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The Creepy Reason Evolution Split Humans Into Different Blood Types (It’s Not Random). — Transcript

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0:00If you ever need a life-saving fluid
0:02transfer in an emergency room, your own
0:04sibling might be biologically toxic to
0:07you.
0:07That makes zero sense on the surface.
0:10Every person on Earth shares 99.9%
0:13of the exact same DNA.
0:15Our hearts pump to the same beat. Our
0:18lungs pull in the same oxygen. Yet, if a
0:20doctor transfers a single cup of fluid
0:22from a type A brother into a type B
0:25sister, her immune system reacts as if
0:27she just swallowed a pint of hornet
0:29venom. Within seconds, her defense cells
0:31lock onto her brother's red cells and
0:33clump them into microscopic brick walls.
0:36Now add an even stranger twist.
0:38Genetically speaking, if you carry type
0:40A blood, the molecular tag on your red
0:42cells has more in common with a wild
0:44gibbon swinging through a Malaysian
0:46rainforest than with your own type B
0:48neighbor across the street. Evolution
0:51spent millions of years making sure
0:53human kidneys, livers, and eyeballs all
0:56run on one universal blueprint. Yet, it
0:59intentionally shattered our bloodstream
1:01into rival incompatible camps that
1:03cannot stand the sight of each other.
1:05For centuries, physicians had no idea
1:08those rival camps existed.
1:10In the 1600s, doctors in Paris and
1:12London actually tried perking up weak
1:14patients by hooking them up to calm
1:16sheep, figuring gentle lamb blood would
1:19soothe the restless human mind. It went
1:21about as poorly as you would expect.
1:23Even when doctors switched to human
1:25donors in the 1800s, the procedure
1:27remained a terrifying coin toss. One
1:30patient would sit up rosy and energetic,
1:33while the patient in the next bed
1:34received a transfer from the exact same
1:36donor and suffered immediate organ
1:38failure. The mystery finally cracked in
1:411900 inside a quiet Vienna laboratory
1:44run by a 32-year-old Austrian physician
1:47named Karl Landsteiner. Instead of
1:50guessing inside hospital wards,
1:52Landsteiner drew tiny fluid samples from
1:54himself and five of his lab assistants,
1:57separated the clear liquid serum from
1:58the red cells, and mixing them on glass
2:01slides like a bartender testing cursed
2:03cocktail recipes. Some combinations
2:06glided together smoothly, others
2:08instantly curdled into thick red clumps
2:10right on the glass. Landsteiner realized
2:13human blood was not a single uniform
2:15liquid at all, winning him a Nobel Prize
2:17and saving millions of modern patients.
2:20What Landsteiner could not answer in
2:221900 was the question that kept
2:24evolutionary biologists awake for the
2:26next century. Why on earth would natural
2:29selection design a species where half
2:31the tribe cannot share life-saving fluid
2:33with the other half?
2:35To see why that split exists, you have
2:37to shrink down to the size of a single
2:39red blood cell. Right now, you have
2:42roughly 25 trillion of these tiny cells
2:44racing through your vessels at about 3
2:46ft per second. Your bone marrow prints 2
2:49million brand new ones every single
2:51second just to keep up with demand.
2:53Unlike almost every other cell in your
2:55body, a mature red blood cell has no
2:58nucleus and zero DNA inside it. It
3:00ejects its own control center before
3:02leaving the bone marrow, so it can pack
3:04itself wall-to-wall with iron-rich
3:06hemoglobin, turning into a hollowed-out
3:08delivery van for oxygen. Because the
3:11inside is just cargo space, all the
3:13identity badges have to hang on the
3:15outside of the van. And despite what
3:17people usually picture, those A, B, and
3:20O badges are not complex proteins. They
3:23are microscopic chains of simple sugars
3:25sticking out from the cell's outer
3:27membrane like festive bakery sprinkles.
3:29Every standard red cell starts by
3:31building the exact same foundational
3:33sugar stock on its roof, known as the H
3:36antigen. Think of the H antigen as a
3:39plain wooden signpost planted on top of
3:41the cell. What happens next comes down
3:44to a single gene sitting on chromosome 9
3:46that codes for a tiny molecular builder
3:48enzyme. If you inherit the A version of
3:51that gene, your builder enzyme grabs a
3:53specific sugar molecule called N-acetyl
3:57glucosamine and glues it onto the tip of
3:59the wooden signpost.
