 and blah, blah, blah, blah, blah, blah. We're here to do a weekly science show that we call This Week in Science. It kind of explains itself. And if you're here right now, you're watching live or maybe you're watching the video of what we recorded live, things will get, oh, you're gonna wear a beanie too, yay. Well, I saw you were wearing a hat and I'm having a bad hair morning, so I thought. Let's just, yeah, this is good. Let's beanie it up. Things will get edited for the podcast. So this is the whole truth, nothing but the truth, and all of the errors and other stuff with nothing taken out. The podcast will be different. We hope that you subscribe to this, that, and the other because we're all over the place. And right now is the time to hit all the likes and shares and tell people that we're live. Everybody pause, if you're seeing this on the YouTubes. Right now. Take the second, hit the thumbs up button. Thumbs up. Because there's a guy named Algorithms. And the only way he will tell anybody about this show is if you have hit the thumbs up button. You don't even have to say anything. Just click on that thumbs up little thing down there and all will be handled by this fella Al. That's how it's been explained to me anyway. Hey Al, what's up? Thumbs are up, that's right. Okay, we're gonna start this show, you ready? Oh yeah, let's do it. Let's start this show, okay. So starting the show in a three, two, two, this is Twist. This Week in Science episode number 948 recorded on Wednesday, October 18th, 2023. How do the days keep going? Oh my gosh, title of the show is Are Snoozers Losers? I'm Dr. Kiki and tonight on the show we are going to fill your heads with MAPS Dementia and a snooze button, but first. Disclaimer, disclaimer, disclaimer. There is a baby crying, my baby. He is sick, fever, rash, blisters on his tongue. His mother is trying to sue them. He cannot be appeased, will not be calm. The discomfort is too great. I would have written a typical disclaimer here, something topical or sciency, but I couldn't. Thinking is impossible under these conditions. There's a baby crying, my baby. At some point he will sleep. For how long? Not long, but in the moments in which he sleeps there will be silence. A blanket of peace thrown over the household, we will step cautiously avoiding the creaky boards, open drawers and cabinets with delicate care, speak in hushed tones, knowing that there is a baby sleeping. Our baby, but not for long. Who upon waking will again be crying. He will get better, be his happy, healthy self again in a few days, but until then there will be more cries, more tears. And at least one episode of This Week in Science, coming up next. ["Science To You 2"] I've got the kind of mind I can't get enough. I wanna learn everything. I wanna new discoveries that happen every day of the week. There's only one place to go to find the knowledge I seek. I wanna know- Good science to you, Kiki. Good science to you too, Justin. I feel like I need to be whispering even though you're hearing me in your headphones. Yeah, you're fine. You can do that disclaimer. And good science to everyone who is joining us this week. Thank you so much for joining us for another episode of This Week in Science. We have so much good science ahead to discuss. Woo! I brought stories about mapping the universe, mapping the brain, new, old evolution ideas, and fighting cancer with bacteria. Ooh! Yeah, what did you bring, Justin? Let's find out. Oh, I brought that, Snoozers Aren't Losers story. There we go. I've got an ancient stone tool captured in a painting, but it's not a cave painting. It's 15th century painting. I have Why Lawns Are Evil, and a story that I think is making the rounds, at least about antacids and dementia risk. And it's- Interesting. Yeah, and we're gonna talk a little bit about how you could even try to determine causality and something like that. All right, yeah. Cause versus correlation. Just a correlation and maybe some, maybe, well, we'll get into it, but it's a- We'll get into it. Yeah. Yay, okay. I'm excited for your stories. I'm excited to talk about the science. So glad everybody is here. And just a reminder that if you are not yet subscribed and you're here, subscribe to This Week in Science on YouTube, Facebook, Twitch. We are there streaming live weekly, Wednesdays, 8 p.m. Pacific time-ish. And additionally, we are on a lot of podcast platforms. We are podcasters. This is a podcast. It goes, you look for twists this week in science. You could just find it, you know, go on your phone, go trip, trip, trip, and then subscribe. It's so easy. And then if this is just too much for you, you can go to twist.org. It's our website. We have links to shows, links for subscribing, links for all the stories that we cover. That's where it is. It's where it's at. But we're here now. It's a gateway website to having all the podcasting apps on your phone devices. You could go old school and just listen to the show on our website that works to whatever. But, you know, if you subscribe, that's awesome because you get it weekly. So anyway. Websites are old school. Oh, gosh. Yeah, I know, right? Oh, it's a really interesting time we're in right now. Everything new is old. No, old, everything old is new. Anyway, time for the show. Let's talk about science. All right, yeah. Me? Yeah, if you wanna do that. Okay. Let's do it. I would like to start with mapping the universe. That's gonna take a while. I think it'll be very long. And then you gotta draw in 3D and, oh, that's tricky and then what's the scale? How do you even have a legend on one of those things where it's like, all right, this line represents. There's so much to be thinking about, I know. The size of a million solar systems. A million solar systems, oh my goodness. All right, well, this last week there were a few efforts in the research world, astrophysics specifically to map the universe published and there's some interesting stuff out there. First, I'm gonna start with a publication from the Australian National University researchers who say in the abstract of their paper that's called All Objects and Some Questions, they've presented an overview of the thermal history of the universe. So in terms of mapping everything, it's more of like two plots against each other of the thermal history and the sequence of objects as they have appeared in the universe. And what they say is that these comprehensive pedagogical plots draw attention to a triangular region forbidden by general relativity and quantum uncertainty. They go. Who are those? Yeah, but they dive into a place which is the thermal and like what we would call a singularity, the center of a black hole where space, time, mass, all kind of the quantum world loses, things get weird and wacky there. They say that at this point, there is what they call an instaton. So it's like a new particle, which is their replacement for a singularity, but this instaton, which would be a plonk mass black hole. So basically like if you were to go under the empty space and you have a black hole, it's like the smallest black hole that you could possibly have, that would be at the plonk scale, which is the tiniest, tiniest thing. This is like getting in a string space. When you get into the space where matter is popping into being and out of being, that's the plonk scale. And so this is this place where they're like, if a black hole were to form there, they're gonna call it an instaton, not a singularity. But anyway, they ask, do these the plonk density and plonk temperature make them good candidates for initial conditions of the universe? They say the plot of all objects also seems to suggest that the universe is a black hole. However, they map out mathematically how that's unlikely. So it's a very interesting paper that is published in the American Journal of Physics, kind of talking about the mapping of temperature and time and objects in the universe. Like in their mapping, it's fantastic. They've got the log of mass, log of physical radius. And along some of these trajectories, these vertices, they have atoms, bacterium, flea, human, whale, planets, main-sinquents stars. You know, so there's some very interesting stuff. They go off into this certain areas past black holes that are forbidden by gravity because what happens inside of a black hole? When it's the supermass, we think gravity breaks down at the singularity. There's also a Compton limit in which there's quantum uncertainty that we can't really get past at this point with our technology and our math. But it's a very, I think it's an interesting paper in that it just takes a look at things that we already know and maps them out in a way that possibly opens up a space for asking new questions. Yeah, and one of the interesting things to me too is that whether it is a map of your living room or a map of the entire universe, you still cannot fold it in half more than seven times. It's a fun bar bet. It is, okay, I'm not gonna, I'm not an origami person, so. Yeah, you can't fold it in half more than seven times in any piece of paper. Whenever like, okay, this is so typical of the field of physics though. I can't ignore the fact that. I have more coming later with, yeah. So first we're gonna do, we're gonna create a black hole that can't exist because it's too small, so there's nothing that was gonna collapse down to the side. And we're gonna make it a new particle. We're gonna create a new particle while we're at it. And we're gonna forget about singularities. No, no, no. Which is gonna ignore it for the moment. This is a new particle. And try to build the universe from that starting point. Okay, I guess you had the time to do that. And yes, I mean, these are the ways that these theoretical models of spherical cows are the way that discoveries are made because you're placing these sort of constructed the artificially-ish limits on things based on things that are limits that have been observed and then you see what are the ramifications of this and does it fit with anything? Right. So it's a fun field. It's a fun field because it's almost limitless in the ways that you can tear apart the universe and put it back together again. Does it do anything? Maybe not, but... But I do like some part of the way that they've looked at things are in these transitions from matter to dark energy after the Big Bang. Like there's the changes in the energy and how things are there. Like they do take aspects of reheating, electron annihilation, things that have happened physically into account. This isn't just making everything up. It's just taking account of everything that we know so far and plotting it. So you can look at it visually and go, oh, that's nice, that's really great, good job. Yes, anyway, next story of mapping is this last week. We also