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Dr. Bill Andrews and U.S. Transhumanist Party Chairman Gennady Stolyarov II Discuss Transhumanism and RAADfest at Sierra Sciences

Dr. Bill Andrews and U.S. Transhumanist Party Chairman Gennady Stolyarov II Discuss Transhumanism and RAADfest at Sierra Sciences

Gennady Stolyarov II
Bill Andrews


On October 12, 2019, Brent Nally recorded this discussion between Dr. Bill Andrews – the Biotechnology Advisor of the U.S. Transhumanist Party / Transhuman Party – and U.S. Transhumanist Party / Transhuman Party Chairman Gennady Stolyarov II regarding recent news in the field of longevity (including pet longevity), techniques to slow down the rate of telomere shortening, changes to public perceptions of aging and longevity, transhumanism and technologies of life enhancement, and how to be rigorous and appropriately skeptical when evaluating various ideas and hypotheses in medicine.

Watch this discussion here and be on the lookout for a special visitor from a different species!

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

Show Notes by Brent Nally

0:35 Dr. Andrews links:

Facebook: https://facebook.com/telomere.bill.andrews;

Linkedin: https://linkedin.com/in/william-h-andrews-5455b45/;

Wikipedia: https://en.wikipedia.org/wiki/William_H._Andrews_(biologist);

Sierra Sciences Website: https://sierrasci.com/;

Sierra Sciences YouTube Channel: https://www.youtube.com/channel/UCB9UFIxyD9VUHjuNQzpLzeA

1:08 Brent’s RAADfest 2019 YouTube playlist. Go to RAADfest primarily to network https://www.raadfest.com/

2:35 USTP concluded its presidential primary elections: watch Gennady Stolyarov II & Johannon Ben Zion at RAADfest 2019; watch Brent interview Mr. Ben Zion at RAADfest 2019; watch Brent interview Mr. Ben Zion and his VP running mate Charlie Kam at RAADfest 2019.

3:10 Bill’s dog Dash makes his cameo appearance.

4:35 Long-distance running and recovery.

7:20 Bill hosted a pet-longevity panel at RAADfest 2019.

12:15 Quacks and charlatans have discredited human longevity for centuries.

13:26 How has the public’s perception of human aging changed in the last decade?

15:10 Buy Bill’s 2 books: Curing Aging and Telomere Lengthening. See Brent’s book review of Telomere Lengthening: Curing all diseases including cancer & aging by Dr. Bill Andrews

15:25 Inflammation is the number one cause of human aging.

16:47 Do fun activities, meditate, practice yoga, eat a healthy diet, reduce stress to decrease the rate of telomere shortening.

18:48 Caldwell Esselstyn – Wikipedia

19:10 Watch Brent’s interview with Dr. Sandy Kaufmann.

21:33 Funding is needed to cure human aging and all chronic diseases.

24:03 Bill is hoping the telomerase gene therapy clinical study by Libella Gene Therapeutics (which is scheduled to start in November 2019) will show age reversal in the human Alzheimer’s patient in every measurable way.

24:18 Mice telomerase gene therapy study by Dr. by Ron DePinho

26:13 Animals age in different ways.

30:35 Life enhancement should be our focus.

33:08 Most humans living in the 1st world have been transhumanists for quite some time.

35:38 Nanobots

38:02 Get involved in the longevity movement in any way you can – follow thought leaders; donate.

39:40 Dr. Jason Williams

40:30 A race to cure human aging is a great idea to educate people.

43:26 Watch Brent’s interview with USTP Presidential candidate Johannon Ben Zion.

45:15 Spinal-cord repair, prosthetics, stem cells, etc.

51:01 Bill is impressed by stem-cell therapies but warns of charlatans. Watch Brent’s playlist on stem cells.

52:38 Use PubMed to do a meta-analysis of scientific peer-reviewed studies.

Rejuvenation Research Is Now a Mainstream Topic – Article by Steve Hill

Rejuvenation Research Is Now a Mainstream Topic – Article by Steve Hill

Steve Hill


Editor’s Note: In this article, originally published on August 26, 2019, by the Life Extension Advocacy Foundation (LEAF), Mr. Steve Hill reviews an MIT Technology Review article authored by David Adam. Mr. Adam gives his view of the research field of aging, and Mr. Hill is impressed by the factualism compared to the MIT Technology Review’s previous articles that covered the topic. Mr. Hill goes on to discuss aging and lifespan in other species and address the question: Is aging a disease, and does it really matter?