4:01If you inherit the B version, the
4:03builder enzyme differs by just four tiny
4:06amino acids, which causes it to grab a
4:08slightly different sugar called
4:10galactose and glue that onto the
4:12signpost instead. If you inherit from
4:14both parents, you stick both sugars on
4:17the roof and become type AB.
4:19And if you are type O, your chromosome
4:21nine carries a tiny genetic typo,
4:24a missing single letter of DNA that
4:26breaks the builder enzyme completely.
4:29Nothing gets glued to the top of the
4:30signpost. Your red cells roll through
4:33your veins, displaying only the bare,
4:35undecorated H antigen stock.
4:38Four letters of protein code and a pinch
4:40of sugar are the entire difference
4:42between life and death in an operating
4:44theater. That leads straight into the
4:46first genuinely creepy puzzle of human
4:49immunology.
4:50Normally, your immune system only builds
4:53targeted weapons after it gets ambushed
4:55by an invader. You do not carry
4:57antibodies against chickenpox or measles
4:59until you either catch the virus or get
5:01a vaccine. Yet a baby born with type A
5:04blood starts manufacturing heavy-duty
5:06attack antibodies against type B sugar
5:08within the first six months of life,
5:10even if that baby has never received a
5:12transfusion or touched a single drop of
5:14type B blood.
5:15Why is your body preloading weapons
5:17against a neighbor's blood type it has
5:18never met?
5:20The answer is sitting inside your lunch.
5:22Those exact same A and B sugar chains
5:24are not exclusive to human red cells.
5:27They also coat the outer walls of
5:28trillions of common bacteria living
5:30inside your intestines, along with dust
5:32particles, plant pollen, and bits of
5:34food you swallow every day.
5:36Within months of being born, as milk and
5:39solid food populate a baby's gut with
5:41microbes, the infant's immune system
5:43inspects all the new bacteria moving
5:45into the neighborhood. If the baby has
5:47type A blood, the immune system
5:49recognizes A-shaped sugars on gut
5:51bacteria as friendly household furniture
5:54and leaves them alone. When it spots a
5:56gut bacterium wearing a B-shaped sugar
5:58coat, the immune system flags it as a
6:00foreign trespasser and builds a
6:02permanent stockpile of anti-B antibodies
6:05to patrol the bloodstream.
6:07Type O individuals, who have neither A
6:09nor B sugars on their own cells, treat
6:12both bacterial sugar coats as
6:13trespassers and spend their entire lives
6:16patrolling with both anti-A and anti-B
6:19weapons locked and loaded.
6:21For decades, pop science books and
6:23late-night talk shows tried to explain
6:25this setup with a neat, tidy story that
6:27millions of people still believe. In the
6:301990s, a massive diet craze swept the
6:32world, claiming that blood types were a
6:34recent calendar of human eating habits.
6:37According to that popular myth, Type O
6:39was the original Paleolithic
6:41hunter-gatherer who lived on mammoth
6:43steaks. Type A popped up 10,000 years
6:45ago when Neolithic farmers started
6:48boiling wheat and lentils, and Type B
6:50appeared later among Eurasian cattle
6:52herders drinking milk.
6:53It sounded great on the back of a
6:55cookbook.
6:56There is just one problem. When
6:58geneticists actually sequenced the DNA
7:00across primates, that entire timeline
7:02fell apart in about 10 seconds.
7:05In 2012, evolutionary geneticist Laura
7:08Segurel and her colleagues at the
7:10University of Chicago and the French
7:12National Center for Scientific Research
7:15compared the exact DNA sequences of the
7:17gene across humans, chimpanzees,
7:21bonobos, gorillas, orangutans, gibbons,
7:25and Old World monkeys like baboons and
7:27macaques. If Type A and Type B had
7:29evolved recently inside human farming
7:31villages, then human A and human B genes
7:34should look almost identical, like two
7:36sibling branches that just sprouted at
7:38the very top of a tree. Instead,
7:41Segurel's team found the exact opposite.
7:44The genetic code that makes Type A in a
7:46human is far closer to the code that
7:48makes Type A in a gibbon than it is to
7:51the Type B gene sitting inside another
7:53human. Even baboons and macaques carry
7:55the exact same two core amino acid
7:58switches distinguishing A from B.
