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September 5, 2023 85 mins

There’s no denying that human imagination is a powerful thing. It has led us to create incredible works of art, literature that transports its readers to other realms, technology that revolutionizes the way we communicate and travel, music and film that makes us laugh, cry, and hit repeat. But our imagination often falls short when trying to conceive of the world from another person’s perspective, especially when it comes to senses. In this episode, we delve into one of the most prominent examples of this: color vision and color vision deficiencies. First, we take you through how color vision works and just how non-universal this experience is. We then explore the origins of color vision and what evolutionary significance it may have held before getting into the discovery of color vision deficiency and its impact on industry. We close out this colorful episode by chatting about some of the latest developments and products geared towards those with color vision deficiency.

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Episode Transcript

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Speaker 1 (00:00):
So I guess it all started really before I was
ever born. When my parents were dating, it sort of
naturally came up that my dad has color vision deficiency,
and my mom at the time acknowledged that she had
experienced with that because her dad has color vision deficiency
as well, and at the time, they really didn't think
too much of it. It was something cool they had

(00:21):
in common and really didn't devote a lot of consideration
to it. But eventually they got married and they had
my brother, and then they had me. So when my
brother was, I want to say, a toddler, he started
displaying some patterns that would be consistent with color vision deficiency.
And funny enough, my mom is an optometrist, so she's
really well versed in how this works, so she knew

(00:44):
that this was a consideration, and so they went and
they had my brother tested and it turns out he
had color vision deficiency.

Speaker 2 (00:51):
Now he's a.

Speaker 1 (00:52):
Couple years older than I am, and so I have
two X chromosomes. It's not totally normal for people like
me to have this, and so my parents were really
not concerned until I started displaying those same patterns, and
that's when it all finally clicked. That my dad having
colored vision deficiency, my grandpa having color vision deficiency, pretty

(01:12):
much created this scenario that normally doesn't occur until your
ninth grade biology class, where I had the possibility to be.

Speaker 2 (01:21):
A female with color vision deficiency.

Speaker 1 (01:24):
So growing up, it was a household of my dad,
my mom, my brother, and myself. So actually, color vision
deficiency was the quote unquote.

Speaker 2 (01:32):
Normal way to be.

Speaker 1 (01:34):
So we all have Deutero anomaly, so that's the red
green color vision deficiency, and so it's the most common
I think of all of them.

Speaker 2 (01:43):
The three of us all have it.

Speaker 1 (01:44):
My mom doesn't, but she's an optometrist, so this is
always the ideal scenario. So there's going to be one
person in your house that doesn't see the way you
all do. It's kind of nice that she's at least
an expert in this situation. I would say growing up,
it was never really a concern. It may be came
up on occasion, but my parents were very proactive about
letting my teachers know that this was just something.

Speaker 2 (02:05):
We all had.

Speaker 1 (02:06):
But one of the best parts of being a female
with color vision deficiency is that it's on both sides
of my family.

Speaker 2 (02:11):
So on my mom's side, I have a bunch.

Speaker 1 (02:13):
Of cousins and they have it too, and so we
all like to say we're better than the other cousins
or whatever it is you do in families. And then
on my dad's side, he's somewhat unique, but his maternal grandfather,
so my great grandpa lived a very long life and
we all had the opportunity to get to know him.
So it was this big thing that we were all

(02:33):
kind of proud to have. So one of the stories
that we were always told about my great grandpa is
that in World War Two, when they were trying to
get people to enlist, he volunteered early, hoping they would
look the other way and allow him to fly planes.
They definitely did not allow him to fly planes.

Speaker 2 (02:50):
But something they.

Speaker 1 (02:51):
Always tell us is a supposed advantage to having color
vision deficiencies that camouflage doesn't work as well, and so
one of the things had him doing was trying to
spot really any sort of activity that other members of
his squadron really couldn't see, and so he was the
designated see the camouflage guy. So this is always just

(03:12):
sort of an interesting story that was told to us.

Speaker 2 (03:14):
But I do want to take it with a grain of.

Speaker 1 (03:16):
Salt, because I never actually heard it from my great
grandpa himself. He did not like to talk about his
experiences during the war, but it was always kind of
a funny side note growing up with color fission deficiency
in my family, again, it was so normal.

Speaker 2 (03:29):
But then getting out into this supposed real world.

Speaker 1 (03:32):
Now that I've moved out, gone to college and everything,
there have been a couple things that are very challenging.
So I'm working on my PhD and we do nutritional
immunology and microbiology, and so a lot of that encompasses
some microbiome research and heat maps are a big part
of it, and most heat maps usually go from red
to green. But being red green colorblind, that's really challenging,

(03:54):
and you can't be the person at the conference who
stands up and can't read their own data. So my
really awesome collaborators actually came up with a new color
scheme that would work for me, and according to everyone else,
it's really really ugly. So I think it goes from
blue to black to yellow, and I.

Speaker 2 (04:13):
Can see it really well.

Speaker 1 (04:14):
But I've definitely been at conferences or given talks in
my department where people have actually said that's all great,
but your colors are ugly or these are really really bad,
and that puts you in this really awkward situation where
you have to stand up in front of all these
people and say, yes, I understand they might look bad,
but those colors are for me, they're not for you.
And so it does end up becoming sort of an

(04:35):
awkward teachable moment where they have to acknowledge that there
are people in the room and there's a good likelihood
that there are people in the room who just don't
see colors the same way as you, but then also
having to stand up and say, yes, I am a female,
I'm colorblind, and then that starts a whole different conversation
that isn't about the science I just presented it, It's
about me. And then the other biggest challenge I would

(04:58):
say is that because it's.

Speaker 2 (05:00):
Not likely for females to be colorblind or to.

Speaker 1 (05:03):
Have this sort of color vision deficiency, is that some
people were taught, most simplistically, that it's impossible. So it's
not that they were told it's unlikely. They were just
told by some teacher along the way that it was
totally impossible. And so when you tell them this about yourself.
They look at you funny. They come at you as
sort of a negative approach, like you.

Speaker 2 (05:25):
Must be lying to get attention, you're making this up.

Speaker 1 (05:29):
So that always is really a challenge because it's trying
to overcome that impression that didn't really need to be
an impression in the first place, and.

Speaker 2 (05:37):
So all of that has been somewhat of a challenge.

Speaker 1 (05:40):
But ultimately, I think the best thing that comes out
of it is just being part of this community. I
think it's really funny when you catch people off guard
with it, because it's not you can't look at someone
and see this, So it's nice to get a few
jokes in there. A lot of times I'll tell my
friends that my favorite eminem's are the great kind. Even
though I can see those colors, it's still just always
catches people off guard. I think my biggest thing that

(06:03):
I get asked is if I would ever consider using
those color vision correction lenses, And my biggest answer is
a resounding no. I was born this way, I've always
seen the world this way. I don't want anything different.
The glasses aren't guaranteed to work, and so I don't
want to run the risk of seeing things differently and
ending up unhappy. So I would say that's kind of

(06:26):
the main part of my story is that I just
love being this way. It's a challenge most times, but
it's a lot of fun when you can make it
fun and just proves that my brothers were always wrong
when they said I was adopted. So yeah, I think
that's pretty much the main part of my story.

Speaker 3 (07:30):
Thank you so much, Kristen for sharing your story with us.

Speaker 4 (07:33):
We really appreciate it.

Speaker 2 (07:35):
Hi.

Speaker 4 (07:35):
I'm Erin Welsh and I'm Erin Almond Updink.

Speaker 3 (07:38):
And this is this podcast will kill you.

Speaker 4 (07:41):
Welcome Today we're talking about the whole spectrum get it
of color vision deficiencies.

Speaker 3 (07:49):
That actually took me a second to get it. I
think I'm too close to this thing, Erin.

Speaker 4 (07:56):
That's the only joke I have for the whole episode.

Speaker 3 (07:58):
So yeah, I don't think I have any which is
really surprising. Again, I was like too much in the weeds.
I lost the forest for the trees.

Speaker 4 (08:07):
Yeah, whoops, we're really selling it.

