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0:55

Infamous International, The Pink Panther's

0:57

Story takes you into the world of Serbia's

1:00

most infamous jewel thieves. Infamous

1:02

International, The Pink Panther's Story premieres

1:05

Thursday, September 14 on exactly

1:07

right. Listen on Amazon Music, Apple

1:09

Podcasts, or wherever you get your podcasts.

1:12

So I guess it all started really before

1:15

I was ever born. When

1:17

my parents were dating, it sort of naturally

1:19

came up that my dad has color vision deficiency.

1:22

My mom at the time acknowledged

1:25

that she had experience with that because her

1:27

dad has color vision deficiency as

1:30

well. And at the time, they really didn't think too

1:32

much of it. It was something cool they had in common

1:34

and really didn't devote a lot of consideration to

1:37

it. But eventually they got married and

1:39

they had my brother and then they had me. So

1:42

when my brother was, I

1:44

want to say a toddler, he started displaying

1:47

some patterns that would be consistent with color vision

1:49

deficiency. Funny enough,

1:51

my mom is an optometrist, so she's really

1:53

well versed in how this works.

1:55

So she knew that this

1:58

was a consideration.

1:59

they went and they had my brother tested, and

2:02

it turns out he had color vision deficiency. Now

2:04

he's a couple years older than I am, and

2:07

so I have two X chromosomes. It's not

2:09

totally normal for people like me to have this,

2:11

and so my parents were really not concerned until

2:14

I started displaying those same patterns, and that's

2:16

when it all finally clicked that

2:18

my dad having color vision deficiency,

2:21

my grandpa having color vision deficiency,

2:25

pretty much created this scenario that

2:27

normally doesn't occur until your ninth

2:29

grade biology class, where

2:32

I had the possibility to be a female

2:34

with color vision deficiency.

2:37

So growing up, it was a household of my

2:39

dad, my mom, my brother, and myself,

2:41

so actually color vision deficiency was

2:44

the quote unquote normal way to be.

2:47

So we all have Deuter Anomaly, so that's

2:50

the red-green color vision deficiency, and

2:52

so it's the most common, I think,

2:55

of all of them. The three of us all

2:57

have it. My mom doesn't, but she's an optometrist,

2:59

so this is always the ideal scenario, so there's

3:01

going to be one person in your house that doesn't see the

3:03

way you all do. It's kind

3:05

of nice that she's at least an expert in this

3:08

situation. I would say growing

3:10

up, it was never really a concern. It

3:12

maybe came up on occasion, but my parents

3:14

were very proactive about letting my teachers

3:16

know that this was just something we all had,

3:19

but one of the best parts of being a female

3:21

with color vision deficiency is that it's on both sides

3:23

of my family, so on my mom's side, I have a bunch

3:25

of cousins, and they have it too, and

3:27

so we all like to say we're better

3:30

than the other cousins, or whatever it is you

3:32

do in families. And then on my

3:34

dad's side, he's somewhat unique,

3:36

but his maternal grandfather, so

3:38

my great-grandpa, lived a very long

3:41

life, and we all had the opportunity to get to know him.

3:43

So it was this big

3:45

thing that we were all kind of proud to have. So

3:47

one of the stories that we were always told about my

3:49

great-grandpa is that in World War II,

3:52

when they were trying to get people to

3:54

enlist, he volunteered early, hoping

3:57

they would look the other way and allow him to fly planes.

3:59

They definitely did not allow him to fly

4:02

planes, but something

4:04

they always tell us is a supposed

4:06

advantage to having color vision deficiency is

4:08

that camouflage

4:09

doesn't work as well.

4:11

And so one of the things they had him doing

4:13

was trying to spot really any

4:15

sort of activity that other members

4:18

of his squadron really couldn't see. And so

4:19

he was the designated see

4:22

the camouflage guy.

4:24

This is always just sort of an interesting story that

4:26

was told to us, but I do want to take

4:28

it with a grain of salt because I never actually heard it from my

4:30

great grandpa himself. He did not like

4:32

to talk about his experiences during the war,

4:34

but it was always kind of a funny

4:36

side note. Growing up

4:39

with color vision deficiency in my family, again,

4:41

it was so normal, but then

4:42

getting out into the supposed

4:44

real world now that I've moved out on to

4:46

college and everything,

4:48

there have been a couple of things that are very challenging.

4:50

So I work, I'm working on my PhD

4:52

and we do nutritional immunology and

4:55

microbiology. And so a lot

4:57

of that encompasses the microbiome research and

5:00

heat maps are a big part of it and most heat maps

5:02

usually go from red to green, but being red,

5:04

green colorblind, that's really challenging.

5:07

And you can't be the person at the conference who stands

5:09

up and can't read

5:11

their own data. So my really

5:13

awesome collaborators actually came up with

5:16

a new color scheme that would work for me. And

5:20

according to everyone else, it's really, really ugly. I

5:22

think it goes from blue to black to yellow

5:25

and I can see it really

5:27

well, but I've definitely been at conferences or

5:29

given talks in my department where people

5:31

have actually said, that's

5:33

all great, but your colors are ugly

5:35

or these are really, really bad. And that puts you in

5:37

this really awkward situation where you have to stand up in

5:39

front of all these people and say, yes,

5:41

I understand they might look bad, but those colors

5:43

are for me. They're not for you. And

5:46

so it does end up becoming sort of an awkward

5:48

teachable moment where they have

5:50

to acknowledge that there are people in

5:52

the room and there's a good likelihood that there are people

5:54

in the room who just don't see colors the same way

5:56

as you, but then also having to

5:58

stand up and say. yes, I

6:01

am a female, I'm colorblind, and then that

6:03

starts a whole different conversation that isn't

6:05

about the science I just presented, it's about

6:07

me. And then the

6:09

other biggest challenge I would say is

6:11

that because it's not likely for

6:14

females to be colorblind or to

6:16

have this sort of color vision deficiency is

6:18

that some people were taught most

6:21

simplistically that it's impossible. So

6:24

it's not that they were told it's unlikely,

6:26

they were just told by some teacher along

6:28

the way that it was totally impossible.

6:31

And so when you tell them this about yourself, they

6:34

look at you funny, they come at you as sort of a negative

6:36

approach, like you must be lying

6:38

to get attention, you're making this up.

6:41

And so that always is really a challenge

6:44

because it's trying to overcome that impression

6:46

that didn't really need to be an impression in the first

6:48

place. And so all of that has

6:51

been somewhat of a challenge, but ultimately,

6:53

I think the best thing that comes out of it is

6:55

just being part of this community.

6:58

I think it's really funny when you catch people off

7:00

guard with it, because it's not you can't look at

7:02

someone and see this. So it's nice

7:04

to get a few jokes in there. A

7:06

lot of times I'll tell my friends that my favorite M&Ms

7:09

are the gray kind, even though I can see those

7:11

colors, it's still just it always catches

7:13

people off guard. I think my biggest

7:15

thing that I get asked is if I

7:17

would ever consider using those color vision correction

7:19

lenses. And my biggest answer is

7:21

a resounding no. I was born this

7:24

way. I've always seen the world this way. I

7:26

don't want anything different. The

7:28

glasses aren't guaranteed to work. And

7:30

so I don't want to run the risk of seeing

7:33

things differently and ending up unhappy.

7:36

So I would say that's kind

7:38

of the main part of my story is that I just love

7:41

being this way. It's a challenge most

7:43

times, but it's a lot of fun when

7:46

you can make it fun and just

7:48

proves that my brothers were always

7:51

wrong when they said I was adopted.

7:53

So yeah,

7:55

I think that's pretty much the main part of my story.

7:58

You

8:30

You

8:42

Thank you so much Kristen for sharing

8:44

your story with us we really appreciate

8:46

it Hi, I'm Erin

8:49

Welsh and I'm Erin almond update

8:51

and this is this podcast will kill you

8:53

welcome today We're talking about

8:56

the whole Back drum

8:58

get it color vision

9:00

deficiencies It actually

9:02

took me a second to get it. I think I'm too close

9:05

to this thing, Erin That's

9:08

the only joke I have for the whole episode so

9:11

yeah, I don't think I have any jokes which is really Surprising

9:14

again. I was like too much in the

9:17

weeds. I lost the forest for

9:19

the trees. Yeah. Yeah, we're

9:21

really selling it Yeah, no, but no I

9:23

mean that's the thing though that there is just

9:26

so much to go into with this

9:28

and it's all really interesting like honestly,

9:31

it's like you could throw a dart dart

9:33

board and Find a thousand

9:36

interesting things about one aspect

9:38

of the history or the biology of color

9:40

vision deficiencies So yeah, you

9:43

might have to open like no

9:45

less than 50 Wikipedia pages to

9:47

understand one paper I Know

9:50

I could not tell what was like on my chrome.

9:53

I was like, oh my gosh way

9:55

too many tabs deal

9:57

with this Well,

10:01

it's going to be a great episode. But before

10:03

we get into the meat of

10:05

it, it's quarantine time. It

10:08

is. What are we drinking this week? We're

10:11

drinking True Colors. And

10:13

I love this title because

10:16

is there any such thing as true

10:18

color?

10:19

That's that's how the song goes, right? I

10:22

see your true colors shining through. There you

10:24

go. That's why

10:26

I love you. Not going

10:28

to keep that in. What is

10:30

in True Colors?

10:33

In True Colors,

10:35

there's a fun little summary concoction.

10:38

It has basically as many colors as

10:40

we could try to fit in there, which

10:43

is not that many because I'm not a skilled layerer

10:46

when it comes to quarantine-y

10:48

making. But there's grenadine and

10:50

then there's orange juice and then there's blue

10:53

curacao and there's lime

10:55

juice and rum. Yum. It's

10:58

great. We'll post the full recipe

11:00

for that quarantini as well as our non-alcoholic

11:03

Plessy Burrito on our website, thispodcastwillkillyou.com.

