Andy Dobson on Disease Ecology & Conservation Strategy

Episode Notes

Physics usually gets the credit for grand unifying theories and the search for universal laws…but looking past the arbitrary boundaries between the sciences, it’s just as true that ecological research reveals deep patterns in the energy and information structures of our cosmos. There are profound analogies to draw from how evolving living systems organize themselves. And at the intersection of biology and physics, epidemiology and economics, new strategies for conservation and development emerge to guide us through the needle’s eye, away from global poverty and ecological catastrophe and toward a healthier and wealthier tomorrow…

This week’s guest is SFI External Professor Andy Dobson of Princeton University, whose work focuses on food webs, parasites, and infectious diseases to help us understand and better manage the complexities of climate change and urban growth, human-wildlife interactions, and the spread of pathogens. In this episode we talk about how network structures can inhibit or accelerate disease transmission, the link between biodiversity and economic growth, and how complex systems thinking leads to better wildlife conservation.

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Episode Transcription

Michael: Andy Dobson, it’s a pleasure to have you join us on Complexity Podcast. What are you doing at SFI this week? What's your visit?

Andy: This week we are in a workshop that's part of the 'hour of time sequence'. And so specifically we're looking at immunity and aging. Trying to understand how your ability to fight diseases or fight cells in your body changes as you age and my own particular interest, that is how species of different body size handle that problem.

Michael: Yeah. Actually your work on scale as a variable in the primate disease paper, I thought that was an interesting thing. We'll touch on that. But first before we start I'd like to ask how you got into the research that you're doing, how you became a scientist and how you ended up working with diseases.

Andy: I think I was very lucky in that I was playing in a rock group in London. I was actually starting a Masters in Oceanography in Southampton and I was having to hitch lifts up and down in the classic British pouring rain. So I thought it would be better to find a job in London. And I was lucky enough to start working with a brilliant scientist called Roy Anderson at the beginning of his career. And he, together with that Bob May, who has a long association with SFI were developing theory, a better theory for understanding the population dynamics of infectious diseases. So in order to live in London, I started working as Roy's research assistant and I just realized that was going to be so much more interesting than working as a musician.

Michael: Well, in spite of some of the comments that you make in this paper on the Yellowstone wolf population, there's probably more stable funding as a researcher than as a musician.

Andy: Not certainly the case. Any form of funding is never stable. But I think long term there's more funding, particularly when you get a faculty job that funding, knowing that you've got finances to at least put food on the table helps.

Michael: So given that obviously universality and thinking across disciplines is a key theme here at SFI and on this podcast in particular, I'd like to start with some statements that you made in this paper for PLOS on Yellowstone wolves and the forces that structure natural systems. You made a really interesting comment that comparing the kind of theoretical work that you do to the kind of theoretical work that's being done at CERN and other physics institutions seeking these general principles. And I'd love to hear you discuss that a little bit and how you see those things as related to one another.

Andy: Well, I do have immense respect for the work that's done in CERN and work that's done by physicist. I feel that the urgent problems we have, I try to understand how natural biological systems work and how can we take tools, particularly mathematical tools from physics and apply them to natural ecosystems. And straight away when we start trying to do that, we realize that they fit perfectly into the SFI mandate and the natural systems such as Yellowstone or the Serengeti are naturally complex. They have many components that interact with each other at different nonlinear speeds. So we need to develop the type of mathematics and approach that's used at SFI to understand these systems.

Michael: Yeah. I like that you compare the search for the Higgs boson to trophic network research and the idea that really the main thing differentiating these two forms of research are the scale of the phenomena that are being explored. Can you get in a little bit more about that.

Andy: Yeah. The physicists are very much focused on doing things at heroic scales. The scale of the universe or tiny, tiny little scales. So I think ecologists are tended to be perceived as not doing things that are heroic because we doing them on physical sizes that are similar to ourselves. Yet the irony of that is that understanding how those systems work and having a deeper theoretical understanding so as we can manage them better is crucial. As people like Greta Thunberg will tell us we have about 10 years to solve those problems. Whereas the wait for Higgs boson can go on for a century. It can go on if we haven't solved those problems of how we manage the natural world properly.

Michael: I don't know if you would find this a fair line to draw, but I'm sure you're familiar with some of the work that Jessica Flack has been doing lately and her provocative comments, that rather than complexity of being a sort of informational hierarchy of emergence that it may have more to do with us being at the center of this hourglass. That we're at an information bottleneck and that when our tools improve, we find as much complexity in the microscopic or the macroscopic as we do at the meso level.

Andy: Yeah. I think that's a very important insight. And we see that and in particularly with the workshop this week, once we realized that there's this whole community of organisms living in humans or other animal and plant species, the microbiome, we realized there's as much biodiversity inside us as there is outside that we're trying to save.

Michael: On that note, it seems like a good place to start exploring your research and discussing it in this paper that you co-authored for Science Magazine’s Research Reports on a general consumer resource population model.

