There’s no cure for the world’s deadliest disease. And you have it right now.

Katie Silverman
9 min readOct 4, 2020


Symptoms include hearing loss, cataracts, arthritis, heart disease, diabetes, depression, and dementia — and that’s just the beginning. It kills 100,000 people every day, and there’s a 67% chance that it will kill you (90% if you live in an industrialized nation). No, it’s not the flu, it’s not HIV, and it’s not alcohol or cigarettes or suicide or pollution. It’s aging.

Now, I know what you’re thinking. Why would I scare you like that? Aging’s not a disease. It happens to everyone. It’s natural. And it’s nothing to be afraid of.

But what I listed in the first paragraph are just the most common age-related problems — not the worst. Of course, there are strokes, and cancer, and Alzheimer's — in fact, old age is a risk factor in practically every disease. And if car crashes or social media killed 100,000 people a day, you better believe we would be taking note. So what makes aging any different?

The answer is our cultural viewpoint. There has been a tendency, throughout history, to cope with the inevitability of aging and death by embracing it.

Christianity advertises the afterlife like a Sandals resort, philosophers frantically work to either comprehend death or overcome the fear of it, and edgy teenagers scream along to emo songs about how dying is quirky and avant-garde.

But that’s because until now, death has been something we can’t fix. Sure, we’ve tried — Gilgamesh was trying to be immortal 150 years before the Pyramids of Giza were built (or at least, that’s when the king whose life the Epic of Gilgamesh is loosely based on lived).

But alas, we’ve failed, and every time we fail, we go back to accepting that aging is just part of the human condition.

But wait. Smallpox originated at least 3,000 years ago, but there was no vaccine for it (or any disease) until 1796. Today, smallpox is one of only two globally eradicated diseases, along with rinderpest (or cattle plague). That said, we’re so close on many more, such as African trypanosomiasis (sleeping sickness), polio, and guinea worm disease.

The Black Death, which killed 60% of Europe’s population in the 4th Century, can now be treated with antibiotics, and today it’s about as deadly as SARS (a coronavirus that appeared in 2002 and has not been transmitted since 2004).

The people of the past would have looked at these diseases and felt hopeless, but I highly doubt you know anyone who’s died of smallpox in the last 70 years.

Aging is the same. While aging is as old as life, its symptoms could still be manageable, if not completely curable. And the next big step in medicine could be not just preventing individual diseases before they occur, but preventing the degenerative effects of aging that make us susceptible to these diseases in the first place.

However, there’s still a major question that we don’t quite know the answer to.

Why do we age?

If we’re going to come up with anything like a cure for aging, first, we’re going to need to understand how aging works. After all, you can’t have antibiotics without germ theory. But we are starting to understand how it works. Well… how it works in yeast.

Of course, scientists have plenty of theories — as scientists tend to — and it's pretty likely that some combination of these, possibly along with other factors we don’t yet understand, are key catalysts behind aging. So let’s talk about some of the major players.

Cellular Senescence

No, this has nothing to do with Evanescence, although these cells could use a little waking up inside. Senescent cells are zombie cells that accumulate with age. They form when a healthy cell is damaged or has a DNA mutation.

Luckily, cells are pretty cooperative, so rather than dividing to produce unhealthy daughter cells, these cells will send out a metaphorical smoke signal, basically telling the immune system that it’s in distress and needs to be… erm… taken care of.

While the signals are going out, the cell is inactive, but still alive. However, these signals could inflame nearby cells. Under normal circumstances, this isn’t a problem — Grimm Reaper cells come along and put the damaged cell out of its misery before it can cause any real problems.

But as we get older, our body gets worse at this process. Your immune system becomes bored of looking after all of these fragile, sensitive little cells, and starts ignoring the signals.

With no one to regulate them, the senescent cells start building up, all emitting a cry for help louder than changing your Facebook relationship status to “Desperate.” And this cry for help comes in the form of pro-inflammatory cytokines, chemokines, and extracellular matrix proteases.

What are these? Cytokines are just signaling molecules. Pro-inflammatory means they inflame other cells. They can cause fever, inflammation (not surprisingly), tissue destruction, and, with enough buildup, shock and death, but they’re also necessary to alert your immune system when something’s wrong.

Chemokines specifically call over white blood cells to come help, and are what your body uses to let your immune system know when you’ve got an infection.

Extracellular matrix proteases break down proteins in the extracellular matrix, which surrounds and supports your cells.

None of these sound all that bad, and normally, they’re not, because they’re emitted for a short period of time before your immune system puts the offending cell to bed. But as your senescent cells build up, these chemicals form something called the senescence-associated secretory phenotype, or SASP, which contributes to aging and cancer.

So why don’t we just take them out? You see, it’s not that simple. Even if we could remove senescent cells from the body 100% effectively, we wouldn’t want to. Senescent cells are important in healing wounds, and in cellular reprogramming.

