Speaker 1: Welcome to Thrilling Threads. This is the show where we
take those wild claims you see online, those confusing threads
of information, and we just.
Speaker 2: Keep pulling and we pull on them until we find
the real and usually far more fascinating truth that's tangled
up inside.
Speaker 1: And today we are diving into something that is literally
inside all of us. Our blood, specifically the reesis factor.
You know, whether you're A positive or O negative.
Speaker 2: It's just a tiny genetic difference, but it has somehow
become the seed for some of the most out there
theories I have ever come across.
Speaker 1: Oh absolutely, And if you're listening to this and you
happen to be RH negative, you've probably heard them.
Speaker 2: You've definitely seen them.
Speaker 1: They are everywhere. The big question, the one you've all
sent us, is this, does having RH negative blood mean
you're not entirely human?
Speaker 2: I mean, does it mean you're descended from aliens or
maybe from the Nephlum, those giants from the Bible.
Speaker 1: Some sources even claim reptilian ancestors that you have this
special bloodline that sets you apart.
Speaker 2: It's this idea that RH negative blood is a kind
of genetic marker, an anomaly that proves non human entities
meddled with our DNA at some point in the distant past.
Speaker 1: And that's our mission for this deep dive. We're taking
all of your sources, from the ancient astronaut guys and
the biblical myths all the way to the really dense,
cutting edge genetics research.
Speaker 2: And we're going to conduct a really thorough analysis to
figure out the actual evolutionary puzzle here.
Speaker 1: So first we'll establish the basic biology, no aliens involved,
just the science of the reesis factor.
Speaker 2: Then we're going to directly address and will dismantle those
alien of the gaps arguments.
Speaker 1: After that we get to the really good stuff, the
hard data, the global distribution is genuinely weird and tells
the story of its own.
Speaker 2: And finally we'll get into the real scientific debate, the
intense evolutionary battle between random chance and some kind of
hidden advantage that might explain why this trait even still exists.
Speaker 1: Yeah, and we're drawing from a lot of great sources
medical reviews, specific genetics papers, from researchers like Perry and Flagger,
population data, and of.
Speaker 2: Course the fringe sources themselves. We have to understand what
they're claiming to see why it's so compelling. So, yeah,
let's get into it.
Speaker 1: Let's do it. Where do we even start, I guess
with the discovery itself.
Speaker 2: Yeah, let's start at the beginning. You have to remember,
for a long time, we didn't understand our own blood.
It was just this red fluid.
Speaker 1: Right, and then Karl L. Einsteiner comes along in nineteen
hundred and discovers the Abo blood girks.
Speaker 2: A massive Nobel winning breakthrough. But even after that, blood
transfusions were still a bit of a gamble.
Speaker 1: Sometimes they work, sometimes they didn't, and people got very
sick or died exactly.
Speaker 2: Doctors knew something else was going on. There was another
factor they were missing.
Speaker 1: So Lansteiner went back to the.
Speaker 2: Lab he did. He and a colleague, Alexander Wiener. They
were working on this problem through the late nineteen thirties.
Speaker 1: And it wasn't until nineteen forty that they finally nailed
it down.
Speaker 2: Right. They were at Rockefeller University and they were looking
specifically at these strange immune reactions, especially in pregnant women
or in people who'd had multiple transfusions.
Speaker 1: Okay, and this is where the monkeys come in, right.
Speaker 2: The name the Reesis macaque. Yeah, it's actually a pretty
simple story. They injected blood from the macaques into rabbits
and guinea pigs.
Speaker 1: And that created antibodies.
Speaker 2: They created an anti serum. So then they took that
anti serum and mixed it with human blood samples, and
what happened. They found that about eighty five percent of
the human blood samples clumped up. They reacted, So.
Speaker 1: They called it the Reesis factor or rh factor after
the monkeys.
Speaker 2: Simple as that, if you're blood clumped, you were RH positive.
If it didn't, you were RH negative.
Speaker 1: And just like that, the four known blood types instantly
became eight, a.
Speaker 2: Huge leap forward for medicine. Fundamentally, your blood type ABO
whatever is about antigens.
Speaker 1: These are just substances on the surface of your red
blood cells, little.
Speaker 2: Flags exactly, little flags made of proteins or carbohydrates. For
the Rees's system, we are mostly talking about one specific flag,
the d antigen.
