Aging is far more than wrinkles—it’s a complex biological process driven by twelve interlinked mechanisms like genomic instability, mitochondrial dysfunction, and telomere attrition. In my latest video, I explore how these hallmarks accelerate aging and the science behind interventions that may slow them down—ranging from fasting and NMN supplementation to hormetic stressors and key pathways like mTOR and AMPK.
While full-body age reversal remains out of reach, strategies like caloric restriction, targeted exercise, and certain supplements are showing promise in extending healthspan. Watch the full episode on YouTube channel for a clear, science-based look at what aging really is—and what we can do about it.
Transcript
00:00:00
Aging is a biologically complex multiffactorial process driven by molecular, cellular, and systemic whole body changes that accumulate over time. This ultimately culminates in physiological decline and an increased risk of disease and death. While perspectives on aging vary, ranging from biogentologists who study aging at the cellular level to clinicians and medical doctors who focus on age related diseases to biohackers who aim to intervene in the aging process. Fundamentally, aging is an interplay of
00:00:30
genetic, metabolic, and environmental factors that regulate the body’s ability to function. Today, we’ll explore the molecular hallmarks of aging, the biochemical pathways involved, and the extent to which interventions can modulate these processes. At its core, aging results from the gradual disregulation of key pathways leading to systemic decline. There are 12 major mechanisms or causes of aging. Some of which include genomic instability, telmir attrition, epigenetic alterations, loss of proteostasis,
00:00:59
mitochondrial dysfunction, deregulated nutrient sensing, cellular scinessence, stem cell exhaustion, altered intracellular communication. There’s a lot. These hallmarks are interdependent, creating a self-reinforcing cycle of damage that accelerates the biological aging process. We’ll go over these mechanisms in death in a future episode, but for now, let’s cover a few at a high level. One of the primary drivers of aging is genomic instability, which arises from cumulative DNA damage due to oxidative stress, replication of DNA
00:01:31
errors, and environmental insults. DNA repair mechanisms become less efficient with age, leading to mutations, chromosomal rearrangements, and loss of genomic integrity. The accumulation of mutations particularly in stem cells contributes to the functional decline of tissues and increases cancer risk. Another central aspect of aging is telomeir attrition which is a process where the end caps of our chromosomes which protect our DNA become progressively shorter with each cell division. Telmir shortening leads to
00:02:00
another cause of aging cellular scinessence commonly referred to as zombie cells. We’ll leave that mechanism of aging for another video. Epigenetic alterations, which includes a process known as DNA methylation, plays a key role in gene regulation during aging. The DNA methylation process essentially determines which parts of the DNA should be readable and which should not, ultimately determining gene expression. If your genes are a piano, the epiggenome is the music being played on it, which is heavily determined by your
00:02:30
lifestyle and environment, and the tune changes as we age. Biological age clocks known as epigenetic clocks such as the Horvath clock, rim age clock or the Dunid and Pace clock measure the shifts in the DNA methylation patterns or the epiggenome or the music that correlate with biological age and these changes impact processes involved in how our bodies cope with inflammation, oxidative stress and cellular repair. Next is loss of proteostasis, the failure of protein quality control systems. This
00:03:01
contributes to aging through the accumulation of misfolded proteins and aggregated proteins. With age, these protein folding pathways become disregulated and it leads to the accumulation of toxic protein aggregation seen in neurodeenerative diseases such as Alzheimer’s and Parkinson’s. Next is mitochondrial dysfunction and metabolic aging. Mitochondria are the power plants of our cells. They convert the food we eat into energy and they play a critical role in aging through their involvement in the
00:03:32
production of ATP, the energy currency of our cells, as well as a process known as apoptosis, a process of cellular suicide that is needed when a cell becomes old and dysfunctional. A decline in mitochondrial function, often termed mitochondrial dysfunction, leads to increased production of reactive oxygen species, which cause damage to DNA and to cells and their proteins, bringing us back to the initial point of genomic instability, which leads to cells turning scinesscent, which results in a new cell having shorter telomeres, and
00:04:06
so goes the process. A key regulatory pathway of mitochondrial health is the AM activated protein kinace. For short, it’s known as EMPK. You may have seen it online. It senses when a cell has low energy levels, and this can be the result of exercise, fasting, or even some supplements and prescription drugs. EMPK can signal other pathways like PGC1 alpha, which can result in new mitochondria being created. But with age, AMPK signaling declines, leading to poor mitochondrial function and increased oxidative stress. The mtor
