SGU Episode 821

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SGU Episode 821
April 3rd 2021
SGU 820	SGU 822
Skeptical Rogues
B: Bob Novella
E: Evan Bernstein
J: Jay Novella
C: Cara Santa Maria
S: Steven Novella
Quote of the Week
When I was a kid we’d rent Indiana Jones movies on VHS tapes. It inspired a whole generation of scholars because we saw the excitement, and the passion, and the drama. What’s amazing to me about archaeology is the stories are even better than what you see in a Hollywood movie.
Sarah Parcak, an American archaeologist and Egyptologist
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Introduction

Voice-over: You're listening to the Skeptics' Guide to the Universe, your escape to reality.

B: Hello and welcome to the Skeptics' Guide to the Universe. Today is Thursday April 1st 2021, and this is your hostess with the mostess Bob Novella. Joining me this week is Evan Bernstein...

E: Hey everybody

B: Jay Novella...

J: Howdy.

B: Cara Santa Maria...

C: Hey guys.

B: ...and Steve Novella.

S: How is everyone doing this evening?

B: Doing good. Well, yeah, Jay, I noticed your back. Where the hell were you last week, bro? What happened?

J: Yes. So I got a virus and I didn't know if it was covert or not and it was very scary and we got tested like I had to get tested. Because why would I catch a virus while I'm quarantined at home during a pandemic? So we figured out that, my daughter got a virus in school, like some cold head cold. You know, when you feel virus symptoms coming on, you got to get the test because-

B: Oh God yeah.

J: Because of COVID. You know, once we decided like we're getting the test I realized I could have COVID.

S: And so you have to quarantine that.

J: Oh, yeah. We double secret quarantined. And I got a wicked bad head cold. And as the symptoms got worse, I really, I mean, I just got scared. I got a little scared. I'm like I'm 52 years old and a lot of people, a lot younger and a lot healthier than me died. You know, like you just can't help but think about it.

S: Yeah. You don't want to make that constitution saving throw.

J: Yeah, definitely not. But luckily, luckily it was it was just a head cold. And you know, we went and got COVID tested twice. You know, it was a huge swing. So as we record this five days ago, I was feeling very ill and thinking I'm going to miss my COVID appointment. And wow this would be terrible if I actually got COVID while I was at home. But so the bottom line is I ended up getting my my vaccination yesterday, which I didn't think I was going to be able to get for a couple of more months because I had a reschedule. But my wife pulled an amazing miracle and found us vaccinations like Tuesday. So it was it all turned out awesome. But I mean last week I was like, oh this could be it for me.

S: Yeah. We keep saying like we don't want to get sick now like the end is in sight.

B: Yeah.

S: We need to get a little bit more patient hunkered down.

E: Yeah. So now Connecticut's on the rise, though, unfortunately. So it is a time to be extra cautious, especially around here.

J: And during the live stream, I was like falling asleep while I just wanted to do the live stream. But that was not even close to as sick as I got. So just be careful, guys, like if you get a virus you have to go get tested for COVID. You don't know what virus you have.

S: Yeah. The hospital where I work is preparing for a possible surge another wave. The numbers are starting to go up. The hospital admissions, et cetera. And this is just when they said that the new variants like the UK variant was supposed to be peaking. They said in March. I guess it is.

J: Now, Steve, when the hospital's preparing, does that mean that there are a bunch of doctors in white lab coats running around with their hands up going out saying, I'm sterile, I'm sterile?

S: Yeah, that's exactly right. It's like it's like you've worked in the hospital before, Jay.

E: Or saw it on TV.

J: The doctors stand around, just look at each other and go, doctor, doctor, doctor.

E: Everything I know about hospitals, I learned from St. Elsewhere.

S: St. Elsewhere? So I always know, like when the hospital is gearing up, because one of the first things they do is put the neurologists on standby. They basically ask, so who is going to cover us when we get swamped? You know, who like who's not normally like an internal medicine doctor? So that's so that's that's happened. They can set the word down and say, all right, guys, we're getting ready for another wave. You know, we need to have you waiting in the wings when we get overwhelmed.

B: So are you an external medicine doctor?

C: There are like pediatric nurses working in the ER at the hospital.

S: Yeah, it's all hands on deck.

J: Oh, yeah. My sister in law, she was a she is a nurse that specializes in treating patients after open heart surgery. That comes with a ton of training. You know, that's a very, very difficult thing to do. And they walked up to her and said, you now work in the ER when COVID hit. That was it. And she's been in the ER for a year.

B: During the worst times that we had in the pandemic. So, yeah, she was hit hard. Not one person on her floor got sick. Not one nurse got sick. That's amazing PPE usage.

J: But here we are, guys. We're not out of the woods, man. You know, like we got about 150 million people in the United States got the vaccine. You know, there's a ton of people about to get the vaccine with the scheduling going off the rails. But it's still like it's getting worse because spring is coming and people are getting that itch and they're over it. And that's part of it.

B: And states are opening just prematurely, like trying to outdo each other and how open they are. I know they want their economies to open and get money back in there. But yeah, but Jesus, not cool. All right. This week, we also have a what's the word segment, Jay, what do you have for us this week?

What’s the Word? (5:19)

• phenotype

J: Well, I've got a fun one for you guys today. This word is a word that you've heard before, but I don't know how well you know it. Everybody's heard the word phenotype, right?

C: Oh, yeah.

E: I've heard of that.

J: And I'm sure, Cara, you and Steve are probably well acquainted with it. But when I was looking for a word, I'm like, I want to find a word that I know, but I don't know. And this was one of those words. I had a very loose understanding of it, and now I have a very good understanding of it. So here it is. Here's the definition. The observable and measurable characteristics of an organism as a result of an interaction of the genes of the organism, environmental factors and random variations. So not to be confused with a trait, because a trait is actually an attribute of the organism's phenotype. So you could say the fish is blue, right, as a trait. But that's not really, that is not anywhere near as big as what the phenotype is, right? So traits are underneath phenotypes. This word was coined in 1911 by a scientist called Wilhelm Johansson. Of course, he created the word in German, Würfi. So the-

E: Mark your cards, people.

J: The original word is P-H-A-E-N-O-T-Y-P-U-S, and I think it's pronounced phenotypus.

C: Yeah, why not.

J: Close enough. But it is originally in German. So phenotype is actually a translation from the German. Now Wilhelm was a Danish pharmacist, a botanist. He was a plant physiologist, a geneticist. So he coined the word phenotype. He coined the word genotype. And then, oh, this other word that you probably may or may not have heard of before, the word gene. And they all came out of one book that he wrote.

C: Wow.

J: I know. Isn't that cool? So it's, please, I'm not even going to like, anybody that speaks German just does not want to hear me try to say this. But the translated German book title is Elements of the Exact Doctrine of Heredity.

C: Well, there you go.

E: That's pretty straightforward.

J: And that book became one of the founding texts of genetics, which I think is very cool. So to give you like the real, real, real origin, of course, we're going to go back to the ancient Greek. And that word was phino, P-H-A-I-N-O I probably pronounced it wrong. That means to shine, to show, to appear. And then the second part was tutak or tupos, which means mark or type. So to shine, to show, to appear, mark type. That's phenotype.

C: Right. So it's appearance.

J: Right. Yeah.

C: As opposed to its genetic coding.

J: Yeah. Cara, that would be the genotype.

C: Yeah. Yeah.

S: And in medicine, when we're talking about a phenotype, we're usually talking about a disease, right? So not everybody, not all genetic diseases have 100% penetrance, meaning that they don't always, if you have the gene, that doesn't mean you have the disease. And they're not always as severe. You might have a mild manifestation of it or extremely severe. So we talk about, yeah, this is your genotype, you have this specific mutation, but this is your phenotype. This is like how you manifest that you do or do not manifest the disease.

C: Right. And we often talk about evolution and we talk about how genes can have neutral, positive or deleterious mutations. And one of the ways that we know what's going on in a mutation is that there may be a deleterious phenotype. So a gene mutates, and then now this creature has no melanin, for example, or this organism, you know, ends up with an extra set of wings that prevent it from being able to fly. Neutral mutations often make changes, but those changes might not even be observable from the outside. And so there may be something going on that we can't see. But I think one thing that's important too, to remember is that phenotype is not always just how it looks on the outside. There's a phenotypic expression under a surgical knife. There's a phenotypic expression. It just has to do with what we're observing, right?

J: Yeah.

S: Well, it's also, I think, like physiology. So whereas morphology would be entirely anatomy, what it looks like, morphology. Phenotype includes that, but also biochemistry and physiology and all the other stuff that's how does everything work? Exactly.

C: So it's the expression. It's the way that the gene-

S: It's the expression.

C: Yeah, yeah.

B: Right. And if you want to throw out some very geeky flattery you could throw around the word phenotype as well. Just throwing that out there. Thank you, Jay. I feel confident saying that that's the best what's the word you've ever done. (laughter)

News Items

Satellites and Light Polution (9:58)

• Study finds nowhere on Earth is safe from satellite light pollution

B: Evan, I believe you're about to talk about some pesky light pollution. What have we learned?

E: Oh, pesky, pesky light pollution, indeed. New news about that this week. However, first, I would like to put a little poll out there, a little question for the rogues. As of January 1st, 2021, how many artificial satellites are in orbit around the earth as of January 1st this year?

B: A quintillion.

J: 30,000, I think. Oh, wait, wait, wait, wait.

S: You mean functional and non-functional, or just-

E: Artificial satellites, I believe they're counting the functional ones.

J: 30,000.

S: 3,000. 3,000.

E: Steve's pretty close. Yep.

S: 3,000.

B: Yeah, I think there's a lot of thousands.

E: 3,372.

C: Wow.

J: I got the three right.

