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Hank hates death, so he helps us understand the process of aging, informs us of how scientists are studying ways to prevent it and brings us the exciting news of current research in longevity... for mice.

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References for this episode can be found in the Google document here: http://dft.ba/-2dUq
I hate death.

More than a hundred and fifty thousand people die on this planet every freaking day, and some of those people are getting hit by buses, or dying of how cute a puppy is or something, but in most cases their bodies are just succumbing to the dirty work of aging.

And I'm tired of it. And I don't want George R. R. Martin to die before he finishes the "Game of Thrones" series.

Obviously we all have to die eventually. I mean, it's something that we have in common with every other person who has ever lived, but some organisms can live to be very, very, very old.
And scientists are beginning to understand better how they do it, and what it might take for us to live to be very, very, very old. 

And I'm not just talking about doing squat thrusts or eating kale or whatever... glass of white wine every day, although those things probably help. I'm talking about discovering how our cells die, why they do it, how our genes make us age and yes, how our behavior influences our longevity.

So like come on scientists: make me live forever! Please!

(INTRO)

You and I are just collections of cells, albeit magnificent and really complicated collections that exist as animated blobs for a while, hopefully long enough to reproduce. And when it gets to though for ourselves to keep these masses of cells together: plrrrppppp! we die. 

It happens to the best of us. And also the worst of us. And also everybody in-between.

For humans and for most animals there is a process of aging that happens over the course of our lives culminating in the buying of the proverbial farm.

This process has a lovely little name. It's called "senescence". And at an organismal level we see senescence take place after our bodies reach sexual maturity. After that we begin to lose the ability to combat physical stress and to maintain homeostasis, the internal balance of all of our organ systems and body fluid concentrations, and most importantly: we start to lose the ability to combat disease.  

Because technically there is no such thing as dying of old age.
Everybody dies of something.

But, this is good news. Not all animals do this. Not all animals age this way. Some, particularly some cold blooded animals exhibit whats called "negligible senescence". They don't lose their ability to reproduce over time and their death rates don't necessarily increase with age.

These animals basically stay at a certain level of fitness until something terrible happens to them, like a disease or predation, or a really big, fast truck barreling down the road that they're about to cross.      

So, for instance, Galapagos tortoises have been known to live for a hundred and seventy years, and lobsters can live to be a hundred and forty, and the oldest quahog clam ever collected was about four hundred and five years old.

Freaking Shakespeare was writing Hamlet when that clam was born!

So that's totally unfair. Why do some animals get to start to die as soon as they reproduce, but others get a hall pass to near immortality?

Scientist don't know for sure, they're trying to figure it out by studying senescence at a cellular level. And it turns out that our stupid cells have their own deaths programmed into them.

Our somatic cells, the cells that aren't sperm or eggs, are constantly dividing and making copies of themselves. In fact, there are whole armies of cells being made in your body right now.

In the 1960s, a young researcher named Leonard Hayflick was studying human fetal cells when he noticed that after a while, human cells just stop dividing and then they die. He came to realize that they all quit dividing after about 50 divisions, which took around 9 months.

If he put healthy, dividing cells into the freezer, the division would slow down and even stop, but if he warmed them back up, they'd remember exactly where they left off and start dividing again until they got to that magic number.

It was in this way that Hayflick discovered that human cells have death programmed into them-the number of times a cell can divide is now called Hayflick limit-and although it's 50 divisions for human fetal cells grown in a culture, the number for some animals is less and for others it's more.

For instance, mice, which can live for 2 or 3 years, go through anywhere from 14-28 divisions. A Galapagos tortoise, on the other hand, has a Hayflick limit of about 125.

So, there may be a correlation between an animal's average Hayflick limit and its life span, but as with everything in science, it is not this simple.

Because even though we're always making more new duplicate cells, as we get older, that Hayflick limit gets older. Studies of people in their 80s and 90s found that their cells only divided about 20 times. So since our cells have expiration dates, we, in turn, also have expiration dates. 

By now, scientists are asking "Okay, yes there's a limit, but what causes the limit?"

It turns out, the answer is, uh, probably its chromosomes. A human cell quits dividing after it stops being able to completely replicate its Telomeres, the little caps of non-coding DNA on the end of each chromosome that protect the genes from errors and copying. (4:44)

Telomeres are originally made with the help of the enzyme telomerase when we're just little zygotes. But after that, every time a cell divides the telomeres on the chromosomes of a new cell are a tiny, tiny but shorter than those in the parent cell.

A cell reaches its Hayflick limit when the telomeres become so short that they can no longer protect the chromosomes and the cell becomes unviable.