Speaker 1: So if you're RH positive, you have the d antigen
flag waving on your red blood cells, and if you're.
Speaker 2: R negative you don't. The flagpole is bare.
Speaker 1: Okay, that seems straightforward enough, But the genetics behind why
the flagpole is bare. That's where things get really weird.
Speaker 2: That is where the entire evolutionary mystery begins. Because being
D negative or RH negative isn't from a small mutation.
It's not a typo in the genetic code.
Speaker 1: What is it?
Speaker 2: Then? It's caused by a massive, all or nothing genetic event.
It's the homozygous deletion of the entire RhD gene.
Speaker 1: Okay, whoa, let's break that down. Homozygous deletion. What does
that mean for a person's DNA.
Speaker 2: It means the entire instruction manual for how to build
that d antigen flag. It's been completely ripped out of
your genetic.
Speaker 1: Book, not just smudged or misspelled.
Speaker 2: Gon and homozygous means you inherited that missing page from
both of your parents. You got a book with the
page missing from your mom and another one with the
same page missing from your dad.
Speaker 1: So to be RH positive, you just need one good
copy of that page.
Speaker 2: One good copy is all it takes. But to be
RH negative you need to have zero copies. The gene
has to be completely absent from both of your chromosomes.
Speaker 1: That's kind of shocking that a huge deletion like that
is so common in some parts of the world. How
does a whole gene just disappear?
Speaker 2: Well, the how is actually one of the most fascinating
parts of the story. Researchers like Wagner and Fleegel figure
this out. The RhD gene sits on the chromosome, but
it's sandwiched between two other little segments of DNA.
Speaker 1: What are they?
Speaker 2: They're called recis boxes. And the crucial detail is that
these two boxes are almost identical to each other. They
have about ninety nine percent sequence similarity.
Speaker 1: So it's like having the same complex paragraph at the
start of chapter five and at the end of chapter five.
Speaker 2: That's a perfect analogy. And so when your cells are
copying or repairing your DNA, a process that happens all
the time, the machinery can get confused. How So it
sees the first racist box, the identical paragraph, and starts reading,
but then it accidentally skips over the entire RhD gene
in the middle and jumps straight to the second racist
box because it looks the same, and.
Speaker 1: It snips out everything in between.
Speaker 2: It snips out everything in between, thinking it's just getting
rid of a duplicated bit of code. It's a type
of error called non allelic homologous recombination.
Speaker 1: So the gene disappears because of a structural vulnerability in
our own DNA. It's an accident waiting to happen.
Speaker 2: A catastrophic copy paste error basically, and that one error
is the source of everything we're talking about today, the
medical problems, the pregnancy risks, and all the alien theories.
Speaker 1: It's a molecular smoking gun. It wasn't a gradual change.
It was a sudden, huge dilution that happened and has
just stuck around ever.
Speaker 2: Since, and that region of the genome is just it's unstable.
The same error that causes deletions can also cause duplications.
Speaker 1: What do you mean.
Speaker 2: Well, the hat map project, which was this huge effort
to map human genetic diversity, found some people, one from
West Africa and one from Japan who actually had three
copies of the RhD gen.
Speaker 1: Three, so they're like super rh positive in a way.
Speaker 2: Yeah, it doesn't really cause any major clinical problem for them.
They're just strongly rh positive, but it shows that this
specific spot on the chromosome is a hot spot for
these massive structural changes. It can delete it can duplicate
just a very active area.
Speaker 1: A genetic roller coaster. Okay, so that's the how, But
the why it matters comes down to the clinical side
of things. This is the part that fuels the fringe theories, right,
the rejection phenomenon exactly.
Speaker 2: We're talking about hemolytic disease in the newborn HDN. This
is the life or death consequence of that gene deletion.
Speaker 1: Explain how it works.
Speaker 2: It happens when an RH negative mother is pregnant with
an RH.
Speaker 1: Positive child, which would happen if the father is RH positive.
Speaker 2: Right. The mother's body doesn't have the de antigen, so
her immune system has never seen it before. To her body,
it's a foreign invader, like a virus or bacteria.
Speaker 1: But the mother's and baby's blood systems are separate, aren't there.
Speaker 2: They are for most of the pregnancy, but during childbirth,
especially with the first RH positive baby, a small amount
of the baby's blood can leak into the mother's.
Speaker 1: Bloodstream and her body sees the d antigen on those
baby blood cells for the.
