Microchimerism with Amy Boddy
2026-03-03 13:00:00.000 +00:00

David, this is Evolutionary Psychology the podcast. Actual Evolutionary Psychology by Actual Evolutionary Psychologists. David, today we have uh a guest, Amy Boddy, who is in the anthropology department at UC Santa Barbara, and she studies microchimerism. Yes. And I did not really know what microchimerism chimerism was before going into this. And I learned uh during the episode all about it and a bunch of other crazy fascinating things, like um cancer biology and whether rates of cancers you know differ across different animals, whether mammals have more of it than other uh types of animals, um, and even contagious face cancer and the Tasmanian devil. We talked about that. Lots of really interesting stuff.

Yeah, and tons of stuff on I didn't realize about like the placenta and moms and babies, and how um your um you might have the cells of your mom and your grandmother in you, like just oh yeah, cool crazy stuff. Yeah, and and maternal offspring conflict that manifests itself in weird ways with genes expressed from the father's side versus the mother's side. Super interesting stuff. Yeah, no, this is this is mind uh uh expanding, uh bending stuff that um it's so fun to do these things. Like I'm I'm I'm learning a lot. Yeah. Yeah, no, no, no, me too. This was um just as much of a treat for for Dave and me as it will be for you. Um so I think you will enjoy this one. Yeah, without further ado, here's Amy Body and David and I discussing all things um

cancer and microchimeric. I don't know if that's the right way to end that. Cancerous and microchimerical. Yeah. Yeah, we'll we'll we'll Dave and I will work on this, but in the meantime, enjoy that. So Yeah, enjoy it. So we can just go right into it. Um I I labor under the false uh cartoonish impression that um I am an organism and I'm pretty much like all related to my like I am just like an individual thing. I have this idea that sort of you know when when mothers get pregnant the p the relatedness between like the placenta and the mom gets kind of confusing. And I have like intro bio, like I know that like snails, like the expression of like which direction the snail's shell will twist is like a function of the mom and not the

baby. So like you can have the extended phenotype of like phenotypic expression downstream. And of course, all of um uh and I'll shut up in a second, but like all the all the sort of like methylation or um I can't even think what is the term for when um yeah, these things that my methylation or like the epigenetics. Epigenetics. Yeah, people are like, oh, epigenetics like changes the way we think about natural selection. I mean, obviously, if you think about extended phenotypes, they extend across generations. So anyway, this is all long-winded preface to I still have this, I feel like, and I don't know, but I feel like you're going to disabuse me of my cartoonish view that I'm pretty much a uniform uh thing related to myself, and I I I'm not

made up of I don't even know what. So so so where do we start with like uh or or if there's two questions. One is like, what do you do? Because I also feel like like when we talk to like outside people, like we're psychologists, people like, oh, are you analyzing me, you know? But I think what you do, I don't even understand exactly what you do. So I think you have a very particular interesting thing where most people don't even understand what you do. So either can you talk about what you do or am I completely wrong about how I think about the unity of myself? Great questions. Um I don't know I don't even know if what I know what I do, but I'll try and explain it. But that's a great answer. Yeah, me neither.

I've been in every department from like uh the school of medicine to psychology to to anthropology. So yeah, I am um bouncing around interdisciplinarily. Um, but I mostly study um pregnancy and I study cells that cross between mother and the baby called microchimerism. Um and I also st study cancer biology and so sorry, cross between mother and the baby. Could you walk me through how that works? So I do not actually know anything about microcamerism. I'm very excited to learn about it. So what does that mean for a cell to pass between uh the mother and the offspring? Yes. Um so during pregnancy, um the and Dave, you started with the placenta and the blurred boundaries. So the placenta is actually a fetal organ.

It's mostly derived by by fetal tissue. And it invades the maternal endometrium. And it and across species, across mammals, this integration of the tissues is super diverse. It's so cool. It's like the site of evolutionary conflict. So the placenta is one of the most diverse mammalian organs. And it's, of course these two genetic entities that are uh fighting for survival of both of each other, but one wants more than the other. And so it's like a super diverse. Yeah, we actually haven't talked about parent off-burn conflict. So some of our basic evo bio we haven't covered on the podcast. Yes, yes. So so ideally in in many of these scenarios, you can see it driven Paternal genes would like more resources.

Um, and maternal genes, it's in their best interests to save resources not to bleed fully because they want to save resources for offspring in the future, right? Classic, putting it all on the yes, yes, exactly. So you see this like tug of or um, and you can see it playing out at the genome level with um genomic imprinting. So genes that are specifically turned on just in the paternal lineage versus genes that are just turned on in the maternal lineage. And so right there at the site of you know resource transfer is the placenta, it's transferring resources to the offspring. It's communicating with the mother. It's doing all this. And so across mammals it's quite diverse in its its shape, its size, how it diffuses,

how it integrates into tissue. And so humans have one of the most invasive placentas. And so our placentas actually the specialized fetal cells like invade the the tissue so much that it widens the maternal spiral arteries that kind of embed the endometrium and completely remodels it, has direct access, taps the resource. I think the baby, and when we think about invasive placentas, the paternal genes won, like it got the upper hand in that scenario, actually, because um, because then once there's direct access to resources and it's hooked on, when suddenly there could be lack of resources, what the baby does is ramp up maternal blood pressure. And so we see this with pregnancy complications and stuff like that.

So when we're thinking about, you know, cooperation conflict, yeah, um, humans are unique in that, but yeah, our placenta might have um evolved to be quite invasive in that of course was adaptive, but um the the the downside to that is it's costly on the maternal body. Wow. Yet another thing women can blame men for. Yes, exactly. Is is the is the idea that men won in the sense of still that's like still naturally selected, like in the sense of if there's differential reproductive success out in the world among variants of this like sort of offspring production system, is it that the uh the babies that are extracting more are doing better. And that's sort of the um the the check. I mean, because obviously like you can't kill the mom, like right, like yeah.

Well, it's it's it's so complicated because if you have we know birth weight matters, right? Birth weight matters. A bigger baby um is gonna survive better. It has more fat. It's got more resources, right? We see this all the time that it matters. But on the other extreme, a bigger baby means more potentially obstructed labor and birth complications. So there is this, you know, um really stabilizing selection on birth weight. And it's on average like seven pounds. And I think it's so cool. Like there's just not a lot of wiggle room that you have. And it might be um yeah, pun intended. Um the um yeah, and it might have to, you know, our birth is the timing of birth is just interesting too, because as mammals, um, comparatively you are

termed like at full term at 37 weeks, but you can go up to 42 weeks. And I think that is mind blowing that like we have basically this five, six-week window where like baby could come anytime, and we don't know. And we actually, from a biological medical standpoint, don't really know what triggers labor. We know there's like a cascade of things, but we can't predict it. Yeah. We don't know it when it's coming. And it's I think, yeah, all of this negotiation between the mother and the baby actually. That's really cool. Yeah. You would expect there's tremendous selection pressures on the determine pregnancy or a but determine birth like activate birth program. Yes. Uh that's really interesting.

Yeah. Yeah. Yeah. Um if we could if we could get uh into um the logic of of the conflict here, because it's not it's not parent offspring conflict. So that's when, you know, parents are uh you know equally related to all their children, but uh siblings are twice as related to themselves as they are to their siblings and to future siblings. And so that creates conflict where the siblings or where the children are going to want more resources or twice as much for themselves as for their siblings, whereas parents are gonna want to distribute resources and investments equally. And that's the fundamental conflict that that Robert Trivers talks about. Fascinating idea. But this is not that. This is uh paternal and maternal conflict.

And I want to see f see if I can um walk through the logic of how this works. Because I I'm I'm I confess I don't I don't quite fully understand it. So is it is it the idea that um men have or the males have a greater um ability to invest in say other uh reproductive opportunities, and that's why they want more investment from the mom. That that uh if uh uh like so so why why is it in the male's interest to for the mom to put more resources into the offspring than than would be otherwise beneficial to her or helpful or healthy for her? It actually builds on parent offspring conflict. And I believe David Haig coined the term it's maternal fetal conflict at this point. Ah, okay but it is, you know, again the under the same principles that the fetus shares

half the maternal genes, but then the other half are paternal genes or from the paternal point of view. And it's those that are driving the conflict uh you know, as in, you know, the um the paternal genes the best interest is to invest in that pregnancy and to get that baby the most resources as possible while the mother is only half you know related obviously important for survival of the baby um although she will have more babies right and so the idea is that you're going to invest as much as you should not as much as you can in this baby. And but yeah, and just to be clear, like that's that's really helpful. What is the logic though behind the the dad? Like let's, you know, I'm the dad. Right.

Why why do I want the baby to invest more for this particular pregnancy? Why do I want why do my genes want to invest extract more from the mom than the mom wants to extract? Is it because actuarially I might be mating with somebody else in the future? She might be mating with somebody else in the future. Like is that the okay yes, that's that's the idea, but I think it goes back farther than humans. Um in terms of looking at genomic imprinting um that arose with the evolution of the placenta. Um only placental mammals have imprinting, where the again there's like this allelic expression that really depends. There's about 120 imprinted genes. Um and some are paternally imprinted um and some are maternally imprinted.

So that means some are just expressed from the paternal genome and it matters. They have different uh physiology they have different impacts on on the the development of the baby. And there's, and we learn this from there's various diseases where if you delete the maternal allele versus the paternal allele, those are two different phenotypes that arise in the baby. So it's it's super interesting when you think about it from that. And so, but that arose really, really early in our evolutionary story in terms of um maybe a hundred million years ago with the evolution of the placenta. Wow. And even, I mean, the other thing I'm sure this is, I'm sure you've thought of this. I'm just saying it out loud.