had the Sienna Galaxy Atlas compiled by NSF's Noir Lab Telescopes. And this is a digital galaxy atlas for large galaxies. It has just been published in the Astrophysical Journal Supplement Series and this Sienna Galaxy Atlas is great because it's data from three surveys between 2014 and 2017, the DESI Legacy Surveys identifying targets for dark energy spectroscopic instruments. Like they're trying to like figure out, okay, where's the matter? Where's the dark energy? Where's the matter? What's happening? They used a dark energy camera legacy survey. I mean, we don't know what dark energy is, so I don't know how we have a dark energy camera. But anyway, that's beyond me. They used ground-based telescopes in Chile. We've also got Beijing, Arizona Sky Survey. There's a bunch of other stuff involved. And the science platform has opened this all up to community science and data center. And it had these surveys, 400,000 new objects galaxies in our cosmic neighborhood that they have taken pictures of. And so this is a total area, optical and infrared of 20,000 degrees, square degrees, half the night sky. It's one of the largest galaxy surveys ever and it's precise location shapes, sizes of these galaxies, allowing people to be able to take a look at these large galaxies. It's the preeminent library for this, for people to be able to see what's out there in the night sky and to confirm the things that they are seeing. This is a higher resolution, much larger survey than we've ever done before. And so, I mean, I'm just astounded, 400,000 new galaxies to be looking at. And it's freely available for anyone to look at, not just university researchers. It's available for you and you and you and you and you, anyone can look at it. And it is this great- Where would I go to look at such a thing? And you can go to sga.legaciesurvey.org where they have the data portal. You can take a look at the bits of the night sky that they have been able to map. You can look at particular galaxies that are in this trove of data. So if you're looking at a part of the night sky, you can see what's there and compare it against what they've looked at. So amateurs and researchers alike, it's a massive trove of data. We're gonna need a better telescope. I'm gonna need, I don't have one at all, so this is absolutely easy. Get your telescopes. And then also in the last couple of weeks, Gaia, which is ESA's mission, recently released a whole bunch of data, half a million new stars in a massive cluster, over 380 possible cosmic lenses. And they pinpointed the positions of over 150,000 asteroids in our solar system. It's Gaia is mapping our galaxy and beyond, but it's also taking a picture of close-in. So our solar system is very important. The third release recently contained over 1.8 billion stars of the Milky Way and beyond. And they've got clusters and clusters of, they look like stars in the sky when you look at them, but really these stars in the sky, it's a star cluster. And that star cluster reveals that there's a whole bunch of stuff going on and it increases the resolution so that there's 10 times more stars that we're seeing in the cluster core. Additionally, there's 15 times the brightness. So they're seeing, that's how they're seeing all these things. But I'm excited about also the lensing that they've identified because by observing lensing, what that suggests is that we're able to see back further in time. We're seeing things magnified from back behind objects that are between us and whatever it is. Yeah, it's so nice when black holes or gravity clusters can operate like a better telescope, way deep out in space. It's pretty handy. So the old image of Gaia looking at Omega Centauri was fairly dark and now the center of this image is just fully bright and they have magnified in on it. They're able to see much so many more stars, which means more possible planets, more things out there. It's just the, I'm so excited about these observations, the mapping that we're doing to be able to put ourselves in our place in the universe and see what else is out there. And I don't know, to some people it might make you feel small, but to me, it just makes me appreciate how wonderful the fact that we're here is. Yeah, it doesn't make me feel insignificant in any way. For me, it's awe and wonder. However, there's more than one to that, but I actually, I'm so certain that because physics and chemistry seems to be the same everywhere in the universe, that all of the Earth's like planets that are out there are gonna have a form of life. I don't expect that life might be much more than a bacteria, something without mitochondria. Like that might be the kind of high bar for life most places. However, the way it got started here so quickly and everything that we've learned about how the basic elements of chemistry interact to give the rise of life, although those components, all the organic material that turns out to be so common that we can find it on asteroids floating around in the dark, cold of space. Yep. Probably all of those planets that are Earth-like and even going beyond the Earth-like, somewhat unearth-like rocky planets will likely have a form of life on them. That's really the exciting thing when I see. Yeah. They might not even have to be rocky. Or icy planets that are having methane oceans. Like, there's so many possibilities. There are more possibilities, but even just limiting it to water and rocky planets, there's a lot of them. Right, there's a lot. And one of the, I know we're side-burning, but one of the things too is the building blocks for DNA seem to be somewhat naturally occurring, right? All over, yeah. The form of DNA, that double helix, is just a structurally sound version of those. So that it's not that it's like, oh, but if it, how could you even have it be the same as on Earth with a double helix? That seems like it would take all this. The double helix prevents things from being pulled apart lengthwise and side to side. It's just more stable. So if anywhere else found that stable medium of these combining elements of chemistry and physics, it should persist. So I wouldn't even be surprised to find out that DNA as we understand it here on Earth was also, I think, so that life might not even be that different anywhere else. I swear, yeah. I think that's the interesting question. Yeah, I don't know. Not that we found life anywhere else yet, but I think it is pretty commonly accepted that based on all of the chemistry, the physics and stuff, if the conditions are right, life will happen. But yeah, I think that's the big question. How different will it be? But, I know. Yeah, and I've heard like there's a way that life could have started here where one of the nucleotides was swapped out for another or something like this, but I don't know. Chemistry being chemistry, I have a feeling. And we can talk about this a bit later because I have a story about old evolutionary ideas being new again. So yeah, so we're gonna come back to this in just a few moments. In the meantime, though, I didn't hit a snooze button. Yeah, you snooze, no, I didn't hit a snooze button. I just slept through my alarm. You snooze, you lose, what? Is that true? Okay. So if you're like me, and let's face it, you are nothing like me, where your hobby of collecting your own nail clippings is limited to your own nail clippings. But if you're a little bit like me, you don't wake up all the way after a first alarm. You hit the snooze button. You drift off for a few more minutes of sweet, sweet, sweet. To be all the way like me, you would have to set three alarms spaced out so that all the snoozes that you hit for these set alarms build up to create a crescendo of unending noise. Finally, or your child comes in and jumps on you. At some point, you just can't figure out how to turn the alarms off of your phone and you hand the phone to the child. So snoozing is a little ridiculous. Everyone who snoozes regularly, the snoozers, the snoozers have to plan ahead for snoozing. If you're a snoozer and you know you're a snoozer, you have to plan ahead. So a non-snoozer has to get out of bed at 11 a.m. So the non-snoozer sets the alarm for 11 a.m. But a snoozer might have to set the alarm for 10.30 a.m., 10.15? Yes. Way too early in the morning and losing considerable time in deep sleep compared to the non-snoozer. So the debate has been, I don't know where this debate took place, it exists. Do the snoozers get less restful sleep and suffer consequences from the self-indulgent snoozing behavior? Right, because snoozing is self-indulgent as opposed to just hearing the alarm and throwing yourself out of bed. Yeah, you're like, oh, that alarm is for common folk. Not for me, I deserve more sleep and I will take it. I feel like this is a Western culture capitalist, whatever. But anyway, let's discuss more about these snoozers. Well, a Swedish study finds that the snoozers, on average, do, of course, sleep slightly shorter and do feel more drowsy in the morning compared to those who never snooze. However, there were no negative effects of snoozing on cortisol release, morning tiredness, mood, or sleep quality through the night. According to the lead author of the paper, Tina Sundelin, researcher at Stockholm University, they looked at 1,732 individuals who answered questions about their morning habits, including how often they hit the snooze button. Many reported snoozing regularly. The snoozers tended to be young adults and evening people. I used to be both of those. Now, I'm just the evening people. The most common reason for snoozing? Feeling too tired to get out of bed when the alarm goes off. Yep. Completely relate. That's it. Totally. Oh, God, it's too early. No, snooze, just five more minutes. So they did a second study. They invited 31 regular snoozers to spend a couple of nights in a sleep lab and they measured their sleep in some more detail. One of the mornings, they were allowed to snooze for 30 minutes and the other, they had to get up right when the alarm went off. So even though sleep was disturbed during the half hour of snoozing, most of them actually did get another 20 minutes of sleep. So that whole, you're sacrificing the amount of time you sleep by doing the snooze routine. And not so much. They actually got most of that back. The snoozers also weren't waking up when they did get up from a deep sleep. So that snooze sleep is a much lighter sleep. Right, so it's more of the REM type sleep. It's not the deep sleep that would be more important because we know that a deep sleep cycle takes like 90 minutes. You need like an hour and a half to go through to get into it and get out of it. It's like hour and a half cycles. And when people know they have to get up at certain times, like you go to work, you have a cycle, circadian rhythms