The Naked Scientists explore the discovery that super hot, burning chillies can be used for pain relief; how holes in the asteroid belt show scientists how the planets got to be where they are; why things smell the way they do; the new clue into the cause of Alzheimer's; how our reaction to an unpleasant taste is the basis for our reaction to things we find objectionable; how arsenic exposure can be monitored in your toenails.
Plus in 'Stuff and Non-Science', are the sea and the sky blue because they reflect each other?
Chris Smith: Coming up this week, pain relief from super-hot burning chillies.
Kat Arney: Chillies are a crucial ingredient in a fiery curry and if you don’t wash your hands carefully after handling them, you will discover exactly how burning hot they can be. Now this is because chilli peppers contain capsaicin, this the chemical that gives them their fiery heat, and in fact this burning power could be used to reduce pain and research published in the journal PloS Biology this week has explained how this might be happening.
Chris Smith: Indeed. Kat Arney with the way in which chilli can switch off pain.
Also on the way, how holes called Kirkwood Gaps out in the asteroid belt beyond Mars have shown scientists how the planets in our solar system got to be where they are today.
David Minton: The other three gas giant planets, Saturn, Uranus and Neptune, when they were first born they were closer to the sun and at some point the giant planets began to migrate, and during that migration the locations of these resonances in the asteroid belt which sculpts the Kirkwood Gaps, they had themselves also moved. What we see today in the distribution of asteroids is almost the footprints of the migration of these planets.
Chris Smith: And David Minton will be following those giant footsteps later in the show. Plus, in this week’s ‘Stuff and Non-Science’, we’ll be reflecting on the myths that tell us why the ocean and the sky are blue.
Hello, I’m Chris Smith and this is Breaking Science, which is produced in association with the Open University.
First, with news from across the scientific globe it’s time to join our science reporter, Dr Kat Arney, to find out why things smell the way they do and also to hear about a new clue as to the cause of Alzheimer’s Disease. But to kick us off, Kat, the headline in Science is quite funny but it only really works with an American accent which is ‘from oral to moral’, scientists are saying that the way we react to things that we find objectionable is all based originally on foods that we don’t like the taste of.
Kat Arney: Yes, we often use the phrase ‘it left a bad taste in my mouth’ to describe an activity or a situation that we find quite unpleasant. But now researchers writing in the journal Science have shown that there may actually be more to this metaphor than meets the eye.
Chris Smith: Pray tell why?
Kat Arney: Well the researchers, led by Hannah Chapman, wondered if there was any kind of link between the facial movements made when we eat disgusting food, you know, that sort of ‘urgh’, and when we see disgusting pictures or when we experience really unpleasant behaviour so they carried out some intriguing experiments using volunteers.
Chris Smith: I thought you were going to say for a moment you’ve been sampling my mother’s cooking. But go on, tell us, what did they do with their volunteers?
Kat Arney: Well to start with the researchers gave the volunteers different drinks, they were either neutral tasting, sweet or bitter, and then they took close up video images of their faces. And in particular they focused on the actions of a group of muscles called the levator labii, and these are the muscles that make us wrinkle up our noses and raise our upper lips when we taste something nasty. Now unsurprisingly they found that the bitter taste caused a big movement of these muscles compared to sweet or neutral tastes.
Chris Smith: Yes, but how does the disgust at things and the behaviour bit of it come into this?
Kat Arney: Well next the scientists showed people pictures of disgusting things, including poo, injuries, insects, things like that, and they compared these with pictures of sad things and then some neutral pictures for contrast, and the team found that only the disgusting pictures led again to the movement of these levator labii muscles, and the stronger the disgust that the person felt the more their muscles moved. So this is quite intriguing, and the team went on to look at situations where people experienced unpleasant or unfair situations. These were met with these same facial movements of disgust, say, seen with a nasty liquid or unpleasant pictures.
Chris Smith: So give us the bottom line, taking a financial analogy then, what does this mean in terms of how this behaviour maps onto what we actually do in real life?
Kat Arney: Well, the researchers think that this means that moral disgust and outrage actually has similar evolutionary roots to physical disgust, and they think that this physical response to something nasty has probably been co-opted during our social evolution to express our disgust at social and moral situations that we don’t like.