Speaker 2: First time, and it freaks out. It mounts a massive
immune response, creating armies of antid antibodies designed to find
and destroy that foreign d antigen.
Speaker 1: So the first baby is usually okay.
Speaker 2: The first baby is usually fine because the exposure happens
right at the end. But now the mother is sensitized.
She has those antibodies for.
Speaker 1: Life and for the next pregnancy.
Speaker 2: If the next baby is also our age positive. Those
maternal antibodies are small enough to cross the placenta. They
enter the baby's circulation and do what they were designed
to do.
Speaker 1: They attack the baby's red blood.
Speaker 2: Cells viciously, causing severe anemia, jaundice, brain damage, and very
often death.
Speaker 1: I saw statistic from before modern medicine intervened, around the
nineteen forties.
Speaker 2: I think I know the one you mean.
Speaker 1: It said mortality from HDN was one in every fifty
six berths to D negative women in European American populations.
Speaker 2: It's a staggering number. That is a massive, massive evolutionary penalty,
a huge selective pressure.
Speaker 1: It means that for thousands of years, before the road
jam shot was invented in nineteen sixty eight, being an
RH negative woman carried a significant risk of losing your children, a.
Speaker 2: Huge reduction in what we call reproductive fitness. And that's
the central.
Speaker 1: Paradox How could a trait that is so dangerous for
reproduction survive and even thrive in certain populations.
Speaker 2: It's the multimillion dollar question. And that paradox, that gap
in our easy understanding is the perfect breeding ground for
other explanations.
Speaker 1: The fringe theories. Okay, let's go there, let's tackle them
heat on the core question from the sources, does RH
negative blood come from reptiles from gods?
Speaker 2: The scientific consensus is, and I want to be really
clear about this, a hard no zero evidence zero, as
outlets like the tech Interactive put it, there is just
no evidence to support any of this. It's an ordinary
trait that comes from simple biology. It's a gene deletion,
that's it.
Speaker 1: But the reason it's so compelling, the psychological hook is
the biology we just talked about.
Speaker 2: Absolutely, the idea of a mother's body attacking its own baby,
it just feels wrong, It feels unnatural.
Speaker 1: It feels like rejection. As if, and this is the
key phrase, the mother and child are from different species.
Speaker 2: That's the emotional leap. If her body thinks the baby
is a foreign invader, maybe it's because the baby is foreign,
Maybe it has some non human DNA from the father's side.
Speaker 1: And poof, you have an opening for an extraordinary claim.
Speaker 2: You have a vacuum, and the fringe theories rush in
to fill it. It's a rhetorical trick we call the
Aliens of the Gaps argument.
Speaker 1: It's like the old God of the Gaps, but for
eupology exactly.
Speaker 2: You find a genuine scientific puzzle, a gap in our
knowledge in this case, why does this costly gene persist?
And instead of saying, well, the evolutionary dynamics are complex
and we're still figuring it out, you just say.
Speaker 1: It was aliens.
Speaker 2: It was aliens. You credit it to an external, supernatural
or extraterrestrial source. It's an easy answer to a hard question.
Speaker 1: And you see this on shows like Ancient Aliens.
Speaker 2: Right.
Speaker 1: They're masters of this, they are.
Speaker 2: They'll start with a perfectly accurate description of HGN or
the unique distribution of our age negative blood. They'll give
you real science.
Speaker 1: To build credibility, to build.
Speaker 2: Credibility, and then in the very next sentence they'll pivot
to an author who wrote a book about the Anonachi
seating a special bloodline on.
Speaker 1: Earth, and it creates this false equivalence as if a
geneticist from Harvard and a guy who thinks he talks
to Pleiadians are two equally valid sources of information on
the same topic.
Speaker 2: It's a very effective technique for blurring the line between
fact and fiction.
Speaker 1: And this gets tied up with the Nephlim myth too.
Speaker 2: All the time. The Nephilim are from the Book of Genesis,
the offspring of the sons of God, often interpreted as
fallen angels and human women.
Speaker 1: So the theory goes that RH negative blood is the
genetic echo of that union, the angelic bloodline.
Speaker 2: Right, But you know biblical scholars and theologians who actually
study these tech people, like doctor Michael Heiser, they just
laugh at this.
Speaker 1: I think his direct quote was that it's nonsense and silliness.