~Bobby Ridge, Assistant Editor, September 9, 2019


It is a sure sign that the tide has turned when mainstream news outlets and magazines start publishing positive articles about aging research and the prospects of rejuvenation.

A refreshing change

Today, I want to highlight an article in MIT Technology Review in which the author, David Adam, gives a sensible and measured overview of what is happening in the field and manages to sidestep the usual negativity and misconceptions that often plague popular science pieces.

Since ancient times, aging has been viewed as simply inevitable, unstoppable, nature’s way. “Natural causes” have long been blamed for deaths among the old, even if they died of a recognized pathological condition. The medical writer Galen argued back in the second century AD that aging is a natural process.

His view, the acceptance that one can die simply of old age, has dominated ever since. We think of aging as the accumulation of all the other conditions that get more common as we get older—cancer, dementia, physical frailty. All that tells us, though, is that we’re going to sicken and die; it doesn’t give us a way to change it. We don’t have much more control over our destiny than a Cyclops.

But a growing number of scientists are questioning our basic conception of aging. What if you could challenge your death—or even prevent it altogether? What if the panoply of diseases that strike us in old age are symptoms, not causes? What would change if we classified aging itself as the disease?

The article skips the sensationalism and assumptions that many journalists typically make about aging research; instead, we get a solid piece of factual journalism. This is in stark contrast to the reporting done by this outlet a few years ago, as it had published irrationally skeptical and frequently negative coverage of the field and the science behind it.

This may be partially due to changes to the editorial staff at the magazine, which happened in 2017, but it is also indicative of the wider acceptance of the idea that we may be able to do something about aging. The same magazine has even published a special issue entitled Old Age is Over! – If you want it, which takes a deeper dive into the topic, though this is paid content.

There may be a choice about how we age

For millennia, it has been assumed that aging is a one-way street and that we must simply accept that there is nothing we can do about it, aside from facing age-related ill health with stoicism. However, the situation has somewhat changed. As researchers have discovered more about how aging works, the processes driving it, and the results from model animals, it has become increasingly clear to many people that something might be done about aging in order to delay, prevent, or potentially reverse age-related diseases.

We already know that a number of species do not age; this phenomenon is known as negligible senescence. This simply means that the organism does not show a decline of survival characteristics, such as muscle strength, mobility, and senses. Such species also do not experience an increased mortality rate with advancing age or a loss of reproductive capability with age.

These species tend to have much more efficient repair systems that are capable of offsetting and repairing damage rapidly enough to prevent it from accumulating and snowballing out of control as it does in humans. We are relatively long-lived as a species, but, compared to some longevity champions, such as the bowhead whale at 200 years plus, the Greenland shark at 400 or more years, and the ocean quahog clam, which lives at least 507 years, our lifespan is relatively brief.

So, the race is now on to see if we can develop therapies to repair age-related damage, slow down how fast that damage accrues, and see if we can emulate these kings of longevity. The key take-home message here is that there is no biological reason that humans might not live longer, healthier lives if such therapies are developed.

Exactly how long that might be is a matter of speculation; it could be a few years, a decade or two, or perhaps more. The key point is that the researchers who are developing these therapies are aiming to make those extra years healthy ones, and that is surely something that most people can get behind.

Is aging a disease, and does it really matter?

Some researchers propose that aging is a disease, and while this is a somewhat contentious view, it has some merit and is absolutely worthy of further discussion. We discussed if aging is natural or pathological in a previous article, and while the case can certainly be made that aging is a disease, it may more accurately fit the description of a co-morbid syndrome: a group of symptoms that consistently occur together and a condition characterized by a set of associated symptoms.

Whether or not they believe in either the disease hypothesis or maximum life spans, most experts agree that something has to change in the way we deal with aging. “If we don’t do something about the dramatic increase in older people, and find ways to keep them healthy and functional, then we have a major quality-­of-life issue and a major economic issue on our hands.” – Dr. Brian Kennedy

This matter is largely a matter of semantics, and the important thing is that, from a regulatory point of view, including aging as a disease state or syndrome would make it easier to develop therapies that directly target the aging processes themselves. Currently, therapies must focus on single diseases in order to progress through clinical trials, which is not the most optimal approach.