E: With more satellites comes an increase in the risk of collisions, obviously. They're concerned also about the number of licenses that are being allowed for new satellites to be launched, that it's not just this gradual increase, but rather a sharp spike that can exacerbate the potential for accidents and collisions and other satellite-related problems. They're also concerned that radio frequencies will be pushed to their practical limits throughout the next decade coming up. And they're concerned that the satellites are interfering with ground-based astronomy, which if you think about it, is something countries around the world have invested many hundreds of billions of dollars on, and it puts those investments to a certain degree at some risk. But we can add perhaps a new concern to that list, and it comes to us because of the recent published paper in the Monthly Notices of the Royal Astronomical Society Letters, which has found that objects orbiting the Earth elevate the brightness of the night sky by at least 10% over natural light levels. And this increase in brightness is not limited to certain parts of the planet, but rather it's having a global impact. So no matter where you are, your nighttime sky observations are being impacted by not just these 3,300 or so satellites. It's in concert with the other bodies, the space junk, debris, and other things that are up there that are all reflecting the sunlight. Tens of thousands of these objects that are large enough to reflect the light are having this impact. The title of the paper is called The Proliferation of Space Objects as a Rapidly Increasing Source of Artificial Night Sky Brightness. And you only need to really point to the abstract to pick up the highlights of the story and really what they're talking about here. They say that the population of artificial satellites and space debris orbiting the Earth imposes non-negligible constraints on both space operations and ground-based optical and radio astronomy. This ongoing deployment of several satellite mega constellations, that's something we've definitely spoken about in recent episodes, and the ones that are coming up in the 2020s, this coming decade, they represent an additional threat that raises significant concerns that can no longer be ignored or just kind of brushed off. We have to put it into really the spotlight. They're reporting that a new sky glow effect produced by space objects increased night sky brightness caused by sunlight reflected and scattered by this large set of orbiting bodies whose direct radiance is a diffuse component when observed with the naked eye or with low angular resolution photometric instruments. And according to their preliminary estimates, the zenith luminance of the additional light pollution source may have already reached a 10% increase over the brightness of the night sky determined by natural sources of light. Now that 10% is important. 10% is the critical limit that was adopted in 1979 by the International Astronomical Union for the light pollution level not to be exceeded at the sites of astronomical observatories. And according to their study and their calculations, it's there and it's there right now and it's going to get worse. Dr. Miroslav Kosifaj of the Slovak Academy of Sciences and Cominius University in Slovakia, and forgive me, I mean, that's probably a terrible pronunciation of his name by me. I'm sure he's listening right now. So I apologize. He was the leader of the study and he said that our primary motivation was to estimate the potential contribution to night sky brightness from external sources such as space objects in Earth orbit. We expected the sky brightness increase would be marginal, if any, but our first theoretical estimates have proved extremely surprising and thus encouraged us to report our results promptly. What he's basically saying there is they were, when he says surprising, I believe he means alarmed. And they said, we have to make people aware of this a lot sooner than later. Their work is the first to consider the overall impact of space objects on the night sky by modeling objects' contribution to overall brightness. And their inputs for their modeling are the known distributions of the sizes and brightness of the objects. So they actually took these physical measurements, phenotypes, can I say that? Would that be accurate? These include both functioning satellites as well as the other debris and spent rocket stages and other things that are reflecting the light. Now we have John Barentine. He's the director of public policy at the International Dark Sky Association. Cara, have you interviewed him before for your show?

C: I haven't, but I have done a lot of research on that concept.

E: I could have sworn that you had some folks.

C: What's his name again?

E: John Barentine or Barentine.

C: Yeah, no, I haven't had him on, but I've definitely, I don't know, I have talked to some people about dark sky initiatives before.

E: And they were involved in this study and this analysis as well. He particularly said, unlike ground-based light pollution, this kind of artificial light in the night sky can be seen across a large part of the earth's surface. As space gets more crowded, the magnitude of this effect will only be more, not less. I think he's absolutely right. You know, we've talked about the Starlink communication satellite arrays. And since 2019, SpaceX has launched more than a thousand Starlink communication satellites and obviously for use for global internet service. But how about this? Over the next 10 years, tens of thousands more, they already got the licenses for them. They're going to come from SpaceX and other companies, including Amazon. And those those are just two big companies and there are others. So you're about to see a real significant increase in this traffic.

B: Well, I was disappointed with SpaceX because in response to a lot of this outrage, the SpaceX engineers, they managed to actually dim the satellites that they were working on by about a quarter of the brightness, 25% of the brightness of the that was exhibited from the first prototypes. And that's great that they did that. But my reaction is that they shouldn't have had to have waited to outrage to do this. This should be part of their ethos of like, hey, we're doing all we're putting all these satellites up there. Let's do what we can to make sure it doesn't mess with the glow of the atmosphere or the impact on other astronomers. And if they could, if they could whack it back 75%, I think that should have been in their minds before people started really complaining about it.

E: Yeah. Is there a reason why these satellites can't be coated with either material or a special paint or something that would absorb all that sunlight rather than reflect it? There may be practical reasons or just the material itself doesn't exist, but.

S: No, just weight probably.

J: I would say weight and possibly, possibly heat, right? Because reflecting it is bouncing the energy away. And if it's absorbing all of that energy a black satellite might just get too hot.

E: Hmm.

B: I mean, just redirect it away from the earth. If that's maybe how about some metamaterials that could probably do it, but that's probably expensive.

E: Yeah. But what would that do to add right to the cost? And then they'd have to increase the cost of the users and then the practicality aspects kind of go off the charts, I suppose, at that point, guys, even at the darkest possible sites on the earth the sky itself has this natural glow in the upper atmosphere. You know, you got ionized particles among other things happening up there, but on top of that background glow, the objects already in orbit add about 10% more diffuse light as per these estimates. But this impacts the work of astronomers, the ground-based astronomy equipment that is searching for the faint objects, the dim galaxies. They're relying on that delicate data for collecting and studying, getting clues about, physics of the galaxy, formation of dark matter, other things. And it puts those – it does put those things in jeopardy and there is a lot invested in that. I mentioned there's like many, many billions, in fact, tens of billions of dollars that has been invested towards these projects and it is going to put some of these things at some level of risk. The number of space objects orbiting the earth is expected to increase by more than an order of magnitude in the next decade because – and largely because of these constellation satellites. So this has to become something that comes to the forefront of the conversation. That was the purpose as to why they got this paper out in pretty quick order.

B: So things are crappy for human stargazers on earth.

Heart Size and Space Travel (19:11)

• Biological Effects of Space Travel

B: Cara, how are things for humans in space?

C: Not great.

E: Well, with all that radiation and whatnot.

C: Right. Yeah, not awesome. Not as bad as we thought though. So there's an interesting new study that was published in the journal Circulation. I love that.

E: It's a journal named Circulation. I love it. That's like double – yeah, double meaning. Love it.

C: Right? And so what do we think it's about? Of course, cardiac effects of repeated weightlessness during – this is the best part – extreme duration swimming compared with space flight. So not only are we going to talk today about what space flight does to the heart, we're also going to talk about what weightlessness during extreme duration swimming does to the heart. Because you guys may remember that Benoit Lecomte actually swam over a course of 159 days attempting to break a record 2,821 kilometers. And during this time, he was mostly horizontal. He was mostly weightless in the water. And then at night, he slept in a boat, also mostly horizontal. Interestingly, we saw similar effects from Benoit Lecomte's swim to Scott Kelly's flight. Scott Kelly famously spent 340 days in space. And I know we've talked about him before, astronaut Scott Kelly, because of course he had a twin brother. So there's some really cool twin studies that could be done here. And he spent so much time in space and has been so open, of course, as part of his job, but also with being poked and prodded to really understand what is space doing to this man's body. And so we've got some new data now about what happened to his heart. And what do you guys think would happen to your heart in microgravity?

J: It shrunk.

B: Oh, in microgravity, yeah, it shrank for sure.

C: Yep. It shrunk. Cardiac atrophy. We saw that most of the shrinkage occurred in the left ventricle, which is kind of the powerhouse of the heart. This is where most of the muscle mass is. And the shrinkage was, I think something, let me get the exact number. 27% of its mass.

B: That is scary as hell.

E: Wait, wait, wait. 27. So that is not trivial.

B: That's scary, man.

C: So one thing that we don't usually think about is the heart is striated muscle, which is very similar in a lot of ways to skeletal muscle, unlike most of our organs, which are made of smooth muscle. And the thing about striated muscle is that it builds, it actually builds bulk with work. We know this. We know that in individuals, for example, who have gigantism, that they end up often developing an enlarged heart. We know that in individuals who have narrowed arteries through different types of cholesterol buildup, hardened arteries, different reasons that their hearts sometimes become enlarged because it's working harder. But in microgravity, it doesn't have to work as hard because it's not fighting against gravity. And interestingly, we see something similar if you're swimming for many, many hours horizontally in the weightlessness of the ocean.

B: The same thing? The heart shrinks, even though this person was working out like a madman.

C: And that's the interesting takeaway here.

S: He was not working out like a madman. That's part of the thing. I emphasize that.

B: Well, I mean, you're swimming for eight hours, six hours a day?

S: Average is 5.8 or something, a little bit less than six. But he was pacing himself. He was not swimming all out. He was swimming at a very slow, steady pace in order to be able to keep up.

C: Because this was a long, this was a distance situation.

S: They considered that moderate exercise and what they concluded was, and here's the thing, of course Scott Kelly was exercising as vigorously as his day allowed for on the ISS, that in neither case was that amount of exercise protective.

C: Yes, it didn't make up for it.

S: Six hours of swimming a day was not enough to prevent that from happening because it wasn't vigorous enough or it just doesn't compensate for the fact that the heart does not have to pump against gravity.

B: Right. But I would still say, though, that even though he was doing moderate workouts, I would still say that five hours of moderate activity a day is a lot of effing working out.

C: It is. And so it is to show how much more is necessary. Because Benoit Lecomte lost 25% of his heart mass, Scott Kelly lost 27% of his heart mass. I mean, Scott Kelly lost it over 340 days in microgravity, Benoit Lecomte lost it over after only 159 days swimming. But here's an interesting takeaway that the study authors mention. More research needs to be done, but what they're starting to see that's trending in the data is that a lot of this has to do with pre-morbid functioning. So prior to going to space, prior to swimming in the ocean, if somebody is incredibly athletic, they tend to lose heart mass. But if somebody is not doing much anyway, the strain of working out or the strain of swimming may actually build them. And so the thing is, these people were healthy. They were healthy, so they needed to work harder. Whether Benoit Lecomte needed to swim more intensely to make up for the loss of heart muscle or Scott Kelly, unfortunately, six days a week doing 30 minutes a day wasn't enough. He's going to have to be prescribed a more intensive exercise regimen in space.

B: I'm surprised it was actually that low. My impression was that their workouts in space were far more than 30 minutes a day. I'm doing that every day. They should be working out harder than me.

C: And let's think about where that prescription comes from. It comes from the fact that over decades, we've been collecting data about how space affects our physiology. But that data is really a function of random happenstance. There are certain hypotheses that physiologists working for NASA have been able to come up with. Okay, I'm worried about the bones, right? Our bones work because they keep us upright and they work hard to have our muscles connected to them and to do this kind of work. And the minute that we don't have that kind of pressure, what's going to happen to our bones? We might start to see bone loss. This was a hypothesis that was expected. You know what wasn't expected? That our eyeballs would squish. Nobody saw that coming. But some people's eyeballs squish and it changes their vision. They become more farsighted in space. And they were like, what? When they first realized that. So the thing about space that's so fascinating is we did not evolve there. We evolved here on Earth with 1G.

S: We like 1G.

