The Crazy Evolution of a Universal Blood Type
ALISON STEWART, host:
So we have these morning meetings where everybody comes in and pitches stories. And last week, our video producer, Win, he came in to the meeting with a story he found about a girl in Australia whose blood type changed after a liver transplant. So it's sort of like, okay, that sounds really cool. Let's look into it. Which, of course, during the research for it, led to a basic question where everybody sort of sheepishly looked up and said, um, what is a blood type, really, actually?
RICO GALLIANO, host:
We're journalists, not scientists.
STEWART: You have your A, your B, your O, your AB. But do you know why this blood type is assigned a certain letter?
STEWART: So as we were asking our friendly hematologist all about this, we stumbled on to another story entirely. So, Win, the lady who changed blood types - not so big news, apparently. But a blood type as a malaria reducer and as the result of malaria, that's a little bit bigger. But we do want to start with the basics. Dr. Christine Cserti-Gazdewich is a hematologist in Toronto.
Hi. Good morning, doctor.
Dr. CHRISTINE CSERTI-GAZDEWICH (Hematologist, University of Toronto): Good morning.
STEWART: So can you give us a brief blood lesson? Blood types, I know, discovered a little over 100 years ago. But how is blood type determined?
Dr. CSERTI-GAZDEWICH: So blood type is a fascinating thing. It's actually not just a human thing. The ABO system arose about (unintelligible) ago. And most anciently humans or pre-humans - humanoids - began as group As. A is the most ancient - so-called wild type. That's what we call genes, the way they start before they begin to mutate and turn into things that exhibit selective survival advantages.
So about five million years ago, this mutation pops up called group O. And around that time, and subsequently, group B developed. Group O is actually a non-expression mutation. So A, B and O relate to what kinds of sugars you decorate your cells and secrete into your plasma and other secretions. You're A sugar is something with a messy name called GalNAc of N-acetylgalactosamine. B is galactose. And it turns out that group O is actually a non-sugar or sugar-free status cell.
(Soundbite of laughter)
STEWART: It's not dusted or lightly coated in anything.
Dr. CSERTI-GAZDEWICH: No.
(Soundbite of laughter)
GALLIANO: It's the Splenda of blood.
Dr. CSERTI-GAZDEWICH: Yeah. And it's a bit intriguing too that since 1997, about four books have been published on eating right for your type. You know, the blood group system has been in vogue. Many people have had theories for centuries, or at least since Landsteiner discovered the blood group - the ABO blood group system in 1900.
You know, as to why ABO variations exist and whether or not we should heed at them at all, it's kind of like the dream question of Freud. And…
(Soundbite of laughter)
STEWART: Well, doctor, I've watched enough "ER" and "Grey's Anatomy" to know that you can't mix blood types. Describe what happens to us when you mix A with B.
Dr. CSERTI-GAZDEWICH: So, you know, intriguingly, the ABO blood system, which we had no idea what its original function is, is the one thing that everyone in medicine respects. It's the one blood system that you can't transfuse incompatibly within. And that would be at the peril of killing a patient, even as small as 50 mils - a few bottles of nail polish worth of blood can kill a person.
GALLIANO: My God.
Dr. CSERTI-GAZDEWICH: So ABO mistransfusions are a key cause of transfusion-related deaths. And it's something that we worry tremendously about. And that's - the crux of that is basically because beyond the age of six months, infancy and onwards, we all develop antibodies that naturally recognize the blood type that we're not.
So people who are group O - lacking A or B sugars - make anti-A and anti-B. They're primed already to destroy type A or B or AB blood. People who are type B are naturally primed to destroy type A, and vice versa. The only people who are not primed to destroy any kind of blood are the people who are known as group AB - the double hits for the sugar. And that's only about four percent of the population. They're the so-called universal recipients. But they are terrible blood donors, as far as red cells go because they're basically, you know, unappealing to anyone with - who is non-AB.
GALLIANO: That's what I say about them all the time. They take and they take and they take.
Dr. CSERTI-GAZDEWICH: That's right. There are always some parasites in this world and other people who are natural martyrs and givers.
STEWART: But the O gives and gives and gives.
Dr. CSERTI-GAZDEWICH: Right.
STEWART: It's the universal donor. So there's a ying and yang here. And the O type is the subject of this study. You've published this hypothesis, and you're studying to see if it's right. The O type, as a mutant, we'll say, of the A, without the sugars on the surface, it survived because of this mutation, and it's said to have an advantage in some way.
Tell us about the advantage you've been studying.
Dr. CSERTI-GAZDEWICH: Yeah. It appears there are lines of evidence in support of this hypothesis. And we're going to be putting this to the test in Uganda. There's a clinical trial that we've started back in October. And what we're interested in is whether or not the ABO blood group system indeed influences a child's chance of living or dying with malaria.
The things that are really going to change the gene distribution, you know, the prevalence of certain blood types in populations, are the things that are going to make or break you or kill you before you hit the age of reproduction. And if so, if group O is indeed something that conveys a survival advantage, people who are non-O, we would expect to be rooted out and die in droves from something that we would hypothesize to be the selection pressure at stake. And for us, that hypothesis is malaria.
We're not the first people to come up with this idea. About 24 papers have been published on this subject. And so far, six of them - the ones most rigorously conducted and just two published in the fall - are indicating that it looks like group Os probably have advantage. But the thing is that not a single one of these studies have addressed the mortality question. They've looked at the sickness spectrum, you know, who gets sicker and who seems to only suffer mild disease. And that question, so far, is starting to settle.
Preceding that, there were a lot of animal-based and laboratory-based, so-called in-vitro studies, looking at the impact of these sugars on red cells and how malaria behaves in the test tube.
STEWART: So wait, let me stop for one second. So because the O is sugarless, as we've been calling it…
Dr. CSERTI-GAZDEWICH: Yeah. Yeah.
STEWART: …therefore, it is impervious than malaria?
Dr. CSERTI-GAZDEWICH: So that's a great question. It's actually not a matter as permeability or invadeability. What this appears to be a matter of is how malaria changes your red cells when it infects you. Malaria has this incredible ability to give you something far worse than acne. Malaria makes red cells erupt with these knobs - these so-called sticky knobs. The red cells actually look rumpled and pimply if you take a gander at them through the microscope. And these pimpled out, knob-riddled red cells acquire this ability to stick to blood vessels. Malaria appears to have evolved in this very clever fashion so that it evades immune clearance in the spleen. The spleen is like a giant lymph node, an immune clearance organ in the body. And a lot of the most ancient parasitemias, the parasitic diseases that have infected humans had their first point of clearance in the spleen. And so if a parasite can invade a cell and use a host's own living cells, their own living tanks as…
STEWART: Their own blood as a way to deliver it…
Dr. CSERTI-GAZDEWICH: Exactly.
STEWART: …that's the issue.
Dr. CSERTI-GAZDEWICH: Exactly. It's sort of like camouflage tanks. And they actually seek and sequester away in the vasculature, everywhere…
Dr. CSERTI-GAZDEWICH: …we…
STEWART: …it so - it's interesting, but we've run out of time.
Dr. Cserti-Gazdewich, thank you so much for explaining it off to us here on THE BRYANT PARK PROJECT.
Dr. CSERTI-GAZDEWICH: Thank you very much.
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