8:01That discovery proved that the split
8:02between A and B did not happen when
8:04humans picked up a plow 10,000 years
8:06ago.
8:07It happened at least 20 million years
8:09ago in an ancient primate ancestor long
8:12before humans, chimps, or gorillas even
8:14existed as separate lineages.
8:17In evolutionary biology, this is called
8:19a trans-species polymorphism, and it is
8:22exceedingly rare.
8:24Usually, when a gene mutates into two
8:26versions, one version is slightly better
8:28at helping creatures survive or random
8:31chance in small populations wipes one
8:33version out within a few hundred
8:35thousand years. Keeping both A and B
8:38alive side by side across 20 million
8:40years of extinctions, ice ages, and
8:42continental splits means something
8:44terrifying was actively punishing
8:46primates every time they drifted toward
8:48having just one blood type.
8:50Imagine a neighborhood where every
8:52single house uses the exact same master
8:54key for the front door.
8:56The moment a burglar figures out how to
8:58file a copy of that key, every house on
9:00the street gets robbed in a single
9:02night.
9:03Now imagine a street where a third of
9:05the houses use pin tumbler locks, a
9:07third use magnetic key cards, and a
9:10third have welded the keyhole shut
9:12altogether. A burglar carrying a pocket
9:14full of lock picks might break into the
9:16first house only to hit a brick wall at
9:18the house next door.
9:20For 20 million years, viruses, bacteria,
9:23and blood-borne parasites have been the
9:25burglars, and the sugar sprinkles on
9:27your cells have been the front door
9:28locks. Glycan evolutionary biologist
9:31Ajit Varki at the University of
9:33California, San Diego, demonstrated that
9:36many enveloped viruses, the kind that
9:38wrap themselves in a piece of their host
9:40cell membrane as they burst out of an
9:42infected cell, accidentally decorate
9:44their own outer coats with the blood
9:46type sugars of the person they just
9:47infected. Think about how sneaky that
9:49is. If a virus infects a person with
9:52type A blood, every new viral particle
9:55it coughs out into the air is wearing
9:57stolen type A sugar tags like a stolen
9:59security uniform. If that person sneezes
10:02on another type A individual, the new
10:04victim's immune system sees the familiar
10:06A tags and hesitates, giving the virus a
10:09head start. If that same sneeze lands on
10:11someone with type B or type O blood,
10:14their preloaded anti-A antibodies spot
10:16the stolen uniform instantly and shred
10:18the virus before it can unpack its bags.
10:21That single mechanism explains why
10:23natural selection never let one blood
10:25type conquer the entire human species.
10:27Whenever one blood type becomes too
10:29common in a valley or a city, pathogens
10:31adapt to crack that specific lock,
10:34triggering waves of illness that hit the
10:36majority blood type hardest while
10:38sparing the rare minority blood types.
10:40Over generations, the rare blood types
10:43survive and multiply until they become
10:45the new majority, at which point the
10:47pathogens pivot and start targeting them
10:49instead.
10:51Nowhere is this microscopic tug-of-war
10:53more visible than on a world map of
10:55human blood types today. If you look at
10:57indigenous populations in South and
10:59Central America, nearly 100% of people
11:02carry type O blood, and type O is also
11:05the dominant blood group across large
11:07swaths of sub-Saharan Africa. Why did
11:09type O win by a landslide in the
11:11tropics? Because of a single-celled
11:13parasite called Plasmodium falciparum,
11:15the deadliest form of malaria.
11:17When a mosquito injects Plasmodium
11:19falciparum into a human bloodstream, the
11:21parasite dives inside red blood cells to
11:24hide and multiply. There is a catch for
11:26the parasite. Your spleen acts like a
11:28ruthless quality control shredder at the
11:31end of the bloodstream highway. Every
11:33few minutes, your red cells have to
11:35squeeze through tiny, narrow slits in
11:37the spleen.
11:38Healthy, flexible cells squish right
11:40through. Red cells stiffened by a
11:42bloated malaria parasite inside them get
11:45stuck in the filter and destroyed.
