Nature Podcast

This is a transcript of the 04th February 2016 edition of the weekly Nature Podcast. Audio files for the current show and archive episodes can be accessed from the Nature Podcast index page (, which also contains details on how to subscribe to the Nature Podcast for FREE, and has troubleshooting top-tips. Send us your feedback to


Kerri Smith: This week cleaning out old cells prolongs life.

Darren Baker: All of the mice that were treated to remove their senescence cells had a life span extension neighbouring from 25–35%.

Adam Levy: And the comedian who has a taking on neuroscience.

Robert Newman: Maybe what we've discovered is the bit of the brain that lights up when we spot an elementary conceptual blunder in experimental design. (Audience laughing).

Kerri Smith: Plus, how re-growing forests could help fight climate change. This is the Nature Podcast, February the 4th 2016. I'm Kerri Smith.

Adam Levy: And I'm Adam Levy.


Adam Levy: Save the rain forest! It's a mantra chanted by environmentalists for decades and there are many good reasons why it's a pretty good idea especially when it comes to climate change. Deforestation accounts for up to 20% of global carbon emissions, so, taking care of forests could help stave off climate change, but what if it's too late? What if an area has already been deforested? Well, Lourens Poorter from the University of Wageningen and his team have been studying how the re-growth of forests, called secondary forests, could factor in. Secondary forests regrow after a forest has experienced some kind of disturbance like a fire or logging or clearing for farmland. Poorter and his team are keen to work out a bit more about the regrowth process and Noah Baker gave him a call. Nature 530, 211–214 (11 February 2016)

Lourens Poorter: Forests are very important. They cover a large part of the terrestrial surface area and they store a large amount of carbon and they're responsible for a large part of terrestrial productivity.

Noah Baker: Now that's why people often refer to deforestation as being pretty catastrophic from a climate change perspective. Is it as simple as that?

Lourens Poorter: Well, I think there are two sides to the coin. I think it's very important to stop deforestation because they are indeed very important source of carbon loss. It's about 20% of what we emit as humans is because of tropical deforestation. But you should also think about the potential of forests to take up carbon again and then you talk about stimulating forest regrowth.

Noah Baker: So the idea there is that you plant new forests and they suck carbon back out of the air again?

Lourens Poorter: Indeed, so there's a tremendous potential for forests to regrow and you can either do that actively by planting, yourself, but you can also do it passively by having nature let its leg work be done.

Noah Baker: And in this paper you've been assessing that potential.

Lourens Poorter: Yeah, what we try to do in this study is to get a comprehensive picture of how fast this recovery is in terms of biomass. So, if you have abundant areas that have been used for agriculture or for cattle ranching, how fast the forest regrows naturally and how much biomass has been taken off – we call that the recovery or resilience of biomass. And we've done so by comparing a number of studies: 45 sites across Latin America. You can imagine that recovery rates are slow in dry areas with poor soil and it can be faster in wet areas with very fertile soils. So it is context dependent and it will vary from place to place, with potential of secondary forest regrowth.

Noah Baker: So how much potential do these secondary forests have when it comes to sucking up carbon?

Lourens Poorter: The sequestration potential is tremendous. So if you have one patch of forest, say one hectare, then in one year it can take up three megagrams or three tonnes of carbon per hectare per year. And that's 11 times as fast as what a normal outgrowth forest does.

Noah Baker: So that suggests to me that we should be cutting down forests and planting new ones, because they suck up carbon faster.

Lourens Poorter: Forests fulfil different functions and services. So these old growth forests, they are wonderful because they store large amounts of carbon. They have these huge, big trees that have lots of carbon inside of them. But what these younger forests are good at is capturing lots of new carbon and fixing it into the system.

Noah Baker: And as part of your paper, you've developed a map to try to assess all these potentials across Latin America.

Lourens Poorter: Indeed, we thought that it would be nice – an input for policy makers and governments or NGOs – to share what the potential is across Latin America. If you imagine you have an area where the forest has been removed and you allow it to regrow – where areas that are hotspots of regeneration, where growth is fast, and areas where there are cool spots – we should be careful because if we destroy the system (it's a very sensitive system) it will take a long time to return to its original values.

