June 16, 2009

Synopsis: Bisphenol A and estrogen, Toxoplasma Gondii causing car crashes?, Beware of Robo-Ferret used to sniff out hidden things, RoboGames Redux, Adventures in Popularity, Move Over Silicon!, Go Fly A Kite, TWIS Bits, and Interview w/ Dr. Greg Gibson re: Genes and Illness.

Justin: Disclaimer! Disclaimer! Disclaimer!

It’s no secret, no one gets out of here alive. The question then, if anyone asks, is what if anything we do with the time we have in the great go around. Suggestions are plenty and opinions abound or regardless of intentions of what we do or who we are and why we are doing these things, our opinions, like the following hour of our programming, do not necessarily represent those of the University of California at Davis, KDVS or its sponsors. Still, regardless of self-opinion, this is the moment in which we can do.

In a sense, what we can do is who we are, we are all about to be, This Week in Science, coming up next.

Good morning, Kirsten!

Kirsten: Good morning, Justin! We hear all bright-eyed in science tales?

Justin: I’m ready.

Kirsten: You’re ready?

Justin: I’ve got…

Kirsten: You’re ready for the science rumble?

Justin: I’ve got nothing but big stories today.

Kirsten: I have big stories, too. We have a good show lined up today. We’re going to be having an interview.

Justin: Yeah.

Kirsten: Yeah. We have an interview with Greg Gibson. He is a quantitative evolutionary – empirical evolutionary biologist.

Justin: And we’re going to spend the half hour asking him what that means?

Kirsten: What does that mean?

Justin: What the heck is that?

Kirsten: Basically, he is a geneticist. But he’s written a book called, “It Takes a Genome” all about how our genes are out of whack.

Justin: Mm hmm?

Kirsten: Yeah. Our genes are wacky these days or is it our environment? How do you know and how do you tell the difference? These questions and more, we will ask Greg at the half hour.

And I brought stories about a shrinking giant, World, Robot Domination and the Bisphenol A, we know and love.

Justin: You got a Bisphenol A story.

Kirsten: Yes.

Justin: I feel trunked a little bit. Except…

Kirsten: I have three, actually.

Justin: I’ve got, This Week In T. Gondii.

Kirsten: Whoa!

Justin: Mm hmm. I’ve got a 120,000 year old life form.

Kirsten: Whoa! You do?

Justin: Yes.

Kirsten: Is that catching?

Justin: Come back to life. It could be. It could be easily catching. And good news for planet Earth, yeah.

Kirsten: Yeah?

Justin: Mm hmm.

Kirsten: I like good news.

Justin: Yeah.

Kirsten: We have – I like good news. Good news is good, right?

Justin: Yeah. That’s…

Kirsten: All right. So, let’s kick it off. I think Bisphenol A – I just don’t want to hear about it anymore. But at the same time, it’s big news. And this last weekend, Saturday at the Endocrine Society’s 91st Annual Meeting in Washington D.C., three different groups reported on their research related to this chemical otherwise known as BPA, which is known in a bunch – which is used in a bunch of household plastics. It makes plastics more flexible. It’s also in the lining of some tin cans that kind of a plastic sheet is on the inside.

Justin: Yeah.

Kirsten: Keeps stuff fresh.

Justin: And it produces – when it heats up – this is the unfortunate thing that wasn’t figured out…

Kirsten: Yeah.

Justin: …years and years ago when they first develop this. When it heats up, it can produce synthetic estrogens.

Kirsten: Yeah. Well, yeah, it basically, is an endocrine, an estrogen-like substance.

Justin: Yeah.

Kirsten: So, the BPA, releases things that act on your reproductive system. Yey !

Justin: Yeah.

Kirsten: You know, but okay, so the information has been slow to come out and this is just more research that was reported this last week and the headlines are amazing. So, group – where are they located?

It was funded by the National Institutes of Health and this group from Yale University, injected pregnant mice with a very low dose of Bisphenol A during a sensitive phase of their pregnancy, during days 9 to 16.

And then, after the mice gave birth, they looked at the uterus of the offspring to see what the baby females– what had happened to them. They extracted DNA and they found that the uterus was estrogen sensitive that there was a lasting effect on one of the genes that’s responsible for uterine development and that goes on to fertility.

And so, there are these changes that occurred during development in the uterus of the mother that have a lasting effect on the female offspring.

Justin: Wow!

Kirsten: And so, it’s – the correlative of that is well what happens to humans, you know?

Another study out of the University of Cincinnati Department of Pharmacology and Cell Biophysics, they found that Bisphenol A also has effects on the heart so, that when an animal has exposure to bisphenol A, the estrogenic effects actually lead to a risk of arrhythmias or abnormal rhythms of the heart –skipped beats, all that kind of stuff.

Yey! Fun. And finally, let’s get away from rodents and mice. Let’s talk about what’s actually happening in humans. And this is still – this is taking and extending the conclusion of a study just a little bit.

But some researchers at the University of Missouri, Columbia, they took Bisphenol A and they injected it into, I think it was, rhesus monkeys. And they gave them an amount that was more than 400 times higher than the amount that the FDA estimates that human adults are exposed to.

Justin: Right.

Kirsten: And that’s also eight times higher than the estimated safe daily amount that we should be consuming according to the FDA. They looked at the blood-levels of BPA in these monkeys. And they found that the levels of biologically active BPA over the next 24 hours were lower in the monkeys than the average level that’s found in humans.

Justin: Yeah, there’s some very bizarre thing that they noticed this in some of the first research too that higher levels are actually less harmful than the lower levels.

Kirsten: That’s another – yeah.

Justin: It’s a very sort of bizarre – I don’t understand…

Kirsten: Yeah, that will be…

Justin: …why that would be. That makes no sense to me but…

Kirsten: So, maybe we’re safe then, right?

Justin: As long as we’re getting enough. Now, we’re going to have it in our vitamins. Make sure you’re getting enough BPA because otherwise, it’s going to hurt you.

Kirsten: Yeah. Well, the conclusion from this is that, the average person is probably exposed to WAY MORE BPA than is currently estimated to be safe. So, the FDA has looked at stuff and go said, “Well, this is probably how much people are getting.”

Justin: Right.

Kirsten: “And this is how much it’s safe for you.”

Justin: Mm hmm.

Kirsten: But based on THIS study with these monkeys, who metabolize BPA in a very similar way that the way humans do so, you would expect — the assumption is that, if they’re metabolizing it similarly, they’re going to have a similar amount of BPA in their blood given to what humans would. And they’re finding that we probably get way more BPA than is considered safe by the FDA on a daily basis.