are a big thing, your body kind of wakes up, gets you out of those deep sleeps at a certain time if you're doing it over and over again. Yeah, I got to the point where I had a routine for such a long time that I would wake up like a couple of minutes before my first snooze alarm went off, which was annoying because then I'm like, oh, now I'm awake, I gotta wait for this thing. And if I fall back asleep now, it's just gonna wake me up in like five minutes. Oh, what do I do? It's such a conundrum. So the snoozers performed better on cognitive tests in waking up from the snooze as opposed to waking up from the deep sleep. There were no other clear effects of snoozing on mood, sleepiness, the amount of cortisol in the saliva. Study shows that a half hour of snoozing does not have negative effects on night sleep or sleep inertia, that's the ability to get up and start the day. The feeling of not quite being alert in the morning wasn't affected. If anything, there were some positive outcomes and participants were allowed to snooze. They were a bit more quick thinking when they did get up. So of course, important to remember, the little disclaimer that this study only included people who are regular snoozers and find it easy to go back asleep after each alarm snoozing is most likely not for everyone and should only be attempted by professional snoozers. Totally a professional here. There we go. But if you're a snoozer, that's a nice snooze confirming. You can just have that thought. But next time the first alarm goes off and you go, oh, I'm doing this for alertness later, this will help me start my day and then hit this snooze alarm. Well, I wonder, you know, what's the drowsiness upon waking, right? And if you're snoozing, maybe because you're in that light sleep for just a little bit longer, maybe your brain and all those systems that boot your brain back into alertness and activity, maybe that snoozing gives the brain a little bit of time to actually do that a little bit better. But like you said, maybe it's not for everyone. Some people just need to throw themselves out of bed and that's the way it works. And it made, you know, this is a good indication that there also could be like a, some sort of biological difference going on between the snoozers and the non snoozers. Strategy-wise, if the alarm goes off and you could just get up and you're ready to go, you may not be wired for snoozing. Right. And if you're somebody who always, again, I literally have three morning alarms spaced out. Although initially, initially it was because sometimes in the, that drowsy, not awake brain first waking, I would accidentally turn off the alarm as opposed to hitting the snooze button. So to prevent myself from accidentally not hitting the snooze button, I set a second alarm as the snooze button. But now I've gotten pretty automatic at hitting snooze. And so now it is a constant din of alarms going off at some point. One thing that I really like seeing here in this data though is that the different chronotypes that they've defined, snoozers have the lowest percent of being morning people. Non snoozers have a higher percentage of definitely morning people. So I think that in itself is this very interesting balance of how just people are differently wired and how your circadian rhythm works, how everything works together is very important. And but yeah, let's get rid of this idea of you snooze, you lose because it's not necessarily correct. Unless you're really late for work because you're snoozing all the time and it's impacting your ability to do normal things. And you're not like, maybe you should ask somebody for mental health and depression. This is always, I will just point this out because this is not part of the study, but this is always about it. Yeah, the snoozers, some of us are often late but we're still wide awake at the end of the day. Whereas the non snoozers who woke up three hours before work and got there early and were like, I already are on their fourth cup of coffee when they get there, they're checked out by two and a clock in the afternoon. They're like their brains are done at the end of the day. That's a different, it's different. But you don't get docked at work for mentally checking out at the end of the day. So anyway, pet peeve. Just do the work, get the work done. But I'm wondering also like evolutionarily, the benefits of this. Like it may have been, you know, oh, somebody needs to stay up and make sure the raccoons don't run off with the babies or the bears don't come into camp or whatever the thing was. And so like, okay, some of you need to stay up. Baby thief raccoons. Oh my gosh. Oh yeah. Of course. Somebody might have been like, some of the population, the community would stay up really late. Keeping the fires going, looking out for danger. Other people got to go to bed early and then wake up early and keep the raccoons the way in the morning while the night folk got to sleep in. Yeah. Yeah, different time. And it makes a lot of sense for how a community that is impacted by its surroundings 24-7 would potentially survive the best is to have different people who are better at being alert at different times. That makes absolute sense. We're gonna move on from snoozing to bacteria. Who? Yes. One of the big issues with treating, treating cancers has been whether it's a blood cancer or a solid tumor. Immunotherapy has been really, really good for blood cancers, but it hasn't been great for solid tumors. And researchers that have been trying to figure out how to use CAR T therapy, which we've talked about before, which are these modified T cells that go in to specifically attack cancer cells, how to get them to attack solid tumors better? What can they do? It hasn't been really successful in that solid tumor area. And so Pavers published in Science this last week, researchers used non-pathogenic E. coli to deliver antigens to the tumors, solid tumors and tag them. And so the antigens on the tumors, then that the modified CAR T cells could be attracted to and could grab onto and then destroy solid tumors. They found that when the E. coli probiotic was administered, CAR T cells could be directed to solid tumors. They orchestrated tumor cell killing in mouse models of breast and colon cancer. The system demonstrated cell activation in antigen agnostic cell lysis that was safe, effective in multiple xenograft and syngenic models of human and mouse cancers. So basically human cancers in mouse bodies. But yeah, so this work is using engineered bacteria to basically go and label and infect tumors with little tags so that our immuno, our CAR T immunotherapy can actually work. Yeah, it's a sort of work that like, I guess a B cell would normally do. But it doesn't because the tumor cells are like, hey, I'm fine, don't pay attention to me. And that's like, yeah. Yeah, and so here comes this little bacterial, creation and it doesn't register as the thing that's going to tag it. And so it gets away with it, which is fantastic. Yeah, yeah. So this is a new potential for the CAR T immunotherapy going beyond blood cancers to solid tumor cancers that would be a very specific treatment. So it doesn't have lots of the other problems that come along with chemotherapy and other treatments, drug treatments that kill lots of cells. So the CAR T comes in, is specifically locking on to those cells that have been labeled by the bacteria as tumorogenic and destroys those cells. And so yeah, so it's like the B cells, they selectively attach to the extracellular matrix proteins in the tumor micro environment. They also release a chemokine. So the chemokine is like a signal that's like, hey CAR T cells, come over here. You wanna come over here. This is a good place to be, come on, come hang out over here. And then you have Rosy Perez, like punching someone in a face, you know? And that's how it works. Yeah, well, yeah, I can see that. I was gonna say, this is potentially going to be, they're looking at it for tumors in what they've looked at, mouse models of leukemia, colorectal cancer, and breast cancer. So very much further than just the blood cancers they had previously been looking at. The whole problem with cancer is that it's a survivor. Yep. It's almost like it has gotten off of the, or it's very much like it's gotten off the track of being part of the body. Yeah, it's doing its own thing. And is realizing like, hey, they're gonna get rid of us. That's a little group of cancer cells. If we don't defend ourselves every way possible, and it almost in a weird way acts like it's its own organism because it's not listening to the tissues around it. It's not gonna pay attention to apoptosis signals or anything like this, so. But it's interesting, it's like, it's a weird, it's like a parasite almost too, because it's like, hey, we're gonna stop the virus in here, especially solid tumors. It's like, ooh, I want some of that vascularization. Yeah, come on in here. Well, I don't like the way you talk. The way you voice cancer is very scary. Yeah, yeah, it should be. Oh, yeah, I know, I guess that's it. Yeah, but I think this is gonna be another really interesting tool in the toolkit. And I find it fascinating that as much as we worry about certain bacteria E. coli, people are like, ooh, my spinach has E. coli, and we have to throw it away, or it didn't get washed well enough if somebody has an E. coli infection, they go to the hospital, that's a bad thing. There are ways that we can work with bacteria symbiotically, that we can actually engineer them to do things like this that help us survive better. Bacteria are part of our microbiome naturally, so it's not a big step, and I find this kind of stuff really interesting. And E. coli, too, has been a mainstay of biotechnology for creating things, so it's used probably in every biotech product that you've ever encountered on some level. Involved at some level, yeah. Yeah, at medical or commercial or whatever. Like, that's a very handy. Tool and the tool kit of biology. Speaking of tools, how about handaxes? I like handaxes. Oh, my goodness. I don't know how to use a handaxe. Well, maybe I should learn. Yeah, well, so the handaxe was invented hundreds of thousands of years ago by human ancestors or ancient cousins of some sort. Large stone tools known as the Ashulian handaxes were used to cut meat and wood. They were used to dig with. They were sort of the Swiss army knife of Homo erectus. And they were often made from flint, these prehistoric oval and pear-shaped tools, flaked on both sides with sharp pointy ends, have been found throughout history. So we think of, you know, I always tend to think at least myself that we've just discovered the ancient world. But the ancient world also discovered the ancient or world and it's time. Not always with the