Noah Baker: So instead of saying stop all deforestation, we could instead say a slightly more subtle picture which is choose where we utilise forests in a more informed way?

Lourens Poorter: Yes, that's, in effect, the take home message of the paper. We say, value the potential of the secondary forests, so the forests that regrow after land use. And they're not second-hand: they can fulfil viable functions; they can store carbon but they can also recycle water; and they can build-up fertility in the area again. They can store large amounts of biodiversity so they can play a really important role. So we should benefit, for the potential of nature, and let nature regrow where it can regrow.

Noah Baker: So at the end of last year in the Paris climate talks, forests were very much on the agenda. Do you hope that countries will be making use of papers like yours as they go forward?

Lourens Poorter: Yeah, we really do hope so and we made a start with showing this potential biomass recovery map. And we're working on a second paper in which we really show where these young re-growing forests are and how much carbon they can take up at this moment given their climatic conditions. So we hope to give more finely-tuned information to policy makers and many countries have made commitments in Paris that they're going to reforest large areas that have been degraded. So for example, some commitments are that 50 million hectares should be reforested by 2030 and we hope that these kinds of maps can help them to plan better and see where they can use the potential of nature. So we have a kind of nature-based solution in areas where we have natural forest regeneration – and maybe in other areas where we have to help nature a little by planting trees and kick-starting this regeneration process.

Adam Levy: That was Lourens Poorter from Wageningen University in the Netherlands. You can find out more about his study at and his paper features the map he mentioned of resilient places to plant trees.


Kerri Smith: If you had to describe science in one word, 'amusing' might not be top of the list, but comedian Robert Newman disagrees with you. He has just launched his new show and it's all about neuroscience. It's called The Brain Show and it's just as much about the interpretations of brain science as it is about the science itself. Newman has a longstanding interest in science. The Brain Show follows on the heels of a radio series and a book about evolutionary biology. I went to see the show and then Robert dropped into the studio to tell me more.

Kerri Smith: You've long been interested in science. Your comedy has often had scientific themes; have you got a scientific background?

Robert Newman: Well, none at all, but in his 1940s lectures on the dynamics of perception, Wolfgang Köhler extols the virtues of trespassing as a scientific technique, both between different scientific disciplines and from outside science because something that is of special data in one field, when it's put in another field, can have a wider application, or can be a catalyst somewhere else. I see it as trespassing.

Kerri Smith: You're trespassing on science.

Robert Newman: Yes, I guess I'm coming at both evolution and brain science from a sort of philosophy of science point of view.

Kerri Smith: But aside from any philosophical interest there was one event that features in The Brain Show. Let's have a clip from the show now.“At the beginning of 2014, I was one of 35 volunteer subjects who took part in a brain imaging experiment at the University College of London's Galton Lab, about a half a mile north from here in Gower Street. What nobody knew at that time was that this was going to become a famous brain imaging experiment when it was written up in a paper called 'the neurobiology of romantic love'. And so it stuck in my claw, out of 35 volunteer subjects, I alone was written off as a negative result.”(Audience laugh)

Robert Newman: Claiming dramatic license, I put myself in the experiment. I based the description of the experiment exactly on its methodology, the ESP. They were tracking blood flow to look at blood oxygen level dependence of different bits of different neuronal clusters and yes, people had to bring four photographs. One photograph of somebody you're deeply in love with and three photographs of friends that you're fond of but not in love with.

Kerri Smith: And let's just hear the rest of that clip, where you choose to highlight one methodological problem with the study that you immediately encountered.“When you look at a photograph of someone you are deeply in love with, you have all kinds of emotions including guilt, regret, shame, pity, joy, relief, exasperation, delight, all kinds of emotions, all kinds of thoughts as well. I'm looking at this photo and I'm thinking is this is the best picture of me I could have brought?”(Audience laugh)

Kerri Smith: As the anecdote proceeds, it becomes clear that you found some faults in the brain imaging experiment, and this, I have to say, is the bit that made me laugh loudest on the night.

