SGU Episode 744

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SGU Episode 744
October 12th 2019
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SGU 743                      SGU 745
Skeptical Rogues
S: Steven Novella
B: Bob Novella
C: Cara Santa Maria
J: Jay Novella
E: Evan Bernstein
Quote of the Week
Science doesn't purvey absolute truth. Science is a mechanism. It's a way of trying to improve your knowledge of nature. It's a system for testing your thoughts against the universe and seeing whether they match. And this works, not just for the ordinary aspects of science, but for all of life. I should think people would want to know that what they know is truly what the universe is like, or at least as close as they can get to it.
Isaac Asimov, American writer
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Introduction

Voiceover: You're listening to the Skeptics' Guide to the Universe, your escape to reality.

S: Hello and welcome to the Skeptics' Guide to the Universe. Today is Wednesday, October 9^th, 2019, and this is your host, Steven Novella. Joining me this week are Bob Novella...

B: Hey, everybody!

S: Cara Santa Maria...

C: Howdy.

S: Jay Novella...

J: Hey guys.

S: ...and Evan Bernstein.

E: Hey folks, good to be back.

S: Cara, let me ask you a question.

C: Okay.

S: What planet in the solar system has the most moons?

C: Oh, I know this now.

E: Our solar system.

C: It's now Saturn when it was Jupiter.

S: That's right.

C: Yay.

S: Saturn has overtaken Jupiter because astronomers discovered 20 new moons of Saturn in one fell swoop.

B: Oh, that's getting silly now.

C: Now Steve, what are all of their names?

S: They haven't been named yet.

E: Let's name them.

S: There's like a contest going on to name them if you want to get involved with that.

E: Yes. Mooney McMoonface and among others.

S: 17 of the 20 moons are retrograde.

B: Cool. Opposite direction.

S: They're probably all captured asteroids.

C: That's cool though.

E: That's all right.

B: But what's the best moon?

C: Our moon?

B: Around Saturn.

C: Titan? Yeah.

S: Titan.

B: Enceladus, I'd say.

C: Oh, Enceladus.

B: There's life on that damn moon. They're finding organic molecules spewed out.

C: Yeah, like precursors to amino acids and things are spewing out of its geysers.

B: We've got to get to that moon. Screw everything else. Get to that moon. Come on. I don't understand this.

J: Bob, aren't you scared about what they'll find? I think it's, in my opinion, the best candidate for life outside of Earth.

C: But it looks like Europa, right? It's like frozen and has the geysers where the water spews out.

B: Yeah, it's not frozen on the inside.

C: Yeah, exactly. It's got an ocean.

J: Bob, you're not afraid that they're going to find tentacled monsters on that planet?

B: Oh, how awesome would that be?

C: That'd be cool.

E: Oh, come on.

B: Or something I can't even imagine, even better.

J: Like two tentacled monsters.

E: Nice pair of tentacles you got there.

S: We'll name him Tentacles. After the Greek god, right? So we have a lot of shows coming up. I know we mentioned this, but we've got to keep mentioning it. We have updated our events page. So if you just go to theskepticsguide.org and click on the events button, you'll see all of our upcoming events. There are tickets available for four extravaganza shows. There's a separate page for the extravaganza, but they're also listed on the events page. So get your ticket now before they sell out. They're going fast.

J: Yeah, real quick. So we're going to be in Los Angeles on November 23rd. On January 31st, we're going to be in Pittsburgh, PA. On February 1st, we're going to be in Philadelphia, PA. And on February 2nd, we're going to be in Brooklyn, New York. Those are all the extravaganza shows. If you haven't been to one, they are a ton of fun, and they are science-infused.

E: And interactive. So you will be part of the show as well.

S: They are an exercise in humiliation. But mainly on our part.

E: We take most of the slings and arrows, so don't worry.

"5 to 10 Years" ()

• Fairy Circles - The mystery deepens

S: Nobel Prize time has come around again. It always seems to come around so fast.

E: We had Nobel Prizes last year. What's going on?

S: It just seemed like a year ago that we had the other Nobel Prize. So we're going to get to those in a moment. But Evan, you're going to start us off with a five-to-ten-year update.

E: Five-to-ten-year update. This one takes us back to the year 2012. I recall 2012. Well, and you might recall that back in July of 2012, at the amazing meeting, I brought up a news item about fairy circles in the country of Namibia.

B: Oh, yeah.

E: Do we have anyone on the show who knows anything about Namibia?

C: I love Namibia.

E: Namibia. Cara, did you go see the fairy circle?

C: I don't even know what a fairy circle is.

E: Well, let me tell you a little bit about them.

C: Okay.

E: They are mysterious. You've got to get the word mysterious in there. But they really are. It's a scientific mystery, in a sense. They are mysterious, reddish-hued, circular-shaped patches dotted along about a 1,200-mile-long desert grassland region of the country. And these things, you can see them in satellite images, and individual ones can be as large as several feet in diameter. And there are hundreds of thousands of these things. And there are hundreds of thousands of these things. And they've been studied for quite some time. Now, the tribe's people of Namibia for many centuries attributed them to what else? Supernatural causes. Gods. They were called the footprints of the gods, for example. And there's even a folklore that a dragon or dragons are dwelling underneath the ground, and their poisonous breath is what causes the patches, kills the vegetation up above. Yeah. Scientifically speaking, though, that's not quite right.

S: So that's not true, Evan?

E: No, that didn't really turn out to be the case. You know, strangely enough, I could not find out exactly why these are called fairy circles. Now, I don't know who came up with the designation or where it caught on, but my guess is that this happened because European settlers, when colonization of Africa was all the rage, came over with their language, or our language, I should say, because of terms such as fairy rings, which is something that we do have in Europe and in North America, I should say. So I think it eventually soaked into the culture, and it's still used colloquially today.

C: What are fairy rings?

E: That's just a hunch. Yeah, so fairy rings. These are growths of mushrooms that appear to take on a ring shape. You may have seen them. You may have them in your backyard. I had them in my backyard in my old house in Cheshire. I had a couple of mushroom rings that actually grew, and I'm like, oh, look, fairy rings. Now, for folklores concerning fairy rings, and I'll get back to the fairy circles in a second, the folklores for that dates back hundreds of years, and they're supposedly made by magical creatures such as fairies and elves and gremlins and Eskimos. Yeah. Thank you, Bob.

B: You're welcome.

E: That's a Simpsons reference forever.

C: Oh, I don't remember that.

E: Look it up. Look it up. It's a great one. Now, supposedly these fairy rings, these mushroom rings, were portals, gateways to these creatures' magical realms. Ooh. Yeah. No. They're just mushrooms. They happen to just grow in circular patterns on these grassy surfaces. It's very, very common. So you don't have to apply anything supernatural to them. But, and look, hey, circles are abundant in nature. We like to think that a circle somehow denotes some sort of intelligence must be at hand. Nope. Circles happen all the time in nature. So back to Namibia and the fairy circles in this particular news item. Now, back in 2012, scientists had already been studying fairy circles of Namibia for quite some time, but they were having a hard time figuring out the cause. One of the theories that was alive in 2012 was that insect activity could have been the cause for the rings. And that was true with some other theories, which included plant toxins, radioactive soil, and plant spatial growth patterns. In other words, it's just how these grasses and plants fight for the limited water resources in this desert environment. So all of these scientific theories are at conflict with each other, but really could not hone in on exactly what was going on here. We were talking about it in the context as a news item because there was a new update suggesting that perhaps the mystery had finally been solved because a paper that had been published showed evidence that a specific species of sand termite was responsible for these mysterious dirt rings. So the termites would live underneath the ground, and they would eat the vegetation, essentially, from below. And as the vegetation, because of the sparse rainfall that you'd get, it would collect at the center, and then the termites would eat that, and then it would have to eat out further and further, sort of forming this larger, larger circle pattern, essentially, as the vegetation continued to grow outward. Termites would eat what was in the center and work their way to the outside. So that study was published in March of 2013 in the journal Science. So there you go. There was some more evidence added into the insect bucket, if I may say, as far as what these very circles exactly were. The scientists from Germany, they measured the water content of the soil. They did a whole bunch of experiments, and they determined that there was termite activity in just about all of the fairy circles that they tested, and especially more recent ones, which had 100% termite activity. So these scientists said, okay, it's looking more and more like termites are responsible. But there were issues with that particular theory. For example, why would termites create circular-shaped patches specifically? According to some of the critics, the studies did not address other key questions as to what's the primary factor that suddenly causes a plant to die? In other words, what starts the process of a small circle becoming a larger circle over time? And the study never really addressed that. So it was still not exactly a sealed deal.

S: Evan, did they test control areas that didn't have circles?

E: For the termites?

S: Yeah, maybe there's termites everywhere.

C: There are a lot of termites.

