Did Science Find It Yet?

This is twist. This week in science, episode number 1072, recorded on Wednesday, August 19th, 2026. Did science find it yet? Hey everyone, I'm Dr. Kiki, and tonight on the show, we're looking for stuff that will fill your head with cheese, cancer, and cannibalism. But first, thanks to our amazing Patreon sponsors for their generous support of Twist. You can become a part of the Patreon community at patreon.com/thiswecience. Disclaimer, disclaimer, disclaimer. As scientists peer into the depths of the universe, find fast stars and evidence for glue balls, questions keep coming about the future of science. Who will be able to do science? Who will pay for science? Who will own science? Why do we worry about these questions? Why do we fret about an endeavor that has historically been closed to so many? Well, if science is not free, then neither are we. So, ponder this information in this week in science coming up next. [music] kind of mind that can't get enough. I want to learn everything. I want to fill it all up with new discoveries [music] that happen every day of the week. There's only one place to go to find the knowledge I seek. I want to know what's happening. What's happening? What's happening [music] this week in science? What's happening? What's happening? What's happening this week [music] in science? Good science to you, Kiki. >> And a good science to you, too, Blair, and everyone out there. Welcome to another episode of This Week in Science. We are back again to talk about all the science we decided to bring to the show this week. We got some good We have some good stuff for you. Uh it's been a it's been a decent week. You know, lots of stuff going on. can't rest for a minute these days. But we've got some cancer vaccine success I want to talk about. There are some superpowered centinarians, well superpowered super centinarians that are out there. And I have some cheesy news in addition to how we might actually be able to think ourselves well. Um the impact of being a sugar baby and how you move. What did you bring, Blair? I brought uh Oh gosh. [laughter and gasps] Stand by. I brought holotypes and I brought sexual cannibalism. >> So holotypes, I am going to guess that not everybody knows what they are. >> No, we're going to talk about it. >> And so everyone went hollow what? And then you said sexual cannibalism and everyone went okay. >> Yeah. >> So >> yeah, which is a throwback. I feel like I have not talking about t talking >> talking. >> Wow, this is going to be an interesting show. I've not talked about sexual cannibalism in a long time. I feel like that was my go-to for the first few years I was on this show, but >> very much so. >> It's coming back today. So, >> it's back in vogue. >> Yeah, >> it's kind of chic. [laughter] >> That should be our That should be our meme for the week. Sexual cannibalism. It's kind of chic. >> Yeah. >> Yeah. jumping on the meme wagon, you guys. All right. Well, we are here to bring you this show full of science this week. And since you're here, I want to remind you that you can subscribe to Twist any place that podcasts are found. Look for This Week in Science. Look for that orangey starburst logo and hit subscribe or share it with your friends. Additionally, we are on YouTube, Facebook, and Twitch every week that we are live at 8:00 p.m. Pacific timeish on Wednesday evenings. And then finally, if you have questions about the show, want to know information about stories that we talk about, head over to twist.org where our show notes live. And other than that, well, oh yeah, that's also where our Patreon is. You can click on the Patreon link and get into our Patreon community or also link to our Zazzle store where you can find some of our cool merchandise that's out there. But now it's time for the science. Are you ready for this? >> Bring it to me. >> All right, bringing it down. I know a lot of locations have been talking about this already this week. It is the big story for the week. Even though it really hasn't been published yet, this is early. [laughter] was good. >> These are ear early clinical trial results that have been announced by Merc and Ma. Now you might recognize the name of the company Merna. And when you think Merna, what do you think Blair? >> COVID vaccine. >> Yes. This has nothing to do with a COVID vaccine. It's all about cancer vaccine. >> Okay. >> Yeah. So even before the pandemic came, people were working on the idea of using mRNA to allow for personalized vaccines for many different ailments, cancer being one of them. One of the reasons that we end up with cancers is because we have individual mutations that are hard for the body to overcome. And um in the case that our immune system can't do it by itself, the idea is that maybe we could help it along. And so these vaccines and and we did report, I think earlier on the phase 1 and phase 2 trials, this is now the phase three trial results. They still need to be uh analyzed for sure by independent experts, not just the people at Mercern. But the vaccine that they're using is called in inismaran and it's given in combination with another imunotherapy drug that's called kruda. And the two of them together reduce the amount of time that well it it it increases it I was going to say reduced it reduces cancer risk of the disease. it it reduces the risk of cancer spreading to other organs and it increases the time that patients are cancer free. So if you're going in and you're undergoing a tumor removal or even chemotherapy, this vaccine once they're once they're using it, the way that it works is they take a little chunk of your tumor. So a biopsy of the tumor, they do genetic analysis of the tumor specifically to see what is gone, what's gone wrong, where the mutations are. And so then a very specific mRNA tag can be created and it works will work the same way basically that the mRNA vaccine does where for COVID where it's basically holding the piece of bad stuff like a flag in its hand goes into the cell and says attack this and >> get rid of this. >> Yeah. Yeah. And your body creates a whole bunch of antibodies to attack and get rid of that thing that's bad. Um, and so this is exciting because we know that one of the issues with cancer, in addition to the fact that it's like an eternal cell type, right? It just keeps dividing, dividing, dividing. They also mutate and continue to mutate and divide because the uh the normal checks and balances have been turned off. And so they're they accumulate mutations that are very specific to an individual. So your spec even though you have the maybe you have a liver tumor or a kidney tumor or whatever and okay there's this general type of liver tumor or kidney tumor but you have very specific single point mutations that other people do not. And so because of this, this will allow the uh the power of the vaccine to be much greater for individuals. And so what they were saying is in combination with the imunotherapy drug, it boosts the immune system. It also increases the attack rate on very specific cell types that hold these particular mutations. And it's helping to keep people cancer-free. And this is skin cancer we're talking about. We're not talking about uh for this particular cancer trial, for this particular treatment. Um it is specifically for skin cancer. Um but it's it's just a very exciting uh development because we've been talking about these on being on the horizon for so many years. You know, we were talking about mRNA stuff for a long time and then COVID happened and everything got exciting and yay, this mRNA vaccine stuff is working. How do we get to do it so fast? Oh, because there are decades of work leading up to where we are right now and it thank goodness we have this. And my big question now is knowing how people have been primed to accept or reject mRNA therapies. I am wondering >> if in a cancer situation a doctor and and also not just M mRNA but vaccines. So the name vaccine which would be priming your immune system to fight something [clears throat] off. >> Yeah. >> You have cancer. I can give you a vaccine that will help your cancer go away. What is going to happen, Blair? So, I mean, I have a lot of thoughts. I feel like So, first of all, people's whatever value you want to put on it. Um, theories on uh on certain scientific >> ideas, >> accuracies, I don't really know what to say. people's crazy thoughts about vaccines and how they could be negatively whatever. Anyway, um a lot of those things I feel like disappear when it suits those individuals. And so I do think that no matter what your let's say beliefs about vaccines are, if you have cancer and you are going to die and you're offered a vaccine that might save your life, I think more people than not are going to take it. >> [laughter] >> So, you know, but I think the other thing I wanted to ask you about is I think the mRNA piece of this is the less interesting part to me. The