Robert Newman: It gets a very big laugh and I don't mean to be modest but I am very pleased that I have a punch line which is the words: “maybe, maybe what we've discovered is the bit of the brain that lights up when we spot an elementary conceptual blunder in experimental design”.(Audience laugh)

Kerri Smith: I'm intrigued – what's the creative process like, when you've got something as wildly hilarious as a scientific method as your source material.

Robert Newman: Well, trial and error. For about six months you're going and you're trying out stuff. You do these new material nights and the audience are told to come with low expectations and the ticket price is quite cheap. And also you're seeing what connects with people, what makes people's ears prick up as well as 'okay that got a laugh and that didn't.' But you're also seeing, ah, there's something there in that area. They sort of like that. And also my character in the show gets things. There's this character Natasha – when she says will you do this brain experiment into the neurobiology of guilt…I said, to be honest I don't really think the brain works like that. I don't think there's like different bits of the brain that do different things. And she said that's very interesting. She said your view is what in neuroscience is called 'wrong'.(Audience laugh)

Robert Newman: Audiences want something which has got some ideas in it, rather than let's all cheer… Let's be cheerleaders for those clever scientists and laugh at people that we'll never meet in our lives who live in the Southern Bible Belt or something. That sort of crass dichotomy doesn't interest me at all.

Kerri Smith: Having dipped your toes into the water of evolution and now neuroscience, what's next?

Robert Newman: I don't really know what I'll do next. Maybe something about the history of science – history of certain ideas. One of the things I was interested in doing in this show was to look at how, say, with V. S. Ramachandran's ideas about the evolution of smiling, how they absolutely do not come from evolutionary biology. They come from mid-19th century Romanticism.“V.S. Ramachandran, the Dean of Neuroscience. Time Magazine described him as one of the hundred most influential thinkers in the world. He speculates on the evolutionary origins of smiling, which he says evolved from an aborted snarl. He based his theory on no evidence.”

Robert Newman: And it's quite good to look at these – that the Dean of Neuroscience's ideas do not derive from anything anyone would recognise as science.“Instead he says, when one of your ancestral primates… and right there that's a curious choice of phrase isn't it? Not when one of 'our' ancestral primates, but one of 'your'. Clearly he is cut from a superior cloth. We may have come down from the tress; he descended from the mezzanine… Sorry I'm late, I've been inventing verbs and cutlery…”

Robert Newman: Darwin saw this completely differently. In Expression of Emotions in Man and in Animals, Darwin says 'our long habit of uttering reiterated sounds from a sense of pleasure has evolved into the tendency to contract the orbicular and zygomatic muscles whenever any cause excites in us a feeling which, if stronger, would have led to laughter…'

Kerri Smith: May many future audiences utilise their orbicular muscles to laugh at your jokes in the audience.

Robert Newman: Thank you very much.

Kerri Smith: Robert, thank you.

Kerri Smith: Robert Newman is touring The Brain Show around the UK now. Find details and buy tickets at His most recent book The Entirely Accurate Encyclopaedia of Evolution is out now from all good book places.

Adam Levy: Also entering the annals of fun science this week is our new video all about soft squiggy robots. These things could be much more useful than their hard counterparts whenever a delicate touch is called for. Think things like search and rescue missions and surgical procedures. Hit up to watch them wriggle around in a lab in Italy. There's also a feature about soft robots in this week's magazine


Kerri Smith: Keep listening to hear how a bit of spring cleaning for the body could combat ageing, but before that it's time for the Research Highlights with Corie Lok.