00:04:40
pathway which stands for mechanistic target of raprapamycin is another central regulator of metabolic aging. MTor complex one activated by nutrients and growth factors particularly insulin and IGF-1 promotes anabolic processes and inhibits the cellular cleanup process known as autophagy. This sounds good right? The problem is that chronic activation of mTor complex 1 accelerates aging by driving cellular scinessence and metabolic dysfunction. In our modern-day constantly fed environment, mTor is practically always on. This is
00:05:14
why people are seeing such great effects from fasting and reducing their caloric intake. Doing so lowers the volume on mTor complex one and turns up the process of autophagy cellular recycling thereby clearing damaged cells in organels and prolonging lifespan. The NAD+ certuin axis also plays a critical role in mitochondrial function. NAD+ is trending a lot on Tik Tok and Instagram for health enthusiasts. Well, what is it? It’s a co-enzyme essential for reactions that reduce oxidation in the body and it declines with age NAD+. This
00:05:50
decline impairs enzymes known as certuins which regulate the creation of new mitochondria responses to oxidative stress and damage and helps to repair DNA and restoration of NAD+ levels through precursors like nicotinomide monucleotide also known as NMN has shown promise in reversing aspects of mitochondrial aging. Given our understanding of metabolic pathways involved in aging, several interventions have been proposed. One is caloric restriction and fasting. This reduces mTor complex one activity and
00:06:23
increases and cert. It enhances autophagy and it promotes ketogenesis by increasing a molecule known as beta hydroxybutyrate that our body produces which acts as something known as a histone deacetylase inhibitor. What does that mean? It means improving expression of genes associated with longevity. Number two is supplements. NAD plus precursors like NMN. They may help to restore mitochondrial function and enhance DNA repair. Number three, exercise and hormetic stressors. For example, highintensity interval
00:06:55
training. It improves mitochondrial density and efficiency. Cold exposure and the resultant heat shock proteins that come from the cold exposure activate stress responses and promote cellular resilience. And finally we have the pharmacological interventions pharmaceutical drugs like rapamy and metformin. Rapamycin inhibits mtor complex one. It extends lifespan in every species it has ever been studied in. It’s the gold standard longevity drug that scientists compare all other drugs and supplements to metformin
00:07:28
activates kynisek. It reduces inflammation and enhances insulin sensitivity and it’s prescribed to diabetics. Now, both of these drugs you need to see a doctor about. Don’t take them on your own. So, what can and can’t we do about aging? While significant progress has been made in understanding aging at the molecular level, full body age reversal is not yet possible. We can slow aging. We can improve health span, extend lifespan, we can reverse certain biomarkers of aging as we saw in a study called the Trim
00:07:59
trial. However, irreversible aspects of aging such as neuro degradation, skeletal remodeling like what our faces look like and glycation induced cross-linking which stiffens our tissue including our blood vessels just to name a few. These are major hurdles. The challenge now is translating these molecular insights into effective scalable therapies. Advances in cellular reprogramming, autophagy enhancement, and scinsesscent cell clearance. They all offer hope, but their safety and long-term effects are currently being
00:08:31
studied. We don’t know yet. As the field moves forward, the integration of systems biology, AIdriven biomarker analysis in real time and personalized interventions. These are going to lead to a new generation of longevity strategies. But we’re not there yet. So today what we learned is that aging is a multiaceted biological process driven by interconnected molecular pathways. While we’ve identified key regulators such as mTormp kin certuins and scinsessence pathways the question of full reversal
00:09:04
is still quite a while away. Current interventions focus on slowing aging and mitigating damage but emerging research is promising for more substantial rejuvenation approaches. Until then, optimizing metabolic health through caloric restriction and an ideal diet, sleep hygiene, stress management, certain supplements and exercise, maybe even prescription drugs, remain the most effective approaches to extending health span. So, make sure to like, comment, and subscribe if you’d like to stay in the loop on future episodes in which
00:09:36
we’re going to dig in deeper into what causes us to age, and most importantly, the specifics of what all of us can be doing today to slow down the process of aging. All based on the top science directly from the scientific labs, not crazy claims that are being made by popular influencers nowadays. So, make sure to follow on social, slow my age, on Instagram, Tik Tok, X, LinkedIn, YouTube, all of those networks. Send your questions in. I’d be happy to answer them.