Speaker 2: It is the idea that a gene that causes reproductive
tragedy would be the secret marker of a superior hybrid race.
It just makes no sense textually or genetically.
Speaker 1: But the myth also comes with these claims of superiority.
Doesn't it that RH negative people are special?
Speaker 2: Oh yeah, you'll see lists of traits online. Higher IQs,
more empathetic, more sensitive to the environment, lower body temperature,
lower blood pressure. Sometimes even psychic abilities.
Speaker 1: It's a classic move. You take a group that's a
minority and you label them as special or elite. It's appealing,
it's very appealing.
Speaker 2: We all want to feel like we're part of something unique.
But the key scientific phrase here is far from universally accept.
Speaker 1: It, meaning there's no solid, repeatable evidence for any of
it exactly.
Speaker 2: So we had to set aside the wishful thinking and
the aliens and look at the actual data because the
real puzzle, the geographic distribution, is far more interesting.
Speaker 1: Okay, so this is where it gets good. If this
gene delution is so bad for reproduction, you'd expect evolution
to stamp it out right.
Speaker 2: You'd expect it to be super rare everywhere. Purifying selection
should have gotten rid of it over thousands of years.
Speaker 1: But that's not what we see.
Speaker 2: Not at all. The global picture is patchy, it's really uneven.
Speaker 1: Let's un through the numbers. What's the distribution like.
Speaker 2: Well, in some populations it's as rare as you'd expect.
For people of Asian descent, only about one percent are
our age negative.
Speaker 1: One percent, so very rare.
Speaker 2: Very the gene deletion frequency in Japanese and Chinese populations
is super low, like five to nine percent for the allele.
Speaker 1: What about people of African descent, It's a.
Speaker 2: Bit more common, but still low. Around eight percent are
our age negative.
Speaker 1: Okay, so one percent in Asians, eight percent in black people,
and then you get to Caucasians.
Speaker 2: And the number jumps about fifteen percent of people of
European descent are our age negative.
Speaker 1: Fifteen percent. That's a huge difference. That's way too high
for a trait with such a big downside.
Speaker 2: It's an anomaly that demands an explanation, and it suggests
something different happened in the evolutionary history of Europeans.
Speaker 1: But it gets even more extreme, doesn't it. There's one
group that blows everyone else out of the.
Speaker 2: Water, the Basque people.
Speaker 1: Right tell us about the Basques.
Speaker 2: The Basques are a truly unique population. They live in
the Pyrenees Mountains between France and Spain, and they are,
for all intents and purposes, an island, a genetic island,
and a linguistic one. Their language, Uskara is a total isolate.
It's not related to any other language on Earth. It's
thought to be a remnant of what was spoken in
Europe before the Indo Europeans arrive, so they've.
Speaker 1: Been genetically isolated for a very very long time. Mountains
are good barriers.
Speaker 2: And they have a strong cultural identity that has resisted
assimilation for centuries. They didn't even get fully romanized. The
result is a very distinct, ancient and relatively unmixed gene pool.
Speaker 1: And what does that gene pool say about RH and
negative blood?
Speaker 2: It screams. The frequency of the RH negative phenotype in
the Basque population is the highest in the world. Some
studies put it as high as twenty nine.
Speaker 1: Percent, almost a third of the population.
Speaker 2: And if you look at the frequency of the deletion
allele itself the actual gene one study found it was
at forty seven point two percent.
Speaker 1: Wait, almost half of the gene copies in the entire
Basque population are the deleted version.
Speaker 2: Almost half. It is a staggering number. It's double or
triple the average for the rest of Europe.
Speaker 1: So what's the scientific explanation for that? Not aliens?
Speaker 2: I'm guessing no, not aliens. This is the classic textbook
example of something called the founder effect and genetic drift.
Speaker 1: Okay, explain those.
Speaker 2: Imagine a small group of people breaks off and founds
a new isolated population just by random chance, that small
group of founders might have a higher than average frequency
of a rare trait like the RhD gene deletion.
Speaker 1: So the starting point is already skewed exactly.
Speaker 2: That's the founder effect. Then, because the population is small
and isolated, random chance, which we call genetic drift, continues
to play a huge role. The frequency of that trait
can drift up or down unpredictably from one generation to
the next.
Speaker 1: And in the Basques it just happened to drift way way.
