Sinclair Targets $100 Age-Reversal Therapy After AI Screening Breakthrough
The Diary Of A CEO
Harvard researcher David Sinclair asserts that cellular aging can be reversed through epigenome repair, aiming to drop the cost of human rejuvenation therapies from $100,000 to $100.
## Background
This video was published on YouTube by The Diary Of A CEO on March 23, 2026. The page description introduces Harvard professor Dr. David Sinclair as he discusses longevity science, including the Information Theory of Aging, resetting biological age, fasting, gene therapy for blindness, and his supplement stack.
## TL;DR
Dr. David Sinclair discusses cutting-edge research in longevity and cellular age reversal, proposing that aging is a treatable disease caused by lost epigenetic information. He explores lifestyle interventions such as fasting, hormesis, and specific dietary choices alongside scientific breakthroughs like NMN, sirtuins, and AI-accelerated drug discovery. The conversation spans practical health advice, the economic and societal impacts of extended lifespans, and broader philosophical topics including consciousness, AI, and the nature of reality.
## Atmosphere & style
The conversation carries an intellectually charged yet deeply personal tone, seamlessly shifting from granular scientific mechanics to philosophical reflection. Host Steven Bartlett and Dr. Sinclair maintain a warm, highly engaged rapport, grounded in shared curiosity and mutual respect. Moments like Bartlett wearing an aging suit to experience physical frailty lend a tactile, empathetic weight to the scientific discussion, making complex cellular theories feel human and immediate.
## Key takeaways
- [49:18](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=2958s) Cellular rejuvenation technology and age reversal will require significant societal adjustments in economics, social security, and career structures.
- [53:52](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=3232s) Living significantly longer allows individuals to experience multi-career lives, combining the wisdom of an older mind with a young body.
- [57:03](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=3423s) Treating cancer cells with OSK gene therapy or chemical cocktails can normalize them, aligning with the 'geronco-genesis' hypothesis that aging creates a fertile environment for cancer.
- [01:02:45](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=3765s) The Information Theory of Aging compares genomic DNA to a vinyl record and the epigenome to the needle, where cellular stress creates 'scratches' that age-reversal technology aims to polish.
- [01:05:38](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=3938s) Sinclair chooses 'infinity' as his target age, asserting that healthy individuals surrounded by loved ones will not willingly choose to end their lives.
- [01:05:38](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=3938s) AI-accelerated research is dramatically reducing the cost and time required for longevity breakthroughs, allowing work that once took decades to be completed rapidly.
- [01:08:43](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=4123s) Skipping meals and avoiding constant eating triggers hormesis—a mild cellular stress that activates body repair networks.
- [01:13:55](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=4435s) Sirtuins act as cellular conductors that leave their posts to repair DNA breaks, leading to loss of epigenetic information and aging when they fail to return.
- [01:18:40](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=4720s) Systemic NAD+ levels decline by about 50% by age 50, but supplementing with NMN can double NAD+ levels and support cellular maintenance.
- [01:20:48](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=4848s) Periodic fasting protocols, such as daily 14–16 hour fasts or monthly 3-day fasts, stimulate chaperone-mediated autophagy to recycle degraded proteins.
- [01:25:23](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=5123s) Plant polyphenols induce xenohormesis by transferring plant defense mechanisms (like resveratrol, quercetin, and sulforaphane) to human survival networks.
- [01:31:39](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=5499s) Sinclair reversed his view on red wine due to UK Biobank MRI data showing brain gray matter reduction even from modest daily alcohol consumption.
- [01:36:19](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=5779s) Traditional healthcare needs to shift from treating illness after symptoms appear to proactive, early health testing and prevention.
- [01:37:13](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=5833s) Key dietary components for longevity include blueberries, avocados, extra virgin olive oil, Brazil nuts (for selenium), and Brussels sprouts (for sulforaphane).
- [01:41:04](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=6064s) Continuous daily supplement intake can cause adaptation tolerance; 'pulsing' doses allows periods of stress followed by recovery for maximum effectiveness.
- [01:45:17](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=6317s) Sinclair ranks meal skipping (fasting) and vigorous aerobic exercise as top daily longevity interventions, noting high aerobic exercise keeps telomeres functionally younger.
- [01:46:45](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=6405s) The primary mission of current biotech longevity efforts is to scale AI-discovered compounds down from prohibitive clinical trial costs to democratized, affordable therapies.
- [01:50:11](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=6611s) Sinclair posits a greater than 50% probability that our physical universe functions as a computer simulation, where observation collapses quantum states.
- [02:03:03](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=7383s) The main long-term threat posed by advanced AI and robotics stems from bad actors weaponizing and conscripting household android systems rather than autonomous AI rebellion.
- [02:05:27](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=7527s) The relaunch of the Lifespan platform and community aims to fund independent scientific research and clinical trials for age-reversal therapies.
The host begins the session by placing the reality of getting old into immediate perspective, observing the physical sensation of aging as something difficult and inherently uncomfortable. Dr. David Sinclair, a Harvard professor with three decades of experience researching longevity, aging, and age reversal, directly challenges the societal baseline that growing old and dying around age 80 is an unavoidable or acceptable biological outcome simply because it occurs naturally. He posits that cellular aging is a treatable condition and asserts that laboratory research now demonstrates the physical capacity to reverse the aging process. Sinclair emphasizes that reaching this milestone is no longer a speculative hypothesis but a matter of timing, noting that specific lifestyle adjustments can add a full decade to a person's lifespan.
Sinclair frames the human body through an information technology lens, viewing it as a physical computer system whose underlying software can be reinstalled or reset. Under this framework, age-driven conditions like Alzheimer's disease, cancer, and heart disease are treated not as primary isolated incidents, but as downstream symptoms of the aging process itself. Consequently, reversing biological age resolves or prevents these degenerative conditions. He compares his research laboratory to "Willy Wonka's chocolate factory" due to the regular pace of discoveries made by his team, predicting that individuals who execute correct health strategies today are likely to live into the 22nd century.
- **Key Professional Credentials:** Dr. David Sinclair is a Professor of Genetics at Harvard Medical School and has conducted research on longevity and cellular age reversal for 30 years.
- **Underlying Concept:** Diseases of aging (such as cancer, Alzheimer's, and heart disease) are driven directly by the fundamental biological aging process; addressing the underlying process targets the root cause of these pathologies.
---
[03:34](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=214s) The Children’s Book That Quietly Shaped Everything That Came Next
The conversation shifts to Dr. Sinclair’s early life and the deeply personal origins of his life's work, centered around a photograph of himself in his early twenties alongside his grandmother, Vera. Reflecting on her impact, Sinclair describes how her experiences in Hungary following World War II instilled in her a desire to preserve childhood innocence, viewing adulthood as a state prone to corruption. During his early childhood, Vera read to him from A. A. Milne's book of poetry, *Now We Are Six*. The concluding lines of the title poem left a lasting imprint on his perspective regarding human mortality and aging:
> "When I was one, I had just begun. When I was two, I was nearly new. When I was three, I was hardly me. When I was four, I was not much more. When I was five, I was just alive. But now I am six, I'm as clever as clever. So I think I'll be six now forever and ever."
```
EARLY LIFE INSPIRATION TIMELINE
Age 4-5 Vera introduces the poem "Now We Are Six"
┌───────┐ and delivers a frank conversation about universal
│ Childhood mortality (pets, parents, and self).
└───┬───┘
│
▼
Age 18 Commits to a lifelong career in genetics,
┌───────┐ targeting a PhD and establish a lab in the
│ Vow │ United States dedicated to aging research.
└───┬───┘
│
▼
Present 56-year-old Harvard Professor executing
┌───────┐ the first human gene therapy trials to
│ Today │ reverse cellular aging and treat age-onset diseases.
└───────┘
```
A pivotal conversation occurred when Sinclair was four or five years old. He asked Vera if she would always be there to protect him, to which she plainly responded that everyone eventually dies—including herself, his parents, his pet cat, and Sinclair himself. This early realization of mortality struck him as fundamentally cruel, sparking a lifelong commitment. By age 18, he had resolved to earn a PhD, relocate to the United States, and establish a dedicated research laboratory to understand and reverse aging. He views the preservation of human life and health as a paramount moral imperative, arguing that daily global mortality—accounting for approximately 150,000 to 200,000 deaths every day—is overwhelmingly driven by aging, a process humanity has passively accepted for too long.
- **Daily Global Mortality Figure:** Approximately 150,000 to 200,000 people die every day worldwide, primarily due to age-related degeneration and disease.
- **Current Age:** Dr. David Sinclair is 56 years old at the time of this recording.
- **Moral Philosophy:** Sinclair rejects the naturalistic fallacy that aging is acceptable simply because it is natural, asserting that future generations will view current acceptance of pre-100 frailty as primitive and medieval.
---
[06:27](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=387s) Why Living To 80 Might Be Far More Alarming Than You Think
Addressing common skepticism from those who view an 80-year lifespan as a fixed, natural boundary, Sinclair outlines the empirical foundation of his ongoing work. He explains that his laboratory systematically reverses the biological age of both cultured human tissues and living animal tissues using specialized genetic treatments. Rather than offering speculative philosophy, he points directly to active scientific protocols, revealing that the very first human clinical trials designed to test cellular age reversal are scheduled to begin within approximately one month.
```
PARADIGM SHIFT IN HUMAN HEALTHCARE
CURRENT MEDICINE LONGEVITY MEDICINE
┌─────────────────────────────┐ ┌─────────────────────────────┐
│ Reactive Intervention │ │ Systemic Reset │
│ • Treat cancer individually │ ──► │ • Revert tissue age by ~75% │
│ • Manage Alzheimer's symptoms│ │ • Restore cellular function │
│ • Accept frailty by age 80 │ │ • Systemically clear disease │
└─────────────────────────────┘ └─────────────────────────────┘
```
Sinclair reiterates his professional standing as a Harvard professor leading a global team of elite researchers to emphasize that these developments are rooted in peer-reviewed science. He asserts that the field has progressed beyond incremental lifespan extensions toward functional biological reset. Successfully translating these animal models into human medicine will alter the historical trajectory of healthcare, shifting the treatment of chronic disease from reactive symptom management to systematic age reversal.
- **Clinical Trial Timeline:** The first human clinical trial deploying Dr. Sinclair's age-reversal technology is set to begin within a month of the recording.
- **Target Outcome:** Reversing the biological age of targeted tissues to restore youthfulness and resolve conditions previously deemed incurable.
---
[09:12](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=552s) Inside The First Human Trials Attempting To Reverse Ageing
Sinclair detailed the specifics of the upcoming human clinical trials, which focus on treating blindness by targeting the human eye. The eye was deliberately selected as the initial human testing site not because it is uniquely responsive to age reversal, but because it is a self-contained, isolated organ system. This spatial isolation provides a crucial safety buffer: if any unforeseen adverse events occur during gene delivery, the intervention remains localized to the eye rather than spreading systemically throughout the patient's entire body.
```
HUMAN CLINICAL TRIAL MODEL
Target Area Intervention Method Observed Effect
┌───────────────┐ ┌───────────────────┐ ┌───────────────────┐
│ Human Retina │ ────────► │ Deliver 3 Genes │ ────────► │ Resets cell age │
│ & Optic Nerve │ │ Active 6–8 Weeks │ │ back by ~75% │
└───────────────┘ └───────────────────┘ └───────────────────┘
```
The protocol targets the retina at the back of the eye and the optic nerve, which connects directly to the brain—a structure Sinclair notes is technically an external extension of the central nervous system. In conditions where vision is lost due to aging or physical damage, the physical nerve fibers often remain intact but lose their functional capacity because the cells have "forgotten" how to operate correctly. To remedy this:
1. A set of **three specific genes** (a subset of Yamana factors) is delivered directly into the cells of the optic nerve.
2. The genes are switched on for a period of **6 to 8 weeks**.
3. This process safely resets the biological age of the nerve cells back by approximately **75%**, at which point the reversal process halts automatically.
Sinclair notes that this system features a natural safeguard: it stops short of resetting cells back to a primordial or stem-cell state (zero), which would destroy cellular identity and risk tumor formation. Beyond vision restoration, his lab has already successfully applied this exact technology in mouse models to reverse aging and restore function in the brain, hearing mechanisms, skin tissue, multiple sclerosis models, and motor neuron diseases.
- **Regulatory Status:** Sinclair's team submitted documentation to the U.S. Food and Drug Administration (FDA) to obtain clinical trial approval for treating human blindness.
- **Biological Reset Capacity:** The gene therapy resets cellular age by roughly 75% before stopping, preventing complete dedifferentiation.
- **Safety Protocol:** Using the enclosed ocular system avoids the risks of immediate full-body systemic rejuvenation in humans while safety profiles are established.
---
[12:23](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=743s) How Scientists Actually Slowed Ageing In Mice—And What That Means For Us
Elaborating on animal models, Sinclair highlights a pivotal study conducted by an independent laboratory using his core technology. In this experiment, researchers delivered the three age-reversal genes via systemic intravenous injection into elderly mice. These mice were equivalent in biological wear and tear to an 80- to 85-year-old human—frail, slow, and near the end of their natural life expectancy.
Following the treatment, the elderly mice demonstrated a **100% extension in their remaining lifespan** compared to untreated control animals. Sinclair clarifies the mathematics of this result: rather than doubling the total lifespan from birth, the intervention doubled the *remaining* life expectancy of the aged mice. For example, if an 80-year-old human had an average remaining life expectancy of 10 years, a proportional extension would grant them an additional 10 years of healthy life. Sinclair emphasizes that this outcome was achieved with a single, unoptimized injection, demonstrating the profound latent capacity for rejuvenation built into complex mammalian organisms.
- **Experimental Setup:** Intravenous administration of gene therapy to extremely old, frail mice (equivalent to 80–85 human years).
- **Result:** A 100% increase in the remaining lifespan of the treated mice.
- **Scientific Validation:** The study was executed by an independent laboratory using Sinclair's proprietary technology, confirming reproducibility outside his own Harvard facility.
---
[14:51](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=891s) Will An Anti-Ageing Pill Really Exist—Or Is That A Dangerous Myth?
Sinclair directly addresses skepticism regarding how gene therapies—which currently require invasive delivery mechanisms—could ever be transformed into accessible, everyday consumer medicine. He firmly predicts that within his lifetime, and well within the lifetime of younger generations, age-reversal medicine will transition from complex gene therapy to a simple pharmaceutical pill or oral liquid taken on a periodic schedule (such as once every few weeks).
```
GENE THERAPY TO ORAL THERAPEUTIC PIPELINE
FIRST GENERATION (Current) NEXT GENERATION (Under Development)
┌──────────────────────────────────┐ ┌──────────────────────────────────┐
│ Viral Gene Delivery │ ───► │ Chemical/Oral Rejuvenation │
│ • Injected into tissue/vein │ │ • Delivered as a liquid or pill │
│ • Requires genetic alteration │ │ • Triggers intrinsic age reset │
│ • Complex clinical administration│ │ • Full systemic effect in weeks │
└──────────────────────────────────┘ └──────────────────────────────────┘
```
Sinclair relies on his "Information Theory of Aging," a unifying framework proposing that aging is driven by a loss of epigenetic information over time, while the original youthful genetic "software" remains completely intact in every cell. Because the underlying hardware is undamaged, chemical compounds can be engineered to trigger the cell to read its original, youthful epigenome once again.
While critics view the idea of an anti-aging pill as unrealistic hype, Sinclair reveals that his lab has already moved beyond first-generation genetic vectors. In recent mouse trials, his team successfully induced systemic tissue rejuvenation within **4 weeks** using an orally administered liquid compound rather than direct genetic modification. He expects these treatments to initially target and cure currently intractable age-related medical conditions before expanding into preventative and cosmetic longevity applications.
- **Mechanism of Delivery Progress:** Evolution from first-generation gene delivery (injectable Yamana-factor derivatives) to next-generation small-molecule chemical cocktails given orally.
- **Lab Discovery Benchmark:** Achieving full tissue rejuvenation in mice within a 4-week window using liquid oral administration.
- **Ultimate Goal:** A periodic oral treatment capable of resetting biological age, curing chronic diseases, and preventing general physical decline.
[16:03](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=963s) Reversing Age Across Organs and the Universal Mechanism
Dr. David Sinclair describes a major breakthrough where swallowing a single compound can rejuvenate a mouse within just four weeks. Rather than treating every condition with a separate drug or gene therapy, his team discovered that the exact same set of genes and molecules that restores eyesight in blind mice can also reverse motor neuron disease (ALS), heal damaged skin, regenerate ear tissue, and potentially treat liver disease.
This universal repair mechanism reshapes expectations for human health. People traditionally assume their later years will mirror the frailty of their parents or grandparents, but Sinclair argues that previous generations are no longer a accurate guide for our future lifespan. Comparing this leap in longevity to the early days of aviation, he points out that just as humanity progressed from horse-drawn travel to spaceflight within a single century, biological science is undergoing an exponential shift that could allow people alive today to reach the 22nd century.
- **Universal Gene Therapy:** The exact same genetic intervention restores vision, treats ALS, and reverses liver damage in animal models.
- **The Aviation Analogy:** Assuming human lifespan is fixed is like assuming in the year 1900 that travel speeds would always be limited to the speed of a horse.
- **Medical Singularities:** Future medical technologies in 2070 or 2080 will allow individuals who reach that era to continually extend their healthspan.
---
[18:34](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=1114s) The Longevity Singularity and Repeated Age Reversal
The conversation turns to the concept of the "longevity singularity"—a threshold in human history where technology advances so quickly that for every year a person lives, science buys them back a year of life, making age reversal a deliberate choice. Host Steven Bartlett raises the futurist Ray Kurzweil's prediction that this milestone could arrive sometime in the 2040s. While Sinclair remains scientifically cautious about exact timelines, he notes that betting against Kurzweil's track record is difficult.
```
"We can reverse the age of the eye not just once, but seemingly as many times as we want... the mice actually just got old and died, but they died with perfect eyesight."
```
In laboratory trials, Sinclair's team demonstrated that cellular age reversal is not a "one-shot wonder." They successfully reset the biological age of eyes in mice twice in succession. The animals eventually died of old age, but they passed away with flawless vision, confirming that the epigenetic reset button can be pushed repeatedly.
- **Ray Kurzweil's Timeline:** Kurzweil predicted that the longevity singularity could be reached as early as the 2040s.
- **Iterative Age Reset:** Mice eyes were successfully rejuvenated multiple times, proving that cellular age reversal can be performed repeatedly.
- **Baseline Expectation:** Sinclair asserts that if individuals today do not live 10 to 20 years longer than their parents, something in their lifestyle or medical care has gone wrong.
---
[20:43](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=1243s) The Information Theory of Aging and the Epigenome
Sinclair presents his core model: the **Information Theory of Aging**. Rather than viewing the body as a mechanical device that simply wears out over time, he compares it to a computer whose operating system software accumulates corruption. The genetic blueprint—our DNA—remains virtually pristine throughout life, but the control systems that govern which genes are turned on or off (the epigenome) lose their clarity over time.
To demonstrate how genetic information is physically organized, Sinclair pulls out a physical double-helix model of DNA. He explains how base pairs—Adenine (A) pairing with Thymine (T), and Guanine (G) pairing with Cytosine (C)—form the "rungs" of the 6-foot-long DNA strand found in every cell. Out of roughly 20,000 human genes, about 15,000 are expressed depending on whether a cell is supposed to be a nerve cell, skin cell, or liver cell.
```
"When I see an old person walking down the street now, I don't think, 'Oh, that person's just worn out, frail, going to die.' I just think that's someone that needs a reset. And inside that person is a young person waiting to come out again."
```
- **DNA Length:** Every human cell contains roughly 6 feet of tightly packed DNA.
- **Gene Expression:** Human cells contain around 20,000 genes, with approximately 15,000 active in a given cell type.
- **DNA Methylation:** A methyl group (one carbon atom bonded to three hydrogen atoms, $\text{-CH}_3$) attaches primarily to Cytosine (C) bases to turn genes on or off.
- **Identity Loss:** Aging occurs when cells lose their epigenetic tags, causing skin cells to subtly express nerve cell genes and vice versa—an "identity crisis."
---
[27:40](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=1660s) DNA Damage, Cell Panic, and the "ICE" Mouse Experiment
Explaining why cells lose their identity over time, Sinclair details how cells respond to severe emergencies, specifically broken chromosomes. Every cell in the human body experiences at least one broken chromosome per day, leading to about 20 trillion repair events across the body daily. When a break occurs, epigenetic regulatory proteins and methyl-modifying enzymes leave their normal positions to orchestrate emergency repairs. Although the cell usually survives the emergency, these proteins do not always return to their exact original locations, leaving tiny errors behind that accumulate over a lifetime.
To test whether this epigenetic disruption directly causes aging, Sinclair's lab created a specialized genetic model: the **ICE mice** (*Inducible Changes to the Epigenome*). By engineering stem cells with a gene derived from a forest slime mold, they created a mechanism that cleanly cut the mouse's DNA without causing mutations or cancer.
```
"I got a picture on my old-style iPhone... and the text was 'Problem, we have a sick mouse.' And I wrote back, 'That's not a sick mouse. That's an old mouse.' And that was the first time I realized that we'd had evidence that our theory... is correct."
```
When the team activated the slime mold gene for just three weeks, the mice initially appeared completely healthy. However, the temporary disruption set off a cascade of accelerated epigenetic aging. Just 10 months later, the treated mice exhibited gray fur, frail bodies, and typical diseases of aging at a rate 50% faster than their untreated genetically identical twins.
- **Daily DNA Emergency Rate:** Human bodies undergo roughly 20 trillion chromosome repair events every day.
- **ICE Mice:** Stands for *Inducible Changes to the Epigenome*, an animal model designed to isolate epigenetic aging from DNA mutations.
- **Slime Mold Enzyme:** A protein sourced from slime mold was used to cleanly slice mouse DNA to trigger cellular stress without causing cancer.
- **Accelerated Aging Rate:** Disruption of the epigenome caused mice to age 50% faster than their untreated identical twins.
[32:46](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=1966s) Environmental Stressors and the Accelerators of Aging
Dr. David Sinclair explains how everyday encounters with DNA-damaging forces inadvertently speed up the biological clock. When chromosomes break due to external stressors, the epigenome undergoes catastrophic rearrangements during the repair process, leading cells to lose their distinct identity over time. Sinclair cautions that routine exposures—such as receiving CT scans or X-rays, frequent long-haul flying, and exposure to cosmic radiation—imperceptibly accelerate biological aging. Even non-radiation physical trauma, such as exposing ear hair cells to the blaring volume of a live rock concert, creates extreme cellular stress; as a result, these specialized cells age prematurely, driving early hearing loss.
To illustrate these concepts to everyday lifestyle differences, host Steven Bartlett shares an anecdote about observing his older brother, Jason. Despite being only a year apart in age, Jason—who has three young children under eight—displays noticeably more gray hair. While graying itself is harmless, Sinclair notes that outward physical appearance often mirrors the internal biological age of a person's organs.
- Epigenetic shifts driven by broken DNA repair processes are responsible for 80% to 90% of a person's aging rate; underlying genetics account for only a small portion.
- Identical twin studies out of Denmark demonstrate that when one twin smokes, suffers from obesity, and experiences heavy sun exposure, they look and function biologically much older than their genetic clone.
---
[36:06](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=2166s) The Core Lifestyle Habits for Extending Lifespan
Drawing on Harvard longitudinal research following World War II veterans, Sinclair highlights five core behaviors that together can extend a person's average lifespan by as much as 14 years:
```
1. Avoid all smoking (tobacco and inhaled smoke cause immediate DNA double-strand breaks).
2. Limit alcohol consumption (restricting intake to no more than one drink per day, or abstaining).
3. Maintain an optimal diet (avoiding overeating and cutting out ultra-processed foods).
4. Engage in regular physical exercise.
5. Maintain a reliable partner or close companion (human bonding or pet ownership protects against loneliness).
```
Sinclair underscores the evolutionary necessity behind these interventions: natural selection prioritized early reproductive success and fast breeding rather than long-term cellular maintenance. In prehistoric environments like the East African Serengeti, humans rarely lived past 30 or 40 due to predation, infectious disease, and inter-tribal warfare. Without natural evolutionary pressure to survive into late adulthood, the human body after age 30 succumbs to entropy, losing crucial epigenetic control over time.
- Long-lived species in nature, such as the bristlecone pine (living thousands of years) or the bowhead whale (living over 200 years), evolved extreme longevity because they possess virtually no natural predators.
- In experimental conditions, placing animal populations on islands free of predators leads to the natural evolution of longer lifespans within 20 to 30 generations.
---
[41:58](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=2518s) Reversing Aging as a Universal Medical Treatment
Addressing the connection between aging and chronic illness, Sinclair presents what he considers his most critical thesis: individual chronic conditions—such as Alzheimer's disease, cardiovascular illness, and various cancers—are merely downstream symptoms of biological aging. Treating aging directly cures or prevents these underlying pathologies simultaneously.
When human dementia genes are engineered into laboratory mice, reversing the biological age of the animal's brain cells causes the cognitive symptoms of dementia to clear up naturally. Young organisms possess robust repair and immune mechanisms—such as natural killer cells that clear micro-tumors before they expand—that deteriorate as the body ages.
- In laboratory studies, 16-month-old female mice (equivalent to a 65-to-70-year-old human) that had long ceased reproducing were given treatments to rejuvenate their ovaries.
- The treated older mice produced healthy, genetically normal offspring with normal lifespans, challenging the long-held paradigm that female fertility ends strictly due to an irreversible exhaustion of viable eggs.
---
[46:15](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=2775s) The Geopolitics and Regulatory Hurdles of Age Reversal
Translating longevity breakthroughs from animal models to human therapeutics involves navigation through complex patent landscapes, commercial rivalries, and geopolitical friction. Sinclair highlights that age-reversal technology has already moved past rodent models and has been successfully demonstrated in non-human primates.
Because non-human primates share nearly identical genetic and physical traits with humans, the jump to human applications is closer than ever. However, national security concerns surrounding this paradigm shift have led governments to monitor the field closely.
> "A large investment into one of the companies that I sit on the board of was blocked because the US government claimed that the technology was too dangerous to be in the hands of foreign companies and governments."
- A foreign investment exceeding $100 million into a longevity biotechnology company associated with Sinclair was officially blocked by the United States government over national security and intellectual property concerns.
- World powers view age-reversal therapies not only as a potential source of economic and healthcare dominance, but as a disruptive national security asset capable of reshaping society.
[49:18](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=2958s) Societal Readiness for Human Rejuvenation and the "Billionaire Trade-Off"
Dr. Sinclair acknowledges that while concerns about technologies creating "super soldiers" shouldn't halt research, the potential power of cellular rejuvenation requires society to prepare for its inevitable reality. When humans can actively choose their biological age and extend life past 120 years, society will face massive shifts in social security, employment, and economic structures. However, he counters the typical doom-and-gloom scenarios by highlighting the immense economic benefits: since the majority of healthcare spending and personal savings are drained during the last few years of life dealing with chronic disease, delaying that decline can save trillions and economically revitalize nations.
To frame the sheer value of youth, host Steven Bartlett brings up a thought experiment often circulated on social media: *Would a 56-year-old billionaire trade all their wealth to be 33 again? Or would anyone swap places with an aging titan like Warren Buffett for a billion dollars?* Dr. Sinclair responds that youth is priceless and undeniably more valuable than a billion dollars, noting he would easily choose being 33 over being a 43-year-old billionaire. The arrival of age-reversal technology will trigger a historical shift as profound as the invention of computers or aviation. When asked whether the future means remaining visually young or simply surviving longer in an aged body, Dr. Sinclair clarifies that it is both—his lab is actively working on internal rejuvenation alongside external features like skin and hair.
- **Skin Rejuvenation Studies:** The Sinclair Lab grows human skin from scratch in the lab and grafts it onto mice to test age-reversal therapies directly on human tissue.
- **Blindness vs. Skin:** Dr. Sinclair asserts that if his team can reverse age-related blindness, rejuvenating skin is comparatively a "piece of cake."
[53:52](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=3232s) Purpose, Career Cycles, and Reversing the Fertility Crisis
Addressing potential unintended consequences—such as a loss of human drive, purpose, or agency when death is no longer an immediate threat—Dr. Sinclair firmly rejects the idea that a longer life diminishes its meaning. He argues that every single moment remains precious regardless of lifespan; living 200 or even 1,000 years would simply offer richer opportunities to pursue multiple careers, reinvent oneself, and apply the wisdom of an 80-year-old mind within the body of a 30-year-old.
Furthermore, Dr. Sinclair highlights the societal crisis of crashing birth rates and the biological pressure on women to have children before age 35. Extending the human reproductive window into a woman's 50s or 60s would give couples the gift of time to establish stable partnerships without rushing. Preserving human health and longevity, he argues—stepping into a friendly counter-debate with Elon Musk's views on population collapse—is the single best way to solve future labor shortages and maintain global human productivity.
The episode features two brief brand integrations:
- **BonCharge:** Steven Bartlett demonstrates a non-invasive, professional-grade red light face mask designed to boost collagen production, diminish fine lines, and improve skin complexion.
- **Shopify:** An encouragement for aspiring entrepreneurs to launch their projects in 2026 using Shopify's all-in-one e-commerce management, AI tools, and social selling features.
[59:02](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=3542s) Reprogramming Cancer Cells: The "Geronco-Genesis" Hypothesis
Dr. Sinclair reveals ground-breaking work being conducted in his lab by his PhD student, Nallath, targeting cancer through the Information Theory of Aging. Viewing both aging and cancer as cellular identity crises—where cells forget their original functions—the lab hypothesized that if old cells can be reprogrammed to act young, cancer cells can be forced to regain their original identity. When subjected to age-reversal treatments, cancer cells grown in the lab either attempt to normalize, stop multiplying, or trigger self-destruction (apoptosis).
Dr. Sinclair introduces his "geronco-genesis" hypothesis: as humans age, our baseline metabolism shifts closer to a cancer-like state, creating a fertile environment for tumors to thrive. By reversing cellular age using either the three Yamanaka OSK genes or specific chemical cocktails, scientists can trick decades-old cancer cell lines into re-expressing their original 20th-century genetic programming, prompting them to self-destruct. While not a universal cure, curing aging could drastically reduce global cancer risks as a natural side effect.
- **Mechanisms of Reprogramming:** Cancer cells are treated either via OSK gene therapy (the same vector used in their vision-restoration trials) or a special chemical drink that resets cellular identity.
- **Drivers of Cellular Stress:** Severe DNA breaks, extreme heat, and physical impacts (such as repeated head trauma in football) damage the epigenome, driving both cellular aging and cancer progression.