Andy: Right.

Michael: And this is a really clear example of the idea that really what we're looking for as David Krakauer said in the first episode of the show is compact, elegant, encodings to describe what we observe in nature, as simple as possible but no simpler than adequate. And so what you and your co-authors have done here is put together a really interesting general model for how organisms independent of their... we tend to think in terms of like heterotrophic predator-prey relationships, the Lotka-Volterra model. And you make, I think, a really smart argument here that that's a profound oversimplification. That it's not general enough. So could you explore this for me?

Andy: The goal for doing that very much goes back to work on food webs. Similar things to Jennifer Dunne has been doing here. That is the central core of work we need to understand how places like Yellowstone work, how places like the Serengeti work. We need models for food webs. They will always have two components. The geometry of the web and how different species are coupled together to give some geometric pattern and that geometry will tell you something about stability, but you also need a generalized mathematical function that tells you about the scaffolding poles if you like, the couple the different species together.

And so what we were trying to say is, sometimes those relationships, the predator-prey relationships, sometimes they're virus and host relationships, sometimes they're elk eating grass. Could we have a general form for those equations? Because people have tended to use, starting with the Lokta-Volterra equations, different variants on those. Now is there an underlying set of equations which could collapse them to give you any of the other types of equations, but you could use them for any type of interaction? And hopefully the thing that would determine the way they collapse down would be the relative body size of the predator or prey or more generally the consumer and the resource that they're consuming. So it's an attempt to find a general set of functions that could be used to couple together the geometry of food webs.

Michael: One of things I really enjoyed about this was how it brings to light how these types of relationships may change over the lifespan of an organism. That you get partitioning between different life stages of a single creature or you get even at a single phase in an organism's life, it may have different types of consumer-resource relationships, like the leech, right. Is this example where it's a predator sometimes and it's a micro predator at other times, so how are you seeing or how are you imagining this shedding new light on the way that we understand these trophic networks and how we can start to use this additional dimensionality to explain some of the complexity that we see in ecology.

Andy: We hope that that approach will help in several ways. One, it even relates particularly to the working group we're looking at this week, the age and immunity. Because one of the classic things with consumer-resource, predator-prey relationships is that a predator only eats you once. You spend a lot of your life being scared and worried about the lion that might be out there or a crocodile, but that's a one-off interaction. You may only lose a limb. But in contrast to that, you are steadily accumulating a bunch of parasites and pathogens. You may only have a transient relationship with an influenza virus for a week but it changes your immune system in a way that modifies how it will react to another attack by a tiny little predator type thing, like the next flu virus to come along.

If you get a worm, which is a not too tragic a thing to happen, but you've got that as a companion for the next five to 10 years, and that also modifies the way that A your immune system operates, and B the amount of food that's available to you, you sharing it effectively in the worm through that period of time. And people living in Africa and South America have a whole community of pets living in their guts that they're sharing their food with. So it's looking at how do we understand… from a food web perspective, how much energy is going into the parasitic species, of which there may be a huge diversity versus along the traditional herbivores eating plants, carnivores eating herbivores, lines of the food web. So it gives you a mechanism of looking at the dynamics of those things and understanding how they affect energy flow.

Michael: This seems like it also might illuminate how different lineages have shifted in their strategy over time. Like where a predator or a micropredator may become a parasite over same period.

Andy: Right. Yeah. Well, that does seem to be… One of the things we were able to do in that paper. Was to say, because we can show these general equations class down in different ways, there's effectively a phylogeny in the way that different consumer resource relationships are related. And that very much splits with this bifurcation of being eaten from the outside-in versus from the inside-out. We also find that the evolution of parasitism seems to be very much tied in with the species that were originally living on decomposing bodies.

Most of the species that have evolved to be some form of pathogen are things that have ancestors that were feeding on decomposers and decided just to move into the thing that became their host while it was still alive, and then feed on it while it's still alive. And we're talking in evolutionary time here rather than in the course of the lifespan of an organism. And in the end, having a sort of interaction, a co-evolutionary interaction with it. Let’s keep it alive a bit longer because it'll keep feeding us if it's alive. Whereas if it's dead, we'll have to go and find another one to feed on.

Michael: Right. Kind of similarly, you brought up Jennifer Dunne and the way that she and her colleagues have started including “use webs” into their trophic networks. Not just, “We're feeding on this thing,” but, “We might be harvesting living animals for resources,” shearing sheep and that kind of thing. So, I mean it's not a long jump from this kind of general model to economic evaluations and looking at different kinds of economic relationships, corporate mergers, the way that different human agencies depend on one another, the way different human communities depend on one another. Have you and your colleagues worked much on that?