11:06

We certainly will. On our website,

11:09

thispodcastwillkillyou.com, I'm going

11:11

to pull it up and just see what I can find

11:13

because, you know, it's my

11:16

brain has not been functioning

11:18

very well today. We've

11:20

got transcripts. We've got the sources

11:23

for each and every one of our episodes.

11:25

We've got a first-hand account form.

11:28

I don't think I've been saying that in past

11:30

episodes. We have

11:32

got links to bookshop.org, affiliate

11:35

account, Goodreads list, our merchandise

11:37

page, Music by Bloodmobile, Patreon,

11:40

lots of stuff. Check it out. It's good stuff.

11:43

With that,

11:44

shall we talk about color

11:47

vision deficiencies? I think we should.

11:49

Okay.

11:50

Right after this break.

11:53

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12:59

If you're a true crime fan, you know a lot

13:01

of stories come out of Florida, and unfortunately,

13:03

they sometimes involve alligators. But

13:05

more importantly, you know that things aren't always

13:08

what they seem. And all of these things are true

13:10

in the new season of Wondery's limited series,

13:12

"'Over My Dead Body' Gone Hunting."

13:15

Gone Hunting tells the story of Mike Williams,

13:17

who set off on a hunting trip in the swamps

13:19

of North Florida 23 years ago. He

13:22

planned on being back in time to celebrate his sixth

13:25

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13:27

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13:30

friends and loved ones feared that Mike had been killed

13:32

by alligators, and it would take over two decades

13:35

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13:37

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13:40

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13:43

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13:45

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13:47

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with your free trial at Wondery.com slash

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plus. Goodbye.

13:56

Thank

13:59

you. To

14:16

be able to talk about color vision

14:19

deficiencies, aka color

14:21

blindness, I think we first

14:23

have to understand at least a little

14:25

bit about color vision

14:28

itself, right? It's

14:31

easy, right? So simple

14:33

and straightforward to explain

14:35

on a podcast in under

14:37

two hours. Here we

14:39

go.

14:42

At the most basic

14:44

level,

14:45

just like bare bones in it, we

14:48

as humans are able to distinguish

14:51

between colors in the visible spectrum

14:54

because our brain can

14:57

compare information that it receives

15:00

from three different sets of

15:03

cells that contain photoreceptor

15:05

proteins in our eyes. I'm

15:08

going to go into a bit more detail about

15:10

how that process works. And

15:13

I think once we understand the really

15:15

bare basics of that process,

15:18

I think the many, many

15:20

ways in which this system can have

15:22

deficiencies, aka all

15:24

the variations of color vision deficiency,

15:28

become pretty obvious, or at least

15:30

relatively so, okay? So

15:34

going all the way back to the beginning of

15:36

time, kind of, light

15:40

exists as a spectrum.

15:42

I actually have no idea if that has anything to do with the beginning

15:44

of time, but anyway.

15:49

Light exists as a spectrum. There

15:51

is an infinite number of wavelengths

15:53

of light that exist from ultraviolet

15:55

to infrared, 400 to 800 nanometers. human

16:00

eyes have evolved to see a fairly

16:03

small portion of this spectrum

16:05

of light, visible light, ROYGBIV

16:08

in our rainbows. So

16:10

it goes like this. Light,

16:14

all of its various wavelengths, comes

16:17

into our eyeballs, travels

16:19

through our eye dew, and

16:22

hits onto our retina at the very, very

16:24

back of our eyes. And in

16:26

this retina, which is just the area in

16:28

our eye, there exists a whole

16:31

bunch of different cells that are full

16:33

of photoreceptor proteins. There

16:36

are two main types

16:37

of these photoreceptor cells, rods

16:40

and cones.

16:41

Rod cells express

16:43

a protein called rhodopsin. It mostly

16:46

helps us have vision in dim light.

16:49

So we get to ignore it for this episode. Okay?

16:52

Yay! Yay! So

16:54

I'm finding something. I'm not really marginally involved, etc.,

16:56

but for the purposes of today, rods

16:59

dim light. It's the cone cells

17:02

that allow us, as humans, color

17:04

vision. So these cone

17:07

cells, which are super densely

17:09

packed within our retina, come in

17:11

three different flavors. Or rather,

17:13

they express three different kinds

17:16

of opsins, which are these

17:18

photoreceptor proteins.

17:20

Each one of these opsins is

17:23

most sensitive, peak sensitive,

17:26

to a specific wavelength

17:28

of light.

17:29

Short, medium, and

17:31

long. Huh? Simple

17:34

enough.

17:34

Simple enough so far. So the short

17:37

wavelength sensitive opsin is also

17:39

called the blue cone. The

17:41

middle or medium wave sensitive opsin

17:44

is also called the green cone. And

17:46

the long wave sensitive opsin is called

17:49

the red cone, even though its

17:51

peak wavelength of absorption is actually

17:53

yellow, not red, but let's

17:56

ignore that and call it red. Yeah?

17:59

Great.

17:59

Yeah. So

18:01

the waves of light hit these photoreceptor

18:04

cells. They are absorbed

18:06

by these proteins. Very complex

18:09

chemistry happens. And

18:13

then those wavelengths, that

18:15

energy is translated into

18:18

electrical signals that travel

18:20

via our optic nerve to

18:23

a part in the middle of our brain in

18:25

our thalamus and then

18:27

to the primary visual cortex,

18:29

which is in the back, the occipital lobe of

18:31

our brain. And that's where all

18:34

of this visual information, everything

18:36

that we see, including color

18:39

information, is processed and

18:41

interpreted.

18:42

That is

18:43

the most basic way that we can explain

18:46

how color vision happens. The

18:50

short wavelengths, or blue-sensitive

18:52

cones, respond to

18:54

a much more discrete array

18:57

of wavelength of light. Like, if you look

18:59

at all of the spectra that they can absorb,

19:02

it's more offset. Whereas

19:04

the middle, green, and the long, red

19:07

wavelength cones have much more overlap

19:09

if you look at all the wavelengths that they're sensitive

19:11

to. But they all three

19:13

have different peaks. And this is

19:15

really important because none

19:18

of these cone cells alone

19:20

allow us to see or distinguish

19:23

colors on their own. Our brain

19:25

has to compare the information

19:27

that it gets, the signals, from each

19:30

of these different types of cells. And

19:32

in doing that, it's then able to differentiate

19:35

colors into our human trichromatic,

19:38

or three-color, vision system.

19:41

All right. You need at least two for comparison,

19:44

but three, you just get to compare

19:46

more and split up that spectrum more.

19:49

Exactly. And speaking

19:51

of only two, a lot of mammals, in

19:54

fact, have only two sets of cones.

19:56

That's why people say, like, dogs are colorblind.

19:59

They're not colorblind. blind but they only have two

20:01

sets of cones. Humans

20:03

and some primates have three. What's

20:06

very cool is that fish have like four

20:09

and some birds have five. Oh

20:11

yeah, it's like wild.

20:13

I know. And people thought that fish

20:16

were color blind forever.

20:18

Oh,

20:18

I know.

20:20

I

20:21

love it. I

20:22

mean, they can see UV for goodness

20:24

sake. Right. So many things can see

20:26

UV. I know, but not us. But I don't

20:29

know. Do you know, I learned it's mostly because of our

20:31

lens, not because our cones are not

20:33

sensitive in that wavelength. Oh,

20:36

interesting. Our lenses filter out

20:38

the UV and that's a

20:41

large part of why we can't see UV because

20:43

as like protect from damage.

20:45

Don't ask me about the why's, Erin.

20:49

It has nothing to do with this

20:51

episode. So I didn't dig into

20:53

it. Those are my favorite questions. I know.

20:56

I know. I know. Okay. But getting

20:58

back to it, obviously these cone

21:01

cells therefore are very

21:03

important. And in addition

21:06

to allowing us to perceive color vision,

21:09

cone cells also have a faster

21:11

response time to various

21:14

light stimuli. And they

21:16

help us a lot in fine detail perception

21:18

because they can perceive rapid changes in

21:21

images. So our cone cells are

21:23

very, very important to our

21:25

overall human vision system.

21:29

So color blindness or color

21:32

vision deficiency is what

21:34

happens when there are problems with

21:36

this visual processing. Because like

21:38

we said, you need all three of these cones

21:40

to be functioning and specifically

21:43

to be responding to the specific

21:46

wavelengths of light that we expect

21:49

to be able to distinguish the color spectrum

21:51

that we associate with human color

21:54

vision.

21:55

So

21:57

there's a lot of different ways that this can

21:59

go. little, shall we say, wonky?

22:05

The vast majority of color

22:07

vision deficiencies are congenital,

22:09

meaning they are inherited. They

22:11

are from mutations in

22:14

our genetic code. These mutations

22:16

can happen in genes that encode

22:18

for the cone cells or for the opsins

22:21

themselves, or

22:23

they can happen because of mutations in

22:26

the promoter regions for any of those genes,

22:28

like the regions that tell ourselves

22:30

to turn on or off the expression of

22:32

those genes. And

22:34

that process gets incredibly

22:37

complicated. So this is not by any

22:39

means a one gene,

22:42

one disease

22:43

type scenario that we have here. There

22:45

are many, many, many possible

22:48

mutations that result in a wide

22:50

variety of color vision deficiencies,

22:52

which we'll get into all of the details of. But

22:55

also, in addition to hereditary

22:58

color vision deficiency, is acquired

23:01

color vision deficiency. And that can

23:03

happen from damage to parts of our

23:05

eye during our lifetime. This

23:08

can happen from other

23:10

congenital diseases that aren't directly

23:12

related to, say, our cone cell function.

23:16

But it also can happen just from direct

23:18

damage from various eye illnesses.

23:22

For the purposes of this episode, because that's

23:25

a lot, I'm mostly

23:27

focusing on the congenital rather than

23:29

the acquired color vision deficiencies. But

23:32

I have a couple papers if people want to read more about

23:34

the other side. Let's

23:36

get into what does color vision deficiency

23:39

even mean. Yeah. Okay?

