The team reveals why we pay too much in auctions and how moving continents can cause climate change. In this episode it is also explained how a deadly frog fungus has been spread from pregnancy tests.
Plus in 'Stuff and Non-Science', does shaving your hair make it grow back thicker and stronger?
Chris Smith: Hello. Welcome to the Naked Scientists Up all Night with me, Chris Smith. On the way, why despite the fact that you really didn’t want it you still ended up paying over the odds for that James Blunt CD you bought on an internet auction site.
Kat Arney: Well this suggests that actually the prospect of losing the competition of the auction leads people to bid too high, so it’s a sort of a social oh my God, I’m going to lose, you know, I must kind of go for it and bid as high as I can.
Chris Smith: Yes, scientists have got to the bottom of why we can’t help ourselves in the auction room. That’s coming up. Also this week, a new theory of what causes ice ages.
Dennis Kent: In the Cenozoic, which is the interval of the last 65 million years of Earth history, the first 30 million years or so ago was warm, quite warm in fact, and then the latter half, the last 35 million years has been cold. The key question is why, and then second question is why did it turn cold?
Chris Smith: And apparently it’s all India’s fault, and we’ll be finding out why later in the show when we’ll also be hearing about a deadly disease threatening frogs and toads everywhere.
Matt Fisher: To stem this global decline in amphibians, we’re going to have to take species into captive breeding programmes. But what our study’s saying is that we have to guard against known but we also have to guard against unknown threats because we actually don’t know what’s inside a living body a lot of the time and it only becomes clear later that there was some unknown nasty there that we really didn’t want.
Chris Smith: That’s all on the way in this week’s Naked Scientists Up all Night. First though, let’s take a look at some of the other scientific discoveries from around the world with our science guru, Kat Arney. Kat, scientists are saying there’s potentially a link between a desire to overeat and alcoholism.
Kat Arney: Yes, there is indeed. Now if you’re feeling peckish it is probably down to a hormone called ghrelin which is produced in the stomach. It’s ghrelin that makes us feel hungry by stimulating the urge to eat and now researchers at the University of Gothenburg have discovered that ghrelin might also play a role in addictive behaviours, including alcohol addiction. So scientists have previously shown that levels of ghrelin in the blood change in people with addictive behaviours such as alcoholism and compulsive over-eating and this led Jorgen Engel and his team to suspect that ghrelin might be involved in many addictive behaviours, including addictive gambling and drug dependence, and these involve the brain’s reward system so they set about looking for a link between ghrelin and alcohol dependency.
Chris Smith: Where does ghrelin normally come from?
Kat Arney: Well ghrelin is normally produced in the stomach but there is some produced in the brain as well. It’s a really fascinating hormone so to find out how it was actually involved they recruited 279 healthy people and they also recruited 138 very heavy drinkers who’d been admitted to hospital for treatment, and then they took a really detailed look at the DNA that encoded the ghrelin receptor, called GHSR1A, in these people and the team found that a certain version of the gene was heavily linked to heavy alcohol consumption. They also discovered that another variation of the gene and another variation of the ghrelin gene itself were also linked to an increased body mass in people who drank heavily.
Chris Smith: So what are the implications of this?
Kat Arney: Well this suggests that carriers of these genetic variants are more susceptible to having multiple addictive behaviours such as alcohol dependence along with over-eating, and the researchers hope that their results will shed light on the links between different addictive behaviours. And of course, there’s also the possibility of developing new drugs for alcohol dependence or compulsive eating based on blocking certain versions of ghrelin or its receptor.
Chris Smith: And in these populations such as aboriginals in Australia who seem to have an increased risk of alcoholism, the Pema Indians in the Americas who seem to have a preponderance to develop excess body fat, are they going to study those populations and see if they hold the key to or to see if this particular hormone’s involved there too?
Kat Arney: Well I don’t know what the team’s plans are exactly but that certainly sounds like a good avenue for exploration, definitely.
Chris Smith: Well talking about looking at different populations around the world, there’s interesting evidence surfaced this week and the University of Arizona is saying it’s definitely a woman’s world.
Kat Arney: It certainly is. Well at least when it comes down to genetics. And the researchers at the University have found that women are more successful on average at passing on their genes to the next generation, and this is because over an evolutionary timescale, we’re talking thousands and thousands of years, males tend to father children with multiple females. This is known as polygyny, and this occurs at the expense of less successful chaps.
The researchers have found that polygyny has led to excessive genetic diversity on the X chromosome. Now, females have two X chromosomes, and that determines our sex, and males only have one. In a population with an equal number of breeding males and females you would expect to find an equal amount of diversity on the X chromosomes compared with non-sex chromosomes. Those are autozomes.
So writing in the journal PLoS Genetics, the researchers measured genetic diversity on the X chromosomes and autozomes in 90 people from six different populations. They looked at the Biaka people from the Central African Republic, the Mandenkas from Senegal, San people from Namibia, the French Basques, Han Chinese and Melanesians from Papua New Guinea, and looking at all the variation they found and considering a lot of alternative explanations, they discovered that only polygyny could really account for the patterns that they saw. So this means that over years through our ancestry as humans, it looks like men have, er, been doing it with lots and lots of ladies and this has had implications in our genetic diversity.
Chris Smith: Well the thing is, couldn’t people have said well I could have told you that because women have to have children because men can’t, and therefore if you have any man that doesn’t have a child with a woman then automatically his genes are going to disappear?
Kat Arney: Absolutely, but it does show that, you know, it’s one man to lots of ladies through our evolutionary history. And it’s got quite big implications as to how these sort of subtle sex-based forces can shape our genomes over time, and also it really highlights how mutations will sweep through populations maybe from one man through to many women and their descendants.
Chris Smith: Well certainly food for thought that one isn’t it, but what about this story about breast cancer in the UK and the fact that there’s, although figures are looking more rosy all the time in terms of survival in total there’s actually a bigger and bigger gulf opening up between rich and poor in terms of how people do?
Kat Arney: Yes, that’s very true. The latest statistics do show that long-term breast cancer survival is definitely on the rise in the UK, and now more than eight out of ten women with the disease will survive for at least five years or longer. There’s still a worrying gap in survival between the richest and the poorest. And now writing in a special supplement in the British Journal of Cancer, Professor Michel Coleman and his team have been analysing data from more than 380,000 women who were diagnosed with breast cancer in England and Wales between 1986 and 1999, and after they’d corrected for other causes of death they found that even after one year survival rates were higher among more affluent women compared with the poorest, and this gap doubled five years after diagnosis.
Chris Smith: But why?
Kat Arney: Well, you know, it’s interesting because although many cancers show a gap in survival between the most and the least affluent, breast cancer’s the only one where this gap widens. Researchers think that the initial gap in survival at just one year might be due to late diagnosis; for example, women not going early to the doctor, not going for screening or having delays in diagnosis once they have gone to the doctor, though we really need to investigate this a lot more thoroughly. But when it comes to the longer term survival gap between rich and poor things are slightly more complicated.
Now, it may be that poorer women don’t get the best treatment. For example, it can be very difficult and very expensive to get to hospital on a daily basis for radiotherapy appointments which you have to do if you’re being treated for breast cancer. They may also be more likely to suffer from other diseases such as lung conditions, heart conditions that affect cancer treatment, what you can give people, and also affect survival. But at the moment this is really just speculation.
Chris Smith: I was going to say, do you think it comes down to education as well because people who are probably more affluent may have a slightly higher educational standard and therefore they might know the best way to get treatment, they might know the best treatments to put themselves on, they might even know the best surgeon.
Kat Arney: Well we certainly know that that’s some of it. There’s some very interesting studies being done into attitudes between the richest and the poorest people into cancer, and there’s this prevailing attitude of fatalism among people from the lower social groups, that they think well if it’s going to get me it’s just going to get me, you know, and not really looking into it. But hopefully we should know a lot more about how social groups, demographics influence cancer and cancer survival because recently we saw the launch of the National Cancer Intelligence Network, and that’s a network that’s going to be gathering much more information and statistics about cancer, its treatment and its survival here in the UK, and until we’ve got that data we can’t really work on effective ways to narrow it.
Chris Smith: Well the thing that’s emerged in recent years is that breast cancer isn’t just one disease, it’s a whole collection of different diseases, some people will respond to one drug, some to another. So do you think that the disease that the rich people are getting is a different kind of disease than that which the poorer people are getting, probably because of other risk factors in their lifestyle and that accounts for the difference?
Kat Arney: That’s certainly an interesting idea but at the moment we just don’t have the evidence to support it. It’s really very recently that the idea that breast cancer is many, many different diseases has come about and I don’t think the research has been done to try and pin different types down to different social groups.
Chris Smith: It’s certainly an interesting study. You can follow that one up in the British Journal of Cancer this week. And finally Kat, a paper in Science this week, very exciting as an eBayer myself, scientists have got to the bottom of why we tend to indulge in bidding wars.
Kat Arney: Absolutely. If you’ve ever got into a bidding war on eBay or in a real-life auction house, you’ll know how quickly bids can rise, and economists have known for a while that people tend to over-bid in auctions, bidding more than an object’s worth.
Now, by using brain imaging techniques, researchers at New York University have managed to study this in greater detail, bringing economics and neuroscience closer together than ever before. And writing in the journal Science, the scientists use functional magnetic resonance imaging, known as FMRI, to examine patterns of brain activation as volunteers played either an auction game with a partner or a pure chance lottery game, and in both games participants could win money but in the auction game winning depended on out-bidding a partner. And when the researchers looked at the striatum, that’s the part of the brain involved in reward, they found that a higher response in the striatum was seen when players made a loss in the auction game and it was higher the higher they tended to over-bid.
Chris Smith: So why was the brain’s reward centre getting more active if they lost?
Kat Arney: Well this suggests that actually the prospect of losing the competition of the auction leads people to bid too high, so it’s a sort of a social oh my God, I’m going to lose, you know, I must kind of go for it and bid as high as I can, even if it's subconscious. And to confirm this the economists carried out a follow-up study with three groups of volunteers playing an auction game again. One group just made bids as normal, the second group were told they would get a bonus if they won, while a third group were told they would lose money if they failed to win the auction, and essentially these are basically the same outcomes, the last two scenarios, although they’re framed differently.
In one case you’ll lose and in the other case, you know, you’ll win more money if you win. The researchers found that people in the group that would lose money if they lost the auction consistently bid higher than people in the other groups, and this confirms that the fear of losing is actually driving people to over-bid excessively. And the scientists say that these results are highlighting a role for the contemplation of social loss in understanding the tendency to bid too high in auctions, and it shows that we should consider social factors in economic decisions.
Chris Smith: And of course the fact that, and we almost started on this point, gambling’s addictive.
Kat Arney: It certainly is, and maybe it’s that sort of compulsion not to lose may be a driving force as well.
Chris Smith: Thank you, Kat. That was Kat Arney with some of this week’s top science news stories. And if you’d like to follow up on any of those items, they’re all on the web at open2.net/nakedscientists. This is the Naked Scientists Up all Night with me, Chris Smith. Coming up shortly, the infection that’s threatening frogs and toads worldwide, and we’ll also be finding out whether shaving your legs really does make the hair grow back thicker and faster. First though, to a discovery that might explain what causes ice ages. It turns out that plate tectonics and the movements of continents over millions of years could have a lot to do with it. Here’s Dennis Kent.
Dennis Kent: In the Cenozoic, which is the interval of the last 65 million years of Earth history, the first 30 million years or so ago was warm, quite warm in fact, and then the latter half, the last 35 million years, has been cold. The key question is why, and then the second question is why did it turn cold?
Chris Smith: And how are you trying to get a handle on that?
Dennis Kent: There is mounting evidence this is the CO2 problem, that CO2 is probably the chief cause of this; that is when you have high CO2 contents in the atmosphere the greenhouse effect is higher and the climate is warmer, so this would be applicable to the early stage of the Cenozoic from about 65 to 35 million years ago, and carbon dioxide then presumably went down and this started our present ice ages. So the question then became what caused the carbon dioxide to go up and down, and a story, a hypothesis, a scenario, is that it’s India moving northward and it’s not just India moving north but there’s a vast sea called Tethys that was between Asia and India that was consumed in subduction, and in the consumption of this vast ocean was a carpet of carbonate sediments from micro-organisms that had just in fact evolved and proliferated through the water column and they essentially capture CO2.
When they die, they end up as sediment at the bottom of the ocean but when these ocean sediments with the oceanic crust is consumed in these subduction zones the metamorphism or the heat of being plunged into the Earth allows some of the CO2 to evolve and come back out through volcanoes. And so the net result is there was an increase in carbon dioxide to the atmosphere and this we think was what caused the unusually warm conditions in the early part of the era.
Chris Smith: So India wasn’t always where it is now?
Dennis Kent: No, India’s a far traveller. It started out well in the Southern hemisphere, and from about 120 million years to 50 million years it travelled many thousand kilometres.
Chris Smith: So India starts off way down south near the Antarctic, it’s moving northwards. As it moves northwards the carbonate-rich sea which is in front of it gets swallowed up and that turns into CO2 keeping the CO2 in the atmosphere high, and then what happens when India actually meets Asia and the ocean that it was swallowing up has all gone?
Dennis Kent: That’s a critical point because we know from other evidence that the peak warm period is about 50 million years ago, and this is precisely the time at which India collides with Asia from geologic evidence in the literature, so that when India slams into Asia the subduction or the consumption of oceanic crust stops, there’s no further ocean crust to be consumed.
Chris Smith: And after that global CO2 starts to fall and the temperature falls in sympathy?
Dennis Kent: That’s correct. And the additional factor, which is more speculative but we think it is important, is this occurs very close to the Equator and near the Equator is where, it’s essentially the heat engine of the Earth climatologically speaking, and it’s where due to the higher warmth from the Sun you have also higher precipitation, and this makes conditions ideal for weathering of rocks. And weathering is the primary means by which carbon dioxide ultimately is taken out of the atmosphere to keep it in balance, by reacting with the silicate rocks and eventually being deposited as calcium carbonate.
Chris Smith: So your theory would be then that when we have low CO2 because there’s not much CO2 being produced but it’s all being consumed you then get a big dip in CO2, you get a dip in global temperature and that triggers an ice age?
Dennis Kent: That’s correct. When the weathering machine is enhanced by putting continental crust by continental drift into this regime there’s really no control on how much weathering will occur as long as the continental crust stays there, and so this allows CO2 levels to plunge and this is what may start an ice age. And these ice ages last typically tens of millions of years, as the one we’re in now and as the one that occurred, the last major one was 300 million years ago, and so they last on a same timescale as continental drift occurs so it’s not until continents rearrange their positions and take some of the continental crust out of the high weathering regimes can you get a return to more warmer conditions that more typify the rest of the geologic time.
Chris Smith: Dennis Kent from Rutgers University in the US showing that continental collisions can cause ice ages. That work’s published this week in the journal, PNAS. Now talking of global phenomena, it looks like our efforts to save endangered species can sometimes do more harm than good, especially if we don’t pay attention to, as Donald Rumsfeld referred to them as, the unknown unknowns. Amphibians like frogs and toads are in trouble and it looks like it could be our fault. Here’s Matt Fisher.
Matt Fisher: Globally, amphibians have been undergoing these extraordinary declines, in fact they’re the vertebrate group which is most at risk of mass extinction at the moment. This is the largest mass extinction since we lost the dinosaurs and there’s been huge question marks about why amphibians have been declining so fast. And it turns out, briefly, that there’s been an unrecognised emerging infectious disease which has been sweeping around the world and causing a lot of these species declines, and in some cases indeed extinctions.
The disease is a basal lineage of the fungi, so it’s right at the kind of the origins of when fungi evolved, and it’s a chytrid, which means it’s a swimming fungus that has little tadpole-type zoospores which swim through water and these zoospores infect amphibians and they live in the amphibian skin, and in some cases they cause disease.
Chris Smith: In what way do they compromise the animals?
Matt Fisher: Well it’s still, a lot of question marks hanging over this, but it seems that by interfering with the natural function of the amphibian’s skin they interfere with the absorption of water and of course oxygen, so amphibians because they live in damp environments actually process a lot of their environmental needs through their skin rather than lungs as we do.
Chris Smith: And why is this fungus suddenly becoming a problem, because amphibians have been on Earth for millions of years so why now are they having this problem?
Matt Fisher: The best idea that’s come about so far about where the fungus has originally come from is probably South Africa, because this is where the earliest records of the fungus are from the 1930s. And also there’s been a huge trade in amphibians from South Africa since the 1930s, and this is because the principal species, which is Xenopus, the African Clawed Toad, used to be used as a pregnancy test and they were spread all around the world as a result, and if they were infected with the fungus they could have spread the fungus with them.
Chris Smith: And so this means that we’re now desperately trying to undo that bit of damage we’ve done and basically bring some of these species back from the brink of extinction, and you’re saying there might be a problem with that?
Matt Fisher: Well yes. Alarm bells were raised when we started looking at some of the very rare species in Europe, and specifically this paper is about the Majorcan Midwife Toads. It’s only found in the island of Majorca and until the 1970s was actually thought to be extinct, but then herpetologists discovered these relict populations existing in these very deep inaccessible gorges in the mountains of the far north of the island. So as soon as the species was found then the conservation community went into overdrive and captive breeding programmes were set up, and at this point the fungus became a problem.
Chris Smith: So in what way do you think that the captive breeding programme was fuelling the fungus problem?
Matt Fisher: We surveyed the populations in the island and we found that only two of them had very high levels of infection, so the majority of infection was clustered, very tightly clustered into these two adjacent valleys. So we then asked what was unusual about these valleys, and it turns out that one of these sites had received a large number of animals from the captive breeding programme which had started introducing animals in the 1980s. So we thought ah-ha, maybe this actually explains some of what we’re seeing.
We then went back to the records of the captive breeding programme, and we went back through time and we saw that these animals that had been introduced to the wild in the 1980s had suffered very high mortality in around about 1989 and 1991, and it was at that point that we were able to do our DNA tests and we were also be able to do a microscopy on the skin of these archived amphibians and we showed that they were infected with chytrid fungus.
Chris Smith: So if the programme to spare them was responsible for getting the fungus into them in the first place, where did it come from?
Matt Fisher: Well this is where we really don’t exactly know. What we do know is that this fungus is very, very transmissible so it can jump between species very easily. In 1989 in these zoos there wasn’t this recognition that there is now that there were these infectious diseases which are likely to cause these problems and these diseases in natural populations, so the Majorcan Midwife Toads were co-housed with other species, in particular species Xenopus from Africa. It turns out that those African animals were also infected with the fungus at the same time as these captively-bred Majorcan Midwives, so here it’s very, it’s highly possible that these African Xenopus transferred their infection to the Majorcan Midwives which were then shipped to Majorca to bolster these natural populations of the Majorcan Midwife Toads, and that was when the disease was introduced into the island in this particular site.
Chris Smith: There’s an important conservation lesson in there for us isn’t there?