Speaker 3 (08:10):
Yeah no, but no. I mean that's the thing though,
that there is just so much to go into with
this and it's all really interesting, like Honestly, it's like
you could throw a dart dart board and find a
thousand interesting things about one aspect of the history or
the biology of color vision deficiencies.

Speaker 4 (08:29):
So yeah, you might have to open like no less
than fifty Wikipedia pages to understand one paper. For example.

Speaker 3 (08:37):
I know I could not tell what was like on
my chrome. I was like, oh my gosh, this is
way too many tabs.

Speaker 4 (08:44):
I hate to deal with this my life. Well, it's
going to be.

Speaker 3 (08:49):
A great episode, but before we get into the meat.

Speaker 4 (08:52):
Of it, it's quarantine any time.

Speaker 3 (08:55):
It is what are we drinking this week?

Speaker 4 (08:58):
We're drinking True Color?

Speaker 3 (09:00):
And I love this title because is there any such
thing as true colors?

Speaker 4 (09:07):
That's how the song goes, right, I see your true
color shining through there you go. Yeah, that's why I
love you. I'm not going to keep that in What
is in true Colors?

Speaker 3 (09:21):
In True Colors? It is a fun little summary concoction.
It has basically as many colors as we could try
to fit in there, which is not that many because
I'm not a skilled layerer when it comes to quarantinie making.
But there's grenadine, and then there's orange juice, and then
there's blue currosow, and there's lime juice and rum yum.

Speaker 4 (09:45):
It's great. We'll post the full recipe for that quarantini
as well as our non alcoholic plusy burita on our website.
This podcast will kill you dot Com. We certainly will
on our website. This podcast will kill you dot Com.
I'm gonna pull it up and just see what I
can find, because you know, it's my brain has not
been functioning very well today. We've got transcripts, We've got

(10:09):
the sources for each and every one of our episodes.
We've got a first hand account form. I don't think
I've been saying that in the past. Yeah, most recent episodes.

Speaker 3 (10:19):
We have got links to bookshop dot org, affiliate account,
Goodreads list, our merchandise page, music by Bloodmobile, Patreon, lots
of stuff.

Speaker 4 (10:29):
Check it out. It's good stuff. With that, shall we
talk about coorvision deficiencies? I think we should, okay, right
after this break, to be able to talk about color

(11:02):
vision deficiencies aka color blindness, I think we first have
to understand at least a little bit about color vision itself. Right.
It's easy, right, so simple and straightforward to explain on
a podcast in under two hours. Here we go at

(11:26):
the most basic level, just like bare bones in it,
we as humans are able to distinguish between colors in
the visible spectrum because our brain can compare information that
it receives from three different sets of cells that contain

(11:48):
photoreceptor proteins in our eyes. I'm going to go into
a bit more detail about how that process works, and
I think once we understand the really bear basics of
that process, I think the many, many ways in which
this system can have deficiencies, aka all the variations of

(12:09):
color vision deficiency become pretty obvious, or at least relatively so. Okay, So,
going all the way back to the beginning of time,
kind of light exists as a spectrum. I actually have
no idea if that has anything to do at the
beginning of time, but anyways, light exists as a spectrum.

(12:34):
There is an infinite number of wavelengths of light that exists,
from ultraviolet to infrared four hundred to eight hundred nanimeters.
Our human eyes have evolved to see a fairly small
portion of this spectrum of light, visible light ROIGBIV in
our rainbows. So it goes like this light, all of

(12:58):
its various wavelengths, comes into our eyeballs, travels through our
eyege and hits onto our retina at the very very
back of our eyes. And in this retina, which is
just the area in our eye, there exists a whole
bunch of different cells that are full of photoreceptor proteins.

(13:19):
There are two main types of these photoreceptor cells, rods
and cones. Rod cells express a protein called rhodopsin. It
mostly helps us have vision in dim light, so we
get to ignore it for this episode. Gay yay, so
I'm finally something. It's probably marginally involved, et cetera. But

(13:40):
for the purposes of today, rod's dim light. It's the
cone cells that allow us as humans color vision. So
these cone cells, which are super densely packed within our retina,
come in three different flavors, or rather, they express three
different kinds of opsins, which are these photoreceptor proteins. Each

(14:04):
one of these opsins is most sensitive peak sensitive to
a specific wavelength of light, short, medium, and long. Huh
simple enough, simple enough, so far so. The short wavelength
sensitive opsin is also called the blue cone. The middle

(14:25):
or medium wave sensitive opsin is also called the green cone,
and the long wave sensitive opsin is called the red cone,
even though its peak wavelength of absorption is actually yellow,
not red, but let's ignore that and call it red. Yeah,
it's great. Yeah. So the waves of light hit these

(14:46):
photoreceptor cells, they are absorbed by these proteins, very complex
chemistry happens, and then those wavelengths that energy is translated
into electrical signals that travel via our optic nerve to

(15:06):
a part in the middle of our brain, in our thalamus,
and then to the primary visual cortex, which is in
the back the occipital lobe of our brain. And that's
where all of this visual information, everything that we see,
including color information, is processed and interpreted. That is the

(15:27):
most basic way that we can explain how color vision happens.
The short wavelength or blue sensitive cones respond to a
much more discrete array of wavelengths of light, like if
you look at all of the spectra that they can absorb,
it's more offset, whereas the middle, green, and the long

(15:49):
red wavelength cones have much more overlap if you look
at all the wavelengths that they're sensitive to. But they
all three have different peaks, and this is really important
because none of these cone cells alone allow us to
see or distinguish colors on their own. Our brain has
to compare the information that it gets the signals from

(16:13):
each of these different types of cells, and in doing that,
it's then able to differentiate colors into our human tri
chromatic or three color vision system.

Speaker 3 (16:25):
Right, you need at least two for comparison, but three
you just get to compare more and split up that
spectrum more exactly.

Speaker 4 (16:33):
And many speaking of only two, A lot of mammals,
in fact have only two sets of cones. That's why
people say, like dogs are colorblind. They're not colorblind, but
they only have two sets of cones. Humans and some
primates have three. What's very cool is that fish have
like four and some birds have five. Oh yeah, it's

(16:55):
like wild, I know.

Speaker 3 (16:58):
And people thought that fish were colorblind for ever.

Speaker 4 (17:02):
Oh I know, I love it. I mean they can
see UV for goodness.

Speaker 3 (17:07):
Sake, right, so many things can see UV I know,
but not us.

Speaker 4 (17:11):
Butter I know.

Speaker 2 (17:13):
Do you know?

Speaker 4 (17:13):
I learned it's mostly because of our lens, not because
our cones are not sensitive in that wavelength. Oh interesting.
Our lenses filter out the UV and that's a large
part of why we can't see UV.

Speaker 3 (17:25):
Because as like protect from damage.

Speaker 4 (17:28):
Oh, don't ask me about the whys erin. It has
nothing to do with this episode, so I didn't dig
into it.

Speaker 2 (17:37):
Is there my favorite questions?

Speaker 4 (17:39):
I know, I know, I know, Okay, But getting back
to it, obviously, these cone cells, therefore, are very important
and in addition to allowing us to perceive color vision,
cone cells also have a faster response time to various
light stimuli, and they help a lot in fine detail

(18:01):
perception because they can perceive rapid changes in images. So
our cone cells are very, very important to our overall
human vision system. So color blindness or color vision deficiency
is what happens when there are problems with this visual processing, because,

(18:21):
like we said, you need all three of these cones
to be functioning and specifically to be responding to the
specific wavelengths of light that we expect to be able
to distinguish the color spectrum that we associate with human
color vision. So there's a lot of different ways that

(18:42):
this can go a little shall we say, wonky. The
vast majority of color vision deficiencies are congenital, meaning they
are inherited. They are from mutations in our genetic code.
These mutations can happen in genes that encode for the

(19:02):
cone cells or for the options themselves, or they can
happen because of mutations in the promoter regions for any
of those genes, like the regions that tell our cells
to turn on or off the expression of those genes,
and that process gets incredibly complicated. So this is not
by any means a one gene, one disease type scenario

(19:27):
that we have here. There are many, many, many possible
mutations that result in a wide variety of color vision deficiencies,
which we'll get into all of the details of. They're
also in addition to hereditary color vision deficiency is acquired
color vision deficiency, and that can happen from damage to

(19:48):
parts of our eye during our lifetime. This can happen
from other congenital diseases that aren't directly related to say,
our cone self function, but it all so can happen
just from direct damage from various eye illnesses. For the
purposes of this episode, because that's a lot, I'm mostly

(20:10):
focusing on the congenital rather than the acquired color vision deficiencies.
But I have a couple of papers if people want
to read more about the other side so let's get
into like, what does color vision deficiency even mean? Yeah, okay,
so the mildest forms of CVD, can you just call
it that? Sure, are called anomalous trichromacy. So humans are trichromatic.

