Helping you kill the zombie cells in your body, one by one.
I’ve always been curious. Not specifically about why we die, which I’m assuming you think is the point of this article due to the tags and your inferring skills. Anything, really. Why the sky’s blue to why we’re all so different.
More importantly, I’ve always been inclined to ask ‘Why’?
And I’m sure you’re inclined as well. Seeing as you might’ve clicked on this article, curious as to what I’d be talking about and what the heck senescent cells are.
Or maybe you’re an established longevity researcher, just clicking this to see if my solution is real or not.
Or maybe you’ve done some research about longevity and know what senescent cells are, and want to see if you have a new way to flush them out!
The point is, it doesn’t matter who you are, what you do for a living, what your favorite movie is, whether you’re a world-famous longevity researcher to a student who just wants to learn, etc.
You clicked this article. And in doing this you asked: Why is this article here? What is it going to talk about? What will I learn today?
And I’ll answer your questions. However, we’ll start with a simple one.
‘Why do we die?’
Note: I’m not asking why we age. This is because there are two types of aging. chronological and biological aging.
Chronological aging is easy to define. Think of yourself as 6. Now, think of yourself at 65.
How are they different? I’m sure, unless you’re Dwight Schrute (office reference, yall know what I’m talking about) who believes he’s immortal, you imagined yourself as a bouncy, younger, clear colored hair self when you thought of yourself at 6.
However, I’m sure when you imagined yourself at 65, you thought of yourself as a less-moving, gray-haired person with wrinkles. That’s chronological aging. You, on the outside and inside, “aging” with time.
Now, biological aging is different. It can contribute to chronological aging in some capacity, but they aren’t the same. Biological aging is the compilation of factors such as cellular senescence, free radicals, gene mutations, and more to our bio-age (internal age).
Now, answering the real question. Why do we die? This is because of many many factors.
FYI, biological aging contributes to our “death date” more than chronological aging. This is proven by the fact that we don’t all have the same due date. If chronological aging primarily contributed to it, we would all die at, say, 79.
We die because of our buildup of senescent cells, our free radicals, our gene mutations, and all the biological factors that make up biological aging.
I’m not saying that we wouldn’t die because of a car accident, but this is if it’s a health-related cause.
There are so many reasons we could die, but on the biological level, it’s due to biological aging (and a bit of chronological aging).
Now, of all of these factors that age us, we at Biotein are primarily focusing on senescent cells.
What are senescent cells?
Senescent cells/cellular senescence is a cell state discovered by Leonard Hayflick (my personal idol) in the 1960s.
Senescence is a zombie-like state when cells are still producing fluids, (such as SASP, senescence-associated secretory phenotype) but are supposed to be dead (divided a finite amount of times). It’s a state between alive and dead.
Normal somatic cells can only divide around 50–70 times, the Hayflick limit, before descending, *cough*, oops, I mean progressing into a state of senescence.
Senescence is caused by telomere attrition. To explain what this is, I’d have to start from the beginning.
Around 13.8 billion years ago, a large explosion theoretically happened.
“No, not THAT far back… the beginning of the process.”
Fine. When our cells divide, they copy their DNA (deoxyribonucleic acid, if you were wondering) from chromosome to chromosome.
Quite unfortunately, this process is NOT perfect. When they copy the DNA, a little bit of DNA is cut off from the end of the chromosomes.
But… we don’t want to lose all of this valuable DNA information, right?
Right. So our body has these things called telomeres at the ends of chromosomes. And they’re kind of like the aglets on the ends of our chromosomes. But a repeated DNA sequence cut off after every division.
After around 50–70 cell divisions, our cells become senescent. This is the Hayflick limit (see where I was going with the mentioning of Hayflick?), which is the maximum number of times a cell can divide before turning senescent.
Other than telomere attrition, several factors can induce cellular senescence.
- One is oxidative stress. This is essentially a buildup of free radicals, which are molecules missing an electron.
- Another is mitogenic and oncogenic signaling. When oncogenes (cancer genes) signal, this additionally induces senescence!