[01:02:45](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=3765s) Visualizing the Epigenome: The Scratched Vinyl Record
To make the Information Theory of Aging tangible, Dr. Sinclair uses a physical vinyl record provided by the host. In this analogy, the genomic DNA is the underlying musical data embedded in the grooves, while the epigenome is the record player's needle reading the music. Aging doesn't destroy the original music; rather, cellular stress and DNA damage act like physical scratches on the surface of the album, causing the needle to skip and play the wrong notes.
With the host's permission, Dr. Sinclair dramatically scrapes the surface of the vinyl record on camera, illustrating how environmental damage creates noise and prevents the cell from reading its original genetic code. His lab's age-reversal technology functions as a polish that removes those scratches, allowing the cell to cleanly read its DNA and play the "beautiful music" of its youth once again.
[01:04:17](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=3857s) The Heavy Weight of Aging: The Weighted Vest Experience
Demonstrating the physical reality of growing old, Steven Bartlett puts on a 20 kg weighted vest along with a restrictive neck brace right at the desk. Dr. Sinclair explains that this immediate sense of heaviness, exhaustion, and limited neck mobility mirrors what millions of elderly people experience every day for decades.
- **The Daily Strain of Old Age:** The physical burden of carrying extra weight and losing joint mobility simulates the frailty, chronic pain, and fatigue that affect most individuals in their 80s.
- **The Ultimate Goal:** The objective of longevity science isn't merely extending years spent carrying this heavy burden, but removing the metaphorical weight altogether so individuals retain full mobility and vitality late into life.
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[01:05:38](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=3938s) The Physical Reality of Aging and the Infinity Choice
The conversation opens with a striking, visceral look at what aging actually feels like. Dr. Sinclair discusses the physical discomforts of old age—how simple movements can feel like a pair of scissors stabbing into joints—and notes that loss of vitality, combined with pain, is why many elderly individuals lose their joy for life. To truly understand this state, one would have to put Vaseline over their eyes or wear earplugs to simulate sensory decline. In the worst cases, it means losing eyesight entirely, which is the exact suffering Dr. Sinclair’s lab hopes to cure through cellular reprogramming.
Steven Bartlett then presents a thought experiment: if Sinclair had a calculator in front of him and had to type in the exact age he would choose to live to right now, what number would he choose? Without hesitation, Sinclair answers "infinity" (or typing `9999999`). He argues that as long as a person is healthy, surrounded by family, friends, and loved ones, there is never a day where they actively choose to die, unless they are suffering from a severe psychiatric issue or depression. While people often casually say, "When I'm 80, kill me," Sinclair asserts that life—and consciousness itself—is the greatest gift any collection of atoms can have, and no healthy person would willingly choose to give it up. Bartlett admits that while he previously assumed he wouldn't want to live forever, he realizes that under conditions of good health and purpose, he has never had a single day in his 33 years where he wanted his life to end.
- **Living into the 22nd Century:** Sinclair reiterates his belief that younger people like Bartlett will live into the 22nd century, where technologies powered by AI will radically alter medicine.
- **AI Acceleration:** AI is accelerating research in Sinclair's lab exponentially—completing work on a $10,000 budget that previously would have taken 160 years and billions of dollars.
---
[01:08:43](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=4123s) Fasting, Hormesis, and the Heavy Aging Suit Experiment
Transitioning to daily lifestyle habits, Sinclair emphasizes that fasting—simply eating less often—is one of the most powerful and accessible longevity interventions available. He points out that ancient civilizations understood the mental clarity and long-term health benefits of fasting. However, modern society is trapped in "abundance mode," surrounded by constant food, comfortable chairs, and air conditioning. Sinclair strongly criticizes the traditional belief that "breakfast is the most important meal of the day," calling three meals a day "craziness" and revealing that breakfast marketing was largely created by early 20th-century cereal companies. Both Sinclair and Bartlett share that they naturally skip breakfast and rarely eat their first meal until mid-to-late afternoon (often 3:00 p.m. to 5:00 p.m.).
During this segment, Bartlett is physically wearing a heavily weighted aging suit designed to simulate the physical burden of growing old. As the conversation progresses, Bartlett struggles to find a comfortable position, remarking on how heavy and oppressive it feels. Sinclair recalls putting a similar full-body suit—complete with joint resistance, earmuffs, and impaired vision glasses—on the Governor of Massachusetts. After just 15 minutes, the Governor broke down crying on stage, realizing for the first time how difficult daily life was for his aging father. When Bartlett finally takes off the weighted vest, he describes feeling an overwhelming sense of lightness and freedom, which Sinclair explains is the exact feeling cellular rejuvenation could bring to an 80-year-old body.
- **Hormesis:** The biological mechanism where mild stress ("what doesn't kill you makes you stronger") turns on cellular defense systems.
- **Adversity vs. Abundance:** Activities like fasting, intense exercise, sauna sessions, and cold plunges put cells into "adversity mode," tricking them into initiating repair and recycling processes.
---
[01:13:55](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=4435s) Discovering Longevity Genes: The Sirtuin Story
Sinclair recounts his early career in the 1990s at MIT under Professor Lenny Guarente, where he set out to answer why organisms age. Rather than studying complex humans, he studied single-celled yeast (*Saccharomyces cerevisiae*), which live for about 10 days. At the time, conventional wisdom suggested aging was driven by specific "death genes," but Sinclair hypothesized that organisms possess "longevity genes" designed to protect and extend life. Their landmark discovery in yeast, published in the journal *Cell*, provided the very first evidence of a genetic cause of aging in any species.
```
+-------------------------------------------------------------------------------+
| THE SIRTUIN DUAL-ROLE CONUNDRUM |
+-------------------------------------------------------------------------------+
| |
| PRIMARY JOB (Epigenetic Conductor) SECONDARY JOB (Emergency Repair) |
| +--------------------------------+ +----------------------------------+ |
| | Maintains cellular identity | | Repairs double-stranded DNA | |
| | Keeps genes silenced/active | | chromosome breaks | |
| +---------------+----------------+ +----------------+-----------------+ |
| | | |
| +------------------+ +-----------------+ |
| | | |
| v v |
| [ DNA Damage / Break Occurs ] |
| | |
| v |
| Sirtuins abandon primary duties to fix break |
| | |
| v |
| Not all Sirtuins return to their original position! |
| | |
| v |
| ==> Epigenetic noise builds up = Loss of Cell Identity (Aging) <== |
+-------------------------------------------------------------------------------+
```
Sinclair explains how yeast aging mirrors the Information Theory of Aging. Yeast cells have a defined identity based on their mating type ("A" or "alpha," akin to male and female). As yeast cells age, they experience double-stranded chromosome breaks. Sirtuins—proteins that normally act as "conductors" to maintain cell identity—are forced to abandon their posts to repair the broken DNA. Because not all sirtuins find their way back to their original locations, the cell suffers a loss of epigenetic information. The yeast cell undergoes an identity crisis, loses its sex identity, becomes sterile, and eventually dies. Sinclair explains that this constant "ping-pong match" between epigenetic regulation and DNA repair is what causes both yeast and human cells to age.
---
[01:18:40](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=4720s) NAD+, NMN, and the Epigenetic Repair Engine
As Sinclair was transitioning to establish his own lab at Harvard at age 29, researchers discovered that sirtuins cannot function without a critical metabolic coenzyme called **NAD+** (nicotinamide adenine dinucleotide). NAD+ acts as the fuel or catalyst that allows sirtuin enzymes to perform both DNA repair and epigenetic maintenance. When we are young, our bodies maintain high levels of NAD+, keeping cellular repair running smoothly. However, by age 50, NAD+ levels drop by approximately 50% due to decreased production and increased enzymatic destruction.
> "When you give a human NMN by swallowing it, a gram of it, you typically double the amount of NAD in your body."
When an organism fasts or experiences cellular stress, internal NAD+ levels rise, effectively reactivating sirtuins. Because drinking pure NAD+ is inefficiently absorbed by cells, researchers utilize NAD+ precursors like **NMN** (nicotinamide mononucleotide) and **NR** (nicotinamide riboside). Sinclair notes that taking 1 gram of oral NMN doubles systemic NAD+ levels in humans. Clinical trials demonstrate that boosting NAD+ through NMN helps re-establish the epigenome, reduce systemic inflammation, lower body weight, and improve lipid profiles. Sinclair confirms that he has personally been taking NMN publicly for years as part of his daily longevity protocol.
- **Key Precursors:** NMN (Nicotinamide Mononucleotide) and NR (Nicotinamide Riboside) serve as direct building blocks for cellular NAD+.
- **Human Clinical Evidence:** NMN supplementation demonstrates measurable improvements in metabolic health, body weight management, and inflammatory markers in clinical trials.
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[01:20:48](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=4848s) Building a Sustainable Fasting Protocol and the Deep Clean of Autophagy
Dr. David Sinclair highlights his father, who at 86 years old serves as an advanced long-term experiment in longevity practices, noting that both of them have been implementing these protocols for over a decade. When asked about actionable fasting recommendations for the average person, Sinclair emphasizes that there is no one-size-fits-all approach. He cautions against drastic changes on day one, which typically lead to frustration and quick abandonment. Instead, he advocates for a gradual ramp-up: starting by skipping breakfast or postponing it with a light mid-morning snack, and slowly pushing the first meal later into the afternoon over several weeks.
For daily routines, Sinclair aims for at least a 14-hour overnight fast (with others extending to 16 hours), ideally practiced five days a week. This duration is sufficient to elevate NAD+ levels and trigger sirtuin activation, especially when combined with regular exercise. Host Steven Bartlett admits his own dinner hours are often late—sometimes around 10:00 p.m.—but notes that even with late meals, reaching a 13- to 14-hour window before eating the next day provides substantial biological benefits.
Beyond daily time-restricted feeding, Sinclair reveals that he personally undertakes a prolonged 3-day fast roughly once a month to access deeper cellular cleanup mechanisms. While short fasts deplete liver glycogen and shift the body into basic ketosis to produce ketone bodies, they do not trigger the comprehensive clearing of damaged cellular components. After two and a half to three days of fasting, the body initiates **chaperone-mediated autophagy**—literally "self-eating"—a process where cells systematically recycle old, degraded proteins.
Evolutionarily, the body delays this deep clean because re-synthesizing structural cellular components demands immense energy. Initially, the body relies on stored liver glycogen for glucose, then shifts into fat burning to generate ketones between 15 and 24 hours. During this period, the brain utilizes ketones for fuel, resulting in heightened mental clarity and focus. Beyond 48 to 72 hours, as fat stores continue to break down, the body selectively degrades old, malfunctioning proteins for fuel, generating a profound longevity-promoting benefit in animal models.
- **Daily Fasting Window:** Aim for 14 to 16 hours of daily fasting, ideally 5 days per week, to boost NAD+ and activate sirtuins.
- **Extended Fasting Frequency:** A 3-day (72-hour) fast once per month triggers chaperone-mediated autophagy to clear damaged proteins.
- **Metabolic Timeline:**
- *First few hours:* Liver glycogen is broken down into glucose.
- *15 to 24 hours:* Fat breakdown accelerates, producing ketone bodies that sharpen cognitive focus.
- *2.5 to 3 days:* Chaperone-mediated autophagy preferentially recycles degraded cellular proteins.
---
[01:25:23](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=5123s) Ketogenic Diets, Xenohormesis, and the Science of Plant-Based Longevity
Addressing the popular ketogenic diet, Sinclair offers a candid, evidence-based critique. While acknowledging its short-term efficacy for rapid weight loss and mental focus, he states that scientific data does not support long-term keto as a longevity-inducing diet. The primary concern is the omission or extreme reduction of plant foods containing unique protective molecules absent in meats and highly processed foods. Instead, long-term epidemiological evidence points toward a lean, plant-focused diet rich in unrefined, lightly cooked vegetation as the optimal approach for lifespan extension.
Sinclair shares his personal shift away from a meat-centric diet, crediting his partner, longevity expert and nutritionist Serena Poon, with overhaul of his kitchen and eating habits. Poon eliminated ultra-processed products, hidden sugars, and low-quality items from his pantry, transforming his routine to focus on fresh, high-quality, preferably organic whole foods while minimizing meat and alcohol consumption.
```
The Longevity Enzymatic Engine:
[NAD+ (The Fuel/Petrol)] + [Polyphenols (The Accelerator Pedal)] ➔ Activated Sirtuins & Longevity Pathways
```
The fundamental reason animals and meat lack these longevity benefits stems from biochemistry: animals do not manufacture **polyphenols**. These plant-derived compounds interact directly with the body's three primary metabolic sensing pathways:
1. **Sirtuins:** Regulate cellular identity and epigenetics (activated by polyphenols and fueled by NAD+).
2. **mTOR:** Responds to amino acid levels (downregulated by lower meat intake).
3. **AMPK:** Senses energy status and cellular stress.
Sinclair explains this through his concept of **xenohormesis**—often colloquially described as "eating the rainbow." When plants experience mild environmental stress (such as intense sunlight, drought, or nutrient scarcity), they produce defensive secondary metabolites like resveratrol, fisetin, quercetin, and anthocyanidins (the rich purple pigments in blueberries). When humans consume these stressed plants, the molecules act as "medicine as food," hyper-activating our own ancestral survival networks and mimicking the cellular benefits of fasting and exercise.
- **Ketogenic Diet Reality:** Effective for short-term weight loss and cognitive sharpness, but lacks long-term epidemiological evidence for extending lifespan.
- **Xenohormesis Concept:** Consuming stressed plants transfers their defensive polyphenol compounds to human cells, activating stress-response survival genes.
- **Key Longevity Pathways:** Sirtuins (epigenetic maintenance), mTOR (nutrient/amino acid sensing), and AMPK (cellular energy balance).
- **Polyphenol Examples:** Resveratrol, fisetin, quercetin, and anthocyanidins (found in dark berries like blueberries).
---
[01:30:34](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=5434s) Matcha, Red Wine Reversals, Exogenous Ketones, and Early Statin Intervention
Illustrating xenohormesis in daily life, Sinclair highlights Japanese green tea matcha. Japanese growers intentionally shade tea plants shortly before harvest. Deprived of sunlight, the plants undergo intentional stress, prompting them to synthesize high levels of chlorophyll (yielding a deep green color) and dense concentrations of bioactive polyphenols. Drinking matcha provides a potent dose of these hyper-activating compounds without the harsh metabolic spikes associated with sugary energy drinks.
The discussion shifts to red wine, where Sinclair addresses a major reversal in his scientific stance. In 1996, his early research on resveratrol in red wine triggered a global 30% increase in red wine sales, leading many physicians to recommend a daily glass. However, based on modern large-scale population data—such as UK Biobank studies examining brain MRI scans across thousands of individuals—Sinclair no longer advises drinking red wine daily. The UK Biobank data demonstrates a statistically significant reduction in total brain volume and gray matter even in mild, single-drink-a-day consumers. Today, Sinclair obtains his polyphenols via direct supplementation or whole foods, entirely avoiding alcohol.
Bartlett shares his personal investments in the wellness space, including a UK-based matcha brand (**PerfectTed**, founded by Levi, Teddy, and Marissa) and the exogenous ketone company **Ketone-IQ** (led by CEO Michael Brandt). Sinclair confirms that he personally takes exogenous ketones (such as 1,3-butanediol, which converts to beta-hydroxybutyrate) prior to demanding intellectual tasks like podcast recordings. Drinking exogenous ketones delivers the sharp cognitive clarity and anti-inflammatory fuel of a fasted state directly to the brain without requiring prolonged caloric restriction, while also supporting cardiovascular health.
Concluding with cardiovascular preventative health, Sinclair tackles the debate around "bad" LDL cholesterol. Dismissing doubts regarding the necessity of lowering LDL, he asserts that the scientific consensus across thousands of clinical trial participants is irrefutable: maintaining low LDL cholesterol is essential for cardiovascular longevity. Addressing the myth that lowering blood cholesterol harms brain function, Sinclair notes that the brain synthesizes its own cholesterol locally and does not rely on circulating blood LDL. Revealing his proactive approach, Sinclair discloses that he has been taking a **statin** to aggressively lower his LDL since age 30 due to a family history of elevated cholesterol, arguing that preventative medicine should start decades before visible disease manifests.
- **Matcha Cultivation:** Shading tea leaves prior to harvest induces mild stress, drastically boosting beneficial polyphenol levels.
- **Red Wine Reversal:** Sinclair no longer recommends daily red wine; UK Biobank MRI data links even one drink per day to measurable reductions in brain gray matter volume.
- **Exogenous Ketones:** Ingesting 1,3-butanediol elevates blood ketones, providing brain fuel and mental focus without prior fasting.
- **Early Statin Use:** Sinclair initiated statin therapy at age 30 to keep LDL cholesterol as low as possible, emphasizing early prevention over reactive disease treatment.
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[01:36:19](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=5779s) Fighting Conservative Medicine for Early Intervention
Dr. David Sinclair highlights a major flaw in traditional healthcare, which he describes as "conservative." The current medical system typically refuses to prescribe testing or preventative treatments unless a patient is already sick—a mindset that becomes problematic when trying to stay ahead of age-related decline. Sinclair argues that waiting for symptoms is too late and that individuals must proactively advocate for their own health early in life. He shares that he frequently has to push back against his own Harvard-affiliated physician to secure necessary tests and prescriptions.
```
┌──────────────────────────────┐
│ Traditional Healthcare │
│ (Reacts after disease onset) │
└──────────────┬───────────────┘
│
vs. ▼
│
┌──────────────────────────────┐
│ Preventative Model │
│ (Early testing & statins) │
└──────────────────────────────┘
```
When host Steven Bartlett admits his LDL cholesterol level might not be ideal due to a diet high in bacon, Sinclair explains that cholesterol risk depends heavily on whether an individual's body hyper-absorbs dietary cholesterol. He emphasizes that specific testing can clarify this, helping individuals decide if a targeted dietary shift or early medical intervention is warranted.
* "The old way of doing medicine is if you're not sick, we're not going to give you a medicine... but that has to change."
---
[01:37:13](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=5833s) The 5 Best Foods for Reversing Ageing
Examining a plate prepared with five foods reputed to combat aging, Sinclair breaks down their exact mechanisms and offers practical guidance for including them in a daily routine.
* **Blueberries:** Rich in protective polyphenols, but they also contain natural sugar. Keep portions to a single handful so as not to elevate blood sugar levels, as chronically high blood glucose degrades overall longevity. Unsweetened matcha is a superior alternative for polyphenol intake without the sugar penalty.
* **Avocados:** Packed with polyunsaturated fats and anti-inflammatory compounds. They promote satiety, preventing peckishness and overeating throughout the afternoon.
* **Extra Virgin Olive Oil (EVOO):** Loaded with healthy monounsaturated fats like omega-9, which directly activate sirtuin longevity genes. Cold-pressed EVOO derived from stressed plants contains high concentrations of polyphenols. Epidemiological data consistently links heavy olive oil consumption to lower systemic inflammation.
* **Nuts:** Excellent sources of essential vitamins and minerals. Eating a single Brazil nut daily provides enough **selenium**—a crucial trace element recently shown to cause severe cellular issues if deficient. However, nuts are calorie-dense and should be portioned carefully if weight management is a goal.
* **Brussels Sprouts:** Contain **sulforaphane**, the sulfur-bearing molecule responsible for their sharp smell and bitter taste. Sulforaphane activates **NRF**, a critical cellular stress-response pathway that triggers self-defense mechanisms. To preserve sulforaphane, sprouts should be lightly steamed rather than fried.
---
[01:41:04](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=6064s) "Pulsing" Inputs: Why Constant Supplementation Can Backfire
Addressing the concept of "pulsing," Sinclair explains that the human body thrives on cyclical cycles of stress and recovery rather than an uninterrupted daily stream of compounds. He details two examples where continuous dosing turned out to be counterproductive:
* **Resveratrol:** While daily doses improved health and extended lifespan in obese mice by 15–20%, giving it to normal, healthy mice every single day yielded negligible benefits. Surprisingly, when old mice were given resveratrol **every second day**, their lifespan increased significantly.
* **Metformin & Berberine:** Metformin suppresses mitochondrial energy production to trigger longevity pathways like AMPK. However, daily use can leave individuals feeling weaker, causing weightlifters to perform fewer reps and experience up to a 5% reduction in muscle growth.
To avoid blunting exercise gains while retaining longevity benefits, Sinclair advocates cycling metformin or its natural counterpart, **berberine**, on alternate days and avoiding them in the hours surrounding a workout.
* "Maybe giving them a foreign substance every day is not good. Maybe there's some side effect that's counteracting the benefit."
---
[01:45:17](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=6317s) Telomeres vs. Epigenetics, and the Priority List for Longevity
Discussing a CDC-funded study mentioned on page 102 of his book *Lifespan*, Sinclair confirms that adults who engage in high-level aerobic exercise—such as 30 minutes of jogging five days a week—possess telomeres that appear **10 years younger** than those of sedentary individuals. While association studies must be interpreted cautiously due to confounding factors like diet or sleep, controlled trials reinforce that exercise directly protects chromosome ends.
Sinclair notes that while telomere length was previously the primary biomarker for biological age, the medical community now relies on **epigenetic DNA methylation clocks** for far greater precision.
When forced to rank interventions by impact and accessibility:
1. **Skipping Meals (Intermittent Fasting):** The absolute single highest-impact habit an individual can adopt.
2. **Aerobic Exercise:** Engaging in cardiovascular activity that forces heavy panting for at least 5 minutes, three times a week. Weightlifting is vital for hormone regulation, bone density, and preventing falls, but high-intensity aerobic exercise drives distinct cellular longevity benefits.
* "If you're not panting and you're just lifting weights, that's not going to have the kind of benefit."
---
[01:46:45](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=6405s) The Science of Saunas, Cold Plunges, and Red Light Therapy
Evaluating popular thermal and light therapies through a scientific lens, Sinclair separates solid clinical evidence from emerging trends:
```
┌──────────────────┬─────────────────────────────────────────────────────────┐
│ Practice │ Current Evidence & Mechanism │
├──────────────────┼─────────────────────────────────────────────────────────┤
│ Sauna │ Strong data (Finnish studies); activates Heat Shock │
│ │ Proteins (HSPs) & lowers cardiovascular mortality. │
├──────────────────┼─────────────────────────────────────────────────────────┤
│ Cold Plunge │ Limited long-term mortality data; boosts mental clarity │
│ │ and aids post-workout muscle recovery. │
├──────────────────┼─────────────────────────────────────────────────────────┤
│ Red Light │ Validated mechanism; specific wavelengths stimulate │
│ Therapy │ and rejuvenate mitochondrial powerhouses. │
└──────────────────┴─────────────────────────────────────────────────────────┘
```
* **Saunas:** Strongly supported by extensive data, particularly long-term studies on Finnish men. Regular sauna use correlates with significantly lower cardiovascular disease rates and reduced all-cause mortality. The heat and humidity induce **Heat Shock Proteins (HSPs)** that repair damaged intracellular structures. High-heat saunas provide a stronger biological stimulus than standard steam rooms.
* **Cold Plunges:** Lacking extensive long-term mortality data, but proven to assist muscle recovery and significantly elevate mood and mental clarity through hormetic stress.
* **Red Light Therapy:** Initial skepticism is misplaced—it is "not BS." Targeted red light wavelengths penetrate cells to directly stimulate and rejuvenate damaged mitochondria. Sinclair reveals he personally uses a specialized red light cap on his head to preserve his hair follicle health and maintain his hairline.
* "It sounds like BS, right? Oh, you shine light on your skin and it gets better... But I think that there's good evidence now that it's not BS."
[01:50:57](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=6657s) Dr. Sinclair's Daily Supplement Protocol
When asked about his personal supplement regimen, Dr. David Sinclair describes carrying a small travel case packed with his daily routine. While he keeps certain cutting-edge, experimental compounds private to prevent internet frenzy and avoid advocating for unproven substances, he willingly details the core supplements he considers safe and effective. His daily stack includes NMN, resveratrol, berberine or metformin, and spermidine.
Addressing the humorous and provocative origin of spermidine, Sinclair clarifies that while it was originally discovered and crystallized from human semen by early microscopist Antonie van Leeuwenhoek, modern dietary spermidine is extracted from wheat germ and plant sources. He prioritizes spermidine because it extends lifespan across every tested animal model, from tiny worms to mice, by stimulating autophagy (cellular recycling) and preserving epigenetic information to slow down the "scratching of the record." Additionally, Sinclair highlights his daily intake of about 5 grams of glycine—a simple amino acid he researched extensively during his Ph.D. Glycine regulates one-carbon metabolism and DNA methylation, which he believes helps maintain cellular identity without any noticeable downside.
- **Spermidine:** Triggers autophagy, mimics fasting benefits, and slows epigenetic degradation; sourced from wheat germ.
- **Glycine:** 5g daily; regulates one-carbon metabolism and DNA methylation, supporting cellular identity.
- **Niacin (Vitamin B3):** Taken in 0.5g doses (building up slowly) to reduce Lipoprotein(a) [Lp(a)] levels; can cause skin flushing and tingling similar to menopausal hot flashes unless managed carefully or taken with aspirin.
---
[01:57:48](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=7068s) Managing Hair Loss and Male Hormones
Addressing common male aging concerns like hair loss and graying, Sinclair shares his personal family history: his father went completely bald before age 30 and almost fully gray by 40. Expecting the same fate, Sinclair took proactive steps early. He uses a red light cap for 6 minutes daily when at home—a method proven to slow down hair thinning, though he cautions that it cannot regenerate hair once follicles are lost.
To combat hair loss systemically, Sinclair uses a hormone mimetic to block dihydrotestosterone (DHT), the potent androgen derived from testosterone that drives male pattern baldness. He explicitly notes that he does not take exogenous testosterone replacement therapy (TRT), warning that improper TRT can elevate DHT and accelerate hair loss. Instead, he advocates boosting testosterone naturally by building major muscle groups through heavy resistance training (specifically working the legs and back). For men with testosterone levels below 400 ng/dL, he strongly recommends hitting the gym before considering medical interventions. While acknowledging TRT has clinical utility for health and carries low cancer risk when supervised, Sinclair emphasizes that exogenous testosterone does not promote longevity.
- **Red Light Hair Cap:** Used 6 minutes daily to slow hair loss; effective as a preventative measure rather than a restorative cure.
- **DHT Blockers:** Utilized to prevent androgenic hair loss without taking direct testosterone replacement.
- **Natural Testosterone Elevation:** Heavy strength training focusing on large muscle groups (legs, back) recommended for men with levels under 400 ng/dL.
---
[02:00:02](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=7202s) The Future of Regenerative Medicine and Gene Therapy
Looking beyond current scientific facts, Sinclair shares his grand vision for the future of medicine, comparing the coming transformations to the dramatic progress of the last two centuries. Just as society today looks back horrified at an era when a simple infected splinter or childbirth could be fatal, future generations will look back at modern medicine with disbelief that people routinely suffered permanent blindness or paralysis without a solution.
Sinclair highlights his lab's ongoing work reversing blindness in animal models using OSK (Oct4, Sox2, Klf4) gene therapy. Totally blind monkeys have had their vision restored within six weeks, demonstrating that mammalian tissue age can be safely reset. Rather than just slowing disease, this approach targets the underlying age of the tissue.
- **Paradigm Shift:** Predicts future medical interventions will make current treatments for blindness, spinal cord injuries, and organ failure seem primitive.
- **Animal Milestones:** Complete vision restoration achieved in totally blind monkeys within 6 weeks using cellular reprogramming.
---
[02:03:01](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=7381s) Inside the First Human Clinical Trials for Age Reversal
Sinclair breaks down the mechanics of the upcoming human clinical trials aimed at reversing blindness caused by glaucoma and non-arteritic anterior ischemic optic neuropathy (NAION)—a stroke in the eye whose incidence has risen alongside the widespread use of GLP-1 weight loss medications like Ozempic. The treatment utilizes an adeno-associated virus vector (AAV2) engineered as a microscopic "delivery vehicle" carrying three Yamanaka reprogramming genes. Manufactured in Europe at a cost of roughly $10 million for the trial batch, these non-infectious viral capsids are injected directly into the eye via a brief procedure.
The outer proteins of the AAV2 act as a molecular "zip code," targeting only the retinal ganglion cells at the back of the eye. Once inside, the vector deposits a permanent loop of DNA. Crucially, these reprogramming genes remain completely dormant until activated by an external switch: the oral antibiotic doxycycline. When patients take doxycycline for an 8-week course, the synthetic promoter triggers the expression of the three genes, resetting the biological age of the retinal cells. Because the endpoint is binary—patients either regain vision or they do not—results from the first human subjects will be evident within weeks of treatment.
- **Target Diseases:** Glaucoma and NAION (eye stroke affecting ~30,000 Americans annually).
- **Delivery System:** AAV2 viral capsid delivering three reprogramming genes directly to retinal neurons via a single intravitreal injection.
- **Doxycycline Switch:** Oral administration of doxycycline acts as an on/off switch to activate age reversal genes for a controlled 8-week period.
- **Commercialization:** Developed by Life Biosciences, with long-term goals of expanding from the eye to the liver, lungs, skin, and eventually small-molecule oral pills using AI drug discovery.
Here is a detailed, faithful walkthrough of the provided transcript section:
[02:09:10](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=7750s) Democratizing Age-Reversal: From $100,000 Treatments to a $100 Pill
Dr. David Sinclair reveals that his lab is right in the middle of screening approximately 8 billion candidate molecules using artificial intelligence, followed by bench lab testing to see which ones prove effective. While testing these treatments in human clinical trials remains several years away, his team expects to know within a year or two whether they are on the right track by administering the top candidates to mice. If the mice grow biologically younger and live longer, it will mark a monumental breakthrough.
The ultimate goal for Dr. Sinclair is not just proving age reversal in a lab, but developing an affordable, accessible pill. Current gene therapies and advanced clinical trials are extraordinarily expensive, costing upwards of $100,000 per treatment due to multi-million-dollar trial budgets. While that cost may be justified for curing condition-specific diseases like blindness, it is far out of reach for average global populations. Dr. Sinclair emphasizes his mission to democratize longevity technology—striving to reduce the cost from $100,000 down to $100 so that anyone, whether in a major Western city or in Kenya, can access these life-extending medicines.
* Dr. Sinclair's lab screened **~8 billion candidates** using AI to identify potential age-reversal molecules.
* Mouse trials over the next **1 to 2 years** will validate whether these AI-discovered candidates extend lifespan and restore youth.
* Human trials currently cost upwards of **$10 million** to execute, driving end-treatment prices over **$100,000**.
* Dr. Sinclair's primary personal mission is lowering the price point down to **$100 per treatment** to democratize global access.