(20:37):
So we have three sets of cones, three peak wavelengths
of color vision. A lot of people with color vision
deficiency still have these three separate sets of cones, three
separate sets of options, but they have some kind of
mutation that results in a shifting of the frame, if

(20:59):
you will, the shifting of that peak wavelength of sensitivity
so that there's more overlap between the peaks, so that
the information that your brain gets about those different wavelengths
can't be separated out as easily.

Speaker 3 (21:16):
And so when you say that there's a shift, is
it they're moving closer together and it's all three of
them or is it just one that happens to move
closer to the other one?

Speaker 4 (21:28):
Such a good question. There's three different possibilities. Okay. So
in deter anomaly due to you'll hear me say it
a lot, it's I think it has something to do
with green anyways. In due to anomaly, the middle wavelength
photopigment is mutated so that it's more similar to the
long wavelength photopigment. So when you should be able to

(21:51):
absorb the peak in the green zone, now that specific
cone looks a lot closer to the red zone. Okay.
Now the opposite can happen as well. In protonomally, the
long wavelength photopigment, the red is mutated so that its
peak is really similar to the middle wavelength. So what

(22:12):
should be absorbed in the red zone is shifted to
the green Does that kind of make sense? Kind of?

Speaker 3 (22:20):
So in terms of like the result, like what resolution
you lose in terms of color distinguishing or the colors
that are typically called whatever colors you know we have
in our visual spectrum, you know what I mean?

Speaker 4 (22:36):
Like I totally so yeah, So you're right, you lose
some of that distinction, so you're not able to distinguish
between say certain hues or between certain colors. Okay.

Speaker 3 (22:49):
And so for deter anomaly, you lose the ability to
distinguish between reds and greens, and for protonomally, it's also
reds and greens, but it's slightly the shading is different.

Speaker 4 (23:05):
Okay, that's exactly right, one percent, right, Okay, cool and
those overall are the two most common forms of color
vision deficiency, and so.

Speaker 3 (23:13):
That is not caused by a lack of opsin, but
just a shift in the opsin exactly.

Speaker 4 (23:21):
They often result from unequal recombination. So what you get
are these hybrid gene formations. The details of it, that's fascinating.

Speaker 5 (23:32):
I know, I really thought it was just an absence
of a cone. Oh, we're getting there, We're getting there. Okay,
we are nowhere near done. So there's also tritonomaly, which
would change the peak of the blue cone, right, triton
because we talked about the red cone and the green cone.
Triton means blue. This would change the peak of the

(23:53):
blue cones. Overall, this is far less common. And if
you remember that I mentioned that the the L and
the M have a lot more overlap to begin with,
tried denominally alone may not result in that big of
a deficiency, depending on how much it's shifted, if that makes.

Speaker 4 (24:12):
Sense, right right, yep. Now, overall, those three types again
are called anomalist trichromacy. You still have all three cones.
They usually result in milder color vision loss, but there's
a lot of variation in the ability to distinguish between
shades and colors. Now, then we move on to die chromasy.

(24:36):
You can imagine this means two sets of cones. This
is obviously more severe and means that you're having loss
of function of one of the cone types entirely, either red,
which is called protinopia, green which is called deuterinopia, or
blue tritinapia. Here's where it gets even more interesting, though,

(24:58):
is that this ca happen by, say, the loss of
one of these genes entirely, and for a long time
it was thought that that is how it happens, but
it can also happen by replacement of one of these
genes with the equivalent. Say, for example, during recombination, you

(25:19):
end up with two sets of M genes instead of
an M and an L.

Speaker 3 (25:25):
Right, so you have like two green cones, one red cone.

Speaker 4 (25:31):
Beautiful exactly and then one blue pretty cool. Right, Yeah,
So that is di chromasy. Then there is the most
severe form of color vision loss, and that is monochromasy,
aka the complete absence of color discrimination. Because like we said,
you have to be able to compare to be able

(25:52):
to distinguish between colors. This is by far the most rare,
and there still are several different forms of this. Part
of the reason that true monochromacy is so rare is
because while the M and the L cones, or rather
the genes that encode the M and the L opsin

(26:12):
green and red, they sit right next to each other
on the X chromosome, but the S cone or the
blue cone opsin gene is all the way over on
chromosome seven. It's nowhere near MNL. So to have true
loss of all three of these would be incredibly rare.

(26:35):
There is, however, a form of monochromacy known as blue
cone monochromacy or X linked recessive incomplete a chromatopsia where
you have no functioning M or L cones and you
only have functioning blue cones. Okay, but remember that I

(26:55):
mentioned that cones are responsible for a lot more than
just color vision. They aid in our visual acuity and
things as well. So when we get to the point
of monochromases and incomplete or even complete a chromatopsia where
we have like say, no functioning cones, you're not just
losing the ability to distinguish colors, you're also losing a

(27:18):
lot of visual acuity. So people with monochromacy or complete
a chromatopsia would have significant overall visual field deficits as well.
But if we kind of some all of those fancy
words up, if you hear the term red green color blindness,

(27:40):
that refers to any of those different possible mechanisms of
the loss of distinction between red and green. So red
green color blindness includes deuteranomaly, protonomaly, douteranopia, and protinopia. Okay,
that makes sense, right, because whether we're talking about a

(28:00):
functional loss or just a shift in spectral sensitivity, the
end result is that distinguishing the wavelengths of light that
make it into our eyes between red and green becomes
really difficult because our brain essentially just doesn't receive enough
information to make those comparisons and computations. And all four

(28:25):
of those disorders are X linked recessive traits. So the
presence in general of one X chromosome with a functioning
M and a functioning L gene is enough to result
in quote unquote normal color vision discrimination, with the exception

(28:47):
than that because of X inactivation, which we talked about
all the way back in our Turner syndrome episode. But basically,
what happens when people have two X chromosomes instead of
just one, is that one of those xes gets turned off,
and because that can happen relatively randomly, sometimes it's also

(29:11):
very possible to have color vision deficiency even if you
carry a normal or an M and an L X chromosome.
But in general, that is why we see red green
color blindness be far more common in males who are
X Y than in females who are XX. Yeah. Now,

(29:34):
blue yellow deficiencies called triton deficiencies are overall exceedingly rare
compared to red green color blindness. But these are autosomal
dominant when they are present, because they're on chromosome number seven,
and they generally happen from missense mutations like complete pretty
severe mutations that happen in the blue cone opsin sequence.

(30:00):
Whereas the M and the L which sit again right
next to each other on the X chromosome, they kind
of just get mixed up all the time, and that's
why there's such variation in the possible anomalous expression of
these two genes. Okay, interesting question. Okay, I came across.

Speaker 3 (30:19):
In my reading for this, and I didn't really look
into it too deeply. Tetrachromacy in humans, is it real?
Doesn't exist?

Speaker 4 (30:29):
So glad that you asked, So glad, So that's got
a whole Let me tell you, I can't believe I
can answer your questionnaire. So tetrachromacy would mean four color
vision channels essentially instead of three. So if we remember

(30:49):
what I just said that the most common forms of
color blindness are forms of anomalous trichromacy where you still
have three sets of cones blue, green, red, but the
peak sensitivity of one of these cones, generally a red
or green, is shifted. So here's where things can get fun.