C: We do. We adapted to 1G. And so we're learning slowly but surely, based on these ISS studies, exactly what microgravity does to us. And it seems to do a hell of a lot. Now the cool thing is some things can be prevented or changed or mitigated, like the muscle mass loss. It's very likely that if they exercise more and more rigorously, that muscle mass loss would be prevented. The bone loss can be prevented through certain types of exercise. But there doesn't seem to be a mitigation for things like squishy eyeballs, immunodeficiency, the disorientation that happens within your inner ear, where turning your head ever so slightly makes it feel like you're literally turning your body around in circles. And a lot of these different things come out of space travel. And so physiologists are working on trying to figure out, are there mitigation efforts? We know that, for example, what's it called, the like rotating areas that force fake gravity that we see in a lot of science fiction.

B: Yeah. Like the spinning satellites, like centrifugal force and all that.

C: Yeah, the centrifugal force that keeps your feet on the ground. You know, it has long been thought of as a mitigation. For a while it was abandoned because it's insanely expensive. But it seems to be the case that it may actually be necessary because it might make up for some of the unknowns that could happen months and years.

E: So our health is directly tied to gravity.

C: Our health, everything that we do on Earth, we do in this environment. All of our physiology happens at 1G. And as soon as we change that, everything goes wonky and weird. And we still don't even know what some of the things are that could go extra wonky and weird.

B: So we need to seriously look at having things like rotating sections of spaceships. If we're going to have people out there for months and months and months and over a year or more, we're really going to need to consider that if we can't really get around these things that happen.

C: Right. And that's not to mention basically unlivable conditions of space. Radiation, we talked about, the intense cold, the near vacuum.

E: No Starbucks.

C: No Starbucks. Oh, goodness. You know, don't get me started. So obviously all of those mitigations are in research phases and very, very smart people are spending a lot of money to try and figure out how to solve these problems. There probably is a solution for all of these problems. Whether that solution is feasible financially, whether it's feasible physiologically, that is yet to be seen. Because what we're talking about here are the unknown unknowns when there's no way back to safety very readily. And we're talking about very, very, very long spans of time. And one thing that I want you guys' insight into, because I don't know this very well and I don't seem to see it in most of the coverage here, is pretty much everything we know is based on low Earth orbit. It's microgravity. But when we're talking about going to Mars, isn't it going to be even more intense?

S: What do you mean? Like on the trip to Mars?

C: Yeah. Like the lack of gravity is even less than in microgravity?

S: No. No, no.

C: Okay. It's not.

S: No, microgravity is just being technically correct rather than zero gravity. Because it's not like you're not surrounded by mass that's having gravity on you. But when you're drifting through space and you're in low Earth orbit, it's basically the same. It's essentially no gravity.

C: So I wasn't sure because if you're in low Earth orbit, you're still within an orbital plane, which means there's enough gravity.

B: But you're falling.

S: You are falling.

C: Yeah. You're falling. Whereas once you get out of low Earth orbit, you're no longer falling.

'B: Right.

S: Well, it depends on where. You could be in higher Earth orbit. You're still falling.

C: Right. Right. But once you get outside of Earth's orbit...

B: It depends. If you're accelerating, then that's a different story.

S: You're falling around the sun.

B: But yeah, it's essentially the same. You're yielding to gravity in orbit or you're traveling to... You're not accelerating to Mars. You're still in... You're not affected by mass.

S: Especially, Cara, if you're in an inertial frame. So in other words, you are just traveling without any forces acting upon you. It doesn't matter what gravity is pushing you or pulling you in one direction. The reason why we feel the 1G of gravity at Earth's surface is because the Earth is pushing up against us, right? When you're in orbit, you're falling around the Earth. There's nothing pushing up against you, so you're not feeling any gravity. Same thing would be when you're coasting through deep space would be exactly the same thing. When you said Mars, I thought you were going to a different place. So I think, yeah, spaceships, space stations, you're going to need some kind of artificial gravity, which is basically going to be rotation. It's going to be the big thing.

B: And that can't be small. I mean, I looked into this.

S: No, it's got to be big.

B: That can't be small. There's a lot of diameters and radii being tossed around. I found one study, though, that said that you're going to need... You can go to four revolutions per minute, and that seems like a lot. It's not what's really recommended, but you could adapt to four revolutions per minute. And that means that the diameter would have to be 336 feet.

C: Wow.

B: That's a lot.

C: So that's like the minimum diameter.

B: Well, maybe not minimum, but that's a good one. That's a good diameter. That's a lot. 336 feet. Damn.

E: That's sizeable.

J: So even when you're in Earth's orbit-

B: 56 meters, man.

J: -you're falling, right? So you're constantly in motion because you're not only falling around the Earth, you're falling around the sun in a way, right? So our existence is basically managing falling.

C: Well, that's what walking around on the ground is, too. I mean, we've already fallen.

B: That's right. Controlled imbalance.

S: Cara, did you know that there's already a private company, Orbital Assembly Corporation, OAC, that is planning to build a station that is a rotating station in orbit?

C: Good. Oh, I'm glad.

S: And they plan on starting it in 2025. We'll see.

C: The interesting thing is that really could mitigate a lot of the fundamental problems of low Earth orbit.

S: Totally.

C: There are still the problems of radiation cosmic rays, like all these things.

S: Poop shield.

C: Poop shield. Yeah, there are definitely things that are in research phases and development phases. But one thing that I often like to think about is the fact that when we look at these human trials, these like real-life studies, so much data has been published about one guy. And I'm not saying that Scott Kelly's the only astronaut who we've studied. We've studied many astronauts. But we do not. Our N is very small. And these are people who are very fit. These are people who were trained.

E: Pilots. Military pilots.

C: Yeah, military pilots who went through years of training before they left Earth. And the amount of variability, just for example, in our susceptibility to cancer is so great. You know, you and I, if we get the right dosage of radiation, we'll both get cancer. But there is definitely an in-between where some people are going to get cancer and some people aren't.

E: Well, yeah. I don't know. Is anyone under the illusion that space is for everyone?

C: I think that's the ultimate goal, right?

E: Well, sure, but it's not really attainable.

S: You also wonder, though, how long will it take for a subpopulation of humans to evolve adaptations to living in space?

J: How long would that take?

E: We call them the space race.

C: It's interesting, too, Steve, that you mention that because we're talking about like kind of classic natural selection, right, like populations. But a lot of the researchers, even the researchers of this study, mentioned that there are certain things where we may actually be able to adapt. We've just never given somebody long enough to see if they can. So we're not even talking about evolutionary adaptation genetic adaptation. There may actually be ways that our bodies start to adapt.

S: Just physiological adaptation.

C: Yeah, just physiological. The longer that we're exposed to these certain stressors. And so we still don't know if maybe there would be a rebound effect with Scott Kelly's heart if he was there long enough.

B: Well little footnote, Scott's heart went back to normal within, I think, months of his return to the Earth.

C: It went back to normal. But also, remember, Scott Kelly works out a lot.

B: And we don't know of any long-term effects up to that rebound.

C: Yeah. Yeah. And so the interesting thing is that if somebody who is kind of like lazy and like not doing a lot of work goes to space and has this new exercise regimen that's really intense, their heart may actually grow because the exercise regimen may make up for the shrinkage. But then, of course, they may not rebound the same way either.

E: Like the Grinch.

C: I think the write-up in the New York Times actually referenced the Grinch.

E: Of course. Because that's one of the famous lines from that.

C: Yeah. They said it wasn't from love, though. It was from exercise.

B: All right. Well, thank you, Cara.

Self-Replicating Synthetic Cell (35:08)

• Scientists built a perfectly self-replicating synthetic cell

B: I will now talk a little bit about synthetic cells and replication in the news. So yeah, there's another nicely incremental advance in synthetic cells recently. It's also a little on the milestone-y side, kind of important. Researchers have updated their minimalist synthetic cell so that it can now reproduce itself normally. So this was published March 29th in the journal Cell. The senior author was Elizabeth Strachowski, leader of the Cellular Engineering Group at the National Institute of Standards and Technology, NIST. So in 2016, some of you may remember, we talked about the creation of a synthetic cell by genome sequencing pioneer J. Craig Venter. That name is probably familiar to a lot of listeners. They wanted to create a cell with the minimum amount of genetic baggage required to be alive. That was the goal. So they started with the bacterium Mycoplasma genitalium, and I love that name. It's probably obvious, though, that this is a sexually transmitted microbe. So remember, this is still back like a decade ago when this started in 2010, they started working on this. I believe they used that microbe because it already starts with a very spare genome of only about 985 genes, which is not a lot. I believe some common microbes have somewhere in the thousands. So this is kind of spare. So back in 2010, they replaced them with 901, they reduced it by 84 genes. These are hand-engineered genes that they used, and they dubbed the result Syn1.0. So they basically took out the nucleus and then put in the basically completely hand-engineered genome. So that was like the first minimalist attempt. But 2016, though, was the bigger breakthrough, and that's what we talked about a few years ago. God, a half a decade ago? Damn. So when they brought that total way down to a measly 473 genes, that's from 901 to 473, they called that Syn3.0. Now I'm not sure what happened to Syn2.0, but it might be best if we just don't ask. So that was a nice breakthrough, and they believed that they were close to the minimal genome required to be alive, but they soon discovered a problem. Building proteins and duplicating its DNA, no problem. It did that stuff like a champ. But when it came time for this minimalist cell to divide, it did not go very well. It would not produce... Well, it should have produced these nice spheres like Borg spheres, but they were all messed up. They were different sizes. They were different shapes. Some were huge. Some were kind of skinny, like beaded necklaces, just not at all good. But like all good scientists, they looked at, first, all their processes, and they ruled out the environmental causes for these messed up kids. Since they ruled that out, the cause then was most likely that the previous removal of genes that managed reproduction itself and the resulting shapes of the daughter cells. That was probably the mistake they made. They pulled out some genes that they probably shouldn't have. Now that gets us up to modern day, and they have now produced the new champ, the new synthetic minimalist cell. It's called SYN3A, not 4, but 3A, and this contains 492 genes, a little bit more than 3.0, but that's fine, and it makes sense, of course. Crucially, seven of those genes that were added were absolutely critical for the cell to divide normally. Now the cell is great. It can divide. It creates these nice little uniform baby spheres, and they're just the right size. So it looks like they nailed it in terms of reproduction, at least. So what happened? What did they do? So in the intervening years, they discovered that two of the genes that they had previously removed for 3.0 were involved in cell division. My take was that they discovered, oh, look at this. This gene clearly is doing something involving cell division. Let's throw that into 3A. But the other five, though, there's five more genes, though, that they added back, and they were obviously needed to reproduce because they helped it to be able to reproduce perfectly, but they have no idea what those genes do. Regarding this, Strachowski said, we still don't know the mechanism by which these things divide. That blows my mind. It's one of the basic aspects of life, and it's kind of true. This kind of reproduction is kind of critical to life propagating on Earth, and they still don't have a really good handle on just the minimal amount of genes that you need to make this happen with cells. Now, of course, the scientists point out that determining what those genes do was not within the scope of the study, and it makes sense. They weren't looking to find out exactly what they do. Their goal was to create this minimalist cell that can live and reproduce, and that's what they did. That, of course, leads to the future of this work of finding out what those genes actually do is going to be obviously at the top of somebody's list because once they get a handle on those genes and exactly how they operate, then you could truly say that we know now exactly what's needed for this. But more generally, though, this is important, I think, and the scientists as well. This is important because once you have a truly minimalist cell that can live, make proteins, reproduce, maybe smoke a nice cigar or two, that then, that's the proper foundation because from there, you can build and you could add desirable properties to do truly amazingly helpful things that we're probably going to see in the future with this synthetic cell technology. What can we do? They're talking about building minuscule computers. Imagine molecular scale computation taking place inside of cells. That's just too awesome, and don't even get me started on that. They could also do things like engineer living sensors. These sensors can potentially be aware of the environment that they're embedded in, in terms of acidity, temperature, oxygen levels, et cetera. That could be incredibly helpful. You could potentially make these tiny synthetic cells be drug factories or just tiny generic factories that could produce drugs that could ... Essentially, they're talking about having them detect a disease state in part of the body. Then it could actually make the necessary therapeutics and then stop once the problem is gone. Bam. I mean, that's pretty damn convenient, but it's not just drugs they're talking about. They're talking about synthetic cells creating fuel and food itself. I think this is an amazingly promising industry, that this is going to be an amazingly advantageous industry in the not too distant future. I can't wait to see what these guys can do. Imagine. Imagine basically being able to create a custom-made microbe. Look at everything that bacteria and archaea do on a daily basis. If we could tailor, build these metabolisms and these cellular structures to create what we need, I think it has amazing potential. That's my story, and I'm sticking with it.

