This Podcast Will Kill You - Ep 124 The full spectrum of color vision deficiency

Episode Date: September 5, 2023

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. See omnystudio.com/listener for privacy information.

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your podcast. 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 experience with that because her dad has color vision deficiency as well. time, they really didn't think too much of it. It was something cool they had 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 that this was a consideration. And so they

went and they had my brother tested and it turns out he had color vision deficiency. Now he's a 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 color vision deficiency, my grandpa having color vision deficiency pretty much created this scenario that normally doesn't occur until your ninth grade biology class, where I had the possibility to be a female with color vision deficiency. 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 normal way to be. So we all have

Duter anomaly. So that's the red green color vision deficiency. And so it's the most common, I think, of all of them. The three of us, I'll have it. My mom does. doesn't, but she's an optometrist. So this is always the ideal scenario. So if 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 maybe came up on occasion, but my parents were very proactive about letting my teachers know that this was just something we all had. But one of the best parts of being a female with color vision deficiency is that it's on both sides of my family. So on my mom's side, I have a bunch 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 kind of proud to have. So one of the stories that we were always told about my great-grandpa is that in World War II, 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,

but something they always tell us is a supposed advantage to having color vision deficiencies is that camouflage doesn't work as well. And so one of the things they 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 C-Divor the camouflage guy. So this is always just sort of an interesting story that was told to us,

but I do want to take it with a grain of 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 vision deficiency in my family, again, it was so normal, but then getting out into the supposed real world now that I've moved out, gone to college and everything, there have been a couple things that are very challenging. So I work, 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. 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 can see it really well, 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 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's about me. And then the other biggest challenge I would say is that because it's not likely for females to be colorblind or to 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 with sort of a negative approach. Like, you must be lying to get attention. You're making this up. And 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 so all of that has been somewhat of a challenge, 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 M&Ms are the gray kind. Even though I can see those colors, it's still just, it always catches people off guard. I think my biggest thing that 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 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. Thank you so much, Kristen, for sharing your story with us. We really appreciate it. Hi, I'm Erin Welsh. And I'm Aaron Almond Updike.

And this is, this podcast will kill you. Welcome. Today we're talking about the whole spectrum, get it, of color vision deficiencies. It actually took me a second to get it. I think I'm too close to this thing, Aaron. That's the only joke I have for the whole episode. Yeah, I don't think I have any jokes, which is really surprising. Again, I was like too much in the weeds. I lost the forest for the trees. Yeah. Whoops. We're really selling it. Yeah. No, but no. I mean, that's the thing.

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 dartboard and find a thousand interesting things about one aspect of the history or the biology of color vision deficiencies. Yeah. You might have to open like no less than 50 Wikipedia pages to understand one paper, for example. I know. I could not tell what was like on my Chrome. I was like, oh, my gosh. Gosh, this is way too many tabs. We need to deal with this. My life.

Well, it's going to be a great episode, but before we get into the meat of it, it's quarantine time. It is. What are we drinking this week? We're drinking true colors. And I love this title because is there any such thing as true color? 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? 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 quarantini making. But there's grenadine, and then there's orange juice, and then there's blue cura-sau.

and there's lime juice and rum. Yum. It's great. We'll post the full recipe for that quarantini as well as our non-alcoholic. Plessy Berita on our website, this podcast will kill you.com. We certainly will. On our website, this podcast will kill you.com, I'm going to 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 the sources for each and every one of our episodes. We've got a firsthand account form. I don't think I've been saying that in past. Oh, yeah. We've missed that. We've missed that. We have got links to bookshop.org affiliate account, goodreads list, a merchandise page, music by Bloodmobile, Patreon, lots of stuff. Check it out. It's good stuff. With that, shall we talk about color vision deficiencies? I think we should. Okay. Right after this break. dinner shows up every night whether you're prepared for it or not and with blue apron you won't need to panic order takeout again blue apron meals are designed by chefs and arrive with pre-portioned ingredients so there's no meal planning and no extra grocery trip there assemble and bake meals take about five minutes of hands-on prep just spread the pre-chopped ingredients on a sheet pan put it in the oven and that's it and if there's truly no time to cook dish by blue apron meals are fully prepared just heat them in the oven or might be