Corie Lok: In January of 2014, huge rainstorms and floods hit southern England causing nearly half a billion pounds of property damage. Now researchers have found that human-induced climate change probably contributed to the storms. To figure this out they took a citizen science approach. Volunteers let the researchers use the spare processing time on their personal computers to run simulations of winter weather in southern England. The chance of extremely wet winters was about 43% higher in simulations based on current climate conditions compared to those that modelled pre-industrial times. You can find the study in the journal Nature Climate Change. Nature 530, 8 (04 February 2016)Two species of fungus have survived 18 months in a Mars-like environment on the international space station. The hardy organisms live inside rocks in the Antarctic, one of the harshest places on Earth. So researchers wondered, could the black fungi also withstand a Martian atmosphere? They had dried samples sent up to space station where they were exposed to 95% carbon dioxide and high levels of radiation. Back on Earth the researchers found that less than 10% of the samples were able to divide and form colonies but up to two-thirds of the cells remained intact and even yielded stable DNA. The paper was published in the journal Astrobiology. Nature 530, 8 (04 February 2016)


Adam Levy: Sometimes a theory comes along that makes you think… 'Ah, that seems like such an obvious idea now you've suggested it.' And so it is with Darren Baker and his latest research project. He and his colleagues were interested in ageing and they thought, could we delay ageing and prolong life if we just took out all the old worn-out cells? When cells in the body get old they either kill themselves or they enter a state called senescence: kind of like a suspended animation at the end of their lives. These cells could be harming their neighbours, leading to tissue damage. So the researchers found a way to selectively kill them off in a special mouse model. Darren Baker told reporter Ewen Callaway how he got into doing the study in the first place. It had to do with a particularly haggard-looking mouse. Nature 530, 184–189 (11 February 2016); Nature 530, 164–165 (11 February 2016)

Darren Baker: The way we came into ageing in the first place, we started with a model that was supposed to be a cancer model and instead we ended up looking… The mouse looked awful at five months of age and so that was where our entry into the ageing field came from.

Ewen Callaway: Can you explain what senescent cells are? They kind of sound like worn-out cells.

Darren Baker: That's right. So senescent cells are these damaged, worn-out cells that typically encounter a lot of severe damage. It can undergo basically two distinct cell processes, where one would be an apoptotic response where it just dies and it is removed from the tissue. The other is where it will become a senescence cell and become a permanent resident within tissues and organs. And as you see, if you look in mice, if you look in people, you do see an accumulation of these senescent cells with age, suggesting that they are either efficiently removed early on in our lives or that there is maybe a difference in kinetics later on in our lives where the intrinsic mechanisms that we have to combat these negative cells are maybe failing with age. And then you see these age related accumulations.

Ewen Callaway: And your team tested a, what seems like on the surface a really simple idea: what happens if you get rid of these senescent or worn- out cells. How do you do this?

Darren Baker: We knew that senescent cells were accumulating with age and natural tissues and the thought was, let's just start removing these things starting at midlife in mice and see what the consequences were. We used a transgenic approach. We utilised the expression of a marker that most senescent cells have. That's the expression of a p16 gene that locks cells in this permanent growth arrest and what we used was p16 to drive the expression of a drug-inducible suicide gene. When we add the particular drug it causes activation of the suicide gene and thus triggering the endogenous apoptotic response of a cell to remove it.

Ewen Callaway: And what happens to the health of the mice? Are there any effects from killing off senescent cells?

Darren Baker: There were really no negative consequences. The only thing that we actually found was either no effect in some tissues, but for the most part we found beneficial impacts in a variety of tissues.

Ewen Callaway: So the mice were ageing more healthily? Is that what you say?

Darren Baker: Yes, so what we found is that when we started treating mice at 12 months of age, we just did a consistent treatment to always be removing senescent cells as they were arising. And what we found is that if you looked just at the overall health span of animals that we found at 18 months of age, so after six months of treatment, the treated animals were more exploratory, more active. They had improvements in kidney function and heart function – a variety of things that are benefited in those particular animals and we did some further studies.

Ewen Callaway: Did they live any longer?

Darren Baker: We found that all of the mice that were treated to remove their senescent cells had a lifespan extension, neighbouring from 25 to 35%. In all cases we found that there was a significant health and lifespan extension.

Ewen Callaway: Which is pretty – that's pretty significant. That's what you get from other interventions that have been tested in lab animals, right?