And so, the question now is like, what does that mean?

Justin: And considered safe too, in the first place.

Kirsten: Yeah.

Justin: It’s – why is it considered safe? Because we didn’t have this research that said it did bad things before.

Kirsten: Yeah. Anyway, BPA news, a little bit scary. But the things that you can do to get away from that are use glass containers, try and not use plastics so much. If you are concerned about it, try and limit your exposure to food products contained within plastics.

Justin: Yeah.

Kirsten: I mean, that’s basically, what you can do. It will help. More news, more news, more news.

Justin: This was sent in by minion (Richard Barton). Breaking news from scientists out of the University of Prague, as a two-year old study has just recently now come to my attention that links baby blinding, schizophrenia inducing, national agenda setting parasite Toxoplasma Gondii with a dramatic increase in automobile related traffic fatalities.

Kirsten: What?

Justin: Yeah. Estimates from the CDC suggests that over 60 million people in the United States are infected with T. Gondii. So, this is a lot of us out there. A parasite…

Kirsten: You say, “us”, like you already know you have it.

Justin: Not me. I know actually, I know that I don’t have it, the (parasite)…

Kirsten: All right.

Justin: …I don’t know that I don’t have it. I just assumed because otherwise, I’ll be harboring this horrible parasite which is only complete it’s life cycle in cats, escapes the cat, by the way, of cat scat, is then carried often in locations be clinging to the domesticated paws out of the kitty litter box, so to say. Favorite spot maybe, it ends up on the couch or the bed or ends up on the kitchen counter.

Kirsten: Yeah.

Justin: Can get consumed by people and therefore, the parasite gains an unprecedented opportunity to eventually find itself stuck in a human body where it heads to brain, can cause behavioral changes in the host.

Kirsten: “I’m stuck in here. I must go to the brain. I must find a way out.”

Justin: They go to the brain. And then, rodents like rats and stuff, it causes them not to fear cats…

Kirsten: Yeah.

Justin: …and to be attracted to the smell of cat urine.

Kirsten: Right. Because if you’re a rodent, you go near a cat, cat will eat you and then the parasite gets back into its favorite host.

Justin: Exactly.

Kirsten: Yes.

Justin: Which is also my biggest – I think it’s very plausible that the cat lady is hording so many cats because the parasite is looking at the ratio of human cat and, “We need back up.” Let’s have those gather around. Maybe 18, 20 cats…

Kirsten: Yeah.

Justin: …then, we got a chance of being devoured again. So, the “new to me” study, finds the unexpected correlation between reaction times of those who have the parasite and with those who have traffic accidents more likely to have the T. Gondii infection. Right?

So, reaction time – here it is, now the reaction time is maybe limited also to people with a certain blood type. Jaroslav Flegr – I’m just guessing.

Kirsten: Right.

Justin: …and colleagues at Charles University in Prague, Czech Republic have previously discovered that Toxo affected reaction times, and mostly in people whose blood type was rhesus-negative.

So, they monitored about 4,000 military drivers for a year and a half. And those who have blood types that were RH-negative had Toxo were 2 ½ times as likely to have an accident as those unaffected drivers who are Rh-negative or anybody who is or any positive.

So, even if they had – yeah, if they were Rh-negative but no Toxo, the RH-negative with Toxo, 2 ½ times more likely to get into a car accident.

Kirsten: Mm hmm.

Justin: And then, the Rh-positive, regardless of the Toxo infection were the same as the Rh-negatives who didn’t have it.

Kirsten: Got it.

Justin: So, it’s just affecting the Rh-negatives in this delay time.

Kirsten: That’s interesting. I wonder what about the blood type?

Justin: Yeah. People…

Kirsten: …allows the parasite to get in there.

Justin: The only thing – I mean, he doesn’t really have an answer for this. He says, people with Rh-negative lack a protein on the surface of their blood cells but doesn’t know why this affects the way the parasite operates in the brain.

Kirsten: Yeah. Fascinating.

Justin: And why that protein is involved (yet).

Kirsten: And then…

Justin: Yup. And now, we can see the mechanism.

Kirsten: Yeah. Now, we can look at the mechanism. How does – maybe this has something to do with the way that Toxo gets into the cells, has an effect, but at the same time – yeah, why more car accidents?

Justin: Yeah.

Kirsten: Weird. Just the reaction times were dulled that which if you’re going to be eaten by a cat is good.

Justin: Yeah. It slows you down so, the cats…

Kirsten: I mean, it slows you…

Justin: …are even faster.

Kirsten: Slows you down so you can be eaten.

Justin: It says though, the results suggest that between 400,000 in a million of the world’s annual road deaths might be due to Toxoplasma Gondii infection. Suggesting also that regular testing should be employed on RH-negative pilots, air traffic controllers, truck drivers, people in the, you know…

Kirsten: Right.

Justin: …in the motor-vation departments…

Kirsten: Yeah.

Justin: …for any infection.

Kirsten: If you’re responsible for other people or, you know, in a position that could, you know, cause…

Justin: School bus driver.

Kirsten: Yeah.

Justin: Yeah.

Kirsten: And you’re RH-negative, maybe you should be tested for a Toxo.

Justin: Yeah. So, anybody who has a negative blood type.

Kirsten: Enforced – I’m just imagining enforced Toxoplasma testing for all RH-negatives.

Justin: You know what, look, it might be time. Look, it blinds babies, it induces schizophrenia, alters vast swaths and public opinion, now…

Kirsten: And now causes car accidents.

Justin: …kills a million people a year in car accidents.

Kirsten: Where did you get that?

Justin: It says, between 400,000 – he says – this is the researcher was saying between 400,000 and a million of the world’s annual road deaths might be related to this.

Kirsten: Might be.

Justin: Well, yeah.

Kirsten: Not “are”, might be.

Justin: All right. Well, you know, maybe killing a million, maybe it kills 400,000. I think the “might be” event was on the number.

So, the time has come gentle minions to wage war in Toxicism. If you know anyone who is harboring, Toxicists or simply suspect somebody might be linked to a cat, a tip line has been set up via email, Put TWIS in the subject matter. We’re going to root out this problem.

Kirsten: Toxo-TWIS.

Justin: Yeah. It’s time to turn-in your neighbors.

Kirsten: Oh, dear. This Week in World Robot Domination, who do you have to fear?

Justin: Robots?

Kirsten: Ferrets.

Justin: Ferrets?

