Aging, and the chronic diseases that come with it, is considered just an inevitable part of life. But what if it wasn’t? What if aging itself was a disease – a disease that can be treated? Many scientists are doing just that, and the results are nothing short of shocking. Just how close are we to a cure for aging?


I had a birthday recently, and I’m way past the age where a birthday is something to get excited about. Now it’s just a reminder that your body has decayed one more year.

Yeah, aging is bullshit.

It’s a joke that a lot of comedians have told that once you get past a certain age, doctors just stop trying to fix you.

After a certain point, life is just an endless series of trying to figure out what is causing the random pain today.

And you go to the doctor with that pain and they just kinda give you the shoulders like, I don’t know that’s what happens.

Cool. Thanks guy.

But there are some doctors and researchers doing the opposite. In fact they’re making the argument that aging itself is a disease. And this disease can be treated.

And I think it’s a pretty compelling argument. So today let’s not go quietly into that good night and talk about how we can slow, stop, and maybe even reverse aging.

The Merck Manual defines aging as “a gradual, continuous process of natural change that begins in early adulthood.” And that’s fine. Change is good.

It goes on to say that “bodily functions begin to gradually decline” during a person’s early middle age. Cool.

But people can grow old in several ways:

In 1970, the average life expectancy in the U.S. was 71. Fifty years later, it was 77.

And that sounds great… But it’s kind-of not.

Because yeah, we’re living longer, but those extra years are being added at the end of our lives, when we’re at our most decrepit and in the most pain.

In other words, we may be extending our lifespans, we’re not necessarily shoring up our healthspans.

For example, between 2013 and 2015 the number of years lived in poor health in the U.K. was 16 for males and 19 for females.

More people living longer also increases the risk of more people living with dementia, and Alzheimer’s disease.

And this isn’t just a problem in individual lives, this has societal implications.

These people often need constant care in order to live their daily lives, which may create economic and social burdens for communities, caregivers, and families.
The longer you live also increases the risk of developing other chronic conditions like cancer, diabetes, and heart disease.

It’s like this constant, expensive whack-a-mole we play in the last 20 or so years of our lives until eventually… one of the moles get us.

But what if we change our thinking on this? What if instead of treating these as different diseases, we start thinking of them as symptoms of a bigger, broader disease? The disease of aging.

o a lot of people that sounds crazy, to call aging a disease because I mean, aging is a natural process, how can that be a disease?

But… cancer is a natural process. Arthritis is a natural process. Most diseases are natural processes and we fight them tooth and nail. So why not aging itself?

It’s funny how aggressively people push back against the idea of life extension and age reversal, people call it unnatural as if there’s anything natural about the way we live these days.

It’s weird to me. Like why wouldn’t you want to live longer and healthier? Why wouldn’t you want to be in less pain? It’s like people have some kind of mortality Stockholm Syndrome or something.

We know that different people age at different rates, and different animals age at different rates. So clearly aging is a malleable process that can be sped up or slowed down. And we’re learning how to do exactly that.

So let’s start by talking about how aging works and I should go ahead and disclose that a lot of what I’ll be talking about here is from the book Lifespan by David Sinclair, he’s a Harvard researcher that focuses on aging and he’s got some pretty unique insights; it’s worth a look.

Right off the bat, there’s no unifying theory about aging. Except for the one that Sinclair professes, which we’ll get to in a moment.

One hypothesis is that DNA damage causes aging. There are also theories about mutations to the DNA or that free radicals contribute to aging.

But many of these theories have kind-of fallen to the wayside over the years. These days aging is usually attributed to a handful of cellular processes, including:

  • Attrition of telomeres
  • Genomic instability from DNA damage
  • Mitochondrial dysfunction
  • Senescent cell accumulation
  • Stem cell exhaustion

Researchers work at addressing these aspects as a way to slow down aging, which may mitigate diseases, which could forestall death.

All of this may help us add more healthy years to our lives. But they won’t help us live longer.

