1
00:00:00,160 --> 00:00:03,160
Speaker 1: Welcome to Thrilling Threads. This is the show where we

2
00:00:03,200 --> 00:00:06,440
take those wild claims you see online, those confusing threads

3
00:00:06,440 --> 00:00:08,199
of information, and we just.

4
00:00:08,199 --> 00:00:10,679
Speaker 2: Keep pulling and we pull on them until we find

5
00:00:11,160 --> 00:00:14,960
the real and usually far more fascinating truth that's tangled

6
00:00:15,000 --> 00:00:15,679
up inside.

7
00:00:15,720 --> 00:00:18,839
Speaker 1: And today we are diving into something that is literally

8
00:00:18,960 --> 00:00:23,039
inside all of us. Our blood, specifically the reesis factor.

9
00:00:23,359 --> 00:00:26,039
You know, whether you're A positive or O negative.

10
00:00:26,640 --> 00:00:30,440
Speaker 2: It's just a tiny genetic difference, but it has somehow

11
00:00:30,480 --> 00:00:33,840
become the seed for some of the most out there

12
00:00:34,280 --> 00:00:36,079
theories I have ever come across.

13
00:00:36,119 --> 00:00:37,960
Speaker 1: Oh absolutely, And if you're listening to this and you

14
00:00:38,000 --> 00:00:40,039
happen to be RH negative, you've probably heard them.

15
00:00:40,159 --> 00:00:41,119
Speaker 2: You've definitely seen them.

16
00:00:41,159 --> 00:00:43,759
Speaker 1: They are everywhere. The big question, the one you've all

17
00:00:43,759 --> 00:00:47,159
sent us, is this, does having RH negative blood mean

18
00:00:47,159 --> 00:00:48,960
you're not entirely human?

19
00:00:49,359 --> 00:00:52,280
Speaker 2: I mean, does it mean you're descended from aliens or

20
00:00:52,520 --> 00:00:54,880
maybe from the Nephlum, those giants from the Bible.

21
00:00:55,039 --> 00:00:59,439
Speaker 1: Some sources even claim reptilian ancestors that you have this

22
00:01:00,000 --> 00:01:02,079
special bloodline that sets you apart.

23
00:01:02,359 --> 00:01:05,640
Speaker 2: It's this idea that RH negative blood is a kind

24
00:01:05,680 --> 00:01:09,920
of genetic marker, an anomaly that proves non human entities

25
00:01:10,159 --> 00:01:13,239
meddled with our DNA at some point in the distant past.

26
00:01:13,640 --> 00:01:16,200
Speaker 1: And that's our mission for this deep dive. We're taking

27
00:01:16,239 --> 00:01:19,680
all of your sources, from the ancient astronaut guys and

28
00:01:19,719 --> 00:01:23,799
the biblical myths all the way to the really dense,

29
00:01:23,879 --> 00:01:25,799
cutting edge genetics research.

30
00:01:25,560 --> 00:01:28,000
Speaker 2: And we're going to conduct a really thorough analysis to

31
00:01:28,079 --> 00:01:30,439
figure out the actual evolutionary puzzle here.

32
00:01:30,519 --> 00:01:34,439
Speaker 1: So first we'll establish the basic biology, no aliens involved,

33
00:01:34,560 --> 00:01:36,319
just the science of the reesis factor.

34
00:01:36,439 --> 00:01:40,000
Speaker 2: Then we're going to directly address and will dismantle those

35
00:01:40,159 --> 00:01:41,680
alien of the gaps arguments.

36
00:01:41,840 --> 00:01:44,200
Speaker 1: After that we get to the really good stuff, the

37
00:01:44,280 --> 00:01:47,719
hard data, the global distribution is genuinely weird and tells

38
00:01:47,719 --> 00:01:48,680
the story of its own.

39
00:01:48,799 --> 00:01:51,400
Speaker 2: And finally we'll get into the real scientific debate, the

40
00:01:52,200 --> 00:01:55,640
intense evolutionary battle between random chance and some kind of

41
00:01:55,719 --> 00:01:59,040
hidden advantage that might explain why this trait even still exists.

42
00:01:59,159 --> 00:02:01,480
Speaker 1: Yeah, and we're drawing from a lot of great sources

43
00:02:01,560 --> 00:02:05,280
medical reviews, specific genetics papers, from researchers like Perry and Flagger,

44
00:02:05,359 --> 00:02:06,879
population data, and of.

45
00:02:06,840 --> 00:02:10,400
Speaker 2: Course the fringe sources themselves. We have to understand what

46
00:02:10,439 --> 00:02:14,520
they're claiming to see why it's so compelling. So, yeah,

47
00:02:15,199 --> 00:02:15,919
let's get into it.

48
00:02:16,039 --> 00:02:18,520
Speaker 1: Let's do it. Where do we even start, I guess

49
00:02:18,560 --> 00:02:19,759
with the discovery itself.

50
00:02:19,879 --> 00:02:22,039
Speaker 2: Yeah, let's start at the beginning. You have to remember,

51
00:02:22,800 --> 00:02:25,280
for a long time, we didn't understand our own blood.

52
00:02:25,560 --> 00:02:27,639
It was just this red fluid.

53
00:02:27,840 --> 00:02:30,960
Speaker 1: Right, and then Karl L. Einsteiner comes along in nineteen

54
00:02:31,039 --> 00:02:34,439
hundred and discovers the Abo blood girks.

55
00:02:34,319 --> 00:02:39,080
Speaker 2: A massive Nobel winning breakthrough. But even after that, blood

56
00:02:39,080 --> 00:02:41,280
transfusions were still a bit of a gamble.

57
00:02:41,400 --> 00:02:43,960
Speaker 1: Sometimes they work, sometimes they didn't, and people got very

58
00:02:44,039 --> 00:02:45,319
sick or died exactly.

59
00:02:45,400 --> 00:02:47,879
Speaker 2: Doctors knew something else was going on. There was another

60
00:02:47,919 --> 00:02:48,960
factor they were missing.

61
00:02:49,080 --> 00:02:50,479
Speaker 1: So Lansteiner went back to the.

62
00:02:50,520 --> 00:02:53,759
Speaker 2: Lab he did. He and a colleague, Alexander Wiener. They

63
00:02:53,800 --> 00:02:57,120
were working on this problem through the late nineteen thirties.

64
00:02:56,759 --> 00:02:59,560
Speaker 1: And it wasn't until nineteen forty that they finally nailed

65
00:02:59,560 --> 00:02:59,919
it down.

66
00:03:00,240 --> 00:03:03,080
Speaker 2: Right. They were at Rockefeller University and they were looking

67
00:03:03,159 --> 00:03:07,360
specifically at these strange immune reactions, especially in pregnant women

68
00:03:07,719 --> 00:03:09,759
or in people who'd had multiple transfusions.

69
00:03:09,759 --> 00:03:11,560
Speaker 1: Okay, and this is where the monkeys come in, right.

70
00:03:11,639 --> 00:03:14,919
Speaker 2: The name the Reesis macaque. Yeah, it's actually a pretty

71
00:03:14,919 --> 00:03:18,759
simple story. They injected blood from the macaques into rabbits

72
00:03:18,800 --> 00:03:19,800
and guinea pigs.

73
00:03:19,680 --> 00:03:21,319
Speaker 1: And that created antibodies.

74
00:03:21,319 --> 00:03:23,960
Speaker 2: They created an anti serum. So then they took that

75
00:03:24,039 --> 00:03:26,800
anti serum and mixed it with human blood samples, and

76
00:03:26,840 --> 00:03:29,479
what happened. They found that about eighty five percent of

77
00:03:29,479 --> 00:03:32,879
the human blood samples clumped up. They reacted, So.

78
00:03:32,759 --> 00:03:35,960
Speaker 1: They called it the Reesis factor or rh factor after

79
00:03:36,000 --> 00:03:36,840
the monkeys.