Andy: No. It's something we're starting to work on. I've started working with economists in France. We were beginning to look at, can we make models for decisions that people living in poverty make and that are affected by the economic services they get from the biodiversity around them? Whereas at the same time, some of the decisions they make will reduce that biodiversity. So can we begin to develop economic theory for people living on the economic margins very much embedded in natural ecological systems of people like in the Amazon or in the Serengeti and also including early farming like around the Mediterranean. One of the most curious conversations I had there — and I noticed you had the figure up — that one of the figures that consistently emerges from that work that appeared on that generalized consumer resource models is you always have some saturating function relating the abundance of resource to the amount that gets consumed.

And I was talking to the economists about this and they said, "Well, what's that function? We rarely ever use something like that.” This concept of things saturating was very alien to that man. And I was like, "What?" That is central to all ecological models of the way that species interact together. Yet it doesn't seem to be a common way that the economists think about it. So even bringing that approaching would help. And then one of the things we're trying to do is bring together models that have aspects of ecological models with aspects of economic models and aspects of models for diseases, which is basically, I just think of it as a special case of a predator-prey relationship. But the disease people tend to think of them as a more pure thing. Do we get through the insights from bringing together three different disciplines to see and that's a huge amount of emergent complexity. But how does it change the way each of those disciplines thinks about their problems?

Michael: Yeah. So that paper that you're just mentioning here, this “General ecological models for human subsistence, health, and poverty” in Nature Ecology & Evolution. Yeah. This one was kind of discouraging in some respect. This studying poverty traps and really what the realistic limits of our global sustainable development strategies are. So I'd love to hear a little bit more about how you are applying this kind of thinking to where we can set our expectations for the eradication of poverty and also the risk or the threat of poverty and even more well-to-do nations. Because it really looks like we're all perched on the edge of a precipice all the time.

Andy: It does. I mean those models very much say that there’s a likelihood of going in two different directions and how do we avoid going in the worst possible direction of having lots of people living in poverty? One of our agendas there was we are now entering the period of the sustainable development goals which have set guidelines for what we'd like the world to look like by 2030. There's about 17 of those and we’ve been working, could we start developing a framework initially in those papers, and now they say with an overlapping group of colleagues that were more economists this time, to say, "How can we realistically find ways of taking models for biodiversity and its loss, how that affects people's food and the other things that affect their survival and health and integrate those into a common framework?”

And how many of the sustainable development goals are compatible with each other? And once you start putting them on these frameworks, how many of them are incompatible and how are we going to deal with this, because of the UN goal and people have signed up to this development goals is to have all of those goals met. And it may be that there are incompatibilities or interactions that take you down the wrong trajectory.

Michael: So yeah, one of the things that comes out of the models in this paper is that, “Globally stable poverty,” you write, “represents the largest portion of the perimeter space for all models explored.” And especially for the more complex models, it seems like…

Andy: It's a deeply worrying result, but in fact we have two groups of people working on different aspects of those problems in parallel. And it consistently came up as avoiding that poverty trap is a nontrivial problem.

Michael: And that has to do with reinforcing positive feedback.

Andy: Definitely. And finding ways to focus both on people's health and on their nutrition and the food that's available to them and the fact that lots of that is coming from other species that we need to keep those other species going for those both to reduce disease risk and to enhance food availability.

Michael: So this is linked to Ross Hammond's work on the Global Syndemic, right? That this notion that climate change and malnutrition and obesity are reinforcing one another. And so this seems like it makes pretty clear policy prescriptions about where the best place to put investments are if you really want to lift people out of poverty.

Andy: Well, to a scientist it makes clear recommendations. To a politician, it's intensely inflammatory because it may not fit in with their perceptions of what needs to be done or their perceptions of what their philosophy says needs to be done. Again, one of the largest problems we have with all of the work we do that deals with the environment and health is how do you present the science in a way that it isn't inflammatory from a political perspective.

Michael: That seems like it requires its own kind of complex systems thinking in terms of getting people to think across multiple different timescales rather than just within an election cycle.

Andy: Yes. According to Greta Thunberg, we've probably got two election cycles to go before it'll all be irrelevant.

Michael: So in that sense, that is oddly optimistic because what that means is that the political goal time horizon and the ecological goal or economic goal time horizon are actually getting closer.

Andy: Yeah. What we'd see with things like the fires in Australia at the current time and how that's massively undermining the Australian prime minister's position. That tragically, I think we're going to have to have more environmental disasters like that to turn the political minds to say, "Actually, we really need to start listening to what the scientists are saying." But similarly, there is so much science being done that there's a need for more cogently sharp messages for the people who are protesting on the streets to say, "The scientists specifically say this. We want that to happen. The scientists are saying that. We need that to happen." Rather than just listen to the scientists, the scientists have to put a sharper message out there for the people on the streets to send back to the politicians.

Michael: So that seems like it links nicely into this other piece…you’re the lead author for this piece of PLOS Medicine on sacred cows and sympathetic squirrels. And making a really interesting case looking at how the epidemiology links to the way that different cultures regard different animals. Could you talk a little bit about that?

