Can we live long enough to experience the singularity?
There is a concept that is gaining traction around the world that the exponential progression of technology will reach a point where humankind, as we know it, can not continue any longer, i.e., a future time where humans will have merged with machines and obtained immortality in the process.
So if you are seeking immortality, then all you would need to do is survive long enough for this to happen. At this point, graphically, the rate of emerging technologies in genetics, cybernetics, and nanotechnology will have the appearance of a vertical curve, referred to by futurists as a spike or singularity.
The term “singularity” is adopted from the Black Hole Event Horizon, characterized by the impossibility of ever being able to see beyond other side of the curve. This also applies for the curve of emerging technologies, which are being developed at such accelerating rates that it is no longer predictable as to what kind of society will emerge. This may lead to super intelligence, space exploration or, as transhumanists have proposed, eternal life. Those who endorse this concept are generally called Life Extensionists. American founding father Benjamin Franklin was one of the first to propose that at some point in the future, all diseases, including aging, will inevitably be cured by science.
In recent years, business accelerators like Y Combinator have been financing the first longevity Startups in Silicon Valley. Technology giants like Google and Apple have created anti-aging subdivisions. Jeff Bezos, the wealthiest man in the world, has partnered with the Mayo Clinic to do human studies on reversing aging. While billionaire Peter Thiel has donated 7 million dollars to the SENS Foundation.
Currently the average human life expectancy is increasing at a rate of about 5 hours per day. Once medical technology becomes good enough to give us 24 hours per day, we’ll have, in effect, attained immortality. A common instinctive reaction to the idea of immortality is to respond with the argument that “living forever would be boring.” But I would challenge that notion, since new experiences are being invented faster than we can experience them. So would it even be possible for you to get bored?
When we consider real life, people don’t actually appear to run out of things to do. Perhaps this is because we live in an infinite universe with infinite possibilities, and boredom is just a state of mind. I, personally, don’t really understand the boredom argument because wouldn’t eternal death be even more boring? Even so, the great thing about longevity is that if you ever get bored, you could always just end your own life at any time, i.e., euthanasia. You don’t have to live forever if you don’t want to. Life extensionists tend to be ok with euthanasia, but emphasize the ethical imperative for reverse euthanasia, where people who don’t want to die are given the choice not to.
Some people in their thirties often say that they don’t want to live past 90, but when they turn 90, many still desire to live to be 91. Death anxiety is really just component of human nature. People who say they plan on killing themselves before they get too old, do a lot of talking, but no walking, which is why we need the option of life extension, in case you change your mind.
Anthropologists have pointed out that the desire for immortality is fundamental to all human cultures. It is not an accident that virtually all religions offer some account of an afterlife, because the human desire for self-overcoming is as ancient as humankind itself. Burial ceremonies and preserved fragments from religious writings bear witness to the fact that prehistoric humans were also profoundly distressed by death. In fact, the oldest piece of writing in history, the “Epic of Gilgamesh,” recounts the story of a king who devotes his entire life to seeking immortality, because he believes life wouldn’t be worth living otherwise. Upon learning that there exists a herb at the bottom of the sea which could grant one eternal life, Gilgamesh embarks on a quest, battling fearsome monsters to find it. Today, nothing has changed. We are all Gilgamesh.
Aging, categorically speaking, is technically a form of genetic affliction that we inherited as a result of an outdated evolutionary mechanism. In the words of gerontologist Dr. Aubrey de Grey, “aging is just another disease that can and should be cured…” The sole reason aging isn’t being classified as a disease is simply because it happens to everybody. But that’s not really a scientific reason to have such a classification.
There have been rallying cries throughout the scientific community to launch a “Manhattan Project” to cure aging so that we can save as many people as possible. After all, people will look back in a hundred years and question why we didn’t work harder on anti-aging research, just as we look back a hundred years ago and wonder why they didn’t work harder on antibiotics and vaccines, which could have saved billions of lives had they been developed a few decades earlier.
It is uncertain when this technological spike will occur, but computer scientist Ray Kurtzweil estimates that it might very well be around the year 2045. So the question is, can we actually survive until 2045? How can we push our physical bodies to their limits and buy ourselves as much time as possible?
Although I personally don’t believe that we can cure all forms of biological aging, since cancer tends to correlate with longer lives, perhaps we won’t have to cure aging to reach the singularity. We don’t necessarily have to cure cancer either. All we would have to do is slow down the physical decline of our bodies until 2045. So the real question is, to what degree can we slow down the aging process?
What is the maximum number of years that we can possibly live?
In religion, according to the old testament, the biblical character Methuselah is said to have lived to be over 900 years old. However, many biblical scholars suggest that this is a mistranslation, citing that the timescale in months might have accidentally been counted as years. In actuality, this would make Methuselah over 75 years old, which was still an extraordinarily long life given that the average life expectancy back then was barely above 30. In modern times, the oldest person ever to live was the late Jeanne Louis Calment, who lived to be an staggering 122 years old. So if we really tried, we might be able to buy ourselves 120 years worth of time.