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Visit o'Keefscompan.com slash this podcast and code this podcast at checkout. This season on Dear Chelsea with me, Chelsea Handler, we've got some incredible guests like Kumail Nanjiani. Let's start with your cat. How is she? She is not with a thing. Okay, great, great, great way to start. So this is a great beginning and hopefully you'll be able to, I don't know, maybe you will cry. Amanda Seifred.

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Oh my God. That's so funny. I know. So I'm always like, hi. I try to butcher it up for kids, you know, so they're not confused. Yeah, but you're butching it up is basically like an angry woman.

And Torres Day. Right. No, I turn it to be Arthur. Listen to these episodes of Dear Chelsea on the IHeart Radio app, Apple Podcasts, or wherever you get your podcasts. To be able to talk about color vision deficiencies, aka color blindness,

I think we first have to understand at least a little bit about color vision itself, right? That's easy, right? So simple and straightforward to explain on a podcast. in under two hours. Here we go. At the most basic level, just like bare bonesing 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 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 bare basics of that process, I think the many, many ways in which this system can have deficiencies, aka all the variations of 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. There is an infinite number of wavelengths of light that exist from ultraviolet to infrared, 400 to 800 nanometers. Our human eyes have evolved to see a fairly small portion of this spectrum of light. visible light, Roy G. Biv in our rainbows. So it goes like this. Light, all of its various

wavelengths, comes into our eyeballs, travels through our eye goo, 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. 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. Yay! Yay! So I'm finally something. It's probably marginally involved, etc., but for the purposes of today, rods 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 opcens, which are these photoreceptor proteins. Each one of these opsons is most sensitive, peak sensitive, to a specific wavelength of light. Short, medium, and long. Huh? Simple enough so far. So the short wavelength sensitive opson is also called the blue cone. The middle or medium wave sensitive option is also called the green cone. And the long wave sensitive option is called the red cone, even though it's peak, length of absorption is actually yellow, not red, but let's ignore that and call it red. Yeah. Great.

Yeah. So the waves of light hit these 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 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 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 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 each of these different types of cells. And in doing that, it's then able to differentiate colors into our human trichromatic or three-color vision system. Right. You need at least two for comparison, but three, you just get to compare more and split up

that spectrum more. Exactly. 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 like wild. I know. And people thought that fish were colorblind forever. Oh, I know. I love it. I mean, they can see UV for goodness sake. Right. So many things can see UV. I know. But not us. But don't. I know. Do you know 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. Because as like protect from damage. Don't ask me about the wise, Aaron. It has nothing to do with this episode, so I didn't dig into it. Those are my favorite questions to ask. 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 us a lot in fine detail 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 like we said, you need all three of these cones to be functioning and specifically to be responding to the 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 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 cone cells or for the opsons themselves,

or they can happen because of mutations in the promoter regions for any of those genes, like the regions that tell ourselves 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 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. There also, in addition to hereditary color vision deficiency, is acquired color vision deficiency. And that can happen from damage to parts of our eye during our lifetime. This can happen from other congenital diseases that aren't directly related to, say, our cone cell function.

but it also can happen just from direct damage from various eye illnesses. For the purposes of this episode, because that's a lot, I'm mostly 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 we just call it that? Sure.

Are called anomalous trichromacy. So humans are trichromatic. 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 opposins. But they have some kind. of mutation that results in a shifting of the frame, if 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.

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? Such a good question. There's three different possibilities. Okay. So in Duter anomaly, Duter, you'll hear me say a lot. It's, I think it has something to do with green. Anyways, in Duteronomy, the middle wavelength photopigment is mutated so that it's more similar to the long wavelength photopigment. So when you should be able to 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 protonomily, the long wavelength photopigment, the red, is mutated so that its peak is really similar to the middle wavelength. So what should be absorbed in the red zone is shifted to the green. Does that kind of make sense? Kind of. 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? 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. And so for Duteronomily, you lose the ability to distinguish between reds and greens.