Yes. Is that um there's also just the cold calculation of the mother faces this. Well, if I do invest to a certain level, there's the chance that I might die. Yes. And the the the dad just doesn't have that calculation, right? So there's also just this cold calculation of you just you just snip out even even assuming a monogamous species, there's still just the the the trade-off, the cost benefit of well, if I invest more in the offspring, there's a chance that the mother might die. And if you're the mother, you land on a different trade-off point than if you're not the mother is simply because, you know, like, yeah, the mom might die, but like my offspring might be better off, and it's not me.

So like it's you know, obviously it's not explicit, but it's just cold calculus. So I think even I would I would think, at least off the top of my head, it seems like even that, just because you're not the body risking death or you're not the one investing, there's still a conflict between those two. You don't land on the same threshold. Yeah. Yes. But yeah, I think it it's more of a historical legacy evolutionarily because obviously within humans, we um if there's a tons of data to show if if if mother dies, baby does not have a good chance of surviving. Oh, that's true. Yeah. Um so I think a historical legacy I see um that we have, you know It's why we get sick. Perhaps from an ancestral form in in which maternal uh mortality wouldn't have been such a

death sentence for the kid, perhaps an ancestral form. Or more polyga more polygamy or something. Oh, interesting. Yeah, because we're we're hyper adaptationists. We're like, it must be designed perfectly. That's why is this, yeah. Oh yeah. Yes. Yes. Where I actually don't see the I I s I I don't I see us as like a messy bag of conflict that somehow is still able to reproduce. Yeah. Like we're just like there's all these internal conflicts and and there's adaptive compromises and then it just like yeah. Yes. Ever ever since my child was born, I just like to just slightly editorialize for a second. Like people often celebrate like soldiers and things, and I'm like, you know, it's violence. Like, if you want heroes, if you want to see a hero go to a maternity ward.

Yes. Like there are heroes, real heroes in the world every day. Uh they're in a maternity ward. It's incre I mean, it's crazy. Yes. Yes, yes, absolutely. Um anyway. So yeah, uh, that all to say that there's cells that then get transferred between our like deeply invasive placenta, right? There's fetal cells that get transferred into the mother's body, and there's maternal cells that get transferred into the baby's body. Um, and we used to think this was a spillover effect because we have a deeply invasive placenta. Um, but then it was observed in species that don't necessarily have as a deeply invasive placenta that have that like road, um, that that highway that um our placentas have. Um and also these cells persist decades

after the pregnancy, and they're doing things. So um we think that potentially there is an adaptation there, and they're they're actually um selected for to help with the pregnancy, but also help with that organism afterwards. And that actually sometimes that can still lead to conflict. So that can still lead to problems. So another way to put it, if I understand right, is that the mechanisms in the mother have a have a biochemical sample of the at least the genetics, if not other substances of her offspring inside of her. Yes. Yeah. Yes. Um, and we we think they last last a lifetime and they have like biological impacts. And if you think about it again, thinking from like this, I think about it from a maternal

fetal conflict perspective. it's the baby's insurance policy that the mom will take care of it after birth, right? It's it's been like a really costly negotiation for nine months. Um, and now there's cells inside the mother that could maybe potentially help the mother care for the baby even more. So maybe they're involved in lactation biology, attachment, like all of these things, helping the mother heal after the pregnancy as well, um, in order to make sure they have the best shot at survival. So is it it that's really interesting? Is it because the baby is new and has new genetics and has new stuff? Is it sort of like a it's like a booster rocket of this is a brand new genotype? This is brand like you know, everybody has this model of like babies are fresh, and it's

obviously like there's there's so much here, like the pathogen coevolution and stuff. So the idea is that baby cells are special, fresh. This is the metaphor. And they're coming in and like hyper helping the mom. Is that is that I mean, I realize it's like a I'm it's a metaphor, but is that Yes. I that's the idea. So we don't know, right? This is like um it's it's a newish field. I don't want to say completely not new because we knew about this forever. It was just really hard to study because they're rare cells that are half identical to the host. So we didn't have a lot of genetic tools in our toolkit to actually study this. Actually, what they used to do is look for the Y chromosome. So it was women who had given birth to a son.

And they just like draw their blood and look for Y chromosome and say, oh, these cells are still here. But then they started doing it for a bunch of women that had never given birth to a son and still found Y chromosome in their blood. And then it was like, where are those coming from? And so then they had a bunch of just female lab tax doick that thought it was contamination and still found the same. Um, and what we've realized since then is these cells come over quite early in pregnancy before you even know you're pregnant. And so you could have been had a really early spontaneous miscarriage, never knew about it and had cells seeded into your body. Wow. Um wow. We also learned that obviously you can have that effect if it's twinning

in utero, and then the twin doesn't. Right. But there's this really nice study looking at um um these girl Danish girls and showing that they it was before they went through menarchy. So before they had an opportunity or chance to be pregnant, and they still found Y chromosome in in their blood. And what they've found suggested was maybe it was from their older brothers. So our cells are going into our mother. Oh wow. Right? Yeah. And so the older sibs could actually be seated with. yes. Wow. So there's the the the tr the family tree gets very the very big, yeah, very big after that. So Yeah. And and have we gotten to microchimerism yet? Or are we still walking to that? Because I don't know, I don't know exactly what the definition No no, don't apologize.

I'm just yeah, I'm curious like what is that are those Y chromosomes in the female's body? Is that an example of microchimerism? It is, yes. Okay. Yes. Um, we're still working on the definition definition of it because some people would argue just because you can detect a gene doesn't mean it's a cell. It could just again be a byproduct of a cell, where is it coming from? Is is microchimerism does it have to be an attack cell? Does it have to persist? Does it have to do things where we're actually struggling, not struggling, but debating as a community what the actual definition is. But yeah, what we're getting to is microchimerism is a small amount, small micro of chimeric that's different, different genome within you.

And we are all microchimeric because we're all mammals. And in the genes, I mean, you know, uh I mean you and we talked about how Jurassic Park is one of our favorite movies. Yes. Um obviously everybody knows that like genes code for proteins that builds the animals or organisms, din dinosaurs, for example. Um, but um but why is that significant that the genes are there? like because you could just imagine, well, yeah, the genes are there. Like the null hypothesis is sort of like, well, yeah, there's like leakage of cells. Who cares? Right. Like it's yeah. So yes. Uh I think it's really, yeah, it's important for a few different reasons. One, um, the genes are there and the immune system is not getting rid of them.

Why? Right. Oh, because we've learned self, non-self. You like that's immunology 101. Anything that that's why we can't have these large-scale organ transplants that from anyone, right? Um, even if it's from a sibling, you still have issues, right? You have to have immunosuppression. So why is the immune system fine with this? Um and then the other thing is um we're realizing sometimes the immune system is not fine with this. So women, excuse me, are at a higher risk of developing autoimmune diseases. And some of the idea is that it could be these paternal genes expressed through these baby cells that are triggering an immune response. Wow. That's fascinating. I mean, so that that would predict a higher prevalence of autoimmune

diseases among women who have uh microchimerism. So have, say, Y chromosomes that can be detected. Yes. Um is that, I mean, uh has that prediction been tested? It's been looked at uh often. And so I can I can say autoimmune diseases are complex and there's many pathways to them, right? And so you could just have a genetic predisposition. We know individuals that develop autoimmune diseases in their early ages before pregnancy. There's men that develop autoimmune diseases. Like this is this is not the answer to autoimmune diseases. But along with the genetic predisposition, there are a few papers showing that yes, but it matters on your genetic makeup. One, you I'm gonna simplify it as you have to be predisposed to the autoimmune disease,

right? And then you have to be exposed to a certain paternal allele. Not all per paternal alleles, but certain ones can trigger that reaction. So it's like the perfect match to create the autoimmune disease. And so, yes, I think there's pretty good data to show that in those scenarios it can trigger the reaction. Fascinating stuff. Um so we've gotten to maternal fetal conflict, we've gotten to microchimerism. Yes. Um there's still another area of your research that I'm very curious about, which is uh cancer and the evolution of cancer. Um from an evolutionary perspective, it makes a lot of sense to me why we we would be vulnerable to pathogens like bacteria and viruses. Um, because the bacteria and viruses, they win in some sense.

Like they're evolving to invade us and exploit us. Um, whereas with their tool, we're their food. Yeah. They want to eat us. They want to eat us and have babies. That's their goal. Totally. Uh yeah, and we're just at odds. Um so that I can wrap my head around. But cancer is a little more mysterious and hard for me to have my wrap my head around because those are my cells and they're hurting me. What are they why are they doing that? And how why hasn't evolution gotten rid of that? I love this question. Um okay. Um we we have a few answers for you. Um one is we cells had to suppress their own interest to become a multicellular body, right? We used to be single-celled organisms that could just multiply.

We started having to cooperate once we became a multicellular body. And you suppress your cellular fitness for the multicellular fitness, right? That's crazy. It's so cool. It's such a weird. I mean, it makes total sense when you say it out loud, but it's such a I mean, as a macro, a macro, a micro, a multicellular organism myself, I find it it's it's counter to my personal experience. That would that is tautological, right? But no, that's amazing. Yes, exactly. Yes. And and we have conservation of genes that have persisted since we were single-cell organisms. And so some of that is still in there, right? And so we have these multicellular organisms. And you know, the bigger you get, the more cells you get, um, the better you are at

competing for mates and resources and all this stuff. And so in certain organisms, it's in your best interest to have a lot of cells, right? And cancer is a disease of cells. Okay. And when you have a lot of them, you end up having to control them and they end up when they're proliferating, mutating, and causing mutations that knock out their basically cooperative behaviors. And they become selfish again. And they start dividing. And then there's a different selection going on there where they're now dividing for their own self-interest instead of the interest of the multicellular organism. And that oh go ahead. Oh, sorry. And the reason that we don't get rid of it is because there's trade-offs in that.