Speaker 2: Up, way up, and once it's at that high frequency,
it tends to stick around, even with the negative pressure
from HDN. So for the Basques, the story is likely
one of ancient isolation and pure genetic chance.
Speaker 1: Okay, But the story doesn't end there, does it. There's
another twist with the reciss system, right, because.
Speaker 2: It's not just one gene. The main one we talk
about is RhD, the one that gets deleted, but right
next to it is another gene called RHC.
Speaker 1: And what does that one do?
Speaker 2: It also codes for antigens on your red blood cells,
the CC and E atigens. They can also cause HDN,
but it's usually much less severe than the d antigen.
Speaker 1: Reaction, so it's a related system. What's the twist.
Speaker 2: The twist is that when scientists analyze the rhcee gene,
they found something completely unexpected. They found strong evidence of
positive selection on one of its variants.
Speaker 1: Positive selection meaning evolution was actively favoring it.
Speaker 2: Actively pushing it to high frequency in non African populations,
specifically the coliele of the race gene.
Speaker 1: So it must have provided some kind of benefit. What
was the editors for this selection.
Speaker 2: They used the statistic called FST, which measures how different
populations are genetically. They found a huge FST value banned
zero point sixty four for this coliele between East Asians
and Africans. It's a massive statistical signal that something was
driving this allele to become common in the groups that
left Africa.
Speaker 1: So we have this bizarre situation. On the one hand,
a dangerous gene deletion RhD is hanging around, probably due
to random.
Speaker 2: Drift, and right next door, a related gene rhce has
a variant that it was so beneficial that evolution actively
selected for it.
Speaker 1: It's like two completely different stories happening on the same
page of the genome.
Speaker 2: And that's the mystery. The genetic signal for the cleele
is shouting that it was helpful, that it gave people
a survival advantage. But here's the kicker. What we have
no idea what that advantage was. The paper itself concludes
that the fitness benefits of the cecliel are currently unknown.
Speaker 1: So we know it was good for something, but we don't.
Speaker 2: Know what exactly. It just adds another layer of complexity
and shows how deep this evolutionary story really goes.
Speaker 1: Okay, so this brings us to the big scientific showdown,
the core evolutionary battle.
Speaker 2: Right. We have this profoundly dangerous gene deletion, the RhD gene.
We know it causes HDN. We know that fitness cost.
Speaker 1: Was huge, So why is it still here? Why is
the allele frequency as high as forty three percent in
European Americans? How did it survive?
Speaker 2: There are two main camps, two competing hypotheses, and we
need to really dig into both.
Speaker 1: Okay, Hypothesis A.
Speaker 2: Hypothesis A is basically the story are we told about
the Basques, but applied more broadly, it's genetic drift and
the founder effect.
Speaker 1: It was just chance argument.
Speaker 2: Essentially, Yeah, it's the null hypothesis. It doesn't require any
secret benefit. It just relies on population history and random luck.
Speaker 1: And is there evidence for this.
Speaker 2: There is a big study in twenty twelve by Perry
and his colleagues went looking for the molecular footprint of
recent positive selection on the RhD deletion in.
Speaker 1: Europeans and they didn't find it.
Speaker 2: They didn't find it, which suggests that evolution wasn't actively
trying to make this gene more common. So the argument goes,
the negative force from HDN must not have been strong
enough to overcome the power of genetic drift in those
small early European populations.
Speaker 1: But how could it not be strong enough? One in
fifty six berths seems incredibly strong.
Speaker 2: Well, this is where they brought in some really interesting
data from the Hutter Rights.
Speaker 1: Hotter Rights. Who are they?
Speaker 2: They are a religious community in North America, kind of
like the Amish. They're a founder of population. They've been
isolated for a long long time. They have big families,
and they have meticulous genealogical records going back generations.
Speaker 1: So they're a perfect natural experiment for looking at reproduction
before modern medicine.
Speaker 2: Exactly before. Rogam and the researchers looked at the Hutterighte
family records to see if the risk of HDN actually
reduced the total number of children of family had.
Speaker 1: And what did they find?
Speaker 2: Surprisingly, it didn't. When they compared the at risk families
our h negative mom our each positive dad to the
non risk families, there was no significant difference in the
total number of kids.
Speaker 1: How is that possible if babies were dying.