And for protanomily, it's also reds and greens, but like it's slightly the shading is different. Okay. That's exactly right. 100% right. Okay, cool. And those overall are the two most common forms of color vision deficiency. And so that is not caused by a lack of obson, but just a shift in the air. option. Exactly. They often result from unequal recombination. So what you get are these hybrid gene

formations, if you want, the details of it. That's fascinating. I know. I really thought it was just an absence of a cone. Oh, we're getting there. We're getting there. Okay. We're nowhere near done. So there's also Tritonomily, 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 blue cones. Overall, this is far less common. And if you remember that I mentioned that the L and the M have a lot more overlap to begin with,

Tritonomily alone may not result in that big of a deficiency depending on how much it's shifted, if that makes sense. Right, right, yep. Now, overall, those three types, again, are called anomalous 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 dichromacy. 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, protonopia, green, which is called deuteranopoe, or blue, tritinopia.

Here's where it gets even more interesting, though, is that this can 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 end up with two sets of M genes instead of an M and an L. Right. So you have like two green cones, one red cone. Beautiful, exactly. And then one blue. Pretty cool, right? Yeah. So that is dichromacy. Then there is the most severe form of color vision loss. And that is monochromacy, a.k.a. the complete absence of color discrimination. Because like we said, you have to be able to compare

to be able 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, green and red, They sit right next to each other on the X chromosome. But the S cone or the blue cone opson gene is all the way over on chromosome 7. It's nowhere near M&L. So to have true loss of all three of these would be incredibly rare. 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 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 monochromacy's and incomplete or even complete achromatopsia where we have like say no functioning cones, you're not.

just losing the ability to distinguish colors. You're also losing a lot of visual acuity. So people with monochromacy or complete achromatopsia would have significant overall visual field deficits as well. But if we kind of sum all of those fancy words up, if you hear the term red-green colorblindness, that refers to any of those different possible mechanisms of the loss of distinction between red and green. So red-green colorblindness includes duteronomily, protanomily, duteronopia, and protonopia. Okay, that makes sense.

Right, because whether we're talking about a 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 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, 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 X's gets turned off. And because that can happen relatively randomly sometimes, it's also very much. very possible to have color vision deficiency even if you carry a normal or an M and an L X chromosome. Uh-huh. But in general, that is why we see red-green color blindness be far more common in males who are XY than in females who are XX.

Yeah. Now, blue-yellow deficiencies called Triton deficiencies are overall exceedingly red. 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 mis-sense mutations, like complete, pretty severe mutations that happen in the blue cone opson sequence.

Okay. 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 in my reading for this, and I didn't really look into it too deeply, tetrachromacy in humans. Is it real? Does it exist? 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 question, Aaron.

So tetrachromacy would mean four color vision channels, essentially, instead of three. So if we remember what I just said, that the most common forms of colorblindness 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. 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 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 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 color channel or tetachromacy that, at least in theory, if our brain was plastic enough, could use to interpret and distinguish between additional colors and shades. What do you mean by if our brain was plastic enough?

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? Right. Okay. And but this could happen with any one of those options. Yes, in theory. In practice, it's going to be red or green, most of the same. likely. 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, whether they're able to distinguish among the colors that they, you know, should be able to based on our interpretation of the science behind it. 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 Duter anomaly. So that is red-green colorblindness 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,

we're actually able to separate out tones, distinguish between tones that looked the same to, quote, normal color vision or trichromatic 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 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 trichromatic, how can you determine 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 tetachromacy, meaning that she tests where she can distinguish between additional shades and colors. colors based on wavelengths, then a trichromat can.

Hmm. One so far out of all of the people that I read about that were tested. Okay. Okay. But it's really, really interesting. 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 that point, Erin, where did this color vision deficiency thing come from, huh? Oh, gosh. Yeah.