80
00:03:36,840 --> 00:03:40,000
Speaker 2: Simple as that, if you're blood clumped, you were RH positive.

81
00:03:40,400 --> 00:03:42,080
If it didn't, you were RH negative.

82
00:03:42,439 --> 00:03:46,240
Speaker 1: And just like that, the four known blood types instantly

83
00:03:46,240 --> 00:03:47,639
became eight, a.

84
00:03:47,719 --> 00:03:52,360
Speaker 2: Huge leap forward for medicine. Fundamentally, your blood type ABO

85
00:03:52,599 --> 00:03:55,080
whatever is about antigens.

86
00:03:54,520 --> 00:03:56,800
Speaker 1: These are just substances on the surface of your red

87
00:03:56,800 --> 00:03:58,280
blood cells, little.

88
00:03:58,000 --> 00:04:02,159
Speaker 2: Flags exactly, little flags made of proteins or carbohydrates. For

89
00:04:02,240 --> 00:04:05,599
the Rees's system, we are mostly talking about one specific flag,

90
00:04:06,240 --> 00:04:07,039
the d antigen.

91
00:04:07,280 --> 00:04:09,639
Speaker 1: So if you're RH positive, you have the d antigen

92
00:04:09,719 --> 00:04:11,800
flag waving on your red blood cells, and if you're.

93
00:04:11,759 --> 00:04:13,840
Speaker 2: R negative you don't. The flagpole is bare.

94
00:04:14,120 --> 00:04:17,839
Speaker 1: Okay, that seems straightforward enough, But the genetics behind why

95
00:04:17,879 --> 00:04:21,600
the flagpole is bare. That's where things get really weird.

96
00:04:21,759 --> 00:04:25,639
Speaker 2: That is where the entire evolutionary mystery begins. Because being

97
00:04:25,759 --> 00:04:29,519
D negative or RH negative isn't from a small mutation.

98
00:04:29,959 --> 00:04:31,720
It's not a typo in the genetic code.

99
00:04:31,800 --> 00:04:32,199
Speaker 1: What is it?

100
00:04:32,240 --> 00:04:35,680
Speaker 2: Then? It's caused by a massive, all or nothing genetic event.

101
00:04:36,319 --> 00:04:40,639
It's the homozygous deletion of the entire RhD gene.

102
00:04:40,680 --> 00:04:44,399
Speaker 1: Okay, whoa, let's break that down. Homozygous deletion. What does

103
00:04:44,439 --> 00:04:46,199
that mean for a person's DNA.

104
00:04:46,519 --> 00:04:48,959
Speaker 2: It means the entire instruction manual for how to build

105
00:04:48,959 --> 00:04:52,000
that d antigen flag. It's been completely ripped out of

106
00:04:52,040 --> 00:04:52,839
your genetic.

107
00:04:52,560 --> 00:04:55,040
Speaker 1: Book, not just smudged or misspelled.

108
00:04:54,560 --> 00:04:58,079
Speaker 2: Gon and homozygous means you inherited that missing page from

109
00:04:58,120 --> 00:05:00,240
both of your parents. You got a book with the

110
00:05:00,279 --> 00:05:02,439
page missing from your mom and another one with the

111
00:05:02,439 --> 00:05:03,800
same page missing from your dad.

112
00:05:03,879 --> 00:05:06,319
Speaker 1: So to be RH positive, you just need one good

113
00:05:06,399 --> 00:05:07,319
copy of that page.

114
00:05:07,399 --> 00:05:09,160
Speaker 2: One good copy is all it takes. But to be

115
00:05:09,319 --> 00:05:12,279
RH negative you need to have zero copies. The gene

116
00:05:12,279 --> 00:05:15,000
has to be completely absent from both of your chromosomes.

117
00:05:15,319 --> 00:05:19,000
Speaker 1: That's kind of shocking that a huge deletion like that

118
00:05:19,120 --> 00:05:21,160
is so common in some parts of the world. How

119
00:05:21,199 --> 00:05:23,959
does a whole gene just disappear?

120
00:05:24,120 --> 00:05:26,199
Speaker 2: Well, the how is actually one of the most fascinating

121
00:05:26,240 --> 00:05:29,720
parts of the story. Researchers like Wagner and Fleegel figure

122
00:05:29,759 --> 00:05:33,360
this out. The RhD gene sits on the chromosome, but

123
00:05:33,399 --> 00:05:36,120
it's sandwiched between two other little segments of DNA.

124
00:05:36,519 --> 00:05:37,040
Speaker 1: What are they?

125
00:05:37,160 --> 00:05:40,759
Speaker 2: They're called recis boxes. And the crucial detail is that

126
00:05:40,800 --> 00:05:44,279
these two boxes are almost identical to each other. They

127
00:05:44,319 --> 00:05:47,399
have about ninety nine percent sequence similarity.

128
00:05:47,560 --> 00:05:50,279
Speaker 1: So it's like having the same complex paragraph at the

129
00:05:50,319 --> 00:05:52,839
start of chapter five and at the end of chapter five.

130
00:05:52,920 --> 00:05:55,759
Speaker 2: That's a perfect analogy. And so when your cells are

131
00:05:55,800 --> 00:05:58,959
copying or repairing your DNA, a process that happens all

132
00:05:59,000 --> 00:06:02,160
the time, the machinery can get confused. How So it

133
00:06:02,199 --> 00:06:06,199
sees the first racist box, the identical paragraph, and starts reading,

134
00:06:06,720 --> 00:06:09,759
but then it accidentally skips over the entire RhD gene

135
00:06:09,759 --> 00:06:12,240
in the middle and jumps straight to the second racist

136
00:06:12,279 --> 00:06:13,800
box because it looks the same, and.

137
00:06:13,759 --> 00:06:15,439
Speaker 1: It snips out everything in between.

138
00:06:15,720 --> 00:06:18,839
Speaker 2: It snips out everything in between, thinking it's just getting

139
00:06:18,920 --> 00:06:21,720
rid of a duplicated bit of code. It's a type

140
00:06:21,720 --> 00:06:24,759
of error called non allelic homologous recombination.

141
00:06:25,120 --> 00:06:28,680
Speaker 1: So the gene disappears because of a structural vulnerability in

142
00:06:28,720 --> 00:06:32,399
our own DNA. It's an accident waiting to happen.

143
00:06:32,240 --> 00:06:36,120
Speaker 2: A catastrophic copy paste error basically, and that one error

144
00:06:36,319 --> 00:06:38,360
is the source of everything we're talking about today, the

145
00:06:38,399 --> 00:06:42,439
medical problems, the pregnancy risks, and all the alien theories.

146
00:06:42,480 --> 00:06:45,199
Speaker 1: It's a molecular smoking gun. It wasn't a gradual change.

147
00:06:45,199 --> 00:06:48,040
It was a sudden, huge dilution that happened and has

148
00:06:48,199 --> 00:06:49,360
just stuck around ever.

149
00:06:49,279 --> 00:06:53,279
Speaker 2: Since, and that region of the genome is just it's unstable.

150
00:06:53,360 --> 00:06:57,600
The same error that causes deletions can also cause duplications.

151
00:06:57,920 --> 00:06:58,360
Speaker 1: What do you mean.

152
00:06:58,519 --> 00:07:01,279
Speaker 2: Well, the hat map project, which was this huge effort

153
00:07:01,319 --> 00:07:04,560
to map human genetic diversity, found some people, one from

154
00:07:04,560 --> 00:07:07,360
West Africa and one from Japan who actually had three

155
00:07:07,439 --> 00:07:08,959
copies of the RhD gen.

156
00:07:08,920 --> 00:07:11,680
Speaker 1: Three, so they're like super rh positive in a way.

157
00:07:11,759 --> 00:07:14,759
Speaker 2: Yeah, it doesn't really cause any major clinical problem for them.