more interesting part to me is that you said they're going to sample >> the cancerous cells >> and make what is basically bespoke medicine, right? Like, and I think in my opinion, this is the big >> kind of new revolution, like the next renaissance in medicine is bespoke medicine, right? Like this is where we're going to start to see massive shifts in life expectancy, massive improvements in medical care that we've could never even fathom before is in bespoke medicine. Like this is the thing that I'm really excited about. Longtime listeners of the show know that I want to live forever or at least to like 150 would be great. And the only way we're going to get there is bespoke medicine. I truly believe that the only way is to sequence somebody's genome, sequence problematic cells, like be able to attack it with precision >> so that you can have high efficacy and speed and accuracy, right? So like all of those things together are going to make current >> potential medical intervention so much more effective. And I love the combination of these kind of two ideas together because they make perfect sense. Like mRNA is dealing with genetic code. So like so it's very easy to go, okay, this is your specific cancer cell. Let's go ahead and flag your specific cancer cell. >> Y >> and I love that. It sounds very exciting to me. >> It's very exciting. and and um you know in addition there can also be you know banks of prepared mRNA vaccines right that are genotyped to certain right >> sub subgroups right so within >> a certain kind of cancer skin melanoma skin cancer you're going to have multiple subtypes so which branch of the cell has gone wrong and started having the crazy mutations right so >> you know you we can create and clinically prove that these banked ones work and so you can use overlapped vaccinations to be able to get get there faster. But it's just all about being able to genotype the biopsy and genotype the individual tumor, >> which is awesome. >> It's so exciting. Um, >> and they're not saying, you know, it's going to get rid of it completely. And they don't know because this is early. This is phase three. what they've really been doing is going past just proof of concept and getting actually now into let's look at dosage and let's see how this works. And so they're still only at an early level of a thousand people, but this looks like a really promising trial and should the independent analysts think that it is great, then it'll go forward to phase four. And in phase four, that's when we really see things move more quickly. And so and and a lot of most most trials halt between phase two and phase three. >> You know, it phase three to phase four is really exciting. >> It's very exciting. Yeah. >> Yeah. That's awesome. >> It's And it could work. It's so cool. Yeah. So, good news everybody. Personalized treatments, bespoke medicine. you too can be biopsied and treated and maybe I there was something recently related to aging and um they were saying that based on like tieumirs and cell divisions and other things that most of the cells of the body can go on for a really long time. So like our our kidneys or our liver are almost our liver especially it's like an almost eternal >> cell. Yeah. It's the it's it's the heart, the lungs, and the brain that are the limiting factors. Um, and so, you know, it's really interesting to think of when we talk about tieumirs, you think of yourself as this like homogeneous thing. You know, you are not milk in a milk carton. You are a very exceptional puzzle. [laughter] And so, you're you have a really heterogeneous makeup. And so it's our heart and our mind, our heart and our brain that are going to keep us to maybe a maximum human lifespan of 150 to 190 years so far. Yeah. >> But that's if you do everything right and medicine works and I'll talk about it in a couple of minutes. You you have the uh the stuff to be a super centinarian. Oh >> yeah. >> Okay. Don't give me bad news, Kiki. I can't take it. >> I'm gonna give you your doctor's the one who's going to give you the bad news, not me. Come on. >> Okay. Okay. Okay. [laughter] All right. Do I want to know? I don't know. Anyway. >> Yes, you do. What you got? >> Uh, hey, what's a holotype? >> And I know you like Star Trek and you're not talking about a holiday. >> I'm not talking about a hol deck. You know what a holotype is? >> I do, but why don't you tell us? >> Okay. Well, it's I I like to think about it like [laughter] the breed standard in the AKC for a dog, right? So, it's like >> that's a good analogy. >> Yeah. It's basically like, okay, here's a prehenselletailed porcupine. This is the prehensellet tailed porcupine that we measure all other porcupines to to determine yes, this is a prehensellet tailed porcupine. So, yeah, it's basically you're basically like setting up the species standard. This is um >> we're gonna go we're going to go with US Science gold standards now. >> Yeah, exactly. So, it's it's kind of like this is Yeah, this is how big they are. This is what their skin covering looks like. This is what colors they come in. This is um how much they weigh. [snorts] Um this is how big their teeth are and what kinds of teeth they have. And the reason a holotype is important is a to determine speciation. So like is this specimen that I collected a prehensellettail porcupine as you're looking at on the screen right now or is it something else? And B, before you can do genetic testing, you can develop relationships between individuals based on phenotypic similarities. So you can say like this is definitely a porcupine. It has quills like this prehensel tailed porcupine, but it also has hair. It doesn't have a prehensel tail. Okay, so it's probably related to this, but it is definitely not the same species. So basically a species is discovered, you develop a holotype. You say this is like the the platonic ideal of this species and then you can measure all other species against it >> or uh specimens. >> And this is different from the haplletype which is genetic, >> right? Yes. >> Yeah. So it's it's characteristics versus genetics. >> Yes. The phenotypic stuff. Yes. >> Phenotypic. Yeah. So, why am I talking about holotypes? Well, a study analyzed 1,116 mammal species discovered between 1990 and 2025. So, recent mammal discoveries. 95% of the species were native to what we call the global south, which is south of the equator, Latin America, Africa, Asia, the Caribbean. Um, and 60% of the species holotypes are housed primarily in Europe and North America. >> Not Yeah, I was going to say not the global south. >> Yeah. Yeah. >> So, we've got biodiversity mostly in the global south. >> Yes. >> Where it's all housed or stored in the global north. That's >> Yes. >> Yes. Which you can't be that surprised. Like, think about the British Museum, right? I'm not I'm not surprised. This is how we do. This is colonialism. Yeah. Right. So, >> it's I mean, as much as we love our museums, the Smithsonian, like we've all all our museums are like this. Yeah. >> Yeah. Um, conversely, only 22% of the species native to the north have holotype sword outside their country of origin. Not even whether it's in the north or the south, just outside the country of origin, only 22%. And even then, they're stored in institutions with similar geopolitical domains. And that includes things like Australia and New Zealand. So like colonial [laughter] um more than 90% of all mammal holotypes stored in the global north are collected in a different country. In the global south by contrast less than 8% of holotypes are deposited in countries other than where they were collected. Um >> less than eight. >> Yeah. >> Wow. >> So uh this is higher for charismatic groups. um less for things like fish, [laughter] but it's still a problem. 