Kirsten: Yeah.

Justin: Ferrets and robots?

Kirsten: Robotic ferrets.

Justin: Oh, my goodness.

Kirsten: Dubbed the cargo-screening ferret, there is a new robot that’s being developed in the UK by the leader of the project is a Dr. Tony Dodd. And he says, “It’s essential we develop something which is simple to operate and which Border Agents can have total confidence in. The ferret will be able to drop small probes down through the cargo and so pinpoint exactly where contraband is concealed.”

So, in effect, they’re making a little tiny robotic ferret that can slink…?

Justin: I think, kind of slink, I think they’re slinkers.

Kirsten: Yeah. They make little…

Justin: Some very good ferrets…

Kirsten: I want to know if they make little ferret noises. Yeah, they will have two different types of sensors, laser and fiber-optic based that will allow these ferrets to be able to detect tiny amounts of carbon dioxide which can indicate people, because people breathe, perspire a lot of carbon dioxide…

Justin: (Unintelligible).

Kirsten: …emissions. So, they can actually use these little ferrets where border agents and dogs can’t get in. These little ferret robots will be able to kind of sneak into smaller spaces, be able to delve their probes into the cargo containers potentially finding trafficked humans; potentially finding illegal substances and potentially finding, you know, terrorist related contraband.

Justin: Yeah.

Kirsten: Yeah. So, beware of ferrets if you’re on the lookout for the World Robot Domination.

Justin: Speaking of World Robot Domination, I went down to the Robogames…

Kirsten: Oh, yeah, yeah, yeah.

Justin: …this weekend.

Kirsten: Tell me, tell me.

Justin: It’s awesome. Awesome.

Kirsten: Aren’t they great?

Justin: Yeah.

Kirsten: David Calkins who we interviewed on the show a few months ago, December I believe, he is the leader of the gang, the Robogames gang. He’s a great roboticist in the San Francisco Bay area.

Justin: Yeah. I was not really into it. My six-year old…

Kirsten: Was into it.

Justin: Like, at first, like I was – because like this, like robots fighting and pushing each other, and they looked cool but like the six-year old loved it.

Kirsten: Oh, yeah.

Justin: And then – but the one thing that got both of us, was there was a chess-playing robot which is like…

Kirsten: Mm hmm.

Justin: …it’s just basically, it’s like a computer program that you’re playing chess against, right? We’ve all done that.

Kirsten: Right. And then, it’s like a little arm (prosthetic).

Justin: But it has this prosthetic arm that goes and moves the pieces. It was that added element where you have a real chess board made out of wood in front of you and you’re playing this robotic arm. And my six-year old started playing, he doesn’t really know how to move all the pieces yet.

Kirsten: Right.

Justin: And then, the guy – there was like, it doesn’t matter. Whatever he moves, the human is always right. The robot goes from there, right. So, I like that. I like the…

Kirsten: That first assumption, the robot is always right.

Justin: No, the human is always right.

Kirsten: And then, the human is always right. Okay.

Justin: The human is still always right. When that changes, when that robot, when you make a move that’s illegal and the robot moves your pieces back and corrects you, that’s when we know, if the tide has been turn, when the robot stops us from cheating at chess.

Kirsten: Did you see the robot soccer or the…

Justin: I didn’t see…

Kirsten: …robot martial arts?

Justin: No. We didn’t get to see – because we also went to the California Academy of Sciences early in the day. So, we kind of did both things in one day.

Kirsten: That’s great.

Justin: That’s an awesome place. But don’t go in the weekend because there are billion people there.

Kirsten: Yeah, yeah.

Justin: And I think…

Kirsten: Very crowded.

Justin: …there’s a room for like a hundred.

Kirsten: Yeah.

Justin: But it was really cool.

Kirsten: The Robogames though, it’s only once a year. It was this last weekend…

Justin: Yeah? Really?

Kirsten: Yeah.

Justin: You should go next year then, not tomorrow.

Kirsten: Yeah. That’s right. It will be…

Justin: (Unintelligible).

Kirsten: We’ll be back again next year with more robots in the bay area. Showcase, I mean, these are all garage roboticists. I mean, everyone at the robot games, I mean, maybe there are some sponsorship of teams of the larger BattleBots. But really, I mean, there are kids building robots.

Justin: Yeah.

Kirsten: There are – you know, these are high schoolers, college students, you know, people who work in an office during the day and then, get tired of it and want to go home and work on their robots on the weekend. You know, this is, it’s a really neat movement…

Justin: And some of them looked like criminals who are…

Kirsten: Yes, they do.

Justin: …trying to develop robots to take over the world. I mean, there was a couple of mad scientists-looking people there.

Kirsten: Awesome.

Justin: All right. Adventuring writer and poet, Miguel Cervantes once said, “Tell me, what company you keep and I’ll tell you what you are”. Looking around the studio that would make me a scientist with PhD and Kirsten went fair so well. But now, new research by consumer psychologists Arul and Himanshu Mishra from the University of Utah and Dhananjay Nayakankuppam…

Kirsten: Just give up. Just give up.

Justin: …from the University of Iowa is now showing that guilt or specter association translates not just to people but to groupings of objects. It’s kind of an interesting contagion theory that’s being developed by how close things are.

They had – proximity was the hidden motivator in what they were looking at. So, they had the study and they set up ketchup bottles. And they would have one group of ketchup bottles that were all very close together.

Kirsten: Mm hmm.

Justin: And another grouping of ketchup bottles that were further apart from each other.

Kirsten: Mm hmm.

Justin: And what they did was they would tell people, “Okay, in one of the bottles, there is a coupon, a gift certificate.” And what they found is vast majority of people would choose out of the group that things were close together.

Kirsten: Mm hmm.

Justin: And if they were told that, they were defective lids, like three of them have defective lids and you got to open up and pour it out, they would choose from the group that was spread further apart.

So, there was some sort of hidden thing that was happening where, if they wanted something good, they were going for the closely grouped ones because this idea is, it’s somehow could be shared. If it maybe, it’s not this one but it’s close enough to that one, it could be translated…

Kirsten: That there is some kind of translate…

Justin: Yeah.

Kirsten: …transitive property because of proximity.

Justin: Right, right. So, the results as reported in the Psychological Science, a journal of the Association for Psychological Science, and it reveals that we tend to view products that are grouped close together as being “contagious”.

That’s what they’re saying. The group that’s closed together is contagious. So, if there’s something good, maybe it could be in any of the others.

Kirsten: And everything could be good.

Justin: Like it’s bad. Right.