E: There are a lot of termites, and yes, and that's sort of what leads into the current status or the most recent set of data that's been collected and published concerning the fairy circles, 2019. But before I get to that, I got to just get you to 2014, because fairy circles, it turns out, it's not just an African phenomenon, Namibia or otherwise. They're in Australia too, and they were discovered in 2014. Those were being attributed to weather-related processes like heavy rainfall, extreme heat, and evaporation. And yes, there were termites also in the sands of Australia, but not nearly to sort of the degree that was discovered in Africa. In other words, it wouldn't make sense for the amount of termites that they discovered in these rings would be creating these large areas, as large as they would be. It would have been much, much more smaller, essentially. So it wasn't adding up. So they went ahead and did studies, and they released in 2019, brand new, two new papers have been published, one in the journal Ecosphere, and the other in the Journal of Arid Environments. That's cool. There's a Journal of Arid Environments. And we have Jennifer Ouellette to thank for this, because she actually wrote about this earlier this year, in 2019, and brought it to everyone's attention. So I'm referencing her article primarily in that. Thank you, Jennifer, friend of the Skeptic's Guide, of course.

C: Cool.

E: So one of the co-authors of the study, his name is Stefan Getzen of the University of Göttingen in Germany. That's a mouthful. Here's what he said. Overall, our study shows that termite constructions can occur in the area of fairy circles, but the partial location correlation between termites and fairy circles has no causal relationship. So no destructive mechanisms, such as those from termites, are necessary for the formation of the distinct fairy circle patterns. Hydrological plant-soil interactions alone are sufficient. So essentially, they're saying termites need not apply. And because termites are sort of ubiquitous in these areas, you can't say that the termites are necessarily responsible. That's basically what they were able to come up with. So the controversy, 2019, here we are talking about it again, continues. Those in the insect camp and those in the weather camp now, I suppose, are the ones vying for what might really be going on here. So it's a real scientific controversy unfolding before our eyes.

S: So it's back from – it's now unsolved and back to being a mystery.

E: Essentially, yes. And there's calls for more, of course, more studying to be done on this. And we'll see what else they hypothesize out of all of this, if any new theories essentially arise from it. But it's looking like what was once heavy in favor of the insects and the termites being responsible perhaps is really no longer the case, and the balance is tilting in a different direction. So that's basically the update. We were talking about termites being responsible for this in 2012, and now we're talking about weather being responsible for them in 2019. Let's continue to see how this evolves.

S: Yep. We'll have to do this another 5 to 10 years.

E: Basically, yeah.

S: All right. All right, thanks, Evan.

E: Thanks.

News Items

Nobel - Chemistry ()

• Nobel chemistry prize: Lithium-ion battery scientists honoured

S: Now we come to the Nobel Prizes. We have chemistry, physics, and medicine to talk about tonight. And Cara, you're going to start us off with the chemistry prize.

C: The 2019 Nobel Prize in chemistry has been awarded to, I love this guy's name, John Goodenough. Do you actually pronounce it Goodenough?

S: Yeah.

C: Oh, my gosh. Okay, so this reminds me. Yeah, I had a friend in high school whose last name was Bytheway. But it turns out that his parents actually changed it. Like it was Bytheway, but they changed it to Bytheway. They like added the E. I don't know, to make it easier for people to pronounce or something. I wonder if he used to be like Goodenough, and then they changed it.

S: We've talked about him on the show a couple of times before, just because of more recent work that he's doing on batteries.

C: John Goodenough, M. Stanley Whittingham, and Akira Yoshino shared the Nobel Prize in chemistry, and it's all about lithium-ion batteries. There are a lot of really great quotes that came out of the committee talking about their contributions to lithium-ion, so a little bit of background on kind of the lithium-ion revolution. It really began in the 60s and 70s, and that's where a lot of this work actually started. If you think about it, when cars first came on the scene around the turn of the century, just after the turn of the century, they were actually utilizing battery technology in their first designs. Isn't that crazy? But they realized that they were just way too heavy, and obviously we didn't have a way to recharge them. Batteries have been around for quite some time, not lithium-ions. That's what we're going to talk about. It was always an idea within the automotive industry that batteries be involved. Then they just realized that petroleum was much faster, easier, cheaper.

S: Yeah, the battery-operated electric cars at the beginning of the auto industry were great if you're driving around in a city, but there was no way to recharge them between cities. That was the problem. When Ford came out, basically put their chips down on the gasoline engine, that killed the electric cars.

C: Yeah, it killed everything. Petroleum became king. All of the research became in that area. Then in the 60s was really when it started to come to a lot of people's realization that emissions were not good. Cities were becoming smoggy. Air pollution was becoming a real problem. I think there were even some mutterings of climate change this early. That's when researchers started to say, OK, I think we need to take another stab at this battery thing. It took several years to get batteries to a place where they would become a viable option, not just for cars, but also for the ubiquitous electronics that we use right now. If you want to look and maybe just break down really quickly the contributions of each individual to this work, we'll start with Whittingham. In the 70s, he was doing research on superconducting materials and doing classic solid state chemistry research. He actually developed a new cathode material, titanium disulfide. We know that batteries have an anode and a cathode, these two terminals, and that there's a circuit within them. It's the release and recapture of these electrons that actually makes them work. I'm talking about rechargeable batteries now. He was trying to develop a new cathode material because batteries were just not very powerful. He came up with titanium disulfide that was better at the ions moving around. There were a lot more free ions because using lithium really aided in that, and that made these new classes of materials. Then Goodenough, improved on his work, he actually realized that a metal oxide material could hold even more energy than the sulfide that Whittingham utilized. Instead of using titanium disulfide, he decided to use a cobalt oxide cathode, and that actually doubled the voltage and also increased the energy capacity of the battery, which made it more viable in commercial applications. Then after that, Yoshino was focusing on the anode of the battery, and he realized that lithium had always been a problem because they would explode, and that was just not safe in commercial products. The interesting thing is he was actually looking at electroconductive polymers in research that was related but also not related, and it allowed him to come up with this realization that instead of using lithium metal on the anode, he could use something called petroleum coke, which I had never heard of, which is a carbon matrix. When they used Yoshino's new anode with Goodenough's new cathode, all of a sudden we had a safe, lightweight, and very efficient lithium-ion battery. Soon after that, Sony released their first lithium-ion, and we've only seen improvements since then. But as a lot of the Nobel Committee have pointed out, the batteries that we're using, the lithium-ions that we're using right now to power Teslas are based on the very technology that these three chemists developed, even starting in the 70s. So we've seen small iterations, but their developments were altering for the field. So a lot of people are saying the time has come. We're really excited to see this recognition. Almost everybody in the world utilizes a lithium-ion battery in their daily lives. They're everywhere, and they've really changed the way that we interact with our technology. So super cool, and congratulations. Once again, to Drs. John Goodenough, M. Stanley Whittingham, and Akira Yoshida.

S: Definitely deserves it. I hope that in 2039, the Nobel Prize is for whatever the next battery is, right?

C: Yeah.

S: Whatever next battery technology transforms our world again.

C: Yeah, some big change, like a real shift.

E: Oh, yeah.

B: The nano-quantum battery.

Nobel - Physics ()

• Nobel physics prize: 'Ground-breaking' win for planets and Big Bang

S: Okay, Bob, you're next with the Nobel Prize in physics.

B: Oh, yeah. The Royal Swedish Academy of Science announced some Nobel winners for 2019 this week, as we've been talking about. We all have our favorite go-to category for the Nobel Prizes for us. For me, anyway, it's the Nobel Prize for best podcast. Oh, wait. They don't have that yet. Mine, of course, is physics. Hello. So the prize for physics was won by two astronomers, Michael Mayer and Didier Queloz, who shared it with cosmologist James Peebles. Nobel judges said that they, all three, transformed our ideas about the cosmos. So I'll start with one half of the prize going to the two astronomers. Mayer is an astrophysicist and professor emeritus of astronomy at the University of Geneva. And Didier Queloz is a professor of physics at the Cavendish Laboratory at Cambridge University and the University of Geneva. Wow, can you imagine working at Cambridge University and the University of Geneva? I hate my workplace. But the work that they did, they didn't do their work there, unfortunately. They did the work at France's Haute Province Observatory. So let me throw out something. 51 Pegasi b. Mean anything?

S: Yes.

E: That's a star, right?