Chris Smith: Indeed. Well moving from how the brain works when it’s working right to how it can go wrong. Tell us about Alzheimer’s Disease.
Kat Arney: Yeah, Alzheimer’s is a disease that affects more than 20 million people around the world, and it’s basically a degenerative brain condition that’s currently essentially incurable. And we do know that many of the effects of Alzheimer’s are due to the build-up of a protein called amyloid beta and this makes lumps called plaques in the brain. But until now it’s not really been clear exactly how the amyloid protein starts to build up in brain cells or how it really causes the illness. But this week, scientists in the US have discovered that this build-up of amyloid might be aided by a rogue protein, the prion protein.
Chris Smith: It’s the same thing that’s been implicated in mad cow disease and BSE isn’t it?
Kat Arney: Absolutely, yes. This prion protein called PrP is normally found in many different cells and it sits in the cell membrane. And normally it does a useful job, for example in the brain it helps brain cells to respond to changes in the environment around them. But sometimes the prion protein is found in a different shape, a different conformation, and this is where the trouble really starts.
Chris Smith: But how does Alzheimer’s come into it?
Kat Arney: Well writing in this week’s edition of the journal Nature, the researchers discovered that amyloid beta can stick to the normal form of the prion protein and this might be what’s causing amyloid to build up in brain cells. Now importantly they discovered that little groups of amyloid are more likely to stick to the prion protein than single amyloid molecules, suggesting that this really is a key for building up amyloid plaques.
Chris Smith: But does this actually have an effect on the function of the brain? How can we actually be sure it’s really important for the development of the disease itself?
Kat Arney: Well the scientists then went on to look at samples of mouse brains. They were particularly looking at the hippocampus, this is the part of the brain that’s involved in your learning and your memory and it’s badly affected in Alzheimer’s, and they found that brain samples from normal mice, they found the build-up of amyloid protein blocked a process called long-term potentiation, which is basically how the brain builds memories. But in samples from mice that lacked the prion protein, amyloid didn’t cause these problems with long-term potentiation, so this really does show that the prion protein’s a key link in the chain.
Chris Smith: And what are they going to do next about this?
Kat Arney: Well this discovery is pretty exciting because it gives us a whole new angle for new Alzheimer’s treatments. Perhaps if researchers could develop drugs that block the interaction between amyloid and the prion protein, then this might be a good way to prevent the plaques building up.
Chris Smith: Yes, an exciting start but certainly not the whole story. Now let’s move from Alzheimer’s Disease to something I know troubles you enormously. It’s smelly feet. Tell us about smelly feet.
Kat Arney: Yes, they do say a rose by any other name would smell as sweet, but what does make us think that a rose smells nice but my feet smell bad? My feet don’t smell that bad, come on Chris. But until now scientists have known relatively little about how the smelly molecules, known as odorant molecules, are recognised by the receptors in our noses. But new research by Harumi Saito published in the journal Science Signalling this week could shed some light on this mystery.
Chris Smith: So come on then, tell us why does a rose to me smell like a rose and your feet smell, well let’s not go there.
Kat Arney: Well our sense of smell is an amazing thing and our noses have hundreds of olfactory receptors, each of which can pick up a different smelly molecule and this then sends a signal into the brain which gets interpreted as a smell. But we only know around about 50 of these smelly molecules and that somewhat limits our understanding of the whole system.
Chris Smith: So what are the researchers actually doing in this study to try and home in on what’s going on?
Kat Arney: Well they used a technique called high throughput screening which allowed them to carry out many, many experiments in a short time, and this allowed them to test 93 different odorants, these are the smelly molecules, against a panel of 464 different olfactory receptors, and they picked up 52 specific odorants that activate mouse receptors and the screen pulled out 10 new odorants that activate human receptors. So this has, you know, made a big increase on what we know about the number of specific molecules that interact with the smell receptors. And the scientists used the knowledge from their screen to then develop a computer model that can help to predict what kind of odorant molecules might fit with different olfactory receptors. So now it’s probably possible to look at a whole range of smelly chemicals and try and predict which olfactory receptors they might bind to. So this is basically going to speed up the process of research in this area so scientists will have better ideas of which routes to follow rather than just taking shots in the dark.