Andy: That came from a meeting we had at Penn State because there's this controversy within the world of wildlife disease, infectious disease people, about “How important is biodiversity either as a source of new pathogens or as a buffer for old pathogens?” And so we were discussing the various mechanisms by which perhaps for things like Lyme disease in the Eastern US having possums around… Possums are fabulous magnets for ticks. So the possums get covered in ticks but don't get Lyme disease but every tick that attaches to a possum, usually which it then goes on to eat, stops a human being infected if that tick happens to be affected. So there's a benefit to biodiversity there. For other diseases, the more hosts, the more other species are out there, then there's a higher risk that they'll have a pathogen that might come across.

So could we delineate the mathematical structure of host communities that says, under which circumstances will having more diversity of host species increase the risk of humans getting disease or their livestock getting disease and under which circumstances will more host diversity reduce the risk of human disease? And the bottom line is, for things that are transmitted usually by factors, which we tend to think of frequency dependent transmission, having higher biodiversity is usually a good thing. Because it gives plenty of suboptimal hosts for the vectors to go and feed on and that reduces the risk to humans. We tend to live in directly transmitted things. Things like Ebola or SARS or this new SARS like-thing that's here. As long as there's lots of species out there, there's probably lots of diseases we haven't discovered yet that may pop over from them. And so we should be slightly more worried about directly transmitted diseases in terms of new things emerging than we should from better transmitted diseases.

Michael: So yeah. So just as an example,  you make this supposition, which you acknowledge as a controversial supposition, that that's where the tradition of the sacred cow comes from, right?

Andy: Right. Now well, it comes from work done in India with Mercedes Pasqual who's on the board of trustees here. But we noticed going around some of these towns in the very impoverished parts of India. That there would be a huge difference between one house would have a cow in the backyard, another couple of houses wouldn't have a cow. Now the kids in the house with the cow, were much much healthier. That could be the fact that if you had a better job and had more money to feed your kids then your kids would be healthier and you could buy a cow as well.

But it looked as if everybody was financially challenged. But the difference was if you had a cow, the cow is wonderfully attractive to mosquitoes. And so instead of the mosquitoes biting your kids and giving them malaria, they go and bite the cow and the cow doesn't get malaria. Plus you have the advantage of the cows giving you milk, which you can make into cheese. So the kids are better fed and less risk of getting malaria. And indeed when we talked to people they said, "Oh yeah, all those people with cows, their kids haven't got as sick as ours do.”

Michael: It seems like a similar effect too, but through a different mechanism to the work on... like the children that play in the dirt, children that have dogs and cats in the home, there's a number of different ways in which a more biodiverse home environment can be beneficial.

Andy: Oh, yeah. Well, I mean we certainly see it around the Serengeti in East Africa where I work. There's a huge population of dogs which we've been working on with my colleagues there to vaccinate them, prevent those dogs having rabies because the last thing you want is your kid to get rabies. But the dogs do a fantastic job of keeping the kids cleaned up, keeping the area around the house cleaned up and that massively reduces the risk to the children from other diseases. People are thrilled to have a dog because one of the ways of keeping your relationships good with your neighbor is getting a litter of puppies and passing the puppies out to share.

So although you could have quite an effect on reducing the risk to rabies by sterilizing the dogs, that's the last thing that the local people want. Because if you sterilize the dog, it's useless to them, it's not going to have puppies anymore. So they want both the benefit which may be subconscious to them of the dogs cleaning up the area around the house and preventing quite a lot of diseases for their kids plus a constant production of puppies to use to keep yourself in with your neighbors and other friends in the village.

Michael: Yeah. One of the things that comes up again and again in these papers of yours though, is that it's not clean cut simple linear relationships. You mentioned that cattle create new environments for mosquitoes to breed.

Andy: So we were looking at both Gujarat and Delhi. But if you go across from Gujarat into the desert regions of Pakistan, their having cattle may increase the risk of malaria, because there are pools of poop and everything, a great breeding ground of mosquitoes. So all these relationships and nonlinear, right back to the generalized predator-prey model. At the heart of that is that nonlinear relationship which the wonderful book on the Serengeti Rules goes right back to Michaelis-Menten saturating functions of what cause nonlinearities in food webs and many other processes.

Michael: I'm glad that you're bringing up the Serengeti stuff because I meant to ask you…You’re not really discussing explicitly in any of the papers that I've read of yours, but you do mention on your website that you do this work with the Serengeti Biocomplexity Project and I'd love to hear more about that.

Andy: Well, as I said, initially my interest there was to go and work on different diseases. Particularly diseases that were shared between wildlife and domestic livestock. Initially focusing on rinderpest, which is one of the two diseases that have ever been eradicated by vaccination. And then all the early work on that was done around the Serengeti and then up in Nairobi by a wonderful guy called the Walter Plowright. That then led to work looking at vaccination of domestic dogs because they have rabies, which can be transmitted to children. And we're getting 50 to 60 children a year dying from rabies, which is a horrible way to die. So if you could vaccinate the dogs against rabies at the same time, you could vaccinate them against another disease, canine distemper, which was spilling over from the dogs into wildlife and causing outbreaks in lions, leopards, hyenas, and another disease called canine parvovirus, which was causing declines in the in the wild dogs.