Perhaps the best approach to slow the aging process would be to determine what causes aging in the first place. One possible approach is to take the genomes of millions of old people and the genomes of millions of young people, then have artificial intelligence (AI) analyze the difference to identify where aging takes place. So far, 60 genes involved in the aging process have been found. All we need to do now is to find the correct molecules to activate or deactivate those genes.
To summarize the past 25 years of gerontology research, we now know of three main biochemical pathways responsible for aging. One it’s called the AMPK pathway, which can be targeted by the drug Metformin. Second, there’s the Sirtuin pathway which can be targeted by Resveratrol, NMN, caloric restriction and nicotinamide riboside. Third, there’s the MTOR pathway which can be treated by the drug Rapamycin. Gerontologists aren’t certain about how much of aging each of these pathways are responsible for, so just to be safe we may want to consider utilizing all three.
First we have AMPK, which we have been able to manipulate using a diabetes drug called Metformin. Studies of over 10,000 people have shown that those who take Metformin are not only protected from diabetes, but also from heart disease and aging in general. While Metformin is an FDA approved drug, it’s still illegal to prescribe it for aging, since aging isn’t considered a disease. And that’s a real shame because there have been some very strong arguments from respected medical doctors to classify it as such. The minimum dose of Metformin to get any significant benefits should be about 500 milligrams, twice a day. However, it might just be better to take 250 milligrams of it four times a day to make sure it’s in your body all the time.
This may seem obvious, but exercise is also recognised as a method for boosting AMPK. So if you aren’t exercising every day, then perhaps it’s time to start. Our bodies were meant to be used and if you don’t use them, the body can trick your biochemistry into doing disastrous things.
Next we have the Sirtuin Pathway, discovered by Harvard aging scientists David Sinclair and Dr. Leonard Guarente. The Sirtuin pathway involves a set of seven aging genes, called the Sirtuins, which affect cellular respiration and thus affect aging. But there’s a catch. The Sirtuins actually need a molecule called NAD in order to function. In fact, without NAD in your body, you’re very likely to just drop dead, because NAD is the molecule that enables your cells to create energy. By the time you’re middle-aged your NAD levels will have dropped by about 50% of what you had in your 20s and your rate of aging will start to accelerate, unless you supplement with NMN.
NMN is related to Nicotinamide Riboside, which is what creates the NAD that’s so essential to the Krebs cycle. Dr. Guarente has gotten the backing of several Nobel Prize winners and launched a drug called Basis, which is centered around NMN and Nicotinamide Riboside supplementation. Dr. David Sinclair, a colleague of Guarente at Harvard, has famously stated that NAD is the closest we’ve ever gotten to the fountain of youth. He personally takes a gram of NMN every morning along with half a gram of a drug called Resveratrol, the famous compound in red wine.
You may have heard about Resveratrol through the media, but I it has nothing to do with antioxidants. Rather, it’s a molecule that greatly enhances the functioning of your Sirtuin genes. Dr. Sinclair says to think of the human body like a car where Resveratrol is the acceleration pedal and NMN is the fuel. Without also taking NMN on the side, it is more difficult for Resveratrol to regulate your epigenetics. The most scientifically sound thing you can do for your Sirtuin pathway is either Caloric Restriction or Intermittent Fasting.
Regarding caloric restriction, a multi-decade long-term study called the Madison Monkey Experiment, was just completed several years ago demonstrating that caloric restriction is the one scientifically confirmed method for extending lifespan in primates. More studies that followed also championed intermittent fasting, which is kind of like caloric restriction, but with the added benefit of giving your body a break from using energy for digesting all the time.
Intermittent fasting means skipping breakfasts and even sometimes lunch if you’re busy; but the consensus is that a black coffee is still ok. Intermittent fasting involves compressing your feeding window to between four and eight hours and eating about one or two meals per day. This gives your body time to regenerate and induces Autophagy which clears out Senolytic Cells, nicknamed by the media as “Zombie Cells.” If you’re younger, you probably don’t have to be concerned about senolytic cells. But if you’re an older person, then the drug Dasatinib and the nutrient Quercetin just may be the route to take. Older people in the life-extension community tend to take them about twice a year to purge senescent cells. But generally, the best benefit of intermittent fasting is that it not only slows down aging, but it can also increase productivity by freeing up more time to perform other acivities. It also simplifies caloric restriction because if you’re limiting yourself to eating one 1200 to 1500 calorie meal per day, the damage to your cellular respiration mechanisms will be minimized.