However, it is my personal view that this situation will not change much until the first successful human demonstration of rejuvenation therapy occurs. Until then, researchers will continue to work within the current regulatory system, and while this is, by its nature, slower, it does not prevent progress being made. Fortunately, there are now a lot of companies working in this space, and a number of therapies are quite far along in development.

A therapy that works in humans against one age-related disease by targeting an aging process directly could potentially treat a slew of other related diseases, and so any successful therapy making it through the system would likely rapidly see off-label usage for other, similar conditions.

Conclusion

In closing, it is refreshing to see more balanced and fair reporting on the field and the science of aging rather than the negative and highly biased material that this outlet had published prior to 2017. Reasonable skepticism is perfectly understandable, especially in a field as cutting-edge as rejuvenation biotechnology, which is charting unknown waters and attempting to do what has long been thought impossible.

However, the weight of evidence, the results of a myriad of animal studies demonstrating age reversal, and the rapid increase of scientific understanding should balance that skepticism in anyone interested in science and the actual facts. A magazine devoted to science really should be at the top of its game when reporting the facts, and this and other recent articles on the topic have been much closer to this mark. Oh my, how times have changed.

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.

Human Pilot Study Results for Senolytics Published – Article by Steve Hill

Human Pilot Study Results for Senolytics Published – Article by Steve Hill

Steve Hill


Editor’s Note: The U.S. Transhumanist Party features this article by Steve Hill, originally published by our allies at the Life Extension Advocacy Foundation (LEAF) on January 7, 2019. This article presents the results of a human pilot study that involved the consumption of two promising senolytic drugs, dasatinib and quercetin, to target idiopathic pulmonary fibrosis. The results are promising and constitute a great step forward for senolytics being tested in human clinical trials. Another promising approach is the TAME trial, which is a double-blind randomized controlled clinical trial, to test if Metformin can treat various age-related diseases. 

~Bobby Ridge, Assistant Editor, July 4, 2019

The results from a human pilot study that focused on treating idiopathic pulmonary fibrosis with senescent cell-clearing drugs has been published. The drugs target aged and damaged cells, which are thought to be a reason we age and get sick, and remove them from the body.

Senescent cells and aging

As we age, increasing numbers of our cells become dysfunctional, entering into a state known as senescence. Senescent cells no longer divide or support the tissues and organs of which they are part; instead, they secrete a range of harmful inflammatory chemical signals, which are collectively known as the senescence-associated secretory phenotype (SASP).

Dr. Judith Campisi from the Buck Institute for Research on Aging, along with her research team, identified that senescent cells secreted the various harmful chemicals that characterize the SASP in 2008, which was when interest in senescent cells really began [1]. In 2010, building on this initial research, Dr. Campisi went on to show the link between the SASP and cancer [2].The SASP increases inflammation, harms tissue repair and function, causes the immune system to malfunction, and raises the risk of developing age-related diseases such as cancer. It can also encourage other nearby healthy cells to become senescent via the so-called bystander effect. Therefore, a small number of these cells can cause a great deal of harm.

Normally, senescent cells destroy themselves by a self-destruct process known as apoptosis before being cleared away by the immune system. Unfortunately, as we age, the immune system becomes weaker, and senescent cells start to build up in the body. The accumulation of senescent cells is considered to be one of the reasons why we age and develop age-related diseases.

It has been suggested that the clearance of senescent cells might help address a number of age-related diseases at once, as senescent cells are thought to be one of the fundamental reasons that we age. Drugs that can remove these unwanted, damaged cells are known as senolytics.

Human trial results for senolytics

This new publication by researchers at the Mayo Clinic, including James Kirkland, one of the pioneers of senolytic drugs, shows the results of a pilot study that uses dasatinib and quercetin to treat idiopathic pulmonary fibrosis [3].

Pulmonary fibrosis causes scarring of the lung tissue, which leads to the progressive loss of lung function over time. When the disease’s origin is unknown, it is called idiopathic pulmonary fibrosis, or IPF. The treatment options for this disease are extremely limited with no currently known cure.

The researchers in this new study tested a combination of dasatinib and quercetin, one of the earliest senolytic drug combinations that was tested in mice and shown to have beneficial results, particularly for the cardiovascular system [4-5]. It was also shown in a previous study that clearing senescent cells using dasatinib plus quercetin was able to alleviate idiopathic pulmonary fibrosis (IPF)-related dysfunction in a mouse model of the disease.

