How Do We Get Old? It’s Not as Simple as You Think.

I’ve been developing an accelerated aging device to use as a weapon against my arch nemeses. It’s some of that cool merging of science and occult magic shit like what UAC and Nazis like to use. Basically, I’ve stuck a weaponized false grail from Indiana Jones and the Lost Crusade into what amounts to a high-tech squirt gun. It’s like having a reverse fountain of youth. I call it the Boomerinator™. I have absolutely no idea how it works. Jesus magic or something. But I know for certain that it does. A lot of guinea pigs and T-Class had to retire early to enjoy their golden years.

I may be mad, but I’m not stupid. I know I should definitely have some sort of antidote on hand before using this sort of thing in combat. My arch nemesis is absolutely the kind of dickwad that’d just pick up my 30-ton death ray and shoot me with it. Then he’d extol platitudes about having a strict moral code and never killing, ignoring the fact that several dozen of my hard working staff that he’s viciously beaten are bleeding out or have been paralyzed from the neck down. 

If you follow my Twitter, you’d know that my previous antiaging project based on the late Queen Elizabeth II’s DNA has been foiled. Apparently, she wasn’t actually immortal. She just was fantastically wealthy and lived in a country with a good healthcare system. The fact that she didn’t even live past 100 means she didn’t even have fantastically good longevity genes. Which makes sense now that I think of it. Royalty aren’t exactly known for having the best genetics if you know what I mean.

So it’s back to the drawing board. I’m doing a literature review of aging to get an idea of what the problem is and how I can fix it. The problem with creating an anti-aging serum is that aging is really complicated. If you had aging described to you before, they might’ve made it seem like we know how it works and that it’s all caused by one thing. You’ve probably heard the terms “telomeres”, “antioxidants”, or “accumulated cell damage”. But the truth is that aging is caused by a least a dozen completely unrelated things happening simultaneously, with new ones being discovered all the time.

Table of Contents:

• Anti-antioxidants
• Antagonistic Pleiotropy
• Senescence and Yeezys
• Death by a Thousand Mutations
• Why Do We Age?
• Dr. MILFlove or: How I Learned to Stop Worrying and Love the Hormonal Effects of Aging
• Addendum
• Comments

Anti-antioxidants

Oxidatidants are one of the more popular and publicly known causes of age. The story goes that the mitochondria (aka powerhouse of the cell) occasionally produces an oxygen free radical or a Reactive Oxygen Species (ROS), as an accidental byproduct. 

If you’ve been following my Chemiballs series for a while you’d know that Oxygenball is not to be messed with on a good day. ROSballs are never having a good day. These molecules immediately react with the first thing they bump into. Specifically they react with and damage proteins, fats, and DNA. This can cause an accumulation of cell damage, deteriorating our senescent cells, and cause mutations which may lead to cancer or other age related cellular malfunctions.

Antioxidants are molecules which ROSs prefer to react with over proteins, fats, and DNA. Certain foods, such as dark chocolate and many fruits, are high in antioxidants. So the conventional wisdom is that you should eat lots of those foods to increase your body’s supply of antioxidants while also decreasing your overall calorie intake to decrease the amount of ROSs produced by the mitochondria.

What I have just said makes perfect sense and there seemingly is no logical reason why it shouldn’t be the case. But… science has yet to find definitive proof that antioxidants and oxidative damage actually are the cause of aging in humans in a meaningful way.

Health Fad?

I know, it’s really weird. There have been many studies that did find a correlation between lifespan and oxidative damage, many of which you may have heard from news anchors taking them out of context so they can sell you a new and exciting way to drink a plant. 

However, more recent studies have shown that those studies were based on false assumptions or bad data, and that they don’t actually show what they thought they did. There just isn’t any good statistical evidence that aging from oxidative damage is anything more than negligible in humans.

There are many animals whose aging certainly is caused largely by oxidative damage. But there are also many which don’t. This may just be because our own natural antioxidants are good enough. But then you look at naked mole rats who suffer from very high levels of oxidative damage evidenced by all the oxidized molecules we find in them, but they also live for like 70 years and don’t really seem to mind all the oxidizing going on. 

The take away here, from my understanding, is that we have no understanding of how the fuck metabolic aging works. But as far as we can tell we also don’t really need to since it doesn’t seem to matter all that much.