B: Close. Planet around a star. So they published a paper in 1995, and this was not the first exoplanet discovery that was actually a planet that was orbiting a pulsar, and it was very bizarre. But it was actually the first planet around a sun-like star, the very first exoplanet around a star like that. Not a dead star, but an active star. So a huge milestone, obviously. Now, the idea to actually find these exoplanets came out in the 50s, earlier than I thought it was. Their idea just did not have the technology to make it work, and it did prove ultimately to be workable. The idea is that an orbiting planet will tug on a star gravitationally while it's in orbit around it, or basically they tug on each other. But it's giving the star a tug, and that will Doppler shift the light, so blue when it's pulled towards the Earth and then red when it's pulled away from us. And detecting that was extremely subtle, but that was what they were able to finally do in the 90s. The scientists realized, I think, in the mid to late 80s, that, yeah, the technology is getting there, we're really close, let's start really trying to do this. And eventually they did do that for the first time in 95. And what they found was a Jupiter-mass exoplanet that completed its orbit only in every four days, which was so fast that they doubted it. They actually studied their results for a really long time, they went back and forth, and they just really had a problem with it because it didn't make a lot of sense based on what they knew at the time, which, of course, was so great about science. One of the greatest things about science is that you can make these amazing discoveries and often it's not even believed because it doesn't go with the zeitgeist of the time. And the rest, of course, was history. Now we've discovered over 4,000 exoplanets, an amazing number, it just keeps getting bigger and bigger. We've devised multiple methods to detect them, and we're even beginning the earliest investigations of examining exoplanet atmospheres. Just an amazing, amazing discovery, well-deserved. The second half of the Nobel Prize for Physics goes to James Peebles, he's a professor emeritus at Princeton, and he's also the Albert Einstein Professor of Science at Princeton. What an amazing title, oh boy. So every year the Academy puts together basically a scientific background paper to describe their reasoning. So for this one they said that Peebles wrote a 1965 paper talking about how dark matter is necessary for galaxy formation. And that, they said, was the moment when cosmology embarks on its way to become a science of precision and a tool to discover new physics. So that was a milestone, clearly a milestone to really understand the universe, cosmology, at its biggest scales. Michael Turner of the University of Chicago said, Jim's been involved in almost all of the major developments since the discovery of the cosmic microwave background radiation in 1965 and has been the leader of the field for all that time. Peebles and his colleagues, so here's some of the things that he and his colleagues did, amazing. Peebles and his colleagues predicted cosmic background radiation, they predicted it. And the minute variations found in that is where matter was clumped, they predicted that as well, and they also proposed the accelerated expansion of the universe that was due to dark energy, also key predictors of that major discovery, which also won its own Nobel Prize years ago. But I've got to end on a little bit of a downer on this one because people are rightly complaining about this and a lot of it has to do with Vera Rubin, who was an astrophysicist who was the first person, a woman who discovered, who gave us the first evidence of dark matter. Come on, how amazingly important was that? And she did it by solving the galaxy rotation problem. Spiral galaxies often will rotate in a way that makes no sense based on the luminous mass that we could detect. There had to be some hidden mass in there, a lot of it, to explain the rotation, and that is dark matter. And she didn't predict dark matter initially, that was from Swiss astrophysicist Fritz Zwicky in the 1930s. She was the first one to have verified solid evidence for this. So for years people were saying, oh, she's going to get nominated this year. Never happened. She died in 2016, and it really is a slap in the face, as I see it. It really is a shame. Chandra Prescott Weinstein is an astrophysicist, and said, it's a shame that the Nobel Prize committee brazenly refused to give Vera Rubin the prize for finding the first concrete evidence of dark matter, and now she's dead and ineligible to receive it forever. Thomas Zubushin, Associate Administrator for NASA's Science and Mission Directorate, said, I too wish this would have come earlier so that Dr. Rubin could have been included. Her work has fundamentally changed how we think of the universe. And it's just really, yet again, here we go. We've only had three women win the physics Nobel Prize, three in all this time. And so it really is the bias, I think, is still there. It's really disappointing, and hopefully we can get past it at some point and recognize people that essentially aren't white old guys. I mean, that's the bottom line. If you're not that, it's clearly harder for you to be recognized the way people have been recognized for decades, over a century now.

S: Yeah, Vera Rubin really was an oversight. It's hard to rectify that one.

Nobel - Medicine ()

• Nobel Prize in Physiology or Medicine 2019

S: All right, one more. We got the Nobel Prize in Physiology or Medicine, and this one goes also to three researchers, also three guys, William Kaling, Sir Peter Ratcliffe, and Greg Semenza, for their discoveries of how cells sense and adapt to oxygen availability. So this is extremely wonky and technical, which is what I love about it. This is good, solid, basic science, good old reductionist research, figuring out how stuff actually works at a cellular level, and then going a step further, and then going just totally closing that loop at the most fundamental level that you can get to. And of course, oxygen, kind of important to biology, you know.

E: Just a little.

S: Yeah. So animals, of course, who emerged 500 or so million years ago, breathe oxygen. And so we've had about 500 million years for evolution to tweak our physiological equilibrium and how we deal with oxygen. So I'm going to very quickly go over the science. I'll try to make it as interesting as I can. But if you really want to look at the details, then I wrote sort of like an executive summary kind of thing on science-based medicine. And from that, I link to an even more in-depth discussion on the Nobel Prize site, which links to original research if you really want to get details. You can go as deep as you want. But here's the quickie summary. Scientists knew for a long time, back to like the 1920s, that obviously the body responds to oxygen, and there are mechanisms to equilibrium mechanisms to maintain the delivery of oxygen to every cell in the body. One of those mechanisms is the carotid bodies. These are sensors in the carotid arteries. They respond to pressure, but they also respond to oxygen. When oxygen levels drop, they send signals to the heart to say pump more blood up to the brain. But we didn't know how they sense oxygen. Another very important homeostatic mechanism is in the kidneys. The kidneys produce a hormone called erythropoietin, or EPO, or EPO, we can just call it EPO. And EPO increases the body's production of red blood cells. You may have heard of this because athletes, especially like marathon, long-distance type athletes, will dope with EPO to increase their red blood cell count to give them an edge. So it's illegal to use it as a performance-enhancing hormone. But it's obviously essential to just normal life. It's how you maintain your red blood cell count. If you, say, moved to Denver or went to a higher altitude, part of adapting to that higher altitude is that your body senses the decrease in oxygen. It releases more EPO. You make more red blood cells so that you can deliver more oxygen to the tissue, right? But again, how does it know? How does it know how much oxygen there is? There must be a specific mechanism. So these three guys were all involved in discovering the details of that cellular mechanism. For example, Semenza discovered a protein complex, which he called hypoxia-inducible factor, or HIF, which is comprised of two transcription factors. Those are proteins that regulate the transcription of DNA into proteins, right, into messenger RNA, and then ultimately into proteins. He called those transcription factors HIF1-alpha and ARNT. Now, that's very intriguing because if you, a transcription factor is exactly what you would expect would be a regulatory mechanism. If the oxygen levels drop, for example, this protein might be involved in increasing the transcription of proteins that enact whatever the homeostatic mechanism is. So going further, his work led to other research who discovered that when oxygen levels are decreased, HIF1-alpha levels increased, which increased the transcription of the EPO gene. So that's one link in the chain. But how did that work? How did decreasing levels of oxygen increase HIF1-alpha levels? So other researchers discovered another enzyme, one that degrades HIF1-alpha, and that is oxygen, ultimately oxygen-dependent, right? So when oxygen levels are low, the rate at which HIF1-alpha breaks down is decreased, so levels increase, thereby increasing EPO levels, right? So that was the next link in the chain. This is then where Kaelin comes in. He was researching the effects of oxygen on cancer cells, specifically in a disease called von Hippel-Lindau disease, or VHL. This is a genetic disease that predisposes to cancer. The VHL gene prevents the onset of cancer and is linked to higher levels of hypoxia-regulating proteins. There's a link now between cancer and hypoxia. Solid tumors, cancers, generally tend to be hypoxic because it's hard to deliver enough blood and oxygen to this growing clump of tissue, right? And so cancer cells usually have mutations which make them relatively hypoxia-tolerant. And this von Hippel-Lindau disease, VHL, is a genetic mutation that basically gets you one step there already, so you're already predisposed to having cancer. He found out that the VHL protein, the one that's mutated in this disease, is needed to tag other proteins with ubiquitin, which marks them for degradation.

B: Did you say ubiquitin?

S: Yes, ubiquitin is a protein.

B: It's everywhere!

S: Yes, it's everywhere. So without VHL, the degradation of certain proteins is decreased and their levels will rise. Does that make sense? So now you see where the connection is being made. This is where Ratcliffe comes in. He discovered that VHL interacts with HIF-1-alpha and is necessary for the degradation of HIF-1-alpha at normal oxygen levels. And then finally, Ratcliffe and Kalin, at this point, they're like, hey, our research is intersecting, so let's just do this together. They simultaneously published that at normal oxygen levels, hydroxyl groups are added at two specific positions in HIF-1-alpha, allowing VHL to bind and mark HIF-1-alpha for degradation. So that's the connection with oxygen. It's a chemical reaction that causes hydroxyl groups to be added to the protein, which then allows for the binding and then the whole chain of events that we talked about. So that was the final connection. So that connects oxygen, a few multiple steps to increases in EPO levels, which then lead to more red blood cells. So again, as I said, very wonky, very technical, but that's science, in my opinion, at its best, right? Just these curious scientists without really thinking about what purpose is this going to serve, just how does this work? How does that work? And then what happens? Let's just keep digging and digging until you get to the total base.

B: Gold!

E: How long were they working on these questions, Steve?

C: Whole career, yeah?