Why No Lyme Vaccine (42:26)

• Lyme disease vaccine: the frustrating reason there isn’t one for humans

B: So Jay, got a question for you. You need to tell me why my dog can get a Lyme disease vaccine, but I can't. What's going on?

J: You dog. So I don't know if any of you have had Lyme disease. Steve, did you ever have it?

E: My goodness, no.

S: Nope.

J: I thought somebody had it that we knew, but it's bad. It could be really bad, especially if it goes untreated. So Lyme disease started in Connecticut. I remember talking about this on the show before, right? It started not too far from where me, Bob, and Steve, and Evan are right now. Cara, it's very far from you. But there is a place called Lyme, Connecticut, and I guess that was the first place that the disease was identified, and there you go. So the way people get it is by a deer tick bite, and those little bastards carry a disease and they infect as many as 300,000 people a year. Now most of those are unreported cases, but that's the estimate. We have confirmed cases averaging about 35,000 a year. So out of those cases, some people get very serious symptoms and get permanent damage because the disease, if left alone, can do very serious things to the human body. It's caused by four main species of bacteria. Like I said, the deer ticks transfer the bacteria and they love grassy and heavily wooded areas. So that ends rolling in the hay, I guess, right? Because if you're in New England, you know that you're not supposed to walk in tall grass unless you're wearing long clothing. Sometimes I'll tuck my pants inside my socks because they're so small, you really can't even feel them. And then you have to-

E: We do regular tick checks on ourselves as we go out.

S: Tick check.

E: Do the tick check.

S: We did that with the kids all summer. Tick check.

J: And that means basically get naked and let somebody look at every crevice that you have. So yeah, it's true, Cara, you would be surprised.

B: Don't ask me to do that anymore, Jay.

S: Jay, a couple of points. So that is effective because it takes about 24 hours for a tick bite to transfer the bacteria. So if you get it off in a day, you're probably good. And also the bacteria, these bacteria are called spirochetes because they look like little corkscrews, little spirals. They're related to the bacteria that causes syphilis. So Lyme is actually a very similar disease to syphilis in that not that it's not sexually transmitted, it is tick-borne, but it has a primary, a secondary, and a tertiary kind of infection. And the tertiary infections are very similar. They can chronically affect the heart or affect the nervous system. There's differences obviously, but a lot of overlap, very, very similar kinds of organisms and infections.

J: And did you guys know that there are, so there's four different kinds and there are two of the bacteria are in North America and two of the other bacteria are in Europe. So it's not all the same. So to add to what Steve was saying, there are many different types of symptoms that you can get. You can get a rash. You can get fever, chills, fatigue, body aches, headache, neck stiffness, swollen lymph nodes, which are that could be very painful. And then later on, if untreated, you can get arrhythmia, migraines, joint pain, and neurological problems, which Steve would probably know a lot about, but you don't want any of this. And then the really bad stuff, heart problems, eye inflammation, irregular heartbeat, liver inflammation, severe fatigue, hepatitis, all sorts of nasty things. So what do we do? We use antibiotics to treat Lyme disease. And it works. For the most part, it works. Now, like Bob was saying, though, if you were a dog, you can get a vaccine because they have a vaccine for dogs. But did you guys know that there was a vaccine for people for Lyme disease? And not that long ago. This was back in the early 2000s, and the name of the vaccine was Lymerix, L-Y-M-E-R-I-X.

S: I think Lyme-rix.

J: Lyme-rix. Whatever. I have to say Lyme-rix because that's basically what they were going for. So it was developed and started in the late 1990s. It was up to 92% effective against infections. Several hundred thousand people got the vaccine, but this ended because of the anti-vaccine movement. So Alan Barber, who was one of the people who helped discover the cause of Lyme disease and also a co-inventor of the vaccine, said eventually, he said that even though the patent has run out on the vaccine now, because it's been quite a while since it was being formally produced, no companies are trying to sell it. And it's very unlikely that it will ever be sold. And this is because this particular vaccine had gotten not only just a lot of negative baggage attached to it from the very beginnings of the anti-vaccine movement, it probably was one of, if not the first vaccine to get completely crushed by the anti-vaccine movement. The Food and Drug Administration did approve this vaccine back in 1998 and the vaccine had three doses. They were about $50 each, which if you think about it today, like I'd get that in a heartbeat to like never have to worry about ticks again, 150 bucks. Yes. You know, I mean, it's like a daily problem. If you live in the spring, summer, and fall, you live in New England, it's a part of your life and I don't want that in my life. So I would have spent the money. So these vaccines were given over the course of a year and by all accounts, it was extremely effective against the North American strain and the bacteria. On top of that, it had little to no side effects. With all the good things that science knew about the vaccine, it was unfortunately marketed at the beginning, like I said, of the anti-vaccine movement. So of course, the anti-vaccine movement goes back a very long way. But the modern anti-vaccine movement really did come into existence in the late 90s. And of course, many of you know of the infamous Lancet publication that falsified a study about the MMR vaccine and the link to, the false link to autism. And that study was done by Andrew Wakefield, whose name, he will forever live in infamy and I'm not kidding. You know, we had it in the Lancet and it got pulled out. But the anti-vax movement was already created. And in my personal opinion, he is responsible for the death of every single person that died from a lack of these vaccines because he did it. So Wakefield had his own measles vaccine that he was trying to sell and he put down and discredited the MMR vaccine because he wanted to make money. So that's really where the anti-vax, the modern anti-vaccine movement came from. So word started to get around that there was possibly autoimmune reactions from the Lyme disease vaccine. Now, this was originally brought up by a few members of the FDA that actually approved the vaccine. There was, of course, no evidence of this. And I think that they were being very cautious because the anti-vaccine movement was happening. And it seems to me like they were trying to hedge their bets. But in the end, they gave it full approval and the clinical trials showed no sign at all of any autoimmune effect. A study published in the year 2000 found that the vaccine contributed to autoimmune arthritis in hamsters and not in humans. Then other researchers claimed that it might be possible that some people had a genetic disposition to develop the autoimmune response to the vaccine. And then people who received the vaccine started to report complaints. They filed a class action lawsuit and the vaccine was pulled from the market. And after all of that, the FDA continued to do research on all of the claims that were made. They spent four years doing it and they never, ever found any conclusive evidence that there was any connection between the vaccine and arthritis or autoimmune or anything.

S: In fact, the people, the number of people who reported it, that was at the background level, right? There was, it was exactly what you would predict just from the background incidents of those, those illnesses.

J: So the numbers are 1.4 million doses were eventually ultimately given. And out of all of that, 59 people that got the vaccine developed arthritis. And like Steve said, this exactly matched the rate in which unvaccinated people got the virus. So any grouping of 1.4 million people that were not vaccinated, you would find about 59 people that got arthritis. So what does that mean? That means that they had no effect. It wasn't the vaccine. So of those people, 905 people reported side effects out of the 1.4 million doses given. And again, this is an incredibly small fraction of people who got who got the shots. Like there's a lot of other vaccines and medications that do a hell of a lot more damage than that. This vaccine was good and it was safe and highly, highly effective. So the media frenzy killed the vaccine. The media frenzy completely fueled the anti-vax movement.

C: Ugh, what a bummer.

J: I know, Cara right? It's disgusting. Yeah. So they, and they pulled it from the market because it wasn't making money. It went we went from like hundreds of thousands of people in one year getting vaccinated down to 10,000 people the next year.

E: Yikes.

J: And again keeping, keep this in mind, the FDA did follow up testing and they found nothing. You know what I mean? Like they cleared it. It doesn't matter though, because once marketing hits, man, forget it. So since then, partly due to climate change, Lyme disease infections have done what? They've gone up. They continue to increase in number. Many people in the medical community, of course, want an effective vaccine, right? Doctors are going, Hey, I'm getting lots of patients coming in here. What the hell? Where's the vaccine? But no pharmaceutical companies are biting because they don't want to go back to that "poisoned well", whether it was a good vaccine or not, they have to make money. So I get it. But unfortunately we don't have the Lyme disease vaccine today, which we absolutely could have. I mean, we could have another 20 years of freaking research and understanding of it. And they probably would have even modified it and made it even better. And you know, look, and I'm not kidding when I say this. And the downside is people are getting really sick and it just affects day of life here in New England. Like I have to like really think about my kids every single time they go outside. So good news. I mean, now that I've totally depressed you, let me throw some good news your way. Yes. You know, we all agree that the anti-vaccine movement has compromised public health. But there are other companies now, one particular in France that is developing a new vaccine for I think all of the different strains. Other companies are going to pick it up, but they're not going to take this existing technology. They're going to build something new and it'll be new enough where it probably won't follow the same path. I really don't think it will at all. But unfortunately this is the harm the whole question, that whole thing that we've been talking about for the last 20 years since the internet. What's the harm? The harm is that there are people walking around with permanent neurological disorders from a little bug that bites you, that passes you a bacteria. And you know, the anti-vaccine movement very happily killed that vaccine because they don't like vaccines because one man wrote a BS paper for the Lancet over 20 years ago.

S: Yeah. Did you know that they're doing it? They're already, the anti-vaxxers are building the same kind of bullshit story for the COVID vaccines?