best understanding of what they had found. So there's some texts from the 15th century of Ashulian handaxes being referred to as thunder stones shot from the clouds. They were thought to be some sort of natural phenomenon. Researchers from Dartmouth, I don't know how to say Dartmouth. Dartmouth, Dartmouth, Dartmouth. Say it again. Dartmouth. Dartmouth, okay. I should rewrite how they spell it. Everyone, so I should update spelling to conform. Oh, it's probably British though. University of Cambridge have identified the Mulan diptych, circa 1455, painted by Jean Fouquette, depicts what is likely the earliest artistic representation of an Ashulian handaxe demonstrating that these objects had even earlier place in the modern world. And they published this in Cambridge Archaeological Journal. So the Mulan diptych. Oh, and there's a good picture of it. You got there. You can see you got the guy there in the red who actually commissioned this work of art. He was the accountant or head of the treasury for the king. And so he had a nice painting of himself next to the taller gentleman there who is supposed to be a saint who's holding some sort of red and gold book. And on top of it is this very large stone, which seems to be very jagged and sharp and oval shaped or pear shaped kind of. And actually, now they think this is an Ashulian handax that has found its way into this painting. Now, I guess it's St. Stephen is the one who is the tall one there. Bearing the handaxe. Bearing the handaxe on top of the book. Whatever book that is. So apparently St. Stephen was stoned to death for being an early Christian. I don't really know the story, but that's why the stone has been placed in here. Although, unlikely, I would say, that he was stoned to death by homo erectus. Probably not. It's still possible. I don't know. I wasn't there. 1555, maybe not. Just think. But I do love this story for a few reasons. Stephen Kangus, senior lecturer in the Department of Art History at Dartmouth and the study co-author, had always looked at this painting and thought, that looks like a stone tool to me. That doesn't look like a natural stone. There's something too odd about it. Look at the edges. Look at its surface. It looks like somebody cracked at it. He says, according to him, was always sort of struck in the back of my mind as something that I needed to pursue in the future. And sure enough, the future arrived in 2021. So it's past now. It's now the past. That was the future once. And now it is a publication. Okay. Kangus attended a seminar about an archaeological site in Tanzania, which has a lot of handaxes. And afterwards talked to the presenter and another professor who he had them look at this painting and they went, ah, there's a study there. And so they studied this stone in this painting. Turns out the artist actually spent a lot of time working on this. They did that thing where they can look below the surface of the paint and they can see the drawing on the canvas before the painting and they can tell how many times the paint has been reworked. And they could tell that the stone was especially reworked compared to the rest of the painting. The stone object in the painting similar within 95% to other Acheulean handaxes from the region where the paintings were made. That's important. The researchers counted the flake scars on the surface of the painted stone object. Wow. On average, they found 33 flakes on the surface which was consistent with the average identified on 30 handaxes that were randomly selected from their French handax assemblages. So within a bound of error, it fit. Yeah. And the stone was painted. Had a few, like if you look at that thing too, it's kind of a little brown and a little yellow and there's some reddishness to it which I wouldn't have thought a stone tool has but apparently that color variation is very like the stone Acheulean axes found in the region. They have these discolorations to them. So it all looks like it fits. Yeah. It all looks like it fits. And they say about the artist who painted it. Forquette, I can't, I don't know French translation. Forquette seems to have taken special interest in the stone object probably because he had seen one that stuck his attention and imagination. So if that is so, it's then also likely that the artist had never seen a female breast. The other panel of the painting. We're gonna go there, huh? Yeah, because there's like, they could count the number of chips that were flinted into this 500-ish, or you know, ancient stone tool. This hundreds of thousands of year old stone tool count the number of the flakes they could see the coloration, the detail level was so great. But the next panel, there's a woman who appears to have just or is about to breastfeed a child and there's no nipple. And also the breasts aren't quite in the right place. They're like in her armpits and- One's in the armpit, one's like more standard. Absolutely zero detail. No detail, because honestly, I bet it was not, it was probably blasphemous or looked down upon to have been like gazing upon a woman who was show, maybe he just kind of glanced and was like, okay, I saw enough and then just sketched it and I don't know. And also that painting is supposed to be a virgin and her child, which I don't know how well science was understood in 1455, but I think that would be also unlikely. But it's just, the juxtapose between the level of detail in this rock that we can actually now attribute to an ancient stone Ishmaelian handaxe versus the lack of biological information on the woman in the next panel is just, to me, it says something about the people of 1455. I think it really does. I think that is, yeah. People can make their own conclusions from there. Yes. Since 1455, we have moved on, we've moved on through years and years. Medieval ages, dark ages, on the types of Darwin and Newton and scientists were like, I've got ideas and they wrote their ideas down and these big writings and, yeah, it took a long time for us to really start thinking about how to incorporate all of these ideas together, but now we have the law of evolution, theory of evolution. We have laws of thermodynamics. We have an understanding of natural selection which was addressed by Darwin. This past week, there were a couple of papers that came out that I find very fascinating because of who's publishing them and what they're talking about. And okay, from my perspective, as a biologist who has studied evolution, ecology, all these things, I'm like, and how is this new? Yes. We have a paper published in Nature and we have a paper published in the Proceedings of the National Academy of Sciences. Both of them by individuals who are mostly chemists, astrobiologists, astrophysicists and not so much of the biology background. So either they will have a lack of deep knowledge to assist them in their conclusions or a complete lack of bias to look at things clearly and clearly. It could be in a way. Right, exactly. So I've been asking questions of people who are experts in evolution and biology about their thoughts about these papers. And the first paper, which was published on October 4th in Nature, relates to a topic that they present and call Assembly Theory. And they believe that Assembly Theory is what explains and quantifies selection and evolution. So both of these papers are trying to take physics and chemistry and bind it together with biology because similar to general relativity and quantum theory, there's like the math is lacking. There's no binding equations that anybody's really been able to come up with that are like, and this is how it all works. You know, at a certain point, it comes like, it's like, oh, physics is nice and explainable. Oh, yeah, chemistry, that all works. Biology, ooh, that's mushy, you know. And so there's this, even though we can all look at natural selection and genetics and we can look at genes and chromosomes and DNA and the physics and the chemistry of how those molecules interact and everything. So we know like there's stuff happening in there at the basic level and one of the big tenets of biology form follows function. So the function, what's needed, dictates what the thing looks like, right? Form follows function. This is a tenant and this is something I've learned over. Like this is ingrained in my mind at the same way that ontogeny recapitulates phylogeny is ingrained in my mind. These are statements that anyone who's studied biology is gonna be like, oh, yeah, I know exactly what it is. So I'm gonna go ahead and say, biology is gonna be like, oh, yeah, I know exactly what you're talking about. But these people are funded in a way that what they're trying to do is reconcile in this assembly theory paper says that, you know, reconciling biological evolution with the immutable laws of the universe defined by physics. These laws underpin life's origin. Wait, if they're immutable, how come they're always trying to mute them? Yes, exactly. So assembly theory, I find interesting. One of the researchers, Lee Cronin, he has been working at the edge of chemistry and kind of this chemical life field for a very long time, like creating molecules that self-assemble, creating molecules that assemble to do certain functions. Like, this is the place and he's the last author on this paper. He's been doing this work for a long time and he's well-versed in all this stuff. But so this assembly theory, they're presenting as a framework that doesn't alter the laws of physics, but redefines the concept of an object on which these laws act. So these objects are not point particles, but what they say is that they're entities defined by their possible formation histories. And in saying this, what they're saying is that this allows objects to show evidence of selection within boundaries of individuals or self, or selected units, and that those histories lead to, so basically what an object is, is because of what's come before and what an object is now is gonna lead to what it's going to become later, that these objects are characterized through forward dynamical processes considering their assembly. Yeah, but is that, that's not anything new. I mean... Right! So here I am going, everything old is new again. Okay, so this is the first paper that I'm talking about and everybody in the evolutionary area is like, okay, I'm saying these things. We think a horse previously was a four-legged animal that turned into a horse and in the future, it's unlikely to be a six-legged animal, like, I mean... Yeah, the last sentence of their abstract, it discloses a new aspect of physics emerging at the chemical scale, whereby history and causal contingency influence what exists. But yeah, what's there just going to influence what is... Okay, so now I want you to take this in your head and we're gonna