When will we be able to live forever

Based on the rate at which medicine is evolving, the answer to this question is a resounding “Now!”

Almost every disease has a cure or a cure-in-testing, and aging is just one of those diseases.

In the book How To Live Forever, I wrote four sections on ways that we already know to slow or even reverse aging, including telomere extension, senolytics such as FOXO4-DRI or UBX0101, calorie restriction, and increasing NAD+.

Of the four, three of them are in human trial at the moment, and the fourth has already been shown to reduce the incidence of tumours in humans.

Telomere extension has already been shown by Elizabeth Parrish to increase telomere length by 9%. This equates to about 10-15 years of life extension. This year, it was shown that telomere extension treatment in progeria sufferers results in decreased inflammation and decreased β-galactosidase almost immediately after treatment. Because humans live so long, it is hard to know for sure if live extension works. Progeria is basically a disease that increases the speed of aging in humans – if you can slow or cure progeria, there’s a good chance you’ve also made huge steps towards curing aging itself.

Senolytics are drugs that kill senescent cells – cells that have stopped replicating and producing new young cells, but which also refuse to die. Instead, they stick around spewing out inflammation proteins and causing other nearby cells to also go senescent, resulting in more and more of your cell population becoming old and useless. Senolytics such as FOXO4-DRI or UBX0101 work by covering the part of the FOXO4 gene which is stopping the cell from dying, thus forcing the cell into apoptosis (cell death), making room for new young cells.

Calorie restriction is shown in lab animals to reduce the incidence of tumours (cancers), and leading to longer (up to 50% longer!) lives as a consequence.

And finally, NAD+ is a catalyst which helps the mitochondria of your cells to work with oxygen to produce energy. In older people, the amount of NAD+ in your cells reduces, making it harder for the cell to produce energy, and sometimes resulting in DNA-replication errors. To increase NAD+ in your cells, you can either inject NAD+ directly, or ingest NMN (a precursor molecule that turns into NAD+ in the body).

There are a lot of other methods of living forever, but these are the big four at the moment.

Progress on the workshop/lab

I mentioned last month that I’m starting work building a lab for (eventually!) protein synthesis of FOXO4-DRI to reduce senescent cell build-up and NMN to promote NAD+ production in cells, etc. There’s no point writing a book on how to live forever if you’re not going to get working on the answers yourself!

Because I’m working completely on my own, and have no experience in construction, this is taking longer than I thought!

I have the foundation 95% completed now. The structural parts (the load-bearing bits) are completed. I just need to fill in some gaps in the foundation wall, then add some plastic damp proof coursing between the wall and the wood of the workshop floor, then I can start on the frame of the thing.

The plan with this is to start off with some simple things – a 3D printer and some electronics, and use those as a base from which to build up a proper lab, one tool at a time, building as many as possible from scratch.

Critics might say (and they do…) that the only way to do good work is with good tools, but they appear to forget that everything we see today was built from the ground up using nothing much more than a rock hitting another rock. You use bad tools to make better tools. I am doing the same.

I was asked why I didn’t just get some people in to do the building for me. Partly, it’s cost, but it’s mostly because I want the satisfaction of knowing exactly where every nail and knothole is, and I want to design every aspect of the building to my own specifications.

I have had to learn a lot along the way so far – how to do mortaring, how to drain an accidental pool (siphoning through a hose. muddy water doesn’t taste nice 😉 ), how water travels through concrete.

I’m still learning some things, like how to connect two pieces of wood together. Nails and nail plates appear to be the solution.

This weekend, I start on the frame of the build. I think that will go up very quickly.

Telomere lengthening as a treatment for Progeria

Telomeres are end-caps that keep your DNA from fraying. Over the years, they get smaller and smaller, until they’re so small the cells go into senescence mode and stop splitting.

When a cell is in senescence mode, it refuses to die, and instead just hangs around giving out inflammation-inducing proteins. Senescent cells are useful for helping healing wounds, but other than that, they’re a nuisance.

A study by John P. Cooke and associates found that telomeres in progeria sufferers tend to shorten much quicker than usual. This leads to very quick aging of the body, and usually death by age 15 or so.

In normal cells, telomeres cause death by aging by about age 120 (the Hayflick limit). The observation that telomere shortening is highly linked to aging in progeria makes that all the more obvious.