S: Yeah, this is like a career's worth of research we're talking about. Decades.

E: Many decades, okay.

S: But, of course, there's obvious applications for this. We don't know how exactly it's going to translate, but understanding all of this can have implications for cancer. Obviously, now, anything that allows cancers to thrive is an opportunity to intervene and prevent them from thriving, right? Reversing their adaptation to hypoxia, for example. But also a lot of infections are dependent on oxygen levels. It also could have implications for recovery from stroke, anemia, wound healing, and other things as well. So there's a lot of understanding things at a fundamental level, of course it's going to have implications. You don't have to really worry about that when you're doing the research. Now it's the job of clinicians to try to translate this into some kind of specific treatment. But I also like this research because you will notice that nowhere in this chain of events do the scientists invoke chi or life energy.

E: My goodness.

S: Or at no point is there, and then a miracle happens. Like this is all strictly mechanistic, right? Because our bodies are machines. And that's sort of the meta experiment always going on in the background of this kind of biological basic science research. Our bodies are freaking machines. And you don't have to invoke any kind of magical energy in order to make them work. Also, it's humbling, right? This is complex, and I went into enough detail. Really, the thing you're going to walk away from this is, because you're not going to remember anything I said tomorrow, but the thing that you're going to walk away with is, wow, this is complicated, right? The body is a complicated, homeostatic, dynamic equilibrium, right? And that's how the body works. And simplistic notions of, oh, this is low, so let me increase it, or this is good, so more is better. Any of that kind of stuff is hopelessly naive. Sometimes that works out, but we've already picked all that low-hanging fruit, and we're way beyond that. Now, trying to interfere with these complex homeostatic systems is complicated, and yet basically the entire supplement industry is based upon a ridiculously simplistic notion about how the body works, which is belayed by all this kind of research, you know? This is why pseudoscientists fail, right? Because they are not operating at this level, and this is the level at which the body is actually functioning. So very, very cool. It's great. There's problems with the Nobel Prize, which we've talked about in the past, but it's great that every year we get to celebrate just straight-up science, you know?

B: Absolutely.

S: I think it's a good thing for science communication, ultimately.

E: Definitely.

S: All right. Thanks, guys, for helping me present the 2019 Nobel Prizes in science. We have a couple of other quick news items that we're going to do. Then we have a great interview actually coming up later in the show with Bruce Hood, who's a developmental psychologist. He's been on the show before. He's awesome, another great science communicator. So stay tuned for that interview. Before we get to that, we're going to do two quick news items.

Electric Jet Engines ()

• NASA is Working on Electric Airplanes

S: Jay, can we run a jet on electricity without jet fuel?

J: This is a little bit more complicated because we could be talking about hybrid solutions. It's a hybrid.

C: I was waiting for that.

J: Yeah, I know. But because I said it, I usually don't say that if I say the word hybrid. But I haven't said it in so long. So anyway, NASA is indeed working on electric airplanes. This is great news because air travel represents up to 9% of the anthropogenic greenhouse gases. So I said that jet fuel is very expensive. It is very expensive. It's probably only going to get more expensive. So this is a big challenge for NASA and the commercial industry because many components of electric motors and batteries are super heavy. These things are not light. When you build an electric motor, it's got a ton of weight to it. So NASA's Advanced Air Vehicles Program, or the AAVP, they're already trying to solve the problem like developing lightweight and small inverters. You keep reading about these inverters. So what are they? These components convert alternating current known as AC into direct current known as DC, AC-DC, right? Remember the band?

E: Oh, yeah, Back in Black.

J: So the existing technology today, like motors, generators, and power conversion electronics, they're much too heavy and large to not only fit but to work on an aircraft. Technology is enormous, and it just won't work with what we have today. So the weight issue is similar to rocket technology. Remember we've talked about this? It takes more fuel to bring more fuel up, and you just get into this fuel loop where if you want to bring more fuel, you've got to spend more fuel. And you can get to a point where it's just not worth it anymore. You just stop. Well, that's the problem that's going on right now with our current technology and the idea of building a fully electric airplane. So NASA realized that they need a state-of-the-art lightweight material that will help create lighter and much smaller electronics. General Electric has signed a $12 million contract with NASA to develop silicon carbide technology, or to advance the existing technology is more accurate. This material is used today to create these high-temperature, high-voltage electronics, and GE is trying to make silicon carbide meet the efficiency and power and size requirements NASA has outlined. So for example, NASA wants an inverter that is no larger than a normal-sized suitcase and capable of generating a megawatt of electricity. And don't forget, a megawatt of electricity is a huge amount of power. It could power up to 1,000 homes. So a suitcase that can generate one megawatt, amazing.

S: Well, Jay, it's not generating a megawatt. It's handling a megawatt.

J: You're right. It's handling a megawatt. You're right. I'm sorry.

S: Just to be clear. It's not a power generator, but you need that in order to make an engine work. You also need something that can generate that much energy or store it or whatever. That's another limiting factor we're going to run into. But if the electronic equipment itself can't handle enough power to run the engines without being too heavy to fly, it's a no-go, right? So that's kind of the problem they're trying to solve right now.

J: So this proposed new technology will reduce energy consumption. It'll reduce noise and operational costs. And the industry reports that advancements in power electronics and new materials are making it possible to reach these goals sooner than you might think. So NASA has a goal of reaching this tech by 2035. And the GE researchers are saying that they have prototypes that meet the power, size, and efficiency requirements today. Now, don't get excited when I say today. They've got some of the puzzle pieces but not all the puzzle pieces. And they're not ready for commercial use but are the foundation of some of this exciting new technology that's going to be coming soon. Now, these systems are being developed at NASA's Electric Aircraft Testbed, also known as the NEAT, in Sandusky, Ohio. They're saying that this technology can one day be used from a two-person aircraft all the way to a 20-megawatt airliner. A 20-megawatt airliner. That is really cool, man. So we'll likely see a hybrid version of these new aircraft first and then as the technology continues to improve, they can move it to 100% electric.

Who's That Noisy? ()

• Answer to last week’s Noisy: _brief_description_perhaps_with_link_

S: Okay, Jay, it's Who's That Noisy time.

J: Guys, last week I played this noisy. [plays Noisy] Now, I said that this was a data set that had been interpreted into music. That was my clue. I got a lot of emails. A lot of people were like, what the heck? And they gave me these guesses, so check it out. I got a guess from Josh Gister. He said, hey, this week's sound has to be an audio interpretation of Twitter's data stream with notes played when people are suspended for being jerks.

B: Oh, God.

J: Love the show and hope you all can swing up to Boston sometime after your big Melbourne trip.

S: We are coming to Boston. We are negotiating for an extravaganza in Boston. That date will be announced as soon as it's finalized.

E: Stay tuned.

J: Got another email from a listener named Brett Kruger. Brett said, I've been listening to the SGU for about two years now, and this is my first guess at Who's That Noisy. It sounds like it is the sea organ located in Zadar, Croatia, which turns the movement of incoming waves into harmonic sounds.

C: Cool.

J: That's not correct, but I did get multiple people who wrote that one in. Now, I did play this on the show a couple of years ago, and if you don't know what it is, check it out. The sea organ located in Zadar, Croatia. It's a beautiful sound, very cool thing. There's pictures and videos. You can see of it working, but that is not correct. I got a couple of more guesses here. James Hodson wrote in. Hi, Jay. James from Melbourne, Melbourne, Melbourne, Melbourne, Melbourne, Melbourne, Melbourne, all the different ways we pronounce it. The most recent Who's That Noisy sounds like an installation I heard in Alaska by the composer John Luther Adams called The Place Where You Go to Listen in Fairbanks, which takes data from weather systems to create a kind of aural environment. That is also not correct, but this guy James says me and my brother Barbaro are booked to see you guys in a few months when you're down here in Australia. Catch you all then. Hope you're well. We are well. We're excited, and we're coming to your house for dinner.

E: Can't wait for that.

C: Invite or not, we'll be there.

J: But we have a winner, and there is one winner this week, and there can only be one winner. Why? Because emails are time stamped, and it's the person that writes in first. I don't care if yours came in two seconds afterwards. I have to have a cutoff somewhere, and that's the cutoff, my friends. So Justice Smith wrote in and said, Hey, Jay, I knew this week's noisy. As soon as I heard it, a team from NASA took a Hubble deep space image and turned it into sound. Check this out, guys. Different parts of the image produce different kinds of sound. According to the team, stars and compact galaxies make shorter and clearer sounds, while spiraling galaxies produce more complex, longer notes. Time flows left to right, and the frequency of sound changes from the bottom to the top, ranging from 30 to 1,000 hertz. Objects near the bottom of the image produce lower notes, while those near the top produce higher ones. Pretty cool. So let me play it again. This is a very, very cool noisy. [plays Noisy] Very science fiction-y. Very, very science fiction-y.

B: Love it.

New Noisy ()

J: I have a new noisy for you guys this week. Are you ready?

S: Sure.