move to the next study from the Proceedings of the National Academy of Sciences that was just published this last, ooh, just, yeah, just published October 16th. Daniel Smith, did they just reinvent time? Yeah, they're like, there are moments where things are a certain way and there's a before and there's an after. Yeah. That's time, thank you Daniel. And so this new study is called On the Rules of Function and Selection in Evolving Systems and the media that you might see in the popular stories revolving around this are these researchers just made a theory of everything which makes my alarm signals go ping-tink-tink-tink-tink because, okay, whatever. And in this study, researchers have, they've basically been like, hey, there are these laws of nature, okay, and we suggest that all evolving systems, including but not limited to life and maybe this is the thing that separates their thing from all the other things since they're looking at it from like a everything point of view are composed of diverse components that can combine into configurable states that are then selected for or against based on function. Their big idea, their big idea is that they propose- So there's stuff? There's stuff. Yeah, their big idea is that they propose a law of increasing functional information. And this is kind of interesting. The functional information of a system will increase and evolve if many different configurations of the system undergo selection for one or more functions. Okay. So I was thinking about this in the sense of like, okay, biochemistry. You have chemical interactions. These two things, chemicals, they maybe can do an interaction if the heat gets high enough or the pH changes enough or whatever. But ooh, an enzyme comes around that goes, you get to do this interaction for free. And suddenly the molecules do the extra interaction. They are boosted to a different energy state, we'll say. But it's not like a plateau. It's like they went up a hill to the peak and then down into a little valley. But that little valley is like a pond where it's higher than where they started before, but now it's a new pond. So you can have entropy within that pond. But it's not necessarily gonna make the entropy go all the way back down to the bottom again. So, you know, I'm looking at this going though. I learned about this like over 20 years ago in biochemistry and I don't understand how you think you are making new words here that make new senses. I think I figured it out. I think I did. Can you tell me what's happening? Yeah. Physics and physicists have nothing to work on right now. They're in that entropy valley you're talking about. It's higher. It's higher than our understanding of physics was 50 years ago, but they're waiting for the enzyme. They need a catalyst. Yeah, they need that catalyst. Maybe we should turn the heat up on them. It does sound like they're now, hey, what do we do? We can do the spherical cow thing again. Right, so I feel like there's some stuff happening here. These are big journals who are publishing these papers that are reworking old concepts. And so what I'm wondering is, is it the fact that they're a new reworking that might potentially reframe the way that people think about stuff to allow new questions to be asked? Because I mean, call me naive. Call me that I don't know what's happening. I don't understand what they're talking about, but I'm honestly at a loss here as to why these are big papers getting big attention in big journals. I don't get it. You know, it could be, like, okay, so if I was gonna lead credence to why these would be big papers without really knowing anything about the scenario, but a good hypothesis would be there's a lot of ground that's been covered in science over the last couple of hundred years, thousand years, however far back you wanna go. A lot of ground that's been covered. You know, maybe there are places where we just learned a thing and have an assumption that this has been documented or has been defined or been, like, well-explained by science. Maybe the writers of this paper go, you know what, we know this is taking place, but nobody's written a paper saying it, stating it. Putting it into the record. Right, maybe that's, maybe it's as simple as that. And that's- It really could be. It's possible. And if they've done so more articulately than has been done in the past, more specifically, more narrowly, without having it be about the evolution of a woodpecker in a specific forest, or, you know, like maybe that's been done, right, specific to a life form or another system, but never done without reference to a specific scenario. Like I could see there being some- Yeah, I mean, maybe that's what it is. And when I hear that, I see this old professor being like, you know, a student being like, ah, I don't know, I gotta do a thesis paper and say I gotta do a paper. And then he's like, well, you know, Sonny, or Mr. Whatever, I don't know today, I don't care. Back in my day, we never actually looked into or wrote a paper about just the thing that there's time or that there's stuff. People just assumed it. Right. I mean- We have two papers, one that says there's time and one that says there's stuff. Now we can move on from there knowing we have written papers on these. Yeah, and I imagine as well, there is some amount of now that we're looking beyond Earth and we're looking into the possibility of the emergence of life from chemical and physical systems, potentially different than ours or similar to ours, that maybe this is a place where, you know, because we've only been looking at it here on our own planet and everybody like equates evolution with Darwin, which is not the only part of evolutionary theory, and I just want to tell you- That's like the early part. It's like one little part of our understanding. But it's like, yeah, and I wonder if there's, you know, some aspect of, like you said, physicists going, hey, this is kind of new, oh my gosh, I didn't learn this because they didn't take the advanced biology classes that explained evolution beyond just a Punnett square. You know? Yeah, so there's- And to clean things up and make it a hard science as opposed to those wishy-washy biologists. Running around curing diseases while your businesses are still trying to figure out, I was like, well, I spent 10 years studying string theory and that didn't work and I spent 20 years looking for a particle that we never found. Oh, I know, let's just clean up the biological life sciences. Yeah, that's what we'll do. Also, by the way, I will be the, not probably the first person to ever say this, but, you know, function can follow form. Form can follow function. For sure, but usually- It's not one direction necessarily, yeah. Well, you know, it's like- Like usually, but not always. Well, when you say usually, I don't know. I guess biology is mushy-mushy-mushy-mushy-mushy. It is, it's like, oh, I've got this, I've got this ability to see in the dark for this one thing and now I can use it for all these other things or whatever. You know, like, I always think it's such a two-way street. You know, when change happens over time, as is explained in these papers, new functions can be, new opportunities are there to be exploited by life. And that's- Exactly, and that's why it's so good. Novelty, right? New functions, novelty is a core aspect of what allows progress or change, not even progress, just change to take place. Yeah, but it's, I just found it very interesting that these two studies, you know, kind of on the heels of those mapping studies that I brought up at the beginning of this part of the show, you know, just, it's just very interesting. There's, you know, people looking at old things, maybe in new ways, maybe putting them together in ways that people have thought about, but not put into words in the same way previously, I don't know, it's very, it's interesting. New people coming across old ideas for the first time, thinking they're new, like, I don't know. And to be fair- I think nature and PNAS would actually be like, hey, you know, this isn't new. To be fair though, a lot of research isn't new. You know, actually it's a story I'm gonna do later, the one on the Alzheimer's, the dementia and antacid connection is an example of something that has been studied and seen a bunch of times. So there's not really a problem with seeing it again, reporting on it again, just not discovering. Like we think of science as like, this is the first time anybody's ever even thought of this. But a lot of the times it's, here's another confirmation of the thing in the way things work that we've seen before. There's just another- The wonderful thing about science, right? Replication, doing it over again, confirming results, making sure that we know is what we know. And also looking at old things through new- I think your problem, Kiki, is with the science- No, no, is with the science reporting. I think that's what- Is with the science reporting telling everybody, this is the first time they've just explained the universe. No, no, it's not. No, we've been talking to people who've been doing this. It's not new. And like I know Lee Cronin, he's been doing working on assembly theory for a very long time. This is not new in this year. Just, come on everybody. But media wants to do what media wants to do. So anyway. What if it's the first time you've heard of it? It's new for you. Oh wow, somebody just explained everything. Oh my gosh. Now I get it all. Someone just explained the whole universe and everything. Oh my gosh. It's all sorted out now. Now what do we do? Now I tell everybody that this is This Week in Science. Thank you so much for joining us. If you were just tuning in, I hope that you're gonna stay with us for the rest of the show. And additionally, if you're enjoying the show, please share it with a friend because that's how we spread the word is friend to friend to friend to friend, colleague to colleague to colleague. Hopefully you're telling people about twists so that more people know that it's okay to talk about this stuff, that we can have fun talking about science and the stories that happen every single week from the lens of information and understanding what we're talking about. Let's go there. Let's go to the source. Okay, if you want to help us grow beyond just helping telling friends to subscribe, head over to twist.org. You can go to our Zazzle link. The Zazzle store is where you can purchase all sorts of twists related items, got hats, mugs, towels, great things for you and your friends, pillows you can put on your couch. Also just some of the proceeds go back to help twists keep doing what we're doing. Additionally, if you would just like to support twists directly, click on the Patreon link, become a Patreon supporter, those who support