Chris Smith: It’s interesting because before Christmas I spoke with a perfumer who makes smells for a living, nice smells, and he had the chemical equivalent of synaesthesia, he could imagine a smell and see the molecule in his mind’s eye that would smell like that, so I guess he’d be very interested in a function or a model like that.
Kat Arney: Absolutely. Fascinating.
Chris Smith: Now, let’s finish up on something which is ultimately my favourite thing, which is a hot curry, and you’re going to tell me now why it is that I have to keep adding more and more chilli to my curry every week in order to get the same mouth watering, face burning, eye tingling burn that you get with a really hot vindaloo.
Kat Arney: You feel the burn don’t you, Chris, you love it. Yes, chillies are a crucial ingredient in a fiery curry and if you don’t wash your hands carefully after handling them you will discover exactly how burning hot they can be, especially if you rub your eyes or go to the toilet. Now this is because chilli peppers contain capsaicin, this is the chemical that gives them their fiery heat, and in fact this burning power could be used to reduce pain. And research published in the journal PloS Biology this week has explained how this might be happening.
Chris Smith: It sounds a bit counter-intuitive, you take something that gives you pain and you’re saying at the same time it can relieve pain?
Kat Arney: Yes, this is work by Feng Qin and Jing Yao, and they’ve been investigating how capsaicin can shed light on how our bodies respond and adapt to painful stimuli. But it’s not clear in the case of pain receptors whether they truly adapt or whether they just get completely desensitised to any stimulus and shut down when they get overloaded.
Chris Smith: But you mention that capsaicin might actually relieve pain, so what’s going on there?
Kat Arney: Well the pain and the heat effect happens with relatively low concentrations of capsaicin, and other scientists have discovered that if you rub large amounts of capsaicin onto the skin it also causes nerve cells to show a drop in the levels of a molecule called PIP2, and this causes desensitisation to pain in the end. And in fact, this effect is so powerful that capsaicin creams are sold in pharmacies as treatment for muscle and joint pain, and even for the pain caused by arthritis and neuropathy.
Chris Smith: But how do the researchers actually answer that question about desensitisation and what’s going on?
Kat Arney: Well they used a range of techniques to measure how the pain receptors responded to capsaicin and they found that this drop in PIP2 is directly linked to the activation of the nerve cells by capsaicin, and the scientists also showed that even when the receptors are apparently desensitised by capsaicin they can still respond to new higher doses of the chemical. So this tell us that they’re not being truly desensitised, otherwise they wouldn’t respond at all, but in fact these pain receptors are adapting, they’re getting used to a certain level of stimulation from the capsaicin and that gives a sensation of pain relief. But higher doses of capsaicin or more intense pain would still leak through.
Chris Smith: And so what are the implications for this in terms of exploiting it for pain relief?
Kat Arney: Well it does have big implications. Effectively the intensity of the pain that you experience depends on the pain that you’ve recently felt. So at a very trivial level this suggests that if you kick someone in the leg you should kick them twice because it will hurt less the second time. But it’s also very important for doctors because finding ways to manipulate these pain-sensing nerves could develop better painkillers and anaesthetics in the future.
Chris Smith: And there was me thinking that hot curry causes stomach ulcers. Next time I have a stomach ache I’ll have to eat some chilli. Thank you, Kat. That was Kat Arney from the Naked Scientists taking a look at some of this week’s top science news stories. And if you’d like to follow up on any of those items, the details and the references are on the OU’s website at open2.net/breakingscience.
In just a moment, how holes in the asteroid belt are showing scientists how the planets arranged themselves in the early solar system over four billion years ago. But first, to a new use for your toenail clippings. Scientists can now analyse them to find out how much exposure you’ve had to heavy metals like arsenic. Here’s Gawen Jenkin.
Gawen Jenkin: Okay, well all around the world there are areas where the underlying geology means that people living there are exposed to rather higher levels of arsenic than perhaps they would like, and really it’s finding ways to be able to monitor the contamination that they may be exposed to, to see whether it really is a risk and whether any remedial action needs to be taken in the area.
Chris Smith: But why is arsenic bad news? Why don’t we like arsenic?