23:42

So the mildest forms

23:44

of

23:45

CVD, can you just call it that? Sure.

23:48

It's called anomalous trichromacy.

23:51

So humans are trichromatic.

23:54

So we have three sets of cones, three

23:56

peak wavelengths of color vision. A

23:59

lot of people with color vision deficiency

24:01

still have these three

24:04

separate sets of cones, three

24:06

separate sets of opsins, but

24:09

they have some kind of mutation

24:12

that results in a shifting of the

24:14

frame, if you will, the shifting

24:17

of that peak wavelength of sensitivity

24:20

so that there's more overlap between

24:23

the peaks. So that

24:25

the information that your brain gets

24:27

about those different wavelengths can't

24:30

be separated out as easily.

24:32

And so when you say that there's a shift,

24:35

is it they're moving closer

24:38

together and it's all three of them, or

24:40

is it just one that happens

24:42

to move closer to the other one?

24:44

Such a good question. There's three

24:47

different possibilities. Okay. So

24:49

in deuter anomaly, deuter,

24:52

you'll hear me say a lot. I

24:54

think it has something to do with green anyways. In

24:57

deuter anomaly, the middle

25:00

wavelength photo pigment is mutated

25:02

so that it's more similar to the long

25:05

wavelength photo pigment. So when

25:07

you should be able to absorb the peak

25:09

in the green zone, now that

25:12

specific cone looks a lot closer

25:14

to the red zone.

25:16

Okay.

25:16

Now, the opposite can happen as well.

25:19

In proton anomaly, the long

25:21

wavelength photo pigment, the red, is

25:24

mutated so that its peak is really

25:26

similar to the middle wavelength.

25:28

So what should be absorbed in the red

25:31

zone is shifted to the green.

25:34

Does

25:34

that kind of make sense?

25:36

Kind of. So in terms

25:39

of the result, what resolution

25:41

you lose in terms of color distinguishing

25:45

or the colors that

25:48

are typically called whatever colors

25:51

we have in our visual spectrum. You know what I mean?

25:54

Totally. So yeah, so you're

25:56

right. You lose some of that distinction.

25:58

So you're not able to. distinguish

26:00

between, say, certain hues or

26:03

between certain colors.

26:05

Okay.

26:06

And so, for deuter anomaly,

26:09

you lose the ability to distinguish between

26:12

reds and greens.

26:14

And for protanomaly, it's

26:17

also reds and greens, but it's slightly,

26:20

the shading is different? Mm-hmm. Okay.

26:23

That's exactly right. 100% right. Okay,

26:26

cool. And those, overall, are the two most common forms of color vision

26:28

deficiency. And so, that is not

26:31

caused by a lack of

26:33

opsin, but just a shift

26:35

in the opsin. Exactly. They

26:38

often result from unequal

26:40

recombination. So, what you get are

26:42

these hybrid gene formations,

26:45

the details of it. That's fascinating.

26:48

I know. I really

26:50

thought it was just an absence of a cone. Oh,

26:53

we're getting there. We're getting there. Okay.

26:55

We are nowhere near done. So,

26:57

there's also tritonomole,

27:00

which would change the peak of the blue

27:02

cone, right? Triton, because

27:04

we talked about the red cone and the green cone,

27:07

triton means blue. This

27:09

would change the peak of the blue cones.

27:11

Overall, this is

27:12

far less common. And if you

27:15

remember that I mentioned that the L

27:17

and the M have a lot more

27:19

overlap to begin with. Right. Tritonomole

27:22

alone may not

27:24

result in that big of a deficiency,

27:27

depending on how much it's shifted, if that makes

27:29

sense. Right. Right.

27:32

Yes. Now,

27:32

overall, those three types, again,

27:35

are called anomalous trichromacy. You still

27:37

have all three cones. They usually

27:39

result in milder color vision

27:41

loss, but there's a lot of variation

27:44

in the ability to distinguish

27:46

between shades and colors.

27:49

Now,

27:50

then we move on to dichromacy.

27:53

You can imagine this means two sets

27:56

of cones. This is obviously more

27:58

severe and means that you're having a very long time. having loss

28:00

of function of one of the cone types

28:02

entirely, either red, which is called

28:05

protonopia, green, which

28:07

is called deuteronopia,

28:09

or blue,

28:10

tritonopia. Here's

28:13

where it gets even more interesting though, is

28:15

that this can happen by

28:17

say the loss of one of these

28:20

genes entirely. And

28:22

for a long time it was thought that that is how

28:24

it happens. But it

28:26

can also happen by replacement

28:29

of one of these genes with

28:32

the equivalent, say for

28:34

example, during recombination, you end up with

28:36

two sets of M

28:39

genes instead of an M and

28:41

an L. Right, so you have like

28:44

two green cones, one

28:46

red cone. Beautiful,

28:49

exactly, and then one blue. Pretty

28:51

cool, right? Yeah. So

28:54

that is dichromacy. Then

28:56

there is the most severe form of

28:58

color vision loss, and that is monochromacy,

29:01

aka the complete absence of

29:03

color discrimination. Because like we said,

29:05

you have to be able to compare to

29:08

be able to distinguish between colors. This

29:11

is by far the most rare,

29:14

and there still are several different forms of this. Part

29:17

of the reason that true monochromacy

29:20

is so rare is because while

29:22

the M and the L cones, or

29:24

rather the genes that encode

29:27

the M and the L opsin, green

29:29

and red, they

29:31

sit right next to each other on the

29:34

X chromosome. But the

29:36

S cone, or the blue cone

29:39

opsin gene, is all the

29:41

way over on chromosome seven. It's nowhere

29:44

near M and L. So to

29:46

have true loss of all three

29:48

of these would be incredibly rare. There

29:52

is, however, a form of monochromacy

29:54

known as blue cone monochromacy,

29:57

or X-linked recessive in-

29:59

incomplete

30:00

A-chromatopsia, where you

30:03

have no functioning M or L-cones

30:05

and you only have functioning blue cones.

30:08

Okay. But,

30:11

remember that I mentioned that cones

30:13

are responsible for a lot more than just

30:16

color vision. They aid in our visual

30:18

acuity and things as well. So

30:21

when we get to the point of monochromases

30:23

and incomplete or even complete

30:26

A-chromatopsia, where we have like say no

30:28

functioning cones, you're not just

30:30

losing the ability to distinguish colors.

30:33

You're also losing a lot of visual

30:36

acuity. So people with monochromacy

30:39

or complete A-chromatopsia

30:41

would have significant overall

30:43

visual field deficits as well. But

30:47

if we kind of sum all of those

30:50

fancy words up, if

30:52

you hear the term red-green

30:54

color blindness, that

30:57

refers to any of those

30:59

different possible mechanisms of

31:01

the loss of distinction between red

31:04

and green. So red-green

31:06

color blindness includes deuteronomily,

31:09

protonomily, deuteranopia,

31:12

and protanopia. Okay. That

31:14

makes sense. Right. Because

31:16

whether we're talking about a functional loss

31:19

or just a shift in spectral sensitivity,

31:23

the end result is that distinguishing

31:25

the wavelengths of light that make

31:27

it into our eyes between red and

31:30

green becomes really difficult because

31:32

our brain essentially just doesn't receive

31:34

enough information to make those

31:36

comparisons and computations. And

31:41

all four of those disorders are

31:44

X-linked recessive traits.

31:47

So the presence in general of

31:50

one X chromosome with a

31:52

functioning M and a functioning L

31:55

gene is enough to result

31:57

in quote-unquote normal color-based

32:00

vision discrimination with

32:03

the exception, dun dun dun dun, that

32:06

because of X inactivation,

32:08

which we talked about all the way back in

32:11

our Turner syndrome episode, but

32:14

basically what happens when people have

32:16

two X chromosomes instead of just

32:18

one is that one of those X's

32:21

gets turned off. And because

32:23

that can happen relatively randomly

32:25

sometimes, it's also very

32:27

possible to have color vision

32:30

deficiency,

32:30

even if you carry a

32:32

normal or an M and an L

32:35

X chromosome. But

32:37

in general, that is why we

32:39

see red-green colorblindness

32:43

be far more common in males

32:45

who are XY than in females who

32:47

are XX.

32:49

Yeah.

32:50

Now, blue-yellow deficiencies,

32:53

called triton deficiencies, are

32:55

overall exceedingly rare compared

32:58

to red-green colorblindness. But

33:00

these are autosomal dominant when they are

33:02

present, because they're on chromosome

33:04

number seven. And they

33:07

generally happen from missense mutations,

33:10

like pretty severe mutations that

33:12

happen in the blue cone opsin

33:14

sequence. Whereas

33:17

the M and the L, which sit,

33:19

again, right next to each other on the X chromosome, they

33:22

kind of just get mixed up all the time.

33:24

And that's why there's such variation in the

33:26

possible anomalous expression

33:29

of these two genes. OK, interesting.

33:32

Question. OK.

33:34

I came across in my reading for

33:37

this, and I didn't really look into it too deeply,

33:40

tetrachromacy in humans.

33:43

Is it real? Does it exist? So

33:46

glad that you asked.

33:49

So glad. So that's got a whole,

33:51

let me tell you,

33:53

I can't believe I can answer your question, Erin. So

33:58

tetrachromacy would mean.