If you still want to use the whole “dark chocolate is high in antioxidants” excuse, be my guest. It couldn’t hurt. The antioxidants that is. Eating chocolate every day probably isn’t a great diet plan.

Antagonistic Pleiotropy

There are several hypotheses blaming age on evolution itself. I will only be explaining one of them, which I have chosen based on how hard it’s name is to pronounce.

Evolution works by the simple fact that genes that are better at spreading and passing on to the next generation will generally do that more than genes that aren’t. This is the concept known as the ‘selfish gene’. Your genes don’t really give a shit about what happens to you after you’ve done the whole spreading-your-genes thing. So my virginity is totally on purpose, because I’m not gonna do what some genes tell me to do. Totally.

Genetic diseases and other bad genes which only harm the individual after they’ve reproduced don’t impact their reproductive fitness. So by the time those individuals are selected against (i.e.: they die) the deleterious gene has already been passed on to the next generation. Hence, evolution doesn’t really have a way to get rid of those.

An extreme example would be ALS which Stephan Hawking famously had. It eventually caused him to be confined to a wheelchair and only be able to communicate through that cool robot voice. The symptoms of ALS don’t start kicking in until later in life, generally after the age when most people already have kids. Hawking was lucky to live a relatively long life, most with ALS die not long after diagnosis. 

However, these genes might also be good. Perhaps the gene that causes “old people smell” is also the gene that makes teenagers horny all the time. That’s just an example, I have no idea if that’s the case, but genetics can be weird and intertwined like that. In fact, it almost always is. An example my professor used was a single mutation may cause both male infertility and digestive issues because the cilia which help move stuff through the intestines and tails sperm use to swim both rely on the same gene. Intestinal cilia may just be repurposed sperm tails or vice versa.

Because those antagonistic pleiotropy genes are evolutionarily beneficial when it counts, they spread through the gene pool, and now we all have them. The only real way for any of these genes to be selected against would be in a species that needs to continue reproducing for as long as possible, such as tortoises. Or that benefits from having surviving elderly around, such as humans. I cover why humans evolved grandmas and menopause in an earlier article about gayness.

Senescence and Yeezys

Your cells don’t last long and are constantly dividing to replace old damaged cells. To do that they need to replicate their DNA. But, because of the way that DNA works which is very technical and boring, whenever DNA is copied a small bit off the end is lost. The new strand of DNA will always be slightly shorter than the old strand of DNA. 

Telomeres are a bit of complete gibberish DNA that gets stuck to the end of the DNA strands to solve this problem. What the telomere DNA actually says doesn’t matter as long as it doesn’t actually code for anything, so it’s always just a repeating sequence. In vertebrates, including humans, it just says “TTAGGG” over and over again.

Since telomeres don’t do anything (except for when they do) it doesn’t matter if a bit of it gets cut off each time the cell divides. Think of them like the soles of your shoes. You’d rather your shoes get beaten up by walking on sharp gravel or hot asphalt than your feet. After all, your little piggies are very dainty and are the one thing holding together your relationship with your foot enthusiast life partner, I presume. Though eventually your shoes will be too worn out to use anymore. You can just buy new ones. But can your cells buy new telomeres?

Some cells, such as stem cells, can buy new shoes. There is an enzyme creatively named telomerase which rebuilds the telomeres by adding more TTAGGGs onto the end. But in humans and most other things, unfortunately, stem cells lose the ability to use telomerase after they become normal body cells. 

When you’re a kid you get spoiled by your rich parent’s buying you new shoes every time you get a little dirt on the old ones. But now you’re a broke-ass adult who can’t afford new shoes and have to live with the same cringey, beat up Yeezys you had in highschool for the rest of your life. 

You can’t afford to get new shoes even after the soles of those Yeezys inevitably get worn down to nothing and your big toe is comically poking out of a hole. You are a millennial; you are biologically compelled to spend that money on avocado toast and student loan debt. So you kinda have to just stop walking. Same thing for cells. Instead of cutting into important DNA they just stop dividing, which is called senescence. 

The Hayflick Limit

The Hayflick limit is the number of times a cell can divide before it grinds its telomeres so short that it becomes senescent. Different cell types hit the Hayflick limit at different times, but the process generally starts in your late 20s and gets progressively worse from there.

Once a cell goes senescent, you have to live with that same cell for the rest of your life. Unless it dies before then. This means that any toxins or damage that accumulates in them is mostly permanent. 