There has been speculation that telomere lengthening would help improve life-span, but very little evidence in humans, because we live so long compared to lab animals.

In 2015, Elizabeth Parrish, head of the company Bioviva, became the first person to undergo a telomere-lengthening treatment, and follow-up tests showed that she had indeed lengthened them by 9%, but there was nothing noticeable to show that the treatment had any positive effect.

The study done by Cooke showed that extending telomeres in progeria sufferers has an almost immediate effect, with a decrease in senescence-related beta-galactosidase staining, and reduced secretion of inflammatory cytokines. In Elizabeth’s case, it is possible she just had not reached the age where those would be measurable.

Telomere extension is one of the most important treatments that we will need to get into local clinics. It’s great to see it making some proper traction!

quantum immortality and old age

The idea behind quantum immortality is that there are infinite universes, and everything that can happen, happens in at least one of those universes. Thus, if you were to fall from a building, for example, then you would, in at least on of those universes, land in a bush or tree, or get blown onto a canopy, etc.

The scenarios described in quantum immortality usually only cover drastic events, though, where the “decision” between live and die is obvious. A gun fires, a bomb explodes, you fall from a building, etc.

But old age is not quite as obvious as that. It’s a lot more gradual.

Having said, that, though, maybe old age is the same?

When we say that someone died of old age, what comes to mind is that someone gradually declined until either they just stopped breathing, or their heart stopped.

Those are definitive moments that, if we’re talking about old age degeneration, and not something traumatic, has no obvious cause and is random in nature. Will the heart stop now, or in a minute? Will this be the last breath? It’s impossible to predict, making this ideal for quantum immortality.

You see, with quantum immortality, the fact that something is random means that it will happen in some universes, and won’t happen in others.

So, in many universes, the person that’s lying on the bed dies this hour. In some others, in a few hours, and in even rarer universes, the person lasts the day and is still hanging on tomorrow.

Quantum immortality relies on there being a universe for every possibility. Not just most. Every. So, if there is a random chance that the person will survive the day, even if the chance is one in billions, then it will definitely happen.

And because every death has some cause behind it, even if we don’t yet know what the cause is, the person that is dying on the bed just has to last long enough for the cause to be found and its cure applied.

Quantum immortality guarantees that the person will survive long enough, even if it’s tens (or hundreds!) of years. Luckily, though, we are living in very interesting times, and all causes of death are being discovered and cured, with new cures available almost every week.

With quantum immortality, old age is not to be feared – it just means you’ll be sick for a while until the cure for aging (*cough*senolytics*cough*) is found.

If you want to read more, read the chapters on Quantum Immortality in my “how to live forever” book.

longevity escape velocity

The main part of this website is the book, “how to live forever“, and even as it was written, I kept changing my mind about what the “thrust” of the thing was – is it simply a list of diseases? Is there a central premise? Does a step-by-step instruction set even exist?

I believe that I have the premise now (and will need to rewrite parts of the book now…), which is based around “longevity escape velocity” (note to self: good chapter name)

In the past hundred years, life expectancy at birth has increased in parts of the world from about 64.75 years in 1928, to 89.5 years today. The “life expectancy at birth” is the age at which actuarial calculations predict that humans will die, based on current conditions and past performance.

64.75 to 89.5 is an increase of about 25 years in one century. 25 extra years that a person might live.

While that sounds like a lot (25 years is almost half again of 60 years), it’s not enough to guarantee immortality.

Even if we repeat the trick this century, and tack on an extra 25.25 years to the expected 89.5 years (that a person in Monaco might expect to live), we still have an expected age at death of only 114.75.

As I pointed out in that previous post, though, life expectancy predictions are usually pessimistic, because they rely on the technology of the time, and cannot predict accurately what the future will bring.

The biggest change that we have made in the last few years is one that has not yet filtered down to the world’s clinics – instead of treating old age as a simple winding down and inevitable end to the body, we are now beginning to treat it as a disease that can be treated and cured.

The full “cure” for old age is not likely to appear for a very long time, but that does not matter, as we can concentrate on the more accessible “longevity escape velocity” as a near-term goal.

So what does “longevity escape velocity” mean?