Fourteen patients with IPF were recruited for this pilot study, and the initial results, while leaving room for improvement, are promising.

Physical function evaluated as 6-min walk distance, 4-m gait speed, and chair-stands time was significantly and clinically-meaningfully improved (p < .05). Pulmonary function, clinical chemistries, frailty index (FI-LAB), and reported health were unchanged. DQ effects on circulating SASP factors were inconclusive, but correlations were observed between change in function and change in SASP-related matrix-remodeling proteins, microRNAs, and pro-inflammatory cytokines (23/48 markers r ≥ 0.50).

It should be noted that this was only a small pilot study and that the optimal human dosage and frequency is yet to be established. Typically, the next step is to launch a larger-scale study to establish this dosage.

The researchers also note that these results warrant evaluation of dasatinib plus quercetin in larger, randomized, and controlled trials for senescence-related diseases. In other words, they would like to test senolytics in larger studies for various age-related diseases, and the results certainly support doing exactly that.

Conclusion

These initial results are positive, despite there being plenty of room for improvement. The combination of these two drugs also appears to favor particular cell and tissue types over others, much like other senolytic drugs, which were discovered after dasatinib and quercetin were originally shown to clear senescent cells. It may be that a combination of different senolytics will be needed as a “cocktail” of sorts to fully clear out all the unwanted senescent cells, as different senescent cells appear to use various survival pathways to evade apoptosis, and no single drug can target them all.

We greet these early results positively and look forward to the beginning of larger-scale studies for multiple age-related diseases. Given how senescent cells appear to be implicated in most if not all age-related diseases, there are some exciting possibilities ahead.

Literature

[1] Coppé, J. P., Patil, C. K., Rodier, F., Sun, Y., Muñoz, D. P., Goldstein, J., … & Campisi, J. (2008). Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS biology, 6(12), e301.

[2] Coppé, J. P., Desprez, P. Y., Krtolica, A., & Campisi, J. (2010). The senescence-associated secretory phenotype: the dark side of tumor suppression. Annual Review of Pathological Mechanical Disease, 5, 99-118.

[3] Nambiar, A., Justice, J., Pascual, R., Tchkonia, T., Lebrasseur, N., Kirkland, J., … & Kritchevsky, S. (2018). Targeting pro-inflammatory cells in idiopathic pulmonary fibrosis: an open-label pilot study of dasatinib and quercitin. Chest, 154(4), 395A-396A.

[4] Zhu, Y., Tchkonia, T., Pirtskhalava, T., Gower, A. C., Ding, H., Giorgadze, N., … & O’hara, S. P. (2015). The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs. Aging cell, 14(4), 644-658.

[5] Roos, C. M., Zhang, B., Palmer, A. K., Ogrodnik, M. B., Pirtskhalava, T., Thalji, N. M., … & Zhu, Y. (2016). Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice. Aging cell.[/column]

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

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.

Meet the Naked Mole-Rat: Impervious to Pain and Cancer, and Lives Ten Times Longer Than It Should – Article by Ewan St. John Smith

Meet the Naked Mole-Rat: Impervious to Pain and Cancer, and Lives Ten Times Longer Than It Should – Article by Ewan St. John Smith

Ewan St. John Smith


Smithsonian’s National Zoo/flickr, CC BY-NC-ND

Ewan St. John Smith, University of Cambridge

The naked mole-rat is perhaps one of the most bizarre beasts on the planet. At first glance, it looks like little more than a cocktail sausage with legs and teeth. But beneath its wrinkly pink skin, this creature’s strange and beautiful biology has me fascinated – so much so that I set up a whole research group devoted to studying them. Largely immune to cancer, impervious to some forms of pain, and seemingly blessed with the elixir of life, you may well owe your life to them one day.

As the name might suggest, naked mole-rats buck the mammalian trend by almost completely lacking hair or fur. Living underground in complex networks of tunnels in East Africa, their thermally stable environment means that a few orientation-aiding bodily hairs and facial whiskers are all they need. Lacking evolutionary pressure to regulate their body temperature, they’re also the only known cold-blooded mammal on the planet.

The way naked mole-rats mate and socially organise is more akin to certain insect species than to mammals. Like some species of bees and ants, naked mole-rats are eusocial, living in 100-strong groups headed by a sole breeding female, the queen. But while insects command their colonies with pheromones, the naked mole-rat queen uses physical aggression to keep their groups digging tunnels, foraging, and defending entrances.