J: Of course.

E: Of course. We had to predict that.

S: Saying that, oh yeah, there's this preclinical animal study and whatever, where they get like an immune reaction to it. It's like, okay, but what about the actual clinical human trials where we did placebo-controlled studies and found that if you get vaccinated, your chances of surviving were much greater. You're talking about a theoretical problem based upon animals versus clinical data in humans.

J: Steve, do you want to hear like more details about that? So we've distributed about 145 million COVID vaccines in the last four months. So anyone who died after they got the vaccine and this is after exhaustive research and following up on all the patients and everything, there was absolutely no link to death so far from the COVID vaccine. That's number one. But there was also there was also this whole thing about this nurse who did a YouTube video about the vaccine saying that it causes autoimmune or potentially is giving people autoimmune problems because from her understanding of her reading of the research, she did read that one of the developers of the vaccine and a researcher that had a lot to do with it, and this was a doctor called, let me just get this because I took some notes. This was a doctor called Dr. Drew Weissman. He wrote about an earlier version of the mRNA technology. And he said, it's possible that we could see a few different side effects. And one of the things that he listed was an auto possible effect on autoimmune but that was versions ago of this technology.

S: Yeah, this is like, there's always going to be a phase where scientists are looking at the basic science research are saying, these are the possible things that can happen. These are the things we need to look out for when we do the clinical studies, then we do the clinical studies and we see what actually happens with large numbers of people. And then when millions of people get it, we have lots of data we could look at to see if there's any epidemiological correlations. And they're going back to this preclinical animal data that was theoretical possibilities that have already been disproven by human clinical data, because they're anti-vaxxers, right? They don't look for the truth. They're cherry picking whatever they can in order to build the case they've already decided they want to make.

C: They love to talk about it as if we did studies and the studies were done. Like this idea that we're not still collecting data, that the the vaccine companies, the pharmaceutical companies, and also governments around the world are continuing to look at the data to keep an eye on how things are changing. How is it active in the real world? We're seeing a 90% effectiveness within the real world. This is huge, but there's this mentality like, oh, they didn't do enough research. It's like the research is not over. It's continuing.

J: Yeah, but it's cost versus benefit, right? You know, it's like, yes, of course, wouldn't it be great if we could do 30 years of testing? We can't, and the world is dying, you know?

C: We'll die first. Yeah, exactly.

J: So we, this is what scientists and researchers are good at. They figure out here this is where we begin giving the vaccine. We've done excellent research. It's showing this. Sure, stuff can show up. But man, we'll save way more people than people that will die, right? That's the whole point.

Origins of SARS-CoV-2 (57:07)

• The Origins of SARS-CoV-2

B: Steve, I read your blog on science-based medicine about the origin of SARS-CoV-2.

S: Proud of you.

B: What say you?

S: Yeah, so this, I know this has been an issue since the pandemic began, but a major new report has come out from the World Health Organization, the WHO, and Chinese researchers who collaborated for this investigation. It's actually been, this started last summer, and they've the in-person part of it happened earlier this year. They reviewed the literature, and they produced a pretty thorough report about just where did this virus come from. So SARS-CoV-2, it was a novel coronavirus, right? A new virus that has not been previously detected. So they wanted to know what is the very first evidence that this virus existed, and where, and what was the epidemiology of the spread early on, and they're trying to marshal this evidence in order to determine where it came from. There's basically four hypotheses, right, in terms of where it came from, and they were exploring all of these. One is direct zoonotic spillover, and so zoonotic means coming from animals. Spillover means it goes from the animal population to the human population. The second is introduction through an intermediate host, so it was in an animal population, and then it didn't go directly to humans, but it mutated on its way through an intermediate host and then to humans. The third is...

B: Why isn't that still zoonotic? It's still an animal to human.

S: It is, but it's through... It is zoonotic, but it's not direct. It's through an intermediary. That's it. It's a little difference.

C: It's about the difference in the reservoir. Did a bat bite a person if the bat was the reservoir, or did a bat spill it over to a pig?

S: A pangolin, or whatever.

C: And then the pig got it and passed it on to the person, because then the pig's not the...

B: All right, so the pig is in the reservoir.

C: Well, it's like the temporary, you know? It's not the actual natural reservoir.

E: The pangolin.

S: And that's important, because you want to know the path that this virus took. So the third would be introduction through cold food chain products.

C: So stuff that's not cooked.

S: Yes. So basically, this comes from the meat market, right? And then the fourth is introduction through a laboratory incident. So they looked at all four of those possibilities. Here's what they found. We'll break it down a little bit. So epidemiologically, they found that there was evidence that the virus was circulating in the area, in and around Wuhan, in late November, early December. They can't rule out that it wasn't going around a little bit before that, as early as October of 2019. But the peak of that probability curve is in late November, early December. Of course, it was first discovered in December. And then... But even in the... There was an outbreak in the Wuhan meat market, but that outbreak showed multiple strains. And so that outbreak wasn't the origin. It had already had time to mutate into more than one strain before that outbreak. And the other thing is...

C: They thought at the time that that was the origin though, right?

S: Yeah. Right. Right. But they know that it had to be before that. It still could have come from the market. It just wasn't that outbreak. The other thing is, this is very cool, they calculated the most recent common ancestor of all the earliest strains. So they used basically evolution to figure out, okay, well, how much time would it have taken for these strains to have emerged? And that's also where you get that sort of November, probably sometime in November, can't rule out October sort of timeframe. So multiple lines of evidence are telling us, yeah, probably late November is when this thing broke into the human population and definitely was first spreading in Wuhan. And then after that, it was spreading to the larger province that Wuhan is part of. They also looked at just evidence for the pathway it took from animals to humans. And there's definitely... There's a huge reservoir of SARS viruses, not SARS-CoV-2, but related coronaviruses endemic to the bat populations of Southeast Asia and also the pangolin populations of Southeast Asia. However, they could not find any evidence of SARS-CoV-2 itself.

C: Oh, interesting.

S: In China, in any animal population, wild or domestic.

C: Oh, how frustrating.

B: Wow.

E: So the search continues.

S: Yeah. So, yeah, so a related virus is there the related coronavirus, but not, but not CoV-2, not SARS-CoV-2.

C: Right.

S: All right. So they could not find any evidence of any introduction from outside China, but they can't rule it out either because there's that possibility of the cold chain product, meaning a frozen meat from Italy found its way to that Chinese market. That's very plausible because that market gets cold chain meats from 20 different countries. So it's not just all locally sourced. So even if that was one of the part of that early pathway of the virus, it still could have come from somewhere else.

B: They'd have to investigate all 20 countries then.

S: Yeah, which they did and they couldn't find any smoking gun, right? So frustratingly, at the end of all this, there is, as I said, there's no smoking gun. There's no like, we have discovered the origin of SARS-CoV-2. It's more probability. But here, so here's what they say. Direct zoonotic spillover is considered to be possible to likely. Introduction through an intermediate host is considered to be likely to very likely. So that is the most common pathway they think that it came about. Introduction through cold food chain is considered possible. So not likely, but possible. Introduction through a laboratory incident was considered to be extremely unlikely. So again, but they can't "can't rule it out", which is scientific speak for, well, we can't prove it wrong, but there's no evidence for it. But of course, it always gets picked up by the public and by the media as they said, they can't rule it out. So it's still a possibility. It's like, yeah, we got to put it into perspective.

B: Of course they can't rule it out.

S: It's extremely unlikely.

B: I can't rule out that Santa Claus exists.

C: There are no unicorns in Ecuador. Yeah. I can't prove that.

S: So they also concluded that we need to do more research. So now here is where things get a little tricky because 14 countries, the United States plus 13 other countries wrote a letter to the World Health Organization, essentially complaining about the report and pointing out, what they were complaining about was that access to the data was delayed and was not complete. So they're basically complaining about China not being 100% transparent in this process. And-

B: That's my biggest concern.

S: So that then puts that question mark next to the conclusions. And unfortunately is a big reason why the lab released or lab accident theory is not going to die with this report.

E: Right. Because it leaves open this question mark.

S: Now I just updated myself on what research has been published about just looking at the virus itself to say, does the virus have features of genetic manipulation that would indicate that it was part of laboratory research? And there are studies which say yes, and there are studies which say no. And so I don't know that there's any consensus of expert opinion on that specific question. So again, no smoking gun, but it can't be ruled out essentially is what the research is showing and what the WHO team concluded from reviewing that research, which again I look at myself just to see what it said.

B: Steve, you say in your blog post that some studies have concluded that the virus is incompatible with a lab origin.

S: Yes.

B: And then you say that other studies conclude that genetic manipulation cannot be ruled out. Those are not necessarily incompatible statements though, because that's just like you said-

S: Well, yes they are. Because incompatible means you are ruling it out. And so some studies say you can rule it out and other studies say you can't rule it out. And in fact, there's some evidence that maybe it could have been lab created. So there are studies which come to incompatible conclusions. So it's technical detail about the sequence of the genes and stuff. I didn't want to get into that. But it's looking at the minutia of the organization of the genes in the virus basically. Some people point to the fact that, well, isn't it a coincidence that the Wuhan Institute of Virology is right there where the outbreak occurred? And they are the world's leader in research into coronaviruses in bats, right? So they are studying the virus that SARS-CoV-2 came from. But yeah, as I pointed out in the study, which you were alluding to, Bob, is the fact that well, yeah, the lab is there because that's where the virus is.

C: In nature.

S: Yeah, they both could relate to that both the origin of SARS-CoV-2 and the lab could be in the same region because that's where the virus is. So yeah, you can't assume the cause and effect there. But just the fact that the lab is there still makes it plausible, which is why, again, the WHO said it's possible. It's just extremely unlikely because there's no evidence for it. And the evidence actually suggests this zoonotic pathway and the virus itself doesn't have any fingerprints of genetic manipulation.

E: I have a question about the intermediary one, Steve. So with this intermediary factor, how wide does that open up the possibilities? Does it make it almost infinite? Like we're going to have a real hard time figuring it out if there is an intermediary involved?

S: Yeah, I think that's the problem, Evan, is that there's so many possible candidates. And we haven't found that, what that path is. There's a lot of plausible pathways, animals that could have gotten it from the bat that then spread it to humans. We just don't know what the one is that did it.

C: Yeah. We have to think, though, about what are typical animals that we use for food? What are typical animals that we interact with? Spillover events rarely happen with like super exotic animals. It's usually going to be more likely that it's an animal that's in close proximity to human beings. I'm wondering, Steve, is it likely then that the bats that have the non-SARS-CoV-2 related version of SARS are the actual carriers? So when it spilled over to the intermediate, if this is what happened, it evolved enough within the intermediate to then come?

S: That's what they think. It combined with the virus that was in the intermediate to become SARS-CoV-2.