30% of species described after 2000 have holotypes outside of their country of origin. Reptiles 50%. The mammal figure is so high. Um the problem >> I bet birds is are really high too. >> Yeah, they didn't talk about birds. Uh always >> I would imagine. Yeah. >> Yeah. >> Migration. They fly up here. They're ours too. No. >> Yeah. Right. Depends. Some things migrate, [laughter] some things don't. Um, but yeah, so this is a this is a symptom of what is ter termed as parachute science, which is uh when you know scientists come in, they study, they collect, they go out. That's it. They kind of just parachute in, grab a specimen, and scoot. Um, and so why this is a problem is remember what holotypes are used for. When you are describing what is potentially a new species, plant or animal, you have to have access to the holotype so that you can compare and you can decide whether this is a new discovery or not. That means that if I collect a new South American porcupine and I am native to South America and I'm like, "Yes, I think this is a new species." I have to get on a plane with my specimen and go to the place that is holding this holotype to do that comparative study. >> So, so I'm just curious. I mean I I know having done biology, morphology, um these studies there, you know, there the colonial aspect and where things are housed. It's it's a big deal and it needs to be addressed and it's being very slowly addressed, right? But there are going to be infrastructural issues in >> addressing all this, right? But >> yeah, of course >> with modern technology, >> yeah, >> why do you have to go anywhere? Why can't we do Why can't we do 3D scanning and put it all online and just do comparisons with [clears throat] people? Yes. >> Be like, "Hey, put yours online. I'll put mine online, you know, and then we can be friends." >> Well, it's you certainly could, but you would have to have a relationship with that other organization. You'd have to have the abilities to have that communication and do the comparative study >> overseas. And you have you have to have all the digital assets, you know, you have the technology to digitize and >> Exactly. And that's one of the things they talk about in the study too is genomic analysis techniques that are sometimes used that one institution will have and another institution will not. Um, and so yeah, basically just scattering these different specimens causes a lot of kind of logistical questions aside from just like the ickiness of it too, which exists, right? There's an emotional ickiness because it does feel very similar to like the pyramids in the British M or the sphinx, the mini sphinxes in the British Museum, the mummies in the British Museum. Like why are they there, right? like why can't they be in a museum in the place that they're from, right? Um and so there's a few different ways that you can um kind of attack this problem. [snorts] There's a few different measures with different success rates and and kind of costs and and results. So uh one of them is uh governance. So that means they want scientific journals to adopt mandatory specimen deposit plans to the current editorial policies so that they can make data and codes available. So this is similar to what you were just talking about Kiki like making the data available so that um you don't have to pay to go there or to uh retrieve the data in some way. The the next one is infrastructure. So uh basically that means that you want to uh create better infrastructure in the locations where these animals are found [laughter] because that's the other piece is that like the institutions that are taking these animals these specimens are usually very well funded. They have very fancy facilities. they have like temperature, climate, and and humidity control where they're holding these things. And so, uh, most of those are in the global north, quote unquote. >> So, you need to improve the infrastructure in the areas where you are parachuting in and taking specimens and and leaving, right? Um, >> this seems like this seems like such a a place for philanthropies to step up and step in and whether it is in concert with existing colonial museums, you know, who have the knowhow and the ability, but like to do a a knowledge transfer, a data transfer to create >> infrastructure that actually allows for the transfer of these, you know, the the the the basic assets and a trusted transfer of assets. You know, I there's just I there there seems like there should be so many conversations happening to create, you know, infrastructure so that oh, your country is at war right now. We'll take care of your stuff. You know, let's get all of the the good stuff out and save it and we'll give it back. You know, there's going to be a record of everything. You know, there's so many things so many ways that we we really should be doing things better. >> Yeah. >> Oh, you don't have infrastructure yet? Well, let's help you do it. Do you want infrastructure or do you want us to hold it for you? Well, it seems pretty basic to me that if you are um an institution that wants to send researchers to a place where there are not state-of-the-art facilities, then you need to have a satellite facility there. >> Or you need to provide assets to a local university >> or a scientific center that you can partner with then like >> Yeah. Not just you fly there, take things away and take them back to your museum. the whole the whole parachute science idea is, >> you know, that's abhorrent. We can't do it anymore. >> Yeah. And then of course the last one is access. Um just improving the access of researchers from the countries where these animals are native to being able to get to those. So providing scholarships to fly researchers out to the holotype if it is not housed in the country of origin. Y uh and yeah, just you know, basically removing barriers to access. Um but ultimately I was pretty I not surprised but also bothered by this information. [laughter] >> Yeah, I get that. >> I feel like there's a lot of that lately. Not surprised but bothered, right? Um because there's >> I feel like that's me every day. >> Yeah. That like you can't just be like send them all back, repatriate all the holotypes. you can't do that because they don't have a place to go yet. A lot of them um they don't have the right facilities and uh it's like logistically it's a whole mess. Although I will say like I don't understand why you need I understand why. Okay, so hold on. [laughter] >> I wish in one >> I wish you didn't need a singular holotype. I understand why you need a singular holotype. It is for statistical analysis. If you are measuring similarities and differences and you have a different baseline for one measurement versus another measurement, >> your data is all messed up. So, I understand why statistically you have to have one. I wish it wasn't that way because it would be great if you were like there's the North American holotype and there's the European holotype and there's the South American holotype and there's the African holotype. all of the same animal. And so they're all similar. They all have the things that this animal has. Why can't you just use that one? And yes, it's math. Math is the reason. [laughter] >> It's because of math. >> Yeah, of course. Which we love math, but sometimes it gets in the way. >> It doesn't get in the way. It just creates a short-term barrier that as humans we must creatively overcome. [gasps] Yeah. And we're creative so we can do that. And I think that's the big thing you're talking about logistics and everything. It's like anybody who comes up with reasons why not is just being a gatekeeper is just you know just blocking the path. Because what we need now are people who are figuring out solutions to so many things. >> Of course there are going to be oh we can't do that because but I want yes and everywhere. >> Yes and therefore yes please. [laughter] This would be a good place to start. [snorts] I mean it would be pretty cool um to be able to live for another hundred years and see some of these changes take place >> you know um right so having been here for a good portion little bit half a century um >> it [snorts] would be like you you want to live to 150 Blair >> like if you were my age right now you'd still be looking at another hundred years So that's a lot of time to be able to solve these logistical problems and to be able to do this. So how do we get there? How do we get to be the people who live to 150? Right. >> Tell me. >> Yeah. Okay. So uh study just out in cell reports has been uh making the news related to super centinarians. What are super centinarians? Well, super centinarians are people who live more than a hundred years. So if and and it's not even just centinarians, they have inched it upwards. And so now it's people who live more than 110 years. >> Whoa. >> So they're not just So a hundred years is a centinarian, but just people go in more. So super centinarian. And there are people living to 116, 119, 126 I think is like getting like the numbers keep going up although they are still >> uh controversial because right yeah >> because of recordkeeping 120 years ago who was who was paid the whole problem. Yeah. >> Yeah. Who recorded that birth certificate? Um, I don't know that but I'm I mean I know lots of people who started counting backwards in their age when they reached 50 or 60 and so maybe they went backwards and then went forwards because they forgot. [laughter] So maybe they're even older than that. Who knows? >> Oh my god. >> Um, regardless, these provably over 110 year old individuals, researchers have been trying to study them and figure out what is it? Is it that you do exercise every day? It's your social? Is it the whiskey you drink? What happens in your life? >> These researchers uh published in cell reports CD4 CTLs in super centinarians. Say that three times fast. CD4 cells. Do you recognize what a CD4 cell is, Blair? No. CD4 cells are immune cells. They're cytotoxic T-ymphosytes. TE-C cells are the attack cells >> in our bodies. And so our and and TE-C cells are the things that attack