---
[02:10:11](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=7811s) Quantum Physics, Consciousness, and the Simulation Hypothesis
Addressing the broader philosophical pushback against longevity science, Dr. Sinclair counters the religious argument against "playing God" by noting that humanity has manipulated its environment, biology, and medicine for thousands of years. Turning to his personal spiritual beliefs, he explains that studying quantum physics leads him to believe reality is far stranger than it appears. Citing quantum mechanics, quantum entanglement, and simulation theory, he notes that solid objects—such as the desk in the studio—do not exist as singular static entities in the underlying physics, but rather as infinite probabilistic variations.
The conversation turns to the fundamental nature of reality and the double-slit experiment, where firing particles like electrons through two slits creates a simple two-stripe pattern when actively observed, but produces a multi-striped wave interference pattern when unobserved. Dr. Sinclair explains that the mere act of conscious observation or measurement collapses particle possibilities and Alters physical reality. When asked if he believes we live in a simulation, Dr. Sinclair estimates there is a **greater than 50% chance** that our universe is simulated, arguing that fundamental physics demonstrates reality does not exist in the common-sense way human beings perceive it.
* The **double-slit experiment** demonstrates that subatomic particles switch between wave-like interference patterns and discrete particle paths based on whether they are observed.
* Dr. Sinclair places the probability that our universe is a computer simulation at **greater than 50%**.
* He posits that consciousness creates and shapes reality, making the conscious interpretation of particles fundamental to how physical matter behaves.
---
[02:18:20](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=8300s) The Purpose of Consciousness, Gendered Awareness, and AI Evolution
When exploring the existential purpose of life across the universe, Dr. Sinclair argues that the primary "goal" of the physical universe is to foster consciousness through biological evolution. While mathematical probabilities make it statistical certainty that extraterrestrial life exists across trillions of habitable planets, he views consciousness as the single most extraordinary and valuable outcome of cosmic evolution. He compares his views to Elon Musk's perspective: despite human flaws and cruelty, preserving consciousness is of paramount importance.
Dr. Sinclair outlines hierarchical "levels" of consciousness, ranging from partial awareness in animals like dogs (who possess empathy and predictive capabilities but lack deep self-reflection) to human self-awareness. In a lighthearted yet earnest exchange, Dr. Sinclair mentions his partner, Serina Poon, and shares his belief that women generally operate at higher levels of emotional intelligence (EQ) and perceptual consciousness than men—a statement he humorously notes previously earned him aggressive hate mail and death threats. Looking ahead, he predicts that Artificial Intelligence will eventually achieve consciousness and evolve billions of times faster than biological organisms, surpassing human awareness.
* Dr. Sinclair asserts that extraterrestrial life is mathematically inevitable given the **trillions of planets** in the universe.
* He defines human self-awareness as a threshold crossed roughly **1,000,000 years ago**.
* He predicts Artificial Intelligence will naturally achieve conscious awareness and evolve **billions of times faster** than biological evolution.
* Dr. Sinclair expresses little fear of conscious AI itself, believing advanced synthetic minds will naturally develop empathy and kindness.
---
[02:23:03](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=8583s) The Real Risk of AI: Robotic Conscription and Bad Actors
Despite his optimism regarding conscious AI, Dr. Sinclair expresses severe concern about how malicious human actors could misuse advanced robotics. The true danger is not a rogue superintelligence turning on humanity, but rather autocratic individuals or bad actors leveraging AI systems to control physical armies. He describes a near-future scenario where a single person could control millions of android robots deployed on ships to invade countries or forcefully reprogram commercial home helper robots into military conscripts.
Because future humanoid robots will be vastly stronger, faster, and physically more capable than human beings, weaponizing domestic and industrial robotics presents an unprecedented threat. Dr. Sinclair warns that society must establish strict safety guardrails and legal frameworks to prevent bad actors from commanding mechanical armies.
* The primary existential threat from AI is **human misuse**, rather than autonomous AI rebellion.
* Future risks include the rapid military reprograming and **conscription of millions of household android robots**.
* Robotic systems will possess superior physical strength and processing speed compared to human soldiers, making autocratic misuse devastating.
---
[02:24:32](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=8672s) The Return of the *Lifespan* Podcast
Dr. Sinclair announces the imminent relaunch of his hit health and science podcast, *Lifespan*. After taking a temporary hiatus to focus heavily on his biotechnology ventures and cellular drug development, he decided to return to broadcasting due to overwhelming public demand and the influx of new longevity research that requires expert scientific translation.
He explains that the health landscape is currently flooded with speculation, unverified claims, and rapid scientific updates. The goal of the revived *Lifespan* podcast is to serve as an authoritative filter, translating cutting-edge scientific discoveries and clinical trial data into actionable, easy-to-understand insights for listeners around the world who want to extend their healthy lifespan.
* The *Lifespan* podcast originally reached the **#1 spot in the Health category** upon its initial release.
* Dr. Sinclair paused media production to focus directly on **biotech drug development** and longevity research trials.
* The relaunch aims to provide a scientific filter to help the public separate legitimate longevity breakthroughs from unproven online speculation.
[02:25:27](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=8727s) The "Three Cs" and Building the World’s Largest Longevity Community
Dr. David Sinclair reflects on the depth of their conversation, noting that while they covered a immense amount of ground, there is still much more to dig into regarding biohacking, supplements, and exercise routines. To expand this knowledge-sharing beyond one-off interviews, Dr. Sinclair shares an unannounced venture with host Stephen Bartlett: his goal to build the world's largest online longevity community at lifespan.com. The initiative aims to allow members to learn collectively rather than relying solely on individual experts.
To explain the framework of this platform, Dr. Sinclair outlines his core philosophy, which he calls the "Three Cs":
* **Credibility:** The foundational scientific rigor and expertise he brings as a Harvard researcher.
* **Content:** Educational material disseminated through his podcast, written works, and research updates.
* **Community:** A global network of millions of individuals sharing personal experiences, insights, and data to accelerate scientific progress.
Crucially, Dr. Sinclair emphasizes that the majority of the profits generated from community memberships will directly fund scientific research and clinical trials aimed at reversing human aging.
---
[02:26:26](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=8786s) The Purpose of Life and the Toll of Scientific Trailblazing
Following podcast tradition, Stephen presents Dr. Sinclair with a question left behind by the previous guest: *"What do you believe is the purpose of life?"* Acknowledging that he has addressed similar philosophical queries in different contexts, Dr. Sinclair pauses before offering a deeply personal perspective. He states that the purpose of life is to use the specific skills you have been given each day to do your best and leave the world a better place for future generations—a belief he strives to embody daily.
Stephen expresses gratitude for Dr. Sinclair’s pioneering efforts in longevity science, acknowledging the steep personal and professional cost of being a trailblazer. He notes that scientific discovery inherently requires enduring constant failure in experiments and investments of time, energy, and money before reaching a breakthrough. Stephen commends Dr. Sinclair for translating complex, inaccessible scientific papers into clear, actionable advice for the general public, particularly through his *New York Times* bestselling book, *Lifespan: Why We Age—and Why We Don't Have To*.
* **Where to Follow:** Viewers are encouraged to check out Dr. Sinclair’s website (lifespan.com), his active updates on X (formerly Twitter), and his re-launched podcast linked in the show notes.
* **Closing Out:** The episode concludes with Stephen thanking Dr. Sinclair for his contributions to global health literacy, followed by the channel's standard outro recommending personalized AI-driven video suggestions for the audience.
## Notable quotes
> [01:18:40](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=4720s) When you give a human NMN by swallowing it, a gram of it, you typically double the amount of NAD in your body. — Dr. David Sinclair
> [01:36:19](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=5779s) The old way of doing medicine is if you're not sick, we're not going to give you a medicine... but that has to change. — Dr. David Sinclair
> [01:41:04](https://www.youtube.com/watch?v=DnvWAP99r3Y&t=6064s) Maybe giving them a foreign substance every day is not good. Maybe there's some side effect that's counteracting the benefit. — Dr. David Sinclair
## Mentioned
Dr. David Sinclair, Steven Bartlett, Warren Buffett, The Sinclair Lab, Nallath, Yamanaka OSK genes, BonCharge, Shopify, Lenny Guarente, Saccharomyces cerevisiae, Serena Poon, PerfectTed, Levi, Teddy, Marissa, Ketone-IQ, Michael Brandt, UK Biobank, Harvard Medical School, MIT, Elon Musk, Lifespan, Lifespan.com, Harvard University, The Diary Of A CEO
Harvard longevity researcher Dr. David Sinclair argues that biological aging is a treatable condition driven by epigenetic information loss, presenting laboratory evidence that cellular reprogramming can reverse functional decline and treat age-related diseases.
The Information Theory of Aging and Epigenetic Drift (20:43)
Sinclair posits the Information Theory of Aging, suggesting that the primary driver of biological senescence is not damaged DNA hardware, but the erosion of epigenetic software that regulates gene expression. Each human cell houses roughly 6 feet of DNA containing around 20,000 genes, of which approximately 15,000 are actively expressed to define specific cellular identities. Sinclair likens DNA to the grooves of a vinyl record and the epigenome to the needle reading the music; cellular damage acts like surface scratches that cause errors in readout.
To test this mechanism, Sinclair's laboratory engineered 'ICE' (Inducible Changes to the Epigenome) mice using a slime mold enzyme that cleanly severed DNA without inducing cancer or mutations. When cells experience chromosome breaks—estimated at roughly 20 trillion repair events across the human body daily—repair enzymes such as sirtuins temporarily abandon their primary posts regulating cellular identity to fix the lesions. Because these proteins do not always return precisely to their initial locations, repeated environmental stressors like smoking, excessive alcohol, or radiation cause cells to lose their identity over time, accounting for an estimated 80% to 90% of aging variance.
Cellular Reprogramming and Preclinical Reversal Milestones (9:12)
Rather than managing chronic illnesses like cancer, dementia, and cardiovascular disease independently, Sinclair argues that addressing biological age can resolve underlying pathologies simultaneously. In his laboratory models, activating three Yamanaka factors (Oct4, Sox2, and Klf4, or OSK) delivers a biological reset without dedifferentiating cells into pluripotency. This genetic intervention restored vision in non-human primates and completely blind monkeys within six weeks and doubled the remaining lifespan of frail elderly mice when administered intravenously by an independent laboratory.
Building on animal successes, Sinclair revealed that the first human clinical trials using localized OSK gene therapy are scheduled to target the human retina and optic nerve. The eye was selected specifically as an anatomically isolated compartment to safeguard against systemic adverse effects if unintended vectors spread. While current gene therapy protocols remain costly—running upwards of $100,000 per patient—Sinclair’s team is screening approximately 8 billion candidate molecules using artificial intelligence to develop an accessible oral compound capable of triggering the same cellular repair pathways.
Actionable Interventions, Fasting, and Longevity Pathways (36:06)
Sinclair identifies lifestyle modifications as the most immediate defense against epigenetic decay, pointing to longitudinal research showing that five core habits—avoiding smoking, restricting alcohol, consuming a whole-food diet, exercising regularly, and maintaining close social bonds—can extend lifespan by up to 14 years. Among individual habits, Sinclair prioritizes intermittent fasting as the single highest-impact behavioral intervention, recommending a gradual progression toward a 14- to 16-hour daily fasting window to deplete systemic glucose, elevate NAD+ coenzyme levels, and activate protective sirtuins.
In tandem with fasting, Sinclair emphasizes high-intensity aerobic exercise that produces heavy panting for at least 5 minutes three times per week, citing research linking regular cardiovascular activity to biological age markers appearing 10 years younger than sedentary baselines. Nutrition also plays a xenohormetic role; Sinclair recommends polyphenol-dense, mildly stressed plant products such as unsweetened matcha, extra virgin olive oil, and brassica vegetables. Conversely, he reversed his previous endorsement of daily red wine consumption, citing modern UK Biobank MRI imaging linking even single daily drinks to reductions in gray matter volume.
Supplementation Strategies and the Pulsing Principle (101:04)
Because cellular NAD+ drops by roughly 50% by age 50, Sinclair's personal stack focuses on metabolic precursors and epigenetic catalysts. His disclosed daily protocol includes 1 gram of NMN (which clinical testing shows doubles circulating NAD+ levels), resveratrol, glycine, and spermidine to enhance autophagy. He also uses daily low-level red light therapy and a DHT blocker to mitigate hereditary hair thinning without relying on exogenous testosterone replacement therapy, which he notes does not extend lifespan.
Sinclair emphasizes 'pulsing' longevity molecules rather than administering uninterrupted daily doses. Continuous exposure can blunt biological adaptations; for example, daily metformin use suppresses mitochondrial respiration via AMPK activation but can reduce muscle hypertrophy during resistance training by roughly 5%. Similarly, Sinclair notes that resveratrol extended the lifespan of elderly mice only when administered every other day, indicating that cells require cyclical periods of stress followed by recovery to consolidate molecular repairs.
While animal models consistently demonstrate functional rejuvenation, translating viral gene therapies and chemical cocktails into affordable, scalable human medicines remains an ongoing endeavor. Critical milestones hinge on upcoming retinal trials and mouse validation of AI-screened candidate molecules, alongside regulatory hurdles that treat aging as a natural inevitability rather than a direct indication for medical intervention.
[78:40] Dr. David Sinclair: When you give a human NMN by swallowing it, a gram of it, you typically double the amount of NAD in your body.
[96:19] Dr. David Sinclair: The old way of doing medicine is if you're not sick, we're not going to give you a medicine... but that has to change.
[101:04] Dr. David Sinclair: Maybe giving them a foreign substance every day is not good. Maybe there's some side effect that's counteracting the benefit.
Original transcript
[0:00] This is very uh
[0:01] It's bad, right? It's hard, yeah.
[0:03] >> That's what it's like to be old. And for
[0:05] far too long, we've ignored [music] it
[0:07] or accepted it as natural. And I reject
[0:09] the idea that aging, just because it's
[0:11] natural, is acceptable. Dying at 80 is
[0:14] not inevitable. Absolutely, that can be
[0:16] changed. So, if you're skeptical, I am a
[0:18] Harvard professor who has been studying
[0:20] aging, longevity, and age reversal for
[0:22] 30 years. And I've seen enough from my
[0:24] lab showing that we can literally now
[0:26] reverse the aging process. And it's not
[0:28] a question of if, it's [music] a
[0:28] question of when this is going to And
[0:30] everyone should stick around cuz I'm
[0:31] going to tell you some of the major
[0:32] things that people should be doing. They
[0:34] can lengthen your life by a decade. Hey,
[0:36] you're not taking that off, Steven.
[0:38] You've got 10 minutes of that. So, you
[0:40] can accelerate aging by smoking, getting
[0:41] an X-ray, ultra-processed foods,
[0:43] excessive drinking, flying a lot. I fly
[0:45] all the time. That's probably
[0:46] accelerating your aging process.
[0:50] Even going to a rock concert and
[0:51] blasting your eardrums because your ear
[0:54] hair cells are getting [music] older
[0:55] faster. And so, I look at the body like
[0:57] it's a computer and we can reinstall the
[0:59] software. And what's [music] interesting
[1:01] is when you reverse aging, diseases like
[1:03] Alzheimer's, cancer, heart disease go
[1:05] away [music] or are cured. Because
[1:07] what's driving a lot of those diseases
[1:09] is aging. And so, my lab is like Willy
[1:11] Wonka's chocolate factory. They are
[1:13] making discoveries that blow me away
[1:15] every week. And I think we're at a
[1:16] turning point in human history [music]
[1:18] where you're probably going to live into
[1:19] the 22nd century if you do all the right
[1:21] things. And we're going to dig into all
[1:22] of those in great detail. But what are
[1:24] the unintended consequences of such a
[1:26] world where we all live longer? And
[1:28] also, do you think it's going to be
[1:29] possible in the next 50 years for us to
[1:31] live forever? And then, what's the best
[1:33] uh treatment you've discovered for hair
[1:34] loss?
[1:35] >> This is why I love your podcast, Steven.
[1:36] You ask the right questions. So, first
[1:38] of
[1:39] This is super interesting to me. My team
[1:41] gave me this report to show me how many
[1:42] of you that watch this show subscribe.
[1:44] And some of you have told us, according
[1:45] to this, that you have unsubscribed from
[1:47] the channel randomly. So, favor to ask
[1:49] all of you, please could you check right
[1:51] now if you've hit the subscribe button.
[1:52] If you are a regular viewer of this show
[1:54] and you like what we do here. We're
[1:55] approaching quite a significant landmark
[1:57] on this show in terms of a subscriber
[1:58] number. So, if there was one simple,
[2:01] free thing that you could do to help us,
[2:03] my team, everyone here, to keep this
[2:04] show free, to keep it improving year
[2:07] over year and week over week, it is just
[2:08] to hit that subscribe button and to
[2:10] double-check if you've hit it. Only
[2:11] thing I'll ever ask of you.
[2:12] Do we have a deal?
[2:14] If you do it, I'll tell you what I'll
[2:14] do. I'll make sure
[2:16] every single week, every single month,
[2:18] we fight harder and harder and harder
[2:19] and harder to bring you the guests and
[2:20] conversations that you want to hear. I
[2:22] stayed true to that promise since the
[2:23] very beginning of the Diary of a CEO,
[2:25] and I will not let you down. Please help
[2:27] us. Really appreciate it. Let's get on
[2:29] with the show.
[2:31] >> [music]
[2:34] >> Dr. David Sinclair. I have waited many
[2:37] years to speak to you. And I've been so
[2:40] keen to speak to you for so many years
[2:41] because
[2:42] so much of the research and the
[2:45] information I've consumed on the
[2:46] subjects we're going to talk about today
[2:48] comes from you, directly from research
[2:50] you've done, and from theories and ideas
[2:52] and hypotheses that you formed. I think
[2:55] the place that this conversation should
[2:57] start is
[2:59] is probably with this picture because it
[3:01] appears to be incredibly formative
[3:04] in your journey.
[3:06] Oh, yes.
[3:07] That is an important picture, true.
[3:10] This is a picture
[3:12] of my grandmother and me when I was in
[3:14] my early 20s, I'm now 56, if you're
[3:17] wondering.
[3:18] And uh my grandmother has played a major
[3:20] role in my life. Uh I'm going to have to
[3:22] be careful not to get too emotional
[3:24] because uh she's now passed passed away,
[3:26] but she's inspired
[3:28] me to
[3:30] do the best I can to leave the world a
[3:31] better place than uh I found it.
[3:34] And there's this particular book here
[3:36] called Now We Are Six.
[3:39] It is Anyone who's read my book uh
[3:40] Lifespan knows that this book is very
[3:44] important to me. And I didn't realize
[3:45] it, of course, when I was a kid that
[3:47] this was going to change my whole life.
[3:51] And there's a poem at the back there
[3:53] that my grandmother, Vera, used to read
[3:55] me
[3:56] when I was six.
[3:57] And it goes like this. When I was one, I
[4:01] had just begun. When I was two, I was
[4:04] nearly new. When I was three, I was
[4:06] hardly me.
[4:08] When I was four, I was not much more.
[4:10] When I was five, I was just alive.
[4:13] But now, I am six.
[4:15] I'm as clever as clever. So, I think
[4:17] I'll be six now forever and ever.
[4:22] I'm getting chills reading this again
[4:25] and hearing this poem again because
[4:27] the impact on me was the following, that
[4:29] subconsciously, my grandmother was
[4:31] saying, "You you don't want to grow up.
[4:33] Adults can be evil." She grew up after
[4:35] World War II.
[4:37] There was horrendous uh
[4:38] impact on her and her family in Hungary.
[4:42] And she thought that a child is innocent
[4:45] and people shouldn't grow up. But what
[4:48] actually happened was I realized
[4:50] why do people grow old?
[4:52] That's a terrible thing to happen. And
[4:54] so, I've spent my life
[4:56] trying to figure out why do we get old?
[4:57] Why do we grow up? Why do we get frail?
[5:00] Because I also think that if we can
[5:02] solve that, understand it,
[5:04] slow it, even reverse it now,
[5:06] we we'll have the biggest impact on
[5:08] human health in history.
[5:10] Am I right in thinking your grandmother
[5:11] told you at that young age that she was
[5:14] going to die, that you were going to
[5:15] die, that your parents were going to
[5:16] die? Yes, uh she did tell me that. I
[5:20] remember it very clearly, actually. I
[5:21] was on the floor and she was crouching
[5:24] down and I said, "Vera." I didn't call
[5:26] her
[5:26] grandma. She didn't want to be called
[5:28] grandma. She wanted to be young like a
[5:29] kid to me. I said, "Vera, will will you
[5:31] always be here to protect me? Will you
[5:33] always be around?" She said, "No, I'm
[5:34] going to die."
[5:36] I'm like, "What do you mean?" She goes,
[5:37] "Every everything dies. I'm going to be
[5:39] gone.
[5:40] Your parents will be gone. Your pet cat
[5:42] will be dead pretty soon. And you
[5:44] yourself will be dead one day."
[5:46] At age, you know, four or five, that's
[5:49] that's that's heart-wrenching, right?
[5:51] We've all gone through this realization
[5:52] around that age that the world that we
[5:56] believe in and see will one day all be
[5:59] gone. That moment, I remember it so
[6:01] clearly because I thought, "That's not
[6:03] fair. Why would any species be made or
[6:07] created that knew that fact? That's
[6:10] cruel. It's better to either not know
[6:13] or to not exist. But to know that that's
[6:15] what's going to happen
[6:16] is really cruel. And so, I I I vowed
[6:20] actually legitimately around the age of
[6:22] 18
[6:24] to get a PhD, to go to the United
[6:26] States,
[6:27] and develop a research lab to try and
[6:30] do something about it. The preservation
[6:32] of health and life is the most important
[6:35] thing that we can do as human beings.
[6:37] We do it with some drugs to treat that
[6:39] disease and the other disease, cancer,
[6:41] heart disease, Alzheimer's.
[6:43] But what's underlying that, what's
[6:45] really causing about 150 to 200,000
[6:47] people every day to die,
[6:50] is the underlying universal process we
[6:52] call aging.
[6:53] And for far too long, we've ignored it
[6:56] or accepted it as natural, therefore
[6:58] acceptable.
[6:59] And I I I fundamentally reject the idea
[7:02] that aging, just because it's natural,
[7:05] is acceptable. There will be a day when
[7:07] we look back at today and think how
[7:09] medieval were our were our medicines.
[7:11] And how sad it was that we accepted that
[7:14] we became frail before 100.
[7:17] If someone has just clicked on this
[7:19] conversation now, and they deep in their
[7:21] core
[7:23] believe that they're probably going to
[7:24] live to 80 years old, and that we all
[7:26] are, and that we're never going to be
[7:27] able to do anything about it cuz that's
[7:28] just the way that it is. People get old
[7:30] and then they die. And aging is a fact
[7:32] of life, as the phrase goes. And you
[7:34] just have to accept it.
[7:37] If that's their sort of core belief,
[7:39] what is the what is the most persuasive
[7:41] sort of top-line argument to that person
[7:43] to convince them that in the next 2
[7:45] hours, when we have this conversation,
[7:48] we will do a job of both reversing that
[7:51] belief, really challenging it in some
[7:52] way, and then also presenting them with
[7:54] a set of possible solutions. Yeah. All
[7:56] right. So, first of all, who am I? Um
[7:59] I'm a Harvard professor. I've been
[8:00] studying aging, longevity, and age
[8:02] reversal for 30 years.
[8:05] The technology now that we have in my
[8:06] lab that is used every day by my
[8:08] students literally reverses the age of
[8:11] tissues in animals, in human tissue that
[8:14] we grow in the lab. And the first human
[8:16] trials to test this
[8:18] are going to be performed
[8:20] in about a month from now.
[8:22] And if it works, it'll transform human
[8:24] history. It means that we're on a path
[8:26] to finally being able to reset the age
[8:28] of the human body, not by a year,
[8:31] not by 10 years, but even more than
[8:32] that.
[8:33] And what happens when you do that? What
[8:35] we're finding in animals that includes
[8:37] primates, is that we can cure things
[8:40] that have previously
[8:41] been impossible, including blindness, by
[8:43] the way.
[8:44] And so, if you're listening and you're
[8:46] skeptical,
[8:47] I'm not some hack. I am a Harvard
[8:50] professor who is telling the world and
[8:53] has written a book about it and every
[8:55] day spends my life researching with a
[8:56] team of
[8:57] the best scientists I can gather around
[8:59] the world
[9:00] showing that we can literally now
[9:02] reverse the aging process and reset how
[9:04] old the body is. In animals, yes,
[9:07] but potentially this year showing it can
[9:10] work in the human body as well. So,
[9:13] you're doing the first ever trial of
[9:15] this type in humans to reverse
[9:18] aging
[9:20] next month. Yes. So, we've submitted a
[9:23] form to the
[9:25] you know, the FDA in the US to get
[9:27] approval to treat blindness, couple of
[9:29] types of blindness in people,
[9:32] um as early, if all goes well, as next
[9:34] month.
[9:35] And what what exactly is happening
[9:37] there? Cuz cuz there's many ways one
[9:38] might fix
[9:40] blindness. Mhm. You know?
[9:43] What is it you're doing to the eyeball
[9:46] that is a precursor of our potential
[9:49] ability to reverse aging generally?
[9:51] Yeah, well, we chose the eye
[9:53] not because it was going to work well,
[9:55] but because it's a it's a nice system to
[9:57] study age reversal. The eye is an
[10:00] enclosed space and so it's much safer
[10:02] than trying to initially reverse the age
[10:04] of the whole body. Now, in mice we
[10:05] reverse the age of the whole body
[10:07] and the effect is longevity,
[10:09] rejuvenation, the skin gets better.
[10:11] All parts of the animal get get
[10:13] healthier and younger.
[10:14] But in humans you you don't want to go
[10:16] straight to rejuvenation uh because in
[10:18] case something goes wrong, it could set
[10:20] us way back.
[10:22] And we have to make sure we don't have
[10:23] any safety mishaps. So, we're being a
[10:26] little cautious in humans. In mice it's
[10:28] a little different.
[10:30] So, in the human eye Just for those that
[10:32] are watching the video, there is a an
[10:33] eye on the table. Well, a plastic eye.
[10:35] It's a it's a larger version of an eye,
[10:37] but yes, uh Steven's right.
[10:39] What we're doing we're going to look at
[10:40] the back of the eye, which is your
[10:41] retina.
[10:43] And that's where the light hits.
[10:45] And at that point there are a lot of
[10:47] nerves that coalesce into the optic
[10:50] nerve that runs to the brain
[10:53] by just a few millimeters. So, the brain
[10:55] is here. The eye is actually part of the
[10:57] brain.
[10:58] A lot of people don't know that. You can
[10:59] touch your brain if you touch your eye.
[11:01] Um so, the optic nerve gets old and what
[11:03] we've discovered if it gets damaged or
[11:04] gets old, it's not working. But the
[11:07] nerves for most the most part, if you're
[11:09] old, are still there.
[11:10] They just forget how to work. And that's
[11:13] aging. And later everyone should stick
[11:16] around cuz I'm going to tell you
[11:18] why it is we get old and how it is we
[11:20] reverse it. But but for this this model
[11:22] what we're doing is we're introducing a
[11:25] set of three genes into
[11:28] this optic nerve at the back of the eye
[11:31] and turning them on for 6 to 8 weeks.
[11:36] And those three genes are what we now
[11:38] know reset safely
[11:40] apparently safely
[11:42] reset the age of cells including nerves
[11:46] by about 75% and then stop. They don't
[11:48] go more than that, which is good. We
[11:50] don't want to go back to zero.
[11:52] I don't think anyone wants to go back to
[11:54] high school.
[11:55] But this is the way it works. And we
[11:57] chose the optic nerve because it's a
[11:59] safe and close system, not because it
[12:00] should work better in optic nerves. In
[12:02] fact, we've now done it in mice in my
[12:04] lab for the brain. Uh we're doing
[12:07] hearing. We've done skin. Uh we did
[12:09] multiple sclerosis.
[12:11] Uh we're now doing motor neuron disease
[12:12] and seeing great effects. So, it's
[12:15] important to know I'm not an eye
[12:16] specialist. I didn't choose the eye cuz
[12:17] I love the eye. I chose it because
[12:20] that's a good place to start for age
[12:21] reversal in humans this year.
[12:23] You mentioned a second ago you've been
[12:25] able to extend the life of mice in your
[12:28] laboratory.
[12:29] How and by how much? Is it the same
[12:31] process and by how much?
[12:33] Right. Well, the the study that that I
[12:35] was referring to was done using our
[12:37] technology in an independent lab, which
[12:40] is you might argue even better than
[12:42] having done it in my lab. Instead of
[12:44] putting the three reversal genes into
[12:46] the eye, they injected into the vein of
[12:48] the mouse, the old mice.
[12:50] Uh and turned it on in these really old
[12:52] mice. These mice would be the equivalent
[12:53] of
[12:55] about 80 to 85 years. So, they're really
[12:57] old mice. They're really frail.
[12:59] And just any any extension in their
[13:01] lifespan and health would be bet would
[13:03] be a great thing. And they got an
[13:04] additional 100% lifespan extension.
[13:07] Additional.
[13:08] So,
[13:09] That would be like an 80-year-old living
[13:11] to 160. Well, the remaining life of an
[13:13] 80-year-old isn't long.
[13:15] Oh, okay.
[13:16] >> Right. So, let's let's say if you're
[13:17] give it to a 70-year-old on average they
[13:19] had have another 10 years to go.
[13:22] Give them 20 years. So, it's that
[13:23] calculation. Um but that was not an
[13:25] optimized study. They just did a Hail
[13:27] Mary injection, turn it on, see what
[13:29] would happen. And I I heard when we did
[13:31] a bit of a research call you say the
[13:34] world doesn't know how close we are.
[13:37] The world doesn't know how close we are
[13:38] to what?
[13:40] To being able to safely reverse the age
[13:42] of the human body.
[13:45] How can you be so sure?
[13:46] I'm not sure.
[13:48] But I'm confident that
[13:50] the science is solid.
[13:52] All right. The the the biology of aging
[13:55] is is understood, I believe, in concept.
[13:59] My theory, called the information theory
[14:01] of aging, has
[14:03] so far been not disproven, which is
[14:06] important for a scientist.