There's selection for growth and survival and reproduction. And we see these genes that are important for cancer are sometimes important for implantation and fertilization. And so they're getting selected early and then they get turned back on later on. Wow. Would this be an example of I uh I think it's Peter Medouar came up with his theory of aging, where the idea is that genes that might give you a fitness advantage early in life but impose a fitness cost later in life will be selected for in an organism. And insofar as those genes accumulate over time, uh the genome will accumulate uh features that will sort of cause the body to break down uh in late age uh the further the organism gets past reproduction and and the the further away from the window of selection that that

um evolution will be focusing on. Um I I always found that theory of aging really fascinating. It seems like this might be an example of that, where genes that that help you with gestation or implantation early in life actually increase cancer risk later in life. And this would actually be an example of Medouarin aging. Yeah, and it is that. And what we see, and it's a little nuanced now because I think there the we're humans and we do things that increase our risk of cancer through our lifestyle, like as smoking and you know, various other things, being out in the sun too much. But in general, cancer is a disease of aging. It is, if you look across many different populations, it's an old age disease,

right? And it's after basically those soma and and the mutations have accumulated. Um, but that's not it. It's not just mutation accumulation, because there's been some really great studies that look at like normal healthy tissue, and they have like the mutation profile of a cancer. And so along with the mutations, there's a breakdown in the body as we age, right? And so suddenly our immune system isn't working as well. Our immune system can clean it all out. The tissue fitness matters. And so suddenly the cancer cells have a competitive edge. Right now, when the cancer cells are in a multicellular body of a really healthy individual, and I say healthy, but a a young individual that has, you know, good luck

too, um, the neighboring cells actually can suppress it. But suddenly the neighboring cells get older as well, and the tissue fitness landscape changes. And that's when cancer cells suddenly have a competitive edge and kind of outcompete the the the healthy non-cancerous tissue. Is this why is there uh I mean this seems like a dumb question, but is there evidence that exercise helps or prevent cancer in the sense of like I always hear Dan Lieberman quote of like diseases of old age are diseases of sedentism. Like, you know, and if you look at populations that are more active all sequel. Is that true? Yeah, it's true with cancer too. It's not everything. Cancer is like genetics. You can have underlying genetics that just predispose you to it.

Bad luck. But there's a lot of bad luck in cancer. And it's just you just like our our genomes, we got three billion base pairs. What mutations that land in an important cancer suppression gene? Yeah. Sometimes just bad luck, right? Um, and then the other component is lifestyle. And so they do see yes, exercise is a huge impact on being protective against against cancer. And presumably that's like the the immune system and maybe health of cells sort of if to again gloss a lot, but that's sort of gloss a lot. And then in general, exercise, even though it could be like while you're exercising, it's it's a acute inflammatory, it pulls in some anti-inflammatory mechanisms afterwards. And so again, our immune system is always our double-edged sword where it can help us fight

the things that are trying to eat us, the bacteria and the viruses. But when it creates too much chaos, it also promotes these cells to survive and thrive in in a cancer rich environment. Yeah. So when you're when you're studying this stuff, are you like have you been thinking so this sounds like a lot like the immune system is important. Like you talked about the immune system. So clearly like the immune system, there's been selection to keep these microchimeric cells in the body and the immune system is has evolved, co-evolved with the presence to allow them. Yes. I don't even know what my question is, but like what what's up with that? I have an answer for that. It's my new project. No cool.

I think, yes. So we looked at cancer. Um, I'm gonna take the long way there though. Um so we looked at when cancer arose across a tree of life. And so we see with most multicellular organisms, there's at least some evidence that they can get cancer or cancer-like properties, okay? Even plants. While plants don't have a vascular system like we do, so it's not so impactful. Um, but once we get into maybe vertebrates or even you know, mammals, we see cancer that is prevalent across the tree. It's ubiquitous across many different animals, but the rates vary, Right. And so I would argue that most organisms are not completely cancer resistant, but some are actually really good at not getting cancer better than humans.

Right. And so if we look across the tree of life, we also see that mammals in particular get more cancer than other groups when we compare them to birds and lizards and various other organisms. And so what is it about mammals that makes us so different? Some of it is one where, you know, we have to internally gestate and we have placentas and placentas look very much like cancer in some sense because they invade and they recruit blood vessels and they do growth in the body. And so is it that because we're placental mammals, we also have this blind spot? And so one of the ideas is potentially, yes, maybe our immune system cannot be as robust as we'd like it to be, because we have to be able to recognize and be okay with different

genomes being in our body. Amazing. That's just what I think though, by the way. No, that's it's not. I don't know if that's like a community wide consensus. That's a fascinating hypothesis. Yeah. I and also I like I my understanding is like and maybe this is just noise, but like things like like dogs, like certain dogs get like like labs get really high rates of cancer. Um and you know, I it's in you know the in the placenta like grows really fast too. Like, you know, I mean it a lot of this feels like it's the a lot of it is sort of maybe developmental things too. So like the immune system has this issue of like, is this a developing offspring? Is this my development, or is it cancer? That's a hard problem, right?

Yes. To tease it. Yes. Yeah. Yes. Yes. Um no and dogs do get more cancer. They're domesticated. We think a lot of it has to do with like inbreeding. So a lot of the domesticated species. And so we bred them to look real cute, but they came with a a baggage in their genetic you know predisposition for disease in general um other species that get a lot of cancer are like ferrets and hamsters we think there is we have this like life history perspective when we're studying cancer where we think like these fast life history strategies that just go reproduce live shortly you will not evolve defenses against cancer because you're not living long enough. You're going to get, you know, eaten by a hawk, right?

Right. And then on the other end, you have these species such as humans, but also elephants and whales that grow really big and slowly. Um, it's in their best interest to maintain their soma, you know, and that means also cancer defense, right? Like making sure you're dividing your cells carefully, there's no mutations, you have in you know enhanced immune activity and various things to prune cancer like cells from them. Is is there any um is there any evidence that like these immune responses or the micro the genetics of offspring, you know, what consequences other than the immune system lets them exist? I mean, it sounds like this might be the edge of science, or we don't know. What what do we know of like what consequence they're having on the on the

mother or on us, you know? Like do we know? Uh yeah, we don't know. Um there's a few papers. So going back to I love that we're jumping from sometimes people think I study these two very distinct topics, but we're yeah, no, it seems like uh it's all related. They relate. So um yeah, the the fetal cell, there's some really great studies to show the mother is sending cells to the baby that are c clearly important for immune education. There's, you know, passive immunity through antibodies being sent to the baby, right? That are really important for survival, especially if it's like an infection that's happening in real time, right? But also immune cells are going to the baby as well. That's an amazing, you know, the immune system is completely naive for the baby, and the

mom has already had this lifetime experience of exposure and is now passing cells on. And then is that through placenta and breast milk? Yes. Okay. Nice. Yes. It goes through the placenta and then again through through the breast milk. Um, there's maternal cells being passed on. Fetal cells get a little bit trickier because those are the baby cells going to the mother. Right. What the heck could they be doing that could actually impact the mother's survival and reproductive success? Um, and again, like you had mentioned, it could be like just this burst of young stem cells that and and there's some data to show potentially yes, or some mouse models that show that these cells can track to sites of injury and help repair it.

There's um these, there was one paper that showed they looked at women in their C-section scars and they were able to find baby cells, fetal cells there. And they were like expressing collagen, which is really important for you know healing the C-section. So yeah, some of it is maybe these, it's just a burst of new cells, like uh, you know. Um, and there's one paper out looking again, broad broad scale at like male origin microchimerism. So not even like being specific about the baby, but just looking at Y chromosome in women. And they found women decades later that tested positive for male origin microchimerism lived longer. Wow. So there could be some potential benefits. And we don't know, we don't know why some women we can detect these

cells in them and other times we cannot detect any cells after they've given birth. I think it's more our method method methodology of not being able to detect rare cells than them not being there. But yeah and how how new I mean this sound like as you alluded to earlier it sounds like this is very much this uh science is very much dependent on genetic sequencing being faster and cheaper or How how old is this? I mean, you said we know we've done some of these things, but like, has is this a case where the change in technology has allowed this research area to proliferate such that it's now feasible to do this at scale? Yeah. Yeah, absolutely. Like it was, you know, 100 years ago we knew that this with potential that cells were

coming over. Everyone just thought it again was a byproduct of this spillover effect, right? Of of being a deeply invasive placenta. Um, and it wasn't until like the early 90s, I believe, was the first paper that showed, oh no, these cells stay around. And that like had a mind shift. Suddenly, evolutionary biologists were interested in it too. Like, wait, like these cells are persisting. Do they have a function? And is it a function that's important for that body actually? Do we and have we co-evolved it? So we expect that right um relationship to to happen. So and then if uh if I can have my mother's um cells in me, can I have my grandmother's cells in me? Yes. We think so there's one paper that has shown it, right?

But of course there's this route, you know. Um and there's one paper that showed that yeah, grandmother cells were in the cord blood. So we think that that's possible. And you can imagine a scenario where there's a group of cells that just get really good at jumping generation to generation. Yeah. Right. Um and it can go on for potentially a really long time. Yeah. Yeah. It's sort of beautiful in a way, right? It's it's yeah. I I to to be slightly like uh poetic about it. But yeah, there's something cool about that. Yeah. Yeah. Yeah. You literally have a you know bits of your your grandma in you, potentially like Yes. I know and and then you hear things like, Oh, she looks a lot like grandma.

Like there's a cousin, you know, and the cousin's like, they look a lot like grandma. And I'm like, what if what if it was more grammar than we know oh yeah for me because these cells are coming over what's the what's the potential that it can actually like be a part of the germline or insert really early into development um and yeah have you know more of a chimerism effect than a microchimerism effect. It's like painting such a messier picture of nature than what I might be accustomed to, where it's just like these cells and DNA strands are just sloshing around and I still got bits of my grandma in me. Like it's just so much messier than than I would think. I don't know. It's it's yeah, horizontal transmission really screws me up too.