cancer as well. So CD4 CTLs have been studied in disease context but not in healthy aging so much. And so these researchers took blood from super centinarians, looked at their tea cells and they discovered that CD4 CTLs which are these cytotoxic tea lymphosytes, so these immune cells that are uh they attack you other cells and they they they clean things up within the body. They discovered that they start to expand get get to be more of them around the age of 100 and they don't get exhausted. Whereas in the majority of people who are not aging to be super centinarians, you do not have an expansion of these cells. So >> So their immune system is better. >> Yes. And so that is what is being suggested here. And so they're suggesting that the these CD4 tea cells, they have um really great cloning where they're able to just make copies of themselves over and over again. And >> cloning is different than normal division. So it doesn't rip up the uh the tieumirs as much. And so you end up with uh you know the clones are healthy, everything's good. And so the um these CD4 helper cells, they can turn themselves into the cytotoxic T lymphosytes. The Tlymphosytes clone themselves and then they can from the clones turn into whatever is necessary to attack cancer in any part of the body. And so the issue is, you know, we know that as you get older, your chance of dying from a cancer related illness increases. Cancer increases as you age because of the number of cell divisions and the greater opportunity for mutations to occur and for increased mutations within your immune system to be able to suppress the ability of your immune system to actually defend your body against cancer or other diseases. And so what they're saying here is that these super centinarians have a an immune system that stays active and it does not slow down and instead of being inhibited it actually expands as you age age and so it is there to address the ills of aging. So the question we have the question long koic is asking how big can their sample be right it's not a huge sample that's for sure um so [gasps] this is there are more and more centinarians and super centinarians in the world however they're not able to get a ton of things and so they've TE-C cells in blood from eight donors in their 70s to 90s, 10 centinarians and 10 super centinarians. >> Mhm. So, you know, they're their starting sample is very low, but because they're able to compare the genetic aspects of each of these cells, they're able to at least give a general understanding of the differences. And this these are the differences that popped out. But >> yeah, we need more super centinarians to give us cells. Well, but also you [laughter] know how we're always talking about how like young blood is very good for you. Now I'm like is super old blood good for you? >> But it's for the same reason or for a similar reason, right? So, so young blood has the markers that refresh the immune system that refresh metabolism to allow it to maintain at uh [snorts] you know a biologically younger age. And so that's why that that works. But this is kind of you're you're on the right track there. This is they're not showing themselves as having an aging immune system in the way that everyone else has aging immune systems. >> Yeah, it's I just Yeah, I'm wondering if you can harness that and give that to people who are of middle age. [laughter] >> And so there is the question, right? as we're talking about personalized vaccines. >> Um, you know, what does a vaccine do? It helps your immune system. So, >> give me those CD4s, >> right? So instead of maybe having the really healthy clonal population of these CD4 CTL cells, maybe instead what you have is very we have treatments or therapies that allow very specific cell populations to be harnessed or created within the body to allow as you know that address the very specific needs of aging. Go. >> Yeah. So, this is about like why people live so long and how we can leverage that, but also there's potential medicine in here for just everyday middle-aged humans also potentially. And so, if we're able to understand exactly what's going on in those cells and why they're different, um, maybe it could help everybody. But the researchers here, they're saying it, you know, this isn't a breakthrough saving our lives, whatever. No, it's just a very interesting data point that could lead to discoveries in the future, right? So, it could lead to specific targets based on, you know, what your genotype is, how your immune cell immune system works at different ages as you're as you're aging. Um, yeah. But anyway, why do some people have an expansion of these cells as they age? I mean, obviously they need it. [laughter] >> Well, there's also the like there's the cause and effect of it, too, right? Like, >> is that what's keeping them alive or is that something that you just see in people that age? >> And that is the that's another point. Yes. Yep. I mean, those people don't have cancer. When they die, it's usually not from cancer. It is just because they died. Um, so >> yeah, >> there's a lot going on there. >> Yeah, aging. It's a whole thing. >> What about aged cheese? [laughter and gasps] >> I love this story cuz really I love cheese. >> Cheese is excellent. >> Yeah. So uh this study came out of the University of Reading Reading and um these researchers in the food microbial sciences unit. Um we're looking at bacteria in cheese. So, we've done a few reported on a few studies where we're like, "Oh, yeah, meat's bad for you. Dairy is bad for you, but it looks like some cheeses and ice cream might be good for you." And like there's all these weird results where we're like, >> "What does this really mean?" And we have no idea really. It's just, you know, large data sets of people who ate certain foods and did not have health problems, right? or or did have health problems. But anyway, they uh looked at biochemical and micro microbial changes that happened in local cheeses. They took these local cheeses and they were like, "We like this. You like the cheese. How does the bacteria affect your gut?" So, it doesn't just impact the flavor and aromomas of the cheese itself. Apparently, um the fats and proteins because of the way they're broken down in the gut, they it makes cheese really good at delivering bacteria to your gut. So you so that instead of it the bacteria being killed and broken down in your stomach because the fats and other things that are protecting them, they actually can make it into your gut to have benefit down lower in your digestive system. Um, cheese rind. If you eat cheese rind, not not wax, the wax wax necess, but the cheese rind, >> white mold, penicyium, candidum, candidium, it puts rind on soft cheeses like brie and others. Um, it produces kiten, which is a dietary fiber that's a prebiotic. >> That's great. Of course, like myself and other people who are lactose intolerant may understand, >> mature cheeses, cheeses that have been aged over longer periods of time have less lactose. So there's less of that sugar milk in there as well. And so um the bacteria being involved in that were able to um help people eat more cheese. And it's actually and those bacteria then are more prevalent in the gut of people who have eaten the cheese which can help to over a long term minimize that lactose intolerance to a degree. So, like eating yogurt, eating cheeses that are mature and have the bacteria that break down lactose, um, that may actually benefit the gut of people who are lactose intolerant and cannot break down lactose on their own. >> Nice. >> Yeah. So, anyway, I thought this study was really fun. Um, >> cheese is good for you. Got it. >> Cheese is good for you. Oh yeah, they are there are other cheeses that have um bacteria that produce propriionic acid which is associated with anti-inflammatory properties. >> Um and some people have said eating cheese can help with appetite regulation. Propriionic acid is one of the signature signalers to your brain and gut to stop eating. Oh, >> and so pro. Yeah. So, the pathway can actually be involved in reducing inflammation and helping to regulate your appetite. So, >> the French were on to something. >> Cheese diet. I see. >> We're We are on the cheese diet now, Blair. That's where we're going. Yum, yum, yum. >> Lactose intolerance be damned. >> Just got to buy your your lactase in bulk and you're all set. >> Full cheese ahead. >> Yes. >> [laughter] >> Oh my god. Okay, moving on up to that's it for the start of the show. So, it is time for us to take a very quick break, which is very quick because really it's just me saying thank you for being here for this week in science. We're so glad that you are here. It's just wonderful to see you in the chat room, to see you um wherever your comments are, and to know that you're listening. If you enjoy the show, please send your friends to Twist. Make sure that they're subscribed. Help us grow on all the