For that, we need a singular reason why we age, which brings us back to David Sinclair’s theory, which he calls the Information Theory of aging.

Sinclair writes in the book that there are two types of information in biology:

  • Digital: Based on a finite set of possible values, like DNA
  • Analog: Commonly referred to as the epigenome, which are heritable traits that aren’t transmitted by genetic means

As DNA stores genetic information, a structure called chromatin stores epigenetic information.

It’s this information that guides the assembly of a human being from a fertilized egg.

Another way of putting it, if the genome was a computer, the epigenome would be the software.

He also uses the analogy of a scratched DVD. That over time DVDs accumulate scratches to the point that eventually it doesn’t play anymore. But, that information isn’t lost. It’s still there under the scratches. And if you polish the DVD, which I’ve done many times, it’ll play perfectly again.

The epigenome works the same way. Over time little imperfections build up – scratches if you will – that cause cellular processes to deteriorate, which we experience as aging.

So the question is, how do you “polish” the epigenome? Well it turns out we have some genes that are designed to do exactly that.

They’re called “longevity genes” or “vitality genes,” and they’re tied into our body’s survival circuit. And they go back all the way to the beginning of life on this planet.

Life, it turns out, wants to survive, and times are not always plentiful so during times of stress, these survival genes kick in and help the body repair itself.

When things get tough, they hunker down. When things are easy, they tell our cells to grow and reproduce fast.

One of these longevity genes is called target of rapamycin, in us and other mammals it’s called mammalian target of rapamycin, or mTOR.

When under stress, mTOR sends a signal to help improve survival by boosting DNA repair, reducing inflammation from senescent cells, and by digesting old proteins.

When everything is good, it helps with cell growth by managing the creation of proteins.

So, mTOR – target of rapamycin, keep that one in mind.

Another longevity gene is called AMPK, which stands for adenosine monophosphate-activated protein kinase. (a beat) That word salad will make sense in just a second.

So to explain AMPK – let’s step back. First of all, the cells get energy in the form of chemical bonds, delivered by the ATP molecule.

Like when you eat something, the digestion process breaks that food down over and over until it gets down to basic molecules that can be used by the cell, well the basic molecule that delivers energy is ATP – adenosine triphosphate.

This is a nucleoside, adenosine, tied to three phosphate groups. So, triphosphate.

Once ATP gets inside the cell, the cell strips two phosphate groups from the molecule, releasing energy in the process, and leaving behind a single phosphate group, turning ATP – adenosine triphosphate, into AMP, adenosine monophosphate.

You got it? You still with me? You good?

So cells require a steady flow of ATP in order to keep functioning. If a cell uses up all its energy from ATP, it then fills up with low-energy AMP molecules.

It then runs out of energy, collapses, and dies. Unless… A new source of energy is found. This is where AMPK comes in.

AMPK essentially is the gene that tells the body to pull energy from stored sources in the body, like fats and sugars.

So, when there are high levels of adenosine monophosphate in the cells, it activates the adenosine monophosphate-activated protein kinase gene. Word salad explained.

In our youth, we have high levels of activated AMPK, which is why we burn fat so much easier when we’re young. But those levels do drop off as the years go by.

But a side benefit of AMPK activation is that it can slow aging in a couple of ways, by reducing oxidative damage, and protecting against senescence.

Senescent cells by the way are kind-of zombie cells. They’re alive… but not functional. They basically just pump out a bunch of inflammatory signals that causes all kinds of problems.

But AMPK activation can clear those senescent cells out through a process called autophagy.

So, AMPK burns fat and kills zombies. So how do you turn on AMPK and become a sexy zombie hunter? One way is through calorie restriction.

Eating less – seems pretty obvious but if you don’t feel like starving yourself, there’s also a pill you can take.

Metformin is a drug that is used to help treat type 2 diabetes but also activates AMPK. It basically mimics some benefits of calorie restriction without decreasing caloric intake.

Also, it can help improve physical performance, increase sensitivity to insulin, and reduce cholesterol levels. And the best part – it’s super cheap. But you do need a prescription in the US.