33:59

four

34:01

color vision channels essentially instead

34:03

of three. So if

34:05

we remember what I just said,

34:08

that the most common forms

34:11

of color blindness are forms of anomalous

34:14

trichromacy, where you still

34:16

have three sets of cones, blue,

34:18

green, red, but the peak sensitivity

34:21

of one of these cones, generally a red

34:23

or green,

34:24

is shifted. So

34:27

here's where things can get fun. In

34:29

a person with two X chromosomes,

34:32

who is heterozygous for this

34:35

allele, what they can end up with

34:37

is one X chromosome that has a typical

34:40

M and an L, and

34:42

another one with a normal

34:44

M and say an L prime, a

34:47

slightly shifted version of L that's

34:50

closer to M, for example. Now,

34:54

in the retina of this person's eye, in

34:56

every cell, only one copy

34:59

of the X chromosome is actually expressed

35:01

at any given time, but it's

35:03

very possible that in some cells, the

35:06

quote normal X chromosome

35:08

is expressed, and in others,

35:11

the quote mutant X

35:13

is expressed, because it's not always

35:15

the same X that gets inactivated in every

35:17

cell. So that means that this

35:20

person has four types of cone

35:22

cells being

35:22

expressed, or

35:25

blue,

35:26

M, or green, and then

35:28

L and L prime. Right.

35:32

So this can provide essentially a

35:34

fourth color channel or tetrachromacy

35:37

that, at least in theory, if

35:40

our brain was plastic enough,

35:43

could use to interpret and

35:45

distinguish between additional colors

35:48

and shades. What do you mean by

35:50

if our brain was plastic enough? Well,

35:52

our brain has evolved to be trichromatic.

35:56

So what we don't know is does our

35:58

optic nerve have a enough to be able

36:01

to distinguish those four color channels,

36:03

can our brain like change

36:06

enough to be able to interpret those

36:08

as separate or does it just collapse

36:10

the L and the L prime together? Right.

36:13

Okay. And but this could happen with any one

36:16

of those options. Yes,

36:18

in theory, in practice, it's going

36:20

to be red or green most likely. Okay.

36:23

Yeah. Okay. Interesting.

36:26

We've talked about lots of animals that have more

36:29

than three cones,

36:29

but it's unclear with tests,

36:34

whether they're able to distinguish among

36:36

the colors that they should be able to

36:40

based on our interpretation of

36:42

the science behind it.

36:44

So I love that you said

36:45

that because I do feel like one thing that's

36:47

so important when we talk about these color vision

36:50

deficiencies is that whenever

36:52

we're talking about color vision, it's like in

36:54

comparison to who or

36:56

to what, right? Right.

36:59

There's another paper that I will link to that

37:01

looks at specifically people with deuter

37:03

anomaly. So that is red green colorblindness

37:06

from a shifted green cone

37:09

that they call

37:11

L prime because it's now closer to a typical

37:14

L or red cone, right? The green shifts to red.

37:17

And what this shows is that some people

37:19

with this type of color

37:22

vision, quote unquote deficiency,

37:24

were actually able to separate out

37:27

tones, distinguish

37:29

between tones that looked the same

37:32

to quote normal color

37:34

vision or trichromatic color vision

37:36

observers. So

37:39

there's a theoretical basis both

37:42

with certain types of deuter

37:44

anomalies and with this theoretical

37:47

trichromacy that

37:49

people could be distinguishing between

37:51

shades and between colors

37:54

differently. It's very,

37:57

very difficult

37:58

to test for.

37:59

be honest, I don't understand

38:02

the tests that they describe

38:04

in these papers because

38:07

to the vast majority

38:09

of the population who's trichromatic, how

38:12

can you determine if someone

38:14

else can distinguish something that you cannot

38:17

distinguish? Right. Right? Yeah.

38:20

It's very difficult. I will say

38:23

there is like one person,

38:25

I think, that I read about

38:27

who happens to live in San Francisco,

38:30

who in tests seems

38:32

to have an actual functional

38:34

tetrachromacy, meaning that

38:37

she tests where she can distinguish

38:39

between additional shades and colors based

38:42

on wavelengths than a trichromat

38:45

can. One so

38:47

far out of all of the people that I read

38:49

about that were tested.

38:50

Okay. Okay. But

38:53

it's really, really interesting. That's

38:56

fascinating. And I feel

38:58

like there's so much there

39:01

in terms of the evolutionary

39:03

history of color vision period

39:05

where it's like

39:07

the information that color gives

39:09

you. Uh-huh.

39:11

Yeah.

39:14

Yeah.

39:14

Anyway,

39:15

interesting. Oh, to that point, Erin,

39:19

where did this color

39:21

vision deficiency thing come from? Oh,

39:24

gosh. Yeah. You're

39:27

going to say the word evolution, huh? Yeah.

39:29

We're going to have to go way further back than

39:32

just that. And I

39:35

guess we should get started right after this break.

39:37

Okay.

40:02

So, Erin,

40:03

you just took us through how

40:06

we see color and what happens

40:08

when people see color differently or

40:10

not as many colors or no

40:13

colors at all. And later

40:15

in the history section, I want to explore

40:17

when we first learned about these variations

40:20

in color vision and color vision deficiencies.

40:23

But before we get into that more like

40:25

medical history side of the story, I

40:28

want to try to answer the question, why

40:31

do we see color? Humans,

40:34

other primates, birds, dogs,

40:37

fish, other animals, why

40:39

did color vision evolve? What

40:42

purpose does seeing in color serve?

40:45

Multiple purposes? You betcha. And

40:49

of course, not everything in biology has

40:51

to serve an evolutionary purpose, but

40:54

the fact that there's variation in

40:56

color vision and patterns

40:58

in that variation, the fact that it

41:01

has evolved multiple times independently

41:03

and in different ways, these things

41:06

all suggest that color vision does

41:08

serve a purpose. But

41:10

color vision, even dichromacy,

41:13

is not universal among animal

41:15

species. Sloths,

41:17

armadillos, whales, raccoons,

41:20

cephalopods, many animals

41:22

are monochromats and they do just fine.

41:25

Stop it. Raccoons? Raccoons,

41:27

apparently. I mean, I guess they're

41:29

nocturnal.

41:30

Yeah. So that

41:33

kind of tracks, but I did not

41:35

know that about those little buggers.

41:36

Yes. And sloths.

41:38

I know.

41:40

I know. Okay. I'm learning

41:42

a lot. Color vision

41:45

is not necessary for survival

41:47

as an individual or as a species.

41:50

And in fact, some research suggests that

41:52

red, green color vision deficiency has

41:55

been selected for in some

41:57

animals.

41:58

So what does color vision do? color vision give

42:00

us? In a word, information.

42:04

For those animals that have evolved color

42:07

vision, whether that's trichromacy,

42:09

like most humans, dichromacy,

42:11

like some humans, heterochromacy,

42:14

also like some humans, being

42:16

able to distinguish among colors

42:19

gives them valuable information that

42:21

they can use to help them, for

42:23

example, evaluate a mate, forage

42:26

for food, navigate, or

42:28

identify predators or

42:29

poisons.

42:31

Initially, when color vision first arose,

42:34

maybe 500 million years ago, it provided

42:37

constancy in vision. The

42:40

ability to sense borders around

42:43

different shapes, being able to track

42:45

that this dark red blob was the

42:47

same dark red blob in shade as

42:49

it was in sun. Is

42:51

this thing a thing or is it just part

42:54

of the background, if that makes sense? Because

42:57

if you cannot distinguish among colors whatsoever,

43:00

just light and darkness, and something

43:02

that is dark moves into dark,

43:05

how can you sense it against the background? And

43:09

so this ability to see color

43:11

to distinguish among not

43:14

just the light and dark, but also colors

43:16

would have been helpful for the animals living

43:18

in shallow waters that had to deal with

43:21

a lot of shifting light and shadows.

43:25

So skipping ahead millions of years from

43:28

that 500 million years ago, the

43:30

first mammals were thought to be

43:32

nocturnal, which

43:35

helped them to avoid predators. So

43:38

color vision wasn't as helpful in dim

43:40

light. And so some researchers think

43:42

that these early mammals lost

43:45

this full color vision from their

43:47

ancestors. And

43:49

then the re-evolution, quote

43:51

unquote, of color vision occurred

43:54

as some mammals shifted to

43:56

diurnal life.

43:58

Interesting.

45:59

of blues and yellows

46:02

until one day for one lineage

46:04

a gene was duplicated. This

46:08

happened to be the long opsin gene

46:11

and over time one of those

46:13

copies of the gene stayed the same

46:16

while the other accumulated mutations

46:18

slightly here and there shifting

46:21

so that it changed from the long opsin

46:23

gene to the medium opsin gene. To

46:27

these primates which were the ancestors

46:30

of old-world primates the world

46:32

was no longer just blues and yellows now

46:34

there were also reds and greens. What

46:38

did these additional colors do for them?

46:41

One of the major hypotheses is that this

46:43

new gene allowed these primates

46:45

to detect red or orange or

46:47

yellow fruits or new reddish

46:50

slash purplish early leaves also

46:52

a good food source against the

46:55

green backdrop of foliage not

46:58

only helping them to find the

47:00

fruit but also tell when it was ripe.

47:03

Why is ripe fruit often red?

47:06

Probably evolved to help with seed dispersal

47:09

so the fruit would turn red when it was ripe when

47:11

the fruit was at its sugariest and when

47:13

the seeds were well developed for survival.

47:16

It's a two-way street at least

47:18

for information. If color

47:21

is used as information something has

47:23

to be producing that information for a

47:25

reason and something else has to be

47:27

receiving and processing that

47:29

information.

47:30

That is

47:32

wild. Right? Yeah.

47:35

I don't know why it like

47:36

hadn't occurred to me. Yeah

47:40

I remember talking a lot

47:43

about this hypothesis

47:45

in that evolution of human health class

47:49

but never did we talk

47:51

or did I think about the plant side of

47:53

it. Right and I know that's

47:55

like results studies

47:58

are mixed or at least like opinions

47:59

are mixed as per usual.

48:03

But I think in general, it's

48:07

easy to just think of colors as

48:09

existing statically.

48:12

That is how they are.

48:14

That is what has happened, especially

48:17

for things that we interact

48:19

with frequently. But we can study

48:22

plumage and birds and stuff like that. But

48:24

also, when we study plumage

48:27

and birds, we're not seeing what the birds see.