So looking at those disease control projects also got me thinking, like, when we get these disease outbreaks in wildlife, it completely changes the structure of the natural food web. And once the disease is eradicated, we get an opportunity to see how the whole ecosystem responds to the removal of one particular pathogen. So one of the amazing things about the Serengeti is that it was completely different 100 years ago than it is today, because this rinderpest hugely reduced the abundance or wildebeest, buffalo almost disappeared. That meant there was less food for the predators, the lions and the hyenas. Once it was eradicated in the early 1960s, we get this huge increase, almost a factor of 10, in the abundance of the herbivores and that leads to an increase in the abundance of the carnivores. So again, this wildlife management perception that predators are controlling prey is completely turned on its head by that.

It says actually diseases are controlling the abundance of these things. Once you remove the diseases, you get an increase in the herbivores and that leads to an increase in the predators, so they couldn't possibly have been controlling the prey. It was the abundance of food for the predators that was controlling their abundance. And then that got sketchy thinking, well, how are all those things coupled together in the food web and to understand it, do we need to have every single piece of the food web or can we just look at the main branches, that grass that the wildebeest eat, the wildebeest, the zebra and the buffalo, the commonest species, and then the commonest species of carnivores. And how much of an understanding do we get just by looking at that core 10 species rather than the 10,000 other species that are there?

Michael: It seems akin to some of the counterintuitive results that you discuss in this PLOS One piece you coauthored on social structure, demography and transmissions, the interactions between these things determining disease persistence in primates. Can you talk a little bit about how you put these models together and how they yielded surprising results?

Andy: Yes. That was a project I was doing within an undergraduate at Princeton, Sadie Ryan, who's now a tenured faculty member at the University of Florida, Gainesville. We were interested in, what is the relationship between social systems and disease? I played around with some theoretical models for that and then decided it would be interesting if we could focus in on one group of species. And I should step back and say that interest in social systems and disease really started emerging when HIV appeared.

Because up until then people hardly talked about sexually transmitted diseases. And there was very little information on social systems. We knew a little about the social system of like, the British Royal family, but we had no other data on, not particularly good data on human social interactions, because people were quite quiet about it. So we thought it'd be interesting to look across primates because of fantastic field studies of primates where individuals have been followed through time, and there's a variety of different social systems that are also very good databases on the different types of parasites and pathogens that go through different primates.

So we wanted know, as social systems become more complex, does that allow more pathogens to establish in them? And what type of pathogens appear in different social systems? And of course one of the instant ironies that emerge is that the ultimate social system that many people would like us to live in is this sort of monogamous territorial system that will be characterized by some sort of top carnivore in a system. If you have a system like that, the only diseases you're going to get are sexually transmitted diseases, because the only time you have any interaction with another member of your species is when a male and female meet to mate. And that's the only opportunity for disease transmission. The rest of the time there's no contact, so there can't be any disease transmission. Now you will pick up things, if you're a carnivore, from your food, but you then translate that in some ways back to your food.

It's only when you have these more complex social systems like the chimpanzees and gorillas and the baboons where you have promiscuous systems, but you've actually got the abundance of interactions that allows non-sexually transmitted diseases to establish. So we wanted to look across primate social systems and see how much of those patterns emerge. And it was quite a strong signature that as you go from the smaller primate species, which tend to be monogamous and territorial, they mainly only have STDs. Once you go up to the larger primate species that live in large groups, there's a much larger diversity of diseases.

Michael: So this seems like you would find very distinct patterns in disease ecosystems between like the chimps and the bonobos, right?

Andy: Well, the chimps and bonobos do seem to have fairly similar pathogens because the other thing with diseases, you have the diseases you come down through evolution with quite a lot of the time. And these chimps and the bonobos probably only split like four to five million years ago, maybe even later, more recently than that. So they have subtly different social systems, but they're still living in groups with lots of interactions between them. And body size is roughly the same thing and they're living in similar habitats. But the difference then between, say the chimps and the baboons that are out in the Savannah is much more dramatic, but the split between them is much deeper.

Michael: So one of the things that you mentioned in this is that this has a lot to do with whether the organisms in question develop an immunity or not, right. So like exposure may actually be beneficial if you're developing an immunity?

Andy: Yeah.

Michael: And so I wonder, surely there have been thoughts to what this means in terms of how economic changes affect the kind of decisions that… Like, a lot of people in my generation now are doing co-housing, the way that the suburbs are populated is changing with like multiple families living in a single home and so on. What do you see as emergent concerns given the shifts in lifestyle and demographic and that kind of thing among human beings?