Gawen Jenkin: Well it is just basically poisonous and it’s been associated with a number of cancers and skin hardenings, etc, so it’s really not something that you want to have any more than you can get away with in your diet.
Chris Smith: The Victorians were pretty fond of it though, weren’t they?
Gawen Jenkin: Certainly, yes, and they even made wallpaper out of arsenic and used arsenic dyes in some of their fabrics, so they were exposed to rather high quantities and that probably didn’t do them any good in general, although specific cases of arsenic poisoning are actually very difficult to pin down.
Chris Smith: I suppose one of the big problems with arsenic, though, is that if it’s something you’re exposed to in the environment it’s quite hard to know actually how much people are getting into their body and therefore to work out how it is associated with ill health.
Gawen Jenkin: That’s right, and that’s why we need to use these biomarkers. Looking at toenails may be the thing to do for arsenic. We could, of course, analyse blood and urine, but we’d have to do that very frequently because arsenic passes through the body fluids very rapidly and so therefore we’re only monitoring exposure over the last few days, whereas looking at something like toenails allows us to monitor exposure over a longer period of time.
Chris Smith: How does the arsenic actually get into the toenail? Obviously it goes into the blood and goes there, but then how does it end up staying in the toenail?
Gawen Jenkin: Because arsenic likes keratin-rich material, so it will bind to keratins in hair or nails, and keratin is basically the flexible protein that makes up these parts of your body.
Chris Smith: So it’s almost like tree rings, you’ve got exposure to arsenic written into your toenails and fingernails.
Gawen Jenkin: Yes, potentially we could keep analysing somebody’s toenails and get a time record of their overall exposure. At the moment we’ve just been testing out the method and just taking some samples to see whether we can pick up the arsenic that we think might be there.
Chris Smith: So what did you actually do in this study to prove that toenails are a good way to measure environmental arsenic exposure?
Gawen Jenkin: Okay, as in all good scientific studies, we had a control group that we thought hadn’t been exposed to any environmental arsenic and they lived in Nottingham, and then our exposed group lived close by to an old abandoned arsenic mine and we suspected that they had been exposed to some arsenic contamination. We asked them for samples of their toenails and then we took them away and analysed them.
Chris Smith: And how do you actually analyse them? How do you work out how much arsenic’s there?
Gawen Jenkin: The first thing you have to do actually is to scrape off the gunge. This is the sort of bit that you get underneath that probably doesn’t smell too good, but that may reflect local contamination that’s in dust etc that you’ve been exposed to externally and we don’t want that. What we want is the true arsenic that’s actually within the toenail. So we scrape off that outer layer, we then clean the toenails very carefully and then we powder them down, which is not a straightforward thing to do because you know that toenails are quite elastic and so what we actually have to do is we have to do is we have to powder them in a freeze drying apparatus, the sort of thing that you’d use for freeze drying fruits and things.
Chris Smith: I had visions of you there with a giant emery board scraping away at these toenails. But when you powder them down and then analyse them, what did you find when you compare the people who live near the old arsenic mine and those people who are in the non-arsenic laced environment?
Gawen Jenkin: Okay, so we found significantly higher concentrations within the exposed group, up to 26 parts per million within the toenail, whereas the control group the maximum value was 0.3 parts per million, so that’s nearly a factor of 100 times higher in the exposed group.
Chris Smith: So the method works and you can pick up environmental arsenic exposure you think by this method, but what does that actually mean clinically? Is 100 times more arsenic really that important, does it make a real health difference or are we talking about something that’s so low anyway that 100 times more of it is still not going to make a difference?
Gawen Jenkin: Well that is the thing that we just don’t know, and the first thing we’d need to find out is how widespread this is, so we need a wider scale study. We have confirmed exposure but what we don’t know is if there are any associated health risks, associated with these enhanced levels.
Chris Smith: So if you’ve got some toenails hanging around then please send them in to – no, no, I’m only joking. Don’t send your toenails quite yet, but possibly before too long the scientists are going to be wanting to hear from you. That was Dr Gawen Jenkin who’s at the University of Leicester, and he was describing work he’s done with his PhD student, Mark Button, and they’ve published that work in Environmental Geochemistry and Health this week.