Like if we if when you add that in, you're like, oh my god. Yeah. this might seem like a dumb question, but I'm curious. Um would you expect differences between mammals and marsupial mammals where the gestation isn't quite as internal? Uh would you expect, say, less microchimerism, less autoimmune diseases, perhaps less cancer? This is a great question. Um we we're trying to look at that. Um we don't know if there's microchimerism in marsupials. I think there is. I'm I've I've had some leads on some mars marsupial blood before, but we haven't had a chance to look at it. Um, but but potentially. Um, and then the other thing that is complicated is yeah, you could maybe suggest um less cancer. So there's marsupials that have a very um placenta-like structure

that's really quick, and then they go to the pouch, right? And then across mammals, there's basically three different invasion types of placentas from a very um surface invasion to some kind of integration into a superinvasive placenta. And it's assumed that organisms that have the super invasive placenta have the most microchimerism. And there's also predictions that those organism or those organisms have the most cancer. Like there's a stepwise. The more invasive a placenta gets, the more cancer we should see. We do not see that in my data. No. It's like a really nice theory. It's in evolutionary medicine textbooks. It's much messier than that. And so with the marsupials, what we see is that um they

could have went through some genetic bottlenecks and um actually um some of them get a lot of cancer but it might have nothing to do with their relationship with the placenta it could be just other factors And actually, um, the Tasmanian Devils. Have you heard of the Tasmanian Devils? Well, I've seen Looney Tunes, so yes, I'm totally familiar with it. Yes. These these creatures actually, they're not like the Looney Tunes character in the sense that they spin all around, but they are a little crazy in that in their they're very bitey creatures. And they have developed a transmissible cancer. Whoa. So that is they have a tumor on their face that existed on a devil hundreds of years ago, um, and it still persists.

And they just transfer cells, not a virus, cancer cells from an individual that is no longer alive. Whoa. And it's pretty uh detrimental to the Tasmanian doubles. They may go extinct because of this. Um not only once has this evolved, but now there's a second strain of transmissible cancer. So again, it's cancer cells that are hopping from host to host to host. Wow. And they can't, um it wouldn't does it cross species, like if a Tasmanian double bit uh on their organism, it's not it has not crossed species. There's transmissible cancers in bivalves too, like muscles. Oh wow. And those have crossed species. Wow. Oh man, I mean that's a great topic for a the next pandemic movie is a contagious cancer

right? Yes. Gets spread from the Tasmanian devil. Well, you have to be bitey, right? Like we've talked a lot about like why don't we have contagious cancer, right? And there dogs have uh contagious cancer as well, and it's sexually transmitted. Um, and it's treatable. Um, but it's from a dog that again lived like 10,000 years ago, and the cells still persist. Yeah, it's really mind blowing. Um, but um yeah, the the routes to transmission, if you wanted to pass cancer cells back and forth, you need to either be bitey or it has to be a sexually transmitted type of thing, right? Right. Um so is the clam biting people? No, but well here's the other thing that or you live in the ocean. Uh right, of course.

Because the 'cause you're like we're not just like sucking in cells as we move through our environment. Land, land animal. Oh yeah, that's true. Cause I always think about like you know, vectors, like mosquitoes. But yeah, the ocean is like a whole vector. It's a whole thing. It's a whole another world. Yes. That's true. Truly wild and bizarre this contagious face cancer business. Um it's like put that on a t shirt or something. It's very weird, yeah. Yes. Uh but I i I'm struggling to wrap my head around it because it it makes sense that cancer might evolve in in me if I'm really old and my tissues are damaged, my immune system isn't so great, uh, and there's been a lot of time for the cells in my body to accumulate

mutations that might serve the the self-interest of the cell at the expense of the rest of the body. And so it makes sense that my body might have a hard time tamping down on the cancer. But once it gets into someone else's body, particularly someone else who's young and healthy, then it's a whole different ballgame. And so how how does the cancer survive once it gets to someone else's body? Yeah. Yeah. So there's been studies looking at humans, and there's only been a few cases. One is transferring through pregnancy. Unfortunately, cancers can metastasize. Um, but other than that, we're pretty good at saying, no, that is not me. Um, I, you know, I reject it, the immune system rejects it. When it comes to the Tasmanian devils, um, and sorry, I'm I didn't complete

the the the full story because we talked about genetic bottlenecks. Seems like the Tasmanian devils went through a genetic bottleneck and they have reduction of their MHC receptors, their self non-self receptors. And that reduced genetic diversity has allowed them to not be able to recognize that as non-self as much as it should. Um so unfortunately that was the it was like a combination, the perfect storm for the test, as you said. Like it's just this example of just a species level bad luck, basically. Exactly. Yeah. Yeah. Yeah. Wow. I I love this new picture of of nature where just shit happens, there's bad luck, things are sloshing around, everything's messy all over the place. And somehow we survive.

I know. Yeah. No, again, as a mach as a multicellular organism. And we live for a really long time too. Yeah, no, it's a miracle. It's amazing. All this anything works at all. It's really Yes. When you um uh you mentioned evolutionary medicine. We haven't really talked about that. Um, you know, I don't want to go away from what you're an expert in or what you're, but can you talk about sort of like how you view I don't know, I don't even know enough about you. You're the expert in evolutionary medicine. You're sitting, you're you are an instance of sitting in that Venn diagram of basic research, and then people maybe doing medicine. Can you talk a little bit about that, and I don't even know what to ask because I don't

know enough. Yes. For it's so funny. So I teach evolutionary medicine. I'm teaching it right now at UCSB. And the first day I always ask the students, even though there's a description, they don't know what the class is. Yeah. And I always ask them what they think evolutionary medicine is. And it says how evolution evolved over you know time. and it that's not what evolutionary medicine is how medicine changed over time yeah how medicine changed over time um but evolutionary medicine um is you know the the why we get sick okay so a lot of the medical field so I did my PhD in a med school and so it was a lot of the mechanisms you know this protein this gene this you know factor the you know, proximate

mechanisms of the disease. And then evolutionary medicine takes a step back and says, well, why are we vulnerable in the first place? Why are we vulnerable to cancer? Why are we, you know, vulnerable to these specific diseases? What is it in our evolutionary history or past? Are there trade-offs? Are there constraints that we're vulnerable for this sickness? And I think it's a really powerful way to view diseases. Some have argued that maybe it doesn't have such a practical impact sometimes, where it's like, oh, cool, it's because we're multicellular. Like, what now? Right. In terms of cancer. But then other times it does have a really um interesting point of view because then it's like, oh, but other species that have also are multicellular get less

cancer than humans. So what have they done? So we can take this comparative approach when we're looking deep in the phylogenies. But then also some really great ways evolutionary medicine is moving forward in like a clinical sense is trying to understand both antibiotic resistance and chemotherapy resistance because they're following principles of evolution, right? Bacteria, we provide a selective pressure, they respond, they evolve resistance. Same thing with cancer cells, actually. That that mass that's in your body can start evolving, right? It's operating on principles of natural selection. And um, when it comes to treatment, we could maybe harness these principles of evolution to do a better job at avoiding resistance.

Because the problem with medicine such as antibiotics or chemotherapy, we hit a dead end when we hit resistance. And we don't have any more drugs to provide the patient, right? Um, so if we could avoid resistance, we might be better off. Um, and the patient might do better. And so there's such great work looking at how you steer um the evolution of a bacteria population or a cancer cell population to where you want it to go in terms of their evolutionary trajectory. And I think that is so cool. So like domesticating the Yes, exactly. Yes. And there's all these ecologists that have jumped in, especially in the like cancer world, where it's like, okay, here's a scenario that I see in ecology. So you have, you know, a rabbit, right, that's out in the the savannah

and there's a hawk coming for it. Okay. And so the rabbit, what does it do? It darts under a bush. Where are all the snakes? are hiding in the bush? Right. How do we do that same principle for cancer? Like how can we switch the ecology to end up tricking them into their own demise, basically? So like so yeah. So like an example just like concretely would be some I mean, like this is still I have no no idea, but just to make like make sure I understand, would be something like you have bacteria that feed on something, and you select for those bacteria that are really efficient at feeding on this thing, but then that thing that you've selected those bacteria for, then if in a generation later is the

vehicle of drug delivery. So you've selected for the bacteria that are super good at uptaking this material. Let's give you all the resources. And you Trojan horse the drug later, and then you're like boom, and they just take it up super well. Yeah. Yes. So there's these ideas circul circulating. Another one that's really prevalent um right now is actually let's give less drug. Let's not create resistance in the first place. Because what we realize, especially I'm gonna just gonna the same principles apply to both, but I'm just gonna talk about cancer biology is in a tumor, you have a bunch of cells that maybe can respond to the drug, but there's already cells that are resistant to the drug. And so you're benefiting the tumor if you kill all the cells that are responding to your

drug. Because in the cells that are resistant, we have this competitive release. And then all of a sudden, oh no, your drug doesn't work anymore for that population. But what if you kept the resistant cells and the sensitive cells within the same tumor and they competed for resources. And what you did then was just knocked down the tumor smaller. Wow. Um but still had control over the tumor. Yeah. That's right. Like it's all about staying, but but that psychologically will have to change our our way of how we think about cancer. Because right now there's like the war on cancer, like all of these metaphors about you got to get rid of everything. It's like a contamination. It's like it's like dirt and you've got to clean it out.