Andy: Well, that raises a fascinating bunch of questions. If we look over, just human history and when different types of diseases have emerged. Most new diseases don't appear at random, they usually arise because the opportunities for transmission change as human social organization changes. So if you think of all the biblical plagues, those all arose when people started living in cities and they were bigger aggregations of people living together, providing enough people for chains of transmission not to be broken so as things like measles, whooping cough could establish in those situations. Changes in agricultural practices allow other diseases to come in and like the sacred cows begin to start creating taboos in societies that live in certain ways to prevent exposure to certain types of diseases. We don't know what people living in the suburbs is going to do to different types of diseases.

It may be a mix, plainly, we have much stronger tools for dealing with disease now. But with good tools for dealing with many of the diseases and pathogens we're familiar with, if something new appears, we have to ramp up quite quickly to know how to deal with it. But we're also getting better at that. I mean the new SARS-like thing that's appeared in China. And then there was a case in Japan yesterday and I think a case in Thailand, it's killed two people. But there's a group of people who really understand those diseases on it to try and work out what do we do next? Is this a big threat or is it something we can deal with in a similar way that we dealt with SARS?

Michael: Relatedly, there is this when Lauren Ancel Myers gave her community lecture here a while back, one of the things that it makes sense would be preoccupying epidemiologists now is the just explosion of Intercontinental air travel. But one of the things that comes out of the models that you're making for this paper are that there's a suggestion that there's a threshold of within group infection before the disease can disperse to another group. And so I think this reminds me of a few years ago, Spotify bought the musical big data company, Echo Nest, and one of the things that they were looking at is where the viral pop hits come from.

Andy: Right.

Michael: And it seemed like the incubators for innovative new music were island nations like the UK, like Iceland, Australia, places where... and this makes sense with island biogeography.

Andy: It needs people talk with each other to take off, yeah.

Michael: Right. These tightly connected local networks. And this is related to work that the military has done on engineering viral media. So the question to me is it seems like while we have reason to be concerned about the increased rate of international travel, that it may be that the flattening of the world in this way is actually inhibiting the local saturation and incubation required for certain forms of disease transmission.

Andy: Well, again, those initial models on the primates were instructive. We were using a static framework there. We assume the social systems were relatively static and then compared what type of pathogens could be sustained by hosts with different social systems. More recently, with work in Yellowstone, we managed to develop a more dynamic framework that allows the abundance and the group size of the host to be dynamic and then what happens when you put pathogens into those? And there again you get this thing which is called a social trapping.

Whereas depending on the relative rates of within group transmission and between group transmission, you can have pathogens that get into a social group, affect everybody in that group. But there's not enough between group contact for them to get out of it. So they die out quite quickly in the handful of groups that get infected. Other types of things are like the air travel. Everybody's coupled together and these things can spread quite quickly. In terms of emerging diseases, those would be the things I'd be worried about.

Michael: So to zoom out a little bit from this point, you observe in this work that there is a a broader problem with the way that we're thinking about conservation biology, in terms of the fragmentation of populations and habitats and that we tend to look just at the gross numbers of remaining species rather than the way that the these smaller populations and a fragmented environment lead to this kind of nonlinear relationship.

Andy: Well again, it’s a double edge sword. If you have populations that are divided into social groups or into habitat fragments, if those habitat fragments are well-connected, then a disease that gets in can move from habitat to habitat and social group to social group if it's something that species hasn't seen before, then they can cause you big problems. Although we are desperately worried about fragmenting up nature, if those fragments are not coupled together too strongly, then you can get a disease outbreak in one fragment and it will spread to the others.

So you might lose all the individuals in that fragment, but you may then well, be able to repopulate it from some of the ones where the disease outbreak didn't occur. So again, it's a double-edged sword, and it's interesting from an evolutionary perspective of how the pathogens establish in the host species with different social systems. And then the practical thing is, how is it best to focus on the infected group or is it best just to reduce the rate at which the thing moves between groups.

Michael: This seems like it may have some actionable insights with respect to the growing conversation over the last few years in terms of decentralizing our social architecture.

Andy: Yeah.

Michael: In one sense it seems kind of discouraging that this idea of a global internet for example, is starting to balkanize. But in other respects that seems like it may actually be useful to us in terms of allowing different island networks to devise different strategies for social organization.

Andy: Well, again, it would be interesting. I know they have this wonderful experiment that the SFI Postdocs, when they locked in the house for [72] hours and they have to come up with a publishable paper but they'd came up with, “How would a beneficial pathogen spread?” I think it was one of the first time they did that. But it'd be interesting to take the model they did for that and then put it into one of these social system models and say actually, how do beneficial ideas spread from group to group? Because one of the artifacts we get with this wolf disease model is that the biggest risk for a wolf is another wolf. The wolf groups kill each other all the time. So 75% of the wolves in Yellowstone get killed by other wolves.

