From Death Sentence to World Record in Telomere Extension — My Journey to Becoming a Longevity Pioneer

Disclaimer: The content of this article is for informational and educational purposes only and does not constitute medical advice. It is not a substitute for professional medical consultation, diagnosis, or treatment. Always seek the guidance of a qualified healthcare provider with any questions you may have about your health or before starting any new health regimen. Never disregard professional medical advice or delay seeking it based on information provided here.

Summary: In healthy cells, long telomeres — the end of our chromosomes — are better than short telomeres. With each cell division, telomeres shorten. With aging, the average length of telomeres shortens, increasing the risk for loss of division potential, function and inducing senescence. Therefore telomere extension can be an effective strategy to slow the progress and harmful effects of aging. Two years ago, I was diagnosed with extremely short telomeres corresponding to a biological age of 70 y/old (I was 30 y/old then). This probed me into a journey of research into longevity. I took a data-driven approach to my wellbeing and habits, adopting a plethora of interventions that extended my telomeres by 60%, more than anyone else’s in recorded history.

Introduction

Growing up, I’ve been captivated by the idea of unlocking human potential — like Bradley Cooper’s character in Limitless, who discovers a way to become superhuman overnight. My early career was a whirlwind of 16-hour days, relentless ambition to achieve market leadership in a VC-fueled environment, and a lifestyle fueled by fast food and minimal sleep — a recipe for disaster destroying my health. I became over-weight, which pushed me to start taking conscious care of my health.

In 2017, in my mid-twenties, I stumbled on a blog post of Serge Faguet, and started to connect the dots, the vision that one can indeed become super-human, not with one magic pill, but with the combination of a number of interventions.

Aside from working out and several weightloss challenges, I developed my own supplement routine that I had been running on since c. 2020. You can see my old routine in a previous blog post from 2022, though there is an update coming soon, as many of my views have changed.

As my curiosity deepened, I dove into the science of aging and embarked on the ‘Big 5 Tests’: Whole Genome Sequencing, Extensive Blood Work, Epigenetic Aging assessments, Medical Imaging (MRI), and Telomere Length Testing.

I highly recommend everyone to do these tests. Through bloodwork and genetic testing, I for example discovered I had a mild form of hemochromatosis — a condition causing iron buildup in the blood that can lead to inflammation and cardiovascular disease. It’s highly treatable, and it’s estimated that in the U.S., 5.4% of the population carries the C282Y mutation, and 13.5% carries the H63D mutation, each responsible for a mild form of the disease, and in case both mutations are present, a more severe form of the disease.

In April 2023, it was time for me to take my first telomere test. I was in Los Angeles and did a blood-based test with Novos Age, an American provider of longevity tests and supplements. My expectation was of course that I would have quite healthy telomeres, based on the lifestyle changes already implemented over the last 6 years, and as telomeres are relatively inelastic to lifestyle both on the upside and downside. For example, heavy alcoholics suffer the equivalent of 3–4 years of telomere attrition, according to studies.

However, I remember this day as if it was yesterday. I received my report from Novos Age on 12 June 2023 and it read that I was ranking in the 0th percentile for telomere length of my age group. My average telomere length was 6.8 kilobases (kb). This means that in my age group, almost 100% of people had longer telomeres and my average telomere length corresponded to the average telomere length of a 70 year old. We will get into this later, but this basically meant for me that I was much more likely to suffer from age-related diseases or to even die 10–20 years, a quite bleak outlook for a then 30 year old.

04/25/2023

Rather than succumbing to despair, my diagnosis ignited a two-year odyssey into biohacking and molecular biology — a quest to rewrite my biological destiny. I became obsessed with learning as much as I could about the topic, as well as experimenting on myself. I took the view that extending my telomere length would be the single highest ROI activity I could pursue, and also increased my willingness to just try a lot of things without worrying too much about proven efficacy.

Fast forward two years — the story has an extraordinary ending. My telomeres now mirror those of a teenager — a transformation that not only reversed decades but likely set a world record, reducing my age of telomeres by 50+ years and increasing the length of telomeres by 60%. The change happened gradually, though I was personally surprised by how much and actually found out that I now probably hold the world record in telomere extension, comparing my results to the extensions results of more experimental interventions discussed in section 5.

The images below show two tests. The first, from August 2023, showing that my telomeres, with an average of 7.4 Kb, extended to the average for people my age. The second, from September 2024, shows my telomeres extended to 10.81 Kb (with only 3.47% of extremely short telomeres), which is more than 2 Kb higher than the average for people my age, placing me in the 99th percentile of telomere length compared to others of my same chronological age.