11:47To avoid getting dragged into the
11:49spleen's shredder, the malaria parasite
11:51manufactures sticky protein hooks and
11:53pokes them out through the roof of the
11:55infected red cell. Those sticky hooks
11:57grab onto the A and B sugar chains of
11:59healthy neighboring red cells, gluing 10
12:02or 12 healthy cells around the infected
12:04cell like a clump of grapes in a process
12:07called rosetting. Anchored to the vessel
12:09wall inside that sticky fortress, the
12:11parasite avoids the spleen while
12:13clogging tiny capillaries inside the
12:15host's brain and lungs.
12:17Here is why type O became the ultimate
12:19tropical survival card. Because type O
12:22results from a broken builder enzyme
12:24that leaves the H antigen stalk
12:26completely bare, the malaria parasite's
12:29sticky hooks have nothing to grab onto.
12:31The clumps fall apart. Even better, a
12:33landmark study led by Dr. Kevin Kain at
12:36the University of Toronto revealed that
12:38human immune cleanup cells, called
12:40macrophages, spot and gobble up
12:42malaria-infected type O cells far faster
12:45than infected type A or B cells. You can
12:48still catch malaria with type O blood,
12:51and you will still feel miserable for a
12:52week, but your odds of sliding into
12:54life-threatening cerebral malaria drop
12:56dramatically.
12:58Across thousands of generations in
12:59tropical malaria zones, children
13:01carrying the broken type O gene survived
13:03to adulthood, while A and B carriers
13:06were slowly filtered out.
13:08If type O is so great at dodging severe
13:10malaria, why isn't every human on Earth
13:12type O? Take a flight from West Africa
13:15or the Amazon basin over to South Asia,
13:18right where the Ganges and Brahmaputra
13:20Rivers empty into the Bay of Bengal.
13:22Suddenly, type O plunges to some of the
13:25lowest rates on the planet, while type B
13:27surges to dominate the population. What
13:30changed in the river delta? Another
13:32ancient microscopic killer stepped onto
13:34the stage, Vibrio cholerae, the
13:37waterborne bacterium that causes
13:38cholera.
13:39When cholera bacteria enter the small
13:41intestine, they release a potent toxin
13:44that looks for a molecular dock on the
13:46cells lining the gut wall. Ironically,
13:48the bare, undecorated H antigen sugar of
13:51type O, the exact same bare stump that
13:53starved malaria of a foothold in the
13:55bloodstream, turns out to be the perfect
13:58landing pad for cholera dynamics in the
14:00digestive tract. In people with type A,
14:02B, or AB, the extra sugar molecules
14:05crowding the intestinal lining
14:07physically block and buffer the toxin's
14:09ability to lock in at full throttle.
14:12Studies inside cholera clinics in
14:14Bangladesh showed that while anyone can
14:16swallow the bacteria, individuals with
14:19type O blood are vastly more likely to
14:21suffer rapid, severe fluid loss that
14:24requires immediate hospitalization,
14:26whereas people with type AB blood are
14:28the most resistant on earth, sometimes
14:31drinking contaminated water and walking
14:33away with barely a stomach rumble. Where
14:35ancient river deltas brewed cholera for
14:37millennia, type O became a liability and
14:40type B and AB took over the map. If you
14:43enjoy discovering how invisible battles
14:45from millions of years ago are still
14:47quietly running the rules inside your
14:49own body, hit subscribe right now. This
14:52channel is built for people who never
14:53stopped asking why we are wired this
14:55way.
14:56The plot gets even stranger when you
14:58realize your blood type is not even
14:59confined to your blood. Around 80% of
15:02humans carry an active version of a
15:04second gene called FUT2. In the medical
15:07world, these people are known as
15:08secretors. If you are part of that 80%
15:11majority, your body takes your A, B, or
15:14O sugar tags and sprays them into your
15:17saliva, your tears, your sweat, and the
15:20protective mucus lining your stomach and
15:21intestines.
15:23Essentially, four out of five people are
15:25walking around broadcasting their blood
15:27type out of every pore and salivary
15:29gland they own.
15:30Why would evolution wire 80% of us to
15:33leak our blood type into our spit and
15:35stomach mucus while the other 20% keep
15:38their blood type strictly locked inside
15:39their veins as non-secretors? Because
15:42the stomach lining is another front door
15:44where bacteria and viruses go shopping
15:46for locks. Consider norovirus, the
15:50infamous winter stomach bug that can
15:51turn a cruise ship or an elementary
15:53school into a quarantine zone in 48
15:56hours.