But if you have a disease that reduces the abundance of wolves or reduces the number of wolf groups, then the size of wolf groups goes up because there's less groups to have negative interactions with each other. Now will that turn itself inside out if you had beneficial interactions with the group? Will the groups get bigger, and ultimately the group that was benefiting most kill all the other groups? So what's the upside and the downside of these beneficial and detrimental things that may be detrimental or beneficial to a group. What's their effect once the groups are coupled together? Again, that will give you hopes of insights into social networks and how information spreads through those.

Michael: Yeah, there's so many places to look in the modern news that remind me of the 30 years war and just like, the insane religious mess that Europe was after the protestant reformation.

Andy: Absolutely.

Michael: So do you get that question regarding a particularly successful religious paradigm as a beneficial mutation, and how that ends up shifting the political landscape across the Western world over the last few hundred years.

Andy: Well, McNeill, in Plagues and Peoples, makes this case that the original spread of Christianity through the Roman empire was massively held by measles. That there was measles spreading through the Roman empire at the same time. If you saw someone with measles and gave them a drink of water out of sympathy as the way a good Christian would, the survival rate of those people came up and they thanked God for all that help. But if they hadn't have had the measles to be killing them in the first place, Christianity may well have spread at a much slower rate. And so McNeill talks about that way back in the 60s in Plagues and Peoples.

Michael: To loop back to, we were talking about biodiverse human communities with cows and dogs and so on. I'm reminded of a comment my friend David Titterington made once about the holy water. Like the holy water is the dirtiest thing in the whole church and everybody's putting their hands in it.

Andy: Helps you rehydrate when you're really dehydrated. There's a cost benefit that it may lean towards the benefits.

Michael: So you mentioned being here for the working group on aging and adaptation, all that. Now, what else are you working on at Princeton or?

Andy: Well, as I said, I've been doing lots of work on these social groups and how that affects disease transmission. With a wonderful postdoc I had, we've been doing work on scaling. Very much inspired by the work that Geoffrey West, Brian Enquist, and Jim Brown did here. And then seeing, can we use that in models to look at how does the immune system scale? So as you have hosts of different size and the immune system we have in humans evolved from the immune system that was certainly there in the earliest mammals and simply before that, lizards and then right back to sea anenomes and sponges. So how did the different components of that, the T cells and the B cells, have much smaller variation in size than the hosts they're living in. The T cells and the B cells in an elephant, aren’t three orders of magnitude bigger than the ones in me or in a mouse. They're roughly the same size.

One of the most important functions is keeping a memory of what diseases and what pathogens have you seen before. But if the life expectancy of those cells is a function of their size and their size doesn't change too much, how do they do this business of keeping memory in a finite population of cells that have a finite life expectancy? And so can we look at ways of trying to understand how the immune system kept up with the body size evolution of the mammals and the birds, and can we make simplified models of the immune system that we could use to compare how it functions in a mouse compared with how it functions in a cow or a human or sheep, right up to an elephant.

With the interesting sideline, the birds have much lower mass than mammals because they have to fly. So their immune systems are very similar but subtly different. And then bats have to fly. So how do their immune systems work compared to mammals that don't fly? Because if you have hollow bones, where do you get the bone marrow to make the B cells that are a part of your immune system? And so do these species have immune systems that operate in subtly different ways and how many insights can we get to that from looking at this two levels of scaling, how does the component parts of the immune system scale with their physical size? And how does that operate in different ways in this pool of the host of different sizes?

Michael: So this seems really intimately related to questions about human cultural memory and how human society has scaled and the amount of information that civilization is trying to track. At any given time we've had to come up with new outboard forms, that are written language, or even prior, David Krakauer’s work in the late 90s with Martin Nowak at Princeton on the evolution of syntax emerging as a response to the risk of an error catastrophe.

Andy: Right.

Michael: So what do you imagine we're going to see in terms of how an elephant immune system is operating with similarly sized components across this much larger context?

Andy: Well, part of the things that we’ve been getting glimmers of over this week is that as the host body size gets larger, big parts of the immune system slow down. So they're essentially working at a rate similar to basal metabolic rate. So larger mammals have slower metabolic rates than smaller ones. So having the rate at which your immune cells replicate, slowing down, maybe giving you enough time to have your memory cells last as long as you do. That's the result, we haven't fully tied up yet. That will begin to get to that. We also have something we realized only comparatively recently in humans that some of the diseases, particularly things like rinderpest that we mentioned earlier in the Serengeti or the distemper in dogs or measles in humans, one of the things it does is it causes a disease in you, which itself is really nasty.

But the other thing it does is it completely wipes out your immune memory. So it's like having to restart again at whatever age you have to get measles. And so, often prior to vaccination, people who got measles would get sick over the next two years from all the things they'd had before they had measles because they had to regenerate their immune system. So we're finding these things, that measles and rinderpest and distemper do similar things in other host species of eradicating your immune memory, which means you've got to get sick to everything again to build that memory up again.

