Anthropologist John Hawks of the University of Wisconsin–Madison talks about recent human evolution, especially of our ability to digest lactose. And producer Graham Townsley discusses his three-part PBS NOVA premiering on November 3rd called Becoming Human. Plus, we test your knowledge of some recent science in the news. Web sites related to this episode include www.snipurl.com/t1ivr
Steve: Welcome to Science Talk, the weekly podcast of Scientific American posted on November 3rd, 2009. I am Steve Mirsky. In this episode, we'll talk some more about human evolution with John Hawks, a physical anthropologist from the University of Wisconsin–Madison and Graham Townsley, the producer of a three-part episode of the PBS series, NOVA called, "Becoming Human". First up, John Hawks—he studies the bones and genes of ancient humans. He recently spoke at a meeting of the Council for the Advancement of Science Writing at Austin, Texas. First we'll hear a short clip from his talk about the recent advent of the gene that allows humans to digest lactose. It enabled us to get nutrition efficiently from milk. Then we'll hear an interview with Hawks [that] we did after his talk.
Hawks: When you have a new mutation, one of the things about it is that [if] it is selected [it] increases [extraordinarily] slowly for a long time. Our best [estimate of] the age of the lactase [version] in Europeans is about 8,000 years old. Five thousand years ago, these early Neolithic skulls or skeletons, the ones that were genetic[ally] samples, they don't have it, it is not found in them. So about 5,000 years ago, introduction of agriculture in Europe [it's] not there. That is exactly what we expect. It takes a long time for this to get [to] any substantial frequency, and if you sample 25, 30 or 50 people from that time, you are not going to find it. Today, this is about 80 percent in parts of northern Europe. Which means that the number of lactase-intolerant people is about the square of 20 percent, about 4 percent northern Europe. It means that 80 percent of today's modern Europeans, 80 percent of the population [of] Germany got this gene from 1 percent, early 1,000 years ago. What's the population in Germany? It is like 60 million right? So let's say 80 percent of the 120 [m]illion copies of lactase in Germany now came from this [one person]. [But] I will [tell] you to something else about this, something very interesting, is that there are 40 million copies of this gene [floating] around in Germany now [that] are descended from the people who had a non-tolerant version. They were not 40 million of those genes 5,000 years ago. There probably were 10 million of those genes. So, both versions of this have undergone a massive increase in population, one more than the other. One['s gone] from 0 [up to] 80 percent, the other [one's] gone from not very many to many. All right, so the kind of thing we have looked at it is [we looked at the] genome of life and [asked], how many of these things are there? They look like they will increase in frequency a lot [lately]—how many? It looks like about 3,000. When I started this work in 2006, nobody thought this was unusual—["Well, 3,000 genes out of selection. Well, who knows? How many should there be?". Well, 3,000 genes out of selection—]et me tell you, there are 40,000 amino acid [changes] in humans and chimpanzees and probably only about 12,000 of those are [selected]. So what we are saying is that a fourth of the potential differences between humans and chimps are underway now in [the] human population—that is like 3 million years of evolution [packed] into the last 20,000 years.
Steve: Why so much genetic variability in place so recently? A big reason [would] seem to be that the human population increased so much in the last few tens of thousands of years. More people mean more opportunities for new mutations, which in turn means more genetic variability to select from. After Hawks' presentation, we talked more about the lactase gene's recent arrival on the scene.
Steve: It is possible that single gene arose more than once or can you tell that by the surrounding genetic structure?
Hawks: The lactase?
Hawks: Yes. It looks like from the surrounding structure that it just happened once. It is linked to one haplotype, the haplotypes are widespread. There is in the Caucasus, looks like the same mutational event probably with a slightly different haplotype background. So the idea might be that there was an early recombination, where some of the people sort of stuck around in the [Caucasus] and they sort of like—the whole logic about of Africa is more genetic diversity in Africa than outside; same thing with any given gene. If you find it and it is real diverse in one little area and then everywhere else is uniform, the idea might be [that] it originated there. Now, the African versions of this—[there's] three different ones, three mutational events— and there is an [Arab/]Arabia focused mutational event. So it happened five times and twice at the same mutational change, the same regulatory change.
Steve: But you can tell that they are discrete events because of the surrounding material.
Hawks: Totally different surroundings. Yeah, exactly.
Steve: The haplotype.
Steve: And anywhere where people are adopting milk drinking, you would expect to see this mutation arise, and then be selected for and stabilize.