[_short_vague_description_of_Noisy]

S: Sounds like Mr. Toad starting up his jalopy.

J: So in this particular noisy, I want specifics, because without giving away anything, it does sound like something that we're all kind of familiar to, I bet. Just be very specific. I'm going to be very picky on what's a win on this one. And you can email me at WTN@theskepticsguide.org. If you have guesses or if you have another noisy that you heard. You know you're hearing noisies. You've got to send them in to me, and I will put them into my consideration matrix.

S: All right. Thank you, Jay.

Announcements ()

J: Hey, Steve.

S: Yes.

J: Did you know that the SGU has a Patreon?

S: I was aware of that. Yeah.

C: I'd hope so.

J: So we have something really cool. This is a late-breaking development. We got the phaser rifles that you may have heard us talk about before, and I didn't give all the specifics on what the phaser rifle is and what it means. So here are the details. This Saturday, by the time this show drops or by the time you're listening to this program, Alpha Quadrant 6, our science fiction review show that me, Bob, and Steve do, we did a full build of a custom-built phaser rifle that is in the Star Trek universe that was built by a friend of ours named David Tremont who works at Weta Workshop in New Zealand. And if you don't know who and what Weta is, look them up online. But Weta, in short, is an amazing special effects prop-building company. Our friend David built us a custom-designed phaser rifle, Star Trek phaser rifle from the original series. Now, when I say from, it wasn't actually in the original series. It's just supposed to belong in that Star Trek time frame.

S: In the aesthetic of the original series.

J: Bob, Steve, and I designed the phaser ourselves. David built it.

S: He engineered it.

J: He engineered it. He constructed them. He fabricated them. So we are giving away one of these phaser rifles to SGU patrons, SGU members, and Alpha Quadrant 6 patrons. You are automatically entered if you are a patron. I'm going to have a website up that I will announce next week where you can see the finished product. But you can see us build these phaser rifles on AlphaQuadrant6.com or our YouTube channel. It's going to be the latest video that we have out. But if you're listening to this a couple of months down the road, just go there and take a look at Star Trek Phaser Rifle, and you'll see us build them and talk about it. This is super exciting. Now, David specifically did this for us to help us gain more patrons because we have a goal of 4,000 patrons. And when we hit 4,000 patrons, what we're going to do is we're going to do a couple of very important things. One, we are going to have a 12-hour show, a 12-hour live stream show. You've heard me talk about it before, but it's still happening. We're still getting revved up about it. We're hoping that sometime next year that we can do this. And when we do the 12-hour show, we will be giving away to one lucky winner this amazing hero-level prop. When I say hero-level prop, I mean this prop is as good as they get. This was built by a master prop builder.

S: It's movie quality.

J: It's movie quality. It's amazingly solid. It's beautiful. It does everything that you would want a phaser rifle to do except it doesn't actually disintegrate people.

S: Can you set it to stun?

J: It is really, Evan. It's so cool. I can't wait to show it to you. Next time that you're in the studio, you can take a look. These things are just remarkable how well-built they are. When we built this, when we hand-built it, we got to see how he did it, how he fabricated these pieces. So we go into detail. We interview David on the Alpha Quadrant 6 show, so you can feel free to go take a look at that. But if you want in on this, you have to become a patron of one of our two shows, either alphaquadrant6.com or you can go to theskepticsguide.org. Become a patron. You're automatically entered. If you're a patron of both, you have two entries. That said, we are super excited about the 12-hour show and hitting our goal of 4,000 patrons. And again, if you have any questions, you want to see pictures and all that, all the answers and information will be either in that Alpha Quadrant 6 episode or up on theskepticsguide.org website.

S: All right. Thanks, Jay.

Interview with Bruce Hood ()

• Possessed: Why We Want More Than We Need

S: Okay, guys, we're ready to go on with our interview with Bruce Hood, as is often the case, a longer uncut version of the interview, about 40 minutes or so, will be available as premium content for our patrons. We're going to put about half of that as an excerpt into the show. But if you are a patron, you can skip ahead to science or fiction if you're going to listen to the whole uncut interview. We are joined now by Bruce Hood. Bruce, welcome back to The Skeptic's Guide.

BH: Hi, guys.

S: And Bruce is a developmental psychologist who we've had on the show before, the author of many excellent books. And we're talking to you now about your latest book, Possessed, why we want more than we need. So this is not about demonic possession. This is about owning stuff. Why do people like to own stuff?

J: Wait, this is a problem?

S: So tell us about your research. How did you get involved with this question?

BH: Well, I've been interested in our unusual relationship with physical objects for some time now. And some of my early work on the supernatural thinking and the magical thinking was the way that we have peculiar reactions to objects which we think are possessed by, some kind of supernatural force. We have peculiar reactions to objects which we think are possessed by demons or the evil essence of murderers. So I did that stunt many years ago asking people to put on a cardigan and then say, would you still put on the cardigan if you knew it belonged to Jeffrey Dahmer or something like that. Everyone reacts in a very bizarre way. So I've been very interested in the way that we have this relationship with objects and possessions. And that kind of developed into a kind of appreciation that these are things which are an extension of ourselves in many ways or other people. So we see personal possessions as not just being kind of unconnected to the owner but actually having a deeper psychological connection. That's why we like memorabilia, why we value original authentic items which have a very close connection with people we admire, and conversely why we don't like to come into close contact with things which we feel might be contaminated. So when I started to look more about this kind of work, I mean I was researching where does this start from, where does it begin, and I was very interested in children's first attachment objects or the teddy bear blankets. So I started to do some research with Paul Bloom at Yale, and we were looking at this notion of authentic objects. It comes down to this idea that there is this essence that we attribute to things which makes something irreplaceable or unique. That's why we value original works of art rather over things which are identical or indistinguishable physically. So we have this kind of deep psychological connection with our possessions to the extent that actually part of who we are is kind of extended into all our personal possessions and our wealth and things that we own. This is a point made by William James, one of the kind of fathers of psychology, an American psychologist who said that the self, who you are, is not just your body and mind but everything that you can claim possession of. So this is really the premise of the book. Where does this come from? How does this manifest in different cultures? What is property? Because it's something that we just assume and we don't even think about it. But actually when you start to look about property and ownership and the rights of access, you suddenly realize that your whole life is controlled by laws, so laws of ownership, laws of property, and your whole identity, to some extent, is in the physical extension of the things that you own. But I also address in the book, and this is, I think, a really interesting new territory, is how are these things changing now that the digital revolution is changing the nature of books and recordings and things. So it's a really broad strokes approach looking at the whole relationship humans have with objects, why we accumulate things, what compels us to want things we don't really want in the first place, and what's going to happen in the future.

S: What are some of the basic components of this concept of ownership that first click into place with young kids?

BH: Well, I think in the book I briefly talk about the way that children start to appreciate the way that they can control the world around them, literally young babies. So they start off pretty metorically immature, but they kind of learn to pick up rattles and bang things. So they start to learn the contingency of their actions. And control is actually one of the fundamentals of ownership, because if you suddenly lose control of your body, for example, and you're a neurologist, so you'll know these conditions, where people suddenly have this alien hand syndrome, it suddenly belongs to someone else, it's not theirs. So I think the primeval origins, if you like, of ownership is this appreciation of the contingency of your actions and the control of the world around you. And of course, when you don't own something, that's exactly the point. You can't control it or it's taken away from you. So babies start off literally interacting with the world and banging rattles and sticking things in their mouths and teddy bears and all that stuff. But as they grow up, they learn that they have access to some things, but not others. So initially babies are prevented from touching things which are potentially dangerous for them. But as they get older, they say, no, you can't have that, that's your brother's. Or you can't have that, that doesn't belong to you. So they have to learn to understand the rules that not everything is open access. There are some things that they can own and some things belong to other people. And then they kind of have to work out the rules, like who owns what, who's likely to own what. So you might think, well, that's kind of straightforward. But again, we're talking about very young children here. How do they figure out whose bag that is or whose wallet that is and so on? So there are these kind of fundamentals. If someone's holding it, they're likely to be the owner as opposed to a thief. So there's some basic principles of ownership that children seem to appreciate quite early on, literally two to three years of age. But even that, that develops with experience and develops with cultures because not all cultures operate with the same rules of ownership. So I talk about, for example, in the book, the last hunter-gatherer tribes which are left on the planet, the Hazda of Tanzania. They don't really have the same concepts of ownership that we operate with in the West. So for them, you don't really own anything. You can be in possession of it. But if you're not using it, I can help myself to it. So that's like going over to your neighbors and borrowing their lawnmower if they're not using it, just taking it. Say, well, you're not using it, so I'm going to use it. And that turns out to actually be a very optimal way of thinking about ownership when you're a hunter-gatherer tribe because you can't carry a lot of stuff around with you. And so you have to really kind of be, you have to optimize the usage of things. And it turns out there's been some very interesting studies looking at the emergence of early civilizations and the success of these hunter-gatherer tribes. And they would have had to have had this kind of principle we call demand sharing, where no one actually owns anything outright. It's just a case of what's good for the group.