(31:13):
In a person with two X chromosomes who is heterozygous
for this allele, what they can end up with is
one X chromosome that has a typical M and an L,
and another one with a normal M and say an
L prime a slightly shifted version of L that's closer

(31:34):
to M. For example. Now, in the retina of this
person's eye, in every cell, only one copy of the
X chromosome is actually expressed at any given time, but
it's very possible that in some cells the quote normal
X chromosome is expressed and in others the quote mutant

(31:56):
X is expressed because it's not always the same X
that gets inactivated in every cell. So that means that
this person has four types of cone cells being expressed
S or blue, M or green, and then L and
L prime. Right, So this can provide essentially a fourth

(32:18):
color channel or tetrachromacy that, at least in theory, if
our brain was plastic enough, could use to interpret and
distinguish between additional colors and shades.

Speaker 3 (32:33):
What do you mean by if our brain was plastic enough.

Speaker 4 (32:35):
Well, our brain has evolved to be trichromatic. So what
we don't know is does our optic nerve have enough
to be able to distinguish those four color channels. Can
our brain like change enough to be able to interpret
those as separate or does it just collapse the L
and the L prime together?

Speaker 1 (32:56):
Right?

Speaker 3 (32:56):
Okay, but this could happen with any one of those options.

Speaker 4 (33:01):
Yes, in theory. In practice, it's going to be red
or green most likely.

Speaker 3 (33:06):
Okay, Yeah, Okay, interesting, Yeah, because there are, like we
talked about, lots of animals that have more than three cones,
but it's unclear with tests, Yeah, whether they're able to
distinguish among the colors. That they should be able to
based on our interpretation of the science behind it.

Speaker 4 (33:27):
So I love that you said that, because I do
feel like one thing that's so important when we talk
about these color vision deficiencies is that whenever we're talking
about color vision, it's like in comparison to who or
to what? Right, Right. There's another paper that I will
link to that looks at specifically people with deuter anomaly.

(33:47):
So that is red green color blindness from a shifted
green cone that they call L prime because it's now
closer to a typical L or red cone right the
green shifts to red. And what this shows is that
some people with this type of color vision quote unquote
deficiency were actually able to separate out tones distinguish between

(34:13):
tones that looked the same to quote normal color vision
or tri chromatic color vision observers. So there's a theoretical basis,
both with certain types of deuter anomalies and with this
theoretical trichromacy that people could be distinguishing between shades and

(34:36):
between colors differently. It's very very difficult to test for,
and I'll be honest, I don't understand the tests that
they describe in these papers. Because to the vast majority
of the population who's tri chromatic, How can you determine

(34:57):
if someone else can distinguish something that you cannot distinguish,
right right, Yeah, it's very difficult. I will say there
is like one person I think that I read about
who happens to live in San Diego who in tests,
seems to have an actual functional tetra chromacy, meaning that

(35:20):
she tests where she can distinguish between additional shades and
colors based on wavelengths. Then a trichromat can one so
far out of all of the people that I read
about that were tested, okay, okay, so but it's it's
really really interesting.

Speaker 3 (35:38):
That's fascinating, and I feel like there's so much there
in terms of like the evolutionary history of color vision
period where it's like the information that color gives you,
uh huh yeah, yeah, anyway, interesting, Well to.

Speaker 4 (35:59):
That point, Aaron, where did this color vision deficiency thing
come from?

Speaker 3 (36:07):
Huh oh gosh, yeah, you're not going to be the
word evolution. Yeah, We're going to have to go way
further back than just that. And I guess we should
get started right after this break. So Erin, you just

(36:47):
took us through how we see color and what happens
when people see color differently or not as many colors,
or no colors at all. And later in the history section,
I want to explore when we first learned about these
variations in color vision and color vision deficiencies. But before
we get into that more medical history side of the story,

(37:11):
I want to try to answer the question why do
we see color humans, other primates, birds, dogs, fish, other animals.
Why did color vision evolve? What purpose does seeing in
color serve? Multiple purposes?

Speaker 4 (37:29):
You betcha?

Speaker 3 (37:32):
And of course not everything in biology has to serve
an evolutionary purpose, But the fact that there's variation in
color vision and patterns in that variation, the fact that
it has evolved multiple times, independently and in different ways,
these things all suggest that color vision does serve a purpose.

(37:53):
But color vision, even dichromacy, is not universal among animal species. Sloths, armadillos, whales, raccoons, cephalopods,
many animals are monochromats, and they do just fine.

Speaker 4 (38:08):
Stop it.

Speaker 3 (38:09):
Raccoons raccoons apparently.

Speaker 4 (38:11):
I mean, I guess they're nocturnal. Yeah, so that kind
of tracks. But I did not know that about those
little buggers yes, slots, I know, I know, Okay, I'm
learning a lot.

Speaker 3 (38:27):
Colorvision is not necessary for survival as an individual or
as a species. And in fact, some research suggests that
red green color vision deficiency has been selected for in
some animals.

Speaker 4 (38:41):
So what does.

Speaker 3 (38:43):
Color vision give us, in a word, information?

Speaker 1 (38:47):
Ah?

Speaker 3 (38:47):
Yeah, for those animals that have evolved color vision, whether
that's trichromacy, like most humans die, chromasy like some humans tetrachromasy. Also,
like some humans, being able to distinguish among colors gives
them valuable information that they can use to help them,
for example, evaluate a mate, forage for food, navigate or

(39:11):
identify predators or poisons. Initially, when color vision first arose,
maybe five hundred million years ago, it provided constancy in vision,
the ability to sense borders around different shapes, being able
to track that this dark red blob was the same
dark red blob in shade as it was in sun,

(39:34):
Like is this thing a thing or is it just
part of the background? If that makes sense, Because if
you cannot distinguish among colors whatsoever, just light and darkness,
and something that is dark moves into dark, how can
you sense it against the background. And so this ability
to see color to distinguish among not just light and dark,

(39:58):
but also colors have been helpful for the animals living
in shallow waters that had to deal with a lot
of shifting light and shadows. So skipping ahead millions of
years from that five hundred million years ago, okay, the
first mammals were thought to be nocturnal, which helped them
to avoid predators, so color vision wasn't as helpful in

(40:22):
dim light, and so some researchers think that these early
mammals lost this full color vision from their ancestors, and
then the re evolution quote unquote of color vision occurred
as some mammals shifted to diurnal life.

Speaker 4 (40:40):
Huh interesting, Yeah.

Speaker 3 (40:42):
And the true story is probably much more complicated and
complex than this, But as color vision continued to evolve
in different animal groups, it's unlikely that the same one
thing drove its development or refinement over those millions of years.
Vision was selected for within a species or a group

(41:02):
of animals because it helped out on multiple fronts, and
the utility of trichromatic color vision today, for instance, help
with foraging doesn't necessarily mean that foraging was a driver.

Speaker 4 (41:18):
Yeah, yeah, yeah, yeah.

Speaker 3 (41:20):
Going into what those possible drivers are for different animal
species or different animal groups. Is just a teeny tiny
bit outside of the scope for this particular episode. I mean,
there are textbooks about this, but for anyone who wants
to learn more, I will direct you to the incredible

(41:40):
book An Immense World by ed Young, which was featured
as one of the TPWKY Book series books. And there's
a fantastic chapter in an Immense World, although all the
chapters are fantastic on color vision in the animal world.
But for the purposes of this episode, just going to

(42:00):
stick with what we know or what we hypothesize about
color vision in primates, and last season in our Venomous
Snakes episode, I talked about the snake detection hypothesis, which
deals with many aspects of primate vision, not just color.
But today I'm just going to be talking about color
vision and how that came about in primates as opposed

(42:22):
to like long distance acuity, forward facing eyes, stuff like that.
Between twenty nine and forty three million years ago, something
pretty major happened for a particular group of primates. These
primates were di chromats, so they had just two cones
and they experienced the world in shades of blues and

(42:43):
yellows until one day, for one lineage, a gene was duplicated.
This happened to be the long opsin gene, and over
time one of those copies of the gene stayed the
same while the other accumulated mutations slightly here and there,
shifting so that it changed from the long opsin gene

(43:06):
to the medium opsin gene. To these primates, which were
the ancestors of old World primates, the world was no
longer just blues and yellows. Now there were also reds
and greens. What did these additional colors do for them?
One of the major hypotheses is that this new gene
allowed these primates to detect red or orange or yellow

(43:30):
fruits or new reddish slash purplish early leaves also a
good food source against the green backdrop of foliage, not
only helping them to find the fruit but also tell.