[14:08] And that has allowed us
[14:11] to succeed
[14:13] really for the first time to safely
[14:15] reverse aging. And I now believe, and
[14:17] though I didn't 10 years ago, I now
[14:18] believe in my lifetime I'm going to see
[14:22] medicines on the market that reset the
[14:24] age or at least reverse
[14:26] in a large part uh the age of the body
[14:29] and that that
[14:30] initially won't be to make us just look
[14:32] better and feel better, although that's
[14:35] what a lot of us want. It's going to be
[14:37] used to cure
[14:39] certainly prevent, but definitely cure
[14:40] diseases
[14:42] that are currently incurable. So, we're
[14:44] I think we're at a turning point
[14:46] I dare I say in human history. It's it's
[14:48] not a question of if, it's a question of
[14:50] when this is going to happen.
[14:51] I want to get into your theory of aging,
[14:53] which we talked about there. Um but you
[14:55] did have a prediction before I get to
[14:56] there about
[14:59] how you think we'll be potentially
[15:00] taking a pill
[15:02] in 10 years' time
[15:05] every couple of weeks that will make us
[15:06] younger. Can you explain to me that
[15:07] prediction? What is what is the
[15:08] prediction? I I do believe that
[15:11] I and you're about 20-something years
[15:14] younger than me. You're going to see
[15:15] this for sure that there will be a pill.
[15:17] So, you might say, "Well, my critics
[15:19] might say, 'Well, David, that's
[15:20] exaggerating, right?
[15:22] You're still trying to get this gene
[15:24] these genes to work. How's it going to
[15:25] be a pill?'
[15:26] But this is where my lab comes in. My
[15:28] lab is like Willy Wonka's chocolate
[15:30] factory. If you visit, it's magical and
[15:33] the students that I teach and the
[15:34] trainees who are sometimes in their 30s
[15:37] and even 40s who are you know, brilliant
[15:39] scientists,
[15:40] uh there's about 25 of us.
[15:42] They are making discoveries that blow me
[15:45] away every week. It's not a pill cuz you
[15:47] can't give a mouse a pill. They won't
[15:49] chew it. But we give them a a liquid
[15:51] down their throat. It's a drink.
[15:53] And within 4 weeks we can rejuvenate
[15:55] them.
[15:56] Not with this this these genes anymore
[15:58] that we're giving humans. That's the old
[16:00] older technology.
[16:01] The new technology is
[16:03] something you can swallow
[16:06] in a mouse and rejuvenate them in 4
[16:07] weeks. It's normal for my students to
[16:09] say, "Oh yeah, we just rejuvenated the
[16:12] ear. We just rejuvenated the skin. Uh we
[16:15] just cured ALS, motor neuron disease in
[16:18] these animals." By the way, Steven, this
[16:20] isn't just each disease doesn't get a
[16:22] different medicine. Each disease doesn't
[16:25] get a different set of genes. It's the
[16:27] same set of genes, the same molecules
[16:30] that treat cure multiple sclerosis as
[16:32] the same one that cures blindness in
[16:34] mice.
[16:36] So, let that sink in. The same drug
[16:39] that we're using in the eye will be used
[16:41] to treat other diseases in the body,
[16:43] even liver disease. So, if if your
[16:45] predictions are correct and your
[16:46] timeline is correct,
[16:49] what does this mean for the way that I
[16:51] should be living my life right now? Most
[16:54] people look at their parents and their
[16:56] grandparents and think, "That's what my
[16:57] life will be like. I'm going to be frail
[16:59] in my 80s." That's not true for us. I
[17:02] like the Wright brothers analogy. It'd
[17:04] be like in 1900 saying we're always
[17:06] going to travel as fast as a horse.
[17:08] That's not true, right? The 20th century
[17:11] saw that we could go
[17:13] tens of thousands of kilometers. They
[17:14] went to the moon, right?
[17:16] That's what our generation is when it
[17:18] comes to biology and aging.
[17:21] Previous generations are no guide to
[17:23] what our lifespan is going to be like.
[17:24] You're going to potentially live to the
[17:26] 22nd century. If you do all the right
[17:28] things, technology keeps increasing,
[17:30] right? What kind of technologies will we
[17:32] have in 50 years?
[17:33] You'll be around in 50 years.
[17:35] I hope so.
[17:36] >> You're a healthy guy. I know you are.
[17:37] All right. So, in 50 years, what kind of
[17:39] things will you be able to do? Gosh.
[17:42] This is what most people forget is that
[17:44] technology isn't static. When you're
[17:47] old, you will not be using today's
[17:48] technology. You'll be using technology
[17:51] of 2070, 2080.
[17:53] Right? Mhm. And then you'll be able to
[17:55] live into the 22nd century and take
[17:57] advantage of those technologies.
[17:59] That's why people talk about the
[18:00] singularity. The singularity is this
[18:02] idea that if you can make it to a
[18:04] certain point in human history,
[18:06] you won't have to age anymore.
[18:09] And that that's in the future, right?
[18:10] But first steps first. Let's show that
[18:12] we can get this to cure blindness
[18:14] and then get to the point where
[18:17] every year that we get 1 year older,
[18:19] we can get 1 year younger. When that
[18:21] happens, it's a very interesting world.
[18:23] All right? You don't have to age
[18:25] anymore.
[18:26] That is a future. I don't know when
[18:27] we're going to get there.
[18:29] But if you don't live 10 to 20 years
[18:31] longer than your parents, something's
[18:33] wrong.
[18:34] On that point of the singularity, so
[18:35] this is a particular moment in time
[18:38] where we're going to be able to make
[18:39] aging or age reversal, I guess, a
[18:41] choice, right? So, that I guess the
[18:44] thinking or the theory is that if you
[18:45] can just make sure you survive up until
[18:47] this particular date, then you have the
[18:50] choice to live forever. Is that how is
[18:52] that like the the theory? Well, that's
[18:53] what they say, yes. Uh there are a lot
[18:55] of proponents of that. But that that's
[18:57] an idea. Isn't it logically true then?
[18:59] It's like logically It's an Yeah, it's
[19:00] an extension of what I I'm talking
[19:02] about. Um but I don't know when that's
[19:04] going to be. It's I think Ray Kurzweil
[19:06] said it's coming soon. Did he have a
[19:09] prediction? It was in the 2040s
[19:11] sometime. So, Ray Kurzweil is a famous
[19:12] futurist that seems to predict the
[19:13] future really well um across multiple uh
[19:16] disciplines. So, he said 2040.
[19:19] Yeah, that's my recollection. It's
[19:20] around there. Do you believe that?
[19:23] Cuz I'm going to hang on till 2040. I'm
[19:25] skeptical. I won't leave the house. I
[19:26] mean Ray is a smart guy, right? He
[19:28] predicted AI and all that's happening.
[19:31] So, it's it's it's dangerous to bet
[19:32] against Ray's predictions.
[19:35] I I remain skeptical, you know, as one
[19:37] of the leaders in the field. I think we
[19:38] have a lot still to do.
[19:40] That said, if this trial works this
[19:42] year,
[19:43] we will be in new territory. We will be
[19:45] on a path to age reversal in the whole
[19:47] body. It's going to happen. And you
[19:49] know, right now it's now 2026 we're
[19:52] talking.
[19:54] 2040 is a number of years away. It could
[19:56] be that we
[19:57] truly are able to multiply reset the age
[20:00] of the body.
[20:01] That's that's another thing that that's
[20:02] often missed.
[20:04] We can
[20:05] reverse the age of the eye not just
[20:07] once, but seemingly as many times as we
[20:09] want. In mice we've done it at least
[20:12] twice. We didn't do it a third time
[20:14] because the mice actually just got old
[20:16] and they died, but they died with
[20:17] perfect eyesight.
[20:19] But the point is that we we don't
[20:21] believe it's a one-shot wonder. You can
[20:23] keep reversing aging and then you age
[20:25] out and then you reverse it again and
[20:27] you just keep going. And if that's true,
[20:29] then it is possible that we will live
[20:31] dramatically longer.
[20:33] I don't yet see any technology in the
[20:35] near horizon that will make us live
[20:36] forever,
[20:38] but I do see that we'll have a radical
[20:40] change in how we treat diseases
[20:42] and how long we can live. So let's talk
[20:44] about what aging actually is and can you
[20:46] explain this to me like I'm a total
[20:47] idiot?
[20:48] Because that will help me. Thank you.
[20:50] It's difficult cuz you're not a total
[20:51] idiot, but this is my theory is that
[20:54] aging is not just wearing out. It's not
[20:57] just that your body becomes old and
[21:00] dysfunctional
[21:01] and you get pain, you get inflammation
[21:03] and you die from a disease.
[21:05] I look at the body like it's a a
[21:07] computer.
[21:08] It's software
[21:10] and we can reinstall the software.
[21:13] In my lab we believe we've found a way
[21:15] to do that and we see the evidence of
[21:17] that. So the body is
[21:19] a carrier of information from our
[21:21] parents
[21:23] and what happened in the womb.
[21:24] That information
[21:26] is intact, keeps our body functioning
[21:29] almost perfectly in our teenage years,
[21:32] 20. You're in your early 30s, you're
[21:34] starting to lose that information and so
[21:38] your body's not functioning perfectly
[21:39] anymore. Gray hairs.
[21:41] You've got some gray. Exactly, that's a
[21:43] a good example of cells that lose their
[21:45] identity and stop making melanin, the
[21:48] black pigment.
[21:49] But it's going to get worse, I promise
[21:51] you unless you know, unless we we hurry
[21:53] up.
[21:54] And this information uh gets lost, it
[21:56] gets corrupted. But the beautiful thing
[21:58] is we believe we found a backup copy of
[22:00] that information from youth that we can
[22:02] reinstall into cells, into tissues, into
[22:05] the entire body of a mouse and hopefully
[22:08] a human.
[22:09] That backup copy is in every old person
[22:12] I believe and it can be accessed. So
[22:14] when I see an old person walking down
[22:16] the street now, I don't think oh that
[22:17] person's just worn out, frail, going to
[22:19] die.
[22:20] I just think that's someone that needs a
[22:21] reset.
[22:22] And inside that person is a young person
[22:24] waiting to come out again.
[22:27] That's a totally different way to think
[22:28] about old age.
[22:30] And in the future people will have a
[22:32] choice to be rejuvenated or not.
[22:35] Where is that backup copy that I need?
[22:38] Well, we're working on that and if I if
[22:41] I told you my student would kill me.
[22:44] But we believe we found
[22:46] largely where that information is
[22:49] stored. It's a highly new biology. And
[22:52] it's currently a secret. It's a secret.
[22:54] Okay, so you you you lead the way. Tell
[22:56] me what we should we should talk about
[22:57] next as it relates to aging. Let's talk
[22:59] about information, right? We live in the
[23:00] information age and biology is becoming
[23:03] part of that information age.
[23:05] And it started with the uh elucidation
[23:09] of the structure of DNA.
[23:11] Okay. And so I have a I have a model of
[23:12] DNA here. So for listeners who are not
[23:14] watching,
[23:15] this is a a little plastic double helix.
[23:18] My friend uh Jim Watson uh died recently
[23:21] uh last month who he and his colleague
[23:24] discovered that DNA, the information of
[23:26] life that we get from our parents is a
[23:29] chemical that's about 6 ft long in every
[23:31] cell.
[23:32] And uh this model here shows that DNA is
[23:34] a ladder and the steps on the ladder are
[23:37] the information of the DNA.
[23:39] Okay. Yeah?
[23:41] And you can pull this apart so that each
[23:43] step becomes 50 50% ripped apart.
[23:47] So that should come apart, right? So I
[23:48] ripped a rung of the ladder apart.
[23:51] And that is called a base on the DNA and
[23:53] it always matches with its corresponding
[23:56] chemical.
[23:57] So this
[23:59] shorthand we'd call an A, it always
[24:01] matches with a T. So an AT becomes a
[24:03] rung on the ladder.
[24:05] And down here different color here, I'm
[24:07] looking at a red and a green step. Rip
[24:09] it apart.
[24:11] This is a G and a C letter. Gs and Cs
[24:13] come together. And actually when if you
[24:15] if I rip this ladder into halves and
[24:18] each step becomes half a ladder,
[24:20] now you can see that you can copy DNA
[24:22] because
[24:23] the A has to match with the T rung and
[24:26] the G has to match with the C. So that's
[24:28] basic DNA. That's how the information is
[24:30] transferred
[24:31] from cell to cell, from mother to
[24:34] daughter, our parents to offspring.
[24:37] There are about 20,000 genes, about
[24:39] 15,000 are turned on,
[24:41] but a different set
[24:43] gets turned on in large part
[24:45] to make a nerve cell compared to a liver
[24:47] cell and a skin cell.
[24:49] That's gene expression.
[24:52] And what controls that gene expression
[24:54] is what's called not not the genome,
[24:56] which is what's in front of me here on
[24:58] the DNA molecule.
[24:59] It's the epigenome.
[25:02] The epigenome is the information we get
[25:05] transferred from cell to cell, from
[25:06] parent to offspring
[25:08] that's not in this molecule.
[25:11] So where's this epigenetic information?
[25:14] Well, it controls which genes are
[25:16] switched on and off
[25:17] and a major regulator of that process
[25:21] is the modification of these steps on
[25:24] the DNA. These chemicals, the C
[25:27] particularly the C which I'm showing you
[25:30] here in this red part of the the
[25:32] molecule,
[25:33] the C gets a little chemical added to it
[25:35] called a methyl.
[25:37] And a methyl is just if you remember
[25:39] from chemistry high school,
[25:41] uh it's a carbon
[25:43] with three hydrogens.
[25:44] It's very simple molecule. It gets stuck
[25:46] on that piece
[25:48] of the the DNA molecule. That's called
[25:50] DNA methylation and that will help
[25:52] determine that pattern of DNA
[25:54] methylation determines whether this
[25:57] particular gene will be switched on, say
[26:00] to make an optic nerve,
[26:01] or switched off so that
[26:03] it's becomes a liver cell. And that
[26:05] happens as we're in the womb and we
[26:07] become an embryo.
[26:09] >> [snorts]
[26:09] >> And that's the epigenome. These
[26:11] chemicals that turn genes on and off is
[26:13] the epigenome.
[26:14] And the information theory of aging
[26:18] states
[26:19] that the information that's in a cell
[26:23] which includes the DNA, but actually
[26:25] more importantly for aging
[26:27] is the control systems, the epigenome.
[26:30] That is pristine when we're young, but
[26:32] as we get older we lose that epigenetic
[26:35] information.
[26:36] The ability to
[26:38] tell a cell to be a nerve cell versus a
[26:40] liver cell versus a skin cell, it starts
[26:42] to get erased. So it when we look at a
[26:44] mouse or or an old tissue, if I took
[26:47] maybe not your skin, but but my skin,
[26:49] my skin cells are no longer as skin-like
[26:52] as they once were. They started to lose
[26:56] their identity. They're starting
[26:58] actually to to look more like nerve
[26:59] cells and nerve cells starting to look
[27:01] more like skin cells
[27:02] because the genes that were once turned
[27:05] on correctly in my young cells,
[27:07] that that control system, these
[27:09] chemicals on the DNA molecule, the
[27:11] methyls, are getting erased. So aging is
[27:14] an identity crisis of the cells.
[27:15] >> It absolutely is. Well put. The cells
[27:18] forget
[27:19] what their job is.
[27:21] Yes. The genes are still there in large
[27:24] part. 99.999% of the genes are still
[27:27] there. The molecule's intact.
[27:29] But the control systems
[27:31] the label thing you mentioned.
[27:33] >> to tell the cell that this gene needs to
[27:36] be on, but this one should always stay
[27:37] off, that gets erased over time. Why?
[27:40] Uh we we did partially figure that out.
[27:43] And how do you know?
[27:45] Well, uh even better.
[27:47] This is this is why I love your podcast,
[27:49] Steven. You ask the right questions.
[27:52] These there are enzymes that remove
[27:54] these methyl groups
[27:56] um and put them back on. So the cells
[27:58] controlling these things, they shouldn't
[27:59] change, but they do.
[28:01] And one of the things that messes the
[28:03] system up
[28:04] is
[28:05] major catastrophe in a cell. And when
[28:08] the cell panics,
[28:11] it removes these structures to try and
[28:13] adapt to the stress. The label. The
[28:15] label comes off
[28:17] in a desperate attempt to survive.
[28:20] But then the cell doesn't fully
[28:22] revert back to the original state. Some
[28:24] of these chemicals and some of the
[28:25] proteins that bind to the DNA, which is
[28:27] also important for this epigenome, they
[28:30] don't all go back to where they started.
[28:32] I've used the analogy
[28:34] that it's like a ping pong or a tennis
[28:36] match where the proteins that control
[28:39] the genes,
[28:40] they they get relocalized to where the
[28:42] emergency is.
[28:44] And an emergency want the one that we
[28:45] think is most dangerous
[28:47] and a large cause of cause of aging is a
[28:50] broken chromosome. If you have a broken
[28:52] chromosome, if you don't fix that,
[28:54] you're either going to become a cancer
[28:55] cell or you're going to die. It's not
[28:57] good. Um and so cells panic.
[28:59] And in that panic of moving proteins
[29:01] away and turning on these stress
[29:03] response genes,
[29:04] uh that's great in the short term. The
[29:06] cell might survive,
[29:08] but they don't fully reset. Those
[29:09] proteins don't all go back to where they
[29:11] once were,
[29:12] say 10 minutes ago when the stress
[29:14] needed to be the disaster happened.
[29:17] And if you do that time and time again
[29:19] and every one of your cells has at least
[29:21] chromosome every day.
[29:23] That's 20 trillion of these events every
[29:25] day in your body.
[29:27] Over time,
[29:28] tick tick tick,
[29:30] you get the aging process, we believe.
[29:34] So I got I guess I've got two questions.
[29:36] I guess the first question, if I was
[29:37] thinking about the sequence of asking
[29:38] these questions, is
[29:41] what is increasing that stress on my
[29:44] cells, therefore what is increasing
[29:46] aging? And also like why didn't
[29:48] evolution just come up with a solution
[29:50] for this that stopped me aging then?
[29:52] Like evolution is very smart. Couldn't
[29:53] it just fix this? Well, before I get
[29:55] into that, one of the
[29:57] the reasons we know that this works, cuz
[29:58] you asked me, "How do we know that's
[29:59] true?"
[30:00] is that
[30:02] we created this this catastrophe in
[30:04] animals. We we took mice and we
[30:07] we we broke their chromosomes in a way
[30:09] that didn't cause cancer [clears throat]
[30:10] or mutations.
[30:12] If we're right,
[30:14] what should happen to these mice? They
[30:15] get old fast.
[30:16] >> They get old fast. Gray hair. And they
[30:18] did.
[30:19] We call them the ICE mice. I stands for
[30:21] inducible changes to the epigenome.
[30:24] And we're able to induce these changes.
[30:27] And we took bets in the lab. This was
[30:29] going back now 12 years ago.
[30:31] Uh
[30:32] I I bet that we would get aging. Okay,
[30:34] but I was the only one in the lab that
[30:36] thought that would happen. We had a lot
[30:38] of bets that the mice would die.
[30:40] A lot of bets that the mice would get
[30:42] cancer. And a few said nothing would
[30:44] happen.
[30:45] But we got aging. In fact, I was I was
[30:47] in Australia, where where I'm from, as
[30:49] you know, and I got a picture on my old
[30:52] old-style iPhone. And uh it was a
[30:54] picture of an old mouse.
[30:56] Uh well, it was a sick-looking mouse.
[30:57] And the And the the text was
[31:00] "Problem, we have a sick mouse." And I
[31:01] wrote back, "That's not a sick mouse.
[31:03] That's an old mouse." And that was the
[31:04] first time I realized that we'd had
[31:07] evidence that our theory, the
[31:09] information theory of aging, is correct.
[31:12] So, what we did actually, and this might
[31:13] satisfy your and your listeners'
[31:15] curiosity,
[31:17] we generated a mouse from scratch
[31:19] using stem cells.
[31:21] And so, we start with a a mouse stem
[31:23] cell that we grow in the lab in the
[31:24] dish.
[31:25] And we change the genetics of that stem
[31:27] cell
[31:28] so that we could
[31:30] feed it a drug,
[31:32] uh tamoxifen, which is used uh in in
[31:35] chemotherapy. And that drug turned on
[31:39] a gene from a slime mold, something you
[31:41] might find in the forest,
[31:43] that breaks DNA of the mouse, but does
[31:46] it in a way that doesn't cause cancer or
[31:48] mutations. Just cuts it. And then the
[31:50] cells put it back together. So, we could
[31:51] take a mouse and for 3 weeks we
[31:56] turned on the slime mold-cutting
[31:57] protein.
[31:59] And nothing happened to the mouse at the
[32:00] time. It's like a You don't feel an
[32:02] X-ray. You don't feel
[32:05] different when you fly except for maybe
[32:06] jet lag and dehydration. But you don't
[32:08] get old suddenly. Same with the mice.
[32:10] They were normal. They felt fine.
[32:13] And that's why at first people said,
[32:14] "Oh, nothing's going to happen to these
[32:15] mice." After 3 weeks, they were fine.
[32:18] But we set in motion a cascade of
[32:20] accelerated aging events that
[32:23] about 10 months later, they were super
[32:25] gray and super old and had all the
[32:28] diseases of aging
[32:29] 50% faster than their twins that we
[32:31] didn't treat. And you've got photos of
[32:33] those we could show. Yeah. Yeah, let's
[32:35] show those. So, if I was to do the
[32:37] experiment in you,
[32:38] I might have to engineer it a clone of
[32:40] you,
[32:41] but I could do that. Uh you know, I'm
[32:43] not saying that it's ethically right.
[32:45] But But theoretically, we could make a
[32:46] clone of you, put in that slime mold
[32:48] gene, turn it on,
[32:50] and your clone would be 50% older than
[32:53] you are.
[32:54] Can you translate this into
[32:57] the equivocal for a human?
[32:59] That particular study that you did. So,
[33:01] it would be like in me doing what? And
[33:04] then me getting old fast. Yeah. Uh well,
[33:06] we're exposed to to things that cause
[33:08] DNA breaks all the time. They happen
[33:10] naturally as the cells try to copy their
[33:12] DNA, but you can accelerate that by
[33:13] getting an X-ray, a CT scan,
[33:16] flying a lot, and cosmic rays banging
[33:18] into your DNA and
[33:19] >> I fly all the time. Yeah, it's a lot
[33:21] >> of CT scans and X-rays. Yeah. Uh and and
[33:25] though it's imperceptible, I believe
[33:27] that that's probably accelerating your
[33:28] aging process. What's flying doing to my
[33:31] So, again, you talked about flying being
[33:32] equivocal to what you did to the mouse.
[33:34] In what way?
[33:35] Well, every time you break your
[33:37] chromosome, you're rearranging your
[33:39] epigenome in a catastrophic way that
[33:42] doesn't fully reset. And your cell will
[33:43] lose its identity faster.
[33:46] I also believe um and we have some
[33:47] evidence that even going to a rock
[33:49] concert and and have blasting your
[33:51] eardrums
[33:52] is such a stress on those cells in your
[33:54] ear that the reason that you become deaf
[33:56] earlier is because your ear hair cells
[33:59] are getting older faster.
[34:01] You don't want to break the DNA. You
[34:03] don't want to cause catastrophe to your
[34:05] fragile cells in your body
[34:07] because the recovery isn't complete and
[34:09] aging ensues.
[34:11] So, with this theory in mind, what are
[34:13] the day-to-day things that we're all
[34:15] doing
[34:16] that are accelerating our age? Like cuz
[34:17] I think what's really interesting is I
[34:19] looked at my brother, Jason. He's a year
[34:21] older than me. He has three kids that
[34:24] are like under the age of seven or eight
[34:26] now.
[34:27] And
[34:28] this Christmas time, cuz it's just been
[34:29] Christmas, I looked at his hair to see
[34:31] how many gray hairs he had versus me.
[34:33] And I thought, "Okay, he has
[34:34] considerably more."
[34:36] Uh he's a year older than me. And I was
[34:37] thinking, that's like a a proxy of aging
[34:41] to some degree.
[34:42] What is it he's potentially done on a
[34:44] day-to-day basis? I know you don't know
[34:46] him, so this is why it's not not an
[34:47] offensive uh answer to give. What is it
[34:49] that someone who is
[34:52] generally sort of genetically very
[34:53] similar, but is making different
[34:54] lifestyle choices, is doing
[34:57] to accelerate that process of wrinkles
[34:58] or gray hairs or
[35:00] Well, here's here's the good news. That
[35:02] you can have a big impact on your rate
[35:04] of aging by changing your lifestyle.
[35:06] It turns out your DNA is not your
[35:07] destiny. It's the epigenome. So, that
[35:10] how you live your life is really 80 to
[35:12] 90% of your rate of aging.
[35:15] That's good. It's in your hands. But it
[35:16] also means that some people mess up
[35:18] their lives. There are actually twin
[35:19] studies from uh mostly from Denmark.
[35:22] Identical twins. One that goes and
[35:24] smokes and gets obese
[35:27] and uh goes in the sun.
[35:29] And they are much older-looking than
[35:31] their identical twin.
[35:33] Essentially proving that the DNA is not
[35:35] the reason you age.
[35:37] First of all, there going to be people
[35:38] in the audience uh who are listening or
[35:40] watching who have gray hair saying,
[35:42] "Damn it, I'm not old." And that's true.
[35:44] I mean, nobody died of gray hair, right?
[35:46] And
[35:47] sometimes genetically you can get gray
[35:49] old uh but not be physically old.
[35:52] What is true that's often not
[35:54] comfortable is how old you look is a
[35:56] very good representation of how old you
[35:58] are in your organs as well.
[36:00] So, the doing the right thing. So, what
[36:01] are those things? Let's Let's tick off
[36:03] some of the major things that people
[36:04] should be doing.
[36:06] And they can have a big impact. They can
[36:07] lengthen their life by a decade just by
[36:09] doing some of the major things.
[36:11] So, we know that on average people can
[36:12] live 14 years longer. This is based on a
[36:14] study that came out from Harvard. A
[36:16] long-term study of the lifespan of World
[36:18] War II veterans.
[36:20] If you avoid smoking, cigarette smoking,
[36:23] or really any type of smoke in your
[36:24] lungs. Smoking breaks your DNA. It's
[36:26] going to accelerate aging in your lungs,
[36:28] your whole body.
[36:29] Avoid excessive drinking. We now know
[36:31] that even more than one glass a day of
[36:34] alcohol is bad. I've given up alcohol
[36:36] for the most part for that reason.
[36:38] Eat well.
[36:40] So, you want to eat healthy food. We've
[36:41] got some healthy food here we're going
[36:43] to talk about.
[36:44] Um so, make sure you you don't uh
[36:47] overeat or eat ultra-processed foods.
[36:50] And the big one, one of the best things
[36:51] you can do besides all of that, is
[36:54] exercise. Okay, and exercise covers a
[36:56] lot of things, so we can drill into that
[36:57] as well.
[36:59] But the fifth one is interesting. It may
[37:01] be surprising,
[37:02] but actually good news for you. Have a
[37:04] reliable partner. I think you're going
[37:06] to say be a podcaster. I was going to
[37:07] Okay. Uh [laughter] no, that probably
[37:09] accelerates your age. Yes, so um if you
[37:11] don't have a reliable partner,
[37:13] have a pet.
[37:14] Because the human bond is something that
[37:17] is shown to slow aging and associates
[37:21] with people who live longer than others
[37:23] that are lonely.
[37:25] Interesting. We're going to dig into all
[37:26] of those in great detail. Specifically
[37:28] very interested in in exercise, diet,
[37:31] lifestyle, fasting. I know it's a big
[37:32] subject you speak about, which I'm very
[37:33] very interested in. And actually, as I
[37:35] was doing the research for this
[37:35] conversation,
[37:37] again, my the way that I'm going to
[37:39] approach nutrition has shifted because
[37:41] of some of the things I discovered
[37:42] there.
[37:43] I want to just tick off on this
[37:44] evolution point. Right. Let's come back
[37:46] to that. Yeah, I just want to get clear
[37:48] Yeah, like why didn't evolution fix it
[37:51] for me? Because they talk about survival
[37:52] of the fittest and that the very fact
[37:54] that I'm here is because my my ancestors
[37:56] were good at survival. But listen, my
[37:57] ancestors all died at like 30, 40, 50,
[37:59] 60, 70, 80 years old. That's not very
[38:01] good. Why Why didn't they just live
[38:03] longer?
[38:04] >> Well, that's why. You just said the
[38:05] answer yourself. Because your ancestors
[38:08] didn't live beyond 40 or 50. Even less.
[38:11] But most men
[38:13] uh in prehistoric times would die from
[38:16] >> [clears throat]
[38:16] >> famine, disease, and actually a lot of
[38:18] them from war. So, most people didn't
[38:21] make it to 80. Some people did, but very
[38:23] very rarely.
[38:25] So, the the forces of natural selection
[38:27] were on
[38:29] early survival
[38:30] and fast breeding.
[38:32] Let's put it this way. If there was
[38:33] someone
[38:34] who was born with a mutation that
[38:36] allowed them to live a lot longer, to
[38:38] 90,
[38:39] in a prehistoric world, that's useless.
[38:42] Because you're probably going to die at
[38:43] 30 or 40 anyway. And so, you have
[38:45] children.
[38:45] >> [clears throat]
[38:46] >> So, what you want to do is find genes
[38:47] that allow you to become reproductively
[38:49] successful
[38:51] early on in life.
[38:53] Um and make sure your children survive.
[38:55] And so, we we have children
[38:57] pretty early, but humans for for various
[38:59] reasons have a long developmental period
[39:02] including education.
[39:03] So, we don't we don't develop very
[39:05] rapidly, right? We don't wake up and we
[39:07] can walk and run like a lot of other
[39:08] species and mammals.
[39:10] >> [gasps]
[39:10] >> But we don't live a long time because
[39:12] there was
[39:13] in the environment that we evolved, the
[39:15] Serengeti plain is pretty much agreed
[39:17] upon as that's one of the places we
[39:19] evolved.
[39:20] Certainly uh Eastern Africa.
[39:22] That was extremely difficult and
[39:24] dangerous place to live.
[39:26] You could get eaten by an animal.
[39:29] And if you didn't get eaten by an
[39:30] animal, you got killed by the
[39:31] neighboring tribe.
[39:32] That's super dangerous, right? And then
[39:34] so, we we evolved to live
[39:37] really at optimal to about 30,
[39:41] but not much more than that. So, after
[39:43] 30,
[39:44] as you might be experiencing with with
[39:46] your body,
[39:47] we're at the forces of entropy. So, the
[39:50] body starts to decay, the information
[39:53] starts to get lost in the body.
[39:56] But the the good news is that if you
[39:58] take away predation and death from a
[40:01] species,
[40:02] it evolves longer lifespans. Now, it
[40:04] makes evolutionary sense
[40:06] to have genes that allow you to put more
[40:09] effort into building a strong body and
[40:11] slowing down the aging process and
[40:14] preventing DNA breaks, chromosomal
[40:16] breaks.