S: Yeah, so you talk about that as well, the fact that not them as a specific example but also different cultures have different concepts and strengths of ownership. And so it seems then, therefore, that the concept of ownership may not in and of itself be fundamental and universal but maybe is a manifestation of something deeper, like some deeper psychology. Ownership is just one manifestation of that, and it's very culturally dependent how that manifests. Have researchers been able to dig down deeper as to what, like, the sources of ownership are?

BH: Well, I think I start off by discussing the idea of competition. So, obviously, one goes to Darwin and talks about natural selection. And obviously there's competition between individuals of a species, and so they will compete for resources, territory, mates, food, and so forth. And so that's kind of one basic principle of ownership, which is if you're holding on to it, it's mine, and therefore I have to fight you for it. But ownership is different in the sense that that's a convention, and that operates with kind of third-party punishment. So if we are a member of a group and we recognize ownership, then we understand that even though the owner isn't present, he may have gone off to fight a battle or raid the next village, he still owns the property, so we can't help ourselves to it. And if we do, then we can suffer the consequences of it. Animals don't tend to do that, okay? So if they abandon a territory or they abandon food or whatever, then the next person can just help themselves to it. So they understand possession and that you have to fight for what you have, but the concept of ownership is a convention that really people have to agree upon, and that requires policing and laws, and that would have emerged presumably probably quite early in human development, but I think it really got amplified when we settled down and formed communities. So rather than being hunter-gatherers always on the move, now when you develop agriculture, you start to collect resources, you domesticate animals, you domesticate crops, you start to have reserves, and these need to be protected, and you need to go off on battles and warring parties, but you want to come back and make sure that your homestead is protected. And then, of course, this also allows you to become the establishment, to build up hierarchies of wealth, and then to pass that on as inheritance. So now resources in terms of crops and food and money is starting to appear now. These are things which can form transactions and be used and passed on to give advantage to your offspring and your siblings and all the people that you want to advantage. So some form of possession would have been there very, very early on, as it is with primates and other animals, but the convention of ownership I think actually requires cognitive machinery to kind of work out who owns what and what are the consequences, to almost predict the course of action. So that's kind of sophisticated, and there's very little evidence that you see third-party punishment in animals. There are some reports, like corvids, crows, these guys are very clever. The feathered apes, as they're sometimes called. They may do something like that, but you don't see a lot of very good evidence that there's this third-party punishment, and yet you see it in human children by about three to four years of age.

S: Yeah, and even Jay and I have both raised kids, right? And Jay's younger daughter, who's three now, but even previously, she will take something, whether it's hers or not, and she'll look at it and go, this is mine. Like she totally knows that kind of thing, and she seems like I have to assert my ownership over this to the adults in the room. Like that's a concept that comes in very, very early, but still that's not too early to be learned, right?

BH: No, no, and you're right. And that's actually one of the most common words. Mine is one of the first words that children learn. And so what they appreciate is that possessions are a form of dominance and status. And over 90% of the conflicts in nurseries and playgrounds are over toys and possessions. And very often it's the acquisition of the possession which is the goal, not the actual possession. So a child might fight for a toy, go and take it from another child, and then once they've got it, they'll ban it and then go after another child's toy. So this is how you establish dominance. And it's not too dissimilar to – primates do the same thing as well. So there are these hierarchies. We use possessions as a way of signaling status, and that's no different. We grew up like that in the West. And, of course, that's not the case in all cultures. So I think there is a need to establish acceptance, and there's a need to not be ostracized. And that could be in the form of establishing status. But in other cultures, that's also manifest by how well you integrate with others. So they're more interdependent. That's not to say that they don't have hierarchies. They're just not the same structures that we have.

S: Yeah, so status and being successful in your society are the real goals. The possession is just a means to an end, and that's culturally dependent.

BH: That's right, and that's why I call it social peacocking. So in the animal kingdom, Darwin was really confused by adaptations, which seemed to be so inefficient. So why did the peacock evolve such a ludicrous display? It's really expensive. It's cumbersome, requires a lot of metabolic resources. It means that birds can't effectively fly. Well, this is because of a process in addition to natural selection called sexual selection. So the males typically compete against each other because of the imbalance between the number of potential sperm that a male can produce relative to the cost of raising an egg for the female. The males literally can have many more children. So they compete with each other for the attention of the females. The females, on the other hand, they have to choose the males who have the best genes. So what happened was a war of attrition in terms of advertising your genes. As Darwin said, they developed ornaments and ornaments. So this is the horns and the coloring, and that's why the males in the animal kingdom are the most colorful and show the bizarre displays because these displays are markers for good genetic prowess. And in the case of the peacock, it's true. The elaborate nature of that peacock tail is a direct marker of the genetic immune system. So we know that those with impoverished tails tend to have poor immunity. So in a sense, it's a proxy for genetic fit. Now, of course, humans also developed adaptations to make us more or less attractive to females and vice versa. Females also developed adaptations which are attractive to males. But we also had technology. They could also accumulate wealth. Again, this signals the advantages that you would have if you mate with me if I've got all these resources. And that hasn't changed, of course. And that's why it's not just the beauty of the Ferrari or the fact it's such a wonderful piece of engineering. It also signals a big way up how good your status is. So this is what we call social peacocking. And in another sense, it's also the basis of what we call conspicuous consumption, where people buy and display luxury things. Yes, they're better made goods and they may last longer. But a big factor is you're showing off to other people just how successful you are.

S: Bruce, tell us about the concept of endowment and what that tells us about ownership.

BH: Yeah. Now, I have been doing some research on this because this is getting back into the irrational nature that we value certain objects more than other ones. And it turns out that when objects come into your possession, you immediately, assuming you've got a pretty good sense of self-worth, you start to think your stuff is worth more than anyone else is willing to pay for it. So, I mean, that makes a lot of economic sense that you should always trade and ask more than others and try to buy things and get a deal on something. But there's a psychological process where as soon as you take ownership of it, you value it more. Now, this was established by Danny Kahneman and Richard Thaler, both recipients of the Nobel Prizes in economics. They had both worked on this phenomenon, looking at this imbalance between the price that people are willing to sell things off and the price that others are willing to buy them at. And part of the explanation is to do with what's called the prospect theory. And this is what Kahneman got the Nobel Prize for. And this is the idea that the prospect of a loss weighs more heavily in your mind than the prospect of a gain. So you're always going to bias yourself to make sure you're not losing by asking more for your resources. But another component of this is actually the extent to which that object is part of your identity. And this is why traders, for example, people who do this for a living, they're not as emotionally invested in their products as novices. And so they show less of an endowment effect. And we've been looking at this in children, showing that if you induce an endowment effect in a child by basically getting them to think about themselves or make pictures about themselves, their possessions or the objects that they have, they start to value them more. So we did this really cool experiment where we gave children, first of all, tests to see if they could work out the relative value of these toys. And some of them were really good toys and some of them were a bit rubbish. We used a scale, a smiley face scale. And so the bigger the smile, the more they liked the object. They thought it was good. And if it was frowning, they didn't think it was very good. So once they used the scale, it was a way that they could kind of work out the relative value of these toys. Now, these are three-year-olds. This is well before the endowment effect turns up naturally, which is usually about at least seven to eight years of age. So having established they can use the scale, we then give them two identical spinning tops. OK, so these are two little plastics things that you might get out of, I don't know, McDonald's or something like that. And we asked them, well, how much do you think these are? How much do you like these guys? And they put them on the same point of scale. So that means that they understood at this point these two identical things are equivalent. And then we did the thing is we gave them one of the toys, the spinning tops, and the experimenter took the one themselves. Then we did the manipulation. We got them to draw a picture about themselves and talk about themselves. Or we got them to make a picture of their friend or talk about their friend. Or we had a third controlled condition where they just made a farm scene. After they'd spent some time kind of being primed to think about themselves, someone else, or a farm scene, we then got them to evaluate the two identical tops again. And the children who had been primed to think about themselves, they thought that their top was worth much more than the experimenter's top. But the effect was not seen in the other two conditions. So that fits with this idea that as soon as you're kind of thinking about your possessions, then you start to value them more. And by the way, this was a study which was based on an adult study done with people from Hong Kong done by William Maddox. And a really cool study where they got Hong Kongers to think either as Westerners or to think of themselves as Chinese because they have geonationality. And when they think of themselves as Westerners, they show the endowment effect. But when they saw themselves as being more collectivist Chinese, the effect was more reduced. So in a sense, the endowment effect is this manifestation of this extended self concept, the idea that our possessions are somehow an extension of who we are. And if we have this kind of self-opinion, then we think our stuff is worth that much more.

J: So Bruce, if I buy your book, will you come to my house and take all the crap out of it for me?