And that's a bit like going in and tearing up the library to get rid of all those books and then having to collect them again because that's what that virus has done to you. Which is, I can't think of stronger reason to vaccinate your kids against measles because they're going to get really sick from a whole bunch of other things again. So the older you get those things, pathologically, it's worse to have measles as you get older, but similarly it's eradicating much more memory because you've been around more longer to accumulate that memory.

Michael: So the first part of that, talking about lowering the base metabolic rate of the immune system. I was interviewing Melanie Moses, the same…

Andy: Oh yes, fabulous person.

Michael: Yeah, the same seats and she was talking about this with respect to anthills and how like, as the ant hill gets larger and larger, fewer and fewer of the ants are active at any given time. And we're saying, this looks like, when I was talking, again, with W. Brian Arthur and he was talking about this in terms as production gets, as just our economy scales. Then we put less emphasis on production. Production gets easier with scale and more emphasis on the distribution of resources and how this starts to suggest a universal basic income, the question of maybe at 10 billion people, most people are just watching TV at any given time.

Michael: But then the question in the second part of what you're talking about here, which is that to try and draw an analogy to human civilization from the immune system. That there are ways that we might view the accelerating pace of our technological surround as a measles equivalent type of thing to the extent that the more that we're focused on the Twitter time horizon, the quarterly financial reports, the more imperiled we are by threats that we, at earlier moments in history, have already faced.

Andy: Right.

Michael: Yeah. So I don't know, that's just sort of broad. Well, I think there's multiple analogies to make here. I think one of the things that causes these social networking programs to collapse, if you think of the earlier ones is, the thing that finances them is the advertising. So when you first join in, you've got a handful of friends and you have good interactions with those. As it gets bigger and bigger, it becomes a bit like the dilution effect in these disease things. You're getting more and more advertising, that means it's very hard to find the messages from your friends. And it's got this thing for maybe they'll only send you a message if you talked with that friend in the last couple of weeks, but you're still busy filtering your way through the advertising and all the other fire hose of nonsenses in there.

Andy: Then eventually that particular social network's useless because of the dilution effect of everybody else's information means you can't find what you're looking for in it. And so a new one will arise. So I think now every four or five years the kids in the schools get a new one and then their parents slowly adopt it to see what their kids are doing and then the advertisers pick up on that and it's something nobody wants to use it anymore because there's dilution effect of too much information that's useless to you. That you're spending too much of your time filtering your way through. Kills that whole network. And so I do see in this dilution effect and disease. The real signal you're looking for gets lost in this massive noise.

Michael: And yet this is probably something we're not going to design our way out of, right?

Andy: No. Because it's what pays for it.

Michael: Like there's the whole issue of increasing returns and preferential attachment, right?

Andy: Right.

Michael: So I remember, I think it was, review the future of podcasts, that had Kevin Kelly on. And they were asking him about, the internet seems to reward monopoly. It seems to create these enormous monopolies faster and faster. And they were like, "Well, are you worried about this?" And he was like, "Well, no. Not really. Because it overturns the monopolies faster than it used to." So I don't know

Andy: Yeah. This is interesting. It is amazing how quickly it's developed, but also how rapidly some of the things that were dominating early on have disappeared. Some before they even had time to become monopolies. But it's also massively overturned many of the older monopolies as well. The high streets are a completely different place now than they were even five, 10 years ago.

Michael: So given that almost everything that we've touched on in this conversation is a double edge sword. What provides up your optimism? Where do you feel good about the direction that this planet is heading right now?

Andy: Well, there's two parts onto that. To me as a scientist, these places like Santa Fe Institute, coming here, spending time, talking with intelligent people, working on hard problems will always be stimulating. And the rest of the world disappears I think when I'm here, which is part of your problem, but fabulous for me. And then the thing that's given me huge optimism is actually Greta Thunberg and all these children, young people out on the street saying, "We have to do something about this. Stop messing around with them."

The political discussion that's going on at the moment is so distant from reality and the problems we have to face in the next decade, that actually, for the first time in 25 years, I feel optimistic because these people saying, "Listen to the scientists." And that's why I think the scientists need to sharpen their message for people to say, "This is what we need to have on." And having people, not in the political arena, but outside the political arena, demanding the politicians to see that these are the problems we have to deal with rather than the message they're getting themselves into.

Michael: So basically, like we mentioned earlier, in a weird way, the urgency is its own...

Andy: The urgency is now being felt and hopefully we have enough time to solve the scientific or find solutions to those scientific and health problems in the very little time we have available.

Michael: Wonderful. Well, Andy, thank you so much. Yeah. This has been a real…

Andy: We've covered quite a lot of ground.

Michael: ...a real barnstormer. Yeah. Awesome. Thanks a lot.

Andy: They’ll have confirmed that I have gone mad.  [Laughs.]