Senescence is also why older people heal slower. Wounds heal when cells next to the injury divide until they fill up the empty space. But if most of your cells are senescent, that job is left to just a few cells which haven’t hit their hayflick limit yet, so it takes longer. 

So why don’t all our cells make telomerase like giant tortoises? I dunno. Probably just an oversight caused by antagonistic pleiotropy. Having longer telomeres is easier to evolve, metabolically cheaper, and more reliable than constantly regenerating them, and they work just as well while you’re young.

Death by a Thousand Mutations

As you get older you’ll start accumulating more mutations in your cells which can lead to oncogene mutations. An oncogene is a gene that prevents cancer… as long as it isn’t mutated. Luckily, every cell has many of such genes, so every one would have to get knocked out for cancer to happen. So you probably don’t have to worry unless you have a family history of cancer and may have inherited already defective cancer defenses.

Even if they don’t cause something catastrophic like cancer, mutations can still deteriorate the functionality of a cell. If a cell needs a certain gene to work like it’s supposed to and that gene gets mutated, that cell won’t work right (or probably not at all) and won’t be pulling its weight anymore. 

Imagine if even a small fraction of your cells break like this. It’s like a company that did great in its heyday, but now productivity and profits are down because the old guard retired and left their jobs to their unqualified slacker nephews with worn out Yeezys.

There is no way to completely prevent the accumulation of mutations in your cells as you age. And there’s certainly no way to reverse it. (Yet.) Well, actually there are a few ways to prevent mutations. The famous tardigrades ¹aka water bears evolved to wrap their DNA with armor made of protein and have advanced DNA repair mechanisms. While this gives them completely unnecessary immunity to nuclear radiation, it comes at the cost of severely slowing how quickly they can evolve. Mutation is a key feature driving evolution. Tardigrades have barely changed at all since the Cambrian explosion. Unless you happen to evolve the perfect genome right off the bat, slowing the rate of evolution is a one-way ticket to going the way of the ginkgo tree. Hence why humans don’t have anything like that. (Yet.)

For mere humans, avoidance is the best idea. While you can’t avoid mutations entirely, you can decrease them by avoiding some major sources. Avoid direct sunlight unless you are protected by a sufficient coating of sunblock and/or melanin. Limit the amount of processed, blackened, and unwashed food you consume. Avoid playing with radioactive waste whenever possible. Avoid drinking alcohol, acidic food, strong bases, oxidizers, or catalysts unless you really, really want to. Don’t be born during a time when it is practically impossible to avoid microplastics and industrial pollution because they have permeated the entire surface of the planet. Try not to breathe too much while visiting Los Angeles. If you live in Los Angeles; don’t.

Why Do We Age?

But why does aging even exist? I don’t mean all these technical reasons, I mean the philosophical cause. Like, why haven’t we evolved to just, like, not do that? There is an easy logical explanation; “Out with the old, in with the new”. Aging is a boomer remover that makes room for the next, marginally more evolved, generation. 

But this doesn’t benefit the individuals who are getting old and dying. Evolution is short sighted; it usually only evolves things which are immediately beneficial in the current generation, maybe in the next as well. This is why humans have evolved to be smart enough to create nukes and climate change but not smart enough to not use them.

And yet, almost all species get sick and die from age. There must be another very significant cause. Perhaps the question isn’t “why do we age?”, but rather “why wouldn’t we age?”

Why Wouldn’t We?

Evolving to live longer is a constant struggle against all these previous factors; metabolic aging, mutation accumulation, and antagonistic pleiotropy. While it may be possible to overcome them, it takes a lot more “political capital” or “evolution points” than would other competing adaptations. Such as the “get eaten by lions less often” gene. It’s pretty rare that a species actually evolves to simply not age because most of the time it just isn’t worth doing. 

Even if a species doesn’t age it still isn’t immortal, they just live until something kills them. In the wild, that usually doesn’t take very long. Why devote so much energy and adaptations to increase your species maximum age when your median age is barely any higher than it was before? 

Only species that, for whatever reason, are very unlikely to be killed by a predator or disease would actually benefit enough to justify the cost. For example; the giant island tortoises which exclusively live on islands that have plentiful resources, few diseases, and no predators (until humans came along). Even then, despite being a walking tank, tortoises rarely get beyond 100 years thanks to statistics. If you look at a list of the longest living giant tortoises, most of which also benefited from veterinary care, they tend to only get between 100 and 200 years old and are killed by non-age-related issues like infections or someone accidentally dropping heavy things on them. 