It's like a very it's like a pathogen right. And it's and maybe it's this view that we are this this one uniform thing, right? Instead of this messy thing. And so once there is this idea that oh we can maybe treat cancer as diabetes, where you know it's we're not going for cure, we're going for control of the disease. It's been um really hard to kind of get people wrapped around that mentality. But there are a few clinical trials out there working on exactly doing that. Same drug that is already passed and given to patients, but just at lower doses, um, and only responding when the tumor responds to it. Yeah. It's so interesting. Metaphors of like science or physiology. It's really interesting.

I never thought about like metaphors of like how to think about medicine. But yeah, that's going to totally affect the way you know physicians or the the applied folks are going to use things. And one of the things sort of implicit in a lot of our science is we we change the metaphors we use as we learn more, but maybe that hasn't spread is sort of what I'm hearing. Yeah. Yes. Yes. And and the thing is, unfortunate well, fortunately enough, many times there could be a cure, right? There's many people that I'm not saying this is everyone, like there's many people that get cancer and do chemotherapy and it works. And they're five like five years, 10 years, no, no sign of disease, right? And so it's one figuring out who falls into what category.

When is it a cure case? When is it a case where we're just going to do long-term treatment? And then how do the whole treatment regime should be how do we avoid resistance? So super cool. Yeah. If it's it's sort of it's it's I love this, you know, replacing the metaphor of um destruction and and conquest into like herding and domestication, like dealing with the living organism and and trying to understand how it evolves on its own terms and and using that um to control the disease. Yeah, and I we have a lot of patient advocates that we work with, and some of them just are definitely very open to the the idea, especially when they've been living with the disease for so long. Is it it's like it's a part of me?

Why don't I go ahead and name it? And like we're we're we're like owning this this part of who we are becoming in this stage of our lives, right? And so yeah, I think it can be really impactful. Yeah. Um, in that those are great examples of evolutionary medicine. Um, how uh how how far in, how much has evolutionary medicine invaded medicine? Um so I mean like you know, because a lot of people talk about even things we really know about, like doctors don't do, you know, like like like the basic research and that getting translated to what doctors do, especially in the US, where there's lots of sort of uh decisions made on sort of not getting sued as opposed to what's medically or scientifically best.

Um do you have a sense of either just, you know, uh from the historical perspective of like, is evolutionary medicine being incorporated into day to day medicine, or is that still really a a tragedy and that things could be better? Yeah. I think I I don't think we're there yet. Like when I was in grad school, it was really hard to, you know, I was the evolutionary person in a a sea of, you know, people that weren't interested in the evolutionary perspective. And, you know, we spent most of our time explaining why evolution was useful in human health, right? And I I I still see that potentially the case today, with few excepts exceptions, you know, um, in terms of antibiotic resistance or something, we know that the

bacteria are evolving. And so there is some uptake of trying to understand evolutionary principles for that. But I think in general, it's still a completely different track. It is not taught in med schools or rarely taught in med schools. There's been a big push for evolutionary medicine to be more incorporated into medical school um um course structures and stuff like that but and then at the end of the day I've talked to a lot of physicians and this might be true like they have so much on their plate that they don't care if you were inspired by evolution. Right. They still just want to know what's happening. And so that's the thing. Like, we're working on something that potentially a species in nature, like elephants are

really good at not getting cancer. If we use that mechanism and then suddenly it works to treat human cancers, how many people care that you know we were inspired by evolution? Some people might, but like the the general public's like, can it treat the disease I am seeing patients die of? Right. Right? Yeah. And so I think, yeah, there there's there's room for evolution in the medical curriculum, but also there's there's room for maybe us to do it and then provide the more practical bench side approaches that they get. But I mean, still even in basic research, I mean, uh my understanding is in medicine, there's still like, you know, you don't know if something's gonna become a solution to a problem.

You just don't know, right? So you have to invest in um, you know, things that and there's all kinds of examples of, you know, somebody was studying some like slime mold or um, you know, like a sea cucumber, and it led to like this transformative discovery. Um is there enough of that kind of investment in in from an evolutionary perspective? Because I mean, I I I assume, or maybe it's wrong. Like, I don't know. Um maybe I'll maybe you're gonna tell me something that is terrifying that there's very little investment in basic risky research that might have a payout. I don't know. Yeah. Easy question. Talk to talk to the grant funders. Um NIH, not so much. We've tried, we've been funded by the NIH to study like cancer and animals with the like

eye towards how do we make it, you know, into humans? You know, like how do we translate what we learn from cancer across the tree of life into humans? It's been hard, it's been considered risky, it's been like really uh difficult to provide this. But same thing, we don't know what we're gonna learn in basic biology. So GLP1, which is the drug everyone is obsessed with suddenly, and it's really great for treating individuals with diabetes, was discovered in basic biology studying the Gila monster. Wow. It was one single amino acid change that made it, you know, a difference between the human version and that that has made a difference in human biology. They were not trying to study the Gila monster to treat human and weight loss in

diabetes, right? It was just a basic biology discovery. And so I, yes, I think it's it's a shame that we don't have more funding sources towards basic biology research where it's it's not so driven where you have these deliverables at the at the end of the day. The NSF is obviously more keen to um to uh fund stuff that is on that level of basic biology and just understanding a species biology. But when we try and write grants for there, they're like, whoa, whoa, whoa, you're working on a human disease. Like go to the NIH. And so unfortunately, there is like this evolutionary medicine falls into this, like really in-between that ends up being left behind in many of these uh programs because we were interested in evolutionary percept perspectives on

disease in humans. And there's like, yeah. That's crazy. I mean it really sounds like the funding presupposes what the solution, the best way to get to the solution. And I imagine if you looked the probably evolutionary medicine has a much more efficient track record than though these assumptions. I would affect I mean we argue why are we evolution has provided a roadmap for us to understand cancer. There are some species that do not get much cancer at all. We could almost consider them resistant. Why are we not studying these more and providing so many funds? They're they're mammals potentially like us. It's already proven for millions and millions of years for this species. how can we not translate that better into human biology?

So Yeah, no, natural selection is just an incredible, much much better than any pharmaceutical company at creating uh substances. It's had much longer, uh, much much more RD. Much more RD, more RD than you'll ever have time for. Yeah. So it's crazy. Umthough, I mean, I'm in the academic world, there are tons of startups that are looking at this. They're like bio-inspired medicine that are that are turning to look at species for various things, not just cancer, but tons of different um health issues in in humans. So yeah. Have you uh uh David, were you gonna say something? No, I was just gonna say, like, you know, obviously we're seeing similar resistance to evolutionary perspectives in the social sciences as well, uh in um psychiatry and and

mental health as well. Um there's just the uptake is very slow. Um and you know, it's obviously a big part of the reason why Dave and I have started this podcast is to try to push things along in that direction. Um we're about halfway there. We've made a huge dent we oh yeah. I mean we next next year everyone's fundamentally changed. Hey you guys have a good trajectory. You're getting followers. It's great. Yes. Yes, but yes. No, we're gonna the United States will be fine with evolution by like next spring, you know. Yeah, we'll be fine. Sorry, David. Go ahead. Anyway, yeah, I'm just because of interjections like that. That's why Yeah, we can't even get our names right in the introduction. We think we're gonna change the face of American science.

No. Um uh so yeah, I just uh I wanna know why. Like why w what is the resistance? I mean, I get your point that with medicine there's a certain urgency. And there's a certain callousness to daydreaming about evolution when people are dying, right? Like there you need to get a practical solution right now. And we don't have time for you to think about evolutionary theory and cancer and elephants and microchimerism. Like people are dying, focus on what's happening right now. And like I get that perspective on an intuitive level. Like I understand it. Um there's a bit less of that excuse when it comes to social science and and mental health, I think. Um really with there, there's really no exc like excuse there.

Like the whole point is to understand the human condition, the human mind, uh how hum humans are embedded in their social structures and how they, you know, can achieve you know well-being in their lives. Like I it seems like evolution should be moving at a faster pace as a meta theory for encompassing that stuff. Um so yeah, I don't know. Uh do you have uh an intuition about why the uptake is so slow? I think one, there isn't good, and we know this in this country, um, an evolutionary perspective in general in in in our education. Right. Like, I don't like if you go and I the difference is shocking. If I have colleagues working in the UK, and they I feel like culturally they have a more naturalistic upbringing in their education, where they

everyone, even if you're not teaching evolution, is it's kind of embedded a bit more. And I think there is just such a a divide in the US about even talking about evolution and and bringing it in. And like it's it's it's huge. But I see these differences. Like when I talk to, you know, individuals in the UK about like, oh, species evolution at the zoo and like all like it's just, yeah, it's the same. And then you come here and like it's it's a mess. Like no no one agrees or says you can't say that or you can't do this. And so I I don't know. I wonder if some of it is um how we educate our children and how that is culturally different from the US and other countries as well. Um I yeah, I I don't know why it's such a struggle to

get evolution in more mainstream thinking. I mean, I guess the other thing is there's obviously people who have done things that made it harder for us by by misusing it, right? By misusing how evolution works in in in various ways. We see this, you know, today with um people on platforms saying that like, oh, this is how you should eat or this is how you should think, because evolutionarily that's what we're like made to do, you know, and that's not evolutionary medicine either. Eat a pound of bacon, eat a pound of bacon, yeah. Yeah, like and so that's problematic. You have these these misguided efforts that use evolution as an excuse for terrible things. So yeah. No, it's I mean, that's totally true.