Kirsten: (Toy germs).

Justin: Yeah. It was like…

Kirsten: Yes.

Justin: …they went to contagious. I also would say though it kind of looks like popularity.

Kirsten: Yeah.

Justin: It’s sort, you know, it’s sort of like – the ones that are close together, like it’s like a group of people who are standing closer together.

Kirsten: Mm hmm.

Justin: You think that they’re more closely knit. And so, you’re looking at a group that everybody is close together versus a group that’s sort of disparate and not hanging out with each other so much.

Kirsten: Mm hmm.

Justin: If there is good stuff going on, it’s probably in the group that’s clustered up together because they’re sharing this good thing. And if they are…

Kirsten: Right.

Justin: …standing far apart, there’s probably a problem with somebody. Well, somebody smells in that group and that’s why they’re not standing next to each other. Like that where I would have taken it. But they’ve gone contagion. So, anyway…

Kirsten: It’s probably just because of all the disease talk lately.

Justin: Yeah.

Kirsten: Better for headlines than popularity.

Justin: You think science is about headlines?

Kirsten: I think the media is about headlines. There maybe a replacement for silicon. Those silicon chips that are an integral part of almost all of our technology or all of our technology today, it might be time for it move on over.

Researchers at the Stanford Linear Accelerator – something SLAC, Linear Accelerators – I don’t know that the “C” stands for, I forget.

The National Accelerator Laboratory in Stanford University, they have developed a compound called bismuth telluride which is an unknown material. However, there are properties of this material that have been hypothesized but not actually measured before. And so, what they did is they actually – they used lasers to look at the flow of energy over the surface of this bismuth telluride.

What they’re looking for is something that acts like a super conductor at room temperature or even at above room temperature temperatures. Because that would be more like the average daily life. You could take this kind of a material, it would a free flow of electrons of energy through or over its surface. And it would allow other, maybe smaller or newer chips to be developed.

So, they – this is published in Science Express, it was published on June 11th. And these guys, they looked at the properties of the Bismuth Telluride. And they found that this material allows – it acts as an insulator and it allows electrons to travel on the surface at room temperatures with no loss of energy and it can be…

Justin: What?

Kirsten: …fabricated using existing semi-conductor technologies. So – and they found that it actually acted better than was hypothesized.

Justin: Wow!

Kirsten: So, it actually did better than what they expected it to do. And so, they’re looking at it and they’re like, “Wow!” It can withstand higher temperatures than what was theorized. The energy flows better than what was theorized. “This is really exciting,” they say. This could let them make devices with new operating principles.

They’re talking about using this to create devices that use spintronics, where the electrons are spinning in the same direction that the atoms are spinning so, that when, say a ray of light so, light photon comes in, it doesn’t get damaged itself by bouncing back in the exact same direction. The spin of the electron has actually caused the light to bounce off.

Justin: Reflect.

Kirsten: To reflect in a different direction. So, there’s no degradation of information.

Justin: Wow!

Kirsten: So, it’s a really interesting idea to be able to use this material to potentially create new technologies that use electron spin to carry information.

Justin: That’s awesome.

Kirsten: Yeah.

Justin: But how…

Kirsten: Very cool. And it’s easy to fabricate. So, the next step is just to start fabricating more of this bismuth telluride and starting to see what they can actually do with it.

Justin: Start fabricating information.

Kirsten: Let’s replace silicon, that sounds like fun, right?

Justin: Yeah.

Kirsten: Yeah.

Justin: Yeah.

Kirsten: Yeah.

Justin: Telluride breasts implants, though. It doesn’t quite have the same…

Kirsten: Oh, yeah.

Justin: It’s going to be a while.

Kirsten: No.

Justin: Well, many of us have felt the frustration in the face of formidable climate crisis and have wondered when the world would wake from the unsustainable fantasy of traditional fossil fuel sources, the solution to the trouble maybe best managed by telling humanity to go fly a kite.

Kirsten: Let’s go fly a kite.

Justin: Wind power, to the people. Right on.

Kirsten: Yeah.

Justin: And not just any kind of wind power, oh no. You say, you want a revolution, you need to train your mind to think revolutionary thoughts which is precisely what has been done by – in the study by scientists that Carnegie Institution and the California State University.

Ken Caldeira of the Carnegie Institution’s Department of Global Ecology and Cristina Archer of California State University in Chico compiled the first ever global survey of wind energy available at high altitudes in the atmosphere.

Using some 28 years of data, they discovered that in the high altitudes, there is an incredible density of wind power which they could actually use. “There’s a huge amount of energy available on high altitude winds,” said Ken Caldeira. “These winds blow much stronger and steadily than near-surface winds. But you need to get up near the jet streams around 30,000 feet.”

So, these jet streams – between 20,000 and 50,000 feet, they shift a bit seasonally. But for the most part are pretty persistent features, they don’t – they’re not quite like, you know, we have a windy day and then we don’t for a couple of days.

Kirsten: Right.

Justin: Pretty consistent. They’re usually there. Their down time is like 5% out of the year where they’re not really on in any given area. So, they’re talking though that, if there’s enough energy up there to power all of the Earth’s needs a hundred times over.

Kirsten: This is what they say about so many different kinds of energy though. You know, sun that hits our planet, the wind that’s in our atmosphere, you know, everything. It’s like, “Oh, we can power so much stuff.” But, you know, then, there’s the problem of making it happen.

Justin: Yeah. What they’re talking about here, some of their ideas has been proposed to harvest it. But it’s basically, tethering a giant kite-like wind turbine that would be lofted to the altitude of the jet stream. Forty mega watts of electricity could be generated by the current design.

Kirsten: That’s cool.

Justin: That’s the top end. The average above New York, if you put one above New York, it would be about 16 kilowatts per square meter versus on the ground, the average is about 1 kilowatt…

Kirsten: Yeah. The…

Justin: …for wind turbine to (run).

Kirsten: The high altitude winds turbines are really…

Justin: Yeah.

Kirsten: Amazing idea. And then, the cable that connects the wind turbine…

Justin: Spider silk.

Kirsten: …the kite – no, not spider silk.

Justin: They’re going to make spider silk.

Kirsten: It’s conductive. So, you actually have the cable that’s tethering it or at least part of it…

Justin: Oh, yeah.

Kirsten: …be part of the transfer of electricity from that turbine down to the ground where you can actually store it.

Justin: Yeah.

Kirsten: Very cool. That’s very cool.