Dr. MILFlove Or: How I Learned To Stop Worrying And Love The Hormonal Effects Of Aging

Unlike the previously mentioned parts of aging, the more cosmetic changes (wrinkling, hair whitening, baldness, menopause/andropause) actually seem to be more evolutionarily intended.

Around your 50s you’ll have something like a second puberty where your hormones just give up. For women, this is called menopause and it, among other changes, stops your menstrual cycle and your ability to have kids. This is a good thing evolutionarily, which I discuss in the same part of the same article I mentioned earlier. Here’s another link to that. ²As a refresher to that or if your too lazy to read it the first time; if you can’t make any new kids you will have more time and energy to forcibly overfeed and be judgemental of your grandkids, increasing their chances of survival.

For men, this is called andropause and it, among other things, unwoods your pecker. Your flag will be at half mast. The old soldier isn’t going to stand at attention. Basically; the monkey’s gonna get off scot-free because you can’t administer corporal punishment no more. This is evolutionarily advantageous for the same reason as menopause. Nature’s telling you that you need to stop being a pervy old man and go spend time with your grandkids! Or whatever makes you feel better. To be honest, this is probably another evolutionary cock up if you ask me. That doesn’t happen to everyone.

Going Gray

One of the things we fear most about aging is our hair turning gray. ³And no, I don’t have white hair because I’m old. Prematurely graying hair is a common symptom of Science-Related Memetic Disorder (aka mad scientist madness). Why else do you think so many mad scientists are rocking the Einstein look? Statistically, we can’t all be that old. I’m pretty sure I’m still a twenty-something.

The hair of gorillas also famously loses its color as they age. Silverback gorillas are the oldest males in the troop, which puts them at the top of the gorilla hierarchy. Not only does this mean they are the most experienced, but it also proves they have the best genes by the simple fact that they have survived for so long in such a harsh environment. Being able to clearly denote that makes it obvious to everyone else that grandpa should not be messed with. 

Obviously, this isn’t quite the same with humans, though old man’s strength should not be underestimated. But it’s still important for humans to be able to judge the relative ages of each other. You wouldn’t want to ask an old lady to do a lot of physical labor, but she would probably be a better source of wisdom than the average zoomer twitch thot.

Some people are really into MILFs and silver foxes (I’m talking 30s-40s, not 50+ menopausal/andropausal people anymore). You might write this off as another weird fetish. But it’s actually an important instinct and completely natural, though in your case it might still be a weird fetish. Beauty standards differ between cultures, though are not entirely the product of that culture. Instinct plays a part in what you find beautiful. 

People in societies with low food security tend to find more mature and “thicc” looking people to be more attractive. After all, someone who has experience and is obviously well-fed will be a good sugar daddy/sugar momma for you and your children. 

Inversely, people in societies with high food security tend to find thinner and younger looking people to be more attractive. After all, it’s best to reproduce with someone who is healthier and more fertile so you can make the most of plentiful food and make lots of babies. 

Addendum:

This topic is continued in my next article, How Does Aging Work and How to Fix It (Eventually), which as you might guess from the name is completely unrelated to this article. That was joke, it is very much meant to be the sequel. I talk about some actual constructive solutions about aging in that one.

So yeah, you can probably see why this is such a hard problem to solve. The science of aging is an incredibly complex topic. In fact, I didn’t even cover half of what I had planned for this article. Once I got to 8 pages long I realized I should probably cut back a bit. After spending several hours trimming it down I somehow managed to add another page. 

Did you know that there are several rare genes that give people the real life superpower of being more likely to live a bit longer on average? Or that the calcium leaches out of old people’s bones into their blood which makes their arteries “crunchy”? Go to the comments if you want a part 2 for this article where I go into all those little details. And actually make a comment. You don’t need to have a WordPress account or give your email, or anything like that to leave a comment. At least it shouldn’t need that. If it still does, leave a comment telling me it’s not working right.

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Campbell, et al. (2020) “Integrating Concepts in Biology​” Trubooks: Digital Textbooks and Digital Learning Solutions. ISBN: 978-1-63097-050-5

Fabian, D. & Flatt, T. (2011) The Evolution of Aging. Nature Education Knowledge 3(10):9