I mean, but you also see that in like general, there's like pseudoscience in general. There's perversions of of mainstream science, but it doesn't tarnish our image of science itself when a few crackpots have some stupid ideas. But when a few crackpots and the evolutionary sciences have some stupid ideas, then it it somehow tarnishes the entire evolutionary perspective in a way that it doesn't for other sciences. I don't know. I really don't know why that is. I mean like people it does tarnish science a little bit like going back to Jurassic Park I mean there's like there there's been like 33 decades of like anti-science propaganda movies I mean or like you know or like reasonably enough like for people or like you know the the

Jurassic Park quote of like you were spending so much time thinking about if you should you didn't think about or if you could I totally butchered that I think I should edit that out. Yeah, the the the Ian Malcolm line of like you spent so much time thinking if you could, you didn't spend any time thinking if you should, right? Like that's that's a yes, you know, especially in like a very like we people have been the victims of all kinds of right research, uh especially in the US, um in the 20th century. Like that's pretty historically documented, yeah. And I just think it's so hard to get misinformation away once it's tarnished. I guess the other one, like once it hits mainstream, and I think evolutionary psychology

and all that is sexy enough where it hits mainstream, and then you you really can't. And another relevant one that also hit mainstream that is completely not true is like the vaccines cause autism. Yeah. That researcher and Andrew Wakefield lost his license and was like, Yeah, I made that all up. And people like, yeah, you can read all about it. There's books, there's all this information to prove that that is not true. Yet here we are, and that's tarnished the field. There's such hesitant, hesit hesitancy in in vaccine research, vaccine dis distribution. Um, yeah. Yeah. I think there's these these sticky topics. Yeah. Yeah. Although I yeah. And I guess that's like a for for another episode where we talk about conspiracies and um

redirection of the people who are out to get you. Often the people who are exploiting people are incentivized to have another set of people being the scapegoats of who's exploiting the people. Yeah. Yeah. And it might it might very well be fields most vulnerable where you get this confirmation bias. Right. Like we're really bad at that, where it's like, oh yeah, I knew, yep. I knew a a child that got a vaccine and like, yep. So yes, that's true. And maybe very similar for things in evolutionary psychology where people are like, Yeah, I know like that that that makes sense to me. And like there other things maybe are not so vulnerable to these confirmation biases and so then don't have such a controversy around them, right?

Where you can't get rid of that misinformation. Yeah, that's really interesting. Uh Amy, you're it's just a slightly changed topic. You you're in an anthropology department, but you kind of talked at the beginning about sort of feeling like you're not you're not in any one or you sort of have a um yeah. Um how did you so what is that like? And do you do you do like collaborations with people in the field? Or um and then also uh another question, I don't know, I'm asking you two different questions all the time. But uh the other question is you mentioned you were originally like in medical school. Did you know you wanted to do evolution? Like, how did you get um like I maybe it's the same question, which is sort

of like how did you get to where you are and where are you now? And are you do you still feel like you don't quite fit anywhere? Um is that next question. Yeah. Yeah. Ah no. No, I um I had no idea what I was doing in undergrad. Like I went to a community college, was like, I like biology, went on to like you know, um, a university, um, still didn't know what I wanted to do. So I was like, I should apply to grad school because then I can be a forever student and not have to deal with uh adult life stuff. And so I I did know that I wanted to work with humans and humans somehow. Um, And actually, when I was in undergrad, I was struggling between biology and then anthropology, right? Because all of my biology classes were like biology of plants and, you know, like

things that just didn't excite me in the same way human biology excited me. And then when you want to study human biology, a lot of times you have to be in a med school to study. We really do separate our fields a little weird. So we're using the same principles when we study ecology and all of this stuff, but like humans, we put them in a different room, a different school. It's a silo effect. Um and so just on luck, I applied um to get my PhD. It was still locally, there was no necessarily rhyme or reason to why I went to the school I went to other than I had to stay in the Detroit area. And so but there I I my mind became more open to evolutionary biology. I'd already taken classes. There was a there was a faculty member there kind of looking at evolutionary principles to

cancer already. There was another one looking at evolutionary the placenta. Like all of this was kind of feeding through my graduate experience in terms of, and then of course, uh Randy Nessie at the time, who was one of the big drivers of the field of evolutionary medicine. So I was in Detroit. Um, he was in um Ann Arbor. So that was just an hour away from where we were. And so we as grad students would all drive up when he had evolutionary medicine seminars and watch them. And so, and that's where we were all like, whoa, this putting it together is just so cool. And so, yeah, from there I went to do a postdoc and we ended up at like the Department of Surgery, but it was at such a very specific Posting about studying life

history theory in cancer biology. And I just thought I I I wanted that opportunity and I was able to get it. And yeah, so it's kind of where I went. And so yeah, I there was in the Department of Surgery, and then we went at Arizona State University. Um, we were kind of split between various departments, and there was a center for evolutionary medicine there. So, but yeah, I think anthropology does all that. That's why it's accepting of evolutionary medicine, is that anthropology is already this very broad field that has to take many different perspectives and kind of mush it all together to understand humans. We're we're understanding social circles, we're understanding culture, we look at the

biology, we look at evolutionary history, we're kind of adding all that in. And so yeah. Yeah, that's cool. And do you feel like um is the UCSB anthro department um uh in terms of the biology, hum the human biology, is that sort of a strength in that department? Or yeah, I think so. I there's there's many times where the the students are like, this is biology. And I'm like, yes. I hate that when it's like when you say you're a biological anthropologist, they think you're less of both somehow, you know, like, you know, like the oh, you combined them, you're a hybrid, you're like one of those bikes that can't go like fast on the road, but also is bad at climbing a mountain, you know, like but no, it's like a lot of us are

human biologists. We are biologists. We have wet labs. We have like NIH funding, but also we're studying humans. So we're in the anthropology department. And actually, a lot of the biology is conserved. So when I'm teaching genetics, yes, you're learning fruit fly genetics that will eventually get to human genetics, but yeah. A lot of the the the stuff is conserved biology across systems. Yeah. We we had a recent episode where we haven't released it yet at the time of our recording right now about the microbiome. And that was a case where people's microbiomes, if you look at sort of um more evolutionarily um EA-ish um people, you know, hunter horticulturist, hunter gatherers, their microbiomes look very different than like a Western

modern um is what you study a case where there's less of a sort of mismatchy thing, or do you think there still might be mismatchy stuff? Like, I mean, obviously breastfeeding, um, the the the an absence of breastfeeding or um or like a reduced amount of maternal per leave or um or maybe c sections that are planned. I don't know. Like, is that something you've thought about, or is there potential mismatch-y kind of things? Or are we doing things to violate the good assumptions of these systems that we might not know and inadvertently maybe making our ourselves less healthy, for example? Yeah. Yeah. I yes, mismatch is very much a part of what we're studying. Um in the cancer point of view, I think of mismatch of a long history.

So we're looking at cancer and chimpanzees. What do they get compared to what humans get, right? So it's a broader mismatch in terms of that a little bit. And it's interesting, we're seeing very different patterns of cancer in our closest living relatives. So, like what's going on there? And then, yeah, with with the pregnancy stuff, same thing. Yeah, like mismatch in terms of C-sections. We see maybe more spillover of fetal cells. So there's there's some there's some consequences. Also, yeah, breastfeeding in in general, thinking about it from a a mismatch point of view in terms of how much you're doing, but also thinking about breastfeeding from a maternal fetal conflict kind of view, it's it's interesting because we always

we always say like you know breastfeeding is the best, you know, and the longest is best for the infant, infant, infant focused. What's best for the mother? How long should the mother breastfeed for her own best health and interest? And that is that's missing in our narrative completely. Um and there could be a trade-off at some point where the breastfeeding is still great for the infant, but actually it's not good for the mom anymore because it is a biological process. It has a demand on the maternal body. It's inflammatory. It's got all these other things going on. So yeah. Yeah. Cool. Yeah, that's one of the great um insights of the evolutionary perspective, which is it focuses you on trade-offs.

So even if something is good for the infant, that doesn't necessarily mean it's going to be good for mom. Uh you know. So I I I think that's a really important insight. Um I'm curious, I when I was looking over your uh your research, I saw something called Pito or Pedo's paradox. I don't know how it's pronounced. Uh I'm cu I I don't know what that is. I'd like to learn about what it is. I like a good paradox. Yes. Um The thing about paradoxes is they're very no. Um yeah, it's it's Pedo's paradox and this is great. Um this is was proposed in the 70s. It was an epidemiologist, Richard Pito. Um, he was studying cancer evolution. Cancer um is such an interesting case study for you know how technology really shifted the field.

Because I think in the 70s we knew cancer evolved, right? And cancer cells evolved, and there's these evolutionary principles of cancer. And then within the 80s and 90s, we're all just decided that we're going to sequence everything and try and find the cancer gene and the genetics. And then we got really too detailed, right? Instead of looking at this big holistic picture and trying to fundamentally understand that each cancer is different and it's a whole bunch of different mutation signatures. And it's like this emergent property. We went very molecular, and now we're kind of spit out on the other end where we're back to this, like, oh, we went that route and actually we got to go more holistic.

But in the 70s, it was so amazing. Richard Pito observed that elephants have a hundred more cells in humans. If cancer is a disease of cell division and cell mutation, shouldn't species that have more cells have more cancer? But what I'm seeing is humans have a lot more cancer than elephants. Not all elephants are dropping dead of cancer, right? So what's going on there? And the idea is they must have evolved more cancer defense mechanisms than humans, at least, in order to maintain their soma and maintain the amount of cells that they have for a really long time, too. They can live into their 60s, right? Um, so they have this huge body in Soma. Um, and so that was proposed. And then, okay, so do we test how do we test this?

And so we worked with actually a bunch of zoos. Um, and that's that was a wild ride. Um, because um just different zoos have different protocols, but they all have like I remember just calling zoos and being like, Do you have data on on cancer and your animals? And they're like, oh yeah, yeah, yeah. We could we could work with you and you just gotta fill out a research proposal. Um, what species do you want to work on? And I said, all of them. And they would they were like, no, you can't. It was like silence. Yeah, they're like, no, we don't have the the infrastructure re um to look at that. But we eventually started working with a bunch, like it got it got easier. Um, and then we tested that.

