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  • I hate death.

  • More than 150,000 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 his 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 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 I'm like "C'mon, scientists! Make me live forever...please?"

  • (intro song)

  • 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 too tough for ourselves to keep these masses of cells together...

  • *boof* 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's 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.

  • 'Cause technically, there's 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 what's 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 170 years

  • and lobsters can live to be 140

  • and the oldest quahog clam ever collected was about 405 years old.

  • Frikkin Shakespeare was writing Hamlet when that clam was born.

  • So that's totally unfair.

  • Why do some animals get to start to die 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, the young research named Leonard Hayflick was studying human fetal cells

  • when he noticed that after a while, human cells just stop dividing and then they died.

  • He came to realize, that they all quit dividing after about 50 divisions, which took around 9 months.

  • If you put healthy dividing cells into the freezer, the division would slow down, and even stop

  • but when 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 the 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 to 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 lifespan.

  • But as with everything in science, it is not this simple.

  • 'Cause 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, good scientists are asking, "Okay, yes, there's a limit, but what causes the limit?"

  • Turns out, the answer is 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.

  • 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 chromosomes of a new cell are a tiny, tiny bit 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 biologist 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 divide like crazy and become tumors.

  • Because of that, nobody'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. Scenesence. One thing we have to grapple with as mere mortals.

  • But another thing that's keeping us from playing basketball until we're 500 is our genes.

  • Here, research into extending longevity has focused on a little nematode called C. elegans.

  • These little worms are really good test subjects because their lifespan's only about 14 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 worm 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!

  • Kenyan also found that another gene called DAF-16, that has the opposite role.

  • It keeps the worm young and healthy by regulating the production of antioxidants,

  • germ-fighting proteins and other things that fight off pathogens and the effects of stress.

  • 'Cause, you know, being a worm, stressful.

  • So what Kenyan found is that the aging gene worked by restricting the effects of the longevity gene.

  • And when you damaged the daf-2, daf-16 just keeps on doing its business,

  • keeping the worms young.

  • That's all good and well 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 nemotode 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%

  • 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 of 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 known, actually since the 1940s, that lower caloric intake leads to longer lifespans

  • 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 lifespan for a mouse,

  • doesn't mean 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 freaking forever,

  • cause they're like not dying.

  • The longest running human longevity study have 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 someone's willing to tinker with your cell chemistry

  • or genetic code to help you stay young and spunky forever.

  • But in the meantime, you could take a look at your family: How old are they living to be?

  • How long your grandparents and parents lived probably accounts for about 20% - 30%

  • of your chance of living past the ripe old age of 85

  • Otherwise, life style choices like diet and exercise and whether or not you smoke, play pretty obvious role in longevity

  • Studies show that Seventh-Day Adventists, always great research subjects because they're an actual religion

  • that encourages regular exercise, vegetarianism, and refraining from smoking and alcohol,

  • have an average lifespan of about 88 years

  • About eight years longer than the average US citizen.

  • So, while our best and brightest keep researching senescence, genetics, and calorie intake,

  • just don't smoke like Kate Moss, eat like a pig, or drink like a fish,

  • and you may live longer than those things at least.

  • And one final thing that you can do to increase your lifespan: go to Youtube.com/SciShow and subscribe

  • Proven! We've done the research. We promise.

  • If you have any questions or ideas or thoughts for us, please leave them