So, why don't biologists just fiddle around with our cells and add some telomerase to the mix so that the cells can keep dividing forever? Well, there's actually a kind of cell that already does that really well - Cancer cells. Yes, cancer cells can sometimes create their own telomerase so that they can replicate indefinitely without their chromosomes getting damaged, which is why they divided like like crazy and become tumors.

Because of that, no one's super anxious to start injecting people with telomerase. And in fact, one theory is that programmed cell death evolved in order to keep our tissues from undergoing explosive, cancerous growth.

So, senescence, one thing that we have to grapple with as mere mortals, but another thing that's keeping us from playing basketball until we're five hundred is our genes.

Here, research into extending longevity has focused on a little nematode called C. elegance. These little worms are really good test subjects because their life span's only about fourteen days and they only have about 20,000 genes, so scientists have been able to pinpoint the genes that are most likely in charge of aging.

In 1993, Cynthia Kenyon, a biologist at the University of California in San Francisco, found that there was just one gene that was making these worms age. It's called DAF-2 and when she messed around with that gene, basically mutated it so that it didn't work, her worms started to live 28 days instead of just 14.

Twice as long! If they did that for us, we would live to be like 160. And not only that, the worms were, like, spunky and vivacious all the way until they croaked.

Kenyon also found another gene called DAF-16 that has the opposite role. It keeps the worms young and healthy by regulating the production of antioxidants, germ fighting proteins, and other things that fight off pathogens and the effects of stress.

So what Kenyon found was that the aging gene worked by restricting the effects of the longevity gene. And when you damage the DAF-2, DAF-16 just keeps on doing its business, keeping the worms young.

That's all well and good for the worms, I'm glad that they're having nice, long, healthy lives, but I'm not really too concerned about them. What about us?

Well, in mammals, scientists have indeed found two counterparts to that nematode aging gene, and in humans a lot of research has focused on one gene in particular that creates a growth hormone called IGF-1.

When scientists silence this gene in mice, there is less cell and organ damage caused by oxidation, organs seem to be less susceptible to cancer and other age related illnesses, extending the mice's lifespan by up to 33%!

And now, why aren't we injecting George Martin with this stuff already? Well, for now, scientists aren't ready to start exploding everybody's genes; just because it works in mice doesn't mean it's going to work for people.

But it does lead us to one more final cause for aging that scientists are investigating - Calories. That's right, it turns out that even though we need Calories to live and work, the Calories we take in are also stimulating the aging process.

Scientists have know, actually since the 1940s, that lower caloric intake leads to longer life-spans in mice and other animals, but it wasn't until recently that they put their fingers on the possible cause - that Calorie intake stimulates IGF-1.

How that works isn't exactly clear, in fact it's one of the bigger mysteries in the study of aging. But one theory is that, since IGF-1's ultimate job is to direct food energy toward growth, if you take in fewer Calories, your metabolism shifts gears from growing to simply maintaining existing cells and bolstering your resistance to stress and disease.

So, getting bigger and stronger becomes less important than just staying alive. BUT, before you put yourself on an all celery and watercress diet, DON'T. Because again, just because something increases the life-span for a mouse, doesn't mean that it's going to have the same effect on you. Are you a mouse? If you're a mouse, then do that.

Scientists have been doing Calorie intake studies on animals more like us, monkeys for instance, but it's tough to do longevity studies on long-lived animals because they take freakin forever because they're like not dying. 

The longest running human longevity study has been going since 1921, which is pretty cool; good job doing science back in the day, when our subjects were about 10 years old. Some of the kids involved in that research are indeed still kicking; good work folks. But, as you might expect, many of the researchers have since died as well. One of the pitfalls of studying aging.

So it might be a while before somebody's willing to tinker with your cell chemistry or genetic code to help you stay young and spunky forever.

But in the meantime, you can take a look at your family; how old are they living to be. How long your grandparents and parents live probably accounts for about 20%-30% of your change of living past the ripe old age of 85.

Otherwise, lifestyle choices like diet and exercise and whether or not you smoke play a pretty obvious role in longevity.

Studies show that Seventh-Day Adventists, always great research subjects because they are an actual religion that encourages regular exercise, vegetarianism, and refraining from smoking and alcohol, have an average lifespan of about 88 years, about 8 years longer than average US citizen.

So, while our best and brightest keep researching senescence, genetics, and Calorie intake, just don't smoke, like, cake moss or eat like a pig or drink like a fish, and you may live longer than those things at least.

And one final thing you can do to increase your lifespan - go to youtube.com/scishow and subscribe. PROVEN! We've done the research, I promise.

If you have any questions or ideas or thoughts for us, please leave them below or in the comments, or on Facebook or Twitter. I'll see you next time.