09/29/2023

09/27/2024 — this was my last result, showing my telomere length is significantly above the mean for people my age.

Here you can see a summary of my telomere extension progress over time:

NB: If you consider that 0.65 kilobases (kb) is the standard deviation of telomere lengths in healthy adults (as reported by large cohort studies like Weischer et al., 2013), you can calculate a Z-score to assess how extreme my telomere length is relative to the general population.
A Z-score measures how many standard deviations a data point is from the mean (average). It is calculated as:

Z = (X — μ) / σ

where:

• X = my telomere length = 10.81 kb
• μ = average telomere length = 7.4 kb
• σ = standard deviation = 0.65 kb

Substituting the values:

Z = (10.81–7.4) / 0.65
Z = 3.41 / 0.65
Z ≈ 5.25

A Z-score of 5.25 corresponds to a percentile greater than 99.9999%.
In simple terms: based on this statistical model, fewer than 1 in a million healthy 30-year-olds would naturally have a telomere length as long as mine.

Of course, real-world biological data is not perfectly normally distributed, but this calculation still strongly supports that I am in the >99.9th percentile for biological telomere length among my peers.

Finally, this chart indicates how my chronological versus telomere age evolved over time:

2. Short Telomeres Impair the Replication and Proper Functioning of Cells, Increasing Propensity of Death

In healthy cells, long telomeres are better than short telomeres. Telomere Attrition, meaning shortening telomeres, are one of the hallmarks of aging. Telomeres are protective caps made of repetitive DNA sequences and associated proteins located at the ends of chromosomes. They function like the plastic tips on shoelaces, preventing chromosomes from fraying, fusing with one another, or being mistaken for broken DNA by the cell’s repair mechanisms. With each cell division, a portion of the telomere is lost because DNA replication cannot fully copy the very ends of linear chromosomes. Over time, this progressive shortening leads to critically short telomeres

Figure 1. Our chromosomes end with repeats of conserved ‘TTAGGG’ sequence. These sequences interact with specific proteins and attain a looped conformation which protects chromosomal DNA from degradation. The length of telomeric DNA shortens with each cell division and when it reaches below a critical limit, the cell undergoes replicative senescence or apoptotic cell death. The length of telomeric DNA determines the lifespan of a cell in culture. (Shammas 2012).

Short telomeres have significant negative implications for health and longevity. Cells with short telomeres often lose their function due to the critical role telomeres play in maintaining cellular integrity. When telomeres become too short, they can no longer protect chromosome ends, which triggers a DNA damage response. This leads to cellular senescence (a state where cells stop dividing) or apoptosis (programmed cell death), effectively halting the cell’s ability to perform its normal functions. It has long been thought that telomere attrition is the main cause of aging and death due to the so-called Hayflick limit that imposes a limit on how often a cell can divide. However, by today’s knowledge, this view is too simplistic.

Still, short telomeres increase the risk of age-related diseases such as cardiovascular conditions, diabetes, osteoporosis, and certain cancers. Furthermore, short telomeres impair the function of stem cells, which are crucial for tissue regeneration, and can lead to conditions like bone marrow failure or immune system deficiencies. Telomeric shortening at some point induces DNA damage which lets loose signaling which changes the epigenome disrupting epigenetic silencing and resulting in pro-aging global DNA expression.

Numerous studies have demonstrated the association between short telomeres and increased mortality risk. A meta-analysis of 25 studies, including over 121,000 individuals, found that those with the shortest telomeres had a 26% higher hazard of all-cause mortality compared to individuals with the longest telomeres. Each standard deviation decrease in telomere length corresponded to a 9% increase in mortality risk, highlighting telomere length as a critical biomarker for longevity. Another study found that people with both short telomeres and depression faced a 4-fold increased risk of mortality compared to those without these factors.

Therefore, telomere extension can be an effective strategy to slow the progress and harmful effects of aging. Longer telomeres are a net benefit, potentially adding 3 to 5 years to our lives. Longer telomeres also provide major protection against cardiovascular disease.

In short, you want long and healthy telomeres.

3. Short Telomeres are Caused by Stress, Poor Lifestyle and Potentially COVID-19

Before talking about the telomere extension methods, it’s perhaps important to understand what factors can contribute to the accelerated shortening of telomeres, so that readers can better judge if they should get their telomeres tested.