Do elephants actually get less cancer? Because this was just a really elegant theory, right? And I love this. I love this is why we need more theory in this kind of work. And they do. They do, they still get cancer. Okay. But all else being equal for the amount of cells they have, they get less than what is predicted based on humans. And then we um a colleagues of mine sequenced their genome and discovered there's a gene that we get. We have one copy of this gene, two alleles, one from our mom, one from our dad. And it's called P53, and it's tagline the guardian of the genome. Okay. So if you get a mutation, it turns on and it makes decisions. Does the cell die? Do we fix it? Do we do all these things?

It's a central feature. It's highly conserved. It's an important gene. So we have two copies. It seems like elephants have um 40 copies, potentially, up to that many. Um, and so that was a really neat discovery. It's like, oh, this may be why they get less cancer. They have extras of this gene. This gene is also, um, if it's mutated, um, it's mutated in about 70% of cancers, I think, is the estimate. So if it gets knocked out, that's pretty bad. But if you're an elephant and one gets knocked out and you have backup copies, that might just be fine. So yeah. It's a really good example of theory driven, how efficient theory driven is because if you were just like, well, well, what's the chance that you would just what are all the genes

you could genotype in an elephant or any onion. Right. So if you just did like blind brute empiricism, the sun would explode by the time you made this discovery. Yeah. Yes. Yes. Yes. More funding is needed, yeah. For theory, evolutionary theory in medicine. So is the paradox that we would expect more cancer in organisms with more cells because there are more opportunities for cancer to evolve given that there are more cell divisions and more mutation opportunities. and the fact that we don't see that is the paradox. Yes, correct. Got it. Thank you for vocalizing that because it gets a little bit confusing because everyone's like proving P Pito's paradox. And then like they're like, but wait, did we prove like how do we prove a paradox?

Like so there's been all this like and then there's just been a little nuance because as more data's come out, it does seem like Body size does matter in certain law larger animals might have might have an increased risk of cancer. Like it's a very small effect, but we really like we're talking about such small numbers here. And again, it's not as much as expected for an animal with the many cells they have. And so um it's yeah. Yeah. Is there anything to this? I I remember reading something, it was like a Scott Alexander Blanc post about how uh one reason why whales don't have uh a lot of cancer is that they're so big that their cancer gets cancer. Is that is that totally uh a dumb idea that has been a little bit more than that?

It's not it's not that dumb of an idea. And I I you know, if cancer cells evolve, they mutate and there there's lots of death and selection, and sometimes cancers can collapse in on itself, right? And so the idea that that's an idea that's out there. There's very little research on whale cancer because they live in the ocean and when they die, they end up at the bottom of the ocean. So we don't have a lot of research. We have our group has looked at the P53 gene in whales to see if they've expanded it too, and they haven't. But we do think they live too, some of the these whale species live 200 years. We can we can guess, we can guess from that lifespan that they're pretty good at not getting cancer.

Yeah. Um, what are the mechanisms? That's what's really exciting, actually, about a comparative approach is like there's not just one solution. Yeah. Right. So elephants have the P53 solution. Whales don't. What's their solution? What if P53 is not very translatable to human, you know, cancer therapeutics? There's still like a hot, there's such vast biodiversity that we could we could look at beyond um elephants and even beyond whales, potentially, um, in terms of that. So yeah. Um, but no, it's not a stupid idea to think maybe the cancer gave cancer too. Like we just haven't been able to cool. It's such a fun idea. I'm glad I'm glad there's some truth to it. No one's been able to test it or or prove it.

We have all of you know, again, we're still in the theory based for for that kind of stuff. But yeah. Still though, I mean it's it's an incredible sales pitch for the evolutionary perspective in that um there's literally something like, you know, a a bunch of different mini cures for cancer out there in the animal kingdom that we just don't know about. Uh and like that in itself should be the best sales pitch you could ever get for studying humans in a in a comparative evolutionary context. Yeah. Yeah. There's I mean there's debates and we we could go on about like what's the best species to study, but we tr we always try and stick within mammals because we we hope that that might be the most translatable.

But yeah, there's some really neat species out there. Like have you ever heard of the Greenland shark? No. Is it blind? I think so. Okay. That's all I know. Okay. I don't even know if I know that. Well, I need to learn about this because my daughter's obsessed with sharks, so I'll tell her all about it once we're um it's its uh lifespan is estimated to be around four or five hundred years. Wow. And then its age of maturation. Do you want to guess what the age of maturation is estimated to be? 100. It's 150. Wow. Wow. It is such a slow. And so going back to like life history theory, we think these very slow species are like building their cells really carefully. And so they have these extra, you know, like, which means they have these extra defenses

in them, right? Like they are so slow growing. Um, and I think that's again another if we could go back to the conversation, like why do we get cancer? It's these trade-offs where like, do I have the opportunity to grow slowly? Nope. Well, I'm gonna grow less carefully, but I'm going to get big enough to get resources and access to mates, um, even though it's a little sloppy, right? And that's where a lot of organisms end up. Greenland Shark clearly doesn't have very many predators and has the opportunity to really slow down and take its time and its life history strategy. And it's so cool. Wow. Wow. Really cool. Um for people who are interested in this kind of approach, um, and I can imagine there's two audiences listening.

One is students who might be interested in like learning more about this or studying evolutionary medicine, Uh, in addition to working with you at UCSB, are there other, I mean, how many other people are doing this kind of thing? And like, are the who who, if there was somebody listening who was like, oh, I'm really interested in evolutionary medicine, um, in addition to reaching out to you, who else would you suggest? I mean, not to put you on the spot about an omission doesn't mean you don't think they're doing it, but just first like you have suggestions about like who are people who are currently doing this kind of work? Yes. So we have a we have a society. It's called the International Society for Evolution, Medicine and Public Health.

And there's a journal called the Evolution Medicine and Public Health Journal. So there's a community there and there's tons of resources on the webpage for different groups. But then within the US, there's these little pockets that have like hot spots of individuals that study evolutionary medicine. UCLA has an evolutionary medicine program that's a master's program that's quite great. Arizona State University has the Center for Evolution and Medicine and is invested in has a bunch of different individuals there. There it's interesting. They're always within an anthro or or adjacent to an anthropology program and a psychology. Like it is this interdisciplinary mix. Also Duke has this in the try-sum area has this really great opportunity because there is

a med school, but also there's like zoos and the Duke Lemer Center and all that. And so that's been, but it's within the anthropology department. There's been a really big growth in individuals studying evolutionary medicine. And then outside of the US, there's there's groups in like Zurich and various other countries that are kind of get becoming these hubs for for evolutionary medicine. Awesome. That sounds great. Yeah. And then um, and then for people who are not students but are just interested in maybe like a not terrible popularization, like are there any are there any resources for that? I mean, that's a hard question. I don't even know what I would tell people like for for what I do for like a popular

source, you know. Are there um, you know, are there books you would recommend for people who are interested in? Yeah, uh one of the like land like foundational books is Randy Nessie and George Williams Why We Get Sick. That's a a really great first pass at evolutionary medicine. Um and then there's within the cancer community, there's a really great book by James DeGregor DeGregory called Adaptive oncogenesis. That's a tongue tie, but it's a really great book. Um, Athena Actipus has written a book called The Cheating Cell, which also um is is has an evolutionary perspective. Those two are specifically on cancer biology. Um, but I think within every subfield of evolutionary medicine, there's probably some more

um popular stuff that I'm I'm probably forgetting about, but we'll remember as soon as we that's awesome. Yeah, yeah, yeah. I'll remember it tonight while I'm like laying down. That's great. Oh, I forgot this. And we're gonna we can always add it to show notes if if we think of something. Um do you talk to enough psychologists or are we doing as psychologists a bad job of talking to evolutionary medicine people? Like the body's hooked up to the yeah do we do yeah the mind and body are all it's it's the same thing, you know. Right. I was just thinking that because it is these fields that are quite distinct but have very similar starting points. Yeah. And like within the evolutionary medicine field, there clearly are

evolutionary psychiatrists because that's who Randy Nessie is. And oh, and here's another book. He wrote a book called um good reasons for bad feelings or something along those lines. And I I like I like that title, but again talking about how depression can be an adaptation and anxiety can be an adaptation and all of these things, right? Um but it is interesting that these fields haven't necessarily um merged as much as you would imagine. But I think there is this historical context of like neck up. Yeah, totally. Yeah. You're working in the that area and I'm I'm gonna stay away from humans and how they um make decisions and yeah but you would I mean from a first principles uh evolutionary perspective you would very much expect that the the mind

and the decision making and the control system is very much dependent on like what's the state of the thing I'm in, right? Like so this this thing of uh um like I know there's like work like Josh Schneidgross we should have him on with the lassitude right but there should be all kinds of psychological contingencies with uh what's the state of the body, right? And back and forth. You would expect that on first principles, right? Yes. Absolutely. And and honestly, I see like ways where like, okay, so evolutionary medicine has maybe provided these kind of drastic ways we treat people. It could be different, right? And then we don't see uptake in it, right? Like, for example, like when I talk about the cancer therapy of maybe control versus

cure, we clearly need people to understand why people make the decisions they make and why they avoid the decisions they make. And what in and are there ways you could, you know, tap into that better so they could understand and and be able to? Oh, interesting. So you're even talking about like the psychology of like the intervention and how people metaphors people use to think. That's a really cool idea. That's that's something, yeah. Like how do people think about medicine or the body? Yes. Yeah, that's really cool. I don't know if there are any psychology on that. Like folk folk physiology, more or less. I mean, aside from maybe like how do how do the how do the dumb, wrong natives think about science?