No, this isn’t Star Wars – it’s a naked mole-rat defending a tunnel.
Neil Bromhall/Shutterstock

A key tool for both digging and combat is their teeth. Their incisors are exterior to their lips, so that when they bite through hard soil they don’t get a mouthful of earth each time. Naked mole-rats can also move their lower incisors to manipulate objects, and have a large sensory area of their brains dedicated to their teeth in the same way that hands have dedicated brain space in humans.

The peculiarities of naked mole-rat behaviour are captivating in themselves. However, to most scientists, what makes them really exciting is the potential some of their incredible biology holds for making biomedical breakthroughs.

The naked mole rat’s resistance to cancer, diagnosed in humans every two minutes in the UK alone, is a particular area of focus for researchers. In studying why there are just a few documented cases worldwide in naked mole-rats, scientists are hoping to identify new ways to prevent or treat the deadly disease.

As yet, we’re not exactly sure what gives them their resistance. Some evidence suggests that a key difference in one of the meshwork of substances providing structural and nutritional support to cells prevents them from reproducing uncontrollably. However, others have observed different results, so further investigation is needed.

Not content with just being immune to cancer, naked mole-rats are also impervious to some normally agonising chemical stimuli, such as capsaicin (the substance that makes chilli peppers taste hot) and acid (what gives lemon juice and vinegar their kick). For their acid-insensitivity, researchers are clearer about why. A subtle difference in one particular molecule of the animal’s pain-sensing nerves turns acid into an anaesthetic. That is, rather than stimulating pain-sensing nerves, it actually numbs them – just like an anaesthetic that your dentist administers before the drilling starts. Sadly, this superpower only works with specific chemical stimuli – heat and pressure are just as damaging to them as us.

Scientists are now further studying the naked mole-rat to see whether we might be able to make the human pain system similarly impervious to acid pain. This could be extremely useful for cancer and arthritis sufferers, for whom build-ups of acid in body tissue can be a major contributor to chronic pain. The molecule responsible for insensitivity to acid in mole-rats also plays a role in human genetic conditions that drastically alter pain perception, and as a result of this convergent research, potential painkillers targeting this molecule have made it into clinical trials in humans.

Naked mole-rats are also highly resilient to low oxygen conditions. Their nerve cells can function for almost one hour in the complete absence of oxygen, by instead using fructose to power energy production. In studying this remarkable ability, my lab and others are hoping to uncover novel treatments to prevent brain damage in stroke patients.

Naked mole-rats are also renowned for their longevity. Broadly speaking, a larger body equals longer life in mammals. Standard lab mice weigh around 35 grams, and usually live a maximum of two to three years. Naked mole-rats can be up to twice as heavy, so might be expected to live four to six years, but can actually survive for more than 30 years in captivity. That’s longer than the lifespan of polar bears and giraffes. And while humans experience from many ageing-associated health problems (for example, osteoarthritis), naked mole-rats appear to age without issue. Research into the ageing processes of naked mole-rats is only in its infancy, but could have multiple implications for treating ageing-related conditions in humans.

Newborn naked mole-rats weigh as little as two grams.
belizar/Shutterstock

Naked mole-rats may look comical, but their magical biology is no laughing matter. Studying their hidden powers will not always result in preventions, cures and treatments for human ailments because of fundamental differences between the species. However, every new insight has the potential to lead to a breakthrough – as animal research has continually done throughout recent history. By unlocking the secrets held within their cells in a responsible manner, we may one day improve countless human lives.The Conversation

Ewan St. John Smith, University Senior Lecturer in Pharmacology, University of Cambridge

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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

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

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.

Finally, Rejuvenation is a Thing! – Fresh Interview with Aubrey de Grey by Ariel VA Feinerman

Finally, Rejuvenation is a Thing! – Fresh Interview with Aubrey de Grey by Ariel VA Feinerman

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Ariel VA Feinerman
Aubrey de Grey


This interview was originally published here

Preface

What is ageing? We can define ageing as a process of accumulation of the damage which is just a side-effect of normal metabolism. While researchers still poorly understand how metabolic processes cause damage accumulation, and how accumulated damage causes pathology, the damage itself — the structural difference between old tissue and young tissue — is categorized and understood pretty well. By repairing damage and restoring the previous undamaged — young — state of an organism, we can really rejuvenate it! It sounds very promising, and so it is. And for some types of damage (for example, for senescent cells) it is already proved to work!