Darren Baker: That is correct. It is on par with what we've seen before in all the well-published and well-known studies. And I think what is also pretty remarkable to think about is when we actually try to quantify the amount of senescent cells that are accumulating within tissues, these things represent a small fraction of the overall number of cells within the tissue. But because of the nature of the things that they're secreting and influencing in other cells within the environment, their effects are magnified.

Ewen Callaway: Could these approaches ever be taken to humans?

Darren Baker: That's a great question. The genetic model we used obviously cannot. So even filling you or I with as much of this particular drug as we used in the study, is going to have no impact because we don't have the suicide gene within us. But there are a variety of groups that we know of that are specifically looking for compounds that can selectively eliminate these senescent cells with age that accumulate in you and I. And so it is not a far-fetched idea to think that there will be things that'll be coming down the pipeline that influence or remove the senescent cells. In this particular experiment what we did was more or less a prevention strategy. So we started treating before the senescent cells were actually there but clear follow-ups would be to take now advanced aged animals, do the same sort of approach where we know senescent cells are there, remove them, and see what the consequences are. It may be good; maybe it might be bad. We're not really sure at the moment.

Adam Levy: That was Darren Baker at the Mayo Clinic in Rochester, Minnesota. The research paper is at and there's a news story about that work too at

Kerri Smith: Time now for our News Chat and joining me in the studio, it's chief news editor Celeste Biever and reporter Ewen Callaway. Now, Celeste first of all you're here to tell us about the Zika virus, the mosquito-borne disease that the World Health Organization (WHO) have just called explosive. They've also said it's likely to spread explosively. Can you just give us a briefing first of all on the outbreak? Nature 530, 13–14 (04 February 2016)

Celeste Biever: Zika as you said is mosquito -borne and has been around in the world for quite a while, but things took a turn last year in 2015 when it arrived in the Americas for the first time. And since then there's been a really big outbreak in Brazil and also some other outbreaks in several of the countries in South and Central America.

Kerri Smith: So it's reasonably common to Asia and Africa already and this is the first time we've seen it in the Americas. Is it dangerous?

Celeste Biever: Well people don't really know. Until it hit the Americas, it was mainly thought to have very mild symptoms. In some people it doesn't have any symptoms; in others headache and a rash. What's causing alarm this time around is there's been this reported surge in a type of birth defect called microcephaly which causes children to have small heads and brains, causing Brazilian authorities to report a possible link between the two.

Kerri Smith: So what they've got so far is just a correlation between some quite alarmingly large numbers of microcephaly compared to the average amounts of cases that are reported. And of course they know that the Zika virus is circulating. But is that all – just a correlation at the moment?

Celeste Biever: Some people don't even think there's a correlation. So the story we wrote this week is about a team in Latin America who are responsible for monitoring birth defects, who have looked at this reported surge which is all based on data from the various states of Brazil looking for microcephaly. And they say they're not so sure that there is a massive rise. This increase in reports could be due in part to the fact that people have a heightened awareness to the condition and so they're more likely to go to the doctors, doctors are more likely to look for it and it's just being diagnosed a lot more, combined with the fact that there is probably some misdiagnosis in there as well. So the diagnostic criteria for microcephaly are quite nebulous I suppose. It's difficult to diagnose things like measuring a baby's head, but there's always going to be errors where a child just has a slightly small head, not because it has microcephaly. So, these guys, in a quite provocative report, have raised the possibility that actually there is no surge. There might be a slight rise, but they're saying most of the reported surge can be attributed to these external effects.

Kerri Smith: What do other epidemiologists make of this report?

Celeste Biever: There's a spectrum of opinion. Most agree that some portion of this surge is going to be inflated over what's really happening. Some kind of agree with these scientists that what they're saying is completely possible. Some sort of say they are reserving judgment until we've got more data and others think that there probably is a big rise though not as big as has been reported.

Kerri Smith: And on the question of more data, I presume there are efforts already ongoing to gather more data as to prospective studies of people who are pregnant now, giving birth and what happens to their babies?

Celeste Biever: Well that's what everyone really wants and what the scientists don't yet have. So, a prospective study in which pregnant women in areas of Brazil experiencing Zika outbreaks are monitored to see how many of their children develop microcephaly. And several of those are underway but nothing has been published and several more are starting, so it's in a pretty early stage and you are absolutely right, that's exactly the thing that's missing.