15:57Different strains of norovirus have
15:59evolved specialized molecular claws
16:01designed to grab onto the floating H and
16:04A blood type sugars sitting on the gut
16:05lining of secretors. If you belong to
16:08the 20% of humans who inherited two
16:10deactivated copies of the FUT2 gene,
16:13your gut lining has zero blood type
16:15sugars floating in its mucus.
16:17When the most common strain of norovirus
16:19washes into a non-secretor's stomach, it
16:22slides right down the digestive tract
16:24like a climber trying to scale a greased
16:26glass wall.
16:28You can sit at the same dinner table
16:29while your entire family battles the
16:31winter stomach bug and never feel a
16:32thing. Yet being a non-secretor comes
16:35with its own tradeoff.
16:36Those floating sugars in secretor mucus
16:39also feed friendly gut bacteria, meaning
16:41non-secretors face higher odds of
16:43certain chronic digestive inflammations.
16:46And the system is only the loud
16:48celebrity on the marquee. Most people
16:50only know the four famous letters plus a
16:52positive or negative sign. Yet the
16:54International Society of Blood
16:56Transfusion currently recognizes more
16:58than 45 distinct blood group systems
17:01across over 300 different cellular
17:03surface markers. Every single one of
17:05those lesser-known systems is a
17:07fossilized scar from an ancient
17:08microbial siege. Look at the Duffy blood
17:11group system, named after a patient
17:13named Richard Duffy who helped doctors
17:15identify it in 1950. On most red blood
17:18cells across Europe and Asia, the Duffy
17:21protein sits on the cell surface, acting
17:24as a mop that soaks up excess
17:26inflammatory signals in the blood.
17:28Millions of years ago, a second species
17:30of malaria parasite called Plasmodium
17:33vivax figured out how to use the Duffy
17:35protein as a private revolving door to
17:38slip inside human red cells. In
17:40response, a tiny single letter mutation
17:43popped up in West and Central Africa
17:45that didn't destroy the Duffy gene
17:47completely. It just turned off the
17:49switch that prints the protein on red
17:50blood cells while keeping it working
17:52normally in the rest of the body. That
17:54mutation was such a masterstroke of
17:56evolutionary defense that today nearly
17:59100% of people native to West Africa are
18:02Duffy negative on their red blood cells,
18:04locking Plasmodium vivax out of an
18:07entire region of a continent.
18:09Then there are the ultra-rare blood
18:10types that sound like something out of a
18:12medical thriller. In 1952, in the city
18:15of Mumbai, then called Bombay, a doctor
18:18named Y.M. Pande encountered a railway
18:21worker and a stab wound patient whose
18:23blood violently rejected every single
18:25donor bag in the hospital, including
18:27dozens of bags of universal type O
18:29blood. When Bende investigated, he
18:32discovered the patients carried a double
18:33mutation in the FUT1 gene, the
18:36foundational builder that constructs the
18:38wooden H antigen signpost itself.
18:41Without the H signpost, their red cells
18:43could not attach A or B sugars, even if
18:46they carried the A or B genes.
18:48On a standard hospital test, they looked
18:50like type O because they lacked A and B.
18:54In reality, their immune system saw the
18:57bare H signpost on type O blood as a
18:59foreign invader and attacked it.
19:02Known today as the Bombay phenotype,
19:04this group appears in roughly one in
19:0610,000 people in India and only four out
19:09of every million people worldwide,
19:12forcing carriers to rely on
19:13international rare donor registries if
19:16they ever need surgery.
19:18Even rarer is a condition first spotted
19:20in an indigenous Australian woman in
19:221961,
19:24Rh null, nicknamed golden blood by
19:26hematologists around the world. When
19:29doctors say your blood is positive or
19:30negative, they are usually talking about
19:32a single protein called the RhD antigen
19:35out of a big family of 61 Rh proteins
19:38that help brace the outer frame of your
19:40red blood cells. Someone with Rh null
19:43blood is missing not just the main RhD
19:45marker, but every single one of all 61
19:48proteins in the entire Rh family.