C: So it's still likely that the bat is the ultimate reservoir?

S: Bat's the father. You don't know what the mother was, basically.

E: That's a good way of putting it.

C: Gotcha.

S: So they contributed genes from the virus that was circulating in that population, but it was added to something else.

E: Oh, boy.

S: All right. But here's what I think where there's a pretty strong consensus among scientists, among the WHO researchers, among governments, and this is really where the study winds up, and why it's important that we are spending so much time and effort trying to investigate the origins of this virus, because as terrible as the last year has been, and as hard as COVID-19 has been, this worldwide pandemic, we're still at the hopefully tail end of, this is not the worst virus out there that is capable of causing a pandemic. And there's actually thousands of them out there, and most of them are worse than SARS-CoV-2. This is probably a dress rehearsal for worse pandemics to come. And so the primary conclusion of this report is, to put it euphemistically, is we have to get our shit together. And what that means is we need international institutions, like the World Health Organization, of course. We need international cooperation. We need international treaties of transparency and collaboration and cooperation. There's got to be an international community that is in charge of this, so that there isn't a country that could hide it if they wanted to, because there's the infrastructure, the institutional infrastructure is there for experts, international worldwide experts, to be reacting to any potential new pandemic, so that this doesn't happen again, or it's minimized. You know what I mean? We are ready to pounce if a possible eruption occurs of a virus that could cause a pandemic, and the scientists swing into action, and we just have to have, worldwide, we have to have a better response next time.

B: Yeah, and an example of that is if, a year ago, if we, if China was more forthcoming, and they actually reacted and did what was right, even as little as three, four, five days, or maybe a week at the outset, if they reacted a week earlier, they could, this could have been nipped in the bud so much more easily. This could have this could have died a stillborn death well over a year ago if the reaction was fast enough, and it wasn't, and because of that, what's the worldwide death toll now? I mean, that, that's what that delay brought.

C: Well, and to be fair, you're right that China was a nucleation point, but let's not forget that if the United States, which is a massive global hub, had gotten our act together, and hadn't pretended like this was not a threat to us, and hadn't pretended when we had evidence that this virus was on our shores, that it wasn't actually on our shores, and that kind of overly calm rhetoric of, don't worry, Americans, this is somebody else's problem, hadn't been the case, we would not have carried such a viral load that we know ran back around the world multiple times over.

S: We failed. We totally failed.

C: We failed massively.

B: Yeah, no question about that.

C: And we were a nucleation point for sure.

S: Totally.

C: We could have bottlenecked this thing.

S: And this is not about pointing fingers, I want to say, this is not about pointing fingers or assigning blame. This is about, how can we do better next time?

C: Absolutely. But we need to be a leader in this.

S: Totally. But in medicine, we have something that's called Morbidity and Mortality Report, M&M, and where we go over all the horrible things that happened on our service over the last month or whenever. And the rule of these reports is there's no blame. No one, there's no shame.

E: Not the purpose.

S: There's no blame. Because we want, we need people to be completely honest about what happened so that we can talk 100% about how do we keep this from happening in the future. That's it. So it's like a safe space to talk about what went wrong so that we can fix it. And that's the same thing we need here. This is not about blame or about finger pointing or about politicking. This is about, damn, we cannot let this happen again. The numbers, by the way, 129 million cases, 2.8 million deaths worldwide. That's where we are.

E: And 10 years from now, the next one could go 10 times those numbers.

S: Yes. Yeah. There are viruses out there that if the same thing happened, it could be 10 times as bad. Absolutely. It could be 100 times as bad.

E: Incomprehensible. It really is.

B: Now, I'm just so depressed. I need to feel better about all of this. I know. Evan, I want a quickie. I want a quickie with Evan.

Quickie with Evan: Atomic clocks (1:13:19)

E: Well, thank you, Bob. And all right, let's talk a little bit about atomic clocks.

B: Ooh.

E: Yes. Yes. Redefining the second. So a new clock comparison is the most precise yet accurate to within a quadrillionth of a percent.

B: Nice. I love that number.

E: That is. OK, so you got zero point and then 15 zeros after that decimal point. And then the one is in the 16th place. Right. OK, folks, that is also known as the Bob?

S: Femtosecond.

E: A term we love hearing every time I bring it up in my physics news items. Emily Conover over at ScienceNews.org presented a very nice summary of the story. And she starts by reminding us that back in 2019, the unit of mass, the kilogram, was officially redefined based on a fundamental constant of nature instead of the old metal kilogram known as the IPK, the International Prototype Kilogram. And we covered that on the show. But scientists this past decade have also been focusing on overhauling the fundamental unit of time, which is the second. In order to do so, they are using atomic clocks, three of them, comparing them to one another to squeeze out the last minute bits of discrepancy as to what defines that second. But these are not just any atomic clocks. No, no, no. These are the latest and greatest atomic clocks that makes your grandfather's atomic clock look like a sundial. Since the 1960s, the second has been defined by atomic clocks made of cesium atoms. Now cesium atoms absorb and emit light at a particular frequency that determines the length of a second. Cesium atoms oscillate 9,192,631,770 times per second in their excited state. That's when they were absorbing light, right? Excited state. So from what I have read, there is no variance in this, that they are all the same. Now someone might come back and correct me on something like that. But that's what I've read. They all share this exact frequency. So it makes for a very stable means of measuring time. And of course, an example, the Global Positioning System, GPS, those satellites in orbit, they're using cesium atoms in their atomic clocks. And so since 1967, cesium has been the atomic clock champion element. But until now, cesium perhaps is no longer the undisputed lightweight champion of the atomic clocks. Meet the new atomic clock preferred elements, strontium, strontium?

S/B: Strontium.

E: Strontium, ytterbium. So ytterbium, strontium, and an everyday favorite of people everywhere, aluminum. Yay. All right. So this comes from scientists at the Boulder Atomic Clock Optical Network. And that's Bacon, by the way, Jay, B-A-C-O-N.

J: Thank you.

E: They compared the frequency of light using and measuring the ratios of frequencies of three new atomic clocks. So one made of ytterbium and one made of strontium atoms and one made with a single electrically charged aluminium atom. The results of the most precise clock comparisons yet with uncertainties less than a quadrillionth of a percent. And this was researched. This was reported in the March 25th edition of Nature. The three clocks were in different locations, two at the NIST and the others about 1.5 kilometres away at the Research Institute JILA. Sorry, I don't have the exact names of those, but this is a quickie. The teams compared the clocks by sending information across an optical fibre and through an open air link. So they used, again, fibre and then they used an open air link, which is basically lasers. And they found that there was essentially no difference. So they were able to run these tests. No difference when they measured through the air, right, through space or earth space, and through the fibre network. So that's a very, very good sign. So this ability to compare these distant optical atomic clocks is considered a step forward in atomic clock research and precise measurements. And you're going to use this for helping, well, better characterize Earth's gravity and search for dark matter, defining what dark matter is and testing other fundamentals of physics. So this has been your quickie with Evan. It may have been quick, but we will always have the memories.

B: Nice.

E: Until we don't.

B: Nice. I like it. That was good.

E: Thank you.

Who's That Noisy? (1:18:01)

• Answer to last week’s Noisy: Furby

B: Okay, Cara. It's Who's That Noisy time.

C: Hey, guys. Last week I played this noisy.

[_short_vague_description_of_Noisy]

E: I think I heard that in an episode of Twin Peaks.

C: Yum.

B: Sounds like WALL-E being very high on something.

S: WALL-E got into the hydraulic fluid, huh?

J: I mean, it sounds like, I think it's from a video game.

C: Sounds like it. Could be WALL-E. Could be. No. No. You're wrong. But I did get a ton of emails on this one. People out there, they know. But the question is, what is it? Well, here's our first guest, a listener named Shannon, who also happens to be a close friend.

S: Is this Science Yoga Shannon?

J: Yes.

E: Science Yoga Shannon?

C: So she said, long-time listener, first-time caller, lol, is that an interactive WALL-E toy played backwards? One of you was on it. But no, sadly, that is not the case. And then this next guest is from, why do you do this to me, Tymoteusz Markowski.

J: Oh, my God. I mean, you get these names that are very hard to pronounce. I feel so bad for you.

E: Tymatus.

C: Tymatus. Okay. T-Y-M-O-T-E-U-S-Z.

B: Wow. Tim. Tim!

J: That's a cool name. Tim.

E: Timan.

C: Yeah. Timan Mrakowski.

J: No. It's Tim Rock.

C: Tim Rock. There you go. He says, it sounds like a broken number station. And in case you guys don't know what this is, a number station is a shortwave radio station characterized by broadcasts of formatted numbers, which are believed to be addressed to intelligence officers operating in four countries.

E: I had one of those as a noisy many, many, many years ago. It's still one of my favorites.

C: No way. And did this sound similar if it were broken?

E: No.

C: No. Okay. That's why Tim Rock, sorry, not correct. We've got another guest from a listener named Evil Eye. And they said either Yum Cookie Monster doll or a Gizmo doll from Gremlins. Good guesses. I think we're getting closer.

E: Okay.

C: Yum Cookie. There's really a doll called the Yum Cookie Monster doll. That makes me so happy.

J: I just like the sound of a yum cookie.

C: Yeah. All right. So onto this week's winner. Her name is Hannah Jackson and she wrote, this is without a doubt the horrifying and possessed voice of a Furby. I would recognize it anywhere. And I still remember mine mysteriously turning itself on in the middle of the night speaking from behind the closet door.

S: What's a Furby?

C: What!?

J: Seriously. You don't know what a Furby is?

E: Go ahead. Call him. Call him a boomer. Go ahead Cara.

C: Do you remember this was like the original AI or at least we thought it was. So here's a few facts about Furbies. Maybe this will jog your memory, Steve. It was first sold in 1998 by Tiger Electronics. You can say over 100 words in Furby speak. It's actually called Furbish.

E: It has many dialects though.

C: Yeah. Right. Furbies were actually banned at an NSA base in Maryland because they were able to record confidential conversations. So remember Furbies would listen and react and they would learn. This was a pretty intelligent toy for the time. I was a bit too old to have a Furby, but I knew people that got them sort of "ironically". You know what I mean?

S: Yeah. "Ironically".

C: Yeah. Like in 98, let me think. So I graduated high school in 2001.

E: Wow.

C: So I would have been in high school when the Furby came out. So there were people who had little brothers and sisters who really wanted them. And yeah, there were some people who were like, this seems like a cool toy. I want this toy. But I can definitely imagine being in elementary school and being haunted by a Furby.

S: I think they must have fallen right between me and my kids. You know, like my kids were too young and I was too old for this. But apparently they're Bluetooth connected. So it's great.

B: Oh, God.

J: You know, you could get them on eBay like for about 30 bucks, you can get one that's in good condition. And I was like thinking about getting one at one point just to play with it, just to see what it – because I never held one.