us at $10 a month and more. It's only $10 a month. Oh my gosh, probably less than Netflix. Oh my gosh. You do that. We thank you by name at the end of the show. $15 and more. You get stickers, 25. I think you get a T-shirt. There's like various levels but there's all sorts of fun in there and you get to know that you are a part of making this conversation happen. You're here with us right now. We know you are. Thank you for your support. We can't do it without you. All right, Justin. It's you against the lawn. The long arm of the lawn. So I asked earlier and it turns out we don't have a special effects budget or a live band. So this is audience participation time. I need everyone to imagine a drum roll in their head. Ready? Go. And the Twissey Award for best study title of the year so far goes to Hydrobiogeo-Sociochemical Interactions and the Sustainability of Residential Landscapes, a study on lawns. What? Yeah, you can't, if you still have the drum roll going you can stop now. If you can't stop, I'm sorry for putting that idea in your head. The American residential lawn is, for many, an iconic landscape, heavenly in its brilliance. For others, lawns are mean and rueful of the Western dream. About half of homeowners in the U.S. use fertilizer to keep their yards green and lush. Some proportion of the nitrogen in this fertilizer then works its way into the broader environment and can have negative consequences, including algae blooms and de-oxygenated waters, depending on where those waters end up. So Peter Grofman and colleagues studied residential landscapes in the Baltimore, Maryland metropolitan area, which drains to the Chesapeake Bay, which is already not what you would call a christen, seeking to identify locations, hot spots or times, hot moments, with disproportionately high rates of nitrogen export. The authors went to lawns and exurbans, suburban college campus settings to measure nitrogen export during simulated rainfall events. The authors also used household survey data collected from the Baltimore Ecosystem Study, long-term ecological research that is big going on for almost 20 years. We're at about 20 years. So they also did their own survey of 3,836 Baltimore area households. I thought it was pretty interesting what they ended up finding here. So although all of the export hot spots were found on fertilized rather than on fertilized lawns, the survey data, 48% of the people surveyed incorrectly believed that they did not live in a watershed. More than 60% of those surveyed did not know if nitrogen negatively affected area waterways. Bummer fact, it does. Yeah, it does. And what they then found was that support for policies that would limit fertilizer use among those who were using fertilizer was broadly high. Some types of restrictions, even garnering support among those who fertilize, who love their lawns. So about half of households signaled that they would be interested in converting lawns to features that reduce nitrogen export, rain gardens, if the conversions were subsidized and made as easy as possible. So the idea is somebody's got a house with a lawn, they like the lawn, would they be cool with having a garden that didn't need to be fertilized and didn't need as much water? Yeah, they just don't want to have time and money to tear up a lawn and build a whole thing. Why do you have to tear up a lawn? Just let the weeds take over and then mow those. Yeah, some people do have like, I don't want to call them people superficial, but you know, keeping up appearances and stuff, whatever, you don't want to do that. You have, I mean, you can say that because you live in a place that rains, you know, 250 days out of the year. So you're gonna have nice green, lush looking weeds. Yeah, but except for like the moles, and the moles come through and they have the holes and the moles, oh my gosh. You were talking about moles last week too. These moles really got to you. They're really, I mean, I don't understand how anyone has a nice lawn who does not invest in poison and traps and like the bad things because these moles, they're just there. They do their thing anyway. You just need to get pet ferrets, that's all. Are they legal? I don't know. I should check, not in California, maybe in Oregon. I don't know. Okay, anyway, on with the lawns or off with the lawns. So yeah, the main conclusion of the study really is just that change is possible and even desired. People just didn't know their role in things. You know, the researchers were actually kind of taken aback by the fact that they, how willing people seemed in these surveys to make the changes, they just weren't aware that they were part of a problem. So yeah, people needing to know their role in the larger ecosystem and what the trade-offs are and a little incentive could go a long way. So, you know, sort of think of it as a, if you're a city who's contemplating a multi-million dollar cleanup of your bay and oh, what do we do? We can change the chemistry. We can have these machines. We can have a wastewater project. We could do a thing. Or part of that, you could just offer an incentive to redo people's lawns, like a mobile lawn transformation part of the city. Look at those tree-cutting people. Arborists, they're landscapers for the city. They can't be that busy, especially not in Baltimore. There's not that much open green land there. You know, put some people to work transforming lawns into these water gardens or whatever they're calling it. Anyway, sounds like there could be a win-win there. Yeah, so you have municipal level policies that go to the HOAs and supersede whatever HOAs say. So then it's like, all right, now everybody has to do this kind of stuff. And I really do think that there is a place there. There was another study that came out this week related to more climate-level adaptations. And discussing how the majority of adaptations that are taking place are at the individual level. Like people are doing stuff, but really like it's the government that has to do, like there's a gap between where the government is talking and making regulations and then actually having that passed down through the level, there's like a gap there. And this is one of those places where people are used to the normal, used to the, we're supposed to have a lawn because that's what you do. They don't know that lawns can not be great for the environment. They don't understand what's going on there. I don't know what this is, but in the chat room, Harjar is saying, look into a vibrating mole repeller for us, real nice. Look, I have not- Vibrating mole repellent? I have not gotten into the vibrating mole repellent because I do not want the tremors worm to come and eat my child. So, I mean, Kevin Bacon doesn't live near me at all. So, or Ed, what's his name? Yeah, I don't have any- I gotta go watch tremors again. You do. It's like a, actually several movie series that is fantastic and it just gets better. Is it several? I think I might have seen that first one. The B movie aspect of it is just- It's really well done. Yeah, Chef's Kiss, oh my goodness. Yeah, take us off from lawns to somewhere else, Justin. Oh yeah, it's, I'm up again. Here we go. This is the last one. This is research at Copenhagen University Hospital and Arhus University, Denmark. Look into the potential association between protein pump inhibitors, which is the antacids that are used to suppress stomach acid production and they found increased dementia risk. This is a pretty good size study. This is a nationwide Danish cohort of nearly two million individuals aged 60 to 75, done over two decades. And it included individuals without a prior dementia diagnosis or treatment before being part of the study. So study got narrowed down to 99,000 individuals, 99,384 individuals who developed dementia during the study and another 469,000 who were used as a control group. The antacid use was associated with an increased risk of all causes of dementia, particularly they found in the group between 16, 69 years old. As people got older, there was less of a correlation. Once you get to 90 years old, there was no real correlation that they could find between dementia and antacid use. But it was very significant for the younger groups. And what's sort of interesting about this is there was like the longer you'd used it, the higher the chance of having dementia. But it was also any use. So even if you used it for say three months, it indicated an increased risk of dementia. So I saw this and I'm like, this does not to me look like it could be causal. Like there's that possibility, that's possibility. But it almost looks like an early symptom of dementias will be effects on the gut and increased acid. And so there have been also previous studies that have shown there are in Alzheimer's patients, there is a drastic change, a really identifiable change to gut microbiota. There was a Parkinson's study that also showed that there was early indications of changes in the gut microbiota and in terms. So likely what's happening is there's the enteric nervous system. That's the nervous system that goes from the throat down through your stomach and your intestines. And it's neuronal cells. The gut-brain connection, they've got the vagus nerve that's involved. There's serotonin and there's so much interconnected there. So the authors also point out in this study that further research is needed to explore the mechanisms underlying the association, whether it varies with dementia types, whether what is the causal or reverse causal, possibly. But it looks very much like that's, based on the way I'm seeing it, it looks very much like that increased stomach acid. Might be an early clue of dementia risk, which if that's what they end up finding from this, that in itself could be huge because for some of these individuals, the use is 10 years, 15 years of this. And it's not something that's necessarily prescribed because you can take it into acids just over the counter. You go and get yourself whatever. Which is actually partly why I think it's a little helpful that the Danish cohort study because with the universal healthcare, if your doctor recommends it, you're likely to have it prescribed and paid for as opposed to needing to buy everything over the counter or like to sort of, I mean, you still can, but why would you if it's covered under medical? Because that's one of the hard things in these studies is at a certain point, unless you go back far enough, 90s, I guess, you still had to be prescribed. It was at some point that there in America became over the counter versions. But initially there wasn't. So the problem then is any studies done after that can't find it in just the large data sets because it has to be self-reported kind of a thing. Yeah, or self-reported, yeah. Yeah. But I