channels where we're sending this little show out. We've been doing it for a while, but all of your support really helps keep things going. If you are interested in supporting the show on an ongoing basis, head over to twist.org, click on the Patreon link, and become a supporter. $10 and more, and I will thank you by name at the end of the show, but any amount helps. There's even a link on the website for PayPal. So, if you don't want to get involved long-term Patreon kind of stuff, just click on the PayPal link and it'll send us a send us a donation and that is so appreciated. I mean, every little bit helps. There's also a Zazzle link on our website. The Zazzle link will take you to our store where you can find wonderful merchandise. So many Blair's Animal Corner items that are just incredible. And I really hope that you are looking at them for your holiday gifts this year. You better be. No, I'm kidding. I'm not going to ask you tell you what to do. I mean, ask you. Um, thank you for your support. We can't do it without you. You are what keep us going and keep us unbiased by any commercial influence. So, anyway, really, it's all about you. Now, we're going to come back to that time of the show. we know and love as Blair's Animal Corner [music] with Blair. >> She loves our creatures great and small by [music] pet. No pet at all. >> You want to hear about animals? She's your girl. Except for giant [music] squirrel. What you got, Blair? >> I see what you did. You made a little corner. That's extra cute. >> Um, hey, you know how it is. You're a male redback spider, relative of the black widow. >> Oh, yeah. >> You see a a nice sexy female redback and you're like, that's >> the mother of my future baby spiders, my little spiderlings. And I'm like, I know what I'm going to do. I'm gonna whoop somersault directly so that my abdomen is underneath that female's fangs while we're mating. >> What? >> Which means it'll be all the easier for her to eat me when we're done. >> Oh my gosh. Why would you do that? >> Yeah. [laughter] Well, uh there's there's theories that um this will allow them to mate longer for some reason, I guess, cuz like while she's eating. I don't know. But it allows them to mate a little bit longer and therefore father more offspring. So even if they get eaten, of course, that means they were evolutionarily successful because they have fathered the most offspring. >> That's right. You can go into the void knowing that if you fathered offspring biologically you are successful. >> You won. Yeah. Exactly. Now, uh we've known about this. We've discussed it before. >> Um but this particular study is not about the somersault into death. >> It's not >> that the redbacks perform at the at the the fangs of their lover. >> My god. But it is when an when a a male decides to do it or not do it when he is hybridized with another spider and what that might mean for genetics and evolution. Okay, so let me set the scene. So, aside from this behavior that exists, some redback spiders who do this behavior have also exhibited abdominal narrowing over evolutionary time, which appears to make it more difficult for the female to bite them during mating, which doesn't keep them from getting eaten. >> Oh, but it it surely helps. >> It delays death long enough for the male to do a second mating event. How good is the female How good is the female redback spider's vision close up? Are they like cats where they can't see in front of their nose? [laughter] >> I don't know. >> Probably not because they have eight eyes. But >> yeah. >> Um but yes, so they they are they somehow are able to do a second mating event with that female before they get eaten because they have this abdominal narrowing. [snorts] Um now this is all in New Zealand. A relative of the redback, the cotapo spider does not do the self-sacrifice. The females do not eat the males. They have no cannibalistic mating behavior. But these two species can mate and produce hybrids in the wild. >> What does that do? >> Yes, exactly. Um, and this is only possible with katapo females and redback males since the redback females will just eat the males. They won't mate with them at all. >> Okay. >> No, absolutely not. >> So, um, >> so it has to be the codapo female >> because she won't eat the male. Yes. So, this is these are the only successful pairings that allow for hybrids. >> What are the genetics of these spiders and how what behavior goes forward, Blair? >> Yes. Yes. What's crazy is those male redback spiders of course do the somersault and and they get into the position of like go ahead eat me even female >> that's the male that's the male behavior. >> Yes. And so that means that the somersaults and the cannibalistic behavior have genetic basis because they're doing it >> regardless of the the the the new stimuli of a different female. They're just like this is the only way to be >> feap female eats the males too or no >> no they do not. So that's why this is so crazy that they do that. So they think they're like, "All right, we think this is genetic origins. We do not think this is behavioral. We think it's a genetic thing." Okay. So um they in previous studies there have been um kind of genetic investigations on on mating traits and usually there's a small number of genes or link gene clusters and when you do hybrid studies you can kind of see how those genes get selected or not and what influence they have on their behavior in mating. So they found that first generation hybrid males did not somersault. So it's most likely a recessive trait. So then in order to figure out the genetic basis for these behaviors, they did a backcross hybrid. So they did females with males from either hybrid females with males from either species. Then they filmed mating trials with 104 male offspring to determine whether each male did a somersault, developed abdominal narrowing or both because they also assumed that the abdominal narrowing was related because it was a mating tactic. So they were like these have to be similar genes or similar gene loi or like something related. According to their analysis, the mating somersault is consistent with inheritance from a single gene region on the X chromosome. This is way more simple of an explanation than they thought because a somersault is a complex coordinated behavior. It's not just like >> it's a whole process. It's not it's >> Yeah. >> It's not like the abdominal narrowing where it's just like this is a physiological change. Like no, this is a hard wiring of an entire behavior. Okay. So, we have genes that have led to certain reflexes, right? So, we have genetic basis for innate reflexes. And so, you know, things like hitting your knee with the hammer to see whether you have that reflex. Your tendon has that reflex there in the tendon. It's not even really a nervous thing, right? It's it's within the tendon, >> right? But this is so crazy because this is like visual stimuli. There's a female or it could be, you know, it could be hormonal. Who knows? But there's some sort of stimuli related to >> I'm going to do a a flying through the air maneuver that puts me on my back under her fangs. >> Yes. Yes. Yes. They also found, contrary to what they expected, that the somersault and the abdominal narrowing not inherited together. They were all over the map. About half of the backcross males had only one of the two traits. The traits are not are in in fact genetically separate. Um and unlike the somersault behavior, abdominal narrowing did not fit a simple XL or single gene pattern. It's much more complex, which you would expect the exact opposite. Like this is just a phenotypic change. This should be simple, but that's the complex one. The somersault is the is the simple one. >> Yeah, the somersault. And it's not simple. >> Yeah, >> that's a multi-step process to make the legs move in a certain way to create this movement. I mean, that is a complex neural behavior. How how does one gene >> and spiders do not have a large brain, right? They've got a little tiny ganglia. >> Yeah, they just have like a ball of nerve cells. >> Ball of nerve cells. So there's one gene that's going jump >> right >> across all the nerve cells because of a certain visual stimulus >> which so that is contrary to expectation based on what we're talking about. However, >> the fact that these two species are close enough related, have similar enough genomes that they can hybridize and have offspring. They're true hybrids. That means that evolutionarily they are very closely related and they do not share these behaviors. So it had to happen fast and simply in a short number of mutations. >> Yep. >> They think that they only diverged about a 100,000 years ago. So evolutionarily speaking that's pretty recent. >> So are they still found in over like overlapping regions? Could this even go further to create a uh a hybridized subpop that exists between two separate populations? So are they so this is