Overall, telomere shortening accelerates due to a combination of psychological stress, oxidative damage, and lifestyle factors. Especially chronic stress triggers biological cascades that erode telomeres: a landmark study found women under high stress had telomeres 550 base pairs (bp) shorter than low-stress peers, equivalent to 9–17 years of accelerated aging. Oxidative stress and inflammation amplify this damage — higher C-reactive protein (CRP) levels, a marker of systemic inflammation, correlate strongly with shortened telomeres across age groups, with a 20–37% reduction observed in high-inflammation individuals. Infections further accelerate attrition, as shown in animal models where repeated pathogen exposure reduced telomeres by 15–20% over months. Smoking and alcoholism accelerates telomere loss by 50–100 bp/year. Obesity, a diet high in processed meats and low physical activity compound this effect. Genetic predispositions such as Short Telomere Syndrome can further contribute to these trends.

Moreover, these forces interact — stressed, inactive individuals lose telomeres 4x faster than active peers, highlighting the interplay between environment and biology. Together, these data quantify how stress, inflammation, and lifestyle choices converge to accelerate telomere erosion, with measurable impacts ranging from years of biological aging to disease-specific mortality risks.

There is further emerging research that COVID-19 infection(s) may accelerate telomere shortening, particularly in severe cases and long COVID patients. Multiple studies report 20–37% shorter telomeres in post-COVID survivors compared to controls, with average lengths of 3.03 kb vs. 10.67 kb in one analysis (Mongelli et al. 2021). I personally believe that this may have been the main culprit causing my short telomeres. At the time of my test, I was in good physical shape, while also taking a lot of supplements already curbing inflammation and oxidative stress.

While it can be argued that I’ve been constantly stressed since my early twenties, I’m not significantly less stressed now, compared to two years ago when my telomeres were dangerously short. However, I went through several rounds of COVID-19 infections over the last few years. I believe all survivors of COVID-19, even if the infection was mild, should test their telomeres. I find it likely that excess mortality that we currently see in the post-pandemic world may be linked to a population-wide telomeric attrition and the associated increase in all-cause mortality previously discussed.

4. Telomere Extension is Possible Through Telomerase Enzyme Expression and Lifestyle Changes

Although telomeres are typically thought to shorten with each cell division, there are certain circumstances where they can actually increase in length. This happens primarily through the action of an enzyme called telomerase, which adds repetitive DNA sequences back to the ends of chromosomes, making the cells immortal. This typically happens naturally in specific cells, such as reproductive cells, certain stem cells, and some immune cells, to maintain their ability to divide indefinitely. But in general all cells slow their telomere attrition in presence of telomerase enzymes. With aging, telomerase activity and expression decrease in most human cells, leading to the shortening of telomeres and therefore age-related decline.

Source: genengnews.com

For longevity purposes, I believe that it could be beneficial to temporarily boost telomerase expression to allow telomeres to grow back. Researchers at Stanford, led by Dr. Helen Blau, demonstrated that by temporarily activating telomerase in human cells using modified RNA, they were able to lengthen telomeres by about 1,000 nucleotides (a 10% extension), effectively “rejuvenating” the cells and allowing them to divide more times than they otherwise would.

However, telomerase should not be permanently overexpressed. Its activation is a double-edged sword, as it can grow both telomeres and cancer cells. In cancer cells, telomerase is often hyperactive, contributing to their immortalization by continually elongating telomeres and allowing for unlimited cell division. Telomerase does not cause cancers but can cause them to go into high gear. Therefore, inhibiting telomerase is actually a strategy of cancer therapy, as it makes cancer cells more vulnerable during cancer treatment.

It is likely that an effective longevity regimen would involve cycling phases of telomerase activation to lengthen telomeres and phases of autophagy, to induce apoptosis in (potential) cancer cells that could have benefitted from over-expression of telomerase.

Aside from directly enhancing telomerase enzyme activity, environmental and lifestyle factors can also influence telomere length. For instance, studies have shown that interventions like stress reduction, meditation, Mediterranean or plant-based diets, sleep optimization and exercise can lead to modest increases in telomere length over time. However, it’s worth noting that some of these indirectly act through increasing telomerase.

Another way to improve telomere length is through the activation of the hormetic pathway, which is the underlying mechanism for the health benefits of sauna, cold-plunging and other popular activities. Among others, pulses of laser light, pulsed DC current, heat, cold, restriction of blood circulation, calorie restriction, intermittent fasting, and hypoxia can induce the hormetic activation.