Matt Fisher: There’s a very important conservation lesson here. Yes, I mean what’s increasingly recognised is that to stem this global decline in amphibians we’re going to have to take species into captive breeding programmes, but I suppose what our study’s saying is that we have to guard against known but we also have to guard against unknown threats because we actually don’t know what’s inside a living body a lot of the time and it only becomes clear later that there was something, some unknown nasty there that we really didn’t want to carry along with our reintroductions.
Chris Smith: Imperial College’s Matt Fisher on the pitfalls of species reintroduction. He’s published that work this week in the journal Current Biology. You’re listening to the Naked Scientist Up all Night with me, Chris Smith, and it’s time now for this week’s Stuff and Nonscience where we blitz myths and bash bad science, and this time we have for you a hairy take on the world of waxing, shaving and bikini lines. Here’s Diana O’Carroll.
Diana O’Carroll: Welcome to another bout of 'Stuff and Non-Science', where it’s time to deconstruct the myth of shaving your hair. Legend has it that shaving legs, faces, underarms and everywhere else causes the hair to grow back thicker. Not so, as Professor Des Tobin of Bradford University will tell you.
Professor Des Tobin: Unfortunately it is a myth that the hair grows back any thicker after even close shaving. The reason why the individual may experience what they think is thicker hair growth is because of the sharp edge of the regrowing hair. Normally, your hair tapers to a fine, rather smooth point, therefore if it’s uncut it will feel more fine and soft to the touch but if you cut it you’ll cut it across the thicker regions and also it’ll be sharp to the touch and therefore give the impression of a more robust regrowth, but in fact the hair is exactly the same as if you didn’t actually cut it at all.
Diana O’Carroll: Another bit of nonscience stuffed. Your shaven hair won’t grow back thicker, only sharper. If you want to find the truth behind a science myth, then email me at firstname.lastname@example.org.
Chris Smith: Thanks Diana. That’s Diana O’Carroll from the Naked Scientists. More Stuff and Nonscience next week. Well that’s it for this time, we’re back at the same time next week with another look at the world’s hottest science. The Naked Scientists Up all Night is produced in association with the Open University and that means that you can follow up any of the stories and items that you hear here on the programme via the Open University’s website at open2.net/nakedscientists. You can also get there by following the links in the BBC Radio 5 Live Up all Night pages. Production this week was by Diana O’Carroll from nakedscientists.com and I’m Chris Smith. Until next time, goodbye.
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Pallavi Annand explores climate change in From hothouse to icehouse.
Delve deeper into the stories featured in the programme with these references.
In the news
'Understanding Overbidding: Using the Neural Circuitry of Reward to Design Economic Auctions,'
by M Delgado, A Schotter, EA Phelps and EY Ozbay
in Science (No 5897 - 26 September 2008, pages 1849-1852)
'Peptide ghrelin may be involved in both alcohol dependence and overeating'
from 'Association of Pro-Ghrelin and GHS-R1A Gene Polymorphisms and Haplotypes with Heavy Alcohol-Use and Body Mass'
in Alcoholism: Clinical & Experimental Research (December, 2008)
'Sex-Biased Evolutionary Forces Shape Genomic Patterns of Human Diversity'
by MF Hammer, FL Mendez, MP Cox, AE Woerner and JD Wall
in PLoS Genetics 4(9)
Survival from cancer of the breast in women in England and Wales up to 2001
by M J Quinn, N Cooper, B Rachet, E Mitry and MP Coleman
in BJC (British Journal of Cancer) 99 (2008): S53-S55
Dennis Kent on 'Equatorial convergence of India and early Cenozoic climate trends', by Dennis V Kent and Giovanni Muttoni in PNAS (published ahead of print September 22, 2008)
Matt Fisher for 'Invasive pathogens threaten species recovery programs', by Susan F Walker et al in Current Biology Vol 18 No 18, September 23, 2008
Professor Des Tobin for 'Stuff and Non-Science'