Justin: I mean, this is going to end badly and, you know, if they ever do this, I think. There’s going to be planes running into these things or…

Kirsten: Well, that will be – it will be a

Justin: …the wind will die and the giant kite will crush down and electrocute a village or something.

Kirsten: I think, that’s the question. I mean, if you’re going to put something up in the sky like that, you’re have to sure that the wind is constantly going to be at a rate that will support the structure.

Justin: Right.

Kirsten: You know, you can’t just loft something up there and go, “I hope it doesn’t fall on someone’s head.”

Justin: But on the other hand, I’m sure there are people like, “Electric wires in walls? No, that will burn everybody.

Kirsten: No.

Justin: It will never work.” You know, so, this could be, yeah.

Kirsten: It could be big.

Justin: In ten years…

Kirsten: It could be big.

Justin: I could be talking about out of…

Kirsten: You know there are…

Justin: …we’ve solve the energy crisis through kites.

Kirsten: Yeah. And there’s a company down out of – I think either, it’s Australia or New Zealand that’s talking about a similar idea. I mean, this is an idea that’s being batted around. It’s one of the many ideas and we’ll see what happens. But…

Justin: And Southern Australia has one of the better.

Kirsten: ..we have to also consider what is going to happen with changing climate if any of these patterns are going to change and if wind is going to decrease or increase in certain areas related to how weather patterns are changing.

Justin: Yeah.

Kirsten: We are at our half hour.

Justin: But I’ve got more stories.

Kirsten: I do.

Justin: I’ve got the Earth is going to last another billion years.

Kirsten: Hey, that’s great.

Justin: Isn’t that awesome?

Kirsten: That’s awesome. Betelgeuse is shrinking.

Justin: Then, they found a 120,000 year old ultra micro microbe, three kilometers under glacial and Greenland and brought it back to life. Life could exist anywhere for any amount of time.

Kirsten: Hey, awesome. I’m going to sneeze.

Justin: Okay. So, we’re going to the break. We’ll be back. You’ve been listening to This Week in Science. We have a great guest coming up next.

Kirsten: We do. Stay tuned for more.

Justin: Don’t go away.

Justin: And we’re back with more of This Week in Science.

Kirsten: That’s right. And on the line, we have Dr. Greg Gibson, who – we got the little blurby thing here out of the way. He’s a professor of Genetics and he’s now at the University of Queensland. He was at the North Carolina State University in Raleigh.

Let’s see, yeah. Integrative Biology at the University of Queensland. He is a leader in the new field of genomics studying how interactions between genes and the environment affect human health and organismal evolution.

Justin: Organismal.

Kirsten: Organismal, that’s right. So, without further ado, let’s bring him on the line. Dr. Gibson, are you with us?

Greg: Yes, I am. Good morning, Kirsten and Justin.

Justin: Good morning! Welcome to This Week in Science.

Greg: Thank you very much. Glad to be here.

Justin: This is an exciting topic.

Greg: Well, I’m glad you think so.

Justin: Yes. We’ve entered into this modern era with our old genes.

Greg: We have.

Justin: Is our fashion now completely out of whack with our environment?

Kirsten: These are fashion.

Greg: Well, there’s nothing you can do about it but yes..

Kirsten: Yeah. So, I mean, that’s the basic idea behind your thesis is that we have changed the way we interact with our environment faster than our genes can evolve? Is that basically it?

Greg: Pretty much in a nutshell, yeah. I love to say that there are a lot of new genes out there. Looks like, some people would say, that most of the stuff gets into trouble is all very new stuff. But, you know, the genome have also to keep honest, to keep us stable.

Kirsten: To keep us honest.

Greg: And a lot of pretty good job of it that we’ve insulted it somewhat, I would say.

Kirsten: Yeah. What do you think is the, I mean, what is the biggest insult? I mean, can you…

Greg: Cigarette smoke.

Justin: Yeah.

Kirsten: Interesting.

Greg: You know, it’s just, I mean, I’m not going to lie about this. Change is great. Change is cool. But we have to just accept that there are consequences of that.

You know, it was the greatest insult is the way we eat. It’s the way we approach the world, sitting around watching TV all the time. And sort of, not interacting with each other as human (unintelligible). It just change.

Kirsten: Right. I mean, I hear a lot about in various studies that people are, you know, we’re reasoning behind a lot of what is going on health wise in people’s lives is, is this a difference between our evolutionary history and our current life.

So, once a upon a time, our ancestors were living on the plains either the question is were we scavenging or were we hunting down animals for food; where we, you know, looking for roots and tubers in the ground? That’s different, you’re constantly active whereas now, the couch potatoes syndrome.

Justin: And we don’t probably – we don’t have to even go back that far. I mean, we’ve separated ourselves from the microbial world over the last, really the last 50 years, 60 years maybe. I mean, before then, we didn’t have all the antibiotics, the antibiotic (soaps)…

Kirsten: Mm hmm.

Justin: …and all that sort of thing. So, we were much more in the – in terms of our familiarity with microbes, we were there…

Greg: Yeah.

Justin: …plus the nature. Like, where did nature go?

Greg: In a matter of speaking, we’ve separated ourselves from the microbial world. I mean, we are still 90% microbes.

Justin: Yeah.

Greg: (Out of ten), nine parts bacteria, one part human. But, you know, what? I think, one of the other things that I’d like to get across is the idea that not all humans are the same. We sort of talk about us as species.

Kirsten: Mm hmm.

Greg: I think that’s really to include crucial point to get across (as soon as) – part of what’s the book about is, it’s very complex and we’re all different. So, the notion that, we shouldn’t have a high-fat diet or we shouldn’t, you know, we all be eating McDonald’s or whatever, that’s would probably be (unintelligible) and part of people’s – though a lot of people deal really well with that.

And so, as you go through fat, diet, or fats of this and that, you can’t expect all people to respond in the same manner. And we’ve all got genetic variation which makes better or worse in different circumstances.

Kirsten: Right.

Greg: So, sort of the deeper argument here is it is about variability. So, it’s not about constancy of the species. But it’s the fact that, you know, there’s a normal distribution of absolutely everything. And the notion is that normal distribution has gotten broader, if you like. So, there’s greater exposure at the ends.

Kirsten: Do you think that the rapid advancement of technology which has brought us to the point where we are now, do you think that is adding an extra factor to, you know, the evolution of our genes, like making them, you know, are we going to add some – in some way because of this variability, the way that we’re responding to these new environmental insults or…

Greg: Mm hmm.

Kirsten: …whatever, is it going to make it happen faster? Are we going to change faster now?