Overall, the science suggests that telomeres are not static structures as long thought, but dynamic ones that respond to both cellular mechanisms and external influences. After receiving my diagnosis in June 2023, this gave me hope that there is potential to reverse my telomeric attrition.

5. Main Factors Contributing to Personal Telomere Extension are Mainly Clearance of Senescent Cells, Telomerase Activation and Removal of Toxins

There is a challenge of pinpointing how I exactly increased my telomere length by 60%. It stems from the fact that I was running essentially an n=1 experiment (i.e., an experiment with just one test subject) while changing a hundred variables at the same time. In the following I will try to point out the factors which I believe had the largest contribution to my successful reversal of telomere shortening.

Telomere length can fluctuate widely across the population of cells and short telomere length can be a symptom of improper clearance of senescent cells. Healthy cells have longer telomeres and senescent cells have short ones that bring down the average. Therefore, I went on a daily regimen of senolytics composed of high dose Resveratrol (1000mg/d), Fisetin (1200mg/d), Spermidine (likely the dosage was too low) and Quercetin (750mg/d). Looking at my test results from Sep 2024, the share of cells with very short telomeres has been extremely low. If there was any backlog of senescent cells, it has now been cleared, contributing an increase in average telomere length.

Today, I’m only taking low dose Resveratrol (100mg/d), Spermindine in a higher dose (20mg/d) and cycled Quecetin (750mg/d, one month on/off). There seems to be some evidence that the secretes from senescent cells can induce stem cell driven rejuvenation processes in the body under optimum circumstances, (but the body loses the ability to harness these processes from c. age 30 unless restored). This is a field I’m planning to spend more research on, but for the time being, in young individuals like me, I think permanent suppression and killing of senescent cells could counteract the body’s natural healing processes and have no recognisable benefits.

Aside from senescent cell clearance, there are supplements like L-carnosine (2x500mg/d morning and evening) and Gingko Biloba (200mg/d) that are associated with enhancing telomerase expression. However, I would suspect the effect to be rather mild. Nevertheless, especially L-carnosine has further very compelling benefits, so that it is in my top 10 list of all-star supplements for the purpose of longevity. Aside from this, higher blood levels of omega-3s (3g of DHA&EPA in a 2:1 Ratio/d) were associated with slower telomere shortening over time. I still take all of those supplements today.

EGCG, Resveratrol, Curcumin, Cinnamic acid and Bosweillic acid have been shown to have inhibitory effects on telomerase. Therefore, those should be taken at a distinctly different time of the day vs. the telomerase enhancing supplements to avoid cancelling each other out. Most supplements have a relatively short half-time in the blood, so that spreading out over the day gives you all benefits.

Moreover, NMN (1g/d) supplementation acts through a different, indirect mechanism to enhance telomerase activity. NAD+, the metabolite of NMN, fuels sirtuins, enzymes critical for telomere maintenance. SIRT1 enhances telomerase activity by activating TERT (telomerase reverse transcriptase). SIRT6 stabilizes telomeric chromatin, preventing DNA damage and chromosomal fusions. During 2023/24, I took my NMN in capsule form. These days, following a recommendation of Dr. Andrew Huberman, I’ve switched to a sublingual powder form of ingestion for better absorption. I believe NMN should be cycled to avoid a dependence effect of externally administered NMN, and I currently cycle three weeks on and one week off.

Aside from supplements, I also improved certain aspects of my work routine. I implemented time-boxing, keeping two days a week free for things popping up ad-hoc, therefore giving me more flexibility to react and potentially reducing stress. While I was working out before, in 2023 I started working out 3–4x a week with a personal trainer. Also, in terms of diet, I started to more closely follow a low-carb, high protein diet provided by a private chef and meal kit company.

I’ve also cut out a couple things that may have been harmful to my telomeres and overall health. On 01 January 2023, I implemented a resolution to stop vaping and I haven’t touched a vape ever since. For that, I used the technique of internalising externalities, which I described in another blog post. As of 01 January 2024, I’ve almost stopped drinking diet coke. Research has shown a clear relationship between Coca-Cola (and other sodas) and telomeres, with regular consumption of these beverages being linked to accelerated telomere shortening. For example, drinking a single 20-ounce soda daily is associated with 4.6 years of additional biological aging, a level comparable to the effects of smoking, in a study. Furthermore, I’ve stopped drinking filtered tap water, as I believe filters are not good enough to catch all harmful toxins. Instead I’m opting for bottled water, drinking Lauretana water, the cleanest water in the world.