How do you get rid of them?
Now that you know what these deadly zombie cells are, let’s get into ways to get rid of them.
There are a few significant ways. Reducing stress, initiating autophagy, and senolytics (and potentially biotein, but we’ll get into that in a bit).
The first is…. *tada* reducing stress! Now, this is not as easy as it sounds or looks and is the one that might require the most willpower. But controlling temper, and feeling in control of your emotions is a great start.
Studies have been done where stress has been discovered to cause people to have much shorter telomeres!
The next is initiating autophagy! Now is where we get a little more technical. The protein p26 initiates an immune system that destroys all of your cells and creates new ones.
You can do this by intermittent fasting or doing a ton of exercise. In terms of feasibility, I recommend the first. In terms of willpower, umm… Never mind. Changing the topic.
Another is senolytics. Senolytics are molecules that take away your senescent cells!
Ever heard of metformin, the type 2 diabetes drug? It combats cellular senescence as well.
What’s the problem with all of these?
This’ll only take a minute.
Stress is a tad unreliable and not that effective. Reducing your stress can have a small impact (and I recommend you do it for many many reasons) but it isn’t significant enough to be effective.
Autophagy is cool, but requires quite a bit of willpower and probably isn’t the best option for full efficiency and feasibility.
Senolytics are fascinating and probably the best one on this list, but none except maybe metformin are actually being used, and who’s going to put sketchy molecule-drugs in their mouths?
“What solution do you at biotein propose?”
Wow, thanks for the amazing introduction. We’re currently partnering with The Adam’s Lab to find biomarkers and markers for senescent cells that are specific to them because the markers for cellular senescence currently aren’t specific to senescent cells (meaning other cells can have those markers as well).
We take fluorescence microscopy pictures of senescent cells’, alive cells’, and dead cells’ mitochondria. Then, we run that through ImageJ to find key features, and to compare them effectively. Afterwards, we are planning to use dimensionality reduction methods to consolidate features.
This is a diagram of a fluorescence microscope. There are filters for the lights to go through to the sample, and it’s illuminated by a mercury arc lamp. The detector is the eye.
We chose mitochondria (the infamous powerhouse of the cell) because of the fact that they carry many defining factors of cellular senescence.
Learn a bit more about what we do in further depth in my article about this topic (plus check out the find out more section for some cool resources.
“What does getting rid of senescent cells even do? Why do we even care? It doesn’t do anything for me.”
And that, my friend, is where you are wrong. Senescent cells, as I’ve said before, have a huge impact on us.
Senescent cells cause biological aging, age-related diseases, and are literally the rust that clouds our machines *cough* *cough*.
Biological aging, as I mentioned earlier, is different than chronological aging, If we eradicated our senescent cells, then we would be able to stop a part of biological aging, and make sure that we wouldn’t deteriorate on the inside as much.
Additionally, aging-related diseases are a humongous part of this. Diseases such as Alzheimer’s and dementia, Parkinson’s, kidney failure, and more are mainly caused during old age by senescent cells (as our senescent cells have built up to a large extent).
One in 6 women and one in 10 men who live past the age of 55 will get a case of dementia in their lifetimes. This shows how our bodies deteriorate and hurt us as we age.
If you had a chance not to have dementia or any of those diseases with no consequence, wouldn’t you take it? I would.
Biotein and getting rid of your senescent cells could provide you with that.
How do I find out more?
Biotein has a website at http://bioteinresearch.ca/, contact us there!
- Senescent cells are huge problems for our bodies, and they help cause biological aging.
- Current methods of getting rid of them aren’t effective or feasible enough, and this isn’t good!
- Biotein will find biomarkers + markers and develop targeted therapies for senescent cells.
- Senescent cell eradication is important to stop biological aging or aging-related diseases.
- Find out more about Biotein and our mission at bioteinresearch.ca or check out our one-pager in the ‘Find out more’ section!
We at Biotein would love it if you checked out our website and one pager (in the find out more section) and reached out!