Greg: Genetically?

Kirsten: Yeah.

Greg: No. Actually, there’s a lot of really interesting points wrapped up in that, I think. You know, so, population geneticist, a very quick to point that, you know, there’s sort of no danger to the gene pool from keeping sick people healthy.

Kirsten: Mm hmm.

Greg: That’s sort of the idea is that, God, if you give all of the cystic fibrosis people alive or whatever then, we’re all going to end up with cystic fibrosis. So, that’s sort of not – this is not true because these genes will only invade the population if there’s some benefit to them.

Kirsten: Mm hmm.

Greg: On the other hand, there are people who would argue that actually over time, mutational load will become a very important thing. So, you know what, getting rid of the bad things, as they appear in the same rates that you have in the past. So, there are people that sort of suggest that there will be this mutational melt down of the human species.

And then, some would even argue that they’re even seeing that already that, that the ultimate faith of humanity is to become stupid.

Kirsten: Yeah. I saw “Idiocracy”.

Justin: Become, become.

Kirsten: Justin, you’re already there.

Greg: But that’s not right, that’s not to feel negative. I mean, actually, you know what? The book is about disease. But on the other side, you could just as well be seeing heightened creativity. I mean…

Kirsten: Mm hmm.

Greg: …you know, it’s a two sided thing. And I probably, I should have written the first book about positive side of things instead of the disease side. But…

Kirsten: Right.

Greg: …oh no, nobody likes positive things. So…

Kirsten: They don’t sell so well, yeah.

Greg: But yeah, I mean, it’s actually quite possible that you’re seeing more exposure, more creativity and productivity at the other end because of technology. It’s really interesting thought.

Kirsten: I’m thinking about this idea of disease. And something that’s come up in the past, is that one of the things, I think in the introduction to your book, you mentioned, you know, one of the things, kids not being able to pay attention.

Greg: Mm hmm.

Justin: Mm hmm.

Kirsten: Well, is that really a problem or, you know, autism or ADHD, these things that we consider disorders, are they really disorders or are they just genetic variability that happens to give kids behaviors that don’t fit into our societal construct?

Greg: Oh, well, I’m not qualified to wade into that debate. Yeah, I mean, there’s a lot of the ascertainment, is a lot of it just putting stigmas on things?

Kirsten: Mm hmm.

Greg: I think probably, most practicing pediatricians and so forth would say that it is really a true disorder there.

Kirsten: Right.

Greg: It’s kind of like the depression thing. I mean, you know, when someone is deeply depressed and when someone is sad.

Kirsten: Mm hmm.

Greg: There’s a qualitative distinction there. And I think, with autism, that’s true. You know, this instinct stuff coming out about the genetics of autism and schizophrenia and various some other diseases, one of the things that a lot of your listeners may not be aware of is something called the paternal age effect.

Justin: Mm hmm.

Kirsten: Mm hmm.

Greg: Have you heard of that?

Justin: Yeah. The older the father is…

Greg: Yeah.

Justin: …the more likely the condition is to arise.

Greg: Yeah. It’s the opposite for moms. But then, the argument there is that they’ve got better economic resources to get better education and so forth.

Justin: Mm hmm.

Kirsten: Mm hmm.

Greg: But with the man, it’s probably because there’s so many more divisions in the germline and in the sperm that they’re accumulating mutations and passing those on.

And they’re actually manifesting an increase in the likelihood that kids got sick. But that hypothesis at this point has not been proven. But certainly, that could be an example where what’s happening is should just getting more of this very rare mutations in the gene pool.

And the argument would be is that were less well buffered to absorb the impact of those now so, that more people will sort of show the effects. Whereas in more traditional lifestyle, maybe we were able to just cope with that, the genome was able to cope with that.

Justin: Except in a more traditional lifestyle, we’d already be dead.

Greg: Yeah, well…

Justin: I mean…

Kirsten: Right.

Justin: …these are in age ranges where, you know, was long pass the life expectancy that we use to have.

Greg: Yeah. That’s sort of to have responses to the book and stuff and so, they looked into a little bit more into life expectancies and disease rights and things like that in the middle ages and pre-historic times and so forth.

I don’t see a lot of consensus. But it’s a very much a thing in flux. So, I talked about what’s happening in the last 20 years. That’s probably not the only time in humans, that there’s been this dramatic transition going on in our health is about – in our health outcomes.

But you’re right, yeah. I mean, most humans don’t — haven’t historically lived anywhere to the age that we do now.

Justin: Mm hmm.

Kirsten: Right.

Greg: But that’s most humans. There’s no reason why they couldn’t. I mean, I was recently out in the desert in Morocco doing a study out there with nomads. You know, people would get up and move every three weeks of their life.

And there were people perfectly find in the 70’s and 80’s having kids when they’re in their 40’s and 50’s.

Kirsten: Right. So, it’s not necessarily – I mean, modern technology has helped a lot in the modern society, modern culture has helped a lot to get us to where we are. But that’s not…

Justin: Yeah.

Kirsten: …it’s not unheard of.

Justin: I mean, one of things the genes need to do though, right, is we need to increase now. We need to catch up with our ages, our older ages. We need the third set of teeth for instance.

Greg: Yeah.

Justin: You know…

Kirsten: Yeah.

Justin: Like that’s – we need to start coming out — evolving these new attributes that will help us survive that the longer lifestyle and the new environment that we’re in. Are any of these changes that are turning – that are sort of showing themselves up as diseases, could they be considered attempts for our genes to actually be adjusting into the new world?

Greg: Well, it’s actually pretty interesting that it turns out that, probably the majority view of arthritis and diabetes that have come out.

Kirsten: Mm hmm.

Greg: So, that’s one of the diseases that we’ve made the most progress in the last two years in understanding the genetic basis of. It turns out that many of the variance in the genomes that are protective against diabetes…

Justin: Mm hmm.

Greg: …are actually the derived form. They’re the modern form. So, we sort of go into genetics thinking all mutations are bad. Disease is bad. Therefore, disease is caused by mutations.

But if you read the data as it’s coming out that actually suggests that there have been these things that promote disease in the gene pool and we’re actually in the process of losing them.

So, Asian populations for example have pretty low frequencies of the susceptibility variance, the things will promote disease. So, they’re being replaced by these newer versions that are actually making a (unintelligible). So, in that sense, yeah, we’re evolving protection against some of this…

Justin: Our modern diet.

Greg: Yeah.

Kirsten: That’s fascinating. I hadn’t heard that before.