Like that's I'm I'm aware of work on that. Like but like there's a bit of stuff on like scare quotes for people who couldn't see right. I'm saying like it was a very col it was very like poo-pooing like, you know, yes, ethnographic knowledge that was probably very valuable. But yeah, I don't know. Is there work on sort of like the intuitive psychology of medicine or physiology or mys like in the same way there's like a theory of mind, is there like a theory of body, right? Theory of medicine. Like uh we m there might be very well be folk medicine. Yeah, yeah. Right. There I mean there is folk medicine, but I'm I'm ignorant enough to that to not know if it kind of talks about this broader. There's a bit of stuff I mean about like, you know, medicinal practices and hunter gatherer

societies and how they all they often have pretty impressive you know herbal knowledge and and remedies and and that's intertwined with like you know the study of shamanism and stuff like that. Yes. And you know, it's still there's still some debate about like how much of that is actually effective and how much of it is is just kind of a a a ritual or superstition. And I'm I'm agnostic about that question, but um it seems like a hugely understudied and important topic given how much medicine is interfacing with our lives and with the modern world, just getting a handle on how we think about it and how our representations of medicine you know interact with our own ability to cope with illness.

But I I do see that the there is a divide where people study that as in terms of like folk medicine or, you know, like traditional medicine, but we're not thinking about it in terms of like industrial pop industrialized population in our our m medicine, right? Yeah. Um, where there's not really that crossover. Yeah, it's still important. It's all folk medicine. It's all folk medicine. Yeah. It's still I mean basically, you know, doctor is a large part of the doctor's job is to be a shaman in a white lab coat. You know, like I mean, even from like you don't like if you're a a researcher in a lab, you do so many rituals before you run your experiment to do a discovery. Like you you are just like there is still so much of that psychology

that we just we can't like I can't mess this up. I did it worked yesterday, so I have to wear the same outfit. I have to do this. I have to do that. Like there's still so much of that within with within labs. You know, they have like special like I don't know, this is my good luck pipette, like all of this stuff to get to get things to work that I I don't think we've moved that far away from it. We just call it something different. Yeah. It makes sense. Yeah. Yeah. Yeah. As as Rob Boyd once said, uh, and it always stuck with me, the world is opaque, right? Like the world is opaque. So you have to yeah, it's everything is a mystery. Yeah. Yeah. We we were just talking uh to Clark Barrett about that.

Um uh the episode we just released yesterday about how about uh ritual practices and like uh pre-hunting dances that the Shuar engage in. Yeah, and he made the interesting point that like a lot of our statistical practices are you know have the same kind of logic where we don't really know how they work, we're just accepting them because the ancestors have bequeathed them to us. And it's it's not all that different from a ritual, like a hunting dance or a ritual. Yes, yes, yes. Yeah, which I think maybe, yeah, coming back to thinking about applying that in terms of getting evolutionary medicine or or any evolutionary perspectives into something is it's not already in that ritual doing right. Like it's just like, no, we don't do it that way.

We have to do it this way. And yeah, I think it's really unfortunate because it's probably how we structure medical schools, it's how we structure schools in general, like in terms of silos. Like I want students at UCSB to not have to just take a major classes. I want them to be able to take classes from all over campus and that and it that's just not possible. And I feel like you ask why and people are like, well, because we have departments. And yeah. And then you're like, but why? Why do we have departments? Why do we have departments? And they're like, well, because and like and it's all of this stuff. And it's like, but but we could we could have bigger, better learners if we could have crosstalk across so many different disciplines.

But and I feel like it always lands on it's either because it's difficult and we've always done it this way. And those two things are in a loop. Yes. Right. So we're doing it on the other way is more difficult because we've always done it this way. And we've always done it this way. And that's you know, it's not a good reason to do things, but it yeah, it is hard to change things. Yeah. It is. Yeah. Yeah. How did you um we're we're we're getting closer to the end here. Um, how did you you talked about sort of the way biology is taught in school. And David and I have talked a little bit about how, at least for me, I don't want to speak for David. Like I was like learning parts of the grasshopper in by in like high school bio.

I had a great high school in many ways, but the bio sor like at least at the time I was taking it was horrible. It was just laundry list, it was stamp collecting. There were no principles. Um, were you interested in biology? How did you get interested in in in in like Amy body as a kid? Like, how did you get here? Like, how do you is there a story? Um it's the most boring story. No, I was not inter not necessarily interested in the natural world. I mean, as much as any kid, like I was, you know, in the 80s, you're outside all day long observing things and and doing all that. And I always liked maybe um like math and and lean towards more like quantitative type of analyses and stuff like that, but it

wasn't until a community college class that I took and it was a biology class, and the professor was amazing. And he was so excited about biology. Um, and I was like, oh wow, this is this is great, right? And this is really cool. And the same thing with evolution. I had no evolution in my high school training at all. Like, I don't think we learned about it at right now, I have a 14 year old daughter. She is learning about natural selection. And I'm always like, wait, you're learning that? I'm teaching my undergrad. But there is a disconnect, and you have to like you have to reteach these principles because you don't know if everyone is getting the same education. Um, and so I always start from the beginning when I'm I'm teaching these these classes.

But yeah, I didn't really start studying biology until I was in community college. And it was the same thing. We're doing labs and dissecting mice and various things. And I really liked it. And I really liked evolution too, those those types of classes. It really opened my mind up. Um, so yeah. Steven, you were gonna say something. No, I mean I think we're about getting to that part of the episode where we ask our question about questions. Yeah, should we have asked you anything? Yes. Oh, that's such a tricky question. I know we we often if it if it is a spring, we spring it on you and then we give you a few minutes a few seconds, we we banter about something else to yeah, to um uh um give you a second to think about if there's anything else that we should have asked you

about. Yeah. It's a hard question. I know. Yeah. I can't think of anything. That's fine. Yeah, yeah. That's totally okay. Yeah. Mo I I don't I can't think of a single guest who like totally except for I don't know, maybe maybe like Josh Tiber was like because he's a fan, he like he knew we were gonna ask him he like came with like a great answer. But like we should maybe we should stop. Yeah, maybe we should have a lot of people. No, I think it's a good one because some people could be like, oh wait, we didn't talk about this. People are psychic. I promoted a a book or something like that. Yeah, no, exactly. Yeah, yeah. Yeah. No, grift. This is your chance to grip. No, this was great. I love that we were able to talk about both worlds and of my research and connect them.

And yeah. Yeah, it's it's really great. And I mean one of the things I'm like people are who listen are probably bored by this, but like you and I, Amy, you and I are colleagues, but I never get a chance to talk about science. This is one of the reasons for doing this is just yes. It's a great chance to like talk about science. Absolutely. Yeah. Um well thank you for doing what you're doing. Um you're literally like helping us understand how like cancer works and you're doing you're still, you might, for all we know, a year or two from now, you might discover something in Wales that revolutionizes, you know, what was it? The P35. P53. P53. Uh I tried. Okay, close. Close enough. So uh yeah, no, it's just incredible.

And I hope that um you have lots and lots of students knocking on your doors and lots of funders. And it sounds like the funding agencies really need to get their act together too. I mean, welcome to the the new state of America funding situations. Yeah. But it sounds like even before, like the the binning and the silos and the like kind of presuming the categories of solutions ahead of time made it so that this was sort of an odd man out or not in the Venn diagram, maybe. Yeah. Yeah. And a lot of funding agencies are like, we want something risky, and then they're like, not that risky. It's like their idea of risky and my idea of risky are not in the same category. And so that's unfortunate.

But there's foundations that fund some of this stuff. And yeah. Yeah. So if you if you really if you have a lot, if you're listening, you have a lot of money, then that you would love to have a high risk, hype possible like cancer solution, contact Amy Body. Yes, there you go. Absolutely. We don't do ads, but that's an ad we can do. Yes. Yeah. Do you is there any like seriously? Is there any other things like where people, if they want to like, are there certain projects that you think like if people are interested in supporting them, like are there other ones, or is that the general thing that it's um yeah? Um yeah, I there's tons of like, yeah. There's I mean, the whole world of I mean, we talk a lot about evolutionary medicine, but

the the whole world of comparative biology is just understudied in so many different ways. And then we only study the species that matter for who they matter for and the population. So like, yeah, it's just cool. Yeah, yeah. Lots of incredible things. So um, well, thanks for being on. It was it was a pleasure. Um, it was really good talking, and we'll um I I like that we're as a as an evolutionary psychology podcast, we're also talking to people who are doing an evolution who are adaptationists who are doing evolutionary approach, but studying or and studying, no but, but and studying the rest of the body or the this this issue of the psychology and the and the physiology we need to start talking more.

Yeah absolutely this was so fun. Thank you for having me on. It was wonderful. Thanks so much. Our pleasure. Thanks so much. I learned a lot in this episode and um we know I think people who have been listening to the podcast know they can, you know, subscribe and like uh leave positive comments. Um we have a Patreon page. Um am I leaving anything out? I think those are the big ones. Uh yeah. Just uh support us in in whatever way you can help us push the uh the evolutionary framework wider and farther. Um we also had um we've also gotten some emails from people and some suggestions for guests and that's always appreciated um as well. So um yeah and suggestions for topics. Um and nobody's gotten David a um fanny pack yet.

I am starting to get a little peeved to be honest Dave. I've been waiting on that fanny pack for months now and it has not arrived. I'm starting to think that you know our listeners don't really have a lot of respect for me. Okay. That's them them's fighting words. Um uh and you said green or black? Uh I you know, either one. Have you come around to have you decided ideally green and black? Striped. Okay. All right. Well, that's one way to do it. Okay. Yeah. Um, and French fries, that's the other thing. If you're bringing up the phone, the french fries inside the fanny pack. You you you know what I like, listeners. You know you know your way to my heart. It's so ridiculous. Okay. Um, well, have a good week.

Uh thank you for listening. Uh, and uh, we'll see you next week. See ya