Let’s say that every year, we discover how to let the average person live an extra half year, the current average age of death is 80, and you are 40. How long do you think it will be before you die (on average)? When you are 80 the average age of death will be 100. When you’re 100, the average age of death will be 110. When 110, 115. When 115, 117.5. On average, people will still die by 120, despite the progress.

This is because half a year is /less than/ one year.

But let’s say we discovered how to add on 1.5 years to the average lifespan every year, the current average age of death is 80, and you are 40.

When you are 80, the average expected age of death will be 120. When you are 120, it will be 210. Instead of being almost guaranteed dead at 120, you are now middle-aged!

Even if we have not discovered a total and final cure for old age, if you are 120 and have an extra 90 years to live /at that moment/, you are almost certain to find yet another way to push back that final curtain further, even if it’s not forever.

We are already discovering how to do these things.

The current accepted biological limit to human life is 126 years, because of something called the “Hayflick” limit, which is caused by telomeres shortening on DNA every time it replicates itself. But we have already found ways to lengthen this. Elizabeth Parrish, CEO of BioViva, became the first person to extend telomeres, extending her own by 9%, which equates to between 14 and 20 years extra, bringing her potential lifespan up to 140+ years.

It might even be possible to repeat the same treatment, so she has potentially worked around the Hayflick limit permanently.

This gives us all an extra few years of life to work on whatever the next issue is.

Aging is caused by a lot of different things happening to the cells of the body. Telomere shortening is just one.

Another is that your mitochondria lose the ability to absorb oxygen and convert it to energy as the years go on. By fixing this, we gain another few years. David Sinclair’s research with NAD+ addresses this issue.

Then there are senescent cells – cells which have reached their “end of life”, and yet stick around, taking up space that would be better used by younger cells, and giving out inflammation proteins. We can now selectively kill these cells with FOXO4-DRI and UBX0101 drugs.

All of these are treatments that add on multiple years to your life. And these have all been announced only in the last five years.

It might not be possible to predict the future accurately, but I’m fairly sure it will be a long one!

what is the maximum lifespan of the human body?

It’s amusing to watch people predict things and then see their predictions fall flat almost before the words leave their mouths.

In 1928, Louis Dublin used US life tables to predict an “ultimate figure of 64.75“, saying that it was impossible for a human to live longer than that without the intervention of “radical innovations or fantastic evolutionary change in our physiological make-up, such as we have no reason to assume”.

He was not aware that at that very moment, non-Māori women of New Zealand had a life expectancy of 74.9 years – more than 10 years more than Dublin thought was possible (see Life Expectancy table here).

8 years later, in 1936, Dublin worked with Alfred Lotka on a reassessment, taking New Zealand’s data into account, and predicted a new limit, 69.93. in 1941, only five years later, women in Iceland broke that limit

Undeterred, he tried again, predicting a life expectancy limit of 70.8 years in 1941. Only five years later it was reported that women were reaching into their 80s in Norway.

The error with this kind of prediction, which people keep on doing over and over, is that it is based on information available on how long we lived in the past, but doesn’t take into account that we are always discovering new ways to live longer.

In 1990, S. Jay Olshansky predicted that “it seems highly unlikely that life expectancy at birth will exceed the age of 85“. In 2002, the life expectancy of Japanese females at birth was 85.2 years.

The country with the current highest life expectancy at birth is Monaco, with an expected life expectancy of 89.5 years.

It should be noted that “life expectancy” is not a limit on mortality. It doesn’t state for a fact, that people will not live longer than that. All it says is that this is the age at which most people are expected to die. There will be outliers that live well beyond that, and accidents where people die before that.

But, the fact that the number keeps on increasing, no matter what the experts say, shows that the human race is (very) gradually winning the fight against mortality.

More recent limits are based not on the past indicators of how long people have lived, but on limitations imposed on the human body by biology itself.

A recent prediction is that the biological limit for human longevity is 126 years old, based on the Hayflick limit, which limits how long a human cell can keep replicating itself, because the telomeres at the end of the DNA shorten each time, until the cells stop replicating and go into senescent mode instead.

But, there is now a treatment that can lengthen telomeres, showing that yet again, the naysayers who put limits on what is possible, are consistently low-reaching. And even for those cells that have passed their Hayflick limits, we have senolytics designed for killing senescent cells.

The future is optimistic. We are pushing our mortality further and further into the future. Read more about how we are learning to solve these problems in my book on how to live forever.