Speaker 4 (43:44):
When it was ripe.

Speaker 3 (43:45):
Why is ripe fruit often red probably evolved to help
with seed dispersal, so the fruit would turn red when
it was ripe, when the fruit was at its sugariest,
and when the seeds were well developed for survival. It's
a two way stream. At least for information. If color
is used as information, something has to be producing that

(44:06):
information for a reason, and something else has to be
receiving and processing that information.

Speaker 4 (44:13):
That is wild, right, Yeah, I.

Speaker 3 (44:17):
Don't know why it like hadn't occurred to me.

Speaker 4 (44:21):
Yeah, I remember talking a lot about this hypothesis in
that Evolution of Human Health class back when, but never
did we talk or did I think about the plant
side of it, right, And.

Speaker 3 (44:37):
I know that it's like results studies are mixed, or
at least like opinions are mixed, as per usual. But
I think in general, we it's easy to just think
of colors as existing statically, right, That is how they are.
That is what has happened, you know, for especially for

(45:00):
things that we interact with frequently, Like we can study
plumage and birds and stuff like that. But also when
we study plumage and birds, we're not seeing what the
birds see, so like you know, I.

Speaker 4 (45:13):
Mean it's the same with like colors of flowers compared
to what bees see or what birds see like or.

Speaker 3 (45:19):
Like a coral reef looks completely different to a fish.

Speaker 4 (45:23):
A fish, Oh my goodness, I know.

Speaker 3 (45:26):
It's this is why we were like struggling with this
episode because it's so easy to fall down so many
rabbit holes.

Speaker 4 (45:33):
Oh my gosh, you guys, this episode was the hardest
one I've ever researched. Yeah, it was. It was a
tough fie for sure.

Speaker 3 (45:39):
I felt like I had to relearn a lot of
things that I had or learned them for the first time.

Speaker 4 (45:46):
Well tell me what you learned.

Speaker 3 (45:47):
Yeah, okay, so information two way street at least. Okay,
But getting back to the foraging thing. Researchers have tested
this foraging hypothesis in primates with mixed results. Sometimes trichromats
are better at finding fruit, Sometimes there's no difference between
trichromats and die chromats, and sometimes die chromats outperform trichromats. Huh,

(46:12):
But I want to read you a quote about one
person's experience foraging for fruit who had a red green
color vision deficiency.

Speaker 4 (46:19):
Okay. Quote.

Speaker 3 (46:21):
He observed also that when young, other children could discern
cherries on a tree by some pretended difference of color,
though he could only distinguish them from the leaves by
their difference of size and shape. He observed also that
by means of this difference of color, they could see
the cherries at a greater distance than he could, though

(46:41):
he could see other objects at as great a distance
as they end quote.

Speaker 4 (46:47):
Interesting, isn't that kind of cool? Yeah?

Speaker 3 (46:51):
So there's another hypothesis as to why red green distinction
may have helped us, and I think it's I'm not
entire really sure, but I got the sense that it
has fallen out of favor, and that is that tri
chromacy evolved in primates as a way to help individuals
of the same species communicate with one another.

Speaker 4 (47:12):
So you know those.

Speaker 3 (47:13):
Japanese macaques, like the ones you see pictures of where
they're relaxing in hot springs. Tri chromacy may have helped
species like them to evaluate mate quality or competition or
aggression based on like the redness of their faces, And
for other species it could have been like the shade
of the pelt. But the big question for this would

(47:36):
be did tri chromasy evolve to help them distinguish red
traits in other individuals of the same species, or did
those red traits evolve once tri chromacyved.

Speaker 4 (47:49):
Chicken or egg which came first?

Speaker 3 (47:51):
Yeah, And it turns out to answer this chicken and
egg question, phylogenetic studies suggest that it's it's the latter
that these red traits be came more pronounced to once
trichromacy already existed.

Speaker 4 (48:03):
Interesting, Okay, yeah.

Speaker 3 (48:05):
Predator detection is yet another hypothesis, one that I touched
on in our snake episode, and there are studies suggesting
that trichromats are faster and more accurate when it comes
to detecting predators than di chromats. Full color vision would
have helped primates to distinguish a leopard from a green
background with dappled light, for instance. Studies today evaluating differences

(48:31):
in foraging, predator detection, and social group dynamics have found
support as well as a lack of support for each
of these hypotheses. And in general, we can't reliably say
what the primary evolutionary driver of a particular trait was
based on how it's used today, because it's not possible

(48:52):
to say with certainty whether that trait color vision evolved
because of something like foraging, or if it was later
opted or exploited by that thing, if that makes sense.
Throwing a wrench into this evolutionary story is that tri
chromatic color vision evolved independently in both Old and New
World primates, but in different ways. Stop it right, it's fascinating.

Speaker 4 (49:18):
Let's get into it. Okay.

Speaker 3 (49:20):
So that was just like this brief tour of the
evolutionary history and possible drivers of tri chromatic color vision
among Old World primates, nearly all of which have this
kind of color vision, all a result from that gene
duplication event with seemingly little variation.

Speaker 4 (49:37):
Okay.

Speaker 3 (49:38):
On the other hand, New World primates are just a
quote cornucopia of variation in color vision, as one paper
described it. And instead of that gene duplication, I have
an asterisk here because there's an exception. Color vision in
New World primates is determined by variations in that original gene.

(50:03):
So there wasn't a duplicated gene. It was just there
are just different versions of it. And since this gene
sits on the X chromosome, males within a New World
species have dichromasy, whereas most but not all, females have
tri chromasy.

Speaker 4 (50:21):
Oh okay. I had read that and I was like,
I don't understand, and I just moved on. I did
that a lot. Yeah, yeah, that's why females okay.

Speaker 3 (50:34):
Uh huh. And to make it even cooler, the different
forms of this gene also means that there are different
forms of dichromasy and tri chromasy depending on which versions
of the gene are inherited.

Speaker 4 (50:48):
Wow.

Speaker 3 (50:50):
The exception to this, the little asterisk that I mentioned
in New World monkeys are the howler monkeys who have
the duplicated gene. What so nearly all members of that
species are trichromatic.

Speaker 4 (51:06):
What right? This is cool, Aaron? Isn't that really cool? Yeah?

Speaker 3 (51:12):
I also will say that I found in papers, and
I'm not sure how well this is studied, but I
was curious about whether we have found similar rates or
the existence of period color vision deficiencies in like Old
World apes and primates, similar to the ways that we

(51:33):
see it in humans or the frequencies that we see
in humans. And it appears that we actually don't. The
humans seem to be the exception to this, where we
have a fairly high I know you'll talk about it
rate of color vision deficiencies what and so I don't
know why that is. And there aren't any hypotheses that
I found or explored, but I just thought that was

(51:55):
an interesting little side note.

Speaker 4 (51:58):
Wow.

Speaker 3 (51:59):
Yeah, Yeah, But I think in general, what I wanted
to do in this sort of evolutionary section was to
highlight just how much variation there is in color vision
in primates alone, not to mention the rest of the
animal kingdom.

Speaker 4 (52:16):
My goodness, And this is a.

Speaker 3 (52:18):
Point that ed Yong makes in his book that I
just absolutely loved and like continue to take to heart.
Which is that color vision or any sensory information or
sensory structure or physiology. It's not something to be ranked
in terms of what is better. Oh well, dogs have
better noses or you know, senses of smell or you know,

(52:40):
like that is not a very useful metric or way
to try to understand what another animal or another human
whatever experiences.

Speaker 4 (52:51):
Right.

Speaker 3 (52:52):
So, anyway, monochromacy, di chromasy, trichromacy, tetrachromacy, and beyond, all
of these different types of color vision have evolved and
have been selected for to help with gathering information. We're
not more advanced because we have trichromatic color vision like.

Speaker 4 (53:12):
It is just it's not. It's just more.