found this interesting because it, even if somebody's been using it for a long time, that might then indicate a slow growing form because there were so many that were in the, like only used it for three months or four months or a year or something like this that then had this bump in dementia use. On the other hand, because of that enteric got brain connection, is it possible that antacids are in their disrupting normal microbiota preservative functions? Sure. Are they interact? Yes. Right, are they interacting with the disrupting the lining of the stomach or the... They're changing. They're changing the pH. Are they making changes that could be causal? Yeah. So it could be. A lot of them are like calcium or magnesium related, right? So they're, and you know, non-prescription are, you know, milk and magnesium, you know, kind of stuff or calcium, citrate or there's, the stuff that's going in there is binding up hydrogen and making changes and is adjusting the acidity of the gut. Why is the gut that acid in the first place because the bacteria that are probably there and what's happening in their metabolisms and what they're producing. So there's, is it cause? Is it correlation? That is like for sure something that needs to be determined. But it's... So it is, it does look according to this that it is correlation, but could also be causal. And it could be both depending, it could be both for different people. And it could be the way they work together. Yeah, synergistically, right? It could be accelerating cases. It could be decelerating cases. But the fun thing is, in case you see this, it's cause dementia, it might not be that clear. It might not be that straightforward, but it is really an interesting intersection when you have something that is a real strong correlation find. Yeah. But could be multiple causals still. I find the dementia occurring after 90 years. It's like, if you're making it to 90 years old and then you take antacids, it's like, you're fine. You did everything great. Like you're doing just great, it's good. And then it's also part of why I got the feeling that the direction works from Alzheimer's before use, at least in this cohort that they've got here, because if you hit 90 without having to, address your stomach, and then that's when the dementia hits, it's like, you know, I don't know. It seems to fit better if dementia is causing the stomach acid, which like you say, could be from alterations in the gut microbiota, which could be from the gut brain connection. But again, we don't know which way things start. The other thing I was referencing, I was from one of those, almost made it seem like Parkinson's disease starts in the gut. Like they may have kind of an argument that this was a gut first. And then- I remember that. Yeah, I remember that a while back, yeah. So- Hasn't been confirmed yet, but yes. No, no, but the fact that's even a path, right? The fact that a lot of these correlations and connections lead back to the gut, we really need to understand the effects of the gut on the brain, because it could be the source of the disease, or it could just be an indicator of what's going on in the brain. It could be trying to tell us, gurgle, gurgle, gurgle. Hey, I got a problem up here, and here's how I'm gonna talk to you by using the stomach. Blblblblblb. Yeah. Well, thinking about the brain, researchers at the Salk Institute and a large number of other organizations around the world, the U.S. National Institute of Health's brain research through advancing innovative Neurotechnologies Initiative Cell Census Network, known as the BIKIN, B-I-C-Z-N. Hundreds of scientists working together also with Australian researchers, European researchers, people everywhere, all over the place. They've been working to map the human brain. So they've been mapping fly brains, they've been mapping mouse brains, they've been doing all sorts of mapping, and then they were like, it's kind of like cell types in the human brain, and we've got some little things going on with the human brain, and like, this is really awesome, and then they kind of were like, you know, these techniques that we are using to identify subtypes of cells in mouse brains, we're gonna do it in humans. And so this is like a decade almost in the making these studies. It was like a set of 21 papers that came out to publish all this stuff. But this brain initiative, I love in this Salk Institute PR press release, they have the word, they're describing the full plethora of cells. I think it's honestly a writer's goal to use the word plethora. Whoever. To be honest. Possible. It's one you try to avoid. Plethora. Because it can be used up, but every once in a while you're like, oh. It's a plethora of cells. Plethora is the only word that I could use to describe all of these things. Yes. Well, this menagerie of cells that they have described, they have revealed more than 3000 different cell types. Lots of them are new to scientists and to science. And the way that they are new is not just in what they look like, like their form, but also their genetics and how they work together. So looking at similar genes that are expressed, one cell from the back of the brain might express or have a gene expressed with an on switch, whereas in the front of the brain that same gene gets expressed by an off switch. So the same like cell types and the genetic differences between them are making up what these researchers are using and saying is this atlas that's going to give a much better understanding of the human brain and how different cell types work together. So they're looking at developmental histories, different functions, the mix of neurons and other cell types across different regions. They looked at the brainstem, which is not as studied as other areas in the brain. They found a lot of neuron types that had not been described before in the brainstem, which is the connection between the brain and the spinal cord. Pretty important area, right? You'd think. They use chemical markers that switch genes on or off in more than 500,000 different cells. They found that molecules acted as switches to identify about 200 different brain cell types. They also have genes for, or a different understanding now how different genes might contribute to disease risk. So like we're talking about Alzheimer's, Parkinson's disease, other neuropsychiatric disorders, bipolar disorder, depression, schizophrenia. They're looking at how these different genetics which are able to influence gene regulation and risk of neurological diseases and not just in neurons, but in microglia as well. Microglia are some of those support cells which are involved in cleaning up dead, damaged cells. They're also involved in some local cell signaling. They are very important for basically helping to manage neurons. They keep the neurons in line. And so microglia and understanding how they're working with the neurons themselves is a big aspect. But it's a huge, huge undertaking, like I said, almost a decade in the work that they've been doing. And they've gotten to this point now where they have all sorts of new cells, 3,000 new cell type, new, independent, individual types of cells that they can start looking at. So more questions can be asked. You know, and it's unfortunate that they wasted all that time when physicists, and I think a couple of afternoons, wrote two papers. One that said that time is the thing and the other said that stuff exists which is all that we really needed to know. And slap. Yeah. So it's very exciting. Like who knows where it's gonna go from here? There's this whole package. If you're interested in brain stuff, you can go find it. Anyway. Yeah, where's the gut? Where's the gut brain? It wasn't included in. So this is, they're just looking at the brain itself. They got to the brain stem, right? Right, they got to the brain stem. But those are. And now they're getting. Neuronal cells embedded in the, from the esophagus through the intestines. That's neuronal cells. That's brain. You have a brain in your stomach. You have a brain in your gut. Yeah, and so one of the very interesting things moving forward from here is maybe they can start to address some of those questions about that gut brain connection with or without the microbes and how they're involved and you know, how the vagal nerves, how the vagal nerve innervates and influences the nervous, the enteric nervous system. And they've gotten to a point now where basically they're genetically barcoding these nerve types, these cell types in the brain. And so this barcoding is gonna lead to an ability to compare against other cells, other things that they look at. So maybe the, you know, enteric nervous system is big, big also. Maybe that's the next step. It is. And so here's how I, when you're talking about form following function and all these sorts of things, here's one way to think of it. The brain is connected very directly to some senses, the audio system, the visual system. We have nerves running through our body that allows us this touch system. Before we had a lot of that going on, the way that the body, the brain, sensed the environment was through the gut. What did I just eat? Is that a good thing? Is that not a good thing? This is what I know of the world. This is how I sense the world. This is how I know the world exists in my stomach. To an extent, right? They had these, oh, very primitive forms of, there's a thing that I see it or can hear it or can feel it, sense it in the, and I eat it. But now I have to figure out what it is. Yeah, so I like to think about that also. I mentioned early ontogeny recapitulates phylogeny. It's so the development of any mammalian organism, humans included, it starts with that blastocyst and what happens immediately? It forms a tube through the middle and that is the gut tube. And that's where it all, it's the first thing that starts. From there, everything else goes. It's stomach first. We always think, oh, the brain and then there's all this stuff got attached. No, stomach first. Gut first. So maybe, maybe, maybe we've been ignoring the biggest sensory organ, the biggest, the information back and forth. Maybe the brain that's really running things. It's not as exciting. It's like you're gut. It's the thing that, you know, it makes you feel bad. It's like embarrassing sometimes. It's like, you know. It's just trying to talk to you. It's just trying to tell you things. I know. My final study published in the Proceedings from National Academy of Sciences this last week, researchers at Kyushu University have taken brain immune cells and turned them into neurons and treated stroke injury in mice. So they took microglia, which like I mentioned, they're normally for getting rid of dead or damaged cells. They go to the site of injury. They