48:29

I mean,

48:31

it's the same with colors of flowers

48:33

compared to what bees see or what

48:36

birds see. Or like a coral reef

48:38

looks completely different. To

48:40

a fish. To a fish. Oh my

48:42

goodness. I know.

48:44

This is why we were struggling

48:46

with this episode, because it's so easy to

48:48

fall down so many rabbit holes. Oh

48:50

my gosh, you guys. This episode was the

48:53

hardest one I've ever researched. Yeah,

48:56

it was a toughie for sure. I felt like I

48:58

had to relearn a lot of things that I

49:00

had,

49:01

or learn them for the first time. Well,

49:04

tell me what you learned. Information,

49:08

two-way street.

49:11

But getting back to the foraging thing, researchers

49:13

have tested this foraging hypothesis

49:16

in primates with mixed results.

49:19

Sometimes trichromats are better at

49:21

finding fruit. Sometimes there's no difference

49:23

between trichromats and dichromats.

49:26

And sometimes dichromats outperform trichromats.

49:30

But I want to read you a quote

49:32

about one person's experience foraging

49:34

for fruit, who had a red-green color vision deficiency.

49:37

Okay. Quote.

49:39

He observed also that when

49:41

young, other children could discern cherries

49:43

on a tree by some pretended difference

49:46

of color, though he could only distinguish

49:48

them from the leaves by their difference of size

49:50

and shape. He observed also

49:53

that by means of this difference of color, they

49:55

could see the cherries at a greater distance

49:57

than he could, though he could see

49:59

other objects at as great a distance

50:02

as they." End quote. Interesting.

50:05

Isn't that kind of cool? Yeah.

50:09

So there's another hypothesis as to

50:11

why red-green distinction

50:14

may have helped us. And I think it's,

50:17

I'm not entirely sure, but I got the sense that

50:19

it has fallen out of favor. Okay.

50:22

And that is that trichromacy evolved in primates

50:24

as a way to help individuals of the same

50:26

species communicate with one another.

50:29

So you know what those Japanese macaques, like

50:32

the ones you see pictures of where they're relaxing

50:34

in hot springs? Trichromacy

50:37

may have helped species like them to

50:39

evaluate mate quality or

50:41

competition or aggression based

50:44

on like the redness of their faces. And

50:47

for other species, it could have been like the shade

50:50

of the pelt. But the big

50:52

question for this would be,

50:55

did trichromacy evolve

50:57

to help them distinguish red traits

50:59

in other individuals of the same species? Or

51:02

did those red traits evolve

51:04

once trichromacy evolved? Right.

51:07

Chicken or egg, which came first. Yeah. And

51:10

it turns out to answer this chicken and egg question,

51:13

phylogenetic studies suggest that

51:15

it's the latter, that these red traits became

51:17

more pronounced once trichromacy already

51:20

existed. Interesting.

51:21

Okay. Yeah.

51:23

Predator detection is yet another

51:25

hypothesis. One that I touched on

51:27

in our snake episode. And there are studies

51:30

suggesting that trichromats are faster

51:32

and more accurate when it comes to detecting

51:35

predators than dichromats. Full

51:37

color vision would have helped primates

51:40

to distinguish a leopard from a green background

51:42

with dappled light, for instance.

51:45

Studies today evaluating

51:48

differences in foraging, predator

51:50

detection, and social group dynamics

51:53

have found support as well as a lack

51:55

of support for each of these hypotheses.

51:58

And in general, we can't

51:59

reliably say what the primary

52:02

evolutionary driver of a particular

52:04

trait was based on how

52:06

it's used today. Because

52:09

it's not possible to say with certainty

52:11

whether that trait, color vision, evolved

52:13

because of something like foraging

52:16

or if it was later co-opted

52:18

or exploited by that thing, if that

52:20

makes sense.

52:22

Throwing a wrench into this evolutionary story

52:25

is that trichromatic color vision evolved

52:27

independently in both old and

52:30

new world primates, but in different

52:32

ways. Stop it. Right?

52:34

It's fascinating. Let's get into

52:37

it. Okay.

52:38

So that was just like this brief tour of

52:40

the evolutionary history and possible drivers

52:42

of trichromatic color vision among

52:44

old world primates, nearly

52:47

all of which have this kind of color

52:49

vision, all a result from that

52:51

gene duplication event with seemingly

52:53

little variation.

52:55

Okay.

52:56

On the other hand, new

52:58

world primates are just a, quote,

53:01

cornucopia of variation in

53:03

color vision.

53:04

I love that. As one paper

53:07

described it. And instead

53:09

of that gene duplication, I have an asterisk

53:11

here, so it's an exception. Color

53:13

vision in new world primates

53:16

is determined by variations in

53:19

that original gene. So

53:21

there wasn't a duplicated gene. It was

53:23

just, there are just different versions of

53:25

it.

53:27

And since this gene sits on

53:29

the X chromosome, males

53:31

within a

53:31

new world species have

53:32

dichromacy, whereas most,

53:35

but not all females have trichromacy.

53:38

Oh, okay. I had

53:40

read that and I was like, I don't understand.

53:42

And I just moved on. I did that a lot

53:44

faster than the color vision. Yeah.

53:49

That's why females. Okay.

53:52

Uh-huh. And to make it even cooler,

53:54

the different forms of this gene

53:57

also means that there are different forms

53:59

of dichromacy and trichromacy

54:03

depending on which versions of the gene

54:05

are inherited. Wow. The

54:08

exception to this, the little asterisk

54:10

that I mentioned, in

54:12

New World monkeys are the howler

54:14

monkeys who

54:17

have the duplicated gene. What?

54:20

So nearly all members of that species

54:22

are trichromatic.

54:24

What? Right?

54:26

This is cool, Erin. Isn't that really

54:28

cool? I also will say

54:31

that I found in papers, and I'm not sure

54:33

how well this is studied, but I was

54:35

curious about whether we

54:38

have found

54:40

similar rates or the existence

54:42

of period, color

54:45

vision deficiencies in old

54:47

world apes and primates, similar

54:49

to the ways that we see it in humans or the

54:52

frequencies that we see in humans. And it appears

54:54

that we actually don't. The humans

54:56

seem to be the exception to this, where

54:58

we have a fairly high, I know you'll talk about

55:01

it, rate of color

55:03

vision deficiencies. What?

55:06

And so I don't know why that is. And

55:09

there aren't any hypotheses that I found

55:11

or explored, but I just thought that was an interesting

55:14

little side note.

55:16

Wow. Yeah. Yeah.

55:18

But I think in general,

55:21

what I wanted to do in this sort

55:23

of evolutionary section was to highlight

55:26

just how much variation there is in color

55:28

vision in primates alone,

55:30

not to mention the rest

55:33

of the animal kingdom. Oh my goodness. And

55:35

this is a point that Adyong makes in his book that

55:37

I just absolutely loved and continue

55:40

to take to heart, which is that

55:43

color vision or any sensory

55:46

information or sensory structure

55:48

or physiology,

55:48

it's not something to be ranked in

55:51

terms of what is better. Oh, well,

55:53

dogs have better noses or senses

55:56

of smell or that

55:58

is not a very... useful

56:01

metric or way

56:03

to try to understand what another animal

56:06

or another human, whatever experiences.

56:09

Right. So, anyway, monochromacy,

56:13

dichromacy, trichromacy, tetrachromacy,

56:16

and beyond, all of these different types

56:18

of color vision have evolved

56:21

and have been selected for to help

56:23

with gathering information. We're

56:25

not more advanced because we have

56:28

trichromatic color vision. It's

56:30

just

56:33

more complicated than that. And

56:36

being able to distinguish among colors

56:39

isn't always for the better. And

56:41

there are trade-offs associated with the evolution

56:43

of trichromatic color vision. An

56:46

animal can only take in and process

56:48

so much sensory information. You

56:52

can't max out all the boxes. And

56:54

the least useful sensory feature is

56:57

usually the first to go. In

56:59

the case of trichromatic primates, the

57:02

evolution of trichromacy seems

57:04

to have coincided with the loss of

57:06

genes that are associated with chemical

57:09

sensing via smell, probably

57:12

for pheromones. And

57:14

so, when primates evolved red-green

57:17

color vision, they lessened

57:19

their reliance on this other form

57:21

of chemical information. And

57:24

so, I think, again, this is just to say

57:26

that we have a tendency to place

57:28

humans at the pinnacle of evolutionary

57:30

achievement without considering

57:33

the benefit of other strategies.

57:36

And this failure of imagination has

57:38

led us to make some pretty big assumptions about

57:41

other animals, like how we talked about

57:43

earlier how we thought that fish didn't see

57:45

color for decades, or

57:47

dogs couldn't see color at all. And

57:50

it has also led us to create a

57:52

world where it

57:53

can be difficult to navigate if

57:56

you don't have full color

57:58

vision. Right.

57:59

Which brings me to the other

58:02

part of this history section, the

58:04

how did we learn about color vision deficiency

58:07

in humans part? Of

58:10

course I have to begin with a quote and

58:13

Erin bear with me, it is probably the

58:15

longest quote I have ever read outside

58:18

of like a firsthand account. Oh, okay.

58:20

Okay, but it's worth it, I swear. Okay. All

58:23

right, get ready.

58:24

Quote,

58:26

it has been observed that our ideas

58:29

of colors, sounds, taste, etc.,

58:31

excited by the same

58:33

object may be very different

58:35

in themselves without our being aware of

58:37

it. And that we may nevertheless

58:40

converse intelligibly concerning

58:42

such objects as if we were

58:44

certain the impressions made by them

58:46

on our minds were exactly similar.

58:50

I was always of opinion, though

58:52

I might not often mention it, that several

58:54

colors were indudiciously named the

58:56

term pink in reference to the

58:58

flower of that name seemed proper enough.

59:01

But when the term red was substituted for

59:03

pink, I thought it highly improper.