19:51Because their red cells are stripped
19:52completely bare of every Rh tag on
19:55Earth, their blood is prized like solid
19:57gold by researchers and emergency
19:59physicians. It can be donated safely to
20:02anyone with a rare crisis inside the Rh
20:04system. The catch is brutal. Fewer than
20:0750 human beings on the entire planet are
20:09known to have active Rh null blood
20:11today. Without those 61 structural
20:14proteins bracing the cell membrane,
20:16their red cells are slightly softer and
20:18more fragile as they bounce through
20:20narrow capillaries. And if a person with
20:22golden blood ever gets into an accident
20:24in Tokyo or London, a compatible bag of
20:27blood might have to be flown across two
20:29oceans from a freezer in Brazil or
20:31Europe just to keep them alive.
20:33We can actually see what happens when a
20:35human species loses this wild variety of
20:38blood types by looking inside
20:39prehistoric caves.
20:41For years, anthropologists assumed that
20:43all Neanderthals were universally type O
20:46based on early DNA tests of just one or
20:49two European fossils. Then in 2021,
20:53paleoanthropologist Silvana Condemi and
20:56her team at Aix-Marseille University
20:59decoded the full blood group genomes of
21:01three Neanderthals and one Denisovan
21:04spanning Siberia to Croatia. They proved
21:06that ancient Neanderthals originally
21:08carried A, B, and O blood types just
21:11like modern humans, inherited from our
21:13shared African ancestors. Yet as late
21:16Neanderthals fractured into tiny
21:18isolated bands of 20 or 30 cousins
21:20huddled in Ice Age valleys, inbreeding
21:23caused their blood type diversity to
21:24collapse. Almost all late Neanderthals
21:27ended up carrying the exact same narrow
21:29set of blood markers alongside a weak Rh
21:32variant that would have triggered severe
21:34immune clashes during pregnancy whenever
21:37they mated with outside groups. When
21:39bands of Homo sapiens walked out of
21:41Africa carrying a rich rotating casino
21:43of A, B, O, and secretor shields, our
21:46species could absorb novel plagues while
21:48uniform Neanderthal bands had every
21:50house on their street unlocked by the
21:52very first bug that cracked their single
21:54shared key. And that 20 million-year-old
21:57security system is still shaping your
21:59daily life in ways you can witness on a
22:01warm summer evening. Have you ever sat
22:03outside at a barbecue while one friend
22:05gets eaten alive by mosquitoes and the
22:07person sitting right next to them never
22:09gets a single bite? In controlled
22:11laboratory landing tests, entomologists
22:14discovered that Aedes mosquitoes land on
22:16the skin of type O secretors nearly
22:18twice as often as they land on type A
22:20individuals. Remember that 80% of people
22:23leak their blood type sugars onto their
22:24skin through sweat. Mosquitoes use
22:27chemical sensors on their antennae to
22:29sniff out those invisible H antigen
22:31clues from yards away, zeroing in on the
22:33very same blood group that spent
22:35millennia adapting to survive the
22:37malaria parasites those mosquitoes
22:39carry.
22:40Even inside your own vessels right now,
22:43your blood type is quietly adjusting
22:44your internal plumbing.
22:46Those A, B, and O sugar sprinkles are
22:48not just painted on red blood cells.
22:50They are also attached directly onto a
22:52giant clotting protein floating in your
22:54plasma called von Willebrand factor,
22:57which acts like biological duct tape
22:59whenever you scrape your knee. When A or
23:01B sugars are glued onto that clotting
23:03protein, they act like a protective
23:05shield that keeps your liver from
23:07clearing the protein out of circulation
23:09too quickly. Because type O individuals
23:11lack those extra A and B sugars, their
23:14livers clear out clotting proteins much
23:16faster, leaving type O humans with
23:18roughly 25 to 30% lower levels of
23:21clotting factor in their bloodstream
23:23than type A or B humans. Over a
23:25lifetime, that tiny sugar difference
23:27means type O carriers have slightly
23:29thinner flowing plumbing that lowers
23:31their risk of dangerous blood clots in
23:33modern office chairs, while type A and B
23:35carriers have faster sealing emergency
23:37patches that helped our ancestors
23:39survive physical scrapes in the wild.
23:41Every drop of fluid running through your
23:43veins is a living museum of every
23:45parasite, bacterium, and virus your
23:47ancestors ever outsmarted.
23:49Which camp did evolution put you in?
23:52What is your blood type? And if you are
23:53type O, are you always the first person
23:56in your friend group that mosquitoes
23:57treat like an all-you-can-eat buffet?

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