158
00:07:15,040 --> 00:07:19,079
They're just strongly rh positive, but it shows that this

159
00:07:19,199 --> 00:07:22,720
specific spot on the chromosome is a hot spot for

160
00:07:22,800 --> 00:07:26,680
these massive structural changes. It can delete it can duplicate

161
00:07:26,839 --> 00:07:28,800
just a very active area.

162
00:07:28,560 --> 00:07:31,959
Speaker 1: A genetic roller coaster. Okay, so that's the how, But

163
00:07:32,000 --> 00:07:34,920
the why it matters comes down to the clinical side

164
00:07:34,959 --> 00:07:38,199
of things. This is the part that fuels the fringe theories, right,

165
00:07:38,319 --> 00:07:40,480
the rejection phenomenon exactly.

166
00:07:40,519 --> 00:07:43,800
Speaker 2: We're talking about hemolytic disease in the newborn HDN. This

167
00:07:43,879 --> 00:07:46,680
is the life or death consequence of that gene deletion.

168
00:07:46,879 --> 00:07:47,800
Speaker 1: Explain how it works.

169
00:07:48,120 --> 00:07:51,160
Speaker 2: It happens when an RH negative mother is pregnant with

170
00:07:51,199 --> 00:07:51,879
an RH.

171
00:07:51,680 --> 00:07:55,040
Speaker 1: Positive child, which would happen if the father is RH positive.

172
00:07:55,199 --> 00:07:57,720
Speaker 2: Right. The mother's body doesn't have the de antigen, so

173
00:07:57,800 --> 00:08:00,680
her immune system has never seen it before. To her body,

174
00:08:00,879 --> 00:08:03,720
it's a foreign invader, like a virus or bacteria.

175
00:08:03,879 --> 00:08:07,439
Speaker 1: But the mother's and baby's blood systems are separate, aren't there.

176
00:08:07,519 --> 00:08:10,639
Speaker 2: They are for most of the pregnancy, but during childbirth,

177
00:08:10,839 --> 00:08:14,360
especially with the first RH positive baby, a small amount

178
00:08:14,360 --> 00:08:16,560
of the baby's blood can leak into the mother's.

179
00:08:16,240 --> 00:08:19,920
Speaker 1: Bloodstream and her body sees the d antigen on those

180
00:08:19,920 --> 00:08:21,000
baby blood cells for the.

181
00:08:21,000 --> 00:08:23,480
Speaker 2: First time, and it freaks out. It mounts a massive

182
00:08:23,480 --> 00:08:27,639
immune response, creating armies of antid antibodies designed to find

183
00:08:27,720 --> 00:08:29,839
and destroy that foreign d antigen.

184
00:08:29,959 --> 00:08:31,639
Speaker 1: So the first baby is usually okay.

185
00:08:31,759 --> 00:08:34,600
Speaker 2: The first baby is usually fine because the exposure happens

186
00:08:34,639 --> 00:08:37,559
right at the end. But now the mother is sensitized.

187
00:08:37,840 --> 00:08:39,200
She has those antibodies for.

188
00:08:39,240 --> 00:08:40,720
Speaker 1: Life and for the next pregnancy.

189
00:08:40,919 --> 00:08:44,440
Speaker 2: If the next baby is also our age positive. Those

190
00:08:44,480 --> 00:08:47,759
maternal antibodies are small enough to cross the placenta. They

191
00:08:47,879 --> 00:08:50,039
enter the baby's circulation and do what they were designed

192
00:08:50,080 --> 00:08:50,279
to do.

193
00:08:50,320 --> 00:08:52,120
Speaker 1: They attack the baby's red blood.

194
00:08:51,799 --> 00:08:57,759
Speaker 2: Cells viciously, causing severe anemia, jaundice, brain damage, and very

195
00:08:57,759 --> 00:08:58,879
often death.

196
00:08:59,120 --> 00:09:02,279
Speaker 1: I saw statistic from before modern medicine intervened, around the

197
00:09:02,360 --> 00:09:03,120
nineteen forties.

198
00:09:03,200 --> 00:09:04,240
Speaker 2: I think I know the one you mean.

199
00:09:04,480 --> 00:09:07,399
Speaker 1: It said mortality from HDN was one in every fifty

200
00:09:07,440 --> 00:09:11,639
six berths to D negative women in European American populations.

201
00:09:11,720 --> 00:09:15,879
Speaker 2: It's a staggering number. That is a massive, massive evolutionary penalty,

202
00:09:16,320 --> 00:09:17,840
a huge selective pressure.

203
00:09:18,159 --> 00:09:21,039
Speaker 1: It means that for thousands of years, before the road

204
00:09:21,120 --> 00:09:24,200
jam shot was invented in nineteen sixty eight, being an

205
00:09:24,279 --> 00:09:28,360
RH negative woman carried a significant risk of losing your children, a.

206
00:09:28,440 --> 00:09:31,960
Speaker 2: Huge reduction in what we call reproductive fitness. And that's

207
00:09:32,000 --> 00:09:32,840
the central.

208
00:09:32,480 --> 00:09:35,279
Speaker 1: Paradox How could a trait that is so dangerous for

209
00:09:35,360 --> 00:09:38,919
reproduction survive and even thrive in certain populations.

210
00:09:38,960 --> 00:09:42,919
Speaker 2: It's the multimillion dollar question. And that paradox, that gap

211
00:09:42,960 --> 00:09:46,360
in our easy understanding is the perfect breeding ground for

212
00:09:46,440 --> 00:09:47,440
other explanations.

213
00:09:47,600 --> 00:09:50,279
Speaker 1: The fringe theories. Okay, let's go there, let's tackle them

214
00:09:50,279 --> 00:09:53,799
heat on the core question from the sources, does RH

215
00:09:53,879 --> 00:09:57,240
negative blood come from reptiles from gods?

216
00:09:57,360 --> 00:09:59,759
Speaker 2: The scientific consensus is, and I want to be really

217
00:09:59,759 --> 00:10:03,759
clear about this, a hard no zero evidence zero, as

218
00:10:03,840 --> 00:10:06,159
outlets like the tech Interactive put it, there is just

219
00:10:06,320 --> 00:10:09,200
no evidence to support any of this. It's an ordinary

220
00:10:09,240 --> 00:10:11,759
trait that comes from simple biology. It's a gene deletion,

221
00:10:12,159 --> 00:10:12,600
that's it.

222
00:10:12,639 --> 00:10:15,399
Speaker 1: But the reason it's so compelling, the psychological hook is

223
00:10:15,440 --> 00:10:16,879
the biology we just talked about.

224
00:10:16,919 --> 00:10:19,960
Speaker 2: Absolutely, the idea of a mother's body attacking its own baby,

225
00:10:20,480 --> 00:10:22,639
it just feels wrong, It feels unnatural.

226
00:10:22,440 --> 00:10:25,519
Speaker 1: It feels like rejection. As if, and this is the

227
00:10:25,559 --> 00:10:28,759
key phrase, the mother and child are from different species.

228
00:10:28,960 --> 00:10:32,080
Speaker 2: That's the emotional leap. If her body thinks the baby

229
00:10:32,159 --> 00:10:35,600
is a foreign invader, maybe it's because the baby is foreign,

230
00:10:36,120 --> 00:10:40,000
Maybe it has some non human DNA from the father's side.

231
00:10:39,840 --> 00:10:42,919
Speaker 1: And poof, you have an opening for an extraordinary claim.

232
00:10:43,120 --> 00:10:45,679
Speaker 2: You have a vacuum, and the fringe theories rush in

233
00:10:45,720 --> 00:10:48,519
to fill it. It's a rhetorical trick we call the

234
00:10:48,519 --> 00:10:49,960
Aliens of the Gaps argument.

235
00:10:50,080 --> 00:10:51,840
Speaker 1: It's like the old God of the Gaps, but for

236
00:10:51,960 --> 00:10:53,279
eupology exactly.