59:06

It should have been blue in my apprehension

59:09

as pink and blue appear to me very

59:11

nearly allied whilst pink and

59:13

red have scarcely any relation. Since

59:17

the year 1790, the occasional study of botany

59:19

obliged me to attend more to colors

59:22

than before. With respect to

59:24

colors that were white, yellow, or

59:26

green, I readily assented to

59:28

the appropriate term.

59:29

Blue, purple, pink, and

59:32

crimson appeared rather less

59:34

distinguishable, being, according

59:36

to my idea, all referable

59:39

to blue. I was never convinced

59:41

of a peculiarity in my vision till

59:43

I accidentally observed the color of

59:45

the geranium zonale by candlelight

59:48

in the autumn of 1792. The

59:51

flower was pink, but it appeared

59:53

to me almost an exact sky

59:55

blue by day. In candlelight,

59:58

however, it was astonishing. changed,

1:00:01

not having then any blue in it, but

1:00:03

being what I called red, a color

1:00:06

which forms a striking contrast

1:00:08

to blue. I requested some

1:00:10

of my friends to observe the phenomenon when

1:00:12

I was surprised to find they all agreed

1:00:15

that the color was not materially different from

1:00:17

what it was by daylight, except

1:00:19

my brother who saw it in the same light

1:00:22

as myself. This observation

1:00:25

clearly proved that my vision

1:00:27

was not like that of other persons,

1:00:30

and at the same time, that

1:00:32

the difference between daylight and candlelight

1:00:34

on some colors was indefinitely

1:00:36

more perceptible to me than to others.

1:00:41

I love that

1:00:44

so

1:00:44

much, Erin. Right? Do

1:00:47

you see why I had to do the whole thing? A hundred

1:00:49

percent, yes. Okay, good. I

1:00:51

was like, gosh, this is really long as I'm reading

1:00:54

it. Oh, but it's so good because it also ...

1:00:56

Do you know what that tells you? He's

1:01:00

using his rods that we ignored. Yes,

1:01:02

I know. The rods become more important

1:01:05

when you don't have as many cones.

1:01:06

Yes. It

1:01:09

is so interesting. I loved it

1:01:11

so much, and it's really important

1:01:13

for a number of reasons. First, that

1:01:16

quote was from John Dalton in

1:01:18

his 1794 treatise titled,

1:01:21

Extraordinary Facts Relating to the Vision

1:01:23

of Colors. It's

1:01:26

great for a few reasons, right? Number

1:01:29

one, it's just such a great

1:01:31

systematic retelling of his

1:01:33

thought process, of exactly when he realized,

1:01:36

how he realized everything about

1:01:38

it. Number

1:01:41

two, he mentioned his brother

1:01:43

also experienced this, which is really

1:01:45

good, really interesting.

1:01:48

And number three, it is, as far

1:01:50

as we know, the first scientific

1:01:53

description of color vision deficiency.

1:01:55

Wow.

1:01:57

In honor of his observation, color

1:01:59

vision deficiency ...

1:01:59

was and sometimes still

1:02:02

is called Daltonism.

1:02:04

Oh. But 1794, like, doesn't that seem

1:02:06

recent?

1:02:14

I don't know how to gauge it, Erin. I

1:02:16

know, I know. I mean, I fully

1:02:18

expected to

1:02:20

find like a long list of historical

1:02:22

accounts going back hundreds or maybe

1:02:25

even thousands of years, hinting

1:02:27

at color vision deficiency. But

1:02:30

no. And I will

1:02:32

say that like there are mentions

1:02:35

of confusion in color vision

1:02:38

that were, like,

1:02:40

it seemed fairly well known about, or

1:02:42

at least enough so for like

1:02:44

King George III to make some comment

1:02:47

about it at a dinner in 1785. Like some people have

1:02:49

an ear for music,

1:02:52

some people don't. Some people have an eye

1:02:54

for colors, some people don't, you know, that kind of thing.

1:02:57

And there was also a reference to it

1:02:59

in a German medical science magazine

1:03:02

and also other scattered references in

1:03:05

the 1700s. But Dalton

1:03:07

really seems to be the first to have written

1:03:09

about it scientifically, like

1:03:11

with an analytical

1:03:12

approach.

1:03:15

And I don't know, like,

1:03:18

it does seem

1:03:20

recent, but at the same time,

1:03:23

in a way it does make sense considering

1:03:26

that color doesn't seem

1:03:29

subjective.

1:03:30

Like it seems like it's, it

1:03:33

seems like inherent properties of

1:03:35

objects. You learn your colors at

1:03:37

an early age. If you confuse

1:03:40

colors, it's an easier leap to think that

1:03:42

there's something wrong with your vision

1:03:44

in terms of acuity, like

1:03:46

your sight rather than your perception.

1:03:49

And, you know,

1:03:51

like, like I kind of already mentioned,

1:03:54

as a species in general, we're not great at imagining

1:03:56

the world as it might be perceived by

1:03:58

other species.

1:03:59

alone other humans.

1:04:00

I feel like so tired. So

1:04:03

true. And so it would take a really

1:04:05

keen observer to question

1:04:07

whether color is truly objective

1:04:10

and then also have the opportunity to

1:04:12

publish those

1:04:13

observations. Yeah. Yeah.

1:04:17

It happened when it happened. And

1:04:19

when it happened,

1:04:23

Dalton hypothesized in this

1:04:25

treatise that his and his brother's

1:04:27

color vision deficiency was caused

1:04:30

by the vitreous humor of their eyes

1:04:32

being tinted blue, making

1:04:35

it absorb longer wavelengths. Huh.

1:04:38

Yeah. He requested that after

1:04:40

his death, his eyes be tested to confirm

1:04:42

his hypothesis. And so

1:04:45

the day after he died, July 28th, 1844, that's

1:04:47

exactly what was done. What?

1:04:51

Only the person performing this

1:04:53

autopsy found no support for

1:04:55

Dalton's hypothesis. The vitreous

1:04:58

humor, not tinted. I

1:05:01

don't have the slightest idea

1:05:03

how you would even do that. I don't

1:05:06

know. Wow. I'll include

1:05:08

the paper that mentions this,

1:05:11

goes into more detail about it. Okay.

1:05:14

Okay. Okay. Cool. The alternative

1:05:16

hypothesis was that it came

1:05:19

from a cerebral anomaly, like

1:05:21

the part of your brain that perceives

1:05:24

color

1:05:25

was somehow different, but

1:05:27

that also didn't hold up. Yeah.

1:05:30

The explanation that is generally

1:05:33

accepted today for most

1:05:35

cases of color vision deficiency was

1:05:38

actually first proposed in 1781 by a

1:05:40

mysterious person

1:05:43

named Jirov Svan Gentili.

1:05:46

Oh, okay.

1:05:47

Apparently no one knows anything about who this

1:05:49

person actually was or whether that was like

1:05:51

a real name or just a pen name. What?

1:05:54

Yeah. He's called like an obscure mysterious

1:05:56

figure. I

1:05:58

hope someone calls me that someday.

1:05:59

I'm scared

1:06:02

and mysterious. Oh,

1:06:06

that's hilarious. And

1:06:09

so this Bongentilie

1:06:11

guy wrote in that German science

1:06:14

magazine that I had mentioned that he

1:06:16

thought that color vision deficiency occurred

1:06:19

if one or two of the three

1:06:21

kinds of, quote unquote, molecules

1:06:23

or membranes in the retina was

1:06:26

not functional, either paralyzed

1:06:28

or constitutionally

1:06:29

overactive. It's

1:06:32

interesting that they seem to have known

1:06:34

that there were like three things

1:06:36

involved. Yeah. Well,

1:06:40

okay. And so this is one of the

1:06:42

areas that I did not get into, which is

1:06:45

like Newton and color theory

1:06:48

and, you know, light spectrum,

1:06:51

you know, like all of that. And I was just

1:06:53

like, I don't know how to even begin

1:06:55

to do it. Talk

1:06:58

about that. Yeah. Yeah.

1:07:01

And so I wonder whether that was coincided

1:07:04

with sort of the development of some of those ideas

1:07:06

around what color, what

1:07:08

the visible spectrum of light is. Okay.

1:07:11

Okay. That makes sense. And

1:07:13

so like how you combine, how many colors do you need

1:07:15

to combine in order to make all the colors

1:07:17

that we see? Right, right, right, right, right. Okay.

1:07:20

Yeah. Yeah. I don't

1:07:23

know. That's my guess. Yeah. And

1:07:25

so after this Von Gentile, it's

1:07:27

unclear whether his idea

1:07:31

gained traction then, or we just only

1:07:33

know about it in retrospect, but

1:07:35

it's possible that British polymath

1:07:37

Thomas Young stumbled across

1:07:39

it. And like Thomas Young did one bajillion

1:07:42

things. He proposed the

1:07:44

wave theory of light. He helped

1:07:46

to translate the Rosetta Stone. He

1:07:49

also, right. He

1:07:51

also further developed this hypothesis

1:07:53

about color perception, suggesting

1:07:55

that it was due to the presence of three

1:07:58

kinds of nerve fibers. in the retina.

1:08:02

And over time, this framework for how color

1:08:05

vision worked via cones and rods was

1:08:07

refined with anatomical studies, molecular

1:08:10

studies, advancements in physics, and

1:08:13

just the growth of the field of vision science.

1:08:17

And in the 1990s, the nature

1:08:19

of Dalton's color vision deficiency was

1:08:22

finally made clear when the

1:08:24

Manchester Literary and Philosophical Society

1:08:26

granted permission to a few scientists

1:08:29

to run some tests on the remnants of

1:08:31

Dalton's eyeball. Oh my goodness.

1:08:33

Right? How amazing. I love

1:08:35

it. God would be so worried to drop that little

1:08:38

tube. I'd be like, oh God.

1:08:41

But they confirmed that Dalton

1:08:43

lacked the middle photopigment

1:08:45

cone cell, making him a deuterineope. Wow.