Speaker 3 (53:15):
Complicated than that, and being able to distinguish among colors
isn't always for the better, and there are trade offs
associated with the evolution of trichromatic color vision. An animal
can only take in and process so much sensory information
you can't max out all the boxes, and the least

(53:38):
useful sensory feature is usually the first to go. In
the case of trichromatic primates, the evolution of trichromacy seems
to have coincided with the loss of genes that are
associated with chemical sensing via smell, probably for pheromones, and
so when primates evolved red green color, they lessened their

(54:01):
reliance on this other form of chemical information. And so
I think again, this is just to say that we
have a tendency to place humans at the pinnacle of
evolutionary achievement without considering the benefit of other strategies. And
this failure of imagination has led us to make some

(54:22):
pretty big assumptions about other animals, like how we talked
about earlier, how we thought that fish didn't see color
for decades, where dogs couldn't see color at all.

Speaker 4 (54:32):
And it has also led us to.

Speaker 3 (54:34):
Create a world where it can be difficult to navigate
if you don't have full color vision, which brings me
to the other part of this history section. How did
we learn about color vision deficiency in human's part? Of course,
I have to begin with a quote and air and

(54:56):
bear with me. It is probably the longest quote I
have ever read outside of like a first hand account. Ooh, okay, okay,
but it's worth it, I swear, okay, all right, get
ready quote. It has been observed that our ideas of colors, sounds, taste,
et cetera, excited by the same object, may be very

(55:17):
different in themselves without our being aware of it, and
that we may nevertheless converse intelligibly concerning such objects as
if we were certain the impressions made by them on
our minds were exactly similar. I was always of opinion,
though I might not often mention it, that several colors
were injudiciously named. The term pink in reference to the

(55:41):
flower of that name seemed proper enough, but when the
term red was substituted for pink, I thought it highly improper.
It should have been blue, in my apprehension, as pink
and blue appear to me very nearly allied, whilst pink
and red have scarcely any relation. Since the year seventeen nine,
the occasional study of botany obliged me to attend more

(56:03):
to colors than before. With respect to colors that were white, yellow,
or green. I readily assented to the appropriate term blue. Purple, pink,
and crimson appeared rather less distinguishable, being, according to my idea,
all referable to blue. I was never convinced of a

(56:23):
peculiarity in my vision till I accidentally observed the color
of the geranium zonale by candle light in the autumn
of seventeen ninety two. The flower was pink, but it
appeared to me almost an exact sky blue by day.
In candle light, however, it was astonishingly changed, not having

(56:44):
then any blue in it, but being what I called red,
a color which forms a striking contrast to blue. I
requested some of my friends to observe the phenomenon, when
I was surprised to find they all agreed that the
color was not materially different from what was by daylight,
except my brother, who saw it in the same light

(57:04):
as myself. This observation clearly proved that my vision was
not like that of other persons, and at the same
time that the difference between daylight and candlelight on some
colors was indefinitely more perceptible to me than to others.

Speaker 4 (57:23):
I love that so much, Aaron.

Speaker 3 (57:27):
Right, do you see why I had to do the
whole thing.

Speaker 4 (57:32):
Yes, okay, good.

Speaker 3 (57:34):
I was like, gosh, this is really long as I'm
reading it.

Speaker 4 (57:37):
Oh, but it's so good because it also do you
know what that tells you he's using as rods that
we ignored. Yes, I know. Rod's become more important when
you don't have as many cones.

Speaker 3 (57:49):
Yes, it is so interesting. I loved it so much,
and it's really important for a number of reasons. But first,
that quote was from John Daon in his seventeen ninety
four treatise titled Extraordinary Facts relating to the Vision of Colors.
And it's great for a few reasons, right. Number one,

(58:12):
it's just such a great systematic retelling of his thought
process of exactly when he realized how he realized everything
about it. And number two he mentioned his brother also
experienced this, which is really good, really interesting. And number three,
it is, as far as we know, the first scientific

(58:35):
description of color vision deficiency.

Speaker 4 (58:38):
Wow.

Speaker 3 (58:39):
In honor of his observation, color vision deficiency was and
sometimes still is called Daltonism.

Speaker 4 (58:46):
Wow.

Speaker 3 (58:48):
But seventeen ninety four, Like, doesn't that seem recent?

Speaker 4 (58:56):
I don't know how to gauge it.

Speaker 3 (58:58):
Aaron I know, I know, I mean, I fully expected
to find like a long list of historical accounts going
back hundreds or maybe even thousands of years hinting at
color vision deficiency.

Speaker 5 (59:12):
But no.

Speaker 3 (59:13):
And I will say that, like there are mentions of
confusion in color vision that were it like it was
seemed fairly well known about, or at least enough so
for like King George the Third to make some comment
about it at a dinner in seventeen eighty five, like
some people have an ear for music, some people don't,

(59:35):
some people have an eye for colors, some people don't.

Speaker 4 (59:38):
You know, that kind of thing. And there was.

Speaker 3 (59:40):
Also a reference to it in a German medical science
magazine and also other scattered references in the seventeen hundreds.
But Dalton really seems to be the first to have
written about it scientifically, like with an analytical approach. And
I don't know, like it does seem recent. But at

(01:00:04):
the same time, in a way it does make sense
considering that color doesn't seem subjective. It seems like it
seems like inherent properties of objects. You learn your colors
at an early age. If you confuse colors, it's an
easier leap to think that there's something wrong with your

(01:00:26):
vision in terms of acuity, like your site rather than
your perception. And you know, like I kind of already
mentioned as a species in general, we're not great at
imagining the world as it might be perceived by other species.

Speaker 4 (01:00:42):
Let alone other humans. I feel like sometimes, and so.

Speaker 3 (01:00:46):
It would take a really keen observer to question whether
color is truly objective and then also have the opportunity
to publish those observations. Yeah, yeah, happened when it happened,
and when it happened. Dalton hypothesized in this treatise that

(01:01:08):
his and his brother's color vision deficiency was caused by
the vitreous humor of their eyes being tinted blue, making
it absorb longer wavelengths.

Speaker 4 (01:01:19):
Huh. Yeah.

Speaker 3 (01:01:21):
He requested that after his death his eyes be tested
to confirm his hypothesis, and so the day after he
died July twenty eighth, eighteen forty four, that's exactly what
was done. Only the person performing this autopsy found no
support for Dalton's hypothesis. The vitreous humor not tinted.

Speaker 4 (01:01:43):
I don't have the slightest idea how you would even
do that.

Speaker 3 (01:01:47):
That a mixt Wow, I'll include the paper that that
mentions this goes into more detail about it.

Speaker 4 (01:01:56):
Okay, okay, okay cool.

Speaker 3 (01:01:58):
The alternative hypothesis was that it came from a cerebral anomaly,
like the part of your brain that perceives color was
somehow different, but that also didn't hold up.

Speaker 4 (01:02:11):
Yeah.

Speaker 3 (01:02:13):
The explanation that is generally accepted today for most cases
of color vision deficiency was actually first proposed in seventeen
eighty one by a mysterious person named Giro's von Gentili.
Apparently no one knows anything about who this person actually was,
or whether that was like a real name or just

(01:02:35):
a pen name. What he's called like an obscure mysterious figure.

Speaker 4 (01:02:39):
WHOA Yeah, I hope someone calls me that someday obscure
and mysterious.

Speaker 3 (01:02:49):
That's hilarious. And so this von Gentilly guy wrote in
that German science magazine that I had mentioned that he
thought that color vision efficiency occurred if one or two
of the three kinds of quote unquote molecules or membranes
in the retina was not functional, either paralyzed or constitutionally overactive.

Speaker 4 (01:03:14):
It's interesting that they seem to have known that there
were like three things involved.

Speaker 3 (01:03:22):
Yeah, well, okay, and so this is one of the
areas that I did not get into, which is like
Newton and color theory and oh my god, you know
light spectrum, you know, like all of that, and I
was just like, I don't know how to even begin
to do it talk about that or yeah, and so

(01:03:43):
I wonder whether that was coincided with sort of the
development of some of those ideas around what color, what
the visible spectrum of light is?

Speaker 4 (01:03:53):
Okay, okay, that makes sense, and so.