237
00:10:53,440 --> 00:10:56,360
Speaker 2: You find a genuine scientific puzzle, a gap in our

238
00:10:56,399 --> 00:10:59,799
knowledge in this case, why does this costly gene persist?

239
00:11:00,039 --> 00:11:03,159
And instead of saying, well, the evolutionary dynamics are complex

240
00:11:03,200 --> 00:11:05,799
and we're still figuring it out, you just say.

241
00:11:05,720 --> 00:11:06,559
Speaker 1: It was aliens.

242
00:11:06,639 --> 00:11:11,120
Speaker 2: It was aliens. You credit it to an external, supernatural

243
00:11:11,200 --> 00:11:15,039
or extraterrestrial source. It's an easy answer to a hard question.

244
00:11:15,200 --> 00:11:17,519
Speaker 1: And you see this on shows like Ancient Aliens.

245
00:11:17,600 --> 00:11:17,759
Speaker 2: Right.

246
00:11:17,840 --> 00:11:19,480
Speaker 1: They're masters of this, they are.

247
00:11:19,559 --> 00:11:22,639
Speaker 2: They'll start with a perfectly accurate description of HGN or

248
00:11:22,639 --> 00:11:25,279
the unique distribution of our age negative blood. They'll give

249
00:11:25,320 --> 00:11:26,440
you real science.

250
00:11:26,120 --> 00:11:27,679
Speaker 1: To build credibility, to build.

251
00:11:27,399 --> 00:11:31,440
Speaker 2: Credibility, and then in the very next sentence they'll pivot

252
00:11:31,600 --> 00:11:34,360
to an author who wrote a book about the Anonachi

253
00:11:34,480 --> 00:11:36,519
seating a special bloodline on.

254
00:11:36,440 --> 00:11:39,840
Speaker 1: Earth, and it creates this false equivalence as if a

255
00:11:39,919 --> 00:11:42,639
geneticist from Harvard and a guy who thinks he talks

256
00:11:42,639 --> 00:11:46,200
to Pleiadians are two equally valid sources of information on

257
00:11:46,240 --> 00:11:46,919
the same topic.

258
00:11:47,080 --> 00:11:50,200
Speaker 2: It's a very effective technique for blurring the line between

259
00:11:50,240 --> 00:11:50,960
fact and fiction.

260
00:11:51,279 --> 00:11:53,440
Speaker 1: And this gets tied up with the Nephlim myth too.

261
00:11:53,519 --> 00:11:56,440
Speaker 2: All the time. The Nephilim are from the Book of Genesis,

262
00:11:56,480 --> 00:11:59,600
the offspring of the sons of God, often interpreted as

263
00:12:00,120 --> 00:12:02,039
fallen angels and human women.

264
00:12:02,519 --> 00:12:04,919
Speaker 1: So the theory goes that RH negative blood is the

265
00:12:04,960 --> 00:12:08,159
genetic echo of that union, the angelic bloodline.

266
00:12:08,240 --> 00:12:11,519
Speaker 2: Right, But you know biblical scholars and theologians who actually

267
00:12:11,559 --> 00:12:14,000
study these tech people, like doctor Michael Heiser, they just

268
00:12:14,080 --> 00:12:14,600
laugh at this.

269
00:12:14,799 --> 00:12:18,320
Speaker 1: I think his direct quote was that it's nonsense and silliness.

270
00:12:18,600 --> 00:12:21,960
Speaker 2: It is the idea that a gene that causes reproductive

271
00:12:21,960 --> 00:12:25,720
tragedy would be the secret marker of a superior hybrid race.

272
00:12:26,240 --> 00:12:28,759
It just makes no sense textually or genetically.

273
00:12:29,000 --> 00:12:31,960
Speaker 1: But the myth also comes with these claims of superiority.

274
00:12:32,000 --> 00:12:34,639
Doesn't it that RH negative people are special?

275
00:12:34,720 --> 00:12:38,399
Speaker 2: Oh yeah, you'll see lists of traits online. Higher IQs,

276
00:12:38,679 --> 00:12:42,600
more empathetic, more sensitive to the environment, lower body temperature,

277
00:12:42,679 --> 00:12:46,279
lower blood pressure. Sometimes even psychic abilities.

278
00:12:46,360 --> 00:12:48,559
Speaker 1: It's a classic move. You take a group that's a

279
00:12:48,559 --> 00:12:52,960
minority and you label them as special or elite. It's appealing,

280
00:12:53,080 --> 00:12:53,919
it's very appealing.

281
00:12:54,080 --> 00:12:56,480
Speaker 2: We all want to feel like we're part of something unique.

282
00:12:56,720 --> 00:13:00,679
But the key scientific phrase here is far from universally accept.

283
00:13:00,320 --> 00:13:03,919
Speaker 1: It, meaning there's no solid, repeatable evidence for any of

284
00:13:03,960 --> 00:13:04,879
it exactly.

285
00:13:05,559 --> 00:13:08,000
Speaker 2: So we had to set aside the wishful thinking and

286
00:13:08,039 --> 00:13:11,039
the aliens and look at the actual data because the

287
00:13:11,080 --> 00:13:15,440
real puzzle, the geographic distribution, is far more interesting.

288
00:13:15,480 --> 00:13:17,279
Speaker 1: Okay, so this is where it gets good. If this

289
00:13:17,360 --> 00:13:21,120
gene delution is so bad for reproduction, you'd expect evolution

290
00:13:21,240 --> 00:13:22,159
to stamp it out right.

291
00:13:22,240 --> 00:13:25,639
Speaker 2: You'd expect it to be super rare everywhere. Purifying selection

292
00:13:25,679 --> 00:13:27,720
should have gotten rid of it over thousands of years.

293
00:13:27,799 --> 00:13:29,480
Speaker 1: But that's not what we see.

294
00:13:29,279 --> 00:13:33,200
Speaker 2: Not at all. The global picture is patchy, it's really uneven.

295
00:13:33,440 --> 00:13:35,759
Speaker 1: Let's un through the numbers. What's the distribution like.

296
00:13:36,159 --> 00:13:38,759
Speaker 2: Well, in some populations it's as rare as you'd expect.

297
00:13:39,240 --> 00:13:42,399
For people of Asian descent, only about one percent are

298
00:13:42,559 --> 00:13:43,799
our age negative.

299
00:13:43,519 --> 00:13:45,360
Speaker 1: One percent, so very rare.

300
00:13:45,720 --> 00:13:49,200
Speaker 2: Very the gene deletion frequency in Japanese and Chinese populations

301
00:13:49,279 --> 00:13:52,639
is super low, like five to nine percent for the allele.

302
00:13:52,919 --> 00:13:55,639
Speaker 1: What about people of African descent, It's a.

303
00:13:55,559 --> 00:13:58,960
Speaker 2: Bit more common, but still low. Around eight percent are

304
00:13:59,039 --> 00:13:59,840
our age negative.

305
00:14:00,120 --> 00:14:03,399
Speaker 1: Okay, so one percent in Asians, eight percent in black people,

306
00:14:04,080 --> 00:14:06,240
and then you get to Caucasians.

307
00:14:05,600 --> 00:14:08,960
Speaker 2: And the number jumps about fifteen percent of people of

308
00:14:09,000 --> 00:14:11,039
European descent are our age negative.

309
00:14:11,159 --> 00:14:14,559
Speaker 1: Fifteen percent. That's a huge difference. That's way too high

310
00:14:14,639 --> 00:14:16,639
for a trait with such a big downside.

311
00:14:16,679 --> 00:14:20,399
Speaker 2: It's an anomaly that demands an explanation, and it suggests

312
00:14:20,440 --> 00:14:23,080
something different happened in the evolutionary history of Europeans.

313
00:14:23,120 --> 00:14:25,399
Speaker 1: But it gets even more extreme, doesn't it. There's one

314
00:14:25,440 --> 00:14:27,440
group that blows everyone else out of the.