Kerri Smith: Okay, thanks Celeste and I am going to refer people of course to the News section where we'll be continuing to monitor the Zika story. Ewen Callaway, you're up next and listeners will remember last year's coverage of the researchers who edited genes in human embryos with this technique called CRISPR. The latest is an approval for a similar study in the UK. Nature 530, 18 (04 February 2016)

Ewen Callaway: This week, UK regulatory authorities have given the go ahead to researchers at the Francis Crick Institute to do some experiments using CRISPR to modify the genomes of viable human embryos.

Kerri Smith: Now in the previous case, the team of Chinese researchers had used non-viable human embryos (embryos that were never going to be able to develop into babies). There's a difference here, isn't there, but they will be making sure, obviously, that this is not any attempt to edit the genome of something that will go onto be a baby.

Ewen Callaway: No, these are absolutely, without a doubt not CRISPR babies. The embryos come from IVF clinics in Britain. The people – the couples – who are donating them have agreed to have their surplus embryos donated for research and the research will stop after about a week and it can go no longer than two weeks. This is around the stage when a developing embryo would be implanted on the uterus – the so called blastocyst stage.

Kerri Smith: And what are they studying, these researchers? Why do they need to edit the embryos with CRISPR?

Ewen Callaway: They are interested in very early development, very early human development; what happens in this first seven or so days because when an egg is fertilized by a sperm it starts dividing and dividing and dividing and only a subset of these cells actually go on to form the foetus, the baby. A lot of the cells go onto form placenta, and so they're kind of interested in what's going on, what are the master regulators that are determining these very early cellular fates. It's quite common for pregnancy to terminate early and the hope is that by understanding the biology of the very early stages of pregnancy, maybe you can come up with ways of dealing with problems like early termination. In Britain at least and in some other countries, it's acceptable to do research on viable human embryos. We've made that decision before in the past given what we can learn from them. So a lot of the people are saying with that precedent, this research should be uncontroversial. Of course nothing is uncontroversial when we're talking about CRISPR and embryos. And so, I mean I haven't spoken with anybody who's opposed to this research but I am sure there will be people out there who say we shouldn't be doing any research at all on human embryos even if it has no chance of ever forming a live human being.

Kerri Smith: Do you think that here in the UK where this approval has gone through and perhaps even elsewhere in the world, this kind of project will be more likely to get approval?

Ewen Callaway: Yes. I think a lot of UK scientists were waiting for this decision to be made. One researcher has told me that he's heard from people who'll maybe soon submit applications to do their own research on human embryos. In other countries… there are some countries where, like in Britain, there are regulations that limit it. And this decision might embolden them to apply for permission. In other countries such as the United States, there are no laws prohibiting people from doing this for research. They can't get federal funding for it but there are no laws preventing them. So maybe this could spur them to go ahead and do it. I think the same goes for China where the early experiment you talked about went for it, so we might see some more papers coming out from China reporting efforts to modify the genomes of human embryos.

Kerri Smith: Now of course we've been talking about using CRISPR for research. It's a very important distinction to make between research and then any reproductive use it might be put to. Does this open the door to these other reproductive uses?

Ewen Callaway: Sort of. As you state, this is all about research. Britain's regulators have said… it remains illegal to modify the genome of a baby in Britain and this decision changes nothing. But what people have told me is that in doing this research to understand early pregnancy we can figure out if it's even possible to use CRISPR on human embryos. You'll remember that the one experiment that has been published from scientists in China found that it was both inefficient and error-prone. Research like this could provide tactical information, if you wanted to do germline modification.

Kerri Smith: Okay, thank you to Ewen Callaway and to Celeste Biever for joining me and as always you can find those stories and much more over at

Adam Levy: Don't forget to check out our YouTube Channel as well, where last week's video on the computer that can play the board game “Go” is still getting a lot of attention. Also, because, robots. I'm Adam Levy.

Kerri Smith: And I'm Kerri Smith.