because they're not sexually separated which is the definition of a species. Right. >> Right. So sexual separation question of like are these actually two distinct species or is this one species with different phenotypes? >> Yes. Yeah. that I mean >> and behavioral mating strategies like >> yes >> it's >> I mean the fact that they are together that they're together often enough and mating and creating hybrids often enough that researchers noticed it >> suggests that >> there's a real blending happening and they are not sexually that they are not behaviorally >> separated. >> Yeah. that males and females are still going, "Yep, you work." >> Yeah. And I So, this is also what's crazy is that, >> wow, this is so fascinating. [laughter] >> Gosh. >> Okay. So, X chromosomes are thought to evolve faster um because of their smaller effective population size in this particular, you know, like spider. But they, for some reason, and I don't understand why, I'd have to look into this further, they think that the sacri sacrificial phenotype was lost. that that's the base behavior whether or not there's a somersault involved but the sacrifice is the base behavior that then was evolved out in the in the kotapo spiders >> because the female stopped eating them the fe the fe if the female is not going to eat the male why does the male need to sacrifice anymore >> exactly yes and so that appears to be what happened 100,000 years ago is that the female katapo spider is stopped eating its mates. >> So maybe there always was that and it you know how we talk about beta males but there's beta females. What about just different behavioral traits that there just got to be big enough populations that we're like yeah they're not the same. >> But you have you have a katapo male who's like I'll flip for you. >> [laughter] >> Yeah. [gasps] I mean, what is what is a species? We talk about this enough. Like, I will bring it up one more time. Like, what is a species? >> One of my favorite questions. >> It's it's complicated and there's no clear answer. And in this case, if you can have hybridization and you can back hybridize and you can have um sexually viable offspring over and over and over through hybridization processes, then you most likely have one species. So honestly that's the part of the study that I find the most interesting um is that I I am stuck to wonder [laughter] like is this is this really two distinct species or is it two distinct genotypes within one species that results in phenotypic and behavioral differences? But I don't know. I don't know. I love this. I love that somebody did this. I want to know more about these. I mean, this is just these questions get at the basis of what drives speciation. What uh that question, what is a species? What are we talking about? >> Yep. [laughter] >> That's right, guys. Make sure you keep that somersault trait. Might keep you from being eaten. >> That's right. Wait. No, it'll facilitate you being eaten actually. >> Oh, yeah. >> Yeah. >> Then you Yeah. Well, we won't go any further. >> No. Um, I'll give you a quick two sentence uh story to exit out of the animal corner, which is, hey, you know, Carsonization, how everything underwater is turning into crabs? >> Yeah. [laughter] >> Everybody's so excited about that. >> That's the dramatization. But in reality, there's like five different types of animals that have all developed to look like crabs in the ocean. It's because it's it's a very effective body plan. Well, what about seahorsification? [laughter] >> Uh there are these things called seauppets. Are you familiar with [laughter] this? >> Oh my god. >> Sea muppets have been found deep muppets. Yeah. Like Kermit the frog. um have been found at very deep deep um depths. [laughter] >> Deep deep depths. >> Yeah. And so they haven't really been observed by live humans. Um but they have several spe I think there are three species currently that have been described and they were all kind of assumed to be related to seahorses because they look very seahorsey. But um some CT scanning of these specimens because they don't have a lot of specimens, they can't cut them open has revealed their their body plan. I can't even really say bone structure. They're like exoskeleletal body plan. And it is not a seahorse. It is very different from what we consider seahorses. So, even though they look a lot like a seahorse with Miss Piggy for a face, um they uh they're not they're not seahorses, but they look like seahorses. So, it is a very effective body plan, which seems crazy because seahorses are crazy looking. I don't understand why they're effective at all. They're not like hydrodnamic. They're clunky. They like they can't move very fast. They're not very agile. They have to grab onto like seaweed and just hold on for dear life. They seem very silly, but apparently extremely effective body plan in the ocean because it keeps popping up. >> And I love that though historically everyone's like, "It's seahorses. Everybody's a hippocampus." >> Like a seahorse. It looks like a bad cookie cutter, like a sugar cookie of a seahorse that you got from like Goodwill or something. It's not like quite right. >> These these poor little guys [laughter] >> [gasps] >> They can't hear you. They're dead. [laughter] >> These are dead seahorses, but they're not seahorses. >> No. >> Yeah, >> they're se. >> But I love it. This is I mean, not everything is a seahorse that looks like a seahorse. >> Just like not everything that kind of looks like a crab is a crab. So >> the they say like the similar the similar thing you see with uh mammals is the beaver otter nutria shape. >> Yes. [laughter] Everything becomes like this aquatic hairy weasly thing. [laughter] >> Ro us. >> Yeah, exactly. >> I don't know. I love >> body plans that work. They keep showing up. Convergent evolution. That's the whole thing. >> Not everything has to be a crab. Sometimes they want to be a seahorse. >> Yeah. >> And I think that's important to remember. >> If you can show me a seahorse crab, you got me. How would that even work? >> I don't know. >> Okay, >> send me your drawings every day. >> That's something for your other podcast. [laughter] >> Yes, >> perfect. >> Ah, yeah, we need Tony Steel in here drawing us pictures of the of the seahorse crab, >> the crabby horse, >> and then also a crab seahorse. Yeah, those are two different things. There's the seahorse crab and the crab seahorse. >> Totally. Oh my gosh. Okay, I love it. Not everything is crabs. Seahorses are coming around, too. >> Okay, so I've been thinking about this study this week because I might have gotten um stung by a yellow jacket. And I think this is very interesting because we've also had questions about whether or not you can focus on healing yourself and actually heal yourself. Right? there are all these >> cults of [laughter] of thought. Um >> but there has been through the years you know many many moments where people talk about meditation or you talk about this or that and how you people heal themselves more quickly than other people do. And sometimes people say it's because they thought about, you know, positive thoughts about healing in whatever was injured or whatever needed needed work. Study published August 17th in nature human behavior. It's titled voluntary attention regulates acute immune responses in humans. So they had three pre-registered within subjects experiments using skin inflammation as a model system. I have skin inflammation, you guys. I really think yellow jackets are I don't like them anymore and I don't care if they are pollinators. I'm going to take action on the on the nest that is outside my front door under the maple tree. You can get somebody to relocate it if you really wanted to be nice about it. [laughter] >> You're you're out for revenge now. I understand. >> Oh, they stung me. All I was doing was watering my plants. I mean, >> my goodness. >> Apparently, yellow jackets. My hands like I have I have a big hockey mitt and I have like my normal size hand. It It's not It's not a happy time. I'm on antihistamines and all sorts of things, but maybe I'm also on positive thought because [laughter] according to this study, they found that directing attention toward bodily sensations compared to distraction, attentional distraction, so actually attending to sensation. So this is similar to meditation. in. Breathe in. Breathe out. So, how does it feel when you breathe in? How does it feel when you breathe out? Um, thinking about and attending to the sensation. Oh, there's inflammation here. I am attending to that inflammation. >> Being aware of it and attending to it in a mindful way produced better immune responses. with different temporal dynamics. And I think that is like one of the most exciting aspects of this is that there's a temporal aspect of you putting your attention to the feeling of something in your body and your body responding accordingly. And so they had people um you