315
00:14:27,399 --> 00:14:28,840
Speaker 2: Water, the Basque people.

316
00:14:29,080 --> 00:14:30,559
Speaker 1: Right tell us about the Basques.

317
00:14:30,919 --> 00:14:34,120
Speaker 2: The Basques are a truly unique population. They live in

318
00:14:34,159 --> 00:14:37,639
the Pyrenees Mountains between France and Spain, and they are,

319
00:14:37,960 --> 00:14:41,120
for all intents and purposes, an island, a genetic island,

320
00:14:41,279 --> 00:14:45,399
and a linguistic one. Their language, Uskara is a total isolate.

321
00:14:45,879 --> 00:14:48,679
It's not related to any other language on Earth. It's

322
00:14:48,799 --> 00:14:50,639
thought to be a remnant of what was spoken in

323
00:14:50,679 --> 00:14:53,639
Europe before the Indo Europeans arrive, so they've.

324
00:14:53,440 --> 00:14:56,840
Speaker 1: Been genetically isolated for a very very long time. Mountains

325
00:14:56,840 --> 00:14:58,279
are good barriers.

326
00:14:58,039 --> 00:15:00,840
Speaker 2: And they have a strong cultural identity that has resisted

327
00:15:00,879 --> 00:15:05,360
assimilation for centuries. They didn't even get fully romanized. The

328
00:15:05,480 --> 00:15:10,559
result is a very distinct, ancient and relatively unmixed gene pool.

329
00:15:10,759 --> 00:15:12,840
Speaker 1: And what does that gene pool say about RH and

330
00:15:12,960 --> 00:15:13,679
negative blood?

331
00:15:13,840 --> 00:15:17,159
Speaker 2: It screams. The frequency of the RH negative phenotype in

332
00:15:17,200 --> 00:15:19,720
the Basque population is the highest in the world. Some

333
00:15:19,759 --> 00:15:21,519
studies put it as high as twenty nine.

334
00:15:21,399 --> 00:15:23,200
Speaker 1: Percent, almost a third of the population.

335
00:15:23,320 --> 00:15:24,879
Speaker 2: And if you look at the frequency of the deletion

336
00:15:24,919 --> 00:15:27,720
allele itself the actual gene one study found it was

337
00:15:27,720 --> 00:15:29,279
at forty seven point two percent.

338
00:15:29,440 --> 00:15:32,320
Speaker 1: Wait, almost half of the gene copies in the entire

339
00:15:32,480 --> 00:15:34,679
Basque population are the deleted version.

340
00:15:35,000 --> 00:15:38,759
Speaker 2: Almost half. It is a staggering number. It's double or

341
00:15:38,799 --> 00:15:40,759
triple the average for the rest of Europe.

342
00:15:40,919 --> 00:15:44,039
Speaker 1: So what's the scientific explanation for that? Not aliens?

343
00:15:44,039 --> 00:15:47,720
Speaker 2: I'm guessing no, not aliens. This is the classic textbook

344
00:15:47,720 --> 00:15:50,919
example of something called the founder effect and genetic drift.

345
00:15:51,039 --> 00:15:52,279
Speaker 1: Okay, explain those.

346
00:15:52,200 --> 00:15:54,600
Speaker 2: Imagine a small group of people breaks off and founds

347
00:15:54,600 --> 00:15:59,159
a new isolated population just by random chance, that small

348
00:15:59,200 --> 00:16:01,879
group of founders might have a higher than average frequency

349
00:16:02,120 --> 00:16:05,200
of a rare trait like the RhD gene deletion.

350
00:16:05,360 --> 00:16:07,720
Speaker 1: So the starting point is already skewed exactly.

351
00:16:07,759 --> 00:16:10,440
Speaker 2: That's the founder effect. Then, because the population is small

352
00:16:10,480 --> 00:16:15,039
and isolated, random chance, which we call genetic drift, continues

353
00:16:15,080 --> 00:16:18,039
to play a huge role. The frequency of that trait

354
00:16:18,120 --> 00:16:21,519
can drift up or down unpredictably from one generation to

355
00:16:21,559 --> 00:16:22,240
the next.

356
00:16:22,120 --> 00:16:25,360
Speaker 1: And in the Basques it just happened to drift way way.

357
00:16:25,159 --> 00:16:27,720
Speaker 2: Up, way up, and once it's at that high frequency,

358
00:16:27,759 --> 00:16:30,120
it tends to stick around, even with the negative pressure

359
00:16:30,120 --> 00:16:33,440
from HDN. So for the Basques, the story is likely

360
00:16:33,440 --> 00:16:36,559
one of ancient isolation and pure genetic chance.

361
00:16:36,639 --> 00:16:39,039
Speaker 1: Okay, But the story doesn't end there, does it. There's

362
00:16:39,080 --> 00:16:42,279
another twist with the reciss system, right, because.

363
00:16:42,080 --> 00:16:43,720
Speaker 2: It's not just one gene. The main one we talk

364
00:16:43,759 --> 00:16:46,039
about is RhD, the one that gets deleted, but right

365
00:16:46,080 --> 00:16:47,960
next to it is another gene called RHC.

366
00:16:48,440 --> 00:16:49,240
Speaker 1: And what does that one do?

367
00:16:49,559 --> 00:16:52,399
Speaker 2: It also codes for antigens on your red blood cells,

368
00:16:52,600 --> 00:16:55,799
the CC and E atigens. They can also cause HDN,

369
00:16:56,120 --> 00:16:59,759
but it's usually much less severe than the d antigen.

370
00:16:59,320 --> 00:17:02,000
Speaker 1: Reaction, so it's a related system. What's the twist.

371
00:17:02,279 --> 00:17:06,160
Speaker 2: The twist is that when scientists analyze the rhcee gene,

372
00:17:06,200 --> 00:17:09,920
they found something completely unexpected. They found strong evidence of

373
00:17:10,039 --> 00:17:12,160
positive selection on one of its variants.

374
00:17:12,319 --> 00:17:16,440
Speaker 1: Positive selection meaning evolution was actively favoring it.

375
00:17:16,319 --> 00:17:20,160
Speaker 2: Actively pushing it to high frequency in non African populations,

376
00:17:20,480 --> 00:17:23,920
specifically the coliele of the race gene.

377
00:17:23,640 --> 00:17:25,599
Speaker 1: So it must have provided some kind of benefit. What

378
00:17:25,640 --> 00:17:27,200
was the editors for this selection.

379
00:17:27,720 --> 00:17:30,960
Speaker 2: They used the statistic called FST, which measures how different

380
00:17:31,000 --> 00:17:34,880
populations are genetically. They found a huge FST value banned

381
00:17:35,000 --> 00:17:37,880
zero point sixty four for this coliele between East Asians

382
00:17:37,920 --> 00:17:41,640
and Africans. It's a massive statistical signal that something was

383
00:17:41,680 --> 00:17:44,119
driving this allele to become common in the groups that

384
00:17:44,200 --> 00:17:44,880
left Africa.

385
00:17:45,200 --> 00:17:48,640
Speaker 1: So we have this bizarre situation. On the one hand,

386
00:17:48,839 --> 00:17:53,440
a dangerous gene deletion RhD is hanging around, probably due

387
00:17:53,519 --> 00:17:54,480
to random.

388
00:17:54,160 --> 00:17:59,240
Speaker 2: Drift, and right next door, a related gene rhce has

389
00:17:59,279 --> 00:18:03,160
a variant that it was so beneficial that evolution actively

390
00:18:03,200 --> 00:18:04,079
selected for it.

391
00:18:04,079 --> 00:18:06,599
Speaker 1: It's like two completely different stories happening on the same

392
00:18:06,640 --> 00:18:07,759
page of the genome.