Speaker 3 (01:03:55):
Like how you combine how many colors do you need
to combine in order to make all the colors that
we see?

Speaker 4 (01:04:01):
Ray ray ray ray ray? Okay?

Speaker 3 (01:04:02):
Yeah, yeah, I don't know, that's my guess.

Speaker 4 (01:04:04):
Yeah.

Speaker 3 (01:04:05):
And so then after this Von Gentilly, it's it's unclear
whether his idea gained traction then or we just only
know about it in retrospect. But it's possible that British
polymath Thomas Young stumbled across it, and like Thomas Young
did one bajillion things. He proposed the wave theory of light.

(01:04:28):
He helped to translate the Rosetta stone. He also right,
he also further developed this hypothesis about color perception, suggesting
that it was due to the presence of three kinds
of nerve fibers in the retina.

Speaker 4 (01:04:43):
Okay, okay, yeah.

Speaker 3 (01:04:45):
And over time, this framework for how color vision worked
via cones and rods was refined with anatomical studies, molecular studies,
advancements in physics, and just the growth of the field
of vision science.

Speaker 4 (01:04:59):
And in the.

Speaker 3 (01:05:00):
Nineteen nineties, the nature of Dalton's color vision deficiency was
finally made clear when the Manchester Literary and Philosophical Society
granted permission to a few scientists to run some tests
on the remnants of Dalton's eyeballs. Oh my goodness, right,
oh amazing God. I was so worried to drop that
little tube. I'd be like God. But they confirmed that

(01:05:25):
Dalton lacked the middle photopigment cone cell, making him a deuteroope.

Speaker 4 (01:05:30):
Wow closed, Yeah, love it.

Speaker 3 (01:05:36):
Dalton may not have been the first person to notice
that the way he saw colors was not the same
as most other people. I mean, he was definitely not
the first. We've kind of established that, but his careful
scientific analysis of what he suspected was going on caught
the attention of other scientists and For years, color vision

(01:05:56):
deficiency was seen as kind of ann just this curious
thing that some people had, that some people were born
with or acquired later in life, and it certainly prompted
more research into the structure and function of the eye
and how vision worked, as well as philosophical musings over

(01:06:17):
how we are each in our own little world and
can never truly experience life from someone else's perspective.

Speaker 4 (01:06:24):
Oh my goodness.

Speaker 3 (01:06:26):
But color vision deficiency took on a practical importance starting
in the second half of the eighteen hundreds, coinciding with
the rise of industrial transportation ooh, the so called Golden
Age of rail travel, growth in maritime travel, and of
course automobiles and airplanes. With all of these forms of travel,

(01:06:48):
people had to use certain signals to determine when it
was safe to proceed, when to stop, when to proceed
with caution, when to back up, and this signaling was
done primarily with colors. Suddenly, color vision deficiency was not
just a medical curiosity, but, according to one physician in
eighteen eighty quote, daltonism can be cause of discussions, arguments, battles,

(01:07:14):
industrial and commercial losses, dreadful accidents, and irreparable miseries. Wow, yeah,
strong words. And this fear was realized in November eighteen
seventy five when two express trains on a single track,
one heading from Stockholm to Malmo and the other from

(01:07:37):
Malma to Stockholm collided headfirst in the middle of the night.
Nine people were killed in this collision, and about a
year after the accident, when they were trying to like
figure out what had happened, who was at fault, how
can we prevent this from happening again, an ophthalmologist named

(01:07:58):
freethiof I don't know how you say at Holmgren suggested
that either the engineer of the northbound train or his
oiler was color deficient and misinterpreted the signals leading to
the crash. Neither of them could be tested because they
had both died in the accident, but this didn't stop

(01:08:18):
the speculation, and the lager Lunda collision, as it was called,
has been referenced over and over again as a case
study of the tragedies that could result from having someone
with color vision deficiency in charge of transportation or in
charge of interpreting those signals.

Speaker 4 (01:08:36):
So, just to be clear, yeah, that was just one
guy's idea that this is what happened. Yeah, but nobody
knows for sure.

Speaker 3 (01:08:45):
No, So okay, there is a paper from twenty twelve
that goes into it's an incredible in depth analysis of
like the different trains, how the lights would have worked.
And they did this in depth, like super detailed examination
of this crash, and they concluded that even if color

(01:09:07):
deficiency was a factor, which it's not clear that it
was at all, it was far from being the only
factor responsible, and probably there was some sort of like
problem with one of the trains themselves. Okay, so but
despite this, yeah, this was like a real catalyst, the
lager Lunda collision. You'll find it in so many references

(01:09:29):
to anything related to color vision deficiency in industry and regulations.
It was this huge catalyst for the introduction of color
vision screening and restrictions on what jobs in the transport
industry that people with color vision deficiency could hold. And
most of the time it was just like, nope, sorry,

(01:09:50):
we have to perform these tests beforehand, and I just
I think that's I'm not an expert in anything related
to industry and and transportation and stuff like that, but
like it just seems like another solution could be to
change the signals.

Speaker 4 (01:10:09):
Right, Like, I don't know. Maybe that's a very naive
thing to say, but I mean, I don't know, someone
someone tell us otherwise, Yeah.

Speaker 3 (01:10:20):
Like maybe there's I don't I don't know, yeah no,
but but yeah, this was like a really formative moment.
And one of the things that they used to test
people who were applying for these jobs was the home
gren named after that guy wool Strands test, where you
had to match woll of different colors. And I actually

(01:10:43):
couldn't get a very good sense of how many train
or maritime or aviation accidents were definitively attributed to someone
misreading the signals due to color vision deficiency. I think
it did happen, Like I think there are at least
a few confirmed cases of that happening, but even the

(01:11:05):
ones where it was just pure speculation absolutely captured the
public's imagination and fear and led to these regulations being
quite strict for a very long time. And only recently
have some of these restrictions become a little more relaxed
or more specific. And that's part of that is a

(01:11:27):
result of us learning more about the different types of
color vision deficiency and being able to test for those differences, using,
for instance, those Ishihara tests, which I'm sure many of
you are familiar with. You know, where it's like that
circle of bubbles and some of the bubbles are a
different color, and they make up the shape of a number,
and you if you can determine what that number is,

(01:11:49):
then you don't have color vision deficiency of that particular kind,
or something to that effect.

Speaker 4 (01:11:55):
I just made my child take that test.

Speaker 3 (01:11:58):
I've taken that test a number of times.

Speaker 4 (01:12:00):
Me too, I took it at the same time.

Speaker 3 (01:12:05):
But anyway, since color vision was first put out there
into the scientific world, we've come a really long way
towards understanding the mechanisms and genetics of color vision. And
we finally, i think, at least in small ways, have
started to move away from exclusionary practices like limiting what

(01:12:26):
professions you can have and making an effort to be
more inclusive, recognizing that we may not all experience the
world in the same exact way. And maybe that means
something like a package in r that gives you a
color palette for figures that's quote unquote colorblind safe, or

(01:12:49):
maybe that means changing the types of signals used in
transport so that people who have color vision deficiency can
still utilize those signals, or maybe that means creating glasses
or other methods to allow us to distinguish a wider
spectrum of colors.

Speaker 4 (01:13:06):
So, Aaron, a.

Speaker 3 (01:13:07):
Little bit of an abrupt transition. But what can you
tell me about these glasses and other aspects of color
vision deficiency today?

Speaker 4 (01:13:18):
I can do my best to tell you something right
after this break. Pretty much every single paper that I

(01:13:56):
read sites that when it comes to congenital color vision deficiency,
which again is what we're focusing on, the prevalence overall
is eight percent in males and zero point five percent
in females. I saw those.

Speaker 3 (01:14:14):
Numbers over and over again, and I wasn't even looking
for them.

Speaker 4 (01:14:18):
Over and over and over and over and over. I
have no idea where these numbers came from. I don't
know if they're real. I mean, I guess they're real
because they're in every single paper. One paper that I
read said that this is true in people of Northern
European descent, but it varies across the globe. But I

(01:14:41):
couldn't find data like comparing different regions. So but yeah,
that's the numbers that I have Okay, red green color
vision deficiencies, of course, far more common overall. Interestingly, the
deuteronomalies and deuteronopoia are more common than proteonomaly and protinopia.