You're going to say the word evolution, huh? 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. Anyone who works long hours knows the routine. wash, sanitize, repeat. By the end of the day, your hands feel like they've been through something. That's why O'Keefe's working hands hand cream is such a relief. It's a concentrated hand cream that is specifically designed to relieve extremely dry, cracked hands caused by constant hand washing and harsh conditions. Working hands creates a protective layer on the skin that locks in moisture.

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This season on Dear Chelsea with me, Chelsea Handler, we've got some incredible guests like Camel Nangiani. Let's start with your cat. How is she? She is not with a thing. Okay, great, great, great way to start. So this is a great beginning and hopefully you'll be able to, I don't know, maybe you will cry. Amanda Seifred. Life is so short. If you feel something like that, you have that. in you for this experience. It's not for a guy. It's for the experience of being in love. And like, it's bigger than a guy. Elizabeth Olson. I love swimming naked so much. And I know you love taking pictures of yourself naked. Yes. I love to be naked. I just want to be in my

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Apple Podcasts or wherever you get your podcasts. So, Aaron, you just 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 like medical history side of the story, I want to try to answer the question, why do we see color? Oh, humans, other primates, birds, dogs, fish, other animals. Why did color vision evolve?

What purpose does seeing in color serve? Multiple purposes? You betcha. 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. 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. Stop it. Raccoons? Raccoons apparently. I mean, I guess they're nocturnal. Yeah. So that kind of tracks. But I did not know that about those little buggers.

Yes. And sloths. I know. I know. Okay. I'm learning a lot. Color vision 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. So what does color vision give us? In a word, information. Ah, yeah. For those animals that have evolved color vision, whether that's trichromacy, like most humans, dichromacy, like some humans, tetachromacy, 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. for food, navigate, or identify predators or poisons. Initially, when color vision first arose, maybe 500 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. 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, but also colors, would 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 500 million years ago, the first mammals were thought to be nocturnal, which helped them to avoid predators. So color vision wasn't as helpful in 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. Huh. Interesting. Yeah. 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. Color vision was selected for within a species or a group 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. Yeah, yeah, yeah. 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, like there are textbooks about this. Yeah. But for anyone who wants to learn more, I will direct you to the incredible book, An Emense World by Ed Yong, 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, I'm just going to stick with what we know or what we hypothesize about.

about color vision and 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 to like long distance, acuity, forward-facing eyes, stuff like that. Between 29 and 43 million years ago, something pretty major happened for a particular group of primates. These primates were dichromats, so they had just two cones, and they experienced the world in shades of blues and yellows. Until one day, for one lineage, a gene was duplicated.

This happened to be the long-obson gene, and over time, one of those copies of the gene stayed the same, while the other accumulated mutations slightly here and there, shifting, that it changed from the long obseng gene to the medium opson 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 fruits or new reddish-purplish or leaves, also a good food source, against the green backdrop of foliage, not only helping them to find the fruit, but also tell when it was ripe. 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 sugaryest, and when the seeds were well developed for survival. It's a two-way street, at least for information. If color is used as information, something has to be producing that information for a reason and something else has to be receiving and processing that information. That is wild. Right? Yeah. I don't know why it like hadn't occurred to me. Yeah. I remember talking a lot about this hypothesis in that evolution of human health class. We might have. back when, but never did we talk or did I think about the plant side of it? Right. And I know that's like results, studies are mixed or at least like opinions are mixed as per yuge. 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 things that we, we interact with frequently. But 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 mean, it's the same with, like, colors of flowers compared to what bees see or what birds see. Or, like, a coral reef looks completely different.

To a fish. To a fish. Oh, my goodness. I know. This is why we were, like, struggling with this episode because it's so easy to, to fall down so many rabbit holes. Oh my gosh, you guys, this episode was the hardest one I've ever researched. Yeah, it was a toughie for sure.