Now from trimming nails to clipping asteroids out of their orbits. Between Mars and Jupiter is a very large field of orbiting debris, but it contains holes called Kirkwood Gaps where the material that would have sat there has been dislodged by the gravity of giant planets like Jupiter. But when a research duo in the US ran a computer simulation they found more holes than the present theory could account for, and what these empty spaces are actually revealing is how the planets migrated to their present positions when the solar system was very young. Here’s David Minton.
David Minton: The asteroid belt is basically a belt of loose debris and rocks that orbits the sun between the orbits of Mars and Jupiter. What it is, is the leftovers of planet formation, it was a region that, because of Jupiter’s gravity, was too unstable to form planets so all the stuff that went into making a planet elsewhere in the solar system sort of got kicked out and that’s one unstable region and we’re sort of left with the debris at a place where planet formation never really got past a certain stage.
Chris Smith: And is all the debris in that region just uniformly scattered through space, or are there hot spots where there’s more of it and cold spots where there’s less of it?
David Minton: In some ways it’s almost uniformly scattered but there are these gaps, and these gaps were actually noticed about 150 years ago by a scientist and astronomer named Daniel Kirkwood and since then named the Kirkwood Gaps. And they are specific locations where there is, what is called, a resonance with Jupiter.
For instance, there’s a two to one Kirkwood Gap, which is a place where, if you stuck an asteroid there, it would orbit the sun two times exactly for every one time Jupiter orbited, and because of this resonance it’s a very unstable orbit and it’s a very unstable place so an asteroid doesn’t last in that particular place for very long. And so these specific locations, and there are a multiple of them for different resonance locations, get emptied out of asteroids and so there are currently gaps. What we wanted to ask was: how much of the asteroid belt is shaped by the gravity of Jupiter and Saturn?
Chris Smith: So how are you actually doing that?
David Minton: Well it turned out to be a trickier problem than we first imagined, and took a whole lot of computing power because what we ended up doing was we sort of built a computer simulated solar system and in our computer simulation we filled up the asteroid belt region, the sort of region stretching between Mars and Jupiter, with a whole bunch of computer asteroids and then just let it go, let these computer planets orbit the sun and let these computer asteroids orbit and just let the whole belt be shaped by the gravity of the solar system. And after four billion computer years we were left with an asteroid belt that looked a little bit different than the asteroid belt we see today. There are places specifically around some of these gaps, around these Kirkwood Gaps, where the sunward facing side of the Kirkwood Gap had lots of asteroids but the Jupiter-facing side of the Kirkwood Gap seemed to be depleted in asteroids, like there weren’t as many there as there could have been.
Chris Smith: So what do you think’s going on, how would you explain those missing lumps?
David Minton: Well the explanation that we’ve come up with is that this is a record of this migration of the giant planets.
Chris Smith: So are you saying then that the planet configurations we see today aren’t where the planets formed, they didn’t form in that situation, they started somewhere else and they moved and as they moved they effectively made holes in the asteroid belt?
David Minton: Exactly, so the planets formed probably in a tighter configuration, like Jupiter was a little further away from the sun, the other three gas giant planets, Saturn, Uranus and Neptune, when they were first born they were closer to the sun, so all four of these giant planets were in a much closer position to each other than they are now.
And at some point the giant planets began to migrate, and probably due to interactions with a more massive Kuiper belt, which is this icy belt of objects where Pluto lives. And that ancient Kuiper belt actually fuelled this migration and all four of the giant planets started to move from their original location, where they formed, to where find them today. And during that migration, the locations of these resonances in the asteroid belt which sculpts the Kirkwood Gaps, they had themselves also moved and as they moved they tossed asteroids out along the way, and so what we see today in the distribution of asteroids, is almost the footprint of the migration of these planets.
Chris Smith: And is this process, perish the thought, still happening today?
David Minton: No, what happened was that the Kuiper belt which was fuelling all this migration eventually ran out of mass, so the Kuiper belt we have today is like Pluto and Ares and some of these objects that themselves have been causing some controversy, they’re sort of the remnants of this ancient more massive disc and there’s almost nothing left out there, so there’s nothing to fuel the migration of the planets any more. And this migration probably happened over a very short period of time, it was probably very brief. It was probably very violent, you wouldn’t have wanted to have been on the earth when this was going on because all these asteroids when they were kicked out of the asteroid belt had to go somewhere, Earth would have been a major target for some of these objects. But that all ended fairly briefly and a very, very long time ago, probably about four billion years ago.
