” said Dmitry Klokov, an author of the paper and Section Head of the Radiobiology & Health section at Canadian Nuclear Laboratories.

Furthermore, given the massive amount of funding allocated to research into facilitating and optimizing space exploration and optimization, the researchers hope to have shown how research into enhancing radioresistance for space exploration could galvanize progress in human healthspan extension, an area of research that is still massively underfunded despite its potential to prevent the massive economic burden posed by the future healthcare costs associated with demographic aging.

“This roadmap sets the stage for enhancing human biology beyond our natural limits in ways that will confer not only longevity and disease resistance but will be essential for future space exploration” said João Pedro de Magalhães, an author of the paper and a Trustee of the Biogerontology Research Foundation.

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The paper, entitled “Vive la radiorésistance!: converging research in radiobiology and biogerontology to enhance human radioresistance for deep space exploration and colonization”, can be viewed on Oncotarget here.

Citation: Franco Cortese, Dmitry Klokov, Andreyan Osipov, Jakub Stefaniak, Alexey Moskalev, Jane Schastnaya, Charles Cantor, Alexander Aliper, Polina Mamoshina, Igor Ushakov, Alex Sapetsky, Quentin Vanhaelen, Irina Alchinova, Mikhail Karganov, Olga Kovalchuk, Ruth Wilkins, Andrey Shtemberg, Marjan Moreels, Sarah Baatout, Evgeny Izumchenko, João Pedro de Magalhães, Artem V. Artemov, Sylvain V. Costes, Afshin Beheshti, Xiao Wen Mao, Michael J. Pecaut, Dmitry Kaminskiy, Ivan V. Ozerov, Morten Scheibye-Knudsen and Alex Zhavoronkov. Vive la radiorésistance!: converging research in radiobiology and biogerontology to enhance human radioresistance for deep space exploration and colonization, Epub ahead of print. Published online 2018 February 09. doi: 10.18632/oncotarget.24461

About the Biogerontology Research Foundation:

The Biogerontology Research Foundation is a UK non-profit research foundation and public policy center seeking to fill a gap within the research community, whereby the current scientific understanding of the ageing process is not yet being sufficiently exploited to produce effective medical interventions. The BGRF funds and conducts research which, building on the body of knowledge about how ageing happens, aims to develop biotechnological interventions to remediate the molecular and cellular deficits which accumulate with age and which underlie the ill-health of old age. Addressing ageing damage at this most fundamental level will provide an important opportunity to produce the effective, lasting treatments for the diseases and disabilities of ageing, required to improve quality of life in the elderly. The BGRF seeks to use the entire scope of modern biotechnology to attack the changes that take place in the course of ageing, and to address not just the symptoms of age-related diseases but also the mechanisms of those diseases.

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

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

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.

The Hallmarks of Aging: Deregulated Nutrient Sensing – Article by Ariah Mackie

The Hallmarks of Aging: Deregulated Nutrient Sensing – Article by Ariah Mackie

Ariah Mackie


Editor’s Note: In this article, Ariah Mackie explains that there are four key proteins involved in nutrient sensing that might be key contributors to aging.  This article was originally published by the Life Extension Advocacy Foundation (LEAF).

                   ~ Kenneth Alum, Director of  Publication, U.S. Transhumanist Party, February 15, 2018

As part of our ongoing series covering the hallmarks of aging, we are taking a look at deregulated nutrient sensing today and how these four pathways regulate metabolism and influence aging.

To understand studies on nutrient sensing in the context of aging, let’s introduce four key protein groups. In this post, we’ll explore the pathways they help control and how they affect aging. These key proteins are IGF-1, mTOR, sirtuins, and AMPK [2]. We call these proteins “nutrient sensing” because nutrient levels influence their activity [2].

IGF-1 and the IIS pathway: The Basics

Insulin-like growth factor (IGF-1) inhibits the secretion of growth hormone (GH) by binding to a special receptor on the surface of a cell [1]. Like insulin, IGF-1 takes part in glucose sensing. Both it and insulin are part of the aptly named “insulin and insulin-like growth factor” (IIS) pathway [2].

Attenuation of the IGF-1/GH pathway (IIS) appears to improve lifespan in several model organisms [1]. For example, PI3K mice, which have a weakened IIS pathway, live longer [2]. Additionally, FOXO, a transcription factor (a protein that affects the production of RNA), lengthens lifespans in worms and fruit flies by attenuating IIS signaling [2]. In other studies, IGF-1 improves healthspan even when it does not lengthen lifespan [2].

There’s also evidence of a harmful impact when IGF-1 activity is high. Higher levels of IGF-1 are associated with increased risk of some types of cancer [1]. This increased cancer risk might be due to IGF’s ability to promote pathways that result in increased cell production [1].

IIS and the Not-So-Basics

IGF-1 expression and the IIS pathway are a bit of a paradox. Since it looks like turning down the IIS pathway promotes longevity, you might expect the IIS pathway to be very active in old organisms. It looks like high IIS ages us, after all. However, that’s not the case. In both accelerated and normal aging models, we see that the IIS pathway decreases [2].