I felt like I had to relearn a lot of things that I had or learn them for the first time. Well, tell me what you learned. 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 dichromats. And sometimes dichromats outperform trichromats. But I want to read you a quote

about one person's experience foraging for fruit who had a red-green color vision deficiency. Okay. Quote. 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 he could see other objects at as great a distance as they. End quote. Interesting. Isn't that kind of cool? Yeah. So there's another hypothesis as to why red-green distinction may have helped us. And I I think it's, I'm not entirely sure, but I got the sense that it has fallen out of favor.

Okay. And that is that trichromacy evolved in primates as a way to help individuals of the same species communicate with one another. So you know those Japanese macaques, like the ones you see pictures of where they're relaxing in hot springs? Trichromacy 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 be, did trichromacy evolve to help

them distinguish red traits in other individuals of the same species? Or did those red traits evolve once trichromacy evolved? Right. Chicken or egg, which came first. Yeah. And it turns out to answer the this chicken and egg question, phylogenetic studies suggest that it's the latter, that these red traits became more pronounced once trichromacy already existed. Interesting. Okay. Yeah. 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 dichromats. Full color vision would have helped primates to distinguish a leopard from a green background with dappled light, for instance. Studies today, evaluating

differences 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 to say with certainty whether that trait color vision evolved because of something like foraging or if it was later co-opted or exploited by that thing, if that makes sense. Throwing a wrench into this evolutionary story is that trichromatic color vision evolved independently in both old and new world primates, but in different ways. Stop it.

Right? It's fascinating. Let's get into it. Okay. So that was just like this brief tour of the. evolutionary history and possible drivers of trichromatic 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. Okay. 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 duplicates. I have an asterisk here because there's an exception. Color vision in New World primates is determined by variations in that original gene. 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 dichromacy, whereas most, but not all, females have trichromacy. Oh, okay.

had read that and I was like, I don't understand, and I just moved on. I did that a lot for human color version. Yeah. Yeah. That's why females, okay. Uh-huh. And to make it even cooler, the different forms of this gene also means that there are different forms of dichromacy and trichromacy depending on which versions of the gene

are inherited. Wow. The exception to this, the little astros. 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. What? Right?

This is cool, Aaron. Isn't that really cool? Yeah. 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 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 hypothesis. that I found or explored, but I just thought that was an interesting little side note. Wow. 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. My goodness. And this is a point that Adyong 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, like, that is not a very useful metric or way to try to understand what another animal or another human or whatever experiences. Right. So anyway, monochromacy, dichromacy, trichromacy, tetachromacy, 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 it is just, it's not, it's just more complicated than that. And being able to distinguish a among colors isn't always for the better, and there are tradeoffs 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 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 vision, they lessened their 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 pretty big assumptions about other animals, like how we talked about earlier, how we thought that fish didn't see color for decades, or dogs couldn't see color at all. And it has also led us to create a world where it can be difficult to navigate if you don't have full color vision. Right. Which brings me to the other part of this history section, the how did we learn about color vision deficiency in humans part.

Of course I have to begin with a quote. And Aaron, bear with me, it is probably the longest quote I have ever read outside of like a first-hand account. Oh, 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, etc., excited by the same object, excited by the same object. may be very 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 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 1790,

the occasional study of botany obliged me to attend more 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 peculiarity in my vision till I accidentally observed the color of the geranium zonally by candlelight in the autumn of 1992. The flower was pink, but it appeared to me almost an exact sky blue by day. In candlelight, however, it was astonishingly changed, not having 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 it was by daylight, except my brother who saw it in the same light 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. I love that so much, Aaron. Right? Do you see why I had to do the whole thing? A hundred percent. Yes. Okay, good. I was like, gosh, this is really long as I'm reading it. Oh, but it's so good because it also, do you know what, That tells you, he's using his rods that we ignore. Yes.

I know. The rods become more important when you don't have as many cones. 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 Dalton in his 1794 treatise titled Extraordinary Facts Relating to the Vision of Colors.