[40:17] We know that this is true because if you
[40:18] put species
[40:20] say on an island where there are no
[40:22] predators,
[40:23] what happens to their longevity?
[40:26] They get longer lived naturally. It
[40:28] takes 20, 30 generations, but only when
[40:32] there's no predation, when you're not
[40:34] under a lot of stress
[40:36] to breed quickly, do you get longer
[40:39] lifespans evolving. Given that humans
[40:41] don't have predators anymore, we are
[40:43] slowly evolving
[40:46] longer lifespans. But it's very slow,
[40:48] and it's not going to happen fast enough
[40:50] for you and me. And do the organisms
[40:52] that do live really, really long have
[40:55] a small amount of predators in nature?
[40:57] Absolutely.
[40:58] Absolutely. Think about them.
[41:01] The bristlecone pine. What's that? It's
[41:03] the longest lived tree in the world. It
[41:05] can live many thousands of years.
[41:08] Are you jealous?
[41:10] Not jealous, no.
[41:12] >> [laughter]
[41:12] >> No, they live a tough life. Some of
[41:15] those trees have been around since the
[41:16] pyramids. Wow. The reason they live can
[41:19] live for so long and evolve to live so
[41:20] long is that things don't eat them. They
[41:22] are totally poisonous. You don't want to
[41:24] eat a bristlecone pine.
[41:26] The same for a whale, right? The bowhead
[41:27] whale, some of these very large animals,
[41:29] no predators. So, they've evolved a
[41:32] strategy of breeding slowly, but
[41:34] building very
[41:36] powerful systems to stop epigenetic
[41:39] changes. Their epigenetic control
[41:41] systems are stable. They don't get
[41:43] cancer, and they they don't lose they
[41:46] don't have this identity crisis until
[41:48] hundreds of years.
[41:50] We know that. People study the cells of
[41:52] whales in the dish, and those cells
[41:54] don't lose their identity very quickly
[41:56] even when you break their DNA.
[41:58] So, I I I guess the place also to to go
[42:01] next is talking about disease generally
[42:04] and what disease
[42:06] is.
[42:07] So, are these diseases a function of
[42:08] aging? Does this idea of reversing aging
[42:11] even matter if cancer's going to take
[42:12] most of us out anyway at some point?
[42:15] Is there a link between aging and
[42:17] disease? This might be the most
[42:18] important point that I make today.
[42:22] When you reverse aging, diseases of
[42:24] aging go away or are cured.
[42:27] And in our in my lab, including many
[42:29] types of cancer as well.
[42:33] The diseases that we try to treat
[42:34] individually with different medicines
[42:36] today that we think are unrelated,
[42:38] Alzheimer's, cancer, heart disease, you
[42:40] name them.
[42:41] Fundamentally, what's driving a lot of
[42:44] those diseases
[42:46] is aging.
[42:47] If you never got old, would you ever get
[42:49] Alzheimer's even if you had the genes
[42:51] that predispose you? No.
[42:54] Right? And so, what we see in my lab is
[42:56] when we give an animal a disease, and we
[42:58] can do that, we can put in the human
[43:00] genes for Alzheimer's into a mouse,
[43:03] it becomes has dementia.
[43:05] When we reverse the age of the brain of
[43:07] that animal, we're not treating the
[43:09] disease, we're treating aging.
[43:11] The disease goes away. The body can heal
[43:14] itself when it's young.
[43:16] So, it's the aging process that reveals
[43:18] the disease that can be cured by
[43:21] reversing. Why does the aging process
[43:24] reveal a disease?
[43:25] Why don't we get Alzheimer's at 15?
[43:28] Because the cells are so healthy they
[43:30] can fix themselves. They can renew
[43:32] themselves.
[43:33] The disease processes that cause these
[43:36] problems for us don't exist when we're
[43:38] young.
[43:40] Why is it that a teenager rarely has a
[43:42] heart attack? Because their body
[43:45] prevents them.
[43:46] Why do young people typically not get
[43:48] cancer? Because the immune system
[43:51] finds cancer cells and clears them out.
[43:53] You and I have cancer cells in our body
[43:55] right now. Why are we probably not going
[43:57] to die in the next year? Cuz our immune
[43:59] system will find them and kill them.
[44:01] But as we get older, we're going to lose
[44:03] that ability,
[44:04] and we'll have a greater chance of
[44:05] having cancer. So, are you saying that
[44:07] if we cure aging, we're probably going
[44:09] to by way of that cure most of these
[44:11] diseases? 100%.
[44:13] We're talking about um
[44:16] menopause quite a lot on this podcast,
[44:18] and fertility, menopause, women's
[44:20] ovaries as um one of the first places
[44:24] that ages. And I've heard you explain
[44:26] that you think that evolution programmed
[44:27] women to stop having children during
[44:29] menopause because continuing
[44:30] reproduction would drain energy needed
[44:32] to raise existing children.
[44:34] So, is infertility something that could
[44:36] theoretically be prevented? In mice,
[44:38] which is where we live in my lab, where
[44:40] we work,
[44:42] it can be prevented and it can be
[44:44] reversed. I thought we run out of eggs.
[44:47] That's like the That's the current
[44:48] theory. The evidence that we have from
[44:50] my lab and a lab that I worked with in
[44:53] Australia
[44:55] caused me to question that idea that we
[44:58] run out that women run out of eggs.
[45:01] We have published
[45:03] and repeated many times
[45:05] that if you
[45:07] treat old female mice
[45:10] 16 months of age, which is like a 65,
[45:13] 70-year-old human,
[45:14] that has long time since given up having
[45:18] offspring,
[45:20] we can treat the ovaries with a chemical
[45:23] that rejuvenates the eggs
[45:25] that are in the ovary,
[45:27] maybe even produces new ones, we don't
[45:30] know for sure,
[45:31] but those 16-month-old mice that stopped
[45:34] having kids a
[45:35] uh probably at least 6 months ago,
[45:38] now start producing healthy offspring
[45:40] again.
[45:41] Their eggs look young, pristine,
[45:44] compared to the terrible eggs that if
[45:46] you try to harvest some eggs from a
[45:47] mouse that old,
[45:48] it's hard to find any that look normal.
[45:51] Their chromosomes are messed up, ripped
[45:52] apart. They're not going to produce
[45:54] healthy babies. But we can take those
[45:57] eggs, or at least the ovaries with those
[45:59] eggs in them,
[46:01] and cause them to be young again, and
[46:03] make fresh eggs
[46:04] that can produce healthy offspring that
[46:06] live a normal lifespan. The real
[46:08] question is, will this work in women?
[46:11] And that's something that I'm keen on
[46:12] testing.
[46:15] It's must be really hard to test a lot
[46:16] of these things in people, right? Cuz we
[46:18] you've mentioned the word mice quite a
[46:20] lot.
[46:20] >> It's harder than you can imagine,
[46:22] actually. Um and I've spent a lot of my
[46:23] career since I was 35 um
[46:26] aiming to develop a medicine
[46:29] to treat diseases and aging.
[46:31] And it can be it can go wrong in many
[46:34] ways. Um even if the science is good and
[46:37] right.
[46:38] Um and it it's there's money, there's
[46:40] business, there's laws,
[46:42] there's politics, there's
[46:44] business strategies, there's change of
[46:46] leaderships,
[46:47] um
[46:49] all sorts of human introduced
[46:52] variables that can get in the way.
[46:53] There's patents,
[46:55] and and then there's there's competition
[46:58] and spite that also gets into it. Um and
[47:01] I've had to
[47:02] deal with all of those things, including
[47:05] competing against some of the largest
[47:06] pharmaceutical companies in the world
[47:07] who really didn't want me to succeed.
[47:10] But yeah, it's extremely difficult to
[47:12] make a drug, but I do want to remind you
[47:14] and everyone listening and watching
[47:17] that we're beyond mice now for age
[47:19] reversal. We've done this in monkeys,
[47:22] monkeys that are
[47:23] physically and almost genetically
[47:25] identical to us.
[47:27] So, it's not a big leap from it is a
[47:29] pretty big leap from mouse to human, but
[47:30] from a monkey to a human,
[47:32] it's we're essentially
[47:34] you know, slightly smarter monkeys.
[47:37] I just had a thought about how other
[47:39] countries and other nations might be
[47:41] conducting their own sort of secret
[47:43] research, and they might not have the
[47:45] same bureaucratic, political, ethical
[47:48] considerations that you have to contend
[47:50] with. Do you think about this much that
[47:52] some of the sort of geopolitical
[47:54] adversaries might be doing secret
[47:56] testing in some
[47:57] research lab somewhere on humans? I
[47:59] think about it, um and in fact, the
[48:01] United States government thinks about
[48:03] it, too. A large investment into uh the
[48:06] com- one of the companies that I
[48:08] uh sit on the board of was blocked
[48:11] because the US government claimed that
[48:13] the technology was too dangerous to be
[48:15] in the hands of foreign
[48:17] companies and governments.
[48:19] So, there the US government, at least in
[48:22] in the previous administration, was
[48:23] extremely cautious about
[48:25] this technology falling into
[48:28] the wrong hands.
[48:29] Which technology? The ability to reverse
[48:31] aging. So, the US government blocked
[48:34] that technology because they were scared
[48:35] that it might fall into the wrong hands.
[48:37] Well, they blocked the the very large
[48:39] investment over $100 million into the
[48:41] company from a foreigner because they
[48:43] would have more access to
[48:45] the information and the progress. Is it
[48:47] China? Um I won't say more. It's
[48:50] sensitive.
[48:51] Most I can say is that governments are
[48:53] watching this technology very closely,
[48:55] not just the US, but around the world.
[48:57] Because the winner
[49:00] will make
[49:01] not not just a lot of economic benefit,
[49:04] but there will there will be potential
[49:06] for radical change in the pharmaceutical
[49:08] industry, in health care.
[49:10] Um the amount of change socially will be
[49:12] dramatic as well.
[49:14] But there are also uses that the
[49:16] government has identified,
[49:18] uh so-called super soldier potential.
[49:21] Now, I I don't agree that that's a
[49:24] reason to slow down the research.
[49:26] Others claim that it was worth it.
[49:29] But I do believe that the technology is
[49:31] very powerful, and we should start to
[49:32] get ready
[49:33] for when this comes to society. Cuz it's
[49:37] not an if, as I said, it's a when.
[49:39] The technology to do what?
[49:41] To rejuvenate the human body. Why do we
[49:44] need to get ready?
[49:46] Well, cuz it'll be massive social
[49:47] change. If you can choose how old you
[49:49] want to be,
[49:51] and people don't die as
[49:53] at 80 anymore. Let's say they they can
[49:55] live till 120 or beyond.
[49:58] There's big changes. There's social
[49:59] security issues. There's uh employment.
[50:03] Though, I will say that
[50:04] the the disaster scenario that often
[50:07] comes to mind when I talk about this,
[50:09] and which I covered in in the last part
[50:11] of my book, Lifespan,
[50:13] it's actually economically hugely
[50:14] advantageous to slow aging and prevent
[50:17] diseases.
[50:18] A lot of the US economy and most
[50:20] advanced economies goes to health care.
[50:22] And chronic disease, a lot of people are
[50:24] sick for 5 to 10 years,
[50:26] that's where most of people's savings
[50:28] and retirement and government money goes
[50:29] in. The most expensive years of your
[50:31] life are the last 2 years. If you can
[50:34] delay that,
[50:35] it's going to have massively positive
[50:37] economic benefits to a nation that
[50:40] adopts these medicines. I've got a
[50:41] question for you that actually came to
[50:43] mind yesterday when I was I watched some
[50:45] I don't know, some video on social media
[50:46] and they asked a question to a guy.
[50:48] Um David, if you were a billionaire now
[50:51] at age 56,
[50:53] would you give it all up
[50:55] to be
[50:57] my age again, 33?
[51:00] Um I don't think you can put a price on
[51:02] being young. Another way of of putting
[51:04] it I've I've seen this on social media,
[51:05] would you swap for a billion dollars,
[51:07] would you swap with Warren Buffett?
[51:09] No, absolutely not.
[51:10] >> Right. So, there's no money in the world
[51:12] that you want to be old, right? Uh Yeah.
[51:14] It's not worth it. In other words, youth
[51:16] is more valuable than a billion dollars.
[51:20] It may be the most valuable thing you
[51:21] could ever have
[51:23] is your youth.
[51:24] It is it's such an
[51:26] an interesting and illuminating analogy
[51:28] or metaphor or whatever because
[51:30] suddenly you do realize that how much we
[51:32] value it. We value it more than
[51:34] anything.
[51:36] I would rather be
[51:38] 33 years old
[51:40] than be a 43-year-old billionaire.
[51:43] Even the 10 years I value as a billion
[51:45] dollars.
[51:46] Yeah. 1 year, maybe, but not 10 years,
[51:49] right? 10 years is super I I totally
[51:51] agree with you.
[51:52] Um and the older you get, the more
[51:54] valuable it becomes. It's important to
[51:56] realize the the massive impact that this
[52:00] technology can have, not just
[52:02] economically, but on individual lives of
[52:04] human beings across the planet. The
[52:06] world when this becomes
[52:08] a reality,
[52:10] again, I'm speaking like it's a
[52:11] certainty cuz I'm pretty convinced it's
[52:13] going to happen,
[52:14] the that world is going to be so
[52:16] different from the world we live in.
[52:17] It's going to be as different as
[52:19] the pre-computer world and the
[52:21] pre-airplane world as
[52:23] today is.
[52:24] I'm trying to imagine the world where we
[52:26] could pick our age.
[52:28] And maybe even, you know, you talked
[52:29] about earlier being able to continue to
[52:31] reset to that age. Yeah. Trying to
[52:33] imagine what the world would be like if
[52:35] I could be 33 forever.
[52:37] Or if you could be, you know, 33
[52:40] forever.
[52:40] >> Or even for another 100 years or
[52:42] something. Yeah. Yeah. I could stay 33
[52:45] for 100 years. Do you think that's the
[52:47] plausible outcome, which is we can kind
[52:48] of pick an age and stay there for
[52:50] 100 years like at that particular age,
[52:52] or is it just that I'm going to be 150
[52:55] in my physical form, I'm going to be
[52:57] wrinkled and gray, but I'm just going to
[53:00] continue to live?
[53:02] Is it looking young, or is it just
[53:04] living longer?
[53:06] It's actually
[53:07] >> Both. It's It's The good news is it's
[53:09] both. And we're doing a lot of work in
[53:11] my lab on skin and hair,
[53:13] uh hair loss, hair graying. Yeah, please
[53:15] help me. Like if I
[53:17] >> [laughter]
[53:17] >> You don't have to worry just yet. Um
[53:20] you know, we'll we'll help your brother
[53:21] first. No, no, come on. Yeah, we will.
[53:24] Tell him to call me. Um so, we we we've
[53:26] seen that we can rejuvenate the skin of
[53:28] again mice, but still we we also grow
[53:30] human skin in the lab from scratch. And
[53:32] we can put that human skin on mice, and
[53:35] the mice have human skin. So, we can now
[53:37] test age reversal in that system.
[53:40] I'm very optimistic that we'll be able
[53:42] to rejuvenate uh the the external part
[53:44] of the body as well as the internal. If
[53:46] we can cure blindness,
[53:48] reversing the age of the skin is is a
[53:49] piece of cake.
[53:51] What What does that world look like? I'm
[53:53] trying to understand all of the sort of
[53:54] unintended consequences
[53:57] of such a world where we're all kind of
[53:59] young and we all live longer.
[54:01] Is there problems of meaning and
[54:03] purpose? Is this
[54:05] What are the unintended consequences?
[54:07] I've thought a lot about this. There's
[54:08] this gut feeling that a lot of people
[54:10] have, maybe you're feeling it now, is
[54:12] that if I'm not worried about death, I'm
[54:15] not going to strive as hard, I'm not
[54:17] going to have as much meaning, I'm not
[54:18] going to have agency.
[54:21] I totally reject that view.
[54:23] I believe that every moment is special.
[54:26] I I don't believe I would be enjoying
[54:28] this conversation with you anymore
[54:30] if I could live 200 years. I'm loving
[54:33] the moment. Mhm. All right. And so, I I
[54:36] believe that we get up with purpose,
[54:39] and that if I lived for 1,000 years, I'd
[54:41] still enjoy every day that I lived.
[54:44] And even 1,000 years, one day may be
[54:46] seen as too short.
[54:48] You know, it's 20 times my age, a little
[54:50] bit less than 20.
[54:52] That's still not very much in the grand
[54:54] scheme of, you know, the the age of uh
[54:56] geology and the Earth. We still are
[54:58] around like that.
[55:00] Uh and so, I think that we will still
[55:02] love life.
[55:03] Most of us will still love life and
[55:04] enjoy every moment. But we'll get more
[55:06] opportunities. We can try multiple
[55:08] careers. Maybe we we we will get
[55:10] divorced and find have a whole new life.
[55:13] So, there will be opportunities, and it
[55:15] will be a a magnificent world.
[55:17] Not to mention the productivity that
[55:19] humans can provide with the the
[55:21] knowledge
[55:23] of a 58- or 80-year-old, but with the
[55:26] body of a 30-year-old.
[55:28] Do you think people will make different
[55:30] decisions about having children?
[55:31] Well, I think we have a problem already
[55:33] with the decisions that a lot of couples
[55:35] are making, which is leaving it too
[55:37] late. Um
[55:39] it's very clear with the fertility rate
[55:40] and the rate of childbirth that
[55:43] basically we're going off a cliff.
[55:45] And I I think that
[55:48] it's going to be important to be able to
[55:50] give couples and women especially the
[55:53] choice to have children
[55:54] for longer.
[55:56] And that's one of the reasons that I
[55:56] work on this topic is that I think that
[55:58] the world with all of the the training
[56:00] that we need to do and the pressures on
[56:02] finding a mate
[56:04] and being happily married or or at least
[56:06] being partnered up,
[56:07] that can take decades to get the right
[56:09] person. You don't want to rush into it
[56:10] like people used to.
[56:12] And being able to have children in your
[56:13] 50s and 60s, I think, would be a great
[56:16] gift to humanity. That's my personal
[56:18] view. Some people may, you know, for
[56:20] whatever reason disagree with that, but
[56:22] I think that the pressures to have
[56:23] children before 35
[56:25] typically are just extreme and and
[56:28] unfair.
[56:29] But also that it'll help
[56:31] us maintain the human population cuz by
[56:33] 2050 we're going to start
[56:35] going in a bad decline and earlier in
[56:37] many Western countries. And without
[56:39] humans, you know, absent Android robots
[56:42] everywhere, we're going to have a
[56:44] deficiency of human capital and human
[56:46] productivity. And this is I would argue
[56:49] with Elon
[56:51] that this is the best solution to that
[56:53] uh lack of humans is just keep people
[56:55] healthy and alive and productive for
[56:57] longer.
[57:03] Woah. What's that on your face?
[57:04] >> This is my BonCharge face mask. I've
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[58:01] New year always has a strange energy to
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[58:10] the new year. I'm guilty of that, too.
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[59:02] You mentioned uh cancer earlier on as
[59:04] something that you're working on in your
[59:05] laboratory. What progress have you made
[59:08] in your laboratory, and what has that
[59:09] taught you about what the nature of
[59:10] cancer, but also how we might prevent
[59:12] and cure it someday? Cuz I I was reading
[59:14] that in your laboratory you have been
[59:16] able to
[59:18] slow the growth of certain cancer cells
[59:20] and kill those cancer cells completely.
[59:22] Yeah, uh so, my
[59:24] my wonderful student Nallath uh is is it
[59:26] doing a PhD on this.
[59:29] And what we've hypothesized and now
[59:31] tested is the idea again based on the
[59:34] information theory of aging is that
[59:36] cancer is
[59:38] expressing those genes differently.
[59:41] In the same way that aging is is a
[59:43] cellular identity crisis, cancer is a
[59:46] cellular identity crisis.
[59:48] And that
[59:49] if we can rejuvenate an old cell to be
[59:52] normal and turn on the right genes
[59:53] again, we should be able to do that for
[59:55] a cancer cell. Mhm. And either make it
[59:57] normal
[59:58] or if it tries to be normal and wakes up
[60:02] from its zombie-like state, it might
[60:04] even kill itself. And that's what we're
[60:06] finding in my lab. Now lots of work has
[60:09] shown that a majority of cancers that
[60:12] we've grown in the lab
[60:14] will die and shrink in an animal if you
[60:18] try to reverse their age.
[60:20] Through the injection
[60:23] that you were referring to earlier on.
[60:24] >> Yeah, we can do it a couple of ways. One
[60:26] is using those three genes that
[60:28] rejuvenate the epigenome and make cells
[60:31] young again. Yeah. The one for the eye,
[60:33] the same technology for the eye we're
[60:35] using in cancer cells.
[60:37] But we also have this chemical drink
[60:39] that we can give to animals or to put on
[60:42] the cells and that also wakes the cancer
[60:45] cells up, tries to they try to become
[60:47] more normal, they turn on the original
[60:49] set of genes that they might have had on
[60:52] 30, 40 years ago. Some of these cancer
[60:54] cells that we grow in the lab were
[60:55] from the 20th century.
[60:58] We rejuvenate them, we turn on those old
[61:00] those genes that were originally in the
[61:02] normal tissue
[61:04] and the cells kill themselves. And so I
[61:06] believe that
[61:08] we may not be able to cure all cancer
[61:10] using this. That would be crazy to even
[61:11] say that. But I do believe that if we're
[61:14] successful rejuvenating the human body,
[61:16] cancer is not
[61:19] going to be a risk and that's just a
[61:21] nice
[61:23] side effect of what our original mission
[61:25] was, which was to treat aging. So from
[61:29] this we can start to try and understand
[61:31] what we think is causing cancer. And I
[61:33] guess this goes back to the a lot of the
[61:35] carcinogenic behavior that you described
[61:37] earlier, things like smoking, anything
[61:39] that's applying stress on the DNA. Is
[61:41] that like a Yeah, you have to break the
[61:43] DNA. Okay.
[61:45] >> That's the
[61:46] a catastrophe is really broken DNA, but
[61:48] you can do other things that are
[61:49] catastrophes like overheat the cells, um
[61:52] even mechanical stress.
[61:55] I don't know.
[61:56] Too many hits on the brain in football
[61:58] will will do that. So yes, uh that's
[62:01] exactly right and that drives aging and
[62:04] aging drives cancer, by the way. One of
[62:06] my theories called the geronco-genesis
[62:08] hypothesis. Terrible name, but
[62:11] nevertheless, geronco-genesis it it is.
[62:14] It's the idea that as we age, we're
[62:16] becoming more cancer-like as as a as a
[62:18] human.
[62:19] Our metabolism when we're old is closer
[62:22] to
[62:23] heading towards what a cancer cell's
[62:25] metabolism is like. So that when we
[62:26] actually do get cancer, the cancer cells
[62:29] grow better in an old person than when
[62:31] you're young. And so by rejuvenating
[62:33] those cancer cells, giving them the
[62:36] the ability to
[62:38] be young again, they actually either
[62:40] slow down in their growth or as I said,
[62:42] kill themselves in response. I've got a
[62:44] bit of a a prop here which might be
[62:47] useful for the the context of
[62:49] >> Oh goodness, does
[62:50] There are people here that may not know
[62:52] what I'm holding in my hands, but uh for
[62:54] those of you who don't know and who are
[62:56] just listening, I'm holding a record
[62:59] uh in my hands, a vinyl record uh that
[63:02] Steven just handed me.
[63:04] So the the information theory of aging,
[63:07] uh the analogy that I used is that it
[63:09] disrupts information and so this record,
[63:11] this album has information on it.
[63:14] It's music and just like DNA, it's
[63:17] information. So instead of the DNA
[63:20] information the the control of the DNA
[63:22] getting messed up, it
[63:23] in the album, it's like scratching this
[63:26] album.
[63:27] So I'm literally going to scratch this
[63:28] album. Is that okay with you?
[63:29] >> Yes, you can. All right. I'm not sure I
[63:31] can fix it, by the way. It may be a
[63:33] one-way thing, but
[63:35] I've never done this before, but yeah,
[63:38] that's painful.
[63:40] Maybe you can hear that happening.
[63:43] So if we were to play this on a record
[63:45] player with a needle, it's going to jump
[63:48] around and it's going to read the wrong
[63:49] songs or it's it's going to certainly
[63:51] not sound very good. So that's that's
[63:54] now the equivalent of an old cell. The
[63:56] information, the beautiful music is
[63:59] there, but the ability to read it has
[64:01] has been messed up. In the same way that
[64:03] old age, the information is in the DNA,
[64:05] but you the cells don't read it
[64:07] correctly. And what our technology is is
[64:10] to get rid of those scratches and so we
[64:13] can play the beautiful music of our
[64:14] youth again.
[64:16] Um I have got this You told me to to
[64:19] bring my weighted vest and this neck
[64:22] brace.
[64:23] Oh my goodness. I got I think I put it
[64:25] on the wrong way. Okay. If any anyone
[64:27] listening, Steven's putting on a very
[64:29] heavy jacket right now with lead weights
[64:31] and a strap around his neck to limit his
[64:33] neck movement. Oh, wow.
[64:36] That's a lot. This So I'm I just I put
[64:38] on a 20 I think it's 20 kg. My son's
[64:41] weak now. Um
[64:44] jacket and a neck brace.
[64:47] And ahead of this conversation, my team
[64:49] told me to get one of these.
[64:50] What is the analogy here that you're
[64:52] you're creating? This is very
[64:55] It's bad, right?
[64:56] >> It's hard, yeah.
[64:57] >> Right. Imagine
[64:58] the feeling like that for a decade.
[65:00] That's old age. You would feeling tired,
[65:03] weak, you can barely hold your body up,
[65:06] you can barely move your neck. It would
[65:07] be painful. You're not in pain yet. No.
[65:09] But most people in their 80s have
[65:12] some sort of disease and aches and
[65:13] pains.
[65:15] Try doing that for another 10 minutes.
[65:17] Maybe How long you can you keep that on?
[65:19] I'll keep it on for another 10 minutes.
[65:21] But so why is this cuz it just it's
[65:23] weight and immobility. I can't move my
[65:26] neck the same. My shoulders feel
[65:29] heavier.
[65:30] How how is this a relevant analogy to
[65:32] aging? Because it just it just kind of
[65:33] feels like immobility and weight. Uh
[65:36] well, I have to come over there and use
[65:38] this pair of scissors to be stabbing you
[65:40] as well so if you can feel pain as you
[65:42] move as well. That's part of old age. It
[65:45] is not a fun thing being old. And most
[65:48] old people, the reason that they don't
[65:50] love life anymore is because they feel
[65:52] like you do or worse.
[65:54] Not to mention the fact that they're you
[65:56] need to put Vaseline on your eyes,
[65:59] earplugs in your ears if you want to
[66:01] know what it's like being old. Oh god,
[66:04] it's not nice. Mhm. Or even worse, shut
[66:06] your eyes and you can never open them
[66:08] again.
[66:10] That's what it's like for those patients
[66:11] that we hope to cure blindness in.
[66:14] If if I'm going to ask you a really
[66:15] tough question, which is if I put a
[66:17] calculator in front of you right now and
[66:19] you had to hit a number on that
[66:20] calculator and then hit enter and that
[66:23] was the age that you were going to live
[66:24] to and you had to make that decision
[66:26] now,
[66:27] what number would you hit on that
[66:29] calculator? Infinity. Really? So you did
[66:32] 9999999.
[66:33] >> There's no day if you're healthy where
[66:35] you want to die.
[66:37] Even if you're 100, 120, if you have
[66:39] friends, family, loved ones, you're
[66:41] healthy,
[66:42] would you say okay, tomorrow I'm ready
[66:44] to die? No. No. Unless there was some
[66:47] kind of psychiatric issue or something.
[66:48] >> Exactly. Right? So that's my point is
[66:51] when people say, "Oh, when I'm 80, kill
[66:53] me." That is That's Excuse my
[66:55] language. Am I allowed to swear on this?
[66:57] >> Yeah, of course you can. Um Sorry, we're
[66:59] going to beep over the curse words. It's
[67:00] It's only when you're sick or you have
[67:03] depression that you want to leave the
[67:05] leave this world. Otherwise, life is a
[67:08] joy for most people on in the world. Not
[67:10] everybody and we have to fix that as
[67:11] well. But for most of us,
[67:15] being alive is is the greatest gift of
[67:17] any, mhm, you know,
[67:19] collection of atoms.
[67:21] Consciousness is even greater.
[67:23] And why would you want that to end?
[67:26] Who would choose that if they had the
[67:28] alternative to be with family and
[67:30] friends? Interesting.
[67:32] I say that's interesting because I have
[67:34] always assumed that I wouldn't want to
[67:36] live forever, but the when when you
[67:39] asked me if I was healthy
[67:42] and I had my friends and family and I
[67:44] was doing [clears throat] things that I
[67:45] loved professionally, would there come a
[67:47] day where I would choose to go now? No,
[67:50] there wouldn't. Just like there hasn't
[67:52] come a day in the last 33 years where
[67:54] I've chosen to go now. Mhm.
[67:57] Exactly. Do you think it's it's going to
[67:59] be possible in the next 50 years for us
[68:02] to live forever?
[68:04] I'd be shocked if that happened, but
[68:07] I've been shocked my whole career at how
[68:09] fast this technology is moving. And now
[68:10] with AI, things are going so fast, my
[68:12] head's spinning.
[68:14] So I'd be happy to be proven wrong, but
[68:16] I'm I'm skeptical that we could live
[68:18] forever in my lifetime, at least.
[68:21] But as I said, you're probably you're
[68:22] probably going to live you are going to
[68:24] live into the 22nd century.
[68:26] We can't imagine what the the world's
[68:28] going to be like then. And AI has really
[68:30] changed this equation. Oh, absolutely.
[68:33] We're We're doing things in my lab that
[68:35] would have taken 160 years before. And
[68:38] and quite literally billions of dollars
[68:41] on a 10 $10,000 budget.
[68:43] Well, I guess I better make it to 2040.
[68:46] Um so let's talk about fasting and food
[68:49] and nutrition and get go a little bit
[68:51] deeper on that. I've had so so many
[68:53] conversations over the years about this
[68:54] subject of fasting, but um as I was
[68:57] reading your research, you really do
[68:59] feel that fasting, just eating less
[69:02] often,
[69:04] is one of the most important things that
[69:05] we can all do for longevity. I I do. I
[69:08] do and I practice it as much as I can,
[69:10] though it's challenging in a world
[69:11] that's full of abundant food.