One explanation for this weirdness is that it’s a last-ditch measure of the organism to increase its own lifespan. Yet, this short-term decrease in IIS activity can be harmful. In fact, it is so harmful that IGF-1 supplementation is beneficial [2]. What this seems to point to is a dichotomy concerning the expression of IIS. Overall, it looks like turning down the IIS pathway is good over the long term for longevity. This might be because it causes the reduction of metabolism and cell growth, which lessens wear and tear [2]. However, the body’s attempt to do the same in later life goes too far and too late to be truly beneficial.

How IGF-1 affects human lifespan is still fuzzy as well [1]. On one hand, there is an indication of a longevity effect with reduced IGF-1 activity in those with Laron syndrome (who don’t have functional growth hormone receptors), female nonagenarians, and extremely long-lived people [1]. Yet, the epidemiological data is not clear enough to be conclusive on IGF-1’s effects on humans [1]. This is partially due to the difficulty of structuring epidemiological studies on IGF-1, as many external factors, such as nutrition, can confound results [1].

mTOR

Mechanistic target of rapamycin (mTOR) is composed of the mTORC1 and mTORC2 protein complexes. It senses amino acids and is associated with a nutrient abundance [2]. It is a kinase, which means it adds phosphates to molecules [2]. mTOR is a champion regulator of anabolic metabolism [2], the process of building new proteins and tissues. In this way, how it functions is similar to the IIS pathway [2]. At any given moment, the metabolism is either breaking down old parts (catabolism) or building new ones (anabolism). Both mTOR and the IIS are part of the anabolic side of metabolism.

Lower activity of mTOR lengthens lifespan in model organisms, such as mice, yeast, worms, and flies [2]. Along those lines, mTOR activity increases in the hypothalami of aged mice, which promotes late-life obesity. With rapamycin, an inhibitor of mTOR, these effects are ameliorated [2]. As is the case with, IIS, lowered expression of mTOR is not always beneficial. Low expression of mTOR can harm healing and insulin sensitivity and can cause cataracts and testicular generation in mouse models [2].

Sirtuins

Sirtuins are a family of proteins that act as NAD(+) dependent histone deacetylases [2]. To explain what that means, let’s start with histones. Histones are the proteins that DNA wraps around. They serve as a way to compact the DNA (which is very long) in the nucleus, especially during cell division. Histones also help control the expression of genes by spatially making some genes more or less available for proteins like RNA polymerase to attach. On histones, there are lysines, a type of amino acid. It is on these lysines that histone deacetylases remove acetyl groups, which are small molecules. If that sounds too confusing, remember this: adding or removing acetyl groups helps control the expression of genes. In such a manner, sirtuins help control gene expression.

Sirtuins detect when energy levels are low by sensing the coinciding increase of NAD+ [2]. They also help control catabolic metabolism [2]. Upregulating some sirtuins produces anti-aging or health-promoting effects [2]. However, some sirtuins have only weak effects in some species, which makes summarizing their effects difficult. For example, in worms, higher expression of SIR2 yields only slight gains in longevity [2]. Overexpression of SIR2’s most similar counterpart in mice, SIRT1, appears to improve health during aging but not lifespan [2].

Another mouse sirtuin, SIRT6, seems to promote longevity more robustly [2]. Mice deficient in it experience accelerated aging. Conversely, turning it up results in increased longevity [2]. There is also SIRT3, which has been shown to help the regeneration ability of old hematopoietic (blood and immune cell producing) cells when overexpressed [2].

AMPK

AMP-activated kinase (AMPK) senses AMP (adenosine monophosphate) and ADP (adenosine diphosphate). These long-named molecules are present in higher quantities when nutrients are scarce [2].Therefore, it is easiest to remember AMPK as a sensor of fasted or calorie-restricted states and catabolism [2]. Molecularly, AMPK acts by adding phosphates to serine and threonine [3]. By doing so, AMPK helps regulate metabolism [2].

Like sirtuins, higher activity of AMPK has longevity-promoting effects [2]. To illustrate, metformin, a diabetes drug that appears to have a life-extension effect, activates AMPK in mice and worms [2]. Calorie restriction, which is known to increase lifespan in at least short-lived animals, can also increase the activity of AMPK [3]. Conversely, less AMPK sensitivity due to cellular stress results in oxidative stress, reduced autophagy, metabolic syndrome, more fat disposition, and inflammation [3].

Conclusion

In summary, there are four key proteins involved in nutrient sensing that might be key contributors to aging. Turning down the pathways of the first two, IGF-1 and mTOR, promote longevity. Both of these are involved in anabolic metabolism (building tissues) and increase in states of nutrient abundance[2]. Conversely, turning up the activity of the last two, sirtuins and AMPK, helps longevity. They work to promote catabolic metabolism (breaking down tissues) and increase with nutrient scarcity [2].

References

[1] Milman, S., Huffman, D. M., & Barzilai, N. (2016). The Somatotropic Axis in Human Aging: Framework for the Current State of Knowledge and Future Research. Cell Metabolism, 23(6), 980-989. doi:10.1016/j.cmet.2016.05.014

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

[3] Salminen, A., & Kaarniranta, K. (2012). AMP-activated protein kinase (AMPK) controls the aging process via an integrated signaling network. Ageing Research Reviews, 11(2), 230-241. doi:10.1016/j.arr.2011.12.005

About Ariah Mackie

Ariah received a Bachelor’s Degree in Biomolecular Engineering from the University of California in Santa Cruz in 2016. Her career interests are in regenerative medicine for aging, teaching, computational biology, genomics, and bioinformatics.

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.