1:08:48

Face closed.

1:08:51

Yeah.

1:08:52

Love it. Dalton may not

1:08:55

have been the first person to notice

1:08:57

that the way he saw colors was not

1:08:59

the same as most other people. I mean,

1:09:02

he was definitely not the first. We've kind of established

1:09:04

that. But his careful scientific

1:09:07

analysis of what he suspected

1:09:09

was going on caught the attention of

1:09:11

other scientists. And for

1:09:13

years, color vision deficiency was

1:09:15

seen as kind of an anomaly,

1:09:18

just this curious thing that some

1:09:20

people had, that some people were born

1:09:22

with or acquired later in life. And

1:09:25

it certainly prompted more research

1:09:27

into the structure and function of the

1:09:30

eye and how vision worked, as

1:09:32

well as philosophical musings

1:09:34

over how we are each in our

1:09:36

own little world and can never truly

1:09:39

experience life from someone else's perspective.

1:09:41

Oh my goodness. But

1:09:44

color vision deficiency took on a practical

1:09:46

importance starting in the second half

1:09:49

of the 1800s, coinciding

1:09:51

with the rise of industrial transportation,

1:09:54

the so-called

1:09:56

golden age of rail travel, growth

1:09:58

in maritime travel. and of course automobiles

1:10:01

and airplanes. With

1:10:04

all of these forms of travel, people

1:10:06

had to use certain signals to determine

1:10:09

when it was safe to proceed, when to stop,

1:10:11

when to proceed with caution, when to back

1:10:14

up, and the signaling was

1:10:16

done primarily with colors.

1:10:19

Suddenly, color vision deficiency

1:10:21

was not just a medical curiosity, but

1:10:24

according to one physician in 1880, quote,

1:10:28

daltonism can be cause of discussions,

1:10:31

arguments, battles, industrial and commercial

1:10:33

losses, dreadful accidents, and irreparable

1:10:36

miseries.

1:10:37

Wow. Yeah.

1:10:39

Strong words.

1:10:41

And this fear was

1:10:44

realized in November 1875, when

1:10:48

two express trains on a single

1:10:50

track, one heading from Stockholm

1:10:53

to Malmo and the other from Malmo

1:10:55

to Stockholm collided headfirst

1:10:58

in the middle of the night. Nine

1:11:00

people were killed in this collision. And

1:11:03

about a year after the accident, when they were

1:11:06

trying to like figure out what

1:11:08

had happened, who was at

1:11:10

fault, how can we prevent this from happening

1:11:12

again, an ophthalmologist

1:11:15

named Freeseoff, I don't

1:11:17

know how you say it, Holmgren, suggested

1:11:20

that either the engineer of the northbound

1:11:22

train or his oiler was

1:11:25

color deficient and misinterpreted the

1:11:28

signals leading to the crash. Neither

1:11:31

of them could be tested because they had both died in

1:11:33

the accident, but this didn't

1:11:35

stop the speculation. And the

1:11:38

Lagralunda collision, as it was called,

1:11:40

has been referenced over and over

1:11:43

again as a case study of the tragedies

1:11:45

that could result from having someone with color

1:11:47

vision deficiency in charge of

1:11:50

transportation or in charge of interpreting those

1:11:52

signals.

1:11:53

So just to be clear, that

1:11:55

was just one guy's idea that

1:11:58

this is what happened. Yeah. but nobody

1:12:01

knows for sure. No, so,

1:12:03

okay.

1:12:04

There is a paper from 2012 that goes into, it's

1:12:08

an incredible in-depth analysis

1:12:11

of the different trains,

1:12:14

how the lights would have worked. And they

1:12:17

did this in-depth, super

1:12:19

detailed examination of

1:12:21

this crash. And they concluded

1:12:24

that even if color deficiency was

1:12:26

a factor, which it's not clear that it was

1:12:28

at all, it was far from being

1:12:30

the only factor responsible. And

1:12:33

probably there was some sort of problem

1:12:35

with one of the trains themselves.

1:12:38

Okay.

1:12:38

So, but despite this, yeah,

1:12:41

this was like a real catalyst.

1:12:43

Wow. This the Lagar-Lunda collision,

1:12:45

you'll find it in so many references to

1:12:48

anything related to color vision deficiency

1:12:50

in industry and regulations.

1:12:53

It was this huge catalyst for the introduction

1:12:56

of color vision screening and

1:12:58

restrictions on what jobs in the transport

1:13:00

industry that people with

1:13:03

color vision deficiency could hold.

1:13:06

And most of the time it was just like, nope, sorry,

1:13:08

we have to perform these tests beforehand. And

1:13:11

I think that's,

1:13:13

I'm not an expert in anything

1:13:15

related to industry and

1:13:17

transportation and stuff like that. But like, it

1:13:20

just seems like

1:13:22

another solution could be to

1:13:24

change the signals, right?

1:13:30

I don't know. Maybe that's a very naive

1:13:32

thing to say, but. I mean, I don't

1:13:35

know. Someone tell us otherwise.

1:13:37

Yeah, like maybe there's, I don't

1:13:40

know.

1:13:41

Yeah. I don't know, but

1:13:43

yeah, this was like a really formative moment.

1:13:46

And one of the things that they used to test people

1:13:49

who were applying for these jobs was the

1:13:51

Holmgren, named after that

1:13:53

guy, Wool Strands Test, where

1:13:56

you had to match wool of different colors.

1:13:58

Hmm.

1:13:59

And I actually couldn't get a

1:14:02

very good sense of how many train

1:14:04

or maritime or aviation accidents

1:14:08

were definitively attributed

1:14:10

to someone misreading the signals

1:14:12

due to color vision deficiency. I

1:14:15

think it did happen. I think there are at least

1:14:18

a few confirmed cases

1:14:20

of that happening. But

1:14:22

even the ones where it was just

1:14:25

pure speculation absolutely

1:14:27

captured the public's imagination and

1:14:30

fear and led to these regulations

1:14:32

being quite strict for a very

1:14:34

long time and only recently

1:14:37

have some of these restrictions become

1:14:40

a little more relaxed or more specific.

1:14:43

And that's part of that is a result of

1:14:45

us learning more about the different types of color

1:14:48

vision deficiency and being

1:14:50

able to test for those differences using,

1:14:52

for instance, those Ishihara

1:14:54

tests, which I'm sure many of you are familiar

1:14:57

with. There's like that circle

1:14:59

of bubbles and some of the bubbles are a

1:15:01

different color and they make up the shape of a

1:15:03

number. And if you can determine

1:15:06

what that number is, then

1:15:07

you

1:15:08

don't have color vision deficiency of that

1:15:10

particular

1:15:10

kind or something to that effect.

1:15:13

I just made my toddler take that test.

1:15:15

I've taken that test a number of times. Me

1:15:18

too. I don't know why. I took it at

1:15:21

the same time. But

1:15:23

anyway, since color vision was first

1:15:25

put out there into the scientific

1:15:28

world, we've come a really long

1:15:30

way towards understanding the mechanisms

1:15:33

and genetics of color vision. And

1:15:35

we finally, I think, at

1:15:38

least in small ways, have

1:15:40

started to move away from exclusionary

1:15:42

practices like limiting what professions

1:15:45

you can have

1:15:45

and making an effort to

1:15:48

be more inclusive, realizing

1:15:51

that we may not all

1:15:53

experience the world in the same

1:15:55

exact way. And maybe

1:15:58

that means something like a pattern.

1:15:59

package in R that gives you a

1:16:02

color palette for figures that's, quote unquote,

1:16:04

colorblind safe. Uh-huh.

1:16:07

Or maybe that means changing the types of signals used

1:16:09

in transport so that people who have color

1:16:11

vision deficiency can still utilize

1:16:13

those signals. Or maybe that means

1:16:16

creating glasses or other

1:16:18

methods to allow us to distinguish

1:16:20

a wider spectrum of colors.

1:16:23

So, Erin, a little bit of

1:16:26

an abrupt transition. Uh-huh.

1:16:29

But what can you tell me about these glasses

1:16:32

and other aspects of color vision deficiency

1:16:34

today? I can do

1:16:37

my best to tell you something

1:16:39

right after this break.

1:17:11

Pretty much every single paper

1:17:13

that I read

1:17:15

cites

1:17:16

that when it comes to congenital

1:17:18

color vision deficiency, which again is what

1:17:21

we're focusing on, the prevalence

1:17:24

overall is 8% in

1:17:27

males and 0.5% in

1:17:29

females. I saw

1:17:31

those numbers over and over

1:17:34

again and I wasn't even looking for them.

1:17:36

Over and over and over and over and

1:17:38

over. I have no

1:17:40

idea where these numbers came from. I don't

1:17:42

know if they're

1:17:44

real. I mean, I guess they're real because they're in every

1:17:47

single paper. One

1:17:49

paper that I read said that this

1:17:51

is true in people of northern

1:17:53

European descent, but it varies

1:17:56

across the globe.

1:17:58

But I couldn't find...

1:17:59

data like comparing different

1:18:02

regions.

1:18:03

So but

1:18:05

yeah, that's the numbers that I have.

1:18:09

Okay. Red green

1:18:11

color vision deficiencies, of course, far

1:18:14

more common overall.

1:18:15

Interestingly, the deuter

1:18:18

anomalies and deuteronopia

1:18:21

are more common than protanomaly

1:18:24

and protanopia. I don't

1:18:27

know why. And then I don't

1:18:29

even have numbers for things

1:18:32

like the monochromacy or

1:18:34

tritonomole because they're just

1:18:36

that rare. So

1:18:40

that's

1:18:41

epidemiology. I mean, it's

1:18:44

pretty straightforward. Okay. Okay.

1:18:48

I don't know what I expected, but yeah. But

1:18:50

there it is.