S: Yeah, to play with it. Right.

J: You know what I mean? I just wanted to learn about it.

S: I know what you mean.

J: Jesus Christ.

C: I have a friend who – Jay, I have a friend who recently got a Tamagotchi off eBay.

S: Oh, yeah?

C: And was like, yeah. And was like, you know.

J: That was legit. That was like early crack.

C: Yeah.

J: That stuff, man.

B: Oh, man.

C: But yeah, if you – it's so crazy. It is weird. We've talked about this before, Steve, where – do you remember back now I've seen jackals a ton of times in the flesh in Africa. But prior to going to Africa, somebody mentioned a jackal and I was like, I'm not sure what that is. And it was like these gaps in our knowledge. Literally when you said, what's a Furby? I was like, what? Have you been under a rock this whole time?

S: Well the version 1.0 of this, when we were kids, was literally the pet rock. Have you heard of that, Cara?

C: I do. I know the pet rock.

B: You sold a million of those.

E: Oh, my God. A rock in a box.

S: And you can actually get two – you can get two pet rocks and breed them.

C: Would you just hit them together really hard and a little rock would fall out?

S: Yeah. We call them pebbles.

J: I mean like of all the dumb genius things that marketing came up with, like the pet rock. What are you kidding me?

C: Oh, endless supply of rocks. All profit. 100% profit.

E: Yeah. A jar of air. That was a popular one too.

S: Yeah. A jar of air.

C: You still got to buy the jar. Everyone, this was by far the most accurately guessed who's that noisy of all time. The Furby. Iconic.

E: Wow.

New Noisy (1:24:01)

C: I've got a new noisy for you, and it was sent in by Matt Surley. Here it is.

[_short_vague_description_of_Noisy]

Ah. So you may recognize that melody. And obviously this noisy is deeper than that. I don't need to know where you know this melody from. I want to know what is this noisy. And if you think you know it, or if you heard something really cool that you want to send me, you can email me at WTN@theskepticsguide.org.

Announcements (1:24:49)

C: So Bob.

B: Yeah.

C: Bob.

B: Yes. I'm here.

C: We've got some announcements this week.

B: Oh, we're doing announcements. Okay.

C: Okay. Everyone, this is important. Coming up first on the docket, we have NECSS. This is going to be the 6th and 7th of August, and we really hope you will all join us. This is going to be an incredible event. We'll have some amazing speakers, and you can learn more about that by visiting NECSS. That's N-E-C-S-S dot org. After that, we have a rescheduled. We're so excited to get back on the road.

J: That's right. Can't wait. Oh, God.

C: Yeah. The Denver Extravaganza, and there will be a private show as well. And this is going to be in November. The Extravaganza will be on the 18th. The private show will likely be the next day. And you can learn all about it by visiting theskepticsguide.org. And don't forget that you can support the show by becoming a patron. All you've got to do is visit patreon.com/SkepticsGuide. You pledge your support, and we get a little piece that helps us pay people like Jay. It helps us make sure that we've got everything that we need to keep producing this high quality show week after week. And yeah, it's becoming a big part of our livelihood, isn't it, you guys?

S: Keeps the lights on.

J: And as we, the more patrons we have, the farther our reach and the more stuff that we can do. And we have incredibly great things planned.

C: You're right, Jay. Patreon has become a really important part of funding the SGU and for helping us to continue to do not just this amazing show and not just the ancillary events that we do, but also continue on with our skeptical activism. So thank you all so much. Make sure that you visit NECSS.org, theskepticsguide.org, and patreon.com/skepticsguide.

B: Thank you, Cara.

Emails

Email #1: Avi Loeb (1:26:45)

B: All right, we are now going to address a bunch of emails all at once excoriating us for dissing Avi Loeb. Steve!

S: Yeah, so this is my news item from last week. I was talking about an update on ʻOumuamua and that some scientists came up with an alternate explanation for its odd behavior as it was accelerating away from the sun. Now Avi Loeb is a Harvard astronomer who also has recently come out with a book where he propounds his theory that ʻOumuamua might be an alien artifact and that this could be an explanation for a number of anomalies that we observe with ʻOumuamua. So the feedback from a lot of people thought we were being unfair to Avi Loeb. And I listened back to my segment just to remind myself exactly what we said. And I don't know. I think this one's kind of in the middle. So I think the criticism of us was not fair in that they were saying, you were saying that this guy was a crank. We never called this guy a crank. We never were all the things that we were accused of saying about this guy or implying or you're reading between the lines or inferring it from our tone, whatever. We didn't say it. We never said that anything that he was not a legitimate scientist. Our criticism, we also never said this was his only line of evidence. We also never said that he is saying this is absolutely true. But having said that, yes, we were, there was a little snark in our tone. I will say that, absolutely. And maybe people inferred too much from that or we could have been a little bit more balanced. So usually we do, I was very careful to say that this was one of the arguments he was putting forward. It was not the only one. But I also went back and reread a bunch of articles by Avi Loeb where he is being interviewed or where he's talking about this theory. And I thought, when you dig down to what we were actually saying, I thought we were actually totally fair. So Loeb does have a number, he does point to a number of anomalies of ʻOumuamua. The primary one, and he says this is the primary one, was its acceleration away from the sun, which has now been, I think, largely taken away, explained, or at least a plausible explanation has been offered. And his other lines of evidence also are simply anomalies. They are not anything that we could point to that say that's evidence of that this is an alien artifact. And they're not even that convincing. I didn't find, like, one of them was that the velocity of ʻOumuamua was typical of only about one star in 500. So any object, even if it's leaving a solar system, if you compare it to other things swinging around the galaxy, its velocity relative to the other things is going to be roughly the same as the star system that it comes from. And so if you look at ʻOumuamua's velocity relative to us and relative to the galaxy, it's it's coming from a star that whose velocity is only representative of about one in 500 stars. Okay, that's not such a big deal. One in 500, that's like nothing. He also said that we thought that these things should be very rare. Our models all predicted they would be very rare. And yet here we are seeing one and that would be a very, should be a very unlikely event. I think that was undone by the fact that two years later, we found yet another interstellar object. So the idea is, so again, and our criticism of his reasoning, again, he's, yes, it's perfectly legitimate to say these are hypotheses. I never said we should not consider alien technosignatures as, as the explanation. We are always happy to report on them and excited about it. I wanted Tabby's star to be a Dyson swarm as much as anybody. I think that the history is that when you base your argument on the fact that something is an anomaly we don't currently understand, yes, it's legitimate to, among all the other things to say could this be an alien artifact? But you've got to be very humble and careful about that. It's a very weak argument. And I think that Avi Loeb's arguments are falling one by one and, and hopefully they will continue to as we discover more about the universe is ʻOumuamua an alien derelict spaceship with a solar cell? I would love for that to be the case. And if there's a good reason to argue for that, fine. I also stand by my criticism of him publishing a book again, promoting this idea to the public before letting it marinate in the scientific literature for a bit longer. I think that's legitimate as well. So but yes, did he frame all of this as this is just a hypothesis? Yes, of course he did. He's a scientist and he's a legitimate scientist. We never said he was a crank or a fraud or anything. The last thing was that people were saying that one of his primary complaints was that the scientific community is being unfair to any legitimate hypothesis that happens to deal with aliens. And okay, whatever. I don't know. I don't know that that's true. Astronomers come up with this every time there's a there's a potential anomaly. They always throw on the list. Could it be aliens? And it's fine as long as you don't put too much weight on it. And as long as you're careful, here's where I think the bias is, you have to be careful in how you talk to the public and the media about it. That's because it's not just another hypothesis when you're talking about communicating it to the public. It's a special one because it's going to get all the attention. So you have to be careful. And I think that Avi Loeb is being the opposite of careful when it comes to that hypothesis. So okay, we could have been a little bit more balanced and a little bit less snarky. But I actually think that our take on the whole situation was legitimate.

B: All right. Thank you, Steve. Okay, let's go on with science or fiction.

Science or Fiction (1:32:35)

Item #1: April 10 1918 – Alexander M. Nicholson files a patent for the radio crystal oscillator. Item #2: February 23 1918 – Arthur Scherbius applies to patent the Enigma machine. Item #3: January 22nd 1918 – George Eastman is granted a US patent for his roll film camera, for which he registers the trademark Kodak.

Answer	Item
Fiction	Roll film camera
Science	Radio crystal oscillator
Science	Enigma machine

Host	Result
Bob	win

Rogue	Guess
Steve	Enigma machine
Cara	Roll film camera
Evan	Roll film camera
Jay	Roll film camera

Voice-over: It's time for Science or Fiction.

B: Each week, I don't come up with three science news items or facts, two real and one fake. And I challenge my panel of crack skeptics to tell me which one is the fake. There was no crack this week, so we may have a little less energy than usual. Are you ready?

S: Sure.

E: Yes, Bob.

B: Okay. This week, there is a theme. I call it Pandemic Patents. But not the 2021 pandemic, the 1918 pandemic.

C: Crap.

B: Aha. Okay. Number one, April 10th, 1918, Alexander M. Nicholson files a patent for the radio crystal oscillator. Number two, February 23rd, 1918, Arthur Scherbius applies to patent the Enigma machine. And finally, number three, January 22nd, 1918, George Eastman is granted a U.S. patent for his roll film camera, which he registers the trademark Kodak. Okay, I'm going to roll an imaginary dice in my head. Steve, go first.

Steve's Response

S: No, I always go first.

B: Do you?

S: All right. So the first one, Nicholson files a patent for the radio crystal oscillator. There's a lot of that going around then. So I think that sounds plausible. I don't remember this, but that sounds very plausible. The second one, the patent for the Enigma machine. Now, I know that was World War II, right, the Enigma machine, but is 18, is that when it would have started or is that too early? And then Kodak, sure, 18, that sounds about right. So my gut is telling me the Enigma machine is the fake.

B: Okay. Thank you, Steve. Let's see. Cara, you're next.

Cara's Response

C: I don't know.

B: All right. Jay, all right. Let's try you. Oh, sorry.

J: Okay.

C: Okay. So the real question is, which of these would be anomalous for 1918? Unless you literally just made something up and that's extra frustrating, but my guess is that all of these patents exist, but they're not all from 1918. So we've got the radio crystal oscillator. Don't know what that is. Sounds like a turbo encabulator, but it's probably real.

J: It totally does.

C: We've got the Enigma machine, which again is, yeah, World War, but you know what? This technology could have been developed. This is not uncommon, where the technology is developed earlier and then utilized in the next war in kind of in anticipation. And then we've got the roll film camera. So roll film, you mean like the click, click, click, click, like to actually have it in the cassette and move it across the camera. That's what roll film means.

B: Yeah. It's basically, you know.