Speaker 2: Well a couple of ideas. First, infant mortality from other
causes was already high back then, so maybe the HDN
deaths just got lost in the noise, or maybe families
were compensating. If a child was lost to HDN, the
parents might just try to have another child sooner to
replace them. So the total family size at the end
of the day wasn't really affected.
Speaker 1: So the selective pressure was on the individual child, but
not on the family's total reproductive output.
Speaker 2: Right, which would weaken the evolutionary pressure against the gene itself.
The other key point is something called frequency dependence. Okay,
once the deletion becomes really common, like it is in
the basks near fifty percent, the select of pressure against
it actually gets weaker because the chance of a dangerous
pairing an RH negative mom with an RH positive baby
starts to go down relative to all the other possible pairings.
Speaker 1: So once it hits a certain tipping point, it's easier
for it to just stay there.
Speaker 2: And a little bit of genetic drift is enough to
maintain it. So that's hypothesis A. A dangerous gene gets
a foothold by chance in a small population, and the
forces trying to get rid of it just aren't strong
enough to finish the job.
Speaker 1: A story of chance and circumstance. But that's not the
only story, is it.
Speaker 2: No, And hypothesis B is to me much more tantalizing.
It suggests there was a hidden benefit.
Speaker 1: This is the balancing selection idea.
Speaker 2: Balancing selection driven by something called heterozygote advantage.
Speaker 1: Okay, what does that mean.
Speaker 2: It means that while being homozygous for the trait is bad,
in this case, being RH negative carries the risk of
HDN carrying just one copy of the gene, being a
heterozygote actually gives you some kind of survival advantage.
Speaker 1: The classic example of this is sickle cell anemia.
Speaker 2: Right, The perfect example. If you have two copies of
the sickle cell gene, you get the deadly disease, but
if you only have one copy, you don't get the disease,
and you get protection from malaria.
Speaker 1: So the gene sticks around because being in the middle,
the heterozygous state is the best place to be in
a malarial environment precisely.
Speaker 2: So the big question for RI if negative is what's
the equivalent of malaria? What ancient threat was so bad
that it was worth risking hed N to have protection
against it?
Speaker 1: And there's a prime suspect.
Speaker 2: A very strong suspect, A tiny parasite called toxoplasma gandhi.
Speaker 1: I've heard of this. It's the one you can get
from cats, right from cat.
Speaker 2: Feces, yeah, or undercooked meat. It's incredibly common. Maybe a
third of the world's population is infected, and it can
get into your brain and cause seria neurological issues.
Speaker 1: So the theory is that being a carrier of the
rh negative gene helps you fight off toxic plasma.
Speaker 2: That's the theory, and there's some good evidence for it.
One study actually look at this directly. It found that
Reese's positive heterozygodes the people with one normal RhD gene
and one deleted one were protected against some of the
cognitive damage caused by the parasite. Their reaction times didn't
slow down as much as other groups.
Speaker 1: So there were more resistant to the parasite's effects.
Speaker 2: Exactly, which suggests the bodies making a kind of evolutionary bargain.
It's accepting the risk of HTN in exchange for protection
against this widespread brain altering parasite.
Speaker 1: And the sweet spot is having one copy of the
deletion that.
Speaker 2: Seems to be where the major benefit lies.
Speaker 1: Okay, that's fascinating, but that's just one parasite. Is there
any bigger picture evidence for this balancing selection idea?
Speaker 2: There is, and it's a huge study. A researcher named
Jarislav Fleger published a paper in twenty sixteen where he
looked at data from sixty five different countries.
Speaker 1: What was he looking for.
Speaker 2: He was doing was called an ecological regression study. Yeah,
he was looking for correlations between the frequency of Reese's
genotypes in a country and that country's overall disease burden.
Speaker 1: Like mortality rates and things like that.
Speaker 2: Exactly. He was using a measure called daylies.
Speaker 1: Right disability adjusted life years. It's a measure of the
total impact of a disease, not just deaths, but also
years lived with the disability.
Speaker 2: Right, So he was asking a very big question, is
there a link between a country's RH negative frequency and
the overall health of its population?
Speaker 1: And what did he find?
Speaker 2: He found incredibly strong support for the heterozygote advantage hypothesis.
The single most powerful finding was that for any disease
where there was a significant correlation, the effect on RH
negative homozygotes and RH positive heterozygotes went in completely opposite directions.
Speaker 1: So if having two copies of the deletion was bad
for disease X, having one copy was good for disease
X per c cement.