393
00:18:07,440 --> 00:18:10,920
Speaker 2: And that's the mystery. The genetic signal for the cleele

394
00:18:11,079 --> 00:18:13,319
is shouting that it was helpful, that it gave people

395
00:18:13,319 --> 00:18:16,519
a survival advantage. But here's the kicker. What we have

396
00:18:16,599 --> 00:18:20,000
no idea what that advantage was. The paper itself concludes

397
00:18:20,039 --> 00:18:25,039
that the fitness benefits of the cecliel are currently unknown.

398
00:18:25,119 --> 00:18:26,960
Speaker 1: So we know it was good for something, but we don't.

399
00:18:26,720 --> 00:18:29,480
Speaker 2: Know what exactly. It just adds another layer of complexity

400
00:18:29,559 --> 00:18:32,319
and shows how deep this evolutionary story really goes.

401
00:18:32,640 --> 00:18:35,240
Speaker 1: Okay, so this brings us to the big scientific showdown,

402
00:18:35,240 --> 00:18:36,680
the core evolutionary battle.

403
00:18:36,920 --> 00:18:41,200
Speaker 2: Right. We have this profoundly dangerous gene deletion, the RhD gene.

404
00:18:41,440 --> 00:18:44,480
We know it causes HDN. We know that fitness cost.

405
00:18:44,319 --> 00:18:47,000
Speaker 1: Was huge, So why is it still here? Why is

406
00:18:47,039 --> 00:18:49,519
the allele frequency as high as forty three percent in

407
00:18:49,559 --> 00:18:51,319
European Americans? How did it survive?

408
00:18:51,599 --> 00:18:55,440
Speaker 2: There are two main camps, two competing hypotheses, and we

409
00:18:55,480 --> 00:18:56,720
need to really dig into both.

410
00:18:56,839 --> 00:18:57,960
Speaker 1: Okay, Hypothesis A.

411
00:18:58,440 --> 00:19:00,720
Speaker 2: Hypothesis A is basically the story are we told about

412
00:19:00,720 --> 00:19:05,160
the Basques, but applied more broadly, it's genetic drift and

413
00:19:05,240 --> 00:19:06,079
the founder effect.

414
00:19:06,720 --> 00:19:08,680
Speaker 1: It was just chance argument.

415
00:19:08,599 --> 00:19:12,160
Speaker 2: Essentially, Yeah, it's the null hypothesis. It doesn't require any

416
00:19:12,200 --> 00:19:15,920
secret benefit. It just relies on population history and random luck.

417
00:19:16,279 --> 00:19:17,599
Speaker 1: And is there evidence for this.

418
00:19:17,920 --> 00:19:21,160
Speaker 2: There is a big study in twenty twelve by Perry

419
00:19:21,160 --> 00:19:24,240
and his colleagues went looking for the molecular footprint of

420
00:19:24,359 --> 00:19:27,200
recent positive selection on the RhD deletion in.

421
00:19:27,160 --> 00:19:28,920
Speaker 1: Europeans and they didn't find it.

422
00:19:29,039 --> 00:19:32,599
Speaker 2: They didn't find it, which suggests that evolution wasn't actively

423
00:19:32,640 --> 00:19:36,000
trying to make this gene more common. So the argument goes,

424
00:19:36,559 --> 00:19:38,880
the negative force from HDN must not have been strong

425
00:19:39,000 --> 00:19:41,720
enough to overcome the power of genetic drift in those

426
00:19:41,720 --> 00:19:43,599
small early European populations.

427
00:19:43,759 --> 00:19:45,960
Speaker 1: But how could it not be strong enough? One in

428
00:19:46,039 --> 00:19:48,599
fifty six berths seems incredibly strong.

429
00:19:48,680 --> 00:19:50,640
Speaker 2: Well, this is where they brought in some really interesting

430
00:19:50,720 --> 00:19:52,079
data from the Hutter Rights.

431
00:19:52,160 --> 00:19:53,319
Speaker 1: Hotter Rights. Who are they?

432
00:19:53,519 --> 00:19:55,960
Speaker 2: They are a religious community in North America, kind of

433
00:19:56,000 --> 00:19:59,240
like the Amish. They're a founder of population. They've been

434
00:19:59,279 --> 00:20:01,519
isolated for a long long time. They have big families,

435
00:20:01,839 --> 00:20:05,240
and they have meticulous genealogical records going back generations.

436
00:20:05,559 --> 00:20:08,920
Speaker 1: So they're a perfect natural experiment for looking at reproduction

437
00:20:09,079 --> 00:20:10,759
before modern medicine.

438
00:20:10,799 --> 00:20:15,039
Speaker 2: Exactly before. Rogam and the researchers looked at the Hutterighte

439
00:20:15,039 --> 00:20:18,359
family records to see if the risk of HDN actually

440
00:20:18,400 --> 00:20:20,799
reduced the total number of children of family had.

441
00:20:20,680 --> 00:20:21,480
Speaker 1: And what did they find?

442
00:20:21,880 --> 00:20:25,640
Speaker 2: Surprisingly, it didn't. When they compared the at risk families

443
00:20:25,680 --> 00:20:28,440
our h negative mom our each positive dad to the

444
00:20:28,519 --> 00:20:32,000
non risk families, there was no significant difference in the

445
00:20:32,039 --> 00:20:33,079
total number of kids.

446
00:20:33,880 --> 00:20:36,480
Speaker 1: How is that possible if babies were dying.

447
00:20:36,799 --> 00:20:40,359
Speaker 2: Well a couple of ideas. First, infant mortality from other

448
00:20:40,400 --> 00:20:43,119
causes was already high back then, so maybe the HDN

449
00:20:43,200 --> 00:20:46,519
deaths just got lost in the noise, or maybe families

450
00:20:46,519 --> 00:20:49,480
were compensating. If a child was lost to HDN, the

451
00:20:49,599 --> 00:20:51,799
parents might just try to have another child sooner to

452
00:20:51,839 --> 00:20:54,279
replace them. So the total family size at the end

453
00:20:54,319 --> 00:20:55,640
of the day wasn't really affected.

454
00:20:55,920 --> 00:20:59,680
Speaker 1: So the selective pressure was on the individual child, but

455
00:20:59,759 --> 00:21:03,279
not on the family's total reproductive output.

456
00:21:03,039 --> 00:21:06,480
Speaker 2: Right, which would weaken the evolutionary pressure against the gene itself.

457
00:21:07,119 --> 00:21:10,480
The other key point is something called frequency dependence. Okay,

458
00:21:11,000 --> 00:21:13,359
once the deletion becomes really common, like it is in

459
00:21:13,400 --> 00:21:16,640
the basks near fifty percent, the select of pressure against

460
00:21:16,640 --> 00:21:19,559
it actually gets weaker because the chance of a dangerous

461
00:21:19,559 --> 00:21:23,079
pairing an RH negative mom with an RH positive baby

462
00:21:23,599 --> 00:21:26,640
starts to go down relative to all the other possible pairings.

463
00:21:26,680 --> 00:21:28,920
Speaker 1: So once it hits a certain tipping point, it's easier

464
00:21:28,920 --> 00:21:30,359
for it to just stay there.

465
00:21:30,359 --> 00:21:32,880
Speaker 2: And a little bit of genetic drift is enough to

466
00:21:32,920 --> 00:21:37,359
maintain it. So that's hypothesis A. A dangerous gene gets

467
00:21:37,400 --> 00:21:40,440
a foothold by chance in a small population, and the

468
00:21:40,480 --> 00:21:42,480
forces trying to get rid of it just aren't strong

469
00:21:42,599 --> 00:21:43,519
enough to finish the job.

470
00:21:43,720 --> 00:21:46,359
Speaker 1: A story of chance and circumstance. But that's not the

471
00:21:46,359 --> 00:21:47,240
only story, is it.

472
00:21:47,319 --> 00:21:52,359
Speaker 2: No, And hypothesis B is to me much more tantalizing.

473
00:21:52,799 --> 00:21:54,359
It suggests there was a hidden benefit.