Greg: But this is something that goes over millennia…

Kirsten: Right.

Greg: …not decades and generations.

Kirsten: So, yeah. The evolutionary time for mutations either positive or negative to accumulate — technology is moving so quickly. How do you feel that, you know, we’re learning more and more about the genome with human genome project, we’re sequencing genomes right and left these days. We’ve got banks of data related to what genes or where and now, what they do and what proteins they create. I mean, we’re going to get to the point where we can just swap genes in and out. I mean, even though genes are maybe causing us a problem now, are we going to get past that with technology?

Greg: Probably not with gene technology. At least, I’d hope not with gene technology. That’s pretty dangerous game to play.

Kirsten: Mm hmm.

Greg: Actually one of the things I’d like to say is if genes were drugs, nobody would take them.

Justin: Wow!

Greg: Because their effects – it turns out that their effects are really pretty small average across the population. I mean, okay, like it could have a big effect in and there’s some camps who actually think that most disease is due to single genes would have a big effect. But that’s probably not the majority view at this point.

The majority view is that disease is due to hundreds if not thousands of changes in the genome that each have a very, very small effect. And if you just happen to have hundreds of the wrong type, then you’re at greater risk.

And so, changing those, isn’t going to make any difference. I mean, the other thing that we have to realize is that we all have bad genes as it were. I mean, everyone of us…

Kirsten: Mm hmm.

Greg: …would die many times over if we were homozygous, if we have gotten the same chromosome from one parent. So, and we’re protecting that because we have – we’re built from both parents. So…

Kirsten: Right.

Greg: …we have two copies of every gene. But…

Kirsten: And that allows that the variability to come into (play).

Greg: Well, it’s one of the buffering mechanisms that we have…

Kirsten: Yeah.

Greg: …is deploy all the organisms that we can cope with, with these mutations. But the point is that it will be an ever ending game of we’re trying to replace bad genes with good ones. You can never ever hope to keep up. You have to have ten such replacements in every child that was born.

Kirsten: Right.

Greg: It’s just not going to happen. More likely, there will be sort of, you know, human – (unintelligible) will come in, people say, “Oh, well I want my kid to have, you know, 6 foot tall and be an NBA basketball player” and try to engineer that. I think that’s probably easier than trying to engineer a kid that’s going to be healthy in his whole life form.

Kirsten: Right. One of the last chapters in your book is about genetic normality.

Greg: Mm hmm.

Kirsten: What is normal? This normality that you talk about.

Greg: It’s distribution. So, humans – I mean, this is wonderful diversity of so many talents and extroversion and introversion and, you know, they’re all part of the normal spectrum. And I think, that is sort of a conundrum that we have here, how this normality fade into abnormality. There’s no discreet boundary for most of these things.

And an important question that we’re facing as geneticists now is, is abnormality just the extremes of normality? That came up earlier in our conversation.

Kirsten: Right.

Greg: Or is it qualitatively distinct? And if it is qualitatively distinct, is it because of the sort of a face transition in physiology? Or is it just – is it distinct because people with disease literally have different genes that demarcate themselves from others?

Kirsten: Right. So, does it somehow bring them outside of that normal distribution?

Greg: Yeah.

Kirsten: Yeah.

Greg: Yeah. But that, I think, it can’t be that because – it’s just this environmental dependence of disease. You know, you put people in different settings and their susceptibility changes dramatically.

You know, a few – I think I’ve mentioned in the book, if you’d sort of draw a map, draw a map of cancer distribution, a real cancer distribution across United States and you color a state’s, you know, red or blue according to high or low cancer rates then, that map of United States looks exactly like a sort of political map of the United States five years ago.

Justin: Really?

Greg: Yeah.

Kirsten: Wow!

Greg: But it’s…

Kirsten: Great! Yey!

Greg: But those are different cancer actually. So, for lung cancer, it’s actually, you know, high – if you color high incident rates red then, you just get across the southeast.

Kirsten: Right.

Greg: You’ve got this massive red block.

Justin: Mm hmm.

Greg: If you look at all cancer that should turn out the highest in the northeast.

Kirsten: That’s fascinating. Have you heard – there was a study that I think, came out in the media this last week, I think, it was written up in Medical Hypotheses is the journal.

But it’s an idea that cancer is the result of our bigger brains. And so, like the fact of building our brains leads to less apoptosis and it’s a genetic – some kind of a genetic shift that has led – the cancer is related to this treatment.

Greg: Yeah. I haven’t read that. It sounds interesting. I think more generally, that would just be an example of the idea that some of our susceptibility is because of the rapid evolution of the human species.

So, there’s no getting away from it. Humans are different from just about any other species in many ways. Not so different when you add up the amount of actual molecular variance.

But we’re just different in the size of our brain and our glucose physiology and our, you know, going through – the women going through menstruation and menopause – I mean, all of these things have a huge impact on various types of disease. Our immune exposure is different. And we’ve evolved for whatever reason.

Kirsten: Right.

Greg: And a lot – you tend to sort of think introduction as a manner – oh, will if there’s susceptibility to disease in that shaped by genetics, in the shape by evolution then, what evolution must have been acting on is the function of those variance in promoting disease.

But one of the points I’m trying to make in the book is that now that need it be the case that those variants are actually affecting a whole lot of things in our bodies. They do a lot of – most of the time, they’re doing good things. But in the wrong circumstances, those good things can become bad things.

Kirsten: Right.

Greg: So, that would be an example, (if it was the) brain, yes. There’s been dramatic changes in need for energy supplies of the brain. There’s been dramatic changes in control of cell division in the brain and so forth and that’s meant that genes have changed.

Kirsten: Mm hmm.

Greg: And as a side effect of that, you could then see an increase in cancer. I think, it’s viable, sort of thought, yeah.

Justin: Interesting.

Kirsten: Interesting.

Justin: So, have we really that rapidly – did humanity rapidly evolve? I mean – or were our changes just…

Kirsten: Relative to other…

Justin: …completely different than the changes going on in other creatures. But were we – did we do this over a very brief period of time where we have a lot of change versus what other creatures are going through?

Greg: Well, this is just to – you know, and ongoing debate in evolutionary circles was, is human any different from any other species? I think, that general thought is the species go through millions of years with being fairly stable.

And then, the transition into a different species or they split or whatever speciation happens, it’s probably a fairly rapid process. Very rapid meaning, you know, thousands of generations not two or three but thousands. But that’s a small point amount of time relative to the ensuring period of (stasis), what remains of that species.