So how do we know that this approach works? For starters, if you take a regular field mouse with a lifespan of 8 months, you can double its lifespan by simply putting it in a cage and taking care of it. The mouse will then live about 12 to 16 months due to the fact that you’re helping it to avoid predators, disease and starvation. Elizabeth Parrish, CEO of BIOVIVA, calls this “Mouse Squared.” If you take that same mouse, you can double its lifespan again, from 26 to 30 months, simply by just putting it on a calorie restriction diet. Elizabeth Parrish calls this “Mouse Cubed.” If you take that mouse and then use gene therapy to remove just one gene, IGF-1 or FGF21 in humans, then it’ll manipulate the Sirtuin pathway and double the mouse’s lifespan again. This is “Mouse Hyper-Cubed” and it has the best likelihood of living to the singularity. Perhaps we’ll soon be seeing a gene therapy treatment for proteins like FGF21 or some kind of Crispr Cas9 based gene editing technology that can edit our Sirtuin genes, but this has yet to be turned into a viable approach.
The optimum for caloric restriction is to consume about 40 percent of the calories that you would normally eat along with some Metformin, mentioned earlier, which is also a known appetite suppressor. Basically, caloric restriction is simply under eating without malnutrition, not the agonizing starvation that some people make it out to be.
Finally there is the MTOR pathway which can be targeted by a drug called Rapamycin. While Metformin, Resveratrol, NMN and NNR aren’t really dangerous, Rapamycin occasionally could be, given the fact that it’s also an immune suppressant. Rapamycin was originally approved by the FDA for preventing organ transplant rejection. But taking it just to hit the MTOR pathway can also put you at increased risk of infection. So it would be wise to be extremely cautious with this one. Additionally, fasting doesn’t only help the Sirtuins. It also boosts AMPK and suppresses MTOR; not to mention, it also improves bone marrow function and stem cell activity. Likewise GDF11 might also be helpful for this. It’s related to the Parabiosis startups in Silicon Valley where wealthy old people are trying to infuse their bodies with the blood of young people containing way more GDF11 than theirs does. It’s currently being researched by Dr. Amy Wagers at Harvard, but it’s only just one out of 700 proteins in young blood that might be responsible for the anti-aging effects. The effects on MTOR are still unknown.
We should also recognize the process of free radical damage to our mitochondrial DNA. If the human body is like a car, as Dr. Sinclair proposes, then to find out where aging takes place, look in the engine, because that’s where you have the most moving parts, oxidation and combustion. Likewise, the engine of the human cell is the mitochondria, which are the first to be damaged by the aging process. You may have already heard that antioxidants help avoid free radical damage, which is true, but it’s still only a very small part of a much bigger aging problem.
Overall, these are the three main pathways that are currently being explored to extend life expectancy. There is no guarantee that this will completely cure biological aging by 2045, but it can certainly slow down aging. There are also many other ways to accomplish this. For example, don’t take opiates, don’t do overly risky jobs and get plenty of sleep every night. On that note, building muscle is essential for fat burning, so adhere to the big five, which are deadlifts, squats, presses, dips and bench press. Isolation exercises, like bicep curls, are considered by many in the life extension community, to be mostly just a waste of time.
Another thing that can help you get leaner is the Blue Zone Diet, specifically the Mediterranean Diet or the Okinawa Diet, practiced by populations with the highest life expectancy in the world.
Then there is Xenotransplantation research, which sounds a bit alarming, but it could just make or break your very existence. Xenotransplantation is essentially where pig hearts are harvested and then seeded with human stem cells, providing the functional equivalent of a human heart, since pig heart scaffolds are approximately the same size. Another approach may be to create human pink chimeras, which are essentially just regular pigs, but raied with human organs, thanks to embryo engineering. Transplantation of these organs would give you a more natural analog to a human heart. Given that donor hearts from other people are not immune compatible with your genes, a pig heart grown with your stem cells definitely would be.
People will often make the argument that Xenotransplantation is just science fiction and that we shouldn’t bother researching it. However, at one time, heart transplants were science fiction also. People always believed that transplanting a heart was impossible, until 1976, when Dr. Christian Barnard performed the first heart transplant in Cape Town, South Africa. In the past, heart transplants were generally considered disgusting, ghoulish and controversial, just as Xenotransplantation is now. However, once we realize what’s possible, it’s likely that people will reconsider their position, as they always have in the past.
The list of things you can do to expand your lifespan is endless. Some people take IGF-1, some do Ketogenic Diets, LDL Analysis, Testosterone Replacement Therapy, Cryotherapy, or Senolytic Therapy on the side. But don’t just take my word for it. Go do the research yourself. An excellent resource to start with is the website Fight Aging.
Aging probably won’t end in 2045, as Kurtzweil suggests, but rather, we will just keep replacing our organic body pieces one by one until aging just becomes irrelevant.
So just like Gilgamesh I wish you all the best in your quest to either live forever or die trying.