BH: Oh, I'm not Marie Kondo. Spark joy in you. It's kind of funny. Actually, it's interesting that a number of the reviewers have said, well, look, you haven't said anything I don't disagree with entirely. But you haven't provided me with an answer. You know, what do I need to do? And I haven't got a solution. All I've got to say is that just ask yourself, do you really need to be buying that next thing or do you really need that? And I think actually, paradoxically, that actually might make you appreciate what you've got more in the sense that if you just don't think it, if you're on autopilot, a lot of time you think about we tend to buy things because we just think, oh, well, I can afford it. Well I can do this. Why not? But I think if we start to question what is the motivation? Am I doing this because my neighbor's got just bought a new car? And we start to ask those sorts of questions. I think we've become more mindful to use that dreadful term of what actually is the motivation for doing things. And I think that can only be a good thing.

S: Yeah, absolutely. That's metacognition. It's the same thing we're always talking about. It's the difference between being on autopilot, just going along with your culture and your evolved biases versus actually getting outside yourself and thinking about is this rational? Does this really help me? And the people who can do that, like traders who divorce themselves from their emotions and just do things rationally, they have an advantage over you in any kind of transactional exchange because they're not just going with the flow of their psychology.

BH: Absolutely. I mean, you put it beautifully. I mean, metacognition not only is a better way to live. I think it actually bestows benefits to you. You become more appreciative, more grateful of what you've got. I mean, I teach this course, The Science of Happiness, here at Bristol. What I'm doing in a lot of that course is basic cognitive psychology, just getting them to kind of really stop being on that autopilot, as you put it, and actually start to evaluate things, be more critical. I mean, I think critical thinking is really important for happiness. People think, oh, critical thinking, you'll just be miserable. Well, not really.

S: Not at all.

BH: No, I think it's liberating. I think it provides a different viewpoint. It means you're more appreciative of the positive things in life, and you're probably going to be more satisfied in many instances. And I think you can apply that to consumerism and the way that we buy stuff and seem to have this need to have possessions because we aren't really the only species on the planet that does this. I mean, yes, other animals have tools, but they throw them away once they've used them. We, on the other hand, build sheds to hold all the tools and then put them on display and then collect them by alphabetical order and so on. So we have this really strange relationship with physical things.

S: Bruce, it's a fascinating book and a fascinating talk. Thanks for joining us. We really appreciate it.

BH: I really enjoyed it. Can't wait to see you guys again.

J: We'll see you soon, man.

S: Bye.

Science or Fiction ()

Answer	Item
Fiction	HIV for sickle cell
Science	Cystic fibrosis with neb
Science	Polio for huntington's

Host	Result
Steve	clever

Rogue	Guess
Evan	HIV for sickle cell
Jay	HIV for sickle cell
Bob	Cystic fibrosis with neb
Cara	Polio for huntington's

Voiceover: It's time for Science or Fiction.

Theme: Gene Editing
Item #1: A patient was treated for Sickle Cell disease with HIV engineered to deliver a corrected copy of the hemoglobin gene to his blood stem cells.
Item #2: Researchers have used a bubble of fat to deliver gene therapy through a nebulizer to patients with cystic fibrosis, improving lung function.
Item #3: Polio virus was engineered to introduce a new mutation which counteracts the effects of Huntington's disease in one patient whose disease progress has slowed significantly.

S: Each week I come up with three science news items or facts, two real and one fake. And I challenge my panel of skeptics to tell me which one is the fake. We have a theme this week.

E: Theme.

S: The theme is gene editing. And these were submitted by a friend of the show, Kevin Fulta, who is a researcher.

E: Hey, Kevin.

S: Although I did have to swap one of the ones he sent me out because we used it as a news item already. Obviously, we couldn't use that. I just found a different one. So we're good. So two of the three were ones that – so he came up with a theme and two of the three items. Ready?

C: Yes.

S: Okay. Three items about gene editing. Two, of course, are real. One is fake. Here we go. Item number one, a patient was treated for sickle cell disease with HIV, engineered to deliver a corrected copy of the hemoglobin gene to his blood stem cells. Item number two, researchers have used a bubble of fat to deliver gene therapy through a nebulizer to patients with cystic fibrosis, improving lung function. And item number three, poliovirus was engineered to introduce a new mutation which counteracts the effects of Huntington's disease in one patient whose disease progress has slowed significantly. But I think it's Evan's turn to go first.

Evan's Response

E: So we have a patient and they were treated for sickle cell disease with HIV, engineered to deliver a corrected copy of the hemoglobin gene to his blood stem cells. Can you edit your stem cells while they're in there? He's talking about stem cells outside the body being corrected or worked on but inside the body? Is that what the key here is? So I guess I'll move on to the second one where they've used a bubble of fat to deliver gene therapy through a nebulizer. It's an inhaler. People with asthma take these inhalers. Is that the nebulizer? Am I thinking of that correctly?

S: Yeah, like an inhaler.

E: An inhaler. And these patients have cystic fibrosis and it improves their lung function. A bubble of fat. Well, I suppose so to deliver gene therapy. A bubble of fat. That's a pretty small bubble. You have to get it down. Can you get a bubble of fat so small and also a vector or a delivery system for the gene therapy itself? That would be remarkable. It seems improbable because when you think of a bubble of fat, you think there's no way you get that down small enough, engineer that thing small enough to do what it is you want to do. But that could be the case. That's really interesting. I have a feeling that one's going to be science. And then the last one about poliovirus. It was engineered to introduce a new mutation which counteracts the effects of Huntington's disease. I wish my wife Jennifer were here. She could tell me some things about this.

S: No phoning a friend.

E: No phone and no lifelines here. That was the engineering of the poliovirus to introduce a new mutation. Well, it sounds like you could do that. It does sound like you could do that. It sounds like science to me. That just leaves me the one about the sickle cell disease being the fiction. But I really don't have anything solid to offer here on that one because this one's way above my pay grade. So I just will have to go with my gut and say that that one is the fiction. But, guys, please.

S: The HIV?

E: Yeah, the HIV one I think is the fiction. But please, guys, don't just go with me to go with me.

S: No disclaimers. All right, Jay.

Jay's Response

S: So the patient that was treated for sickle cell disease with an HIV engineer to deliver the corrected copy of the hemoglobin gene. That just sounds like with all the different technology that we've developed to treat HIV, I could see that something like that coming out of it. It would be wonderful if it were true as well. Second one here, the bubble of fat that's delivering gene therapy through a nebulizer. So the thing I don't understand is a bubble of fat is delivering gene therapy. When you're saying gene therapy, I just don't know what the mechanism is happening there. So the bubble of fat is delivering gene therapy through the nebulizer. So they're breathing it in and it's doing something. I don't know how, like I don't know what the effect is there. I don't know what's happening to that bubble of fat when it gets into your lungs. Like how is it actually altering genes? And the poliovirus was engineered to introduce a new mutation which counteracts the effects of Huntington's disease. Now if they're going to use the poliovirus, they engineered a poliovirus, they changed it. And now what it does instead of delivering the poliovirus, it's delivering a mutation which counteracts the effects of Huntington's disease. I think out of all of them, that one seems the most likely. So I'm going to say between the first two, yeah, I think I'm going to agree with Evan. I'm going to agree with Evan. I'm not sure about that first one. Something about it just doesn't seem right to me.

S: All right, Bob.

Bob's Response

B: Yeah, these are kind of hard. There's nothing here that I could definitively say that's wrong or doesn't make sense. The closest one is the bubble of fat. I don't know what the mechanism is here. For one in three, they seem to be consistent in that one's using poliovirus, one's using HIV engineered. And like Jay said, I think Jay hit on it. I'm not sure how bubble of fat is going to deliver the gene therapy. But, I mean, any of these could be true. Any of them could be fake for various technical reasons. So it's really shot in the dark. But I'll say that the bubble of fat is fiction.

S: And Cara?

Cara's Response

C: Yeah, I was leaning towards the bubble of fat one too. But then I was thinking people with cystic fibrosis, this is a lung condition, right? So it does make sense that they would nebulize. I don't fully understand. I guess it needs to be lipophilic, right? So they would somehow be able to put the mechanism.

B: I love fat.

C: Yeah, the virus or something like that that they're using to get it into their cells into lipid. And then when they inhale the lipids, it's a more targeted treatment, I guess. Instead of injecting or swallowing something and it going throughout the cells of their body. Because I would assume here that the cells that need to be reached might not be easily reached via the bloodstream. It might be easier to just do it via breathing. So I could kind of see that one. It was the first one that like triggered my spidey sense. But I think that that one, it might be science. And for me, it's like between, okay, engineered HIV for sickle cell treatment or engineered poliovirus for Huntington's disease. Barring any, like all things being equal, the poliovirus one seems the least likely to me. Because there are questions about whether or not we should even be including certain polioviruses in vaccines. Because we're trying to eradicate polio. And it just doesn't seem as prudent to genetically engineer a poliovirus and utilize it for treatment. Whereas HIV will never be eradicated. It has a zoonotic spillover. We know that it has reservoirs in nature. It just doesn't seem as much of a viral profile that we would want to keep safe. So to me, just for that reason alone, I might have to break with the other people and say the poliovirus one seems least likely. But again, this is all a shot in the dark.