Today in our virtual studio, somewhere between cold, rainy Saint-Petersburg and warm, sunny Mountain View, we meet Aubrey de Grey, again! For those of you who are not familiar with him, here is a brief introduction.

Dr Aubrey de Grey is the biomedical gerontologist who researched the idea for and founded SENS Research Foundation. He received his BA in Computer Science and Ph.D. in Biology from the University of Cambridge in 1985 and 2000, respectively. Dr. de Grey 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. In 2011, de Grey inherited roughly $16.5 million on the death of his mother. Of this he assigned $13 million to fund SENS research.

Note: If you have not read “Ending Aging” yet I suggest you to do it as soon as possible, and to be more comfortable with the ideas we are discussing below I highly recommend you to read short introduction to SENS research on their web page. Also if you are interested in recent news and up-to-date reviews about [anti]ageing and rejuvenation research the best place to look for is Fight Aging! blog. Finally, if you are an investor or just curious, I highly encourage you to take a look at Jim Mellon’s book “Juvenescence”.

Interview

Ariel Feinerman: Hello, Dr Aubrey de Grey!

Aubrey de Grey: Hello Ariel — thanks for the interview.

Ariel Feinerman: How do you feel 2018 year? Can you compare 2018 to 2017 or early years? What is changing?

Aubrey de Grey: 2018 was a fantastic year for rejuvenation biotechnology. The main thing that made it special was the explosive growth of the private-sector side of the field — the number of start-up companies, the number of investors, and the scale of investment. Two companies, AgeX Therapeutics and Unity Biotechnology, went public with nine-digit valuations, and a bunch of others are not far behind. Of course this has only been possible because of all the great progress that has been made in the actual science, but one can never predict when that slow, steady progress will reach “critical mass”.

Ariel Feinerman: In 2017 SENS RF have received about $7 million. What has been accomplished in 2018?

Aubrey de Grey: We received almost all of that money right around the end of 2017, in the form of four cryptocurrency donations of $1 million or more, totalling about $6.5 million. We of course realised that this was a one-off windfall, so we didn’t spend it all at once! The main things we have done are to start a major new project at Albert Einstein College of Medicine, focused on stem cell therapy for Alzheimer’s, and to broaden our education initiative to include more senior people. See our website and newsletters for details.

Ariel Feinerman: What breakthroughs of 2018 can you name as the most important by your choice?

Aubrey de Grey: On the science side, well, regarding our funded work I guess I would choose our progress in getting mitochondrial genes to work when relocated to the nucleus. We published a groundbreaking progress report at the end of 2016, but to be honest I was not at all sure that we would be able to build quickly on it. I’m delighted to say that my caution was misplaced, and that we’ve continued to make great advances. The details will be submitted for publication very soon.

Ariel Feinerman: You say that many of rejuvenating therapies will work in clinical trials within five years. Giving that many of them are already working in clinical trials or even in the clinic (like immunotherapiescell and gene therapies) do you mean the first — maybe incomplete — rejuvenation panel, when you speak of early 2020?

Aubrey de Grey: Yes, basically. SENS is a divide-and-conquer approach, so we can view it in three overlapping phases. The first phase is to get the basic concept accepted and moving. The second phase is to get the most challenging components moving. And the third phase is to combine the components. Phase 1 is pretty much done, as you say. Phase 2 is beginning, but it’s at an early stage. Phase 3 will probably not even properly begin for a few more years. That’s why I still think we only have about a 50% chance of getting to longevity escape velocity by 2035 or so.

Ariel Feinerman: Even now many investors are fearful of real regenerative medicine approaches. For example pharmacological companies which use small molecules, like Unity Biotechnology, received more than $300 million, in much more favour than real bioengineering companies like Oisin Biotechnologies, received less than $4 million, even though the biological approach is much more powerful, cheap, effective and safe! Why is this so in your opinion, and when can we see the shift?

Aubrey de Grey: I don’t see a problem there. The big change in mindset that was needed has already occurred: rejuvenation is a thing. It’s natural that small-molecule approaches to rejuvenation will lead the way, because that’s what pharma already knows how to do. Often, that approach will in due course be overtaken by more sophisticated approaches. Sometimes the small molecules will actually work well! It’s all good.

Ariel Feinerman: Do you agree that the small-molecule approach is generally the wrong way in the future rejuvenation therapies? Because they have many flaws — especially their main mechanism via interference with human metabolism. Unlike them SENS bioengineering therapies are designed to be metabolically inert — because they just eliminate the key damage, they do not need to interfere with metabolism, so it is much easier than usual to avoid side effects and interactions with other therapies. They just eliminate the key damage, which means they are easier to develop and test — and much safer.

Aubrey de Grey: Ah, no, that’s too simplistic. It’s not true that small molecules always just “mess with metabolism” whereas genetic and enzymatic approaches eliminate damage. Small molecules that selectively kill senescent cells are absolutely an example of SENS-esque damage repair; the only thing against them is that it may be more difficult to eliminate side-effects, but that’s not because of their mode of action, it’s because of an additional action.

Ariel Feinerman: In recent years many countries gave the green light for regenerative medicine. Fast-track approval in Japan, for example, allows for emerging treatments to be used so long as they have been proven safe. The similar approach works in Russia. What about the EU or USA?

Aubrey de Grey: There’s definitely a long way to go, but the regulatory situation in the West is moving in the right direction. The TAME trial has led the way in articulating an approvable endpoint for clinical trials that is ageing in all but name, and the WHO has found a very well-judged way to incorporate ageing into its classification.

Ariel Feinerman: Do you think of working with USA Army? As far as we know they conduct research on regeneration and are very interested in keeping soldiers healthier for longer. And they have much money!

Aubrey de Grey: The Department of Defense in the USA has certainly funded a lot of high-impact regenerative medicine research for many years. I’m sure they will continue to do so.

Ariel Feinerman: Is any progress in the OncoSENS programme? Have you found any ALT genes? Is any ongoing research in WILT?

Aubrey de Grey: No — in the end that program was not successful enough to continue with, so we stopped it. There is now more interest in ALT in other labs than there was, though, so I’m hopeful that progress will be made. But also, one reason why I felt that it was OK to stop was that cancer immunotherapy is doing so well now. I think there is a significant chance that we won’t need WILT after all, because we will really truly defeat cancer using the immune system.

Ariel Feinerman: Spiegel Lab has recently published an abstract where they say they have found 3 enzymes capable of breaking glucosepane. Very exiting info! When can we hear more on their research? Revel LLC is a very secretive company.

Aubrey de Grey: They aren’t really being secretive, they are just setting up.

Ariel Feinerman: When can we see the first clinical trial of glucosepane breaker therapy?

Aubrey de Grey: I think two years is a reasonable estimate, but that’s a guess.

Ariel Feinerman: What do you think of the Open Source approach in rejuvenation biotechnology? The computer revolution in the early 2000s has taken place only because Open Source caused an explosion in software engineering!

We have many examples when Big Pharma buys a small company which has patents on technology and then cancels all research. In the Open Source approach you cannot “close” any technology, while everyone can contribute, making protocol better and everyone can use that without any licence fee! Anyway, there are countries where you cannot protect your patents. Maybe it will be better to make technology open from the beginning?

Famous biohacker Josiah Zayner said: “In the gene therapy world most treatments are easy to replicate or pirate because you can reverse engineer the DNA from scientific papers or patents. Same exact treatment, same purity and quality I could give to someone rejected from the clinical trial. The cost? Hundreds or a few thousand dollars at most. Same deal with immunotherapy.”

Aubrey de Grey: I think you’ve pretty much answered your own question with that quote. The technologies that will drive rejuvenation are not so easy to suppress.

Ariel Feinerman: Is the SENS RF going to begin new research programmes in 2019?

Aubrey de Grey: Sure! But we are still deciding which ones. We expect that our conference in Berlin (Undoing Aging, March 28–30) will bring some new opportunities to our attention.

Ariel Feinerman: What are your plans for 2019?

Aubrey de Grey: I’d like to say less travelling, but that doesn’t seem very likely at this point. Really my goal is just to keep on keeping on — to do all I can to maintain the growth of the field and the emerging industry.

Ariel Feinerman: Thank you very much for your answers, hope to see you again!

Aubrey de Grey: My pleasure!