So, humans, you know, yeah, I think the thought is that they merged as a species. This modern anatomically modern humans emerged in the period of probably 50,000 years…

Justin: Wow!

Greg: …that ended up 120,000 years ago.

Justin: Yeah.

Kirsten: Right.

Justin: Whenever somebody says, we’re more evolved than something else, I said, “No, we all are exactly as evolved. We just did more with our time.”

Greg: Yeah. I agree with that.

Kirsten: So, we’re coming to the end of our show here. I just would like to know, from a genetic perspective, you know, you’re looking at where we are, all these, you know, disease in humanity like how to – maybe how to – like this clash you say in the subtitle…

Greg: Mm hmm.

Kirsten: …of your book. The clash between…

Greg: They wanted me to say “war”. The publisher wanted me to say, “war”. But I don’t like that.

Kirsten: It’s not a war.

Greg: Yeah. We don’t like war.

Kirsten: It’s not a war, no. You know, people don’t want to get sick. Do you have advice for people living in this modern world with our old set of genes?

Greg: Yeah. Don’t expect too much of your genes, I guess. Take responsibility for your own life. Yeah, I think – I mean, look, we talked about heritability which is sort of the proportion of disease in a population that’s due to our genes. And rarely, it’s not more than 50%. And what that means is, most of the susceptibility is environmental.

Now, in some cases, that’s very clear what that environmental cause is, it’s tobacco. You see, its bad diet. It’s sitting on the beach for too long.

Kirsten: Mm hmm.

Greg: Okay. But we – even when you’re dealt with a bad card there’s things you can do about it. No, not always, it’s obviously, if you’ve come down with cancer then, it maybe too late. But there are treatments you can get. But always the way, your approach that treatment can make a difference. So, don’t expect too much of the genes, I guess would be my advice. You know, there’s – I saw in the news…

Kirsten: I like it.

Greg: …this morning, there was a case of a ten-year old girl, who’s got breast cancer.

Kirsten: Too young.

Greg: And it’s absolutely horrible.

Kirsten: Yeah.

Greg: This sort of news were discussing it. And sort of saying, “You know, she hasn’t got the genes. She hasn’t got the risk factors. How can this be?” Well, it can be because, life is incredibly complicated. And it’s sort of a miracle that it works out so well as often as it does.

Kirsten: Right.

Greg: And so, you’ve got to expect that there will be some individuals who get all of these things. And horrible as it is, that’s sort of a reality. But – so, we can’t eradicate any of these diseases.

We just sort of have to learn to deal with them, I guess. And technology will certainly make it a lot easier to do that, but part of it as well is just the way we approach (our life).

Kirsten: Well, thank you very, very much for talking with us this morning Greg.

Greg: Well…

Kirsten: It’s been great.

Greg: Thanks a lot for having me. It’s wonderful to be on.

Kirsten: You’re welcome.

Justin: Absolutely.

Kirsten: And I know you’re here in up in Seattle right now.

Greg: Up in Seattle, yeah.

Kirsten: Are you on a book tour?

Greg: Sorry?

Kirsten: Are you on a book tour?

Greg: No, I wish I was. No, I’m teaching.

Kirsten: Okay. All right. Well, have a great, great day. Thank you very much.

Greg: Thank you.

Kirsten: Bye.

Greg: Bye-bye.

Justin: “It Takes a Genome: How a Clash Between Our Genes and Modern Life is Making us Sick”.

Kirsten: Yeah. He has also written, “A Primer of Genome Science”, a textbook, if you’re interested in learning more about genetics. Next week, it’s just going to be the two of us. I don’t have an interview lined up yet. Or I don’t know even know if I feel like making to have an interview. Sometimes, I like just talking to you for a whole hour, Justin.

Justin: Yeah.

Kirsten: Mm hmm.

Justin: And we didn’t get through – we’ve been, yeah. There’s a lot of stories…

Kirsten: Lot of stories…

Justin: …building up.

Kirsten: …and emails and…

Justin: That (were) out there.

Kirsten: That’s right. So, I would like to thank (Eric Weaver), (Weavercooper), (Scott) (Snorthcut), (Glenn) from Vancouver. Ed Dyre, thank you so much for sending in all the stories. (Nitty), (Patrick), (Nearamore), (Art), Kalidasa, (Don), (William), (Christopher), (Verina), (David Barton), (Ian), (Jeffrey), (Karen), (Paula), shout outs to all of you. Thank you for writing in during this last week with story suggestions and responses.

Justin: TWIS is also available via the podcast. If you’re listening on the radio, you can go to to subscribe or you can go search for This Week in Science on the iTunes.

Kirsten: That’s right. And for more information, our Show Notes will also be available on our website. It’s We want to hear from you so, email us at or

Justin: Yeah. Put TWIS somewhere in the subject or you will get spam-filtered in oblivion. You can also check this out on the Twitter or @drkiki and @jacksonfly. We love your feedbacks. So, hit us up there or on the internets anywhere that you can find them – find us.

Kirsten: On an internets near you.

Justin: Yeah.

Kirsten: And we’ll be back here on KDVS next Tuesday at 8:30 am Pacific time. And we hope you’ll join us again for more great science news.

Justin: And if you’ve learned anything from today’s show, remember…

Kirsten: It’s all in your head.

It’s not queuing. It’s just blinking at me. I’ve had nothing but grief from this…

Justin: Why do you keep using the same one? That’s what I don’t understand.

Kirsten: Because it’s…

Justin: That one – same player hasn’t worked, three weeks in a row now.

Kirsten: I know.

Justin: And you keep putting your CD in there.

Kirsten: It’s because they come in. And then, this is the one that’s available.

Justin: Because other DJs got their discs in the other ones.

Kirsten: And there are the discs and – yes. I’m going to open it up and we’re going to play a song here in a minute. Yeah, we have some technical difficulties every once in a while. So, I’m swapping this CD out and trying to think of anything else if – yeah, online Twitter, is there anything else that we can tell people about.

Oh, our Forums, if you haven’t been to our Forums, go to our Forums and get involved in some conversations there. It’s a great place to meet with…

Justin: Yeah, Lots of (Forum).

Kirsten: …TWISminion-y people. And like we said, it’s all in your head.

Justin: And it’s a disclaimer again. Why are you playing another disclaimer? It’s so…

Kirsten: I didn’t.

Justin: It sounds like the beginning of the show. Put on music.

Kirsten: Okay. Hold on, hold on.

Justin: One more try, number ten. One more try. There you go. Hit the button! Hit the button, Kirsten! Walk away!

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