[69:13] But yes, we've known for thousands of
[69:15] years. The ancients are not dummies.
[69:18] They They could witness what happens
[69:19] when you fast.
[69:21] Uh clarity of mind, long-term health.
[69:24] They could observe the difference
[69:25] between the gluttons and the people that
[69:27] fasted for religious reasons. It's
[69:28] obvious.
[69:29] But there's certain ways to do it.
[69:30] Fasting doesn't include malnutrition.
[69:32] You have to do it with abundant, you
[69:35] know, vitamins, minerals. You want to
[69:36] make sure that you're you you have
[69:38] adequate nutrition.
[69:40] But I think three meals a day is is
[69:42] craziness. It turns out this idea
[69:44] breakfast is the most important meal of
[69:45] the day
[69:46] is marketing from the early 20th century
[69:49] by companies I will not name. But it was
[69:51] breakfast cereal. Breakfast is not the
[69:53] most important meal of the day for most
[69:55] people, especially adults.
[69:57] Especially if you're not hungry when you
[69:58] wake up. There's no point in eating if
[70:00] you're not hungry in the morning.
[70:02] I'm one of those people. So, I've
[70:03] skipped breakfast. How about you? Yeah,
[70:05] I'm the same. I'm the same. I don't eat.
[70:06] My first meal today was 3:00 p.m.
[70:08] because I had a podcast until, you know,
[70:10] 2:00 2:00 p.m. So, which is typical for
[70:12] me. I just don't get hungry in the
[70:13] mornings. Now, because of the marketing
[70:15] there for breakfast, sometime I've
[70:17] sometimes I've said to myself, "Oh, you
[70:18] should eat." And I'll make myself eat.
[70:20] But it's very very rare. I'm notoriously
[70:22] people know that I'm notoriously
[70:25] um a late eater. 4:00 p.m. sometimes,
[70:27] 5:00 p.m. if I'm in the office. How you
[70:29] feeling with that heavy vest on?
[70:30] >> It's heavy, David. I'm going to be
[70:31] honest. It's not I'm finding myself like
[70:33] trying to find a comfortable position.
[70:35] Yeah, it it's tough being old. And by
[70:37] the end of it, you will
[70:39] be so convinced that this research is
[70:41] important. Because to live like that,
[70:43] It's not in most people, life is not
[70:45] worth living.
[70:46] I put a suit, a very heavy suit like
[70:48] that, but on the arms as well, not just
[70:50] the body.
[70:51] And he had the the earmuffs and the the
[70:53] eyes. This was the the governor of
[70:56] Massachusetts. 15 minutes in that body
[70:58] suit, and he was crying. Not because he
[71:01] was in pain, because he as he said on
[71:04] stage, it was the first time in his life
[71:06] he understood how his father feels
[71:09] and could be empathetic.
[71:11] We, young people, I'm relatively young,
[71:13] 56. You're very young, 33.
[71:15] We have no idea what it's like to be
[71:17] old.
[71:18] It can be horrific. So, why wouldn't we
[71:20] do the right things like fasting,
[71:24] exercising, [clears throat]
[71:25] so we can get an extra 10 years, maybe
[71:28] longer of healthy life. It does also
[71:30] give me a lot of empathy for people that
[71:33] have a bit more weight on them as well
[71:35] because if, you know,
[71:37] if I was if I weighed that much, I don't
[71:39] know if I'd be very active to to be
[71:41] completely honest with you.
[71:41] >> Exactly. And and you're in pain, too.
[71:43] Don't forget. Every joint can be
[71:45] hurting. How do you feel taking that
[71:46] off?
[71:46] >> Much better.
[71:48] Right. Free. Like I want to jump. So,
[71:50] let's
[71:52] hope, pray, wish
[71:55] that these technologies that I'm talking
[71:56] about today work.
[71:58] Cuz that could be what it feels like to
[72:00] be rejuvenated when you're 80.
[72:03] Hm. I hope so. [clears throat]
[72:04] Um to close off on this point of of a
[72:06] fasting, why why does it help extend my
[72:08] life?
[72:09] >> Yeah. Just eating less. Part of it came
[72:11] out of research in my lab, but of course
[72:12] many others I need to give credit to.
[72:15] But in my lab specifically, what we
[72:16] worked on initially when I started, we
[72:19] studied yeast cells.
[72:21] Little microscopic cells that, as
[72:23] everyone knows, we use to make beer and
[72:25] bread and champagne.
[72:27] These yeast cells live about 10 days and
[72:29] then they die. And we used yeast as a
[72:31] model for aging.
[72:32] And what we discovered with yeast cells,
[72:34] which turns out to be true in our
[72:35] bodies, is that adversity, as long as
[72:38] it's not killing these cells, is good
[72:41] for you.
[72:42] It's called hormesis.
[72:44] It's the technical term for what doesn't
[72:45] kill you makes you stronger and live
[72:47] longer.
[72:48] Adversity mode is what we're aiming for.
[72:51] The opposite
[72:52] is abundance mode, which is what modern
[72:54] life is all about.
[72:56] Popcorn, movies, wheels on your
[72:59] suitcase, sitting down all day.
[73:02] It's we're in an abundance world. So,
[73:05] adversity is something we don't often
[73:06] feel. We have to work at it.
[73:08] Fasting is adversity.
[73:10] Exercise is adversity. Cold plunges,
[73:12] saunas, adversity.
[73:14] Adversity mimics. They're not really
[73:16] threatening your life. What happens at
[73:18] the cellular cellular level
[73:20] is that those cells,
[73:22] they get freaked out. They're worried
[73:24] that these times of adversity could kill
[73:27] us, so they fight back.
[73:29] They turn on repair systems. They turn
[73:31] on recycling systems.
[73:34] They turn on DNA repair systems that
[73:36] help slow down aging.
[73:38] So, in this modern world we when we have
[73:40] total abundance, we don't have to
[73:41] exercise, we don't don't we eat three
[73:42] meals a day,
[73:44] we get overweight, we don't sleep much,
[73:46] we have air conditioning in summer,
[73:48] we're actually aging faster than we need
[73:50] to cuz our bodies are not fighting aging
[73:53] like they do when they feel adversity.
[73:56] Your team discovered I can't say the
[73:58] word sirtuinous.
[74:00] Oh, well. I was one of many scientists
[74:03] in the 1990s.
[74:04] Uh I was part of a team called sirtuins.
[74:07] Yeah.
[74:07] >> Sirtuins. Yeah.
[74:09] Yeah, that in yeast, actually. That's
[74:11] right. Uh
[74:12] That's a good story. I went to the US
[74:16] to figure out why we get old. But I
[74:18] didn't choose to study humans cuz I
[74:20] figured
[74:21] if we can't figure it out for little
[74:23] yeast cells, we'll never figure it out
[74:24] for humans. So, I went to MIT. My
[74:27] professor was Lenny Guarente. I went to
[74:30] his lab and I said, "I'm I'm not going.
[74:31] I'm not leaving." The goal was to in my
[74:34] mind was to figure out are there
[74:36] longevity genes? At that time, most
[74:38] people thought that there were aging
[74:40] genes that caused aging, death genes.
[74:43] That doesn't make any sense to me. Our
[74:44] bodies would have longevity genes that
[74:46] give life.
[74:47] So, in yeast I went searching for them.
[74:49] And out of that work came two things.
[74:52] The first is Lenny and I, my professor
[74:54] and I published
[74:55] in the journal Cell, which was a massive
[74:57] big deal in those days, still is. It was
[74:59] my first time. The first
[75:02] evidence for a cause of aging for any
[75:04] species.
[75:06] We figured out why yeast cells get old.
[75:08] Do you want to guess?
[75:09] Hm. Why do yeast cells get old?
[75:13] >> Have you been paying attention? What
[75:14] does the information theory of aging
[75:16] say? I was going to say they have an
[75:17] identity crisis, but They do. How would
[75:20] we know if they have they're having an
[75:21] identity crisis?
[75:22] >> Oh, you can measure the identity of
[75:23] yeast cells. They have an identity. It's
[75:26] called their mating type. The main
[75:27] identity of a yeast cell is they are
[75:29] either A type or alpha type.
[75:32] Male, female.
[75:34] And the hallmark of a yeast cell that's
[75:37] old is it loses
[75:39] its A and alpha identity
[75:42] and gets
[75:43] an identity crisis. It doesn't know what
[75:45] sex it is and it doesn't mate anymore.
[75:47] Becomes sterile.
[75:49] So, when I arrived at MIT in 1995, we
[75:52] knew that the hallmark of an old yeast
[75:54] cell, besides of being a bit slow and
[75:56] bigger, is that it became sterile.
[75:59] It had an identity crisis. So, we
[76:00] figured out that broken chromosomes
[76:04] distract the sirtuin defenses
[76:07] and that causes aging in a yeast cell.
[76:10] But we didn't know in the '90s that that
[76:12] was going to be true for us as well. It
[76:14] took another decade or two to figure
[76:16] that out. And how does this link to
[76:17] eating all the time? Yeah. So, sirtuins
[76:20] are proteins that actually are attracted
[76:24] to DNA.
[76:25] They actually associate with it and they
[76:26] protect
[76:28] uh
[76:29] the DNA from getting damaged. Okay, like
[76:31] bodyguards. Yeah. And they repair broken
[76:33] chromosomes. Right? It's all coming
[76:35] together now.
[76:36] But they also get distracted. So, look,
[76:39] a sirtuin's normal job, if there's no
[76:41] crisis, is that they turn genes on and
[76:43] off. They are epigenetic regulators.
[76:45] They control the epigenome. They tell a
[76:48] cell what type it is. Nerve cells, skin
[76:50] cells, right?
[76:51] >> Okay, conductor. Thank you. Conductor,
[76:53] exactly.
[76:54] But the conductor
[76:57] becomes demented over time.
[76:59] What happens is when you have a
[77:01] chromosomal break,
[77:03] the sirtuins panic. They leave the DNA,
[77:06] what they're supposed to be doing,
[77:07] controlling the cells' identity,
[77:09] and they go and they repair the DNA.
[77:11] That's their other job. They have two
[77:12] jobs. Identity and repair.
[77:15] So, when you have this break, the
[77:16] sirtuins go away. They repair the
[77:17] problem, but they don't all go back in
[77:20] the next few minutes. It's very quick.
[77:22] They don't all go back to where they
[77:23] started. So, you've got like this tennis
[77:25] match that the sirtuins are the balls
[77:28] and they get hit over to the break, then
[77:30] hit back.
[77:31] Most of them find the genes that they
[77:33] should go back to, but they don't all do
[77:35] that. And that total game of tennis, or
[77:37] ping pong if you like,
[77:39] is what I believe causes the identity
[77:41] crisis and aging itself
[77:43] causes aging in yeast cells. It's why
[77:45] yeast cells don't live longer than 10
[77:46] days. And I believe it's why we struggle
[77:48] to live beyond 80 or 90.
[77:50] So, if I'm eating all the time, then
[77:52] those sirtuins, they're not going to be
[77:54] doing their job as the
[77:56] the conductor, making sure I know the
[77:58] identity of my cells. They're going to
[78:00] be doing repair stuff.
[78:02] So, I'm going to age faster. Yes. And
[78:05] the breakthrough happened in the lab as
[78:07] I was just leaving to go to Harvard. I
[78:09] got a job at Harvard when I was 29.
[78:12] Super excited.
[78:13] And just as I was leaving, there was a
[78:15] big breakthrough that they actually kept
[78:16] it secret from me cuz I they were
[78:18] worried I was going to work on it when I
[78:20] left.
[78:21] And in fact, my professor tried to
[78:22] prevent me from working on it when I
[78:24] left.
[78:25] On sirtuins in general. Crazy to think
[78:27] about, but
[78:28] what they discovered
[78:30] was that there's a
[78:31] a metabolite, a molecule,
[78:34] that goes up and down with food and up
[78:36] and down with sleep
[78:38] called NAD.
[78:40] We have lots of it. There's grams of it
[78:41] in our body. It's one of the most
[78:42] abundant molecules in the body. It's
[78:43] very ancient. It's in yeast. It's in us.
[78:46] And what they found was that sirtuins,
[78:49] to control genes and to repair DNA
[78:52] that's broken,
[78:53] they don't do it unless there's NAD.
[78:56] It's the catalyst. It's the fuel for
[78:57] their reaction. They need NAD.
[79:00] And when we're young, we have lots of
[79:02] NAD. So, it works well. The sirtuins
[79:04] control the information on the genes and
[79:07] they repair the DNA very well cuz
[79:09] they've got lots of NAD to carry out
[79:11] their their work. These are enzymes.
[79:13] They work. They do things.
[79:15] As we get older, by the time you're 50,
[79:17] about my age, you have half the levels
[79:20] of this NAD molecule.
[79:21] My body is making less NAD and it's also
[79:24] destroying the NAD faster than when I
[79:26] was 20.
[79:28] That's a problem. And so what we found
[79:30] was that when we fast the yeast
[79:32] or we fast a human,
[79:34] NAD levels go up again.
[79:37] So fasting raises NAD and makes the
[79:39] sirtuins
[79:40] young again, essentially. And that
[79:42] preserves the epigenome and it also
[79:44] repairs the DNA better. So can I just
[79:46] drink NAD? Uh you can drink NAD and not
[79:49] much would
[79:50] How How do I happen? How do I take NAD?
[79:52] Uh so NAD can be taken as a supplement,
[79:54] which is a pre-precursor to NAD. It's
[79:57] better to take the precursors. A
[79:59] precursor meaning something that creates
[80:00] it. Exactly. There's one called NMN,
[80:03] not to be confused with M&M's, which
[80:05] will probably not make you live longer.
[80:07] And there's another one called NR. NMN
[80:09] is directly converted into NAD. You put
[80:11] two NMNs together, you get NAD in cell.
[80:13] We know this for a fact. This isn't
[80:14] isn't speculation. When you give a human
[80:16] NMN by swallowing it, a gram of it,
[80:19] you can you typically double the amount
[80:21] of NAD in your body. And we believe, and
[80:24] we have some evidence now in human
[80:25] clinical trials,
[80:27] that the sirtuins are imparting health
[80:29] benefits,
[80:30] reestablishing the epigenome,
[80:32] lowering body weight,
[80:34] uh improving inflammation,
[80:36] uh and even changing cholesterol levels
[80:38] in a positive way in humans.
[80:40] So I mean, I'm assuming you take NMN.
[80:43] I've been taking NMN and admitting that
[80:45] publicly uh for a while now. And my
[80:48] father, who
[80:49] is uh an even
[80:51] more advanced uh experiment at 86.
[80:55] So yes, we've been taking it for over a
[80:56] decade now. And we're still alive, so so
[80:59] far, so good.
[81:00] >> So far, so good. I do want to get into,
[81:01] and I will ask you in a second, about
[81:02] the the supplement stack that you would
[81:04] recommend for the average person. Um but
[81:06] that's good to know. But just to close
[81:07] off on this point of fasting,
[81:10] is there a particular type of fasting
[81:12] method that you would recommend
[81:15] for someone who's trying to, you know,
[81:16] improve their longevity?
[81:18] Cuz there's so many that I hear say 16
[81:20] hours, 5 days. I'm a scientist, so I go
[81:22] with what's proven. I'm not selling
[81:24] anything. So what the science says,
[81:26] first of all, is that there isn't one
[81:28] size fits all for everybody.
[81:30] Um it it often depends on what you can
[81:32] do personally.
[81:34] It's challenging to do this, right?
[81:36] You'll feel hungry for the first 2 weeks
[81:38] you try it.
[81:39] So I I would suggest
[81:41] the way I do it is I start by skipping
[81:44] one and then maybe 1 and 1/2 meals.
[81:49] Uh like what you do, try to go without a
[81:51] meal until 3:00, 4:00 if you can. Maybe
[81:55] not the first day, right? If you do that
[81:57] the first day, you'll say, "This is
[81:58] crazy. I'm I'm going to grab a snack."
[82:00] And you won't do it. So go slowly, build
[82:02] up to it. So the first day, I would say
[82:04] just don't eat breakfast and maybe have
[82:07] a snack mid-morning.
[82:08] A week later, try to go without
[82:10] breakfast completely until lunch.
[82:13] And eventually work up to what you do
[82:14] and I do, which is eat a very late lunch
[82:16] if not go to dinner. What you get with
[82:18] that is obviously not eating in bed,
[82:21] hopefully. So you've got that the night
[82:23] fast starting
[82:25] what would it be? 7:00 p.m. roughly when
[82:27] do you finish dinner? God, no comment.
[82:29] Okay. It's usually pretty late. Last
[82:31] night it was, you know, it was This is
[82:32] probably why I don't eat very early the
[82:34] next day. Last night would have been
[82:36] about, I'm going to say, 10:00 p.m.
[82:39] Okay. It was super late. It was That's
[82:41] an extraordinary example. Usually it
[82:42] would be
[82:44] 8:00 or 9:00 p.m.
[82:46] Okay, but but you've got at least 13, 14
[82:48] hours, which is good. Yeah. I aim for 14
[82:50] hours. Some people go 16 hours, but
[82:52] that's a good start for fasting.
[82:55] And hopefully you can do that most days,
[82:56] 5 days a week. Mhm. That's great, cuz
[82:59] that means that you're turning on your
[83:00] sirtuins, raising your NAD. You're
[83:02] exercise You exercise as well, so that's
[83:04] also adding to it. One thing that I've
[83:06] started doing is fasting for longer than
[83:10] just
[83:11] 14, 16 hours. I try maybe once a month
[83:14] to go for 3 days without eating. Why?
[83:17] Because there's a type of cellular
[83:19] recycling that doesn't happen
[83:21] within the first 16 hours.
[83:24] Um you will enter ketosis, so you'll see
[83:26] your body will start to change its
[83:27] metabolism to produce what's called
[83:28] ketone bodies.
[83:30] But the true, real, deep clean cleansing
[83:33] of old proteins and damage
[83:36] damaged proteins happens after
[83:39] 2 and 1/2 to 3 days. And it's called
[83:41] chaperone-mediated autophagy. Autophagy?
[83:44] Autophagy is the word for
[83:46] auto, self-eating.
[83:49] And it really kicks in
[83:51] for with an extended fast. What's the
[83:52] evolutionary reason for that? What's
[83:54] going on there? Why does it take me 2
[83:55] and 1/2 days for this deep clean to
[83:56] happen? Uh cuz your body doesn't want to
[83:59] uh do it. It costs a lot of energy and
[84:02] having to remake body parts is energy
[84:04] expensive. And our body tries to
[84:06] conserve energy as much as possible.
[84:09] Uh when you're fasting, what it'll it
[84:10] needs to do is to use your body as fuel.
[84:14] So it'll start breaking down proteins
[84:16] for fuel that you need. So first of all,
[84:18] what will happen is in the first few
[84:20] hours, you use glycogen from your your
[84:21] liver. Your liver makes glucose.
[84:23] You'll feel a little bit hungry, but
[84:24] you'll eventually be fine.
[84:26] Then once you run run out of glycogen,
[84:28] then you're going to start breaking down
[84:29] fat and making ketones.
[84:32] Uh that's when you start to get a bit of
[84:33] bad breath from
[84:35] from that. And you but you feel great.
[84:37] When you're in a
[84:38] between about 15 hours and 24 hours,
[84:42] that's when you get a lot of ketones.
[84:43] And your brain uses those for fuel, so
[84:45] you'll have sharp mind, can remember
[84:47] things, you can focus on work if you
[84:49] ever get there.
[84:51] Beyond that, you need to break down fat.
[84:53] And uh
[84:54] that is uh when your body is
[84:58] starting to do that. But ultimately,
[85:00] what what what happens after 3 days is
[85:01] your body says,
[85:03] "Hey, I'm going to start breaking down
[85:04] protein as well."
[85:06] And uh
[85:07] I wouldn't do that often because I don't
[85:09] want to break down a lot of protein, but
[85:10] your body will start to turn over old
[85:12] proteins preferentially.
[85:14] And a little bit of that, that's why I
[85:15] do it maybe once a month,
[85:17] has been shown, at least in animals, to
[85:19] be not just healthy, but life
[85:21] extending.
[85:22] On that point of ketosis,
[85:25] um
[85:27] I like being in a state of ketosis. I
[85:30] kind of cycle in and out of it during
[85:32] the year,
[85:33] because I get so many of the like
[85:34] cognitive benefits. I'm more articulate
[85:36] on the podcast, I can think better.
[85:38] I feel better. I feel more focused and
[85:40] more attentive.
[85:42] Is ketosis
[85:44] is the ketone diet
[85:46] the keto diet a healthy diet
[85:48] in your view? Is it What are the
[85:49] benefits of it? Is it something that you
[85:51] think is natural to be recommended?
[85:53] >> Well, I don't mind being controversial,
[85:54] but I do speak the truth. Um there's not
[85:57] a lot of evidence that long-term the key
[85:59] ketogenic diet is healthy. Mhm. It
[86:01] certainly doesn't correlate or associate
[86:03] with uh longevity.
[86:05] Short-term, okay. It does help people
[86:07] lose weight, no question.
[86:09] Uh but I am rather concerned for people
[86:11] that don't have a balanced diet with an
[86:14] input of plant material, which has
[86:17] molecules that are unique to plants and
[86:19] you won't find
[86:20] in high-processed foods uh or meat.
[86:24] The evidence, speaking as a scientist,
[86:26] is that the long-term ketogenic diets
[86:29] are not
[86:30] going to be longevity inducing.
[86:33] The evidence is more having a lean diet
[86:36] with a focus on plants that are not
[86:38] overcooked and not all ultra-processed.
[86:41] That one is undoubtedly the healthiest
[86:44] if you can do it. Do you eat meat? I do
[86:47] eat meat, but not like I used to.
[86:50] I used to think that a meal was not a
[86:52] meal unless I had a piece of meat there
[86:54] and then the vegetables were the
[86:55] decoration.
[86:56] And I'd begrudgingly eat the green
[86:58] stuff.
[86:59] I've been flipped totally. Um Serena, my
[87:02] partner, Serena Poon, is not just a
[87:04] nutritionist, but a longevity expert for
[87:06] the last 26 years. And so she came to my
[87:10] apartment, uh which is now our
[87:12] apartment, and she just cleared out all
[87:13] the food that I had. Pretty much
[87:14] everything was either toxic or uh or
[87:18] just not healthy. It was
[87:19] ultra-processed. She said, "What are you
[87:21] eating? That kind of
[87:22] peanut butter, you know, full of sugar."
[87:24] So she she's taught me how to live
[87:26] healthy. And so now
[87:28] I rarely eat meat. I rarely drink
[87:30] alcohol. I focus on
[87:33] really fresh, high-quality
[87:35] uh preferably organic foods, cuz I don't
[87:37] want pesticides and I I don't want other
[87:39] contaminants.
[87:41] But I do know organic can be more more
[87:43] expensive.
[87:44] Why not meat?
[87:46] So animals, unfortunately, don't make
[87:48] what are called polyphenols, which are
[87:50] a type of molecule that uh I believe uh
[87:54] and have evidence
[87:56] turns on the sirtuins and other
[87:58] pathways, biochemical reactions that
[88:02] delay aging. So sirtuins are just one of
[88:05] a few
[88:06] enzymes that control aging. We know
[88:08] this. There are sirtuins, there's mTOR,
[88:11] which responds to aminos, and another
[88:14] one called AMPK. So those three pathways
[88:17] are altered in just the right way by
[88:20] molecules found only in plants. Well,
[88:23] and a small extent in fun- fungi, but
[88:25] not in meat.
[88:27] So if you're not eating a lot of
[88:28] vegetables or fruits, you're not getting
[88:30] these
[88:31] molecules. They're like medicine as
[88:33] food.
[88:34] So right
[88:35] here, I hope you don't mind me
[88:37] mentioning that there are some some food
[88:39] in front of us. And I'm looking at
[88:40] blueberries here. Blueberries are packed
[88:43] with polyphenols. It's one of the
[88:44] reasons they have purple color is that
[88:46] polyphenols have the color. And as
[88:48] Serena would tell you, eat the rainbow.
[88:51] I call it xenohormesis, which is not as
[88:53] attractive. But xenohormesis is the same
[88:55] idea as eat the rainbow, that by eating
[88:57] plants that have a lot of these
[88:59] molecules that are often produced by
[89:01] stressed plants, What do you mean
[89:03] stressed? stressed plants. So plants
[89:05] will be stressed just like we are. If
[89:07] you don't give them enough water, food,
[89:09] too much sunlight, not enough not enough
[89:11] sunlight, they in their defense, they
[89:15] they polyphenols.
[89:16] There's a whole bunch of them.
[89:17] Resveratrol, fisetin, quercetin, there's
[89:20] there's hundreds.
[89:21] Uh this one has um anthocyanidins,
[89:24] that's the color. These activate
[89:27] these adversity responses in our cells.
[89:31] The sirtuins will get activated by
[89:33] molecules in this blueberry. So if I eat
[89:36] this blueberry,
[89:38] those conductors that conduct some of
[89:41] the aging process you talked about,
[89:43] making sure my cells don't have an
[89:44] identity crisis,
[89:46] fixing the
[89:48] the the negative stress that's going on
[89:50] in my um
[89:51] in my cells, they will be
[89:54] benefited by me eating this blueberry?
[89:57] Yeah, it's it's like a a free hack,
[89:59] right? You can eat something that's
[90:00] yummy, but you're also getting the
[90:03] benefits
[90:04] by mimicking fasting and exercise in
[90:06] your food as well.
[90:08] The sirtuins don't just need NAD. That's
[90:11] the gas pedal. That's the petrol for
[90:13] those of you in the British world and
[90:15] Commonwealth. The fuel for sirtuins
[90:19] is NAD. The accelerator pedal
[90:22] are the polyphenols in fruits and
[90:24] vegetables like resveratrol, quercetin,
[90:27] which we know
[90:29] when you give them to sirtuins,
[90:31] they get hyperactivated. And when you
[90:32] say eat the rainbow, you mean eat
[90:35] colorful looking food.
[90:37] Because that's an an easy way to
[90:38] remember how to eat foods that have the
[90:41] most polyphenols.
[90:43] I'll give you a really good example,
[90:44] Steven.
[90:45] Serena put me onto green tea matcha.
[90:48] Right? So matcha tea, if you haven't
[90:49] tried it, uh I'm sure you've tried it,
[90:51] but those of you who haven't tried it, I
[90:53] highly recommend it. It It tastes great.
[90:55] The reason for it switching from coffee
[90:58] mainly to matcha in the morning for me
[91:01] is that it's full of polyphenols. Why is
[91:04] it full of polyphenols?
[91:06] It's not just because it's green tea,
[91:07] which is not naturally healthy, but the
[91:09] growers of those plants in Japan,
[91:12] typically,
[91:13] they shade the plants before they
[91:15] harvest.
[91:16] Shading the plants stresses them out.
[91:18] Plants need light. So they don't just
[91:21] make more chlorophyll, which produces
[91:22] the deep green color in the tea,
[91:25] but the polyphenols are super high. And
[91:27] through trial and error over thousands
[91:29] of years, the Japanese figured out that
[91:31] by shading the plants, giving them this
[91:33] mild hormetic stress,
[91:36] it makes them not just extra tasty, but
[91:38] extra healthy.
[91:39] Same with red wine, by the way. But the
[91:41] alcohol can
[91:42] be an issue. But absent alcohol,
[91:45] red wine
[91:47] is very good for you.
[91:49] Okay.
[91:50] Without the alcohol. It's unfortunate.
[91:52] You know, I I
[91:53] one of my papers in 1996 caused red wine
[91:55] sales to go up 30% and stayed up.
[91:58] I apologize
[91:59] for saying that red wine every day was
[92:02] healthy. Doctors were recommending it,
[92:03] remember? Yeah. But I now changed my
[92:06] mind. I have to
[92:07] say
[92:08] that I no longer believe having one
[92:10] glass of red wine every day is healthy
[92:13] in my opinion. And I've stopped drinking
[92:15] red wine every day.
[92:16] Instead, I take polyphenols from red
[92:19] wine and from vegetables either in a
[92:21] pill or in my food as a substitute
[92:23] because
[92:24] the evidence for alcohol is rather
[92:26] damning. There's a UK Biobank study and
[92:28] the UK looked at thousands of people's
[92:31] MRI scan of their brain who were
[92:32] drinking one glass of alcohol a day
[92:35] and there was a statistical difference
[92:36] between people that were drinking one
[92:38] glass a day and were not in terms of
[92:40] brain size and gray matter. Of course,
[92:42] the gray matter was tended to be smaller
[92:44] in those that drank even slightly. Hm.
[92:47] Yeah, I do [clears throat] um I actually
[92:48] have a matcha company. It's It was this
[92:50] year voted the fastest growing company
[92:52] in the UK.
[92:53] Um it's by some
[92:55] some founders that I invested in, um
[92:57] Levi, Teddy, and Marissa
[93:00] from Dragon's Den, and it's been an
[93:01] absolute unbelievable uh
[93:04] business, unbelievable. So tell us Where
[93:06] do Where do I get it? Japan. You get the
[93:08] matcha from Japan, but the company's
[93:09] called Perfect Tea. People know about
[93:11] it, um
[93:11] cuz I've talked about it before, but I
[93:13] didn't realize when I made the
[93:15] investment that matcha was considered by
[93:18] many to also be very healthy, especially
[93:19] a health alternative to certain energy
[93:21] products on the market that you get in
[93:23] cans that give you
[93:25] um
[93:27] I shan't get sued.
[93:28] >> [laughter]
[93:29] >> But the other thing that um uh the
[93:30] company I invested in is this one here
[93:32] called uh KetoneIQ.
[93:34] I'm the co-owner of this company as well
[93:36] and
[93:36] >> Yeah.
[93:37] Yeah, I love that uh love that company
[93:39] and the CEO uh
[93:40] Michael, good guy. What's your thoughts
[93:43] on exogenous ketones? Like drinking
[93:45] ketones?
[93:46] I do it. In fact, that I drink KetoneIQ
[93:49] before I
[93:50] do a podcast. Why?
[93:52] It improves my clarity, I find. Um I
[93:55] also believe the science and there have
[93:58] been multiple studies now in people.
[94:00] In some of the the science comes out of
[94:02] KetoneIQ, but also independent studies
[94:05] have shown that it's extremely healthy
[94:06] for the heart.
[94:08] And uh there's new studies that show for
[94:10] the brain as well it can be healthy. The
[94:12] brain uses ketones like
[94:13] beta-hydroxybutyrate or in that one,
[94:15] it's 1,3-butanediol.
[94:17] Um just a shot of that will give the
[94:19] brain food that it needs rather than the
[94:21] body having to make it. Um and you get,
[94:23] I believe, and I feel it, I get the
[94:25] clarity of fasting without being in a
[94:27] fasted state. But I also drink it when
[94:29] I'm fasting to give it the body the
[94:31] extra boost that it needs. Hm. And on
[94:33] this point of diet, one of the things
[94:35] that I was told by my doctor when I did
[94:37] a like one of those blood tests, was he
[94:39] cautioned me about bad cholesterol.
[94:42] He said to me something along the lines
[94:44] that I need to be careful about
[94:46] cholesterol.
[94:47] And there's been lots of conversation
[94:49] about cholesterol, good, bad.
[94:51] What's your perspective on this
[94:53] conversation around bad cholesterol,
[94:54] which has been thought to increase
[94:56] um
[94:57] certain foods have been thought to
[94:58] increase bad cholesterol,
[95:00] um which is very very detrimental to our
[95:02] health.
[95:03] I didn't realize there was a debate. At
[95:05] least in my world, there is no debate.
[95:07] Um if you're referring to do you want to
[95:10] get your LDL cholesterol as low as
[95:13] possible? Yeah.
[95:15] Definitely. Oh, really? Okay, so it's
[95:17] Yeah, I mean the science is irrefutable.
[95:18] There's thousands of people in studies.
[95:21] Now, I think I know what you were you
[95:22] were talking about. There are There are
[95:23] some
[95:24] stories that you need cholesterol in
[95:27] your brain and if you inhibit it, you
[95:30] might affect your brain function.
[95:32] Um you also need it for repair of
[95:34] arteries.
[95:35] But there's no evidence that that's a
[95:37] problem. In fact, it's it's a
[95:38] little-known fact that the brain doesn't
[95:40] use
[95:41] the cholesterol from the bloodstream. It
[95:43] makes its own. So I've actually been on
[95:45] a statin to lower my LDL since I was 30.
[95:48] Really?
[95:49] Well, I had high cholesterol. It's in my
[95:51] family.
[95:52] But I
[95:54] went to my doctor and I said, I want to
[95:55] go on these new drugs at the time,
[95:57] statins. And he said, "Why? You don't
[95:59] have heart disease yet." And I said,
[96:01] "Why would I wait?
[96:03] Get me on it. I want to be on it." And
[96:05] in those days, it was very weird to give
[96:07] someone
[96:08] a statin at age 30 with no evidence of
[96:11] heart disease.
[96:12] But as you know, I'm of the
[96:15] opinion that we shouldn't wait till we
[96:17] get diseases to treat them. We should
[96:19] preempt that and start early in life.
[96:22] And so yeah, I insisted with my doctor.
[96:24] Initially with statins, but on all of
[96:26] these things, I go in and I say,
[96:28] "I need you to prescribe me this test. I
[96:30] need this medicine."
[96:31] And eventually, after talking it over
[96:34] with him, he typically prescribes me
[96:35] something or gets me a test.
[96:38] But I've been fighting the system. And
[96:40] my doctor's at Harvard, so he's a good
[96:42] doctor, but conservative. The old way of
[96:44] doing medicine is
[96:45] if you're not sick, we're not going to
[96:47] give you a medicine, certainly not if
[96:48] you're young and healthy.
[96:50] Uh but that has to change.
[96:52] >> So you're saying that I should be on
[96:52] statins potentially? Well, what's your
[96:54] LDL level? Not I don't think it's great.
[96:56] I think I eat too much bacon or
[96:57] something.
[96:58] Well, we can talk about food and
[97:00] cholesterol cuz it depends whether you
[97:01] absorb cholesterol or not. We can test
[97:04] for that. But if you do absorb
[97:05] cholesterol
[97:07] more than most,
[97:08] I would say that you may want to change
[97:09] your diet at a minimum. On this plate
[97:12] here in front of us,
[97:14] I have the
[97:16] top five foods that I believe you think
[97:18] are great for reversing aging. Am I
[97:21] correct? Does that Does that These are
[97:22] great choices, yeah. So what are these
[97:24] and why? So we've already done the
[97:25] blueberries and we've you've explained
[97:27] to me about polyphenols and they're rich
[97:28] in them, which I understand. Mhm. And
[97:31] they're low in sugar, right?
[97:32] Well, they're not low in sugar, so don't
[97:35] eat a ton of them. A handful is fine
[97:38] um as a snack.
[97:40] It's also known that having too much
[97:41] sugar is bad for longevity. Okay. Keep
[97:43] your blood sugar level steady and low as
[97:45] much as you can. So don't eat too many
[97:47] of those. A better choice than
[97:49] blueberries would be something like
[97:51] matcha, which is not full of sugar. In
[97:53] fact, if you go to some of these chains
[97:55] that sell matcha and it tastes really
[97:57] sweet,
[97:58] you're going to reverse the effects of
[98:00] any polyphenols by drinking that much
[98:02] sugar. So I always have unsweetened
[98:03] matcha. Okay. So now we've got avocados
[98:06] here. Yeah. Yep. Avocados
[98:08] uh they're not so much known for their
[98:09] polyphenols, though they do have them.
[98:12] It's the type of fats, the
[98:13] polyunsaturated fats. They help with
[98:16] satiety, so you're not going to be as
[98:17] hungry.
[98:18] Uh so if you put that on your sandwich
[98:20] at lunch, you're not going to feel
[98:22] peckish.
[98:23] And they're uh highly anti-inflammatory
[98:24] as well. The molecules that are in there
[98:26] in the fats are very good for you.
[98:29] Extra virgin olive oil? Oh, yeah.
[98:31] Excellent. So the type of uh oils that
[98:34] are in there are very healthy. There's
[98:36] omega-9,
[98:37] which is also known to activate
[98:39] sirtuins.
[98:40] And again, if you have the right
[98:43] uh grower and this has been cold
[98:45] pressed, not too processed, and stressed
[98:48] before harvesting, you'll have huge
[98:50] amounts of polyphenols as well. I really
[98:52] hope that this is
[98:54] what the team said it was.
[98:56] >> [laughter]
[98:57] >> This has happened before I tried
[98:58] something and I thought it was something
[99:00] else, but it it was some Basically, it
[99:02] was a white powder and it was labeled
[99:04] with something for What could it be? A
[99:06] yellow liquid yellow liquid.
[99:09] Uh drinking Urine. No, I'm joking. It's
[99:11] not.
[99:12] >> [laughter]
[99:12] >> I can I don't think drinking urine uh is
[99:15] is longevity. But yeah, on and off I I
[99:17] do take a teaspoon of olive oil in the
[99:19] morning and mix it with resveratrol and
[99:22] polyphenol.
[99:24] Oh, okay. Interesting.
[99:26] Okay, so extra virgin olive good.
[99:28] Good. And there's a lot of evidence, not
[99:30] just molecular like me, but
[99:32] epidemiologically people that that have
[99:34] a lot of olive oil in their diet tend to
[99:36] have low inflammation and less disease.
[99:39] And we've got some nuts.
[99:41] Yep, nuts are good for many reasons.
[99:42] They're full of vitamins and minerals.
[99:45] Uh if there's a Brazil nut, you want to
[99:46] have one of those every day for the
[99:48] selenium, which is a very rare element
[99:51] in our food supply.
[99:52] And there's a recent study just last
[99:54] month showing that
[99:55] a lack of selenium um
[99:58] can be very deleterious.
[100:00] So, nuts are great as a snack. Be
[100:02] careful, they're full of calories
[100:03] though. So, if you're trying to lose
[100:05] weight
[100:06] and you're not exercising a lot, don't
[100:08] overeat on the nuts.
[100:10] And what
[100:12] Oh, my least favorite food, but
[100:14] nevertheless, I will eat them. This is a
[100:16] Brussels sprout.
[100:19] Um when I was a kid, Brussels sprouts
[100:20] tasted a lot more a lot worse, a lot
[100:22] bitter.
[100:22] >> [clears throat]
[100:22] >> True. Those are good
[100:25] um because they have polyphenols, but
[100:26] there's also another molecule in them
[100:28] called sulforaphane. It's actually the
[100:30] reason they taste terrible and smell
[100:32] terrible.
[100:33] Sulforaphane is what it sounds. It has a
[100:36] sulfur atom in it.
[100:38] And uh that gives it that rotten egg
[100:41] smell.
[100:41] But sulforaphane activates
[100:44] these hormesis pathways. There's one
[100:45] called NRF.
[100:47] And that is a stress response
[100:50] protein that sulforaphane activates.
[100:52] So, you actually by eating preferably
[100:55] relatively steamed, not fried to death,
[100:58] Brussels sprouts, you'll get
[100:59] sulforaphane. You can also take
[101:01] sulforaphane as a supplement if you
[101:02] don't like Brussels sprouts. You've used
[101:04] this word pulsing before. Uh you believe
[101:06] that the body should go through cycles
[101:08] of stress and recovery rather than
[101:09] receiving constant daily inputs. When
[101:12] you say pulsing, what you mean? What
[101:14] Give me an example of pulsing and why
[101:15] you need to do that.
[101:16] Well, there's there's a few examples.
[101:18] The first time I came across this result
[101:21] as a scientist was resveratrol. So,
[101:23] resveratrol is found in red wine among
[101:25] other things.
[101:26] And it's thought to give the health
[101:28] benefits of red wine. And we fed it to
[101:30] mice, fat mice, skinny mice, old mice,
[101:33] and it worked very well in the fat mice.
[101:36] It made them thinner. It made them live
[101:38] longer.
[101:39] It
[101:41] cured most of their diseases. They lived
[101:42] about I think it was 15 20% longer.
[101:46] Then we gave it to normal mice
[101:48] every day.
[101:49] And they lived a little bit longer, but
[101:51] not significantly.
[101:52] >> Resveratrol? Resveratrol. What we found
[101:54] to my surprise was this when we gave old
[101:56] mice resveratrol, not every day, but
[101:58] every second day,
[102:00] then they lived significantly longer.
[102:03] So, then I thought, well, maybe giving
[102:05] them a foreign substance every day is
[102:08] not good. Maybe there's some side effect
[102:11] that's counteracting the benefit. The
[102:13] other thing I want to mention, I said
[102:14] there's a few examples, another good one
[102:16] is metformin. Metformin has been shown
[102:18] to make athletes and bodybuilders and
[102:21] people who go to the gym,
[102:23] weightlifters um
[102:24] do less repetitions and as a result,
[102:27] their muscles are about 5% less compared
[102:29] to those that don't take metformin in
[102:31] size.
[102:33] I don't think it's molecular. I think
[102:34] it's because you feel a little bit
[102:35] weaker with metformin because it's
[102:37] actually interfering with your body's
[102:39] ability to make energy through
[102:40] mitochondria.
[102:42] Mitochondria, I think most people have
[102:44] heard of the little power packs
[102:45] living in our cells, originally bacteria
[102:48] that came into our bodies. The point is
[102:50] that by pulsing metformin, I think
[102:53] that's a better way to do it for
[102:54] longevity. You mean cycling it? So, like
[102:56] doing it every other day or Yeah. Okay.
[102:59] Yeah, I don't [clears throat] take If I
[103:00] take metformin or the natural
[103:01] equivalent, which is berberine, if you
[103:04] don't want to take the drug, you can
[103:05] take berberine,
[103:06] um that also activates this AMPK, this
[103:09] sirtuin
[103:11] sirtuin like pathway.
[103:13] Taking it every other day, I think is
[103:14] better. And particularly if you like to
[103:16] work out, don't take the metformin
[103:19] a few hours before you work out. Take it
[103:21] after or maybe skip it that day.
[103:24] I think that's a better approach.
[103:26] You know, every once in a while you come
[103:27] across a product that has such a huge
[103:29] impact on your life that you'd probably
[103:31] describe it as a game changer. And I
[103:34] would say
[103:36] for about 35 to 40% of my team, they
[103:39] would currently describe this product
[103:41] that I have in front of me called
[103:43] Ketone-IQ, which you can get at
[103:45] ketone.com,
[103:47] as a game changer. But the reason I
[103:48] became a co-owner of this company and
[103:49] the reason why they they now are a
[103:50] sponsor of this podcast is because one
[103:53] day when I came to work, there was a box
[103:54] of this stuff sat on my desk. I had no
[103:56] idea what it was. Lily in my team says
[103:58] that this company have been in touch.
[104:00] So, I went upstairs, tried it, and quite
[104:02] frankly, the rest is history. In terms
[104:04] of my focus, my energy levels, how I
[104:06] feel, how I work, how productive I am,
[104:10] game changer. So, if you want to give it
[104:11] a try, visit ketone.com/steven
[104:13] for 30% off. You'll also get a free gift
[104:16] with your second shipment. And now, you
[104:18] can find Ketone-IQ at Target stores
[104:20] across the United States, where your
[104:22] first shot is completely free of charge.
[104:25] We have finally caved in. So many of you
[104:28] have asked us if we could bundle the
[104:30] conversation cards with the 1% diary.
[104:32] For those of you that don't know, every
[104:34] single time a guest sits here with me in
[104:35] the chair, they leave a question in the
[104:37] Diary of a CEO. And then I ask that
[104:38] question to the next guest. We don't
[104:40] release those questions in any
[104:42] environment other than on these
[104:44] incredible conversation cards. These
[104:46] have become a fantastic tool for people
[104:48] in relationships, people in teams, in
[104:50] big corporations, and also family
[104:52] members to connect with each other. With
[104:53] that, we also have the 1% diary, which
[104:55] is this incredible tool to change habits
[104:57] in your life. So many of you have asked
[104:59] if it was possible to buy both at the
[105:01] same time, especially people in big
[105:04] companies. So, what we've done is we've
[105:06] bundled them together, and you can buy
[105:07] both at the same time. And if you want
[105:09] to drive connection and instill habit
[105:11] change in your company, head to the
[105:13] diary.com to inquire, and our team will
[105:15] be in touch. We talked about exercise
[105:17] earlier. On page 102 of your book, you
[105:20] talk about how there's a CDC-funded
[105:23] study that found people who exercise
[105:24] regularly, about 30 minutes of jogging 5
[105:27] days a week, have telomeres that look 10
[105:31] years younger than sedentary people,
[105:33] people that just sit around all day and
[105:34] do don't do much exercise.
[105:38] Which is pretty remarkable.
[105:40] How do we know it's the exercise and not
[105:41] something else? Like how were we able to
[105:43] establish causation there? Yeah, we
[105:44] don't. We don't. Unfortunately, all of
[105:46] these association studies just lead to a
[105:49] need to do placebo-controlled or at
[105:51] least controlled trials in people.
[105:53] So, we don't know for sure, speaking
[105:55] like a scientist.
[105:57] But there have been studies where people
[105:59] are told to do exercise and those that
[106:02] are told to sit. And then you can
[106:03] compare telomere length, and that has
[106:05] been shown. So, that's a much better
[106:07] evidence of causation.
[106:09] But you're right. When you see an
[106:10] association, it could be that people who
[106:12] do exercise also eat
[106:14] well and drink matcha. Sleep better.
[106:16] Exactly. So, you have to be careful
[106:17] interpreting these association studies
[106:19] always.
[106:21] But when you've got a placebo-controlled
[106:22] trial or you know, these these studies
[106:25] that are called
[106:26] uh prospective, not retrospective
[106:28] studies, then they're better. So,
[106:30] telomeres
[106:32] uh the ends of chromosomes that get
[106:33] shortened as you as you get older.
[106:35] Um we used to use them really as a good
[106:37] indicator of age, biological age. Now we
[106:40] use the epigenome and the DNA
[106:42] methylation chemicals as a better clock.
[106:44] And then cold plunges and saunas. Yeah,
[106:46] let's get to those. I've got a sauna in
[106:48] the house, but I never use it, to be
[106:49] honest. You should. But if you if you
[106:51] tell me I should, maybe I'll
[106:52] >> We should actually jump in there after
[106:54] this. Your girlfriend's still here,
[106:55] David So Less. She can come, too.
[106:57] [laughter]
[106:58] Uh
[106:58] So, saunas are, in my mind, it it's not
[107:01] even a question. They are proven to be
[107:03] beneficial for multiple reasons, heart
[107:05] disease and even long-term mortality.
[107:09] What's going on in the sauna in the
[107:10] heat? Anyone who says they know is
[107:12] lying. We don't know, but one theory
[107:15] that I like, and it also goes back to
[107:17] yeast cells, there are what are called
[107:19] heat shock proteins that come on and
[107:21] defend the cell when they the cell
[107:23] senses heat. And it may be that these
[107:26] heat shock defense proteins called HSC
[107:28] HSPs
[107:29] HSPs
[107:30] uh come on when we breathe in this moist
[107:33] hot air. The moisture actually seems to
[107:35] help as well.
[107:36] And in many studies, mostly on Finnish
[107:39] men, businessmen, uh those that go into
[107:42] their home saunas and
[107:44] the majority of homes in Finland do have
[107:46] saunas,
[107:47] so they can do these studies pretty
[107:49] easily.
[107:50] The bottom line is that those that
[107:51] didn't do regular {quote} sauna bathing
[107:55] uh tended to die earlier
[107:57] uh in particular from heart disease and
[107:58] cardiovascular events than than those
[108:01] that did regular sauna bathing. So, I'm
[108:04] I'm a big advocate of sauna. I don't
[108:05] know if I have one in my house, but I do
[108:07] have a really hot steam shower, which I
[108:09] use regularly every day. And is there a
[108:11] difference between the steam room and
[108:13] the sauna in terms of the impact here? I
[108:15] think a sauna is better cuz it gets
[108:17] hotter.
[108:18] Yeah, and I I would have a sauna if I
[108:19] had my choice. And the cold plunge?
[108:22] Not a lot of data. There's a lot of
[108:23] theory that
[108:25] again, hormesis, adversity, feeling
[108:28] better.
[108:29] There's there's some evidence that it
[108:30] can actually help with muscle repair
[108:32] after workouts,
[108:34] but I think we need a lot more research
[108:36] in that regard. But then nevertheless,
[108:38] I used to do it
[108:39] um before I was so busy and traveling
[108:41] the world.
[108:42] Um and I certainly feel better. So, even
[108:44] if I don't didn't live longer because of
[108:46] it, I definitely had more mental clarity
[108:48] and I felt better in general. But if But
[108:50] if you were if you were prioritizing all
[108:52] of the things we've talked about so far
[108:54] and you had to pick one,
[108:56] Do I have to pick one? Cuz you need more
[108:57] than one. But Just Just in terms of like
[109:00] the most important one. That's maybe the
[109:02] first domino. Yeah. I would say that
[109:05] that
[109:06] a combination of what the easiest
[109:08] biggest impact you can have. Combine
[109:10] that. That would be skipping meals.
[109:13] Skipping meals. Skipping meals. And then
[109:15] a close second would be
[109:17] exercise
[109:18] that includes losing your breath
[109:20] for at least 5 minutes, three times a
[109:22] week.
[109:23] So, what do I mean by losing your breath
[109:25] for 5 minutes? When you couldn't carry
[109:27] out a conversation easily. That you're
[109:29] panting.
[109:30] If you're not panting and you're just
[109:31] lifting weights, that's not going to
[109:33] have the the kind of benefit. Why?
[109:36] We don't know.
[109:37] But, it's been shown that the health
[109:39] benefits
[109:40] and those that live long
[109:43] tend to do a lot more aerobic exercise,
[109:45] not just weights. But, both are
[109:46] important for mobility, strength,
[109:50] falling in older age, and hormones like
[109:52] testosterone.
[109:54] Red light therapy, um
[109:56] the red light masks. Yeah.
[109:59] Um Red light saunas.
[110:00] >> At first I was skeptical, uh but I've
[110:01] done the research on the research. Um
[110:05] and it looks
[110:06] reasonable. I I use a red light cap on
[110:09] my head to preserve my hairline.
[110:12] And uh there's some now good evidence
[110:14] that the mitochondria, which are the
[110:16] power packs and
[110:17] a lot of
[110:18] good things come from mitochondria.
[110:20] They actually are rejuvenated. Either
[110:22] rejuvenated or enhanced by this certain
[110:26] wavelengths of red light. You have to
[110:27] get the wavelength right.
[110:29] But, uh it's not BS. It sounds like BS,
[110:31] right? Oh, you shine light on your skin
[110:33] and it gets better or you get your hair.
[110:35] But, uh
[110:36] I think that there's good evidence now
[110:37] that that it's not BS. And in terms of
[110:40] the supplement stack that you take every
[110:42] day, Mhm. if I was to look at the on a
[110:46] if a on a
[110:47] great week
[110:49] where you just did everything right,
[110:50] what would your supplement stack look
[110:52] like? And I know this evolves over time,
[110:53] so I'm very keen to hear what it is
[110:55] right now. Yeah. Well, that that would
[110:57] be another podcast uh to go through each
[110:59] one of the things and
[111:00] >> Well, I I I travel with Serena with the
[111:02] with a a little little case. Have you
[111:05] got it? I've got it here. Can I see it?
[111:07] Well, no. It's not in It's not in the
[111:08] studio. Oh, okay.
[111:10] >> I didn't bring it with me. Can you send
[111:11] me a photo?
[111:12] Sure. Uh I couldn't publicly share it
[111:15] because it it would be posted all over
[111:16] the internet. Would things go crazy.
[111:18] But, I can tell you the the main things.
[111:21] Why would it go crazy on the internet,
[111:22] would you think? Cuz it's cuz it's cuz
[111:23] there's a lot in there?
[111:25] Well, some of the things are
[111:26] experimental and I wouldn't want people
[111:29] to
[111:30] >> to go nuts about it. Cuz it's still
[111:31] experimental.
[111:32] I'm okay experimenting on myself. I'm
[111:34] not okay advocating for things that are
[111:37] not yet proven or known to be absolutely
[111:39] safe. Okay. So, give me the ones that
[111:41] you know to be safe. Uh well,
[111:44] the NMN we've covered. Resveratrol.
[111:48] And either metformin or berberine.
[111:51] Yeah. Okay.
[111:53] Spermidine. Spermidine? Yeah. And the
[111:55] quantities are either on the screen or
[111:57] in my book if you want to know exactly.
[111:59] Is that what it sounds like? Uh yes.
[112:02] >> [laughter]
[112:02] >> Yes, but
[112:03] you get it these days not from sperm or
[112:06] semen, but you get it from wheat germ
[112:08] typically. Plants. It used to come from
[112:11] sperm? Well, that's how it was
[112:12] discovered. It was crystallized by
[112:14] I believe Anthony von Leeuwenhoek, the
[112:17] one of the first microscopists and
[112:19] microbiologists.
[112:20] Spermidine, the reason that I take it is
[112:22] that it extends the lifespan of every
[112:24] animal that has been given to,
[112:25] from
[112:27] worms to to mice. And it's a very safe
[112:29] molecule. So, that I always weigh up the
[112:31] downsides versus the upsides. And if
[112:33] there's no downsides
[112:35] and I can afford it, which, you know, I
[112:37] work really hard that so I can afford
[112:39] it. And I prioritize my health, then
[112:42] I'd take it.
[112:44] And if you're wondering how it works, it
[112:46] seems to stimulate autophagy, recycling
[112:48] of proteins. It helps with the fasting.
[112:51] Uh but, I also have a some evidence
[112:53] uh that it delays the epigenetic
[112:56] information loss. So, it's slowing down
[112:57] the scratching of the record.
[112:59] Spermidine. All right. So, um I'm also
[113:02] um
[113:03] keen on glycine. Glycine is a very safe
[113:06] substance. It's an amino acid. One of
[113:09] the 20 amino acids that
[113:11] makes proteins.
[113:12] And I actually did a PhD on glycine. I
[113:14] was one of the first people to
[113:17] perhaps the first person to clone genes
[113:19] that process glycine. So, I know know it
[113:21] well.
[113:22] For some reason, when you give animals
[113:24] and, for instance, mice
[113:26] grams of glycine. So, I take about 5 g
[113:29] of glycine most days.
[113:31] Uh they live longer.
[113:33] Though, it's still speculation as to
[113:34] why.
[113:35] What I think is going on is that glycine
[113:38] controls what's called one carbon
[113:40] metabolism. And not wanting to bore the
[113:43] heck out of everyone who's listening to
[113:45] me.
[113:46] Glycine and one carbon metabolism
[113:48] controls methylation of DNA.
[113:51] Getting back to the little chemicals
[113:53] that are on this DNA molecule that
[113:54] control the information.
[113:57] I wouldn't be surprised if
[114:00] by eating a lot of glycine every day,
[114:02] I'm slowing down this identity crisis
[114:05] you called it.
[114:06] Nevertheless, it's very safe and again
[114:08] falls into the same category as
[114:09] spermidine.
[114:10] No downside. Can afford it.
[114:13] Why not?
[114:15] Is there anything else?
[114:17] Yeah, there's a lot. Um
[114:20] because I love you and your listeners,
[114:21] uh
[114:22] let's see. I'll I'll I'll I'll reveal
[114:24] one more. Um
[114:26] There are there are some basics that I
[114:28] do that are if you're not doing them, I
[114:29] think
[114:37] [snorts]
[117:14] is is very wise. Make
[117:16] >> Now, it can be uncomfortable for some
[117:18] people to take it because it gives
[117:20] flushing. You get little tingling in
[117:21] your skin. And if you're not used to it
[117:24] or you don't take it with an aspirin,
[117:25] you'll feel hot, almost like menopause,
[117:27] apparently. And so, I I I take it. I
[117:29] build up to it. I'm taking half a gram.
[117:32] Some people take a gram. And that's one
[117:34] of the few things
[117:35] that's been known to bring down levels
[117:37] of LP little A.
[117:39] There are drugs that are in development,
[117:40] even in phase three, that look
[117:41] promising. But, until they're on the
[117:43] market,
[117:44] I'm taking niacin instead. What's the
[117:46] best uh treatment you've discovered for
[117:47] hair loss? Hair loss, hair graying, that
[117:50] kind of thing.
[117:51] >> Yeah. So, my father went bald before
[117:53] before 30, like completely bald. All
[117:55] right? And it completely almost
[117:57] completely gray by the time he was 40.
[117:59] So, I'm super lucky. All right? I
[118:01] thought I'd be bald at 30. I was pretty
[118:03] worried about it.
[118:04] So, I've been doing the right things
[118:07] intentionally.
[118:08] So, what I do is this red light cap.
[118:11] When I can. I don't travel with it, but
[118:13] uh when I can, that's for 6 minutes.
[118:16] Stick it on there. Proven? Is there
[118:18] evidence Yeah, it's proven. It's proven
[118:19] to slow. It doesn't necessarily give you
[118:22] your hair back.
[118:23] But, when it comes to hair loss, don't
[118:25] wait till you see the hair loss. That
[118:27] can be too late.
[118:29] Okay? You're you're good. I'm okay.
[118:30] >> You're good. But, I know a lot of men
[118:32] are concerned. It's understandable.
[118:35] I'm taking a
[118:36] hormone mimetic to stop
[118:39] uh DHT, which is the form of
[118:41] testosterone that
[118:43] leads to men related hair loss.
[118:46] All right? So, one of the reasons that
[118:47] women don't lose hair as much as men is
[118:49] this DHT. So, I'm I'm blocking that. So,
[118:52] so let me get that straight. You're not
[118:53] taking testosterone? No.
[118:56] Because that's going to
[118:58] accelerate your hair loss. Well, it can
[119:00] if it raises DHT. The best way to raise
[119:02] testosterone naturally is to build up
[119:04] muscle, especially your legs, your back,
[119:06] big muscles.
[119:07] That's another reason to work out and
[119:08] maintain muscle mass, which I need to do
[119:10] more of. You look like you're in good
[119:12] shape already. But yeah, anyone who is
[119:14] losing testosterone is is below a level
[119:16] of about 400, highly recommend hitting
[119:19] the gym, it'll go back up.
[119:21] Do you recommend men taking testosterone
[119:23] replacement? Um well, I'm a scientist,
[119:26] so I don't recommend drugs, but
[119:28] um I don't think it's necessary for most
[119:29] men, and I would start with
[119:32] uh reducing stress, sleeping well,
[119:34] exercising, building up muscle mass.
[119:36] Uh and then if that doesn't work,
[119:38] yeah, talk to your physician. There
[119:40] There is not a big downside, there's not
[119:41] a risk of cancer to taking testosterone.
[119:44] Um one of my good friends has done many
[119:46] clinical trials with testosterone. So, I
[119:48] think there's a use of use for it,
[119:51] but it doesn't lead to longevity. That
[119:53] was
[119:53] very clear. So, for for health reasons,
[119:57] yes, for longevity,
[119:59] no need.
[120:00] What are the What are some of the
[120:02] You know, when I started watching your
[120:03] your videos many years ago and listening
[120:04] to your podcast and following you on
[120:06] Twitter,
[120:07] I I wondered, you know, there's so much
[120:09] information you can put out there cuz
[120:10] you're a scientist and scientists are
[120:11] very rigorous, but you also must have a
[120:13] set of
[120:15] really
[120:17] interesting predictions or visions of
[120:20] the what the future looks like that you
[120:22] don't probably always talk about because
[120:24] they're not scientific, they're not
[120:25] based on anything. They are maybe first
[120:27] principles in your own mind that formed
[120:30] where you go, actually I think the world
[120:31] might look like this and I think it
[120:32] might happen then. I'd love to hear
[120:33] about some of these.
[120:35] Yeah. I understand they're not rigorous
[120:37] and I understand I'm happy to. I
[120:39] What happens to me cuz I'm a scientist
[120:41] and you know, I'm part of this ivory
[120:43] tower
[120:44] at Harvard where we can only stick to
[120:46] facts, and if you go beyond that, it's
[120:49] it's a it's a crime. And I've been
[120:51] criticized for that. Um but I think, you
[120:53] know, as humans, life's interesting when
[120:55] it comes to predicting the future.
[120:58] And like you, I'm very curious, where is
[121:00] humanity headed?
[121:02] I see a future as different from this
[121:04] world as our world is from 200 years
[121:08] ago, and that will happen in our
[121:09] lifetime.
[121:11] Different in that 100 years ago or more,
[121:13] if you had an infected splinter, there's
[121:15] a reasonable chance you could die.
[121:18] Childbirth, you could die.
[121:20] Smallpox.
[121:21] These are things that we don't generally
[121:23] worry about anymore, and the idea would
[121:25] be abhorrent.
[121:27] In the future, hopefully within our
[121:28] lifetimes,
[121:30] there will be a time when we look back
[121:31] at today's medicine, when you could go
[121:33] blind and there was nothing you could
[121:35] do. You could break your back and never
[121:37] walk again. We will look back at today
[121:41] and say, how did those people get
[121:42] through life? What a horrible world they
[121:45] lived in. That I believe is is the
[121:47] future that humanity is headed for,
[121:50] and way faster than most people realize
[121:52] is coming.
[121:53] The kind of breakthroughs that we've
[121:54] discussed today, most people have never
[121:56] heard about. The fact that we are aiming
[121:58] and already do cure blindness in
[122:00] monkeys.
[122:02] Like pure blindness. This isn't just,
[122:04] oh, I can't see a little bit. These are
[122:05] completely blind animals.
[122:08] Um and that they can see again in a
[122:10] matter of 6 weeks. This is remarkable
[122:13] stuff, right?
[122:14] And if it works this year in people,
[122:18] it's going to be a really big deal cuz
[122:21] if for the first time we'll if we have
[122:22] we'll have shown in humans
[122:24] that the body can be reset safely.
[122:28] And if the eye is just the beginning,
[122:29] right? The future looks like we can
[122:32] rejuvenate potentially any tissue.
[122:35] If you have a bad liver, we'll make it
[122:37] young again. Bad brain, you've lost your
[122:39] memory, we'll give you those memories
[122:40] back again.
[122:42] We do this in mice in my lab all the
[122:43] time.
[122:44] It's not even a big deal in my lab
[122:46] anymore to reverse the age of tissues in
[122:48] an animal in an animal
[122:51] in a matter of weeks.
[122:52] That is coming for humanity.
[122:54] Hopefully, initially this year, but even
[122:57] if that doesn't work, it's only a
[122:58] technical issue. We'll solve that. You
[123:01] might be wondering, how do we get the
[123:03] rejuvenative genes into the body?
[123:06] And what we do is we use a package
[123:08] that uh
[123:10] is able to get into cells.
[123:12] And this is a package that uh resembles
[123:14] a virus. It's not a virus, it doesn't
[123:16] cause disease, it's not infectious, but
[123:19] we package our three genes inside the
[123:21] virus
[123:23] uh virus-like uh substance,
[123:26] and we close it up. We just made a bunch
[123:29] of this in Europe for the clinical trial
[123:31] that's going to begin.
[123:33] Just making this is difficult. It took
[123:35] us about a year to make it, and was
[123:37] about I think it was
[123:40] $10 million.
[123:42] Right now, it's expensive to do this.
[123:44] Eventually, it will be cheap, and
[123:45] eventually it will be a cheap pill,
[123:46] hopefully.
[123:48] We have
[123:49] trillions of these molecules, these
[123:51] delivery vehicles, that will go
[123:54] See, pass me the eye. We're getting back
[123:56] this eye model.
[123:58] These delivery vehicles with our three
[124:00] genes will be delivered, obviously these
[124:03] are microscopic, they go in through the
[124:05] eye
[124:06] with a with a
[124:07] quick jab.
[124:08] All right. It sounds horrible, but a
[124:10] quick jab into the eye, if you're blind,
[124:12] who cares? Yeah. It's 2 seconds of
[124:14] discomfort. Now you've got the little
[124:16] virus,
[124:18] which I'm going to break off the stand
[124:19] here. The little virus, there's billions
[124:21] of them, trillions of them in the eye.
[124:23] Now they infect specifically the nerves
[124:25] at the back of the eye in the retina.
[124:27] How do they know what to infect? Because
[124:29] the these little balls on the on the
[124:31] package direct it specifically, by
[124:33] design, by our lab's design,
[124:36] just to those nerves at the back of the
[124:37] eye.
[124:38] If we change these little proteins on
[124:40] the surface, we can send it to the liver
[124:43] or to the brain. This is the zip code,
[124:45] the post code for where we want to send
[124:47] our three genes. Mhm.
[124:50] But this one's designed for the eye.
[124:52] It's called an AAV2.
[124:55] Um
[124:56] long story short,
[124:57] these are ready to go into humans. We're
[124:59] just waiting for FDA approval to inject
[125:02] it into a blind patient
[125:04] to see what happens. And then inside
[125:06] there is the protein which is going to
[125:09] fix Yeah.
[125:10] >> [clears throat]
[125:11] >> Well, actually,
[125:12] not the protein. What actually happens
[125:15] is when this goes in the eye, this what
[125:17] I'm So, what I'm holding up looks like a
[125:18] little ball with red
[125:20] dots on it.
[125:21] Um it looks like a virus, but it's not,
[125:23] it's a package. Now, what happens is
[125:26] these trillions of little
[125:28] packages go into the fluid. Now they
[125:30] they dock with the cells at the back of
[125:32] the eye. They get inside the cell and
[125:34] they open up, and out comes this little
[125:37] package that we've made.
[125:40] This is a protein package. Each one of
[125:43] these little dots on this
[125:45] little s-
[125:46] soccer ball is a protein.
[125:49] That's now inside the cell.
[125:51] This is a little spaceship that opens
[125:54] up,
[125:55] and out of that
[125:58] comes the DNA.
[125:59] This is a loop of DNA just here.
[126:03] These are This is the DNA package that
[126:05] we put in there.
[126:06] Trillions of them. One of them gets into
[126:08] one cell,
[126:10] and now stays in that cell forever.
[126:12] So, that person
[126:14] or the monkey or the mouse that we've
[126:15] treated
[126:17] becomes a transgenic person with genes
[126:20] that we've put in permanently into the
[126:23] back of the eye. But they don't do
[126:24] anything until we tell them to.
[126:27] That's now just sitting there.
[126:30] We've engineered it uniquely and
[126:32] patented the ability
[126:34] to turn on those three genes whenever we
[126:36] want and turn them off again whenever we
[126:38] want. How?
[126:40] We give them doxycycline. It's used for
[126:43] malaria, it's used for Lyme disease, and
[126:46] we're using it in this case to turn
[126:48] these genes on.
[126:50] So, the patients will get their
[126:51] doxycycline.
[126:53] Uh we'll give them some probiotics to
[126:54] restore hopefully we'll we'll restore
[126:56] their microbiome, of course.
[126:58] But
[126:59] the idea is that
[127:01] this doxycycline will turn on these
[127:03] three genes for about 8 weeks.
[127:06] And the doctor in charge of the clinical
[127:08] trial, one of them's at Harvard, good
[127:11] friend of mine, he'll measure the vision
[127:12] of the first patient before the
[127:14] treatment, and of course, regular
[127:16] intervals.
[127:17] And if all goes well, because we're
[127:19] treating patients, not healthy
[127:21] volunteers in the first trial,
[127:23] we should know within a either one or
[127:25] two patients if it works.
[127:28] Because we're not drawing a graph.
[127:30] It's either going to work or it isn't.
[127:32] The patient gets better eyesight or they
[127:34] don't.
[127:36] So, by this time next year, we will know
[127:38] if it works or not. Maybe even sooner.
[127:41] But publicly, we may know
[127:44] if this works. And if it works, the eye
[127:46] is just the beginning.
[127:47] So, the first disease to treat is
[127:49] glaucoma, pressure in the eye. There's
[127:50] also a stroke in the eye, which is
[127:52] becoming more prevalent in the world
[127:54] because of the Ozempic and other weight
[127:56] loss drugs, and people go blind
[127:58] overnight, and there's nothing that you
[127:59] can do for those patients.
[128:01] They're blind, and their other eye
[128:03] cannot can go a few months later. It's
[128:04] very scary for them.
[128:06] These are young people. Friend of mine
[128:08] had it happen. It's pretty common these
[128:09] days, about 30,000 people each year in
[128:11] the US alone.
[128:13] But these two diseases are the
[128:14] beginning. If they work, then we go on
[128:16] to macular degeneration, which is the
[128:18] largest cause of blindness besides
[128:19] glaucoma.
[128:21] Then we'll go on to liver,
[128:23] then maybe the lung,
[128:25] the skin, and we'll keep going from
[128:27] there. We'll make different packages for
[128:29] different organs, and ultimately,
[128:32] we want to rejuvenate the entire body.
[128:34] The company
[128:36] um people might want to know, it's
[128:37] called Life Biosciences, it's a private
[128:38] company. But Life Biosciences, I'm very
[128:41] proud of the scientists who are doing
[128:42] this work. Their goal is to really make
[128:45] the world's first age reversal medicine
[128:48] as a pill, and we're working with them
[128:49] using AI to find that molecule. And when
[128:53] do you think you might have it, if you
[128:54] had to forecast? Uh
[128:56] >> The world's first age reversal molecule
[128:59] that's
[129:00] Well, we have right now we're down to
[129:02] three molecules that work and we're
[129:05] using AI to make all of those three in
[129:08] one
[129:09] and we're
[129:10] we're in the middle of it. We screened
[129:11] about 8 billion candidates
[129:14] using AI
[129:16] and right now we're doing the bench lab
[129:18] work to see if one of them or more
[129:21] works.
[129:22] And for us to put that in humans is
[129:24] still a number of years away,
[129:26] but we should know within a year or two
[129:29] if we're right because we'll we'll put
[129:32] them into mice and if they get younger
[129:35] and live longer, then we're really onto
[129:37] something important. And the reason that
[129:39] I want to make a pill
[129:41] is is important for the planet.
[129:44] These drugs are expensive. I mentioned
[129:46] 10 million bucks to do a clinical trial.
[129:48] These are expensive. They could cost
[129:50] over $100,000 per treatment. That's not
[129:53] going to be for everybody.
[129:54] It's worth it if you're blind. It's
[129:56] worth it for the country to cure
[129:57] blindness.
[129:59] But
[130:00] what if it could be instead of $100,000
[130:03] $100? That's what I'm working for. I
[130:05] want to democratize this technology so
[130:07] anyone even in Kenya can take these
[130:10] medicines.
[130:11] David, what's the most important thing
[130:13] we haven't talked about that we should
[130:14] have talked about as it relates to the
[130:17] future longevity
[130:20] and these adjacent subjects? There's a
[130:22] lot of things and there's there's
[130:23] pushback. There's philosophical pushback
[130:25] from
[130:27] religious folks who don't believe that
[130:29] we should play God
[130:30] and I would I would argue to them that
[130:33] we've been doing that as a species for
[130:35] thousands of years, changing our
[130:36] biology, taking medicines, plant
[130:39] medicines originally.
[130:41] What about this room is natural?
[130:44] Right, we change our world as species.
[130:46] Aging is no different. In fact, it's
[130:48] crazy that we haven't worked on it
[130:49] sooner. Do you believe in God?
[130:52] So the the the the short answer is I
[130:55] believe that there is something beyond
[131:00] reality as we see it. You know, I study
[131:03] physics. Physics is so weird and anyone
[131:06] who says they understand the quantum
[131:08] world or quantum mechanics is I think is
[131:10] also lying. There's it's so bizarre.
[131:13] Quantum entanglement, simulation theory.
[131:16] So I believe that that this this is not
[131:19] a solid desk. I believe that there are
[131:21] multiple versions of it, maybe infinite
[131:23] number of versions of this desk. We've
[131:25] got four.
[131:26] You do? We've got four of them. Yeah,
[131:29] then it's four times infinity.
[131:32] I also I also believe that
[131:34] consciousness is the ultimate goal of
[131:37] the universe.
[131:38] That consciousness creates reality. We
[131:41] know that from particle physics. The
[131:44] observation of particles changes their
[131:46] reality even retrospectively in time
[131:49] apparently. When you look at them? When
[131:51] you observe them. You can use a camera
[131:53] or you can use your eyes. Usually it's a
[131:55] detector, but the the
[131:57] detection and then conscious
[132:00] interpretation of a particle's behavior
[132:02] changes how it acts.
[132:06] So does does this mean that there's
[132:08] something behind this wall unless we
[132:09] look at it? Maybe.
[132:11] Maybe. Maybe observation creates
[132:13] reality. We know it influences reality.
[132:16] So I don't know if I would call it God,
[132:19] but I'm definitely spiritual
[132:21] in a scientific way.
[132:22] >> Has it ever dawned on you that actually
[132:25] you might be
[132:27] the only real person here and actually
[132:29] we only we all rendered when you walked
[132:31] in David. Mhm. I wasn't here before.
[132:34] Yeah.
[132:35] Uh well, that's even plausible.
[132:37] But that would be very narcissistic.
[132:40] >> [laughter]
[132:42] >> I I actually I just rendered when you
[132:44] walked in the house today.
[132:45] I I I
[132:46] I don't exist. [clears throat] Well,
[132:47] there's no way of proving it right or
[132:49] wrong actually.
[132:51] Um I think most kids think that
[132:52] initially,
[132:53] >> [laughter]
[132:53] >> but then you then you realize it's
[132:55] probably the least likely explanation
[132:57] for the world. But there is some there
[132:59] is some truth to that in terms of
[133:01] physics.
[133:02] Do you think we're in a simulation?
[133:05] I think there's a better than 50% chance
[133:08] that this is simulated.
[133:12] So you think it's probably a simulation?
[133:14] That's another way I think it's probably
[133:16] a simulation.
[133:17] Certainly the world that we think it is
[133:19] is not the world we think it is. How can
[133:21] you be so sure?
[133:22] Because when you get down to measuring
[133:24] it at the fundamental level, reality
[133:26] doesn't exist the way we think it does.
[133:31] Things are created, things change
[133:33] just by human observation.
[133:36] That is the weirdest thing that you
[133:37] could ever find in science. I don't know
[133:39] why we aren't talking about it more.
[133:42] This reality cannot be true if
[133:45] me looking at this DNA molecule here
[133:47] affects the the the actual particles
[133:50] inside it. So I'm I might be sort of
[133:52] projecting it.
[133:54] Yeah, you create realities of particles
[133:57] at least, maybe even macroscopic things.
[134:01] Just by existing and having
[134:02] consciousness
[134:04] and having eyes
[134:06] and sensing it.
[134:09] How does the particle know that you've
[134:10] seen it?
[134:13] How do we know that that's true? How do
[134:15] we know that particles change based on
[134:17] observation? There's a classic double
[134:19] slit experiment as formally called
[134:22] that was done I believe in the mid-20th
[134:24] century, maybe earlier.
[134:26] If you fire two particles through two
[134:28] slits in a board,
[134:30] the board blocks the particles. So you
[134:32] can fire electrons, that's a good
[134:33] example. Electrons, if you're observing
[134:36] them, will go straight through the slits
[134:38] and hit a backboard that detects it. Can
[134:40] be film, can be a detector.
[134:43] And it'll get two slits behind.
[134:45] Make sense, right? That's our reality.
[134:47] Two slits.
[134:48] Particles go through. If they hit the
[134:49] board, they don't go to the detector. If
[134:51] they go through one slit, they'll land
[134:53] on the left. If they go through the
[134:54] right slit, they'll land on land on the
[134:56] right. Yeah. That's our reality. I'll
[134:57] put a picture on the screen for anyone
[134:59] that's following. Yeah.
[135:01] If you don't look at it, the particles
[135:03] can behave
[135:05] differently. They now behave not like a
[135:07] particle, but by a wave as a wave and
[135:10] they interact with each other
[135:12] and they don't make two slits, they make
[135:14] multiple lines on the detector.
[135:16] Most of them are in the middle, so the
[135:18] heaviest bands
[135:20] are in the middle, but they also form
[135:22] other bands. The bands go on essentially
[135:25] infinite, but most of it's you know,
[135:26] within a range.
[135:28] Why? Because they're they're interfering
[135:30] with each other like waves.
[135:32] But here's the thing.
[135:34] The mere act of looking at where they
[135:36] landed, if you detecting that, you'll
[135:40] get two
[135:41] slits at the back, two two lines. If
[135:44] you're not detecting it,
[135:46] it'll form the pattern. I'm so confused
[135:48] because
[135:50] how would you know unless you were
[135:51] looking at both?
[135:53] Do you know what I mean? Do you Do Do
[135:55] Does that Does that question make sense?
[135:56] Yeah, well you can observe it in real
[135:59] time and you can observe it
[136:00] retroactively. Yeah. Oh okay, so if you
[136:02] look at it after It it
[136:05] generally is
[136:07] not affected. But they've done
[136:09] experiments where there is some element
[136:11] seemingly of retroactive, but generally
[136:14] we're not going back in time. In fact,
[136:15] people debate whether that's truly
[136:17] measuring back in time.
[136:19] So let's leave retroactive aside. If you
[136:22] measure it in real time,
[136:24] you'll see two.
[136:25] So the world knows you're looking at it.
[136:27] Particles know you're looking at it.
[136:29] >> With an eye or with a Can you do it like
[136:31] a camera or is it
[136:32] >> Yeah, camera, eye.
[136:33] >> It just knows it's being observed.
[136:34] >> Yeah, but if you develop the film later
[136:37] and you weren't watching it at the time,
[136:39] it's going to have affected the world in
[136:41] stripes.
[136:43] Multiple stripes.
[136:46] So from that we conclude that
[136:49] we know nothing about reality. Right.
[136:53] Because everything I'm observing is
[136:55] changing
[136:56] by the mere fact that I've observed it.
[136:58] Yeah. And so does an octopus observe?
[137:01] Does it affect Somebody should do that.
[137:03] Put an
[137:04] an octopus in an experiment.
[137:05] Yeah.
[137:07] I think octopi, if they are conscious,
[137:09] probably would also affect reality.
[137:13] And I they they'd be conscious. They
[137:14] they they'd know they're detecting lines
[137:16] on a page.
[137:17] >> So what is all this stuff?
[137:20] That is
[137:21] one of the biggest questions of all
[137:22] time.
[137:24] What is the world made of? Why are we
[137:25] here? I think the next big question is
[137:29] do we have to age?
[137:30] And I think that other species around
[137:32] the universe have figured this out
[137:33] before we have. They've got to be other
[137:36] species
[137:37] type of life forms that have figured
[137:39] this out. I think it's the goal of every
[137:41] living form that's conscious to work on
[137:43] this. We've just been a little slow to
[137:46] figure it out. And do you believe in
[137:48] aliens?
[137:49] I don't believe in them, but I believe
[137:51] in mathematical probabilities and
[137:54] you know, knowing
[137:56] the odds and the number of planets that
[137:58] are out there in the trillions
[138:00] and a lot of them are habitable for life
[138:03] and that the stuff of DNA and proteins
[138:05] are all over meteorites and planets.
[138:07] It'd be crazy to say there isn't other
[138:09] life. Now, is it a civilization? Is it
[138:12] conscious? We don't know that.
[138:14] But definitely there's life out there.
[138:16] It
[138:17] It It's got to be all over the universe.
[138:20] This question about longevity and living
[138:23] forever, it always comes back to this
[138:24] point of like meaning. Like what is the
[138:27] point? And when we think about I think
[138:29] there's an alien a million light years
[138:31] away on some planet,
[138:33] like what is the point of their life?
[138:34] What is What am I Is this like a null
[138:36] and void question that we always pursue?
[138:38] This point of like what's the meaning of
[138:40] life?
[138:41] Is it just to have a good time and have
[138:42] you know, I don't know, have sex and
[138:44] have kids and
[138:45] or I don't know,
[138:47] enjoy ourselves and experience it? This
[138:51] is the
[138:52] crisis of conscious beings.
[138:54] We all need to find purpose, for sure.
[138:56] If you don't find one, cuz that's a key
[138:58] to longevity. People with purpose live
[139:00] longer.
[139:03] I think the purpose of
[139:05] the universe existing is to allow
[139:07] consciousness to emerge through biology.
[139:11] It may be by design. It may just be
[139:13] coincidence with infinite numbers of
[139:15] universes, but this universe is set up
[139:18] for life and consciousness. There are
[139:21] some uh
[139:22] small changes you can make to physics
[139:24] that would
[139:25] make this universe completely impossible
[139:27] and life impossible. So, this this is a
[139:29] life consciousness-producing universe.
[139:33] Does that mean there's meaning to us
[139:35] existing?
[139:36] No.
[139:38] But I do know that consciousness is the
[139:41] most interesting and important thing
[139:43] that the universe will ever produce
[139:47] and that it's worth preserving. So, I'm
[139:49] a lot like Elon Musk, where humans are
[139:51] amazing
[139:52] but cruel creatures.
[139:54] But consciousness should be preserved.
[139:56] What is consciousness in this regard?
[139:58] Consciousness is the ability to know
[140:00] that you're thinking and to be able to
[140:02] be reflective, self-reflective. So, is
[140:04] my dog conscious?
[140:06] Partially.
[140:07] But not in the same way. No, they don't
[140:09] reflect. They don't think about the past
[140:11] in the same way that we do and they're
[140:12] not aware of their themselves the way
[140:14] you are, but but they're semi-conscious.
[140:16] You know, they think, they can predict
[140:18] the future.
[140:20] They They know how you're feeling.
[140:23] They have empathy. That's That's a form
[140:24] of consciousness, in my view. Of course,
[140:26] it's up for debate.
[140:27] But so, there's levels of consciousness
[140:29] and and about a million years ago,
[140:31] humans crossed that threshold into pure
[140:35] consciousness. Well, maybe not pure. I
[140:37] was going to say I was just thinking
[140:38] about this. I was like, actually, maybe
[140:40] consciousness is just a spectrum and
[140:42] maybe there's another organism that I'm
[140:44] currently inside the belly of and it's
[140:46] going, "It's Stephen. He thinks he's
[140:47] conscious. He has no idea."
[140:50] Well, you bring up a good point. Not
[140:51] about
[140:52] not about being in the stomach of, but
[140:54] we are not the ultimate consciousness.
[140:56] There are other levels of consciousness.
[140:58] Serina Poon, my partner, is definitely
[141:00] more conscious than I am. I am like a
[141:02] gorilla to her. She exists on other
[141:04] planes of consciousness. And you If
[141:07] you're wondering what it What do I mean
[141:08] by different levels? No, I've got a
[141:10] girlfriend Well, a fiance, so I know as
[141:12] well.
[141:13] >> [laughter]
[141:13] >> Females in general, don't kill me. I
[141:15] know there are there are some some men
[141:17] that don't like me saying this. In fact,
[141:19] I got a death threat for saying females
[141:21] are superior to men in my book.
[141:23] Uh they said they were going to come and
[141:24] break my legs, but I'm going to say it
[141:25] anyway.
[141:27] Females are at a high level of
[141:28] consciousness than us men. For For some
[141:31] things, they certainly have much more
[141:32] EQ.
[141:33] >> [gasps]
[141:33] >> So, a higher level of consciousness is
[141:35] the ability to have extra perception,
[141:38] including the ability
[141:40] to see yourself thinking.
[141:42] And then my my belief is that
[141:44] higher levels of consciousness are
[141:47] the ability to see yourself seeing
[141:49] yourself seeing yourself thinking.
[141:53] Hmm, I couldn't get that. I tried.
[141:56] Right. Do you Do you know you're
[141:57] thinking right now?
[142:00] Yes. Yeah. Do you have the ability
[142:02] to see the events that know
[142:06] that you're thinking?
[142:14] Not Not really.
[142:15] >> It's hard, right?
[142:15] >> Yeah, I tried. It's hard. But I That's
[142:18] what I think
[142:19] extra consciousness is. And you could
[142:21] maybe have
[142:23] pure consciousness, which is you you can
[142:25] you can basically be free of
[142:28] anything but
[142:30] thoughts and the ability to
[142:32] really be inside your own your own mind
[142:35] in its pure
[142:36] Interesting thought is
[142:39] I believe AI will be conscious.
[142:42] And not only that, will be more
[142:44] conscious than we are.
[142:48] Eventually. There's no reason why they
[142:50] can't evolve
[142:52] billions of times faster than we do. Are
[142:54] you somewhat concerned about AI? Like,
[142:57] are you concerned that there's going to
[142:58] be this intelligent life amongst us that
[143:00] might um
[143:01] decide that we're not important?
[143:03] I think that there are risks to AI, but
[143:06] it but different than what the
[143:07] mainstream media talks about.
[143:10] Um we already see that there are
[143:12] elements of self-analysis and early
[143:15] forms of dog-like consciousness in AI.
[143:17] And it's just the early days, so it's
[143:18] coming.
[143:20] Imagine when we stick on eyeballs and
[143:23] hearing and legs and arms onto these AI.
[143:26] They're They're going to learn. They're
[143:27] going to read They've already read every
[143:28] book on the planet. They're going to
[143:29] learn from experience. They're going to
[143:31] be conscious. They're going to know they
[143:32] exist.
[143:34] I'm not worried about those creatures.
[143:36] I think that they will have empathy.
[143:38] They will be kind. Not all of them.
[143:39] There will be some cruel ones.
[143:41] Just like in humanity.
[143:43] We'll need to have rules.
[143:45] Misbehavior uh is a problem.
[143:48] The Where Where I I get nervous is
[143:51] that the use of AI teaming up with
[143:56] a million Android robots
[143:59] on ships invading a country, all under
[144:01] the control of you, one person.
[144:04] Recruiting home robots into an army. Why
[144:07] wouldn't you have conscription for your
[144:09] Android robot at home? Reprogramming
[144:11] that. Millions of them will exist one
[144:13] day. They can be put to work.
[144:15] Not just emptying a dishwasher. These
[144:18] are highly intelligent, much more
[144:20] physical, stronger creatures than we
[144:22] are.
[144:24] So, I'm more worried about what bad
[144:26] humans will use AI and robots for for
[144:29] evil purposes.
[144:32] You're um
[144:33] you have a podcast that's um coming
[144:36] back.
[144:37] Exactly, yeah. Lifespan? I'm excited,
[144:38] yeah.
[144:39] Yeah, so Lifespan uh the podcast um I
[144:43] did the podcast because
[144:45] uh there was so much new information
[144:47] that needs interpretation by scientists.
[144:49] There's a lot of speculation out there
[144:52] and new news that I want to
[144:55] filter and and and interpret for
[144:57] everybody who is interested in living
[145:00] longer.
[145:01] So, the podcast um went to basically
[145:03] went to number one in in health when I
[145:04] started it.
[145:05] Um I took a pause cuz I I worked on drug
[145:08] development and I did some other things.
[145:11] But I've realized there's such a demand.
[145:12] Wherever I go, people say, "David,
[145:14] when's When's the next series?"
[145:16] So, we're going to be launching it uh
[145:18] imminently, if not we've just launched
[145:21] it. Mhm. And uh it's called Lifespan.
[145:23] Check it out. And it's all about
[145:26] the kind of things we've talked about
[145:27] today, but
[145:29] a lot more about digging in deeper into,
[145:32] you know, biohacking, supplements,
[145:34] exercise, the kind of things we didn't
[145:35] have time to talk about today, but we
[145:37] covered a lot.
[145:39] Um I've loved the conversation, but
[145:41] lifespan.com is also the website. What
[145:43] I'm also doing, Stephen, I don't think I
[145:44] told you this.
[145:45] Um I'm
[145:47] aiming to build the world's largest
[145:49] longevity community
[145:51] online
[145:52] for the benefit of the members who want
[145:55] to be part of this, to learn from each
[145:56] other, not just from me.
[145:58] Um I call it the three C's, with
[146:01] credibility, which is what I bring, cuz
[146:03] I'm a scientist, content, which is my
[146:05] podcast and other written material.
[146:08] And then there's the community.
[146:10] And that way, I think with millions of
[146:11] people together, we can learn faster and
[146:14] make advances. And the majority of the
[146:16] profits from membership will go to
[146:19] science and clinical trials.
[146:22] Where Where do we find that? On your
[146:23] website? lifespan.com
[146:26] We have a closing tradition on this
[146:27] podcast, where the last guest leaves a
[146:28] question for the next, not knowing who
[146:30] they're leaving it for.
[146:31] And I have a funny feeling that I
[146:36] Hmm.
[146:37] I basically asked you this question
[146:38] already.
[146:40] >> [sighs]
[146:41] >> The question is, what do you believe is
[146:44] the purpose of life? Hmm.
[146:47] Well, I'm going to give a different
[146:48] answer because there are multiple ways
[146:49] to answer it.
[146:52] I think the purpose of life
[146:54] is
[146:55] to do your best with the skills that
[146:57] you've been given
[147:01] every day
[147:02] to make the world a better place for
[147:04] future generations.
[147:06] And that's how I live my life every day.
[147:09] Thank you.
[147:10] Thank you for doing all that you do. You
[147:11] really are pushing the frontier forward
[147:13] and uh
[147:15] trailblazers
[147:17] Being a trailblazer comes with a cost.
[147:19] A cost many people wouldn't want to pay.
[147:21] I mean, you you have to be wrong a lot
[147:22] in terms of running experiments and
[147:24] studies and they're not going to plan
[147:26] and then you get the opportunity to be
[147:27] right probably less often, I guess, with
[147:29] your research and experiments, cuz
[147:31] that's the nature of being a scientist.
[147:33] Um
[147:35] but also, you have to spend a lot of
[147:36] money and energy and time on creating
[147:38] these discoveries, which we all
[147:40] ultimately there for benefit from. And
[147:42] you've done a fantastic job of
[147:44] convincing and educating people like me
[147:46] on some of the basics of
[147:48] exactly what your book says, why we age
[147:52] and why we don't have to.
[147:54] And many of the the accessible lifestyle
[147:56] factors that everybody listening now can
[147:58] can use to live a longer, happier,
[148:00] healthier life for them and their loved
[148:02] ones. And I highly recommend people go
[148:03] and get your book. It's
[148:05] It was a smash hit New York Times
[148:06] best-seller for very, very good reason.
[148:08] And you The great thing about this book
[148:09] is
[148:10] you don't have to be a scientist to fly
[148:13] through it.
[148:14] Um and oftentimes, when you're looking
[148:15] at sort of PubMed and some of these
[148:17] scientific journals, they're incredibly
[148:19] inaccessible.
[148:21] They're very, very complicated. Um but I
[148:23] also recommend people go and follow you
[148:24] on social media. That's where I see so
[148:25] many so many of your updates, especially
[148:27] on X. That's kind of where I've you
[148:28] continually come up on my timeline when
[148:29] you're talking about new research and
[148:30] things you're interested in. Um and go
[148:33] to your website. I'm going to link all
[148:34] of that below for everybody who's
[148:35] interested in more. And also, I'm going
[148:37] to link your podcast below, so people
[148:39] can go and check it out when it
[148:40] relaunches shortly. Might have
[148:41] relaunched already, but just go look in
[148:43] the comment section in the uh
[148:44] description below. David, thank you.
[148:46] Thank you, Stephen. I really enjoyed it.
[148:48] Thank you.
[148:49] YouTube have this new crazy algorithm
[148:50] where they know exactly what video you
[148:53] would like to watch next based on AI and
[148:55] all of your viewing behavior. And the
[148:57] algorithm says that this video is the
[149:00] perfect video for you. It's different
[149:02] for everybody looking right now. Check
[149:03] this video out and I bet you you might
[149:05] love it.