And it's great for a few reasons, right? Number one, it's just such a great, like, systematic retelling of his thought process, of exactly when he realized, how he realized, like, 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 description of, color vision deficiency. Wow. In honor of his observation, color vision deficiency was, and sometimes still is, called Daltonism. Oh. But 1794. Like, doesn't that seem recent? I don't know how to gauge it, Aaron. 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,

but no. And I will say that like there are mentions of confusion in color vision that were, like, it was seemed fairly well known about, or at least enough so for like King George III to make some comment about it at a dinner in 1785. Like some people have an ear for music. Some people don't. Some people have an eye for colors. Some people don't. You know, that kind of thing. And there was also a reference to it in a German medical science magazine and also other scattered references in the 1700s. 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 the same. time, in a way it does make sense, considering that color doesn't seem subjective.

Like, it seems like it's, 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 vision in terms of acuity, like your sight, 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, let alone other humans, I feel like sometimes. So true. And so 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. It happened when it happened. And when it happened, Dalton hypothesized in this treatise that 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.

Huh. Yeah. He requested that after his death, his eyes be tested to confirm his hypothesis. And so the day after he died, July 28, 1844, That's exactly what was done. What? Only the person performing had this autopsy found no support for Dalton's hypothesis. The vitreous humor, not tinted.

I don't have the slightest idea how you would even do that test. Wow. I'll include the paper that mentions this goes into more detail about it. Okay, okay, okay, cool. 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. Yeah.

The explanation that is generally accepted today for most cases of color vision deficiency was actually first proposed in 1781 by a mysterious person named Giros von Gentili. Apparently no one knows anything about who this person actually was or whether that was like a real name or just a pen name. What? Yeah, he's called like an obscure, mysterious figure. Whoa. I hope someone calls me that someday. Obscure and mysterious.

Oh, that's hilarious. And so this von Gentile guy wrote in that German science magazine that I had mentioned that he thought that color vision deficiency, 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. It's interesting that they seem to have known that there were like three things involved. 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 light spectrum, 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. Yeah. Yeah. And so 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. Okay. Okay. That makes sense. And so like how you combine, how many colors do you need to combine in order to make all the colors that we see. Right, right, right, right, right. Okay, yeah. Yeah. I don't know. That's my guess. Yeah. And so then after this von Gentilly, 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. 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. Okay. Okay. Yeah. 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 there's just the growth of the field of vision science. And in the 1990s, 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? How amazing. I'd be so worried to drop that little tube.

I'd be like, oh, God. But they confirmed that Dalton lacked the middle photopigment cone cell, making him a Duteronope. Wow. Case closed. Yeah. Love it. 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 deficiency was seen as kind of an anomaly, 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 how we are each in our own little world and can never truly experienced life from someone else's perspective. Oh my goodness.

But color vision deficiency took on a practical importance, starting in the second half of the 1800s, 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, 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 1880, quote, Daltonism can be cause of discussions, arguments, battles, industrial and commercial losses, dreadful accidents, and irreparable miseries. Wow. Yeah, strong words. And this fear was realized in November 1875 when two express trains on a single track, one heading from Stockholm to Malmo and the other from 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 Freithiof, I don't know how you say it,

Holmgren, suggested that either the engineer of the northbound train or his oiler was colored 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 the speculation, and the Lagerlunda 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. So just to be clear, that was just one guy's idea that this is what happened. Yeah. But nobody knows for sure. No. So, okay, there is a paper from 2012 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 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. Wow. The Lagerlunda collision, you'll find it in so many references 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, we have to perform these tests beforehand.

And I think that's, I'm not an expert in anything related to industry and transportation and stuff like that. But like it just seems like another solution could be to change the signals. Right? I don't know. Maybe that's a very naive. thing to say, but... I mean, I don't know. Someone tell us otherwise. Yeah, like, maybe there's...

I don't know. Yeah. 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 homegren named after that guy, wool strands test, where you had to match wool of different colors. Hmm. And I actually couldn't get a very...