know sitting in a chair. They were using EEG to be able to manipulate the state. They did a skin prick. There was you know allergy stuff that made their their their skin unhappy. And so they were looking at the time of how the body responded based on whether or not people were paying attention to it or whether they were not paying attention to it. The histamine response. So basically there's a real measurable histamine response >> that can be looked at based on your injuries. So, first you have, oh, my body's upset. And then the histamine response is the part is that's the itchy part. And so, that's why antihistamines work or topical things that get rid of the the histamines. It's part of the healing process as uncomfortable as it is. But if you are paying attention to your sight of injury, not saying you because this is still very small study, um it changes the timeliness of the response so that you your body or the bodies of the people involved in this study responded more quickly and more accurately to the the skin offense, the prick. So paying attention to >> the injury made your body's response to it >> faster. >> But that doesn't mean that's not necessarily a better thing. That's not necessarily a good thing, right? Because like you're actually getting >> a histamine response that's bad. That's like >> it's not that's not bad. Histamine overreaction is bad. And so like I have swelling and itching that's going on for multiple days because of this yellow jacket toxin. >> But it's actually normal a normal response. It this is um and this is why the allergic response to bug bites, to be stings, etc. is such a big deal is because of that histamine response, right? And if you get a normal histamine response to just a cut or a pin prick or whatever else, it itches a little bit and then it goes away. >> I see. >> Relatively quickly. But the itching is basically telling your white blood cells and your lucasytes within the body, come here and attack things. >> The histamine is part of telling your immune system that this is a site that needs to be attended to. When you have things that have more of an allergic response to them, that's when you we call histamine response bad. Histamine is not bad. Histamine is part of the normal process. It's when histamine overreacts that it's a problem. >> So, you want a quicker histamine response that improves healing is basically what you're saying. You want a quicker so that it peaks faster and then goes away more quickly. man. Cuz I always feel like >> that's counter to the advice you're given, right? Like those of us who grew up in the walk it off generation was very much like don't think about it. >> Don't think about it. Don't think about it. >> Yeah. >> But also, you would think about like the more I think about it, the itchier it's going to feel. >> And that is true also. So, I'm not going to we're not going to go into the details of the psychology of of itch, which is a completely which is it is actually I think related to this in a way, but it it makes it more complex, right? Like >> I'm try I've been trying to distract myself from the itchy feelings of on my hand all day long for the last two day two and a half days really. And this show is great because I'm talking and I'm, you know, I might be itching occasionally. If you're watching the video, you've probably noticed me like itching my hand a few times already. Um, but when you itch, what you do this or when you scratch the itch, what you're doing is creating more submal or dermal uh issues that more histamines respond to. >> Right. Right. So that's the is not scratching the itch. It's just this what this this study is showing acknowledging the itch, acknowledging the injury, thinking about the injury >> um actually can be beneficial to uh to healing and that it makes it it changes the way that your body responds to an offense, which I think is instead of walk it off and run away from it, There is a certain aspect of attending to the sensations of it >> that that makes a difference to your immune system coming and defending your body from whatever has has happened. If your if that localized skin temperature increases enough, it will keep bacteria from getting in and creating an infection. >> So, this is really interesting because stay with me here. Yeah, [laughter and gasps] >> I have a toddler and uh the current >> and they have higher temperatures than us anyway. >> Well, that's true. I was thinking more about like emotional health and how like the current wisdom related to how to deal with toddlers with their big emotions is very different from how it used to be, right? And instead of teaching them to like distracting them from the pain or or the upset feelings or telling them that it's not a big deal or trying to ask them to calm down or any of these other things, instead you're supposed to let them embrace the emotion, recognize the emotion, work through the emotion, and then be done with it, right? And it's How's that working for you? >> It's working really well. I will say like I I am very impressed that like just like in the moment you're like I can't believe I'm just going to let this happen. But like you you you you hold them, you tell them, you know, everything's going to be okay. I understand you're upset. Like all that kind of stuff. And then when it's done, it's done. It has been resolved. Like this one of the things he says all the time now after he's been crying, he's like, "I'm okay now." It's like, [gasps] "Whoa, you just regulated yourself. That's the coolest." But like that's very similar to this, right? like you you recognize the sensation, you recognize the injury, you attack the injury, the injury is now done as opposed to like ignoring it and putting it off. >> I mean, >> and then it comes back later, right? Like it's just it's it's kind of a similar theory. >> My my st my son was stung by a hornet's nest very like he was throwing rocks at a hillside and then [laughter] the hornets came out. They came and attacked him. >> Oh my gosh. And at the time we acknowledged, we were like, "That is scary. That's bad. Like, you feel bad. Oh my gosh, of course you're crying. This do you hurt? Yes, you hurt. That doesn't feel good. Well, let's try and make it feel better." You know, just let's go through it. And, you know, he's um he he now wants to burn down our house because he knows that there's yellow jackets that close to our front door. [laughter] Well, [gasps] >> two things can be true, you know. >> Yes, I know. >> He's like, "Fire, Mom. We could burn it down." And I'm like, "It's right next to the house." He goes, "We'll wet the house down. Everything will be great." [laughter] >> Fire, Mom. >> I don't think so. I think also you're just going to get some really angry yellow jackets out of that. >> Angry flaming yellow jackets. You don't want little flying insects covered in fire. >> Yeah, that sounds bad. Uh but yeah, that's that's cool. I like it. >> Yeah. So, it's it's we just haven't had enough people talk about these things and we know from anecdotal experience, even maybe our own experiences of how focusing on things or thinking about things in different putting our minds in different mindsets for healing um change things. And so this is like an actual physiological experiment showing evidence that attending to voluntarily attending to a site of injury actually leads to a more regulated faster immune response that's that's better that the outcome is like faster and better. And so this is a it's a kind of it's interesting. So yeah, baby, we won't just ignore these things forever moving forward. >> Yeah, suck it up. Buck up, camper. Um, last couple of stories before we end for the evening. Um, sugar babies. Apparently, this one's fun. Um once upon a time during the depression there especi or I not the depression excuse me this was an a study in England Britain between 1951 and 1956 people who were uh born in Britain 64,000 people during this period of time were raised in a sugar shortage. So rationing of sugar was taking place because we're talking about a world war generation. The researchers studying these 64,000 individuals who spent their first thousand days or a large portion of it under sugar rationing have a different metabolic uh holotype [laughter] than uh than people who were born after the sugar rationing. Although everyone after the sugar rationing ended in 1956 was eating more sugar. >> Mhm. >> What they're saying is that individuals during their first thousand days who experienced longer periods of sugar rationing during that first couple of years of life. Now as older adults have lower incidences of breast, prostate, liver, rectal and lung cancer. >> Okay. [laughter] >> Additionally, they found that biological aging was slower for these individuals. So the individuals who went underwent sugar rationing during the early stages of their life, they are biologically metabolically younger than individuals who