S: Okay. So you guys are spread out.

J: Which you love.

S: That's pretty good. Which order do you want me to take them in?

J: 3-2-1.

B: Just tell me how I did.

S: All right.

C: Doesn't matter.

S: Jay spoke up first. So we'll do 3-2-1.

Steve Explains Item #3

S: Poliovirus was engineered to introduce a new mutation, which counteracts the effects of Huntington's disease in one patient, whose disease progress has slowed significantly.

E: One patient. One patient.

S: Cara, you think this one is the fiction. The boys think this one is science. And this one is the fiction. Good job, Cara.

C: Polio is too dangerous, and Huntington's is too rare.

E: But they were talking about just one patient. I mean, I thought this was isolated enough that this wasn't some sort of universal.

S: Number one was one patient, too.

C: Yeah, but they still would have had to engineer a poliovirus, which is too risky for Huntington's, which almost nobody has anymore. I mean, that's not true.

S: That's not true. Don't say that.

C: But it's a very rare disease.

S: It's a rare disease. But even still, it's a horrible disease.

C: It is horrible.

S: It's definitely beyond my short list of a genetic disease that I want to cure.

C: For sure. Especially because, yeah, you can eradicate it.

S: But polio is not the right kind of virus. It's not the right kind of virus. You can't eradicate it because there's always going to be a spontaneous mutation rate.

C: Oh, in Huntington's?

S: All you can do is minimize it.

C: Oh, you're right. So I shouldn't have said eradicate it. But we can prevent passing it down.

S: You can reduce it. We can reduce it down to its basic mutation rate. That's it, its spontaneous mutation rate. But then, the thing is it shows anticipation. So the first patient in a family to get it will get it later in life. And then we can prevent it from getting worse in each subsequent generation.

C: Yeah, yeah, yeah.

S: Yeah, so it becomes really horrible in later generations. And if we could cure it, we could prevent all of that badness. But we can't.

C: Well, and Steve, is it safe to assume that people are working on genetic therapies for it right now?

S: Sure. Absolutely. Absolutely. But you're right, Cara. The poliovirus wouldn't really be a good virus to use for genetic engineering. So that's a wrong choice of a virus. And also this sort of counteracting mutation I just made up. I don't know if that exists. All right.

Steve Explains Item #2

S: But let's go back to number two. Researchers have used a bubble of fat to deliver gene therapy through a nebulizer to patients with cystic fibrosis, improving lung function. That one is science. Now, the reason why they are using a bubble of fat is because previous research was using a lentivirus and that was causing infections, which was a huge problem.

B: Wait, how do lentiviruses cause infections?

S: Yeah, lentivirus. This is a huge limiting factor on using viruses for gene therapy was this cystic fibrosis research that was being done. Huge problem. So they basically said, we want to find a way to get the genes in there without a virus. This has bypassed the risky part of it. So they figured out a way to get the genetic fix, right, into the mutated gene without the virus using just literally a bubble of fat as the vector. However—

B: How? How's a bubble a vector?

S: It improved lung function, but only by 3.7% in the initial study. So it's not a cure. It may have a modest clinical improvement, but it's really more of a proof of concept.

C: Interesting.

S: But the fact that it worked at all means that maybe they'd be able to tweak and iterate it and maybe get it up to a clinically significant effect.

C: Because even if it's a small improvement, cystic fibrosis is incredibly painful, right? Like it's a horrible disease. And so just being able to feel better for a while might be worth it.

S: Right, right. So anyway, this is like we're at the beginning of that research arc. Maybe in 10 or 20 years, this will be something that will make its way to the clinic. But for now, that was a proof of concept study.

Steve Explains Item #1

S: And number one, a patient was treated for sickle cell disease with HIV engineered to deliver a corrected copy of the hemoglobin gene to his blood stem cells is science. This is probably the most encouraging one of the two real ones here. So they're not calling it a cure yet because it hasn't been long enough. They want him to go five years without symptoms before they say he was cured of sickle cell disease. But he's getting there. So he's so far so good. Evan, they took the bone marrow out, then did the – used an inactivated HIV to deliver the corrected copy of the gene and then did a bone marrow transplant.

J: Wow, that is awesome.

E: OK. So that's why I'm thinking like how do you do this inside of a body?

S: And HIV is a virus you would use for this because it's a retrovirus, right? The virus inserts genes, genetic material into DNA. That's what it does. So that's what you would want to use for this kind of viral gene therapy as a vector. You want to use some kind of retrovirus or some kind of virus that that's what it does, inserts into DNA. But yeah, if you think, oh, HIV, it's scary, right, that you're going to be using that but they inactivated it. So yeah, that's cool. So that – sickle cell may be on the short list of a cured genetic disease. Now you'll notice that none of these used CRISPR, right?

E: Yeah. I was expecting CRISPR to come up at some point.

S: Yeah, CRISPR is a new technology. It hasn't really been approved for treatment of humans yet. We're just starting to get to human trials with it. Using viruses as a vector, that's 30-year-old technology now. We're getting close to 30 years old. But we're just getting to like these – oh, maybe we've had a clinical effect. That's how long it takes to do this sort of stuff, bros. I do think things will move faster with CRISPR. But still, this kind of research takes place on the order of magnitude of decades, unfortunately. But we are seeing the – maybe the light at the end of the tunnel for genetic therapy. And I just hope in our lifetime, we're going to start seeing genetic diseases fall one by one, you know. Because this is a – genetic diseases, like especially these kinds of like single mutation or we know what the mutation is, these kind of diseases, they are potentially curable, man. You can just change that genetic mutation. And in some cases, it's a point mutation like –

C: Yeah, or at the very least, even just straight-up preventable.

S: Yeah, so not only –

C: Like there's a way to just do it in the embryo or something.

S: Yeah, you could do individual fertilization and just correct any genetic problems right then and there, which is what, you remember, the Chinese researcher tried to do.

C: Was trying to do, yeah.

S: Flawed approach. But yeah, then it's like, OK, let's just get rid of all your inheritable genetic diseases before you even fertilize the egg. There you go. You know, we're shortly after fertilizing the egg. I do think that we – in this century, I think definitely, we will see the end of most genetic diseases.

J: Wow. Really, Steve? That's a huge statement.

S: Massive reduction. Oh, yeah.

B: Jay, 80 years to go this century. I mean, look at what Christopher has done in a decade.

S: Oh, yeah. It's totally plausible. There's no reason why it can't happen. It's just a matter of making the technology work. There's no theoretical reason why we can't do it. And we're getting there. We are getting there. Hey, this guy we may have cured him of his sickle cell disease, you know. We're there. All right, guys. Good job Cara.

E: Yeah, Cara.

C: Yay.

E: Well done.

Skeptical Quote of the Week ()

Science doesn't purvey absolute truth. Science is a mechanism. It's a way of trying to improve your knowledge of nature. It's a system for testing your thoughts against the universe and seeing whether they match. And this works, not just for the ordinary aspects of science, but for all of life. I should think people would want to know that what they know is truly what the universe is like, or at least as close as they can get to it.

– Isaac Asimov (1920-1992), American writer, from an interview on Bill Moyers' "World of Ideas", October 21, 1988

S: Evan, give us a quote.

E: "Science doesn't purvey absolute truth. Science is a mechanism. It's a way of trying to improve your knowledge of nature. It's a system for testing your thoughts against the universe and seeing whether they match. And this works, not just for the ordinary aspects of science, but for all of life. I should think people would want to know that what they know is truly what the universe is like, or at least as close as they can get to it." And that was spoken by Isaac Asimov. Yeah, in an interview with Bill Moyers on his World of Ideas show back in 1988. Boy Asimov is just one of those science communicators, obviously science fiction writer, but also a fantastic science communicator. He's just able to bring these concepts to the public much in the same way sort of Carl Sagan did. I think of Sagan a lot when I think of Asimov in the same class of communicator. Just wonderful. He just really lays it out there simply, eloquently, and allows people to really understand what's going on with science.

S: Yeah, Asimov was more prolific. He wrote 500 books.

B: Hundreds of books.

S: Wrote or edited more than 500 books. And many of them were science communication books. I think I probably read more Asimov books that were science books than science fiction. And I've read a lot of his science fiction. All right, thank you, Evan.

E: Thanks.

S: And thank you guys for joining me this week.

J: You're welcome, Steve.

C: Thank you.

Signoff ()

S: —and until next week, this is your Skeptics' Guide to the Universe.

S: Skeptics' Guide to the Universe is produced by SGU Productions, dedicated to promoting science and critical thinking. For more information, visit us at theskepticsguide.org. Send your questions to info@theskepticsguide.org. And, if you would like to support the show and all the work that we do, go to patreon.com/SkepticsGuide and consider becoming a patron and becoming part of the SGU community. Our listeners and supporters are what make SGU possible.

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