Hawks: Well, it is suggestive because it happened five times, but it did not happen in Mongolia and people have been dairying there for a long time. So, you know, it raises a question, how—in the old days, the argument used to be that, "Well maybe this is a classic polymorphism; it is always around a low frequency; it was under a genetic drift, and in populations that adopted dairying, that rapidly changed, like a quantitative trait." And it did not happen that way. You know, these people started drinking milk. [We’ve] have got the milk residue now on these ancient pots, right? It is really cool. It is a good example, but it is a misleading example, because we've got all the facts, right? So, when I [apply it to] anything else, it doesn't work, but with lactose, we know the facts. We know that they started drinking milk immediately after they started keeping cattle and goats and in Arabia, camels. And that these guys, linear band ceramic people, who were in Germany, who they sampled the 5,000-year-old sample, these guys were drinking milk all the time. They didn't have the mutation. So, it was the environment that changed, made the opportunity for an adaptive response, and the adaptive response happened a discrete number of times, but not everywhere, and maybe it didn't happen because it was just a rare event. Maybe it didn't happen because for some reason, I mean, right now lactase is most, the European version—you call [it] that because it is most common in Northern Europe; doesn't mean it came from there, it is common there. Why is it common? Because those guys in Northern Europe depended on milk more because they didn't have the cereal crops with this high productivity. And so we find the same mutation in the Near East. It is not as common, presumably because the selection was not as strong.
Steve: It is very multifactorial.
Hawks: Absolutely. When we look at an allele over space, the things that can contribute to it are its age, its, you know, the selection pressure, however, much it is, how that varies over space, how gene flow varies over space. Some of these alleles are too widespread. If we just say, "How fast are people moving between these places?" There should not have been time for something like lactase to get all the way to Spain and India. It shouldn't move so fast, unless you have got sort of higher order things going on with the gene flow. And we do. I mean, the Roman legions, the Romans picked up this legion from Iran and put them in England.
Steve: Within a few weeks!
Hawks: Yeah, exactly.
Steve: Within months.
Hawks: Listen, you guys we cannot trust you over here. We are going to station you in Britain. And they stayed there for 200 years. And so, you know, we really have this weird gene flow in the last couple of thousand years that affects the distribution of the stuff.
Steve: But as a rule of thumb, that is, you know, those are always, you know, able to be violated, you know, I always try to—when I am talking to people about malaria and sickle-cell, let's say; any place where there is widespread malaria, you will eventually see the introduction and stabilization of sickle-cell.
Hawks: Well look at malaria. Malaria is the best example because there are so many genes that are genetic responses; we know where they are because they are blood things, we test [them].
Steve: Right. There are at least seven discrete introductions, right?
Hawks: Right, in west Africa, you have got sickle-cell. In Pakistan, southern Iran, western India, you have got sickle-cell—different sickle-cell. So that happened twice, except in that same area, you have African sickle-cell, because they came with the slave traders. So you have got African and indigenous sickle cells in the same place. Sickle-cell is nowhere else. [S]tick with Africa for a second: You have got hemoglobin E, you have got a little bit of Alpha thalassemia, you have got a lot of—I said E, but I meant C, hemoglobin C—you have got G6PD deficiency; in the Mediterranean, you have got Beta thalassemia; in Thailand, you have got hemoglobin E.
Steve: And these are all blood conditions...
Hawks: They are all blood things, yeah. Yeah, they are all classic ...
Steve: ...related to the fact that there is malaria in the environment.
Hawks: Yeah, that is right. They are all classic polymorphisms. [Yeah, we've] been looking at those for 50 years. And so each place you have got this different knockout, basically mutation. Why all these knockouts? Because knockouts are easy and that is the first thing that is going to happen is any mutation that breaks the gene, if your fitness—especially, you know, since when it is rare and heterozygotes, the only thing[s] that appear, you know, then it starts going up—then they start interacting with each other ...
Hawks: ...if they get high enough. So in West Africa, you have got these villages where there is hemoglobin C, and you have got other villages where there is sickle-cell. And there is not a great amount of overlap, even though they live in the same place. That is because hemoglobin C and sickle-cell negatively interact with each other, it is a negative epistasis. So, you cannot have both. If one is high, the other one has to be low.
Steve: Just because any children would not survive?
Hawks: That is right. Yeah, yeah exactly. If you would expect and—Frank Livingstone did a lot of simulation, this is early days of computer simulation. He was real interested in this question: What happens when hemoglobin E comes in [in] a place where the other [Thailand] one already is? Because E is really beneficial, doesn't have as much [of] a negative impact and he calculated how fast this should spread against sort of; it is almost like the gene would spread really fast in the absence of any other allele and if there is another allele that is like a little bit of a head wind, it doesn't move as fast, but it still moves. So we understand with, I mean, the malaria example, one of the bottom lines is, it really is just a chance. You[can put] yourself in an environment where you are dying off something and a genetic adaptation is possible, but you still have to have the mutation and mutations are rare events. And good mutations, I mean, with malaria, all these knockouts because malaria is deadly; you know, anything—it is like throwing everything at the problem. Every gene that could interfere with this parasite, we are going to select something. Whereas with lactase, what can you do, to digest milk? You have to upregulate that gene, which means that you have to hit one of its regulatory regions, which are small. So you got to have a mutation, and we know that two populations did the same way, and [three did it] in some other, possibly three different ways. But it is not easy. But when it happened, it was so advantageous that it spread like wild fire, so you have got this sort of combination [of] it is really, really, really good, but it is one in, you know, a hundred million, and if you wait for something that is one in a hundred million, you got to have a hundred million people or you would be waiting a long time.