were maybe born later than them and did not undergo sugar rationing during that first early period of their life. Individuals that had longer periods of sugar rationing during their first thousand days had longer tieumirs. So that it contributes to lower biological age and slowed aging and better general metabolism as you get older. >> And they found that there's a protein called granzyme B that gets higher the older you get with the immune system. It's a sign of slow slower aging at a cellular level. So that grandzyme B was lower in these individuals who had less sugar when they were babies. >> The first the first year well at least the first six months you're not there's no sugar anyway. It's kind of scrapped data. >> Not necessarily. I mean, as soon as kids are able to start sucking on things that aren't a teit, you end up having applesauce packs, you have um >> Yeah, but that's after six months, right? So, like the first six months, but also I think back then, I think people were breastfeeding way longer. >> They were, but the Yeah, there there are very different >> So, >> very different things. But the if the mother also was eating more sugar >> families undergoing sugar rationing >> so the nutrients coming to the breastfed are going to be different. Um, so there are a lot of factors involved in this and the this the researchers they really want to say it's not you know that we're saying sugar is terrible bad whatever it this is just an interesting characterization that they have been able to pull out of the data >> that people who did not have sugar during their first 1000 days >> have better health in later life. Right. >> And so it's kind of like but what happened in between that doesn't matter as much. I mean it matters but what this is the whole old the body remembers the score and so maybe you're setting the body up to >> maybe people don't eat as much sugar because they weren't raised to have a sweet tooth, >> right? >> You know, >> um there's there's so many questions that are still involved in this. But um >> yeah, it's also though like a generational snapshot. So there's like a lot of other potential variables. >> I mean now everybody's, you know, buying groceries at the dollar store. So >> yeah, >> you know, America's. >> Yeah. Sugar's in everything now. >> It's in everything. I have to work to find bread that doesn't have sugar in it. >> Yeah. >> You have to work to find packaged products that do not include sugar. And the fact that that is not the first that that's not the basic state >> of all of your pasta sauces and everything like what sugar and it's the first ingredient and everything. Not my fault. This needs to be changed. >> Yeah. >> All right. Final story. >> Yeah. >> Final story. Sometimes I wonder and worry about, oh, I'm not moving enough. I have a desk job a lot. You know, I'm sitting here not doing enough movement or activity. Would it be better if I got a job that was more active? Like, should I do construction? I'm not going to go do construction. My dad did construction. I saw what was in in that. I'm not going to go do it. But researchers publishing at USC this week have shown that it's not just any type of physical activity that lowers the risk of dementia. It is kind of activity that you're doing. So if you're doing physical activity as part of your job, it's actually linked to a higher risk of developing dementia. If you're doing activities, >> moving for leisure time, that's the movement that is linked with lower dementia risk. >> Interesting. Well, I mean, I know if you're doing movement as part of your job, a lot of the time it's repetitive movement. And so that's also going to cause physical ailments, >> wear and tear, and strain. Yep. But I think that's interesting that um movements for work are related to dementia risk. That's crazy. >> Yep. They found that uh the apparent harms associated with occupational activity are unlikely to be caused by movement itself. They're more likely to involve psychosocial stress, less job control, hazardous working conditions, and greater exposure to air and noise pollution. And independently all these factors have been linked to dementia risk. So they and people in these jobs because they're working and moving their bodies all the time, they may not have that time or energy for relaxing movement activities. So you're, you know, maybe you go out fishing or hunting or whatever, but um are you running and I don't I I don't think running marathons is good for you either. >> No. No. That's like pushing your body to the limit. I I used to kickbox and I loved that. I still do it occasionally. >> Boxing >> just cuz it's very varied movements. It's a social activity. >> Um it's, you know, at the beginning we do it to music. So there's, you know, there's all sorts of different kind of pieces of moving your body in rhythm and then doing different kind of dynamic movements that are actually related to things that you might do with your body at another time, right? Because that's also another thing is like are your workouts something that you could actually use? >> They're called it's called functional functional workouts >> versus vanity or whatever it's called. >> Yeah. >> I know. I All I know is I just need to be able to >> get down on the floor, get off the floor. [laughter] Yes. >> Can I lift things up? Can I put them down? >> Can I turn? Here we go. >> Yes. I look forward to re-engaging in physical fitness hopefully [laughter] soon. >> Oh, life comes and goes with it. Yes, we all need to set a timer once an hour to just like get out of our chairs and do >> squat jumps. 10 squat jumps. [laughter] Just go. Somebody walks by my office at work, they're like, "What are you?" >> Kiki told me to jump, so I'm jumping. [laughter] >> Gotta keep that cardiovascular health going. Come on. >> I was talking to someone in the hallway the other day at work and we decided to do a wall sit while we were talking. >> That's awesome. [laughter] That's great. >> Anyway, I love doing [clears throat] that stuff. I don't have anyone to do wall sits with anymore, so >> I just sit on the floor and pet my cat. Um, >> that's good. >> Eric Nap says, "Sounds like life is bad for your health." And yes, of course, life is bad for your health, but it's understanding what situations are better or worse so that we can ameliate those risks, right? try and try and make workplaces safer, less stressful, better. I mean, if you're going to spend your whole life doing a a rough job, you know, hopefully we can make it safer and better so that you can live older better. Um, >> I don't know. I think everybody deserves the right to age healthily and we should be working toward that. So understanding what leads to unhealthy aging across the board is essential. Oh, wait. I probably just said something that would get like language filtered by NSF NSF AI filters, didn't I? Anyway, >> it's so crazy how politicized it is that we just want people to be able to like live fulfilling, healthy lives. >> Can't Can't we? Oh my gosh. [laughter] That's all we want. I mean, some people want to live forever, and I don't want to live forever. I don't think that would be cool. I think it would be really weird. And I think the psychological aspects of living way past your, you know, best buy date, um, would be weird. >> I mean, I don't want to be a a husk that can't communicate. That doesn't sound fun. But I would like to live forever. [laughter] >> Right. I mean there there are balances. Yeah. We're all I I I want us all to live for everyone. I get it. >> Yeah. >> I want it. [laughter] >> I think no matter what it's live long and prosper. >> Yeah. >> It's not a bad thing to think ethically about. But anyway, that brings us to the end of the show tonight. Have we done it? >> We've done it. >> Woohoo. I'm gonna have a baby in a sugar ration. Hey now. Hey now. Hey now. No, I'm not. I don't know where that song. What? >> I just made up the song. I'm making up songs now. I think we should like come up with old 60s diddy bops related to like modern science. Okay. Uh, thank you all for being here for the show. Everyone in the chat room, thank you for being here for your push-ups, your squats, your wall sits, and your comments. Thank you for joining us for this week in science. It's so wonderful to have you here with us when you're able to join us. It's just a magical moment to be able to share all these thoughts together. Thank you for listening wherever you are. Thank you to everyone for keeping our chat rooms great places to be. I mean, we cannot do it without you, Arin Lure, Gourd, everyone who's in the chat rooms maintaining compassion and respect. Like, come on, everybody. Um, F, thank you for all of your help with social media and show notes. Rachel, thank you for editing the show and Identity 4, thank you for recording the show. And of course, thank you to our Patreon sponsors. 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