One last longevity pathway are a family of enzymes called sirtuins. There are 7 of these, SIRT1 through SIRT7.

These play a major role in cell survival and metabolism, and DNA repair.

If you’ve heard of NAD supplements lately, this is what those are for, sirtuins are dependent on that.

They can also be activated by low-calorie or low-amino-acid diets or exercise.

mTOR, AMPK, and sirtuins are three longevity pathways, according to Sinclair. They were evolved to help protect the body during times of stress by activating survival mechanisms.

And once activated, “organisms become healthier, disease resistant, and longer lived,” Sinclair wrote.

So basically the key to longevity, according to this theory, is for the body to be in a state of stress. I know that sounds fun. But there are some ways of doing that.

The first is through intermittent fasting.

If you want to activate that AMPK gene, you’ve gotta make your cells hungry. And that means not eating. Sometimes.

There are several types of intermittent fasting.

For example, the 16:8 diet (Jason note: This is the one I do.) has you fast for 16 hours and eat within an eight-hour window. For some people that means you start eating at noon and stop eating at 8:00. When I do it I usually go from 2 to 10. Because I stay up late.

The 5:2 diet has you eat 75 percent fewer calories for two days a week.

Whichever one works for you, studies have shown that intermittent fasting can help lower blood pressure, reduce body fat, and decrease weight.

Though in the interest of balance, there have been some studies that show it’s not as effective for weight loss. But, for the anti-aging properties, studies show some pretty compelling results.

Another way to switch on sirtuins is through cold temperatures.

Cold temperatures activate brown fat, or brown adipose tissue.

This is a type of fatty tissue that has more mitochondria than regular fat, and it helps maintain body temperature in cold conditions. And a side benefit is that it helps in DNA repair because again, your body is in stress.

This is why a lot of people advocate for cold showers which I’ll just come out and say it, that’s a nope for me dawg.

I’ve tried it and…. no.

Although it’s mostly carried in our backs and shoulders so if you can lay on an ice pack or a cold pad, that’s supposed to produce some effect anyway.

And then there’s exercise. Yeah, I know, it always comes back to exercise.

Not only does exercise help with blood flow, heart and lung health, and mental health, it can help preserve longer telomeres, those things at the end of chromosomes that help protect them from damage.

Thing is, you don’t have to exercise for a long time to reap its benefits.

One study showed that with just 15 minutes of exercise a day, a person can reduce the risk of a heart attack by 45 percent.

They say the goal is to exercise to the point that you’re breathing hard enough that it would be difficult to talk. If you can just do that for 10-15 minutes a day, that’s enough to make a difference.

But you might be saying, “10-15 minutes! That’s like my whole day, can’t I just take a pill?”

Yes, there are some pills that you can take but before I go any further, this is where I have to point out that I am not a doctor, and what I’m telling you is not medical advice. But these are some of the supplements and pills that are being studied.

You’re in luck because research is being conducted into things like nicotinamide mononucleotide (NMN) and resveratrol to determine their effects on longevity.

First, a reminder that I’m not a doctor, and what I’m telling you is not medical advice.

The first is NMN, or nicotinamide mononucleotide.

NMN is a precursor of NAD+ so when you take an NMN supplement, your body breaks it down into NAD+.

As I mentioned earlier, NAD+ is central to metabolism and is associated with things like downregulation of energy production in mitochondria, inflammatory conditions, and oxidative stress. And its level decreases with aging.
You might have also heard of Resveratrol lately. This is a compound found in several plants, like peanuts, berry fruits, and grapes.

It’s known for being associated with various health benefits, like:

  • Antidiabetic
  • Anti-obesity
  • Antioxidants
  • Glucose metabolism

Other medicines and supplements that show promise in extending lifespans are the aforementioned metformin and rapamycin.

Rapamycin is interesting actually because it was first discovered on a bacterium in Easter Island – the island with the big stone heads on it. And that’s how it got its name the Polynesian name for Easter Island is Rapa Nui.