Steve: Like in the fruit fly work, where they just started churning out huge numbers so that they could get mutations to occur more frequently.
Hawks: Antibiotic resistance is the same way. You know, they test these antibiotics in a lab, they have got it in the dish, and they say this kills it every time, kills it every time, kills it every time. It is nontoxic, and that is like threading a needle, you know, you can use it in humans and it kills them every time, but when you start applying it to ten thousand humans, ten thousand Petri dishes, and the bacteria have a chance every time of having the thing. They used to test pesticides, you know, on insects in the lab and they would find [this] pesticide—kills them every time. And then they would spray it on a field and within a couple of years, there are these flies around that the pesticide doesn't kill anymore.
Steve: They are actually enjoying the pesticide.
Hawks: Yeah, yeah, you know, spray it on... because we can handle this and our wild competitors can't, you know? But that's the way it goes.
Steve: So, now the key question. Was the lactose tolerance genetic structure directly responsible for the increase in survival rate or where the people didn't have it, just so busy spending half the day in the latrine that they were not as efficient as their comrades there?
Hawks: You know, I talked to someone one time...
Steve: You actually have an answer for this!
Hawks: His name, I will not repeat, because it is someone ought to know better—but the field is full of people who ought to know better—who said, "Well, what differences does it make, you can drink milk." You know, what's the big deal, you know what does that do? And I was just like, "Uh, first of all, you know, basically from a system standpoint, of course, milking is more efficient than meat, you know, you get more calories ...
Steve: Sustainable resource, too.
Hawks: But from an individual standpoint, you get 30 percent more calories out of milk if you can digest that yourself, then if you let the bacteria do it. You can drink it in small quantities, you will get energy out of it, but you get more 30 percent more if you can handle it yourself. So, I look at that 30 percent. Somebody could easily say, well you know, but yeah, but 30 percent is a lot to a woman, who is lactating. You know, I mean, there is 700 kilocalories a day that they are putting out through breast milk and if you can get 30 percent more out of what you are consuming, if you can take your child of[f of] that more easily because you are milking in larger quantities—and the kid can handle this initially, so you can see the pathway by which dairying becomes effective culturally—but once the mother can do this, you are saying 30 percent more calories: That means I can get pregnant 30 percent faster, means I can recover from lactation that much faster. I mean, it translates directly to fertility, and I think there is a tendency, you know, people think about selection, it means that you survived the disease or it didn't kill you or would be good if our hearts didn't break down when we [were 70.]. But really it is about how fast can you regenerate, how fast can you have kids, and how fast can you be mature enough to have kids, especially when the population is growing already. When we get to the Neolithic and the population is growing because of food, the things that grow fastest in a growing population are the things that make you reproduce faster. Because the more grandkids you have and if you can have your grandkids competing with other peoples kids, that is twice as many of your genes.
Steve: Beginning on November 3rd the PBS Science Program, NOVA, airs a three-part episode about the last 7 million years of human evolution called "Becoming Human". I spoke by phone to the producer, anthropologist Graham Townsley. So Graham, this is pretty exciting series of programs. Just give us a general idea of what the audience is going to be in for?
Townsley: What we are trying to do in this NOVA series is a number of things. We have tried to create, tell the whole grand story of human evolution starting from the time we split with the apes, leading up to our own species, Homo sapiens, again, but including in it all the latest findings. And of course every five or 10 years the whole landscape shift[s] as new discoveries come in. And we have also tried to incorporate some of the new ideas about the types of things that might have powered human evolution. And one of the things that has really come to the fore—of course this was I was new to lot of these subject matters this was a discovery for me—was this idea that it was wild climate variations which in some way was the engine of our evolution. And there is remarkable fact that if you put a graph of, you know, the speed of human evolution and put it next to a graph provided by paleoclimatologists, [of] how a climate variation happened over the last few million years, the correspondence is [amazing]. Every time there are these bursts of wild climate variability, human evolution takes a big step forward. So it's just a very provocative and interesting idea. It is one of the ones that we made [a] centerpiece of our series.
Steve: And let us talk about that for just a second. I mean it makes sense in that you have will some natural variability among a population of humans or prehumans, and when the climate has done something interesting like shift wildly, all of a sudden there is a big selection pressure on a small group of those within that population. that happens to have an advantage in that new situation.
Townsley: That is exactly right. What they talk a lot about [is] