PostHuman: An Introduction to Transhumanism from the British Institute of Posthuman Studies

This video by the British Institute of Posthuman Studies explores three factors of transhumanism; super longevity, super intelligence, and super well-being.  Its called PostHuman: An Introduction to Transhumanism and it’s a great video to show your friends who have never heard of transhumanism or the technological singularity.  

Runtime: 11:11

This video can also be found at

Video Info:

Published on Nov 5, 2013

We investigate three dominant areas of transhumanism: super longevity, super intelligence and super wellbeing, and briefly cover the ideas of thinkers Aubrey de Grey, Ray Kurzweil and David Pearce.

Official Website:

Written by: Peter Brietbart and Marco Vega
Animation & Design Lead: Many Artists Who Do One Thing (Mihai Badic)
Animation Script: Mihai Badic and Peter Brietbart
Narrated by: Holly Hagan-Walker
Music and SFX: Steven Gamble
Design Assistant: Melita Pupsaite
Additional Animation: Nicholas Temple
Other Contributors: Callum Round, Asifuzzaman Ahmed, Steffan Dafydd, Ben Kokolas, Cristopher Rosales
Special Thanks: David Pearce, Dino Kazamia, Ana Sandoiu, Dave Gamble, Tom Davis, Aidan Walker, Hani Abusamra, Keita Lynch


Aubrey de Grey on Longevity and Nutrition

I’m pretty passionate about nutrition and healthy living so when I stumbled across this little article called Longevity, Methuselarity, Telomere Lengths which presents some of the ideas and research of famed gerontologist, Aubrey de Grey (of whom I am also a big fan), I got sucked right in.  The Methuselarity is now!

Longevity, Methuselarity, Telomere Lengths



What does the 5,000 year old Bristle Cone Pine (Methuselah Tree) and the purported 252 year old Chinese Taoist Li Ch’ing Yuen share in common?

Answer, longevity.

Both the Bristlecone Pine and Li Ch’ing Yuen were aligned to nature’s standards, avoiding common age promoting diseases.

It’s known that clonal species such as the Methuselah Tree, have an innate capacity to avoid common disease promoting pathogens, and that’s also true for Human Beings.  Bristle Cone Pines have a dense resinous bark, which protects the species from invasion by both insects and fungi.

Similarly, Li Ch’ing Yuen’s immune system warded off generations of opportunistic pathogens and errant cancer cells, avoiding the age-related condition called in medicalese “immunosenescence.”

It’s alleged that Li Ch’ing consumed a soup of Lycium chinensis berries, better known as Gogi berries, after encountering an old sage who was twice his age and able to outperform Li in feats of endurance.

The sage shared his secret of longevity and endurance with Li.  Certain herbs like Gogi, Ginseng and Astragalus, increase longevity, and maybe helped Li Ch’ing Yuen slow his cell division clocks, by upregulating his telomerase enzymes within most of his somatic cell lines.[1][2]

Another factor that may have played a role in Li Ch’ing Yuen’s longevity, besides caloric restriction and healthy diet rich in antioxidants, was practicing Taoist philosophy, which mitigates emotional stress, by teaching adherents to cultivate balance and align their biological and emotional rhythms with nature.  Our cells act as sponges, absorbing everything from the environment, including stress, which contributes to aging, by shortening our telomere beads.

This is why I recommend consuming raw, organic, whole foods, such as Gogi berries which are a rich source of vitamins, minerals, antioxidants, sesquiterpenoids and long chain polysaccharides that deliver critical energy packets for optimal cellular processes.

Every known organism that exists well beyond an average lifespan is worth studying its environs, habits and adaptive capabilities.  Interesting studies have shown that intense exercise and caloric restriction increase mitochondrial biogenesis in both fat and muscle cells.  Mitochondrial dysfunction is linked to premature aging, because there’s less energy available to fix cellular damage such as misfolded proteins and antioxidant/oxidant imbalances.[3]

Aubrey de Grey


Aubrey David Nicholas Jasper de Grey, the famed Bio Medical Gerontologist who coined the term Methuselarity, to describe the near future when humans will defy aging by reversing telomere shrinkage using advanced medical technologies and genetic modification, is enthusiastic about advances in our understanding of what causes biological deterioration leading to death and how we can clean up the cellular messes contributing to our finitude.[4] Some of these “therapies” as outlined in numerous articles and publications by Aubrey de Grey and his non-profit organization SENS, which stands for strategies for engineered negligible senescence.

Aubrey de Grey zeroed in on 7 age-related damages that occur in an individual’s lifetime, contributing to degenerative diseases and death.

Below are the 7 age-related dis-eases contributing to our finitude, along with the 7 strategies for mitigating and preventing them.[5]

Aubrey de Grey often uses the analogy of housekeeping, to describe the future therapeutics of gerontology.

If the roof is leaking…. fix it.  If the floors are creaking and buckling…. replace them.  Strengthen the foundations of the home as it still stands and continue the repair processes as needed.  This is what Aubrey de Grey calls “exporting entropy.”

7 Causes of ageing:

  • Cell atrophy as caused by catabolism.
  • Senescent (ageing) toxic cells caused by free radicals and metabolic byproducts such as lipofuscin.
  • DNA mutations leading to metastatic cancers.
  • Damage and genetic mutations to the 13 genes of the mitochondria. Mitochondrial dysfunction is linked to numerous degenerative conditions, especially premature aging.  The outer membrane of mitochondria has many protein based pores which allow large molecules to pass through for energy production.  Toxins can accompany ions and even pass through the inner membrane matrix to the mitochondria’s nucleus and cause gene mutations.
  • Intracellular non-functioning protein aggregates. Junk inside the cell.
  • Extracellular misshapen aggregates. Junk outside the cell.
  • Extracellular crosslinks such as advanced glycation end products (AGES). Sugar/Protein aggregates.

The 7 therapeutic strategies for promoting negligible senescence.

  • Stem cell therapy can replace any of our 200 cell types. Growth factors for the anabolic process of repairing and upbuilding atrophied organs.  Exercise which is considered a hormetic event that stimulates the anabolic repair processes.  Hormesis is a dose-response relationship in which something as a vaccine or high-intensity exercise produces negative biological effects at high doses but beneficial effects in low doses.  “What doesn’t kill you makes you stronger.”
  • Removal of unwanted cells either by invasive techniques such as laser surgery or gene silencing.
  • Utilizing a strategy known as WILT (Whole-Body Interdiction of Lengthening of Telomeres) which means deleting or silencing genes needed for telomere elongation. Now this might seem counterintuitive but Aubrey de Grey thinks that if these genes are silenced and fresh cells are seeded with already lengthened telomeres then cancer will never occur.  The new cells will have their telomeres lengthened outside the body by synthetic telomerase before they are “seeded” within someone.
  • Adding extra copies of the 13 mitochondrial genes with modifications to prevent copy sequence errors. The mitochondrial DNA is much more susceptible to oxidative damage then the heavily walled in nuclear DNA.
  • The breakdown of intracellular aggregates too big for phagocytosis using microbial enzymes. This can be crucial for improving neuronal health by reducing protein aggregates too big for autophagosomes to degrade and deliver to the lysosome.  The breakdown of junk inside the cell is known as autophagy.
  • For extracellular aggregates, Aubrey de Grey suggests immune-mediated phagocytosis by use of vaccines.
  • The breakdown of AGES (advanced glycation end products) which is when sugars crosslink with proteins non-enzymatically. An example of AGES is the browning of meat when it’s cooked.  AGES form when sugars are floating around the blood in excess and negatively interact with cellular proteins.  AGES can damage the clear crystalline proteins of the lens and cornea of the eye contributing to cataracts and blindness.  AGES can damage the delicate endothelial cells of the cardiovascular system leading to cardiovascular disease.  AGES affect ever cell of the body.

The major philosophical question that comes to my mind is can immortality be opened by a technological skeleton key?

Nutrition is the Key

I believe whole food nutrition and nutraceutical supplementation is the answer to achieving longevity and attaining “ageless vitality” throughout anyone’s lifetime.  If you’re 90 years young, or 45 years old, eating a raw organic whole foods diet, composed of fruits, vegetables, herbs and fresh water will reinvigorate you back to physical and mental juvenilia.

There’s much controversy over the question of reversing cellular senescence.   Microbiologist Leonard Hayflick showed in 1961, that human fetal cells divide 60 times before expiring in a biological process known as apoptosis or programmed cell death.  When a cell divides, a protective bead of DNA called a telomere falls off.



Telomeres are static beads of recurring nucleotides that protect genetic sequences on the chromosomes from degradation.  This biological phenomenon corresponds to the three cell phases Hayflick outlined in his research.  First there’s an initial primary culture, followed by an expansive period of growth and uninterrupted division which then inevitably leads to the third and last stage known as senescence or the Hayflick limit.

The word senescence comes from the Latin root senex meaning old.  Cells in senescence are no longer able to divide and carry out cellular processes.  This is because the enzyme telomerase no longer nourishes telomere strands with fresh nucleotides and cell death quickly ensues.

Hayflick performed an experiment in which he mixed aged male fibroblast cells which divided about 40 times before the experiment, into a substrate with young female fibroblast cells that had divided only 4 times prior to the experiment.

Hayflick discovered that the male fibroblast cells stopped dividing at a certain point, even when surrounded by the young female fibroblast cells.  It was as if they had a memory of their past 40 divisions and ceased dividing.

Hayflick concluded that there must be some kind of physical limit to cellular division, and science later empirically discovered telomere caps at the ends of the chromosome which shortened with each cellular division.

Interestingly, telomere shortening doesn’t occur in cancer cells, because of an enzyme known as “telomerase” which nourishes and relengthens the ends of DNA by adding strands of nucleotides from an inexhaustible reservoir within the cell.  This is the reason for Aubrey de Grey’s WILT strategy, which silences the genes in each cell that encode the telomerase enzyme.



Nutrigenomics is another area of study that is showing promise, by empirically verifying old world wisdom that foods shape our physical and emotional wellbeing.  In vitro (glass tube) studies have shown that the Traditional Chinese herb Astragalus membransceus and its two secondary metabolites cycloastragenol and astragaloside IV, activate the telomerase enzyme within healthy lymphocyte and skin cells to repair shrinking telomeres.  In 2005 there was a very small 24-week double-blind, placebo controlled study, involving 36 men, aged 60 and 85 years old which was sponsored by TA sciences.

The results of the study showed slight improvement in visual acuity, immune function, skin integrity and libido.  Studies performed by companies on their own products, subject the results to considerable skepticism and criticism, and ought to be further investigated by independent researchers in a randomized controlled study to prove effectiveness while removing bias.  If the product works in a small prospective study, than it should in most instances be reproducible in a larger independent verification trial.

It’s important to point out that Japanese centenarians have lower blood levels of C-reactive protein, thrombin, interleukin 1 and 6, each of which are involved in the inflammatory cascade that underlies and drives degenerative diseases.  Interestingly, these same Japanese centenarians had increased expression of the protein adiponectin, which is involved in regulating blood glucose levels and fatty acid breakdown.  You could say genes are responsible for their longevity, but research continues to support the notion that a healthful diet, increased activity and a positive outlook, play more of a role in life-extension, than just a good familial blue print.[6]


There has been a lot of buzz surrounding the “French paradox” which is enjoying life ad libitum (at one’s pleasure) and avoiding the common risk factors associated with such a lifestyle.  The answer to the French Paradox is most likely as complex as a post-modernist dissertation from the famed Ecole Superieure in Paris, but I would say the purported one million café’s that dot the beautiful landscape play a central role in France’s longevity paradox.  Eating fresh food rich in antioxidants such as resveratrol, communicating with friends and loved ones and maintaining a stoical threshold for stress, are all keys to a long happy life.

My Favorite Longevity Herbs

Rasayana which means rejuvenation, is an ancient Ayurvedic discipline focused on using herbs like Bacopa Monnieri and Turmeric for increasing longevity and vitality.  Ayurveda (Ayuh-Life, Veda-Science) is the oldest form of medicine, preceding Traditional Chinese and Greek healing systems by over a thousand years.[7]  What we do know about aging is that proper diet, exercise and positive outlooks greatly reduce several risk factors for age related degenerative diseases.  Ayurvedic medicine has found several powerful anti-ageing herbs which are now being used worldwide for their health promoting and anti-stress properties.

Bacopa Monnieri (Brahmi)


According to the Hungarian endocrinologist Han’s Selye, stress is a non-specific response by the body to any demand.  Whether you’re in traffic hearing several jackhammers break up a once three lane road or running from a bear in a National Park, the physiological and psychological reaction produced by the body is stress.  If certain stressors persist for any period of time exceeding your physical and psychological thresholds, it’s considered distress.  How we subjectively experience stress, depends upon multiple factors, such as personality, age, economic and social status.  Stress is ubiquitous, and the reason herbs known as adaptogens are the most popular tonics in traditional healing systems.

Bacopa Monnieri or Brahmi is a potent nerve tonic that is known to rejuvenate cognition and memory.[8]  The founder of stress research Hans Selye, systematized stress research, by outlining the three stages of stress, beginning with the alarm stage, which is followed by the stage of resistance and finally the stage of exhaustion.  In our modern, fast-paced, technological environments, individuals experience the three stages of stress with alarming consistency.

Stressful situations activate the hypothalamic-pituitary-adrenal axis (HPA stress axis) triggering the release of stress hormones such as cortisol.  This is considered the “fight-or-flight mode” which describes a heightened-stress response by the body, where blood sugar levels rise, for fueling energy intensive systems in response to a “perceived” threat.  Some of this fuel is released from the liver or the result of skeletal muscle breakdown.

This is why cortisol is considered a “catabolic” hormone, because it breaks-down and releases energy as opposed to anabolic hormones which build-up and repair cells.  If cortisol is continually elevated there can be increased fat storage in and around organs known as visceral adipose tissue.[9]  Visceral fat releases proinflammatory hormones that increase chronic inflammation and create the conditions for developing degenerative diseases and rapid ageing.

Combating excess cortisol release can be done, by consuming a healthy plant based diet and using adaptogenic herbs such as Bacopa.

Bacopa can raise your physiological and psychological “stress thresholds,” preventing mental and physical exhaustion.  Ancient Ayurvedic practitioners named Bacopa “Brahmi,” after the Hindu mythical creator “Brama the creator.”  This is because Bacopa supports the seat of consciousness and creation.

Cognitive decline is seen often in the elderly and is considered to be a “normal” part of ageing, but more and more individuals in there 8th and 9thdecades are supplementing with Bacopa and noticing an increase in mental acuity, focus and overall feelings of wellbeing.  Bacopa’s major bioactive chemical constituents are the Bacosides A and B.

These phytochemicals are potent antioxidants which can increase the intracellular antioxidant Glutathione Peroxidase, Superoxide Dismutase (SOD) and Catalase, preventing the age related oxidative induced damage seen in aged neurons.

When taken regularly, Bacopa enhances cognitive function, by increasing neuronal cell communication within the cholinergic system.  Loss of acetylcholine which is the predominant neurotransmitter in the hippocampus, is a hallmark of degenerative brain diseases such as Alzheimer’s.  Bacopa has shown an ability to reverse acetylcholine loss and lower brain inflammation.

Ashwagandha (Withania Somnifera)



Is a powerful Ayurvedic herb and considered India’s equivalent to Korean Ginseng, because of its adaptogenic, immunomodulatory, antioxidant and anti-stress benefits.  Also known as Winter Cherry, Ashwagandha is used extensively on its own and with other herb tonics for rejuvenating senescent cells, raising stress thresholds and increasing mental acuity.

Researchers have found that Ashwagandha detoxifies cells, especially in energy intensive systems, by activating antioxidant enzymes such as Catalase and Superoxide Dismutase.[10]  Both of these antioxidant enzymes protect cells from free radicals and reactive oxygen species.  Unregulated reactive oxygen species cause immune imbalances and chronic low level inflammation.[11]

Supplementing with Ashwaganda, which contains the bioactive polyphenols known as glycowithanolides, boosts antioxidant enzymes in energy intensive systems such as the brain, liver and kidney.

Increasing antioxidant enzyme systems in the body, is the number 1 anti-ageing method for promoting radiant health.  Ashwaganda has shown an ability to mimic the body’s own anti-stress hormones which effectively lowers cortisol levels.  Cortisol is a stress hormone released by the adrenal glands which temporarily provides alertness, increased reaction time and memory function.

Overtime, excess cortisol has the opposite effects, causing insulin resistance, memory loss and depression.  The glycowithanolides in Ashwaganda work with the body to combat the negative effects of physical and emotional stress, by restoring our ability to adapt successfully to the demands of everyday life.

Turmeric (Curcuma longa)


By far the most popular herb in the world, Turmeric is an amazing Rasayana (rejuvenative) tonic that protects all 34 trillion cells from oxidative damage.

Free radicals such as the hydroxyl radical are oxygen atoms with unpaired electrons that cause damage to our cells.  Free radicals enter the body from the environment and are produced as a byproduct of energy production within each cell-especially energy intensive organs such as the brain, eyes, liver and kidney.

Turmeric, also known as Curcumin because of the active secondary metabolites called curcuminoids, is a spice in the Zingiberaceae family which includes the amazing pungent, tonic herb Ginger.

Traditionally, Turmeric has been used to treat numerous ailments such as inflammation, cancer, fatigue and pathogenic invasion.[12]

Recently, Turmeric has been under investigation for ability to work through the inflammatory pathways to quench inflammation and protect cell membranes from oxidative damage.  Turmeric has powerful chelating abilities, assisting the body in removing heavy metals which damage cellular proteins and enzymes.  Researchers have also discovered Turmeric’s mechanism of action in quenching inflammation, is by inhibiting the enzymes cyclooxygenase 2 and 5-lipoxygenase.

Both enzymes convert the omega 6 fatty acid arachidonic acid into proinflammatory prostaglandins, accelerating the ageing process into overdrive.

Turmeric is a powerful Rasayana tonic that can begin offering protection, by inhibiting the production of proinflammatory cytokines, reducing pain and increasing mobility.

The byproducts of fossil fuels leach into the environment and bioaccumalate in our bodies, causing damage to our cellular components, especially our mitochondrial and cellular DNA.  Turmeric is a chemopreventative medicinal, meaning it inhibits the destructive effect of persistent organic chemical pollutants that can form adducts (Latin-Drawn-toward) with our DNA, contributing to genomic instability and cancer.[13]  Our DNA is fundamental to our existence and recent research has revealed that our genome is the principle site of memory storage.[14]  Turmeric can protect both mitochondrial and cellular DNA from oxidative damage.

[1] The Lancet: Increased Telomerase activity and comprehensive lifestyle changes: a pilot study, Dean Ornish, Jue Lin, Jennifer Daubenmier, Gerdi Weidner, Elissa Epel, Colleen Kemp, Mark Jesus M Magbanua, Ruth Marlin, Loren Yglecias Peter R Carroll, Elizabeth H Blackburn; November, 2008.  Ornish et al postulated a comprehensive lifestyle change to increase telomerase activity.  Telomeres are static beads of protein complexes at the ends of chromosomes that promote DNA stability.  Researchers have discovered that individuals with poor lifestyle habits such as smoking, inactivity and overconsumption of processed meat and dairy products increase their risk of developing cancer, diabetes and obesity.  Poor lifestyle habits are also correlated with low telomerase activity which effects telomere length leading to genomic instability and increased risk for age-related diseases.  Telomerase is the enzyme which has the potential to re-lengthen telomeres.  Ornish et al postulated that if poor lifestyle habits negatively impact telomere length then healthy lifestyle changes must produce the opposite effect.  Employing a comprehensive lifestyle modification program that included a whole foods diet high in fruits, vegetables unrefined grains and legumes with moderate aerobic exercise and in group support for duration of 3 months-resulted in a 29%-84% increase in telomerase activity.  Telomerase activity was measured in PBMCs (peripheral blood mononuclear cells) which are immune cells.  The significance of increased telomerase activity within white blood cells means healthy lifestyle changes lower inflammation, diabetes and cardiovascular health which are the top three causes of disease and death in the world.

[2] APS Acta Pharmacologica Sinica: Autophagy in ageing-associated diseases, Li-qiang He, Jia-hong Lu and Zhen-yu Yue, February 18th 2013.  Caloric restriction is a key to longevity in many species such as C elegans, mice and humans because it activates autophagy which is the removal of junk inside the cell.  Autophagy (Greek meaning auto-self, phage-eat) is the cells waste removal process that functions best when fewer calories are consumed.  Researchers discovered that autophagy can be upregulated, especially during times of caloric restriction.  The MTOR protein which is involved in anabolism by increasing protein synthesis and alerting cells such as skeletal muscle there’s anabolic building material outside the cell to bring in for repair and growth.  MTOR or mammalian target of rapamycin inversely regulates autophagy, suppresing autophagocytosis when nutrients and growth factors such as IGF1 are present.

[3] PLoS Genetics: Editorial, Entropy Explains Aging, Genetic Determinism Explains Longevity, and Undefined Terminology Explains Misunderstanding Both, Leonard Hayflick, December 2007. An interesting and engaging editorial by famed microbiologist Leonard Hayflick explores the current scientific understanding on biological deterioration.  If you separate the prefix de, from the word generation, you find a meaning with broader connotations such as the generation of cells within our bodies that begin as one cell and degrade as many.  Multicellular organisms eventually die because as Lenard Hayflick points out, energy dispersal can never be entirely eliminated only circumvented for varying time-periods by repair or replacement processes.  This is the second law of thermodynamics which states that entropy is inevitable in closed and open systems.  The trouble with reversing entropy within multicellular organisms such as human beings is that the repair and replacement processes suffer the same fate as the cells they work to keep up and change.

[4] HarperCollins Publishers: Long For This World: The Strange Science of Immortality, Jonathan Weiner, 2010.  Science Writer Jonathan Weiner explores immortality and man’s timeless quest for conquering biological deterioration.  In 1966, Professor Gerald Gruman wrote A History of Ideas about the Prolongation of Life: The Evolution of the Prolongevity Hypothesis to 1800, in which he distinguished two types of thinkers on the issue of life and death.  The prolongevists according to Gruman are optimistic about man’s ability to extend lifespan and the apologists, who according to Weiner reconcile us to our inevitable fate.  Microbiologist Leonard Hayflick who discovered that human cells divide approximately 60 times before expiring, takes a rather sardonic position on the idea of Prolongevity saying: “Everything in the Universe changes or ages with time, and to think that you can reverse it is nonsense.”  Aubrey de Grey is of the former camp, arguing with passion and erudition that immortality is within the future anterior and molecular biology has just about zeroed in on the “causes” of cellular degeneration.  Jonathan Weiner’s book is an excellent introduction to the science of Gerontology and the individuals such as Aubrey de Grey who’re working tirelessly to supply their shoulders for tomorrow’s immoralists.

[5] IOS press: A Strategy for Postponing Aging Indefinitely, Aubrey de Grey Ph.D. 2005.

[6] New York Times Magazine: The Island Where People Forget To Die, Dan Buettner, October 24th 2012.

[7] Taylor & Francis: Rasayana: Ayurvedic herbs for longevity and rejuvenation, H.S. Puri, 2003.

[8] ELSIVIER: Pharmacology Biochemistry and Behavior: Adaptogenic effect of Bacopa Monnieri (Brahmi), Rai, Deepak; Bhatia, Gitika; Palit, Gautam; Pal, Raghwendra; Singh, Satyawan, July 1st 2003.

[9] HINDAWI: Journal of Obesity: Mindfulness Intervention for Stress Eating to Reduce Cortisol and Abdominal Fat among Overweight and Obese Women: An Exploratory Randomized Controlled Study, Jennifer DaubenmierJean KristellerFrederick M. HechtNicole ManingerMargaret KuwataKinnari JhaveriRobert H. LustigMargaret KemenyLori Karan, and Elissa Epel, June 1st 2011.


[10] HINDAWI: Glioprotective Effects of Ashwagandha Leaf Extract against Lead Induced Toxicity, Praveen KumarRaghavendra SinghArshed NazmiDinesh LakhanpalHardeep Kataria, and Gurcharan Kaur, May 28th2014.


[11] ELSIVIER: Ageing Research Reviews, Molecular Inflammation: Underpinnings of ageing and age related diseases, Chung, Hae Young, Cesari, Matteo Anton, Stephen Marzetti, Emaunuele Giovannini, Silvia, January 1st2009.

[12] ACTA, ABP, Biochimica Polonica: Curcumin and curcuminoids in quest for medical status, Grzegorz Grynkiewicz and Piotr Slifirski, May 14th 2012.

[13] WHO: World Health Organization: PERSISTANT ORGANIC POLLUTANTS (POPS) July 2008.  Persistent organic pollutants are synthetic chemicals that “persist” in the environment and bioaccumalate in fat tissue.  This why they are considered lipophilic or fat loving.

[14] NATURE Neuroscience: Cortical DNA Methylation maintains remote memory, Courtney A. MillerCristin F. GavinJason A. WhiteR. Ryley Parrish,Avinash HonasogeChristopher R. YanceyIvonne M. RiveraMaria D. RubioGavin Rumbaugh, and J. David Sweatt, June 2010.


This article can also be found on the Longevity Upgrades website here.

The Singularity and the Methuselarity: Similarities and Differences by Aubrey de Grey

This is a paper written by Aubrey de Grey discussing the technological singularity vs the Methuselarity.  The original paper is entitled, “The singularity and the Methuselarity: similarities and differences” and can be found on the SENS Research Foundation website or you can follow this link:

In: Strategy for the Future (Bushko R, ed.), 2008, in press.

The singularity and the Methuselarity: similarities and differences

Aubrey D.N.J. de Grey, Ph.D. Methuselah Foundation PO Box 1143, Lorton, VA 22079, USA Email:


Aging, being a composite of innumerable types of molecular and cellular decay, will be defeated incrementally. I have for some time predicted that this succession of advances will feature a threshold, which I here christen the “Methuselarity,” following which there will actually be a progressive decline in the rate of improvement in our anti-aging technology that is required to prevent a rise in our risk of death from age-related causes as we become chronologically older. Various commentators have observed the similarity of this prediction to that made by Good, Vinge, Kurzweil and others concerning technology in general (and, in particular, computer technology), which they have termed the “singularity.” In this essay I compare and contrast these two concepts.

The singularity: a uniquely unique event in humanity’s future

“Unique” is, of course, an over-used word to describe momentous events – arguably, even more overused than “historic.” How, then, can I dare to describe something as uniquely unique?

Well, I will begin by pulling back a fraction from that description. There are actually, in my view, two possible events in humanity’s future that merit this description. But I do not feel very bad about this qualification, because I believe that those two events are, in all probability, mutually exclusive. The singularity is one; the demise of humanity is the other. Hence my choice of the indefinite article: the singularity is not “the” uniquely unique event in humanity’s future, because it may not occur, but if it does occur, nothing comparable will either precede or follow it.

The singularity has been defined in many related but subtly distinct ways over the years, so let me begin my discussion of it by making clear what I mean by the term. I adhere to the following definition: “an asymptotically rapid increase in the sophistication of technology on whose behaviour humans depend.” I do not use the word to mean, for example, “the technological creation of smarter-than-human intelligence” (which is the definition currently given by SIAI, the Singularity Institute for Artificial Intelligence1 ) – despite my agreement with the view that the technology most likely to bring about the singularity (and, indeed, the one that was originally used to define it) is precisely the one that SIAI study, namely recursively self-improving artificial intelligence (of which more below). I am sticking to the more abstract definition partly because it seems to me to encapsulate the main point of why the singularity is indeed uniquely unique, and partly because it will help me to highlight what distinguishes the singularity from the Methuselarity.

One aspect of my definition that may raise eyebrows is its use of the word “asymptotically” rather than “exponentially.” I feel sure that von Neumann2 would agree with me on this: the mere perpetuation of Moore’s Law3 will not bring about the singularity. A gravitational singularity, which is of course the etymological source of the term, is the centre (not, I stress, the event horizon) of a black hole: the point at which the force of gravity is infinite – or, to be more precise, the point arbitrarily near to which gravity is arbitrarily strong. The distance between the singularity and any point of interest (inside or outside the event horizon) at which gravity is finite is, of course, finite. This is an asymptotic relation between distance and strength: if point X is distance Y from the singularity, it is not possible to travel from X, along the line between X and the singularity, by a distance greater than Y, and experience continuously increasing gravity. Exponential (though not inverse exponential! – see below) relations are not like this: they have no asymptote. If the force of gravity exerted by a particular body were exponential (though still increasing with decreasing distance from the body), the relation between distance from that body and gravity exerted by it would be defined in terms of distance from the point furthest away from it (“on the other side of the Universe”). Call the gravity exerted at that point X and suppose that the gravity exerted at half that distance from the body is 4X (which is the same as for gravity in real life). Then the gravity exerted by the body at a point arbitrarily close to it is not arbitrarily large – it is just 16X, since that point is exactly twice as far away from the point of minimum gravity as the 4X point is.

Having belaboured this point, I now hope to justify doing so. Will the technological singularity, defined as I define it above, happen at all? Not if we merely proceed according to Moore’s law, because that does not predict infinite rates of progress at any point in the future. But wait – who’s to say that progress will remain “only” exponential? Might not progress exceed this rate, following an inverse polynomial curve (like gravity) or even an inverse exponential curve? I, for one, don’t see why it shouldn’t. If we consider specifically the means whereby the Singularity is most widely expected to occur, namely the development of computers with the capacity for recursive improvement of their own workings,4 I can see no argument why the rate at which such a computer would improve itself should not follow an inverse exponential curve, i.e. one in which the time taken to achieve a given degree of improvement takes time X, the time taken to repeat that degree of improvement is X/2, then X/4 and so on.

Why does this matter? It might matter quite a lot, given that (in most people’s view, anyway) the purpose of creating computers that are smarter than us is to benefit us rather than to supersede us. Human intelligence, I believe, will not exhibit a super-exponential rate of growth, because our cognitive hardware is incompatible with that. Now, I grant that I have only rather wishy-washy intuitive reasons for this view – but what I think can be quite safely said is that our ability to “keep up” with the rate of progress of recursively self-improving computers will be in inverse relation to that rate, and thus that super-exponentially self-improving computers will be more likely to escape our control than “merely” exponentially self-improving ones will. Computers have hardware constraints too, of course, so the formal asymptotic limit of truly infinite rates of improvement (and, thus, truly infinite intelligence of such machines) will not be reached – but that is scant solace for those of us who have been superseded (which could, of course, mean “eliminated”) some time previously. There is, of course, the distinct possibility that even exponentially self-improving systems would similarly supersede us, but the work of SIAI and others to prevent this must be taken into account in quantifying that risk.

Let us now consider the aftermath of a “successful” singularity, i.e. one in which recursively selfimproving systems exist and have duly improved themselves out of sight, but have been built in such a way that they permanently remain “friendly” to us. It is legitimate to wonder what would happen next, albeit that to do so is in defiance of Vinge.5 While very little can confidently be said, I feel able to make one prediction: that our electronic guardians and minions will not be making their superintelligence terribly conspicuous to us. If we can define “friendly AI” as AI that permits us as a species to follow our preferred, presumably familiarly dawdling, trajectory of progress, and yet also to maintain our selfimage, it will probably do the overwhelming majority of its work in the background, mysteriously keeping things the way we want them without worrying us about how it’s doing it. We may dimly notice the statistically implausible occurrence of hurricanes only in entirely unpopulated regions, of sufficiently deep snow in just the right places to save the lives of reckless mountaineers, and so on – but we will not dwell on it, and quite soon we will take it for granted.

A reasonable question to ask is, well, since even a super-exponentially self-improving AI will always have finite intelligence, might it not at some point create an even more rapidly self-improving system that could supersede it? Indeed it might (I think) – but, from our point of view, so what? If we have succeeded in creating a permanently friendly AI, we can be sure that any “next-generation” AI that it created would also be friendly, and thus (by the previous paragraph’s logic) largely invisible. Thus, from our perspective, there will only be one singularity.

In closing this section I return to my claim that the singularity and the demise of humanity are, in all probability, mutually exclusive. Clearly if our demise precedes the singularity then the singularity cannot occur. Can our demise occur if preceded by the singularity? Almost certainly not, I would say: the interval available for our demise between the development of recursively self-improving AI and the attainment by that AI of extremely thorough ability to protect us (even from, for example, nearby supernovae) will be short. (I exclude here the possibility that the singularity will occur via the creation of AI that is not friendly to us, only because I think humanity’s life expectancy in that scenario is so very short that this is equivalent from our point of view to the singularity not occurring at all.) The “area under the curve” of humanity’s probability of elimination at any time after the singularity is thus very small. I am, of course, discounting here the possibility that even arbitrarily intelligent and powerful systems cannot protect us from truly cosmic events such as the heat death of the Universe, but I agree with Deutsch6 that this is unlikely given the time available.

The Methuselarity: the biogerontological counterpart of the singularity

In a recent interview, Watson was asked what would be the next event in the history of biology that would compare in significance to his and Crick’s discovery of the structure of DNA, and he replied that there would never be one.7 I think he was correct. However, I agree with him only if I am rather careful in defining “biology” as the discovery of features of the living world, and excluding biotechnology, which for present purposes I define as the exploitation of such discoveries. In biotechnology I believe that there will certainly be a counterpart, something that will outstrip in significance every other advance either predating or following it: the Methuselarity.

For almost a decade following my graduation in 1985, I conducted research in artificial intelligence. I switched fields to biogerontology shortly after becoming aware that the defeat of aging was vastly less on biologists’ agenda than I had hitherto presumed. I was not, at that time, aware of the concept of recursively self-improving AI and the singularity, though perhaps I should have been. But even if I had been, I think I would still have made the career change that I did. Why?

Humans are very, very good at adjusting their aspirations to match their expectations. When things get better, people are happy – but if they stay better and show every sign of continuing that way, people become blasé. Conversely, when things get worse people are unhappy, but if they stay worse and show every sign of continuing that way, people become philosophical. This is why, by all measures that have to my knowledge been employed, people in the developed world are on average neither much happier nor much less happy now than they were when things were objectively far worse. This is a good thing in many ways, but in at least one way it is a problem: it dampens our ardour to improve our lives more rapidly. In particular, it depletes the ranks of “unreasonable men” to whom Shaw so astutely credited all progress.8 There are far too few unreasonable men and women in biology, and especially in biogerontology. I am proud to call myself an exception: someone who is comfortable devoting his life to the most important problems of all, even if they appear thoroughly intractable.9 In my youth, I felt I could make the most difference to the world by helping to develop intelligent computers; but when I discovered the truth about biologists’ attitude to aging I knew that I could make even more difference in that field.

Why is aging so important? Aging kills people, yes, but so do quite a few other things – and moreover, life is about quality as well as quantity, and intelligent machines might very greatly improve the quality of life of an awful lot of people, not least by virtue of providing essentially unbounded prosperity for all.

Even if we take into account the fact that aspirations track expectations, such that what really matters is to maintain a good rate of improvement of (objective) quality of life, it is hard to deny that the development of super-intelligent machines will be of astronomical benefit to our lives. But let’s be clear: quantity of life matters too. There is a well-established metric that folds together the quality and quantity benefits of a given technological or other opportunity: it is the “quality-adjusted life year” or QALY.10

Historically, mainstream biogerontologists have been publicly cautious regarding predictions of the biomedical consequences of their work, though this is gradually changing. But even privately, few biogerontologists have viewed aging as amenable to dramatic change: they have been aware that it is a hugely multi-faceted phenomenon, which will yield only incrementally to medical progress if it yields at all. This places them in a difficult position when arguing for the importance of their work relative to other supplicants for biomedical research resources. Yes, there is always a benefit to a QALY, and yes, progress against aging will deliver QALYs – but the force of this argument is diminished by two key factors, namely the probability of success (which biogerontologists cannot provide a conclusive case for being high) and the entrenched ageism in society, which views it as “fair” to deprioritise health care for the elderly. This quandary is well illustrated by the current “Longevity Dividend” initiative, which seeks to focus policy-makers’ minds on the ever-dependable lure of lucre associated with keeping people youthful, rather than on the moral imperative.11

But this is in the process of changing – indeed, of being turned on its head. This is for one reason and one only: it is becoming appreciated that aging may be amenable to comprehensive postponement by regenerative medicine.12,13 And the reason that makes all the difference is because it creates the possibility – indeed, the virtual certainty – of the Methuselarity.

Having tantalised you for so long, I cannot further delay revealing what the Methuselarity actually is. It is the point in our progress against aging at which our rational expectation of the age to which we can expect to live without age-related physiological and cognitive decline goes from the low three digits to infinite. And my use here of the word “point” is almost accurate: this transition will, in my view, take no longer than a few years. Hence the – superficial – similarity to the singularity.

I have set out elsewhere, first qualitatively14 and then quantitatively,15 the details of my reasons for believing that the application of regenerative medicine to aging will deliver this cusp; thus, here I will only summarise. Regenerative medicine, by definition, is the partial or complete restoration of a damaged biological structure to its pre-damaged state. Since aging is the accumulation of damage, it is in theory a legitimate target of regenerative medicine, and success in such a venture would constitute bona fide rejuvenation, the restoration of a lower biological age. (The bulk of my work over the past decade can be summarised as the elaboration of that “theory” into an increasingly detailed and promising project plan for actual implementation16 – but I digress.) This rejuvenation would not be total: some aspects of the damage that constitutes aging would be resistant to these therapies. But not intrinsically resistant: all such damage could in principle be reversed or obviated by sufficiently sophisticated repair-and-maintenance (i.e., regenerative) interventions. Thus arises the concept of a rate of improvement of the comprehensiveness of these rejuvenation therapies that is sufficient to outrun the problem: to deplete the levels of all types of damage more rapidly than they are accumulating, even though intrinsically the damage still present will be progressively more recalcitrant. I have named this required rate of improvement “longevity escape velocity” or LEV.14,15

It is important to understand that LEV is not an unchanging quantity, as it might be if it were a feature of our biology. Rather, it will vary with time – and exactly how it will probably vary is a topic I address in the next section. LEV will, however, remain non-zero for as long as there remain any types of damage that we cannot remove or obviate. Thus, the formal possibility exists that we will at some point achieve LEV but that at some subsequent date our rate of progress against aging will slip back below LEV. However, I have claimed that this will almost certainly not happen: that, once surpassed, LEV will be maintained indefinitely. This claim is essentially equivalent to the claim that the Methuselarity will occur at all: the Methuselarity is, simply, the one and only point in the future at which LEV is achieved.

The singularity and the Methuselarity: some key differences

Having described the singularity and the Methuselarity individually, I now examine how they differ. I hope to communicate that the superficial similarities that they exhibit evaporate rather thoroughly when one delves more deeply.

Perhaps the most important contrast between the singularity and the Methuselarity is the relevance of accelerating change. In the first section of this essay I dealt at some length with the range of trajectories that I think are plausible for the rate of improvement of self-improving artificial intelligence systems – but it will have been apparent that all the trajectories I discussed were accelerating. It might intuitively be presumed that, since aging is a composite of innumerable types of damage that accumulate at different rates and that possess different degrees of difficulty to remove, our efforts to maintain youth in the face of increasing chronological age will require an accelerating rate of progress in our biomedical prowess. But this is not correct.

The central reason why progress need not accelerate is that there is a spectrum not only in the recalcitrance of the various types of damage that constitute aging but also in their rates of accumulation. As biomedical gerontologists, we will always focus on the highest-priority types of damage, the types that are most in danger of killing people. Thus, the most rapidly-accumulating types of damage will preferentially be those against which we most rapidly develop repair-and-maintenance interventions. There will, to be sure, be “spikes” in this distribution – types of damage that accumulate relatively rapidly and are also relatively hard to combat. But we are discussing probabilities here, and if we aggregate the probability distributions of the timeframes on which the various types of damage, with their particular rates of accumulation and degrees of difficulty to combat, are in fact brought under control, the conclusion is clear: we are almost certain to see a progressive and unbroken decline in the rate at which we need to develop new anti-aging therapies once LEV is first achieved. (I do not mean to say that this progression will be absolutely monotonic – but the “wobble” in how rapidly progress needs to occur will be small compared to the margin of error available, i.e. the margin by which the average rate of progress exceeds LEV.) This conclusion is, of course, subject to assumptions concerning the distribution of these types of damage on those two dimensions – but, in the absence of evidence to the contrary, a smooth (log-normal, or similar) distribution must be assumed.

The other fundamental difference between the singularity and the Methuselarity that I wish to highlight is its impact on “the human condition” – on humanity’s experience of the world and its view of itself. I make at this point perhaps my most controversial claim in this essay: that in this regard, the Methuselarity will probably be far more momentous than the singularity.

How can this be? Surely I have just shown that the Methuselarity will be the consequence of only quite modest (and, thereafter, actually decreasing) rates of progress in postponing aging, whereas the singularity will result from what for practical purposes can be regarded as infinite rates of progress in the prowess of computers? Indeed I have. But when we focus on humanity’s experience of the world and its view of itself, what matters is not how rapidly things are changing but how rapidly those changes affect us. In the case of the singularity, I have noted earlier in this essay that if we survive it at all (by virtue of having succeeded in making these ultra-powerful computers permanently friendly to us) then we will move from a shortly-pre-singularity situation in which computers already make our lives rather easy to a situation in which they fade into the background and stay there. I contend that, from our point of view, this is really not much of a difference, psychologically or socially: computers are already far easier to use than the first PCs were, and are getting easier all the time, and the main theme of that progression is that we are increasingly able to treat them as if they were not computers at all. It seems to me that the singularity may well, in this regard, merely be the icing on a cake that will already have been baked.

Compare this to the effect of the Methuselarity on the human condition. In this case we will progressively and smoothly improve our remaining life expectancy as calculated from the rate of accumulation of those types of damage that we cannot yet fix. So far, so boring. But wait – is that the whole story? No, because what will matter is the bottom line, how long people think they’re actually going to live.

These days, people are notoriously bad at predicting how long they’re going to live. There is a strong tendency to expect to live only about as long as one’s parents or grandparents did (just so long as they died of old age, of course).17 This is clearly absurd, given the rapid rise of life expectancies throughout the developed world in the past half-century and the fact that, unlike the previous half-century, that rise has resulted from falling mortality rates at older ages rather than in infancy or childbirth. It persists, I believe, simply because the rise in life expectancy has been rapid only by historical standards: unless one’s paying attention, it’s not been rapid by the standards of progress in technology, so it easily goes unnoticed.

This will not last, however. As the rate of improvement in life expectancy increases, so the disparity between that headline number and the age which someone of any particular age can expect to reach also increases. But here’s the crux: these two quantities do not increase in proportion. In particular, when the rate of improvement of life expectancy reaches one year per year – which, in case you didn’t know, is only a few times faster than is typical in the developed world today18 – the age that one can expect to reach undergoes a dramatic shift, because the risk of dying from age-related causes at any given age suddenly plummets to near zero. And that is (another way of defining) the Methuselarity.

To summarise my view, then: the singularity will take us from a point of considerable computing power that is mostly hidden from our concern to one of astronomical computing power that is just slightly more hidden. The Methuselarity, by contrast, will take us from a point of considerable medical prowess that only modestly benefits how long we can reasonably expect to live, to one of just slightly greater medical prowess that allows us confidence that we can live indefinitely. The contrast is rather stark, I think you will agree.

Epilogue: the Methuselarity and the singularity combined

Those who have followed my work since I began publishing in biogerontology may have noticed a subtle change in the way that I typically describe the Methuselarity’s impact on lifespans. Early on, I used to make probabilistic assertions about future life expectancy; now I make assertions about how soon we will see an individual (or a cohort) achieve a given age.

The reasons for this shift are many; some are down to my improved sense of what does and does not scare people. But an important reason is that my original style of prediction incorporated the implicit assumption that the Methuselarity would occur in the context of a continued smooth, and relatively slow, rate of reduction in our risks of death from causes unrelated to our age. I only belatedly realised that this assumption is unjustified – indeed, absurd. And the singularity is what makes it particularly absurd.