replicate. They're like, we're gonna take out the garbage. And so these researchers were like, hey, these microglia are just in the right place and they're dividing. They're doing this cool stuff. And so they gave my strokes. And then afterwards, they used a viral vector, a lentivirus, to put DNA into the microglia cells that created, that made them turn into neurons. It was a DNA for producing what's called neuro D1. It's a protein that leads to the rest of the conversion into a neuron. And so these neurons that had been infected with the lentivirus, they turned into neurons. Eight weeks after, they integrated with the rest of the brain and these mice that had had reduced motor function and deficits related to the stroke. Saw improvements. They were able to move better. They were actually improving faster than mice that did not have the same treatment. So not taking cells from somewhere else in the body, not taking cells from some other animal, not do another, just do it, just minorly shifting the form and function of the cells that are already in place within a site of injury in the brain, led to help. It's interesting. So anyway, yeah, we can help stroke in mice. We'll see if we can do that in humans at some point in the future. We did, I love that we did the brain atlas on mice first. Yeah. Again, someday in the post-human world. And the mice run everything. The mice rise up, become sentient. They will find in the archives and the records the cure to every mouse disease left to them by the ancients, the giants, the ape, the hairless apes that wandered the earth, making the world, preparing the future world of mousedom so that it could be disease-free. Disease-free, mouse kind. At least we can set the environment to help something, some organisms out there in some way. Rachel had a stupid question. Why don't we have teleportation, Justin? Is that stupid? I don't know. I don't think it's a stupid question, actually. She says it would make so many lives so much easier and I think we as a society deserve that. What's the legit science-y reason we can't teleport yet? Well, because you still have to go everywhere. Yeah, we have to put all the pieces back together or you have to figure out what they were in one place and then- If we're talking Star Trek. Star Trek. If you're talking Star Trek, here's the thing that is a problem with the teleporter in Star Trek. They are murder devices. Yes, they murder the person in the place and they recreate them in the next place. That's- You could, you could just as easily, just as easily go into the transponder or the teleporter and have another version of you pop up on the planet surface without killing yourself. Ah, there would be two of you. So when that one wanted to come back, you can't actually transport them back. And then you have to kill the alternate version. You have to destroy them down on that planet and then create a new one up in it. Like what would be the point there? So you would just really what you want to do is have a clone of yourself out there in the world doing stuff and then reporting back and then- No, because then they're not you. They're at the house. There's no- There's no- They're not you. They're a different person. That just is- By the time you can deconstruct a human and teleport them, you don't need to destroy the first version. You could just be cloning and making a second version. Right. That's the problem with it. And then, cause the problem, real problem is you only have one toothbrush. So you've done, you've transported and then the other, you comes back and now- Now you have to share your toothbrush. Now you're like, share your toothbrush with this other person. And then the toothbrush becomes a shiv and that's your device, not the teleporter. Then they go and teleport somewhere and then there's, now there's three of you. And just in a matter of a couple of episodes of Star Trek, that ship is overflowing with curks and sparks and bones and they're all like, I'm the captain. I'm the captain. I'm the science officer. Oh, well, so am I. Yeah, so are we. I'm not a doctor, but I am like, this is nonsense. Yeah, it's complicated, but the legit science-y reason is that we can teleport little atoms and they're happy. It's that quantum, but it's like, entanglement, that's what we're doing. It's not like, yeah, but yeah, no, we're not doing it yet. We're not there yet. And really there is no, that whole thing with the quantum parts, if one is up, one is down. Here's two letters hidden in a secret package. One says up, the other says down. That we know. I can put this one on the moon and open this one and now I know what the other one is. But it doesn't mean that I have transmitted any information over from here to the moon. It just means that if this was up, the other one's gonna be down. It's all it means. We haven't done it yet. We haven't really transported, teleported it. No teleportation. It's entanglement, not teleportation. And entangled just means the information is entangled, which means, so is like, if you put an up in one envelope and a down in the other envelope, that information is now entangled. There you go, quantum physics and like. Oh my gosh, we're having a conversation. We're so entangled, Justin. Oh my gosh. Ah, let's finish this entanglement. Have we come to the end of the show? Oh yeah, is this the end? Yes. I'm trying to think, do we have more? No, there's no more stories. No more stories. We've come to the end of the show. And I would love to thank everyone who's been in the chat room, in the discord, chatting through the whole show. Thank you for your thoughts and your ideas and everything throughout. I know that some of you are here and don't make any comments. Thank you for being here, all the same. Anyone who's here live, thank you to Fada. She's off doing an improv showcase tonight. So. Break a leg. Yeah, but he's still gonna be doing our show notes and social media, so thanks to that. Identity four, thank you for recording the show. Gord, Arun, Laura, others who help everybody really for being nice in the chat rooms. Let's all be good people, okay? Let's all be nice to each other. And of course, Rachel who helps edit the show and our twist patrons, thank you so much for all that you do to help keep the show going. 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There's a topic you'd like us to cover or address, a suggestion for an interview, a haiku that comes to you tonight, please let us know. We will be back here again next week, and we hope you'll join us again for more science news. And if you've learned anything from the show, remember. It's all in your head. This week in science, this week in science, this week in science, it's the end of the world. So I'm setting up shop, got my banner unfurled, it says the scientist is in, I'm gonna sell my advice, show them how to stop the robot with a simple device. I'll reverse below the warming with a wave of my hand, and all it is is coming your way. So everybody listen to what I say, I use the scientific method. This week in science, this week in science, this week in science, science, science, this week in science, this week in science, this week in science, science, science, science, I've got one disclaimer and it shouldn't be news, that what I say may not represent your views, but I've done the calculations and I've got a plan. We have come to the end of the show, it's the after show. And it is into the 10 o'clock hour. I don't know where Justin just headed off to. So I do not know how long this after show will last. Oh, David, huh, is that a time change next week? Cause that's going to be interesting for you. Connecting with Justin. Although I think this time change is better than the spring time change for Justin, and the way that works. Let's see. Not this weekend. It's not on my calendar, so it's not happening. When is the time change? Do we know this? Time change 2023, Sunday, November 5th, 2023. So no. Oh, it's Alaska day? Happy Alaska day, Eric Knapp, yes. Happy Alaska day. Fallback. No legislative changes to daylight savings time have been enacted yet in 2023. So Sunday, November 5th is when we turn back the clocks. The weekend after Halloween, spoopy, spoopy, spoopy. Yeah, I can deal with that. Thank you, though. Don't worry about apologizing, David. It's good for me to know ahead of time. It's also going to be interesting because as we mentioned last week, Justin has gotten a new job in Denmark and we'll have some differences to his schedule. So Blair, I sent a text to Blair and Justin and the idea is that we'll all get together and talk about what we want to do about scheduling. And I know everybody's used to this nice time and I don't know if I can handle marketing a new time for us to be live, but maybe we will change our time of broadcast or depending on what Justin's schedule is going to be like at the new job, maybe I'll get guest hosts for a period of time, but yeah, time change is going to affect that for sure at some point. Yeah, I don't know, but Blair is working on a calendar. So if you're interested in the 2024 twist calendar, Blair is working on that apparently, which is very awesome. She's been posting some stuff on Facebook and probably Instagram too, but I've only seen it on Facebook, but that's exciting. What does Justin do? Justin has gotten, let's see, a long time ago he was a vacuum cleaner salesman, then a car salesman and now he does like biotech work. So he's worked in gene sequencing, he's worked in all sorts of genetic lab, biology, like Genentech type stuff. He's moved into some very interesting things over the time that we've worked together, yes. So this job would probably be, what's your new job doing, Justin? Okay, I think I'm back. I can't hear anything though. Oh, can you hear me now? I can't hear you, Kiki. I don't know what's wrong with my, it's my hearing. I am not muted. I know that for a fact. You went away and turned off your headphones or your headphones died. Hello, hello? Except, hello, hello. I can't, for some reason, my, hello, hello. My earbuds won't kick in. Oh. Oh. Meh. Well. We, it's late. You have a, you have six. Do we say good night? Good morning, Justin. You could do this, maybe. Mm-hmm, mm-hmm, mm-hmm, mm-hmm. Tarun, we've talked about Alpha Fold and stuff on the show previously, is the problem solved. Very interesting. Absolutely not. Yeah. My earbuds will not work. All right, well, I'm gonna have to end it there because I can't hear you. Yeah. Okay, so. Good morning, Justin. Good morning, Justin. Say good night, Kiki. Good night, Kiki. Good night, everyone. Thank you for joining us for another episode of This Week in Science. The tech will work better next time. Stay safe, stay healthy. Please stay kind to each other and stay lucky. We'll see you again next week. Bye.