1:18:51

There it is. It

1:18:54

just means we can spend some more time talking about like

1:18:57

what's being done or what research

1:19:00

are people doing or whatever. These

1:19:02

glasses, Erin, I have to know like

1:19:05

what do they do? You see these amazing videos

1:19:07

and then I'm like, is the hype real

1:19:10

and it doesn't work for some people? How

1:19:12

does it work? Why doesn't it work? Why doesn't

1:19:15

it work? So I guess which glasses

1:19:17

are you thinking about? Like the Enchroma glasses? I

1:19:19

suppose any of them. Yeah. Yeah.

1:19:24

Let's talk about it. There exist things like tinted

1:19:26

lenses that are just literally tinted lenses

1:19:29

that you can wear over one eye or both eyes

1:19:32

that in some studies help some

1:19:35

people with some kinds of

1:19:37

color vision deficiencies. There

1:19:40

are other like these lens

1:19:42

filter type things which

1:19:45

come in the form of glasses commonly called

1:19:48

Enchroma filters. They

1:19:50

have a lot of theoretical

1:19:53

usefulness because what they do, which is fascinating

1:19:56

and way above my head, is that

1:19:58

they modify the perceived. wavelengths

1:20:01

of light. So something, Erin,

1:20:03

like your red sweatshirt that you're wearing,

1:20:05

the wavelength of light that's coming

1:20:07

off of that into my eyes with this

1:20:09

filter would be shifted such

1:20:12

that if my cones

1:20:14

are also shifted I might better be able

1:20:16

to distinguish it as red. Okay,

1:20:19

yes. But in the papers

1:20:22

that I read at least there's pretty limited

1:20:24

evidence of their actual effect

1:20:27

in terms of color discrimination. In

1:20:30

general, at least in the papers that I read,

1:20:32

both the tinted glasses as well as these

1:20:34

various types of filter lens glasses

1:20:38

as well as some experimental contact

1:20:40

lenses, which is interesting, can

1:20:43

show some increases in color

1:20:46

perception and contrast enhancement

1:20:49

in nature, like when given

1:20:51

natural scenes to look at, but

1:20:54

they haven't yet shown to make it

1:20:56

to the level of like someone being able to pass

1:20:58

an Ishihara test who couldn't before.

1:21:01

Okay. At least from what I read.

1:21:04

That's very interesting.

1:21:08

Now even more interesting, or I think

1:21:11

even more interesting, is that

1:21:13

it is also theoretically at least

1:21:15

possible to try and treat color

1:21:18

vision deficiency with gene therapy,

1:21:20

given that most of the time what we talked

1:21:23

about today are genetic disorders.

1:21:25

Yeah. But there

1:21:28

are a lot of possible individual

1:21:30

gene mutations,

1:21:32

but it's also maybe not

1:21:34

necessary to correct the exact

1:21:37

gene mutation in order to restore

1:21:39

typical trichromatic color vision, right?

1:21:42

Because all you would have to do is restore

1:21:45

a fully functional opsin gene,

1:21:48

for example,

1:21:50

with the expected sensitivity,

1:21:52

right? An M opsin if you're missing that one or

1:21:54

an L opsin if you're missing that one, right?

1:21:58

But it's a

1:21:59

lot of

1:21:59

a lot more complicated than that.

1:22:02

I will say that a number

1:22:04

of studies have done this in mice

1:22:07

as well as in some primates. And

1:22:09

they have shown that they can induce some

1:22:12

trichromatic color vision in mice

1:22:14

and in

1:22:16

primates that are missing

1:22:18

it.

1:22:18

Oh, okay. So

1:22:21

it's possible. If at least the theory

1:22:24

is solid, we've done it in animals.

1:22:28

But what's really interesting, and I

1:22:30

think one of the things that makes

1:22:32

the idea of gene

1:22:33

therapy really interesting, is

1:22:36

that

1:22:37

not only does it beg the

1:22:39

questions around the neuroplasticity,

1:22:42

like we talked about, can

1:22:44

you restore trichromatic color

1:22:47

vision in someone whose eyes

1:22:50

developed during embryologic

1:22:53

development with only two

1:22:56

sets of cones,

1:22:57

can they still then be restored? Because

1:23:02

the cone cells are involved

1:23:04

in, again, a lot more than just

1:23:07

color vision. So

1:23:08

can we quote

1:23:11

six these

1:23:12

deficiencies by adding back

1:23:14

those genes after this period of

1:23:16

development when these complex neural circuits

1:23:18

are being formed? Interesting. Okay. So

1:23:21

we can do it in animals, at least

1:23:23

in a couple of studies, but we still

1:23:26

don't know if it's possible in humans.

1:23:28

Interesting. Gene therapy. Gene

1:23:31

therapy. I always love when we talk about it and then

1:23:33

I'm always like, this

1:23:35

is a big thing. It is a big thing.

1:23:37

Especially- There's a lot of implications

1:23:40

and complications and question

1:23:42

marks. Exactly. Yeah. I

1:23:45

love it.

1:23:46

But that, Erin, is

1:23:49

color vision deficiencies and

1:23:51

literally everything I know about them. You

1:23:54

know, I think that as difficult

1:23:57

as it felt sometimes to kind of like...

1:23:59

hone

1:24:01

in on what we wanted to talk about. I

1:24:04

really feel like this was a great

1:24:07

one to do and I learned so much

1:24:09

about color vision deficiency. Thanks. Same,

1:24:12

same.

1:24:12

Yeah. And about

1:24:14

just like color vision in general,

1:24:17

I love it. Yeah, and if listeners,

1:24:19

you have favorite color

1:24:21

vision facts about animals

1:24:24

or about humans or about anything, send

1:24:26

them our way. I wanna know them. I wanna know them.

1:24:29

Yeah. Speaking

1:24:31

of learning more and knowing more, I

1:24:34

have many things to shout out today. First,

1:24:37

I'm gonna shout out some of the resources that

1:24:39

I used for this, just

1:24:41

a few of them, because there are a lot. On

1:24:44

the evolutionary side of things, there

1:24:46

are so many papers by a really prominent

1:24:48

researcher in the field, Gerald Jacobs, about

1:24:51

the evolution of color

1:24:54

vision in primates and animals in general.

1:24:57

There is also a great paper called The

1:24:59

Causes and Consequences of Color

1:25:01

Vision by Girl and Morris from 2008.

1:25:05

And for the history of color blindness itself,

1:25:07

there's a book called The History of Color Blindness

1:25:10

by Philippe Lantheny. And I

1:25:12

did not mention this at

1:25:15

all. I completely forgot to mention this or

1:25:17

include this in my notes. But one of the really

1:25:19

interesting things that I came

1:25:21

across was the discussion of

1:25:23

color vision deficiency in art. And

1:25:27

so being able to look at art

1:25:29

history in different art movements and

1:25:32

detecting what artists may

1:25:35

have had color vision deficiency based on how

1:25:37

they represented the world

1:25:40

in the context of whatever art movement

1:25:42

was popular at the time. So if it was like

1:25:44

during the time when people were painting literally

1:25:47

the world as they perceived

1:25:49

it,

1:25:50

then you might be able to tell more than

1:25:52

if it was at a time when it was

1:25:54

more, I don't

1:25:56

know, up in the air. I don't know anything about art

1:25:58

history. Yeah, abstract, impressionist.

1:25:59

knows. But

1:26:02

that is like a really cool... So there's a paper

1:26:05

by Marmore and Lanthony from

1:26:08

2001 called The Dilemma of Color Deficiency in

1:26:11

Art. And on that note,

1:26:13

further reading An Immense World

1:26:15

by Ed Yong. I'll shout it out again. It's phenomenal.

1:26:18

It'll change the way you perceive the world. And

1:26:21

then there are two books that I did not read for

1:26:24

this. One is called The Island

1:26:26

of the Colorblind by Oliver Sacks. And

1:26:29

this is about a group of people that have

1:26:31

achromatopsia. And

1:26:33

then there is a book that I read years ago called Through

1:26:38

the Language Glass, Why the World Looks

1:26:40

Different in Other Languages by Guy

1:26:43

Dutcher. And there is a chapter

1:26:45

in this book, at least one, on the

1:26:48

evolution of language as it pertains

1:26:50

to color terminology that

1:26:52

I found fascinating.

1:26:54

I shockingly had less

1:26:57

papers for this

1:26:59

episode than usual because the papers

1:27:01

are incredibly detailed. Shout

1:27:04

out to Wikipedia for helping me understand

1:27:06

the papers. So shout

1:27:08

out there. But the

1:27:10

papers that were actually incredibly detailed

1:27:13

once I understood them were a 2003 paper

1:27:16

from Annual Review of Neuroscience just

1:27:19

called Color Vision that was really helpful in

1:27:21

understanding how that works. And

1:27:23

then a paper from the journal

1:27:26

Eye from 2010 called Color

1:27:28

Vision Deficiency. Those

1:27:31

I think were the two that I used the most heavily,

1:27:33

but I have so many more

1:27:35

on the biology

1:27:37

of this, on the lenses

1:27:40

and glasses and gene therapy, on

1:27:43

tetrachromacy and all of

1:27:45

that. You can find the sources

1:27:47

from this episode and every one

1:27:50

of our episodes on our website, thispodcastwillkillyou.com,

1:27:53

under the episodes tab. Check it out. Thank

1:27:55

you again to Kristen for

1:27:57

sharing your story with us.

1:27:59

Appreciate it so much. Yeah, we do.

1:28:02

Thank you to Blood Mobile for providing the music

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for this episode and every one of

1:28:06

our episodes.

1:28:08

Thank you to Liana Scalacci for our

1:28:10

amazing audio mixing. And

1:28:12

to Exactly Right Network. And

1:28:14

to you listeners, thank you. We

1:28:16

hope that you enjoyed this episode,

1:28:19

found it interesting, learned something, have

1:28:22

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1:28:24

anything.

1:28:26

And a special shout out to

1:28:29

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really appreciate it. Okay,

1:28:36

until next time, wash your hands.

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