Roughly speaking, we prioritise our effort to avoid particular risks of death on the basis of the relative magnitude of those risks. Things that only have a 0.01% risk per year of killing us may not be considered worth working very hard to avoid, because even multiplied up over a long life they have only a 1% chance of being our cause of death. This immediately tells us that such risks will move altogether nearer to the forefront of our concerns as and when the Methuselarity occurs (or is even widely anticipated), because the greater number of years available to get unlucky means that the risk of these things being our cause of death is elevated. It seems clear that we will work to do something about that – to improve the efficiency with which we develop vaccines, to make our cars safer, and so on. But there would appear to be only so much we can do in that regard: first of all there are things that we really truly can’t do anything about, such as nearby supernovae, and secondly there are quite a few moderately risky activities that quite a lot of us enjoy.

The singularity changes all that. What the singularity will provide is the very rapid reduction to truly minute levels of the risk of death from any cause. You may have thought that my earlier mention of snow reliably saving careless mountaineers was in jest; indeed it was not. Moreover, the residual risk that our rate of improvement of medical therapies against aging will at some point fall below LEV will also essentially disappear with the singularity. (Clearly the possibility also exists that the singularity will precede, and thus bring about, the Methuselarity – but that does not materially alter these considerations.)

One of my “soundbite” predictions concerning the Methuselarity is that the first thousand-year-old is probably less than 20 years younger than the first 150-year-old. The above considerations lead to a supplementary prediction. I think it is abundantly likely that the first million-year-old is less than a year younger than the first thousand-year-old, and the first billion-year-old probably is too.

The singularity and the Methuselarity are superficially similar, but I hope to have communicated in this essay that they are in fact very different concepts. Where they are most similar, however, is in the magnitude of their impact on humanity. The singularity will be a uniquely dramatic change in the trajectory of humanity’s future; the Methuselarity will be a uniquely dramatic change in its perception of its future. Together, they will transform humanity… quite a lot.


1. Singularity Institute for Artificial Intelligence. What is the Singularity? (retrieved 25th August 2008). 2. Ulam S. Tribute to John von Neumann. Bulletin of the American Mathematical Society 1958; 64(3 part 2): 1-49. 3. Moore GE. Cramming more components onto integrated circuits. Electronics 1965; 38(8): no pagination. 4. Kurzweil R. The Singularity Is Near: When Humans Transcend Biology. New York: Penguin, 2006 (ISBN: 0143037889). 5. Vinge V. The Coming Technological Singularity. In: Vision-21: Interdisciplinary Science & Engineering in the Era of CyberSpace, proceedings of a Symposium held at NASA Lewis Research Center (NASA Conference Publication CP-10129), 1993. 6. Deutsch D. The fabric of reality. New York: Penguin, 1998 (ISBN: 014027541X). 7. Weatherall D. Was there life after DNA? Science 2000; 289(5479):554-555. 8. Shaw GB. Maxims for Revolutionists. In: Man and Superman, 1903. 9. de Grey ADNJ. Long live the unreasonable man. Rejuvenation Res 2008; 11(3):541-542. 10. Pliskin JS, Shepard DS, Weinstein MC. Utility Functions for Life Years and Health Status. Operations Research 1980; 28:206-224. 11. Olshansky SJ, Perry D, Miller RA, Butler RN. Pursuing the longevity dividend: scientific goals for an aging world. Ann N Y Acad Sci 2007; 1114:11-13. 12. de Grey ADNJ, Ames BN, Andersen JK, Bartke A, Campisi J, Heward CB, McCarter RJM, Stock G. Time to talk SENS: critiquing the immutability of human aging. Annals NY Acad Sci 2002; 959:452-462. 13. de Grey ADNJ. A strategy for postponing aging indefinitely. Stud Health Technol Inform 2005; 118:209-219. 14. de Grey ADNJ. Escape velocity: why the prospect of extreme human life extension matters now. PLoS Biol 2004; 2(6):723-726. 15. Phoenix CR, de Grey ADNJ. A model of aging as accumulated damage matches observed mortality patterns and predicts the life-extending effects of prospective interventions. AGE 2007; 29(4):133-189. 16. de Grey ADNJ, Rae M. Ending Aging: The rejuvenation biotechnologies that could reverse human aging in our lifetime. New York, NY: St. Martin’s Press, 2007, 416pp, hardcover (ISBN 0-312-36706-6). 17. Banks J, Emmerson C, Oldfield Z. Not so brief lives: longevity expectations and wellbeing in retirement. In: Seven Ages of Man and Woman (Stewart I and Vaitilingam R, eds.), Swindon: Economic and Social Research Council, 2004, pp. 28-31. 18. Oeppen J, Vaupel JW. Broken limits to life expectancy. Science 2002;296(5570):1029-1031.

Seeking immortality: Aubrey de Grey at TEDxSalford

Hey y’all!  This is a TEDx talk freaturing Aubrey de Grey called “Seeking immortality: Aubrey de Grey at TEDxSalford.”

If you’re not familiar with Aubrey de Grey’s work, he is a gerontologist and Chief Science Officer of the SENS Research Foundation.  His theories have had a major impact in the field of gerontology (aging).  He was the one to make the claim that the first person to live to 1000 may already be alive.  I make it a point to check in on de Grey every once in a while so you’ll hear more about him.  Btw, Aubrey de Grey was the one to coin the term, Methuselarity* (think of it as the mitochondrial singularity).

Here’s a link to a pdf document comparing the Methuselarity and the Singularity.  The document is called, “The singularity and the Methuselarity: similarities and differences.”

The original video can be found at

Runtime: 20:09

Video info:

Published on Mar 25, 2014

Cambridge researcher Aubrey de Grey argues that aging is merely a disease — and a curable one at that. Humans age in seven basic ways, he says, all of which can be averted. Aubrey claims he has drawn a roadmap to defeat biological aging. He provocatively proposes that the first human beings who will live to 1,000 years old have already been born. With his astonishingly long beard, wiry frame and penchant for bold and cutting proclamations, de Grey is a magnet for controversy. A computer scientist, self-taught biogerontologist and researcher, he has co-authored journal articles with some of the most respected scientists in the field.


Curators: Mishal Saeed & Uzair F. Butt
Technical Lead: Mark Earnshaw
Camerawork: Nathan Rae & Team –
Post production: Elliott Wragg –
Audio restoration: Jorge Polvorinos –