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 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 part of that is a 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'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,

then you don't have color vision deficiency of that particular kind or something to that effect. I just made my toddler take that test. I've taken that test a number of times. Me too. I took it at the same time. 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 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 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. So, Aaron, a little bit of an abrupt transition. But what can you tell me about these glasses and other aspects of color vision deficiency today? I can do my best to tell you something right after this break.

Pretty much every single paper that I read cites that when it comes to congenital color vision deficiency, which again is what we're focusing on, the prevalence overall is 8.5.5.5.5.5.5.5.5. percent in males and 0.5 percent in females. I saw those numbers over and over again, and I wasn't even looking for them. 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 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 Duteronopoeia are more common than pro tenomily and protonopia. I don't know why. And then I don't even have numbers for things like the monochromacy's or tritonomaly because they're just that rare. Uh-huh. So that's epidemiology. I mean, it's pretty pretty straightforward. Okay. Okay. I don't know what I expected. But yeah. But there it 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. 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? Yeah. Why doesn't it work? Why does it work?

So I guess which glasses are you thinking about? Like the Enchroma 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 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 Enchroma filters. they have a lot of theoretical usefulness because what they do, which is fascinating and way above my head, is that they modify the perceived wavelength of light.

So something, Aaron, 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 red, I guess. Yeah. But in the papers that I read at least, there's pretty limited evidence of their actual effect in terms of color discrimination. Huh. 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, 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 Ishihara test who couldn't before.

Okay. At least from what I read. That's very interesting. 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 the same. gene therapy, given that most of the time, what we talked about today, are genetic disorders. Yeah. But there are a lot of 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 opson gene, for example, with the expected sensitivity, right? An M-Oxin if you're missing that one or an L-Oxin if you're missing that one, right? Mm-hmm. 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 vision in mice and in primates that are missing it. So it's possible. It's 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 it beg the questions around like the neural plasticity like we talked about. Can you restore trichromatic color vision in someone who's. eyes developed during embryologic development with only two sets of cones. Can they still then be restored?

Because 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 neural circuits are being formed? Interesting. Okay. So we can do it in animals, at least in a couple of studies, but we still don't know if it's possible in humans. Interesting. Gene therapy. Gene therapy. I always love when we talk about it and then I'm always like, this is a big thing. It is a big thing. There's a lot of implications and complications and question marks. Exactly. Yeah. I love it. But that, Aaron, is. Color vision deficiencies and literally everything I know about them.

You know, 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. Same. Same. Yeah. And about just like color vision in general. I love it.

Yeah. And if listeners you have favorite color vision facts about animals or about humans or about anything, send them our way. I want to learn them. Yeah. 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. prominent researcher in the field, Gerald Jacobs, about the evolution of color vision in

primates and animals in general. There is also a great paper called The Causes and Consequences of Color Vision by Girl and Morris from 2008. And for the history of color blindness itself, there's a book called The History of Colorblindness by Philippe Lantany. And I did not mention this at all. I completely forgot to mention this or include this in my notes. But 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 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 anything about art history. Yeah, abstract, impressionist, who knows. But there's, that is like a really cool. So there's a paper by Marmore and Lantany from 2001 called the Dilemma of Color Deficiency and Art. And on that note, further reading, an immense world by Ed Yong, 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 called The Island of the Colorblind 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, on,

the evolution of language as it pertains to color terminology that I found fascinating. 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 2003 paper from 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 2010 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 and gene therapy, on tetachromacy, 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.com under the episodes tab. Check it out. Thank you again to Kristen for sharing your story with us. We appreciate it so much. Yeah, we do. Thank you to Bloodmobile for providing the music for this episode and every one of our episodes. Thank you to Leanna Skulachi for our amazing audio mixing. And to exactly right network. And to you, listeners, thank you. We hope that you enjoyed this episode. Found it interesting. Learn something. Have more facts to share. Have questions. Anything. And a special shout out to our patrons. Thank you so, so much for your support. Yeah, we really appreciate it. Okay. Until next time, wash your hands.

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