C: Instead of like a plate, like a photographic plate in the back. Okay. Yeah. Film. So film on a roll. It's old. Is it that old? Oh, maybe it's not that old. And it's small too. It might've been 35 millimetre, although it doesn't say. Ooh, I think back to tin types, to garo types. They're from that era. I'm going to say the roll film is the fiction.

B: And let's see, Evan, you go next.

Evan's Response

E: Okay. Radio Crystal Oscillator in 1918. Yeah, I think that one is right. As Steve alluded to, there was a lot of tinkering with early radio around that time. So sure. Not a problem there. It's one of the other two, I think. Now the Enigma Machine, 1918. So yeah, we think about Enigma Machine, World War II era, but that doesn't mean that they didn't try to patent something earlier or come up with some earlier version of it. Arthur Scherbius, that could be a Germanic name, assuming it is a German patent we're talking about. I don't know about this one. And then there's the camera one, the roll film camera. Boy, I could have sworn that Eastman grabbed patents as early as the late 1800s, 1890s. But a roll film camera, boy, that just seems... I don't think that came along until much later. Roll film? You know, it was plates. It was still plates. I mean, when they photographed the eclipse in 1919, was it Eddington?

S: It could have been, yeah.

E: We're using plates still then. So that's why I'm thinking...

B: He did the eclipse in 1919, I think.

E: 1919 eclipse. That's right. Yeah. Arthur Eddington. And what was he using? Well, they were using plates. I don't really know about film, let alone roll film. So I'm having... I think Cara's right. I have a feeling this one's the fiction. I'll go with that.

B: Okay. Jay.

Jay's Response

J: The first one here about the filing patents for the Crystal Infabulator. It totally has that sound. 1918, Alexander M. Nicholson. Yeah. I mean, I'm just trying to figure from what I know about this thing, does it seem about the right time? And I'd say, sure. That seems... I couldn't say yes or no definitively, but it seems about the right time. The Enigma machine, I think that that timing works pretty good. I would think maybe it was later, but I wouldn't be shocked if it was created in the late teens, early 20s. The last one here, 1918, George Eastman with the roll film. I would say that this was earlier. 1918 seems actually kind of late for that kind of technology. So I would say that that one is the fiction.

C: Oh, but you think it was earlier, not later?

J: I think it was earlier.

Bob Explains Item #1

B: Well, let's see who's right. Let's start with the number one, since you all agree that in April 10th, 1918, Alexander M. Nicholson filed a patent for the Radio Crystal Oscillator. That is science.

C: Yay! What's a Radio Crystal Oscillator?

B: I should have thrown in something else, but let's go with what I have here in my notes. The first crystal-controlled oscillator using a crystal of Rochelle salt. This was built in 1917 and patented by 1918 by Nicholson at Bell Telephone Laboratories. So this probably wasn't clear enough. I should have added something relating to quartz oscillators. I should have thrown quartz in there because the quartz oscillators, that's what takes advantage of the piezoelectric effect, and that creates very stable vibrations and have just tons of uses, and especially in timekeeping devices.

S: The quartz watch.

B: The quartz watch, right. I mean, accurate to up to one second in 30 years, which is the most accurate time until atomic clocks appeared. It was amazing.

S: Until caesium came along, yeah.

B: It's crazy because even a really good, purely mechanical, beautifully made mechanical watch, even that could lose a few seconds a day. And so one second in 30 years is just an amazing leap. Radio stations, 1920s, 1930s, they used these quartz oscillators so that they wouldn't drift off their frequency, right? Because they had a very narrow range, like 10 kilohertz or whatever, and they couldn't really drift too far. But the quartz devices were big. They were big. It took until 1968 when Juergen Stott invented a photolithographic process for manufacturing quartz crystal oscillators that made it possible for portable watches to be made. So it's 1968. So I was kind of hoping way too much here. I was hoping that you guys would recognize that, first off, that a radio crystal oscillator was related to the quartz, but also that quartz watches didn't really appear until the 60s. So 1918, I was hoping would feel like way too early for that domino to start falling, but nobody bid on that one. So let's go then now to, let's go to number two.

Bob Explains Item #2

B: Steve thought that Arthur Scherbius did not apply for a patent for the Enigma machine in 1918. And this one is science. Steve.

E: Bob, don't ever do that again.

B: I liked your answer though, Steve, because this is exactly what I was hoping for. The Enigma machine, yes, this is the famous, or should I say infamous, cipher device because it was used by the German military in World War II to encrypt countless important communications, and pre-World War II it was used as well. The fact that the Enigma's encryption was cracked, and multiple times, not just once, but many times as it evolved during the 30s and 40s, that probably led to a shorter war and maybe even to a completely different outcome, which of course is a good outcome. The Enigma machine was invented by a German engineer, Arthur Scherbius, at the end of World War I. He called this machine Enigma, which is a Greek word for riddle. Now I was hoping that you would think that Germany probably never patented such a device because why would you make a patent for something like this that could then make it less secure? Because if you're documenting something, you're going to, it's it's essentially less secure because this documentation exists. And I was also hoping maybe even more that, and I think I got Steve a little bit on this, that 1918 seemed a little bit too early to be invented because most people think, when you think Enigma, you think World War II. You know, you think World War II. You're not thinking way back in 1918 when this special type of cipher wrote a machine that ciphered like this. That was, this was the, this is the peak of encryption at the time. And it was pretty sophisticated, but not good enough. And we're very thankful that that is the case.

Bob Explains Item #3

B: So this means that number three, January 22nd, 1918, George Eastman is granted a U.S. patent for his roll fail camera for which he registers a trademark, Kodak. That is fiction. But actually I was too good on this because it's fiction. First of all, it wasn't January 22nd. It was September 4th. Ha, I'm only kidding. It's fiction.

E: You got me there.

B: It's fiction because it was, it was patented three decades earlier. Jay killed this.

E: Jay was right.

C: Whoa, no way.

B: 1888.

E: Well, I mentioned I thought it was in the 1800s, the late 1800s.

B: You did. You both did. You did, you did as well, Evan. So you both did better than Cara did on this, but you both got it because it doesn't matter.

E: Cara knew what a Furby was.

B: It doesn't matter because you both get it, you bastards.

C: Yeah, I don't even have to be that right, and I still get it.

B: You don't, you don't, you don't have to. So the history is interesting by, by 1988, like right before in 1988, all photographers fixed images on wet plates. They were beautiful.

E: 1888.

B: Yeah, 1888. They could be, they could be very beautiful, but it was very difficult to do. Dry plates or a glass that was coated with gelatin emulsion made things easier. Somebody, somebody thought of that in 1871, but in 1877, a bank clerk, George Eastman, experimented with his new, his new wet plate camera because he was, he bought it for vacation. The vacation was canceled. So it gave him time to experiment, which is interesting because what if that, what if that vacation wasn't canceled, what would have happened? So he was, he's poking around with his new wet plate camera, cutting edge. And over the next eight years, he invented the following. He created a coating machine that he patented in 79. He then replaced the glass support with a film made of three layers. It was a paper layer, soluble gelatin and a gelatin emulsion. And then finally in 1885, he added a convenient roll holder. And and that was it. That culminated on September 4th, 1888, when Eastman got his US patent number three, 388,850 for a small handheld, easy to use camera, all of which became almost obsolete for millions of unprofessional photographers once they got their first digital camera. And then of course the cell phone camera. But still an amazing invention that, that held sway that the broad strokes of the technology held sway for many, many decades.

S: A hundred years, right.

B: An amazing amount of time, an amazing advance. I mean, that was such a wonderful, I mean, Steve, remember when a dad's mom gave us our first little tiny, cheesy, little, tiny little roll film cameras. And we were like, we used them all for years, I think we use that. And they were great. So we would just pop it in, drop it off at the, at the cheesy little, little Kodak thing at the Newer Street Shopping Center and get it back like eight, nine months later. It was awesome.

E: You want to hear a very quick story about film? Well, I went back to my high school, it was like the 25th reunion or whatever it was back at the high school itself. And they gave us a tour. One of the students did, current student at the time, like 16 year olds, kind of walked us around the school to kind of show us how things have changed. And we went over to the photography. What was the photography department? And I mentioned film to them. And they actually said, this 16 year old kid, what is film? No, I kid you not. They said that. And I never felt older in my life.

B: Wow.

C: Oh my God.

B: What a punk. What a punk.

E: What is film? Really?

B: Yeah.

E: Really?

S: Punk.

E: Awful.

B: Let's try to forget about that as soon as we can. All right, congratulations. Cara, Evan and Jay.

J: Thanks, Bob.

B: Steve- Sure, man.

Skeptical Quote of the Week (1:45:57)

‘When I was a kid we’d rent Indiana Jones movies on VHS tapes. It inspired a whole generation of scholars because we saw the excitement, and the passion, and the drama. What’s amazing to me about archaeology is the stories are even better than what you see in a Hollywood movie.’

– Sarah Parcak, space archaeologist

B: Steve, I understand you have a quote for us.

S: Yes. This quote comes from Sarah Parsak, who is a space archaeologist, I'll tell you what that is in just a minute.

B: Parsak or Parsec?

S: P-A-R-C-A-K. Parsak.

B: Oh, close.

S: And she said, "When I was a kid, we'd rent Indiana Jones movies on VHS tapes", know what those were Cara? "It inspired a whole generation of scholars because we saw the excitement and the passion and the drama. What's amazing to me about archaeology is the stories are even better than what you see in a Hollywood movie."

B: Whoa.

S: Yep. Real science is even more interesting than Hollywood. Sarah Parcak. So what is a space archaeologist? She also calls this up as a, this is satellite archaeology. So this is still archaeology on the earth, but it's using things based in space. So she combined the technique of high resolution imagery from satellites with thermal imaging and her work has helped find 17 pyramids, 1,000 tombs, and over 3,200 ancient settlements within a single year of work.

J: What is that about?

E: Yeah, because in those jungle environments, it's almost impossible to find those things conventionally.

B: We gotta do a whole news item on that. That's amazing.

S: Yeah.

C: That's cool.

E: I've actually spoken about that before.

S: We should probably have her on the show to talk about this.

B: Oh, even better.

S: This is totally cool. Yeah, but that was a great quote. I looked into her history. I'm like, oh, wow. She's like an awesome working scientist. Her husband, they're both archaeologists. Her husband's also an Egyptologist, Greg Mumford. How great is that?

B: Parcak and Mumford. I mean, gee.

S: Parcak and Mumford, Egyptologists. How awesome is that?

J: That's literally like, that's a TV show right there.

S: Yeah, that's out of central casting, absolutely.

B: Great quote. Thanks, Steve. Well, all righty then. Thanks, guys, for joining me this week.

E: Thank you, Bob.

S: Anytime, Bob.

C: Thanks Bob.

J: You got it, Bob.

B: And until next week, this is Bob's and Cara's, Jay's, Steven's Evan's Skeptic's Guide to the Universe.

Signoff

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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Today I Learned

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References

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