474
00:21:54,480 --> 00:21:56,319
Speaker 1: This is the balancing selection idea.

475
00:21:56,079 --> 00:21:59,160
Speaker 2: Balancing selection driven by something called heterozygote advantage.

476
00:21:59,200 --> 00:21:59,960
Speaker 1: Okay, what does that mean.

477
00:22:00,359 --> 00:22:03,960
Speaker 2: It means that while being homozygous for the trait is bad,

478
00:22:04,440 --> 00:22:07,599
in this case, being RH negative carries the risk of

479
00:22:07,759 --> 00:22:10,519
HDN carrying just one copy of the gene, being a

480
00:22:10,559 --> 00:22:14,119
heterozygote actually gives you some kind of survival advantage.

481
00:22:14,200 --> 00:22:16,920
Speaker 1: The classic example of this is sickle cell anemia.

482
00:22:17,000 --> 00:22:19,880
Speaker 2: Right, The perfect example. If you have two copies of

483
00:22:19,880 --> 00:22:22,720
the sickle cell gene, you get the deadly disease, but

484
00:22:22,759 --> 00:22:25,200
if you only have one copy, you don't get the disease,

485
00:22:25,440 --> 00:22:27,079
and you get protection from malaria.

486
00:22:27,200 --> 00:22:29,359
Speaker 1: So the gene sticks around because being in the middle,

487
00:22:29,519 --> 00:22:32,640
the heterozygous state is the best place to be in

488
00:22:32,680 --> 00:22:34,640
a malarial environment precisely.

489
00:22:34,880 --> 00:22:37,400
Speaker 2: So the big question for RI if negative is what's

490
00:22:37,440 --> 00:22:40,640
the equivalent of malaria? What ancient threat was so bad

491
00:22:40,799 --> 00:22:43,279
that it was worth risking hed N to have protection

492
00:22:43,319 --> 00:22:43,759
against it?

493
00:22:43,799 --> 00:22:45,599
Speaker 1: And there's a prime suspect.

494
00:22:45,240 --> 00:22:49,400
Speaker 2: A very strong suspect, A tiny parasite called toxoplasma gandhi.

495
00:22:50,000 --> 00:22:51,440
Speaker 1: I've heard of this. It's the one you can get

496
00:22:51,440 --> 00:22:52,720
from cats, right from cat.

497
00:22:52,559 --> 00:22:56,119
Speaker 2: Feces, yeah, or undercooked meat. It's incredibly common. Maybe a

498
00:22:56,119 --> 00:22:58,400
third of the world's population is infected, and it can

499
00:22:58,480 --> 00:23:01,359
get into your brain and cause seria neurological issues.

500
00:23:01,519 --> 00:23:03,920
Speaker 1: So the theory is that being a carrier of the

501
00:23:04,039 --> 00:23:07,119
rh negative gene helps you fight off toxic plasma.

502
00:23:07,400 --> 00:23:10,720
Speaker 2: That's the theory, and there's some good evidence for it.

503
00:23:11,039 --> 00:23:14,079
One study actually look at this directly. It found that

504
00:23:14,160 --> 00:23:18,799
Reese's positive heterozygodes the people with one normal RhD gene

505
00:23:18,799 --> 00:23:21,759
and one deleted one were protected against some of the

506
00:23:21,839 --> 00:23:25,880
cognitive damage caused by the parasite. Their reaction times didn't

507
00:23:25,880 --> 00:23:27,720
slow down as much as other groups.

508
00:23:27,559 --> 00:23:30,799
Speaker 1: So there were more resistant to the parasite's effects.

509
00:23:30,319 --> 00:23:34,359
Speaker 2: Exactly, which suggests the bodies making a kind of evolutionary bargain.

510
00:23:35,000 --> 00:23:37,880
It's accepting the risk of HTN in exchange for protection

511
00:23:37,920 --> 00:23:41,880
against this widespread brain altering parasite.

512
00:23:41,279 --> 00:23:43,240
Speaker 1: And the sweet spot is having one copy of the

513
00:23:43,279 --> 00:23:44,119
deletion that.

514
00:23:44,160 --> 00:23:45,759
Speaker 2: Seems to be where the major benefit lies.

515
00:23:45,839 --> 00:23:49,119
Speaker 1: Okay, that's fascinating, but that's just one parasite. Is there

516
00:23:49,160 --> 00:23:52,680
any bigger picture evidence for this balancing selection idea?

517
00:23:52,839 --> 00:23:55,920
Speaker 2: There is, and it's a huge study. A researcher named

518
00:23:56,000 --> 00:23:59,640
Jarislav Fleger published a paper in twenty sixteen where he

519
00:23:59,680 --> 00:24:01,799
looked at data from sixty five different countries.

520
00:24:01,880 --> 00:24:02,720
Speaker 1: What was he looking for.

521
00:24:02,960 --> 00:24:06,079
Speaker 2: He was doing was called an ecological regression study. Yeah,

522
00:24:06,279 --> 00:24:09,599
he was looking for correlations between the frequency of Reese's

523
00:24:09,680 --> 00:24:14,279
genotypes in a country and that country's overall disease burden.

524
00:24:14,119 --> 00:24:15,880
Speaker 1: Like mortality rates and things like that.

525
00:24:16,000 --> 00:24:18,599
Speaker 2: Exactly. He was using a measure called daylies.

526
00:24:18,640 --> 00:24:21,880
Speaker 1: Right disability adjusted life years. It's a measure of the

527
00:24:21,920 --> 00:24:24,480
total impact of a disease, not just deaths, but also

528
00:24:24,599 --> 00:24:26,960
years lived with the disability.

529
00:24:26,519 --> 00:24:29,480
Speaker 2: Right, So he was asking a very big question, is

530
00:24:29,519 --> 00:24:33,279
there a link between a country's RH negative frequency and

531
00:24:33,359 --> 00:24:35,039
the overall health of its population?

532
00:24:35,200 --> 00:24:36,000
Speaker 1: And what did he find?

533
00:24:36,599 --> 00:24:40,839
Speaker 2: He found incredibly strong support for the heterozygote advantage hypothesis.

534
00:24:41,519 --> 00:24:44,720
The single most powerful finding was that for any disease

535
00:24:44,720 --> 00:24:48,119
where there was a significant correlation, the effect on RH

536
00:24:48,240 --> 00:24:53,039
negative homozygotes and RH positive heterozygotes went in completely opposite directions.

537
00:24:53,319 --> 00:24:55,960
Speaker 1: So if having two copies of the deletion was bad

538
00:24:56,000 --> 00:24:58,880
for disease X, having one copy was good for disease

539
00:24:59,079 --> 00:24:59,880
X per c cement.

540
00:25:00,480 --> 00:25:03,839
Speaker 2: That is the statistical fingerprint of balancing selection and action

541
00:25:04,279 --> 00:25:05,839
playing out on a global scale.

542
00:25:05,920 --> 00:25:09,119
Speaker 1: Wow, did he find links to specific diseases.

543
00:25:09,480 --> 00:25:12,079
Speaker 2: He did, and this is where the evolutionary trade off

544
00:25:12,119 --> 00:25:15,279
becomes really clear. He found the countries with more RH

545
00:25:15,359 --> 00:25:19,720
negative people had a lower burden from neuropsychiatric disorders.

546
00:25:19,319 --> 00:25:21,279
Speaker 1: So a potential mental health.

547
00:25:21,039 --> 00:25:24,039
Speaker 2: Benefit a potential benefit, yes, but it came at a

548
00:25:24,200 --> 00:25:28,599
huge cost, which was those same countries had a significantly

549
00:25:28,680 --> 00:25:32,519
higher burden from cardiovascular disease and especially from most types

550
00:25:32,519 --> 00:25:33,039
of cancer.