Stem Cells

Stem cells get quite a bit of buzz, and chances are you’ve heard of them, or at least you’ve heard people arguing about whether it’s ethical to use them. Stem cells are, to put it simply, unspecialized cells. Unlike your brain cells, which are good at thinking, and your blood cells, which are good at… bleeding, stem cells don’t know what they want to be yet.

There are two basic types of stem cells (at least for the purpose of understanding them as they occur in the body): embryonic and adult. Embryonic stem cells were those first few cells that formed in your mom that ultimately became you. They’re found in embryos that are between three and five days old and have the potential to become any kind of cell.

Adult stem cells, on the other hand, are found in children and adults. Their job is to regenerate dying cells and damaged tissue, but they’re more limited than embryonic stem cells — they can become many types of cells, but not every type of cell.

So how do they cause aging? Well, stem cells, like almost everything else in your body, decline as you get older, and certain stem cell populations, such as those of the brain and hair, actually decrease as you age. Could it be that your body losing the regenerative capabilities of stem cells causes aging?

Well, sort of. Certainly not on its own. But it’s very likely that it’s a factor. That said, the depletion of stem cells is more likely a double-down than a root cause; research has suggested that the decline in stem cell functionality is actually a result of stem cells becoming senescent.

Free Radicals

They’re not political dissenters who have escaped prison, but they are some pretty nasty little thieves. Free radicals are highly reactive atoms and molecules that can cause everything from Alzheimer's to cancer to diabetes to wrinkles. And all because of electrons.

Let’s take a quick trip back in time to your high school chemistry class. You may remember learning about orbitals and valence electrons. If you’re like me, you’ve blocked out those traumatic memories, so let’s do a quick review.

Atoms have three key components: protons, neutrons, and electrons. At its center, in what’s called the nucleus, the protons and neutrons basically just chill. On the outside is where the crazy stuff happens.

When atoms react with each other, sometimes they will lose an electron. When this happens, they’ll try to bond with other cells to steal electrons to make themselves stable. This creates a chain reaction of atoms and molecules losing electrons and then stealing them from other molecules, because apparently, atoms suffer from some pretty severe kleptomania.

Now all these electron-swapping shenanigans might seem harmless and fun. “Particles will be particles,” you might say to yourself, remembering fondly all the fun you had back in your sub-atomic days. And free radicals are a natural occurrence that, in small amounts, are safe, and even help fight viruses.

But just like senescent cells or Friends, these chain reactions can go on too long, messing up the chemical components of your cells and causing a host of problems. As you can imagine, this has led scientists to theorize that free radicals are part of what makes us age.


Nicotinamide adenine dinucleotide, or as its friends like to call it, NAD+, is a coenzyme (an organic protein assistant) that’s found naturally in all your cells. NAD+ plays an important role in metabolism, which converts glucose into ATP so your body can use it for energy.

The problem? NAD+ concentrations decrease as you age, which interferes with your mitochondria’s ability to function properly. And considering that the mitochondria is, after all, the powerhouse of the cell, this is bad news. Low NAD+ concentrations associated with aging can result in:

  • Obesity
  • Fatty liver disease
  • Type 2 diabetes
  • Neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease

and other age-related issues. This has caused scientists to single out NAD+ — or rather, lack thereof — as a major culprit of aging, or at least of common complications of aging.


Last but by no means least, telomeres are one of the most obvious causes of aging — but how much do we really know?

Telomeres are usually compared to aglets — the little plastic or metal “caps” at the ends of shoelaces that keep them from fraying. Telomeres do a similar job, but for your chromosomes. However, as your cells divide, your telomeres are worn down. When there’s none left? You guessed it — cellular senescence.

Biologically immortal creatures like lobsters and hydras don’t age because they are able to continually fix their telomeres to prevent them from shortening. This makes telomeres promising for those looking to understand and combat the aging process.

So what’s to be done?

There are many, many proposed solutions to the problem of aging, ranging in feasibility from nonsensical to already-on-the-market. That’s going to be the topic of my next article, so follow me if you want to learn about the future of human longevity, and some research-backed anti-aging methods you can employ at home.

Key Takeaways

  • 100,000 people die of “old age” every day — out of 150,000 daily deaths
  • There are a number of factors that cause aging and age-related diseases
  • Senescent cells are cells that fail to commit suicide. They can inflame nearby cells, and they build up as we age
  • As we get older, our number of stem cells decreases, taking with it our ability to effectively regenerate and repair tissue
  • Free radicals set off harmful chain reactions by stealing electrons from nearby atoms
  • Our NAD+ supply decreases with age, interfering with our mitochondria and cellular metabolism
  • One cause of cellular senescence is telomere shortening, a process that does not occur in biologically immortal organisms

Thank you for reading, and I’ll see you next time!



Katie Silverman

17-year-old human-longevity researcher, actress, songwriter, TKS Innovator, and marshmallow enthusiast