Ariel VA Feinerman is a researcher, author, and photographer, who believes that people should not die from diseases and ageing, and whose main goal is to improve human health and achieve immortality. If you like Ariel’s work, any help would be appreciated via PayPal: arielfeinerman@gmail.com.

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

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

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

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.

From Within Your Own Failing Shell – Article by Nicola Bagalà

From Within Your Own Failing Shell – Article by Nicola Bagalà

Nicola Bagalà


Editor’s Note: In this article originally published by our allies at the Life Extension Advocacy Foundation (LEAF),  Mr. Nicola Bagalà provides a poignant discussion of the suffering associated with the diseases of old age, for which contemporary geriatric medicine can only offer palliative treatments but no lasting solutions. It is imperative to correct this situation by advocating for the advancement of effective rejuvenation treatments which can not only successfully cure the diseases of old age but also reverse biological aging itself.

~ Gennady Stolyarov II, Chairman, United States Transhumanist Party, September 9, 2018

Some time ago, I noticed a stock photo of an old lady seeing her geriatrician, who was a much younger woman. Nothing special was happening in the picture, which showed just two people talking; however, it made me wonder what it must feel like to be an elderly person consulting a geriatrician.

One initial assumption could be that it isn’t much different than seeing a GP, but that seems unlikely. If you are seeing a GP, the odds are your disease or ailment is not debilitating, let alone life-threatening. Whatever it might be, you went to see your doctor knowing that, most likely, he or she would be able to cure you; especially if you are young, it’s probable that just taking a medicine for some time, or doing physical therapy, will make you better. You know that you will recover, and the discomfort or the suffering you’re going through is destined to go away. You will get back to your life as it used to be, healthy as ever.

Things are rather different when you are seeing a geriatrician. A geriatrician is a specialist who takes care of the needs of elderly patients, an activity that can be summarized as ensuring the highest possible life quality of a patient in spite of his or her failing body, which becomes increasingly less resilient and less able to respond to treatment with the passing of time. Existing drugs and exercise programs, for example, can ameliorate the symptoms that an elderly person experiences and improve his or her life quality, but the vast majority of age-related diseases simply cannot be cured right now.

When you go to see a geriatrician, you do so with the knowledge that your doctor will most likely be unable to make you any better, despite his or her best efforts; you simply can’t shovel water with a pitchfork. You are aware that, as you keep aging, your condition is likely to worsen, and all your doctor will be able to do is help you manage your symptoms. You know that you are not going to get back to your life as it used to be and that you are not going to be as healthy as ever—that’s not what old people generally are like. In fact, one day, one of the conditions that brought you to see a geriatrician in the first place is going to worsen to the point that you will die of it.

Most of us are familiar with the feeling of going to see a general practitioner, getting a prescription for some mild ailment, and going back home, thinking about our plans for the rest of the day or the week, which possibly involve a big project that we have been working on for a while and can’t wait to take to completion. What if, instead, you are going home after seeing a geriatrician because of osteoarthritis in your knees? Whatever you might be thinking then, you probably are distracted by the pain that you feel in your knees with every step you take, and the thought that it’s not really going to ever improve doesn’t make it any better. It is unlikely that you have any big project going on that you are looking forward to finishing; it’s not that you wouldn’t like to have one, but your deteriorating health makes it difficult to do anything too demanding. Probably, your much younger doctor is going to go back home thinking about an exciting upcoming trip or her next night out, but you are not.

It’s impossible not to wonder what it must feel like to watch others get back to their own lives from within your own failing shell, knowing that the life that you are getting back to is likely going to be short and decreasing in quality; to hear your doctor say that your ailments can be managed, but not cured; to know that, as time passes, you are more and more likely to lose your independence and cause problems or suffering for your loved ones.

Putting on a smile and trying to look at the bright side of things may help you cope and avoid making things worse than they have to be, but it’s not going to make them better either. A positive attitude is a great prescription for any disease you might have, regardless of your age, but it is not the only prescription that you would be given for any serious illness that might strike you before old age. There is no reason why staying positive and palliative care should be the only medicines against aging—not now that rejuvenation biotechnology is becoming an ever-more concrete prospect.

People of all ages should have the right to go to see their doctors knowing that, most probably, whatever diseases they have may be cured; that any others they might get in the future can be prevented; that their discomfort or suffering is going to go away; and that they are going to get back to their lives as they used to be, healthy as ever.

About Nicola Bagalà

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