And for years it was used as an immunosuppressant for transplant patients until some studies showed that it had anti-aging properties.

You might remember that mTOR gene that triggers DNA repair earlier, well mTOR stands for mammalian target of rapamycin. That’s how they found this gene.

So rapamycin can trigger DNA repair and improve longevity, there have been some amazing studies in mice with this actually.

Though I should also say that as an immunosuppressant, it can have some undesirable side effects so be especially careful with this one.

Research is ongoing, but all or any of these things might just give you some extra years of life. Years that might get you closer to some real crazy stuff.

Because if we have these genes that can trigger DNA repair and other life-extending processes… and we have the ability to edit our genes… maybe someday we can just turn those processes on at will.

One of the wilder ideas in Sinclair’s book is that we could edit our genes to have an age-reversal trigger. One that gets turned on when we take a simple antibiotic.

So we could create this edited gene, spread it throughout our bodies with a viral vector, and then at various times in our lives, as age-related issues start to crop up, we can go on that antibiotic. That age-reversal trigger kicks in and we just… age backward for a few months.

We get more energy, our joints get stronger, skin gets more supple, hair gets it color back, and when we’re at the biological age we prefer, we stop taking the antibiotic, start aging normally again.

This is apparently something they’re already doing in mice.

And of course, if you really want to cheat death, there’s always cryonics, which I’ve done a whole video on before.

Now we’re really nowhere near being able to restart bodies that have been frozen in liquid nitrogen and if we’re being honest, the chance that it could ever work is low. But in 2019, scientists did put a human being in suspended animation for the first time.

This happened at the University of Maryland and the process involved rapidly cooling the brain to less than 10 degrees Celsius (50 degrees Fahrenheit) by replacing a patient’s blood with an ice-cold saline solution.
This gave surgeons some extra time to perform surgery on a patient who had lost half of his blood. He was essentially dead for a while, his brain and heart went silent. But they brought him back to life.

The boundary between life and death has been shifting for hundreds of years now. And now we can actually put people in suspended animation. It’s only for short periods right now but give it another 30 or 50 years… (shrug)

The bottom line is, aging research is still in its infancy. It’s actually remarkable that we know what we do considering how few researchers around the world are studying this. But that’s changing really fast.

We’re about to see an explosion of aging related research. Because as I mentioned at the beginning of this video, we have to change our mindset on aging from being just a thing that’s bound to happen to a disease that we can treat.

And in January of this year a major step was taken in that direction when the World Health Organization’s 11th International Classification of Disease (ICD) revision went into effect.

The ICD is an international standard for clinical diagnosis, epidemiology, and health management in developed nations. They basically assign a code for every disease.

Having a disease recognized with a code by the ICD basically legitimizes it in the eyes of the research world, it allows for drugs targeting that disease to be clinically evaluated and approved.

And the newest addition of the ICD includes for the first time an extension code for “aging-related” diseases.

This means more money for research and just as important, for insurance companies to provide coverage for therapies targeting that disease.

So hey, everybody says I’ve been too doomy and gloomy on this channel lately well how about this, we are about to see massive advancements in life extension over the next 20 years.

You might not live forever. But it might be a lot longer than you think.

So I’ll leave you with one last thought and let you guys debate it in the comments. I’m sure many of you have already started listing all the reasons why it would be terrible if people lived longer. I mean, other people, not you.

The overpopulation problem, the world can’t sustain that many people, economic and labor problems if people never retire, all interesting points and there are counterpoints to all of them, but I just want to ask one thing.

How much differently would people act if they really had to deal with the consequences of their lifestyles?

I’ve heard many a person poo-pooh climate change saying, “oh the worst of it will happen long after I’m dead.” And the same attitude goes for other things, I’m just using climate change as an example.

But what if we did have to live with it? What if instead of thinking about things affecting future generations, we know it would affect us in our own lifetimes? Would we behave differently? And could that produce a better society? I’m curious what you think. Let me know down in the comments.

Add comment

Your email address will not be published. Required fields are marked *