551
00:25:33,359 --> 00:25:37,759
Speaker 1: Ah wow, So what protected you in one area made

552
00:25:37,799 --> 00:25:39,559
you more vulnerable in another.

553
00:25:39,480 --> 00:25:43,599
Speaker 2: A classic evolutionary trade off. An advantage against ancient threats

554
00:25:43,720 --> 00:25:46,839
like parasites or mental illness may have become a liability

555
00:25:46,839 --> 00:25:49,480
in the modern world, where heart disease and cancer are

556
00:25:49,480 --> 00:25:50,200
the big killers.

557
00:25:50,279 --> 00:25:52,400
Speaker 1: Were the numbers significant, they were shocking.

558
00:25:52,759 --> 00:25:55,319
Speaker 2: The data suggested that just a one percent increase in

559
00:25:55,359 --> 00:25:58,799
the number of RH negative homozygotes in a population was

560
00:25:58,839 --> 00:26:02,960
correlated with over eight eighteen hundred more deaths from cardiovascular

561
00:26:03,039 --> 00:26:04,680
disease per one hundred thousand people.

562
00:26:04,799 --> 00:26:06,480
Speaker 1: That's huge, it is.

563
00:26:06,880 --> 00:26:09,000
Speaker 2: And at the same time, a one percent increase in

564
00:26:09,039 --> 00:26:12,480
the heterozygodes was linked to over four hundred fewer deaths

565
00:26:12,599 --> 00:26:13,519
from the same cause.

566
00:26:13,920 --> 00:26:16,920
Speaker 1: So being a carrier is protective, but being fully RH

567
00:26:17,000 --> 00:26:20,200
negative in the modern world appears to carry a serious

568
00:26:20,240 --> 00:26:22,240
health risk beyond just pregnancy.

569
00:26:22,599 --> 00:26:25,440
Speaker 2: That's what the data on a population level seems to suggest.

570
00:26:25,799 --> 00:26:29,200
It paints this incredibly complex picture of a gene that's

571
00:26:29,200 --> 00:26:32,599
caught between ancient pressures and modern diseases.

572
00:26:32,240 --> 00:26:35,160
Speaker 1: Which just makes you wonder what on earth was the

573
00:26:35,200 --> 00:26:38,359
ancient pressure. It must have been something truly terrible to

574
00:26:38,440 --> 00:26:41,359
make this dangerous gene a good bet for survival.

575
00:26:41,480 --> 00:26:44,319
Speaker 2: It must have been a monster, something worse than the

576
00:26:44,400 --> 00:26:47,519
historical risk of HDN. Maybe it was toxoplasma, maybe it

577
00:26:47,559 --> 00:26:49,920
was something else we haven't even identified yet, or maybe

578
00:26:49,920 --> 00:26:53,359
it's tied into that unknown benefit of the rhceec allele.

579
00:26:53,880 --> 00:26:55,079
The puzzle isn't fully solved.

580
00:26:55,119 --> 00:26:57,680
Speaker 1: Okay, let's try to pull all these threads together. This

581
00:26:57,720 --> 00:27:00,359
has been a wild ride, it really has. We start

582
00:27:00,400 --> 00:27:03,960
with a pretty sensational claim rh negative blood as proof

583
00:27:04,039 --> 00:27:06,640
of an alien or nephilim bloodline, and we.

584
00:27:06,680 --> 00:27:09,759
Speaker 2: Ended up deep in the weeds of chromosome one p.

585
00:27:10,000 --> 00:27:14,759
Thirty six point one one talking about gene deletions, population drift,

586
00:27:15,039 --> 00:27:16,279
and global disease.

587
00:27:16,000 --> 00:27:18,920
Speaker 1: Statistics, and the science seems absolutely clear.

588
00:27:18,720 --> 00:27:20,559
Speaker 2: On one thing that it's not aliens.

589
00:27:20,880 --> 00:27:23,640
Speaker 1: It's not aliens, it's not a marker of superiority. It's

590
00:27:23,680 --> 00:27:28,240
a profound, ancient structural error in our DNA, the deletion

591
00:27:28,480 --> 00:27:30,440
of the entire RhD gene.

592
00:27:30,160 --> 00:27:32,200
Speaker 2: An error that created one of the most classic and

593
00:27:32,359 --> 00:27:33,799
enduring puzzles in human.

594
00:27:33,599 --> 00:27:37,599
Speaker 1: Evolution, the puzzle being how does a trait that kills

595
00:27:37,640 --> 00:27:41,359
your offspring manage to stick around at such high frequencies,

596
00:27:41,759 --> 00:27:43,880
especially in places like the Basque Country.

597
00:27:44,039 --> 00:27:47,599
Speaker 2: And we have two powerful competing scientific stories.

598
00:27:48,119 --> 00:27:50,440
Speaker 1: Story one is that it was all just a series

599
00:27:50,480 --> 00:27:53,960
of historical accidents. Genetic drift and the founder effect in

600
00:27:54,039 --> 00:27:57,720
early European populations pushed the frequency up and the selective

601
00:27:57,759 --> 00:28:00,599
pressure from HDN just wasn't quite so strong enough to

602
00:28:00,599 --> 00:28:01,279
push it back down.

603
00:28:01,599 --> 00:28:04,519
Speaker 2: The Hutterright data supports that idea. It's the chance and

604
00:28:04,559 --> 00:28:05,559
circumstance model.

605
00:28:05,880 --> 00:28:08,400
Speaker 1: But Storry too, the balancing selection model is that it's

606
00:28:08,400 --> 00:28:09,440
not an accident at all.

607
00:28:09,559 --> 00:28:12,400
Speaker 2: It's a trade off. It suggests there's a powerful hidden

608
00:28:12,480 --> 00:28:14,759
advantage to being a carrier of this deletion.

609
00:28:14,720 --> 00:28:17,680
Speaker 1: An advantage that gives you resistance to ancient parasites like

610
00:28:17,799 --> 00:28:18,960
toxic plasma.

611
00:28:18,599 --> 00:28:22,279
Speaker 2: Gandhi, and that this advantage was so important for survival

612
00:28:22,680 --> 00:28:26,400
that it outweighed the terrible reproductive cost of HDN and

613
00:28:26,440 --> 00:28:29,039
even the modern risks of heart disease and cancer.

614
00:28:29,680 --> 00:28:31,599
Speaker 1: And just when you think you have a handle on it,

615
00:28:31,839 --> 00:28:35,039
you remember there's that other weird signal, the positive selection

616
00:28:35,079 --> 00:28:39,880
on the related rhgec allele, whose benefit is still totally unknown.

617
00:28:40,160 --> 00:28:42,640
Speaker 2: It just shows that the real story, the scientific story,

618
00:28:42,720 --> 00:28:46,039
is so much richer and more complex and frankly more

619
00:28:46,119 --> 00:28:49,359
thrilling than any simple alien conspiracy theory.

620
00:28:49,440 --> 00:28:52,079
Speaker 1: It really is. So we'll leave you with this final

621
00:28:52,079 --> 00:28:55,559
thought to ponder. Given the evidence, especially from that huge

622
00:28:55,599 --> 00:28:59,319
global study, that being a carrier a heterozygote seems to

623
00:28:59,359 --> 00:29:01,839
be protective against major diseases.

624
00:29:01,319 --> 00:29:04,680
Speaker 2: While being fully rh negative carries these significant risks.

625
00:29:05,000 --> 00:29:09,200
Speaker 1: What kind of invisible ancient threat? What pathogen or environmental

626
00:29:09,200 --> 00:29:12,240
pressure do you think was so powerful, so deadly that

627
00:29:12,319 --> 00:29:15,119
it made keeping this dangerous gene deletion around a winning

628
00:29:15,160 --> 00:29:18,839
evolutionary strategy for thousands of years. Something had to be

629
00:29:18,880 --> 00:29:21,440
worse than HDN. What do you think it was? Let

630
00:29:21,519 --> 00:29:22,279
us know what you think