(01:15:08):
I don't know why. And then I don't even have
numbers for things like the monochromasies or tritonomaly because they're
just that rare. Uh huh. So that's epidemiology. I mean,
it's pretty pretty straightforward.

Speaker 3 (01:15:27):
Okay, Okay, I don't know what I expected, but yeah,
but there it.

Speaker 4 (01:15:33):
Is, there it is. It just means we can spend
some more time talking about like what's being done or
what research are people doing or whatever.

Speaker 3 (01:15:45):
These glasses, Aaron, I have to know, like what do
they do? You see these amazing videos? And then I'm like,
is the hype real? And it doesn't work for some people?
How does it work?

Speaker 1 (01:15:55):
Yeah?

Speaker 4 (01:15:56):
Why doesn't it work? Why does it work? So? I
guess which glasses are thinking about, like the en chroma glasses.
I suppose any of them? Yeah, so yeah, let's talk
about it. There exist things like tinted lenses that are
just literally tinted lenses that you can wear over one
eye or both eyes that in some studies help some

(01:16:17):
people with some kinds of color vision deficiencies. There are
other like these lens filter type things which come in
the form of glasses commonly called en chroma filters. They
have a lot of theoretical usefulness because what they do,
which is fascinating and way above my head, is that

(01:16:40):
they modify the perceived wavelength of light. So something aarin
like your red sweatshirt that you're wearing, the wavelength of
light that's coming off of that into my eyes with
this filter would be shifted such that if my cones
are also shifted, I might better be able to distinguish
it as read. I guess, but in the papers that

(01:17:04):
I read at least, there's pretty limited evidence of their
actual effect in terms of color discrimination in general, at
least in the papers that I read. Both the tinted
glasses as well as these various types of filter lens
glasses as well as some experimental contact lenses, which is interesting,

(01:17:25):
can show some increases in color perception and contrast enhancement
in nature, like when given natural scenes to look at,
but they haven't yet shown to make it to the
level of like someone being able to pass an Issuejara
test who couldn't before. Okay, at least from what.

Speaker 3 (01:17:45):
I read, that's very interesting.

Speaker 4 (01:17:51):
Now even more interesting, or I think even more interesting,
is that it is also theoretically at least possible to
try and treat color vision deficiency with gene therapy, given
that most of the time what we talked about today
are genetic disorders. Yeah, but there are a lot of

(01:18:12):
possible individual gene mutations. But it's also maybe not necessary
to correct the exact gene mutation in order to restore
typical trichromatic color vision, right, because all you would have
to do is restore a fully functional opsin gene, for example,

(01:18:32):
with the expected sensitivity right, an m opsin if you're
missing that one, or an l opsin if you're missing
that one. Right. But it's a lot more complicated in that.
I will say that a number of studies have done
this in mice as well as in some primates, and
they have shown that they can induce some trichromatic color

(01:18:55):
vision in mice and in primates that are missing it. Okay,
so it's possible, is at least the theory is solid.
We've done it in animals. But what's really interesting and
I think one of the things that makes the idea
of gene therapy really interesting is that not only does

(01:19:21):
it beg the questions around like the neural plasticity, Like
we talked about, can you restore trichromatic color vision in
someone whose eyes developed during embryologic development with only two
sets of cones? Can they still then be restored because

(01:19:44):
the cone cells are involved in again a lot more
than just color vision. So can we quote fix these
deficiencies by adding back those genes after this period of
development when these complex X neural circuits are being formed. Interesting? Okay,
so we can do it in animals at least in

(01:20:06):
a couple of studies, but we still don't know if
it's possible in humans.

Speaker 3 (01:20:11):
Interesting gene therapy. Gene therapy, I always love when we
talk about it, and then I'm always like, this is
a big thing.

Speaker 4 (01:20:19):
It is a big thing.

Speaker 3 (01:20:20):
There's a lot of especially implications and complications and question marks.

Speaker 4 (01:20:25):
Exactly. Yeah, I love it, But that Aaron is color
vision deficiencies and literally everything I know about them, you know.

Speaker 3 (01:20:37):
I think that as difficult as it felt sometimes to
kind of like hone in on what we wanted to
talk about, I really feel like this was a great
one to do, and I learned so much about color
vision deficiency.

Speaker 4 (01:20:53):
Thanks same, same, Yeah, and about just like color vision
in general. It Yeah.

Speaker 3 (01:21:01):
And if listeners you have favorite color vision facts about
animals or about humans, or about anything, send them our away.

Speaker 4 (01:21:09):
I want to hear them.

Speaker 1 (01:21:11):
Yeah.

Speaker 3 (01:21:13):
Speaking of learning more and knowing more, I have many
things to shout out today. First, I'm going to shout
out some of the resources that I used for this,
just a few of them, because there were a lot.
On the evolutionary side of things. There are so many
papers by a really prominent researcher in the field, Gerald Jacobs,
about the evolution of color vision in primates and animals

(01:21:38):
in general.

Speaker 4 (01:21:39):
There is also a.

Speaker 3 (01:21:40):
Great paper called the Causes and Consequences of Color Vision
by Girl and Morris from two thousand and eight. And
for the history of color blindness itself, there's a book
called The History of Color Blindness by Philippe Lanthony. And
I did not mention this at all. I completely forgot
to mention this or include this of my notes. But

(01:22:01):
one of the really interesting things that I came across
was the discussion of color vision deficiency in art and
so being able to look at you know, like art
history in different art movements and detecting what artists may
have had color vision deficiency based on how they represented
the world in the context of whatever art movement was

(01:22:25):
popular at the time. So if it was like during
the time when people were painting literally the world as
they perceived it, then you might be able to tell
more than if it was, you know, at a time
when it was more I don't know up in the air,
I don't know any thinking about art history. Yeah, abstract impressionist,
who knows. But there's that is like a really cool

(01:22:46):
So there's a paper by Marmore and Lanthony from two
thousand and one called the Dilemma of Color Deficiency in Art.
And on that note, further reading An Immense World by Edyong,
I'll shout it out again. It's phenomenal. It'll change the
way you perceive the world. And then there are two
books that I did not read for this. One is

(01:23:07):
called The Island of the Color Blind by Oliver Sacks,
and this is about a group of people that have
a chromatopsia. And then there is a book that I
read years ago called Through the Language Glass Why the
World Looks Different in Other Languages by Guy Dutcher, And
there is a chapter in this book at least one

(01:23:29):
on the evolution of language as it pertains to color
terminology that I found fascinating.

Speaker 4 (01:23:36):
I shockingly had less papers for this episode than usual
because the papers are incredibly detailed. Shout out to Wikipedia
for helping me understand the papers, so shout out there, Okay,
But the papers that were actually incredibly detailed once I
understood them were a two thousand and three paper from

(01:23:59):
Annual Review of Neuroscience just called color Vision that was
really helpful in understanding how that works. And then a
paper from the Journal I from twenty ten called color
Vision Deficiency. Those I think were the two that I
used the most heavily. But I have so many more
on the biology of this, on the lenses and glasses,

(01:24:24):
and gene therapy, on tetrachromacy and all of that. You
can find the sources from this episode and every one
of our episodes on our website, This Podcast will Kill
You dot Com under the episodes tab check it out.

Speaker 3 (01:24:38):
Thank you again to Kristin for sharing your story with us.
We appreciate it so much.

Speaker 4 (01:24:43):
Yeah, we do. Thank you to Bloodmobile for providing the
music for this episode and everyone of our episodes.

Speaker 3 (01:24:50):
Thank you to Leana Scolacci for our amazing audio mixing and.

Speaker 4 (01:24:54):
To Exactly Write Network.

Speaker 3 (01:24:56):
And to you listeners, thank you. We hope that you
you enjoyed this episode, found it interesting, learned something, have
more facts to share, have questions anything.

Speaker 4 (01:25:10):
And a special shout out to our patrons. Thank you
so so much for your support. Yeah, we really appreciate it.

Speaker 3 (01:25:17):
Okay, until next time, wash your hands

Speaker 4 (01:25:20):
You filthy animals.
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