Chris Smith: David Minton from the University of Arizona, tracking what could be some of the largest footprints in the known universe. He’s published that work together with his colleague, Renu Malhotra, in this week’s edition of Nature.
You’re listening to Breaking Science with me, Chris Smith, and it’s time now for this weeks ‘Stuff and Non-Science’, where we massacre myths. And somewhere between lost lake and mineral mist is Diana O’Carroll.
Diana O’Carroll: This week on ‘Stuff and Non-Science’, why are the sea and the sky blue? The old wives tell me it’s because one reflects the other, but no, here’s Martin Chaplin to set those wives straight.
Martin Chaplin: Yes, well the sky being blue clearly does not depend on the reflection of the light from the sea, as it is still blue hundreds of miles from the sea.
The light from the sun consists of all the colours of the rainbow and when they hit water droplets in the sky and clouds they are all reflected, making the clouds white. Now on a clear day, they hit molecules of gas in the atmosphere and the light gets scattered. Now, blue light gets scattered far more than red light and therefore as the light from the sun goes through the atmosphere the blue light gets scattered down to the earth and we see the sky as being blue.
Now water, strangely, perhaps, because lots of people don’t realise it, is actually blue itself as it absorbs red light. You can see it’s clearly blue, if you look through a long tube of water you will see that it is blue, and snow and ice can also look blue as well.
Water can also look blue as a reflection of the sky as well, if the sky is blue so it might look a little bit bluer, and also water can look blue if it’s got small particles in it that can scatter the light, in the same way as the sky looks blue the water will look blue because of the scattering of the light.
Diana O’Carroll: And that was Martin Chaplin, water expert, and he’s based at London South Bank University. And as lovely as the true colour of water is, it still can’t hide the brown of the Thames Estuary. I’ll be back with more mythical non-science next week, and you can email me with your suggestions until then, that’s email@example.com.
Chris Smith: And yet the North Sea still looks as grey as ever. That was Diana O’Carroll with this week’s ‘Stuff and Non-Science’.
That’s it for this time, we’ll be back next week with another round-up of global science news. Don’t forget of course that Breaking Science is produced in association with the Open University, and that means that you can look up anything that we’ve covered in the programme, including all the references, on the OU’s website. That’s at open2.net/breakingscience. And you can also find the way to get there by looking at the BBC Radio 5 Live Up All Night website.
Breaking Science was produced this week by Diana O’Carroll from thenakedscientists.com and I’m Chris Smith. Until next time, goodbye.
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In the news
'In Bad Taste: Evidence for the Oral Origins of Moral Disgust'
by H. A. Chapman, et al
'From Oral to Moral'
by Paul Rozin, Jonathan Haidt, Katrina Fincher
'Cellular prion protein mediates impairment of synaptic plasticity by amyloid-ß oligomers'
by Juha Laurén, et al
'Odor Coding by a Mammalian Receptor Repertoire'
by Harumi Saito, et al (2009) 'Interaction with phosphoinositides confers adaptation onto the TRPV1pain receptor.'
in PLoS Biol 7(2): e1000046. doi:10.1371/journal.pbio.1000046
Dr Gawen Jenkin on ‘Earthworms and in vitro physiologically based extraction tests: complimentary tools for a holistic approach towards understanding risk at arsenic contaminated sites’, by Button M, Watts MJ, Cave M, Harrington CF & Jenkin GRT (2008)., in Environmental Geochemistry and Health. In press. DOI : 10.1007/s10653-008-9208-3.
‘Quantitative arsenic speciation in two species of earthworms from a former mine site’, by Watts MJ, Button M, Brewer TS, Jenkin GRT & Harrington CF (2008) in Journal of Environmental Monitoring, 10 (6), 753-759, DOI:10.1039/B800567B
David Minton on ‘A record of planet migration in the main asteroid belt’, by David A. Minton & Renu Malhotra in Nature
Martin Chaplin for 'Stuff and Non-Science'