Speaker 2: That is the statistical fingerprint of balancing selection and action
playing out on a global scale.
Speaker 1: Wow, did he find links to specific diseases.
Speaker 2: He did, and this is where the evolutionary trade off
becomes really clear. He found the countries with more RH
negative people had a lower burden from neuropsychiatric disorders.
Speaker 1: So a potential mental health.
Speaker 2: Benefit a potential benefit, yes, but it came at a
huge cost, which was those same countries had a significantly
higher burden from cardiovascular disease and especially from most types
of cancer.
Speaker 1: Ah wow, So what protected you in one area made
you more vulnerable in another.
Speaker 2: A classic evolutionary trade off. An advantage against ancient threats
like parasites or mental illness may have become a liability
in the modern world, where heart disease and cancer are
the big killers.
Speaker 1: Were the numbers significant, they were shocking.
Speaker 2: The data suggested that just a one percent increase in
the number of RH negative homozygotes in a population was
correlated with over eight eighteen hundred more deaths from cardiovascular
disease per one hundred thousand people.
Speaker 1: That's huge, it is.
Speaker 2: And at the same time, a one percent increase in
the heterozygodes was linked to over four hundred fewer deaths
from the same cause.
Speaker 1: So being a carrier is protective, but being fully RH
negative in the modern world appears to carry a serious
health risk beyond just pregnancy.
Speaker 2: That's what the data on a population level seems to suggest.
It paints this incredibly complex picture of a gene that's
caught between ancient pressures and modern diseases.
Speaker 1: Which just makes you wonder what on earth was the
ancient pressure. It must have been something truly terrible to
make this dangerous gene a good bet for survival.
Speaker 2: It must have been a monster, something worse than the
historical risk of HDN. Maybe it was toxoplasma, maybe it
was something else we haven't even identified yet, or maybe
it's tied into that unknown benefit of the rhceec allele.
The puzzle isn't fully solved.
Speaker 1: Okay, let's try to pull all these threads together. This
has been a wild ride, it really has. We start
with a pretty sensational claim rh negative blood as proof
of an alien or nephilim bloodline, and we.
Speaker 2: Ended up deep in the weeds of chromosome one p.
Thirty six point one one talking about gene deletions, population drift,
and global disease.
Speaker 1: Statistics, and the science seems absolutely clear.
Speaker 2: On one thing that it's not aliens.
Speaker 1: It's not aliens, it's not a marker of superiority. It's
a profound, ancient structural error in our DNA, the deletion
of the entire RhD gene.
Speaker 2: An error that created one of the most classic and
enduring puzzles in human.
Speaker 1: Evolution, the puzzle being how does a trait that kills
your offspring manage to stick around at such high frequencies,
especially in places like the Basque Country.
Speaker 2: And we have two powerful competing scientific stories.
Speaker 1: Story one is that it was all just a series
of historical accidents. Genetic drift and the founder effect in
early European populations pushed the frequency up and the selective
pressure from HDN just wasn't quite so strong enough to
push it back down.
Speaker 2: The Hutterright data supports that idea. It's the chance and
circumstance model.
Speaker 1: But Storry too, the balancing selection model is that it's
not an accident at all.
Speaker 2: It's a trade off. It suggests there's a powerful hidden
advantage to being a carrier of this deletion.
Speaker 1: An advantage that gives you resistance to ancient parasites like
toxic plasma.
Speaker 2: Gandhi, and that this advantage was so important for survival
that it outweighed the terrible reproductive cost of HDN and
even the modern risks of heart disease and cancer.
Speaker 1: And just when you think you have a handle on it,
you remember there's that other weird signal, the positive selection
on the related rhgec allele, whose benefit is still totally unknown.
Speaker 2: It just shows that the real story, the scientific story,
is so much richer and more complex and frankly more
thrilling than any simple alien conspiracy theory.
Speaker 1: It really is. So we'll leave you with this final
thought to ponder. Given the evidence, especially from that huge
global study, that being a carrier a heterozygote seems to
be protective against major diseases.
Speaker 2: While being fully rh negative carries these significant risks.
Speaker 1: What kind of invisible ancient threat? What pathogen or environmental
pressure do you think was so powerful, so deadly that
it made keeping this dangerous gene deletion around a winning
evolutionary strategy for thousands of years. Something had to be
worse than HDN. What do you think it was? Let
us know what you think