6. There are certain advanced techniques that can further increase telomere length — I didn’t try them yet

There are certain methods for telomere length enhancement that I didn’t get to use, mostly for reasons of practicality (Hyberbaric oxygen chambers, near-infrared lasers & peptide injections) or cost/benefit (TA-65 supplementation). I think each of them is promising though. In a future home of mine with a longevity room, both a Hyperbaric Oxygen Chamber and near-infrared laser cabinet would have a space.

Hyperbaric Oxygen Therapy (HBOT) involves breathing 100% oxygen in a pressurized chamber, typically administered daily over 60 to 120 minute sessions and the number of sessions varies depending on your underlying health conditions. Studies indicate HBOT reduces oxidative stress and clears senescent cells, mechanisms linked to telomere attrition. In a trial of adults over 64, HBOT increased telomere length by 20–37% in immune cells — most notably B cells — while reducing senescent T cells by up to 37%. The effects were dose-dependent, with cumulative benefits observed after 30–60 sessions. The high number of sessions required shows why this is totally impractical unless you would have one at home.

Near Infrared (NIR) Laser Therapy uses low-power infrared light to modulate cellular repair pathways. In rodent models of heart injury, a single 10 J/cm² laser exposure increased telomere length by ~25% in damaged tissue. However, higher doses (20 J/cm²) showed mixed results, suggesting a narrow therapeutic window. Human data remains limited, but preclinical work highlights its potential for targeted telomere rescue. There are other benefits to this as well, so it is worth exploring.

Peptides, short chains of amino acids that can regulate biological functions, are increasingly being explored in the field of longevity for their ability to promote tissue regeneration, enhance DNA repair, stimulate telomerase activity, and modulate inflammation, all key processes in slowing and potentially reversing cellular aging. Certain Peptide Treatments such as Epitalon, a synthetic tetrapeptide, activate telomerase. Human trials report a 33% increase in telomere length and a 28% reduction in mortality over 12 years, with improved cardiovascular outcomes. Epitalon also demonstrates antioxidant and anti-tumor effects, though long-term safety in healthy populations requires further study.

One of the best results in telomere lengthening in humans is that of Dr. Bill Lawrence, a pioneer in longevity research. Through the use of peptides and a carefully curated therapeutic protocol of a combination of 20+ peptides, he was able to extend his telomeres from 6.38 kb to 8.65 kb over the span of six years, a remarkable increase of 35%. This change corresponded to a biological age reversal from 75 years old down to 23 years old, setting a precedent for what is achievable with targeted interventions. Dr. Lawrence’s work demonstrates that with advanced therapeutics like peptides, it is possible to not just slow, but actively reverse key biomarkers of aging.

Specialized Supplements such as TA-65, derived from Astragalus membranaceus, act as telomerase activators. In a 1-year RCT, low-dose TA-65 increased telomere length by 530 base pairs versus a 290 bp loss in placebo groups, preferentially elongating critically short telomeres. Higher doses showed diminishing returns, suggesting a bell-shaped efficacy curve.

7. Conclusions and Looking Ahead

Reflecting on my journey, it still feels surreal to think about where I started — at the 0th percentile for telomere length in my age group, with a biological marker that screamed “70 years old” at just 30. That diagnosis was a wake-up call, one that forced me to confront not just my mortality but the intricate interplay of biology, lifestyle, and science. Today, standing here with telomeres that rival those of a 23-year-old — an unprecedented 60% extension — I feel both humbled and empowered. This transformation wasn’t the result of luck or a single intervention but rather a relentless pursuit of knowledge, experimentation, and an unwavering belief that we can rewrite our biological narratives.

Throughout this process, I’ve learned that longevity is deeply personal. What worked for me — a combination of senolytics, telomerase activation, dietary shifts, stress management, and eliminating harmful habits — may not work for everyone. Our bodies are unique ecosystems, and understanding your own biology is the cornerstone of effective health optimization. My experience underscores the importance of regular testing.

What excites me most isn’t just my personal transformation but the ripple effect it’s creating. Friends, colleagues, and even strangers have reached out to share how my story has inspired them to take control of their health. This growing awareness fuels my passion for advocacy and research in longevity science. Looking ahead, I’m committed to pushing boundaries.

Ultimately, this journey has taught me that aging isn’t an inevitable decline but a challenge we can actively confront with science and determination. To anyone reading this: your health is your greatest asset. Embrace the tools at your disposal, stay curious about emerging innovations, and never underestimate your ability to change your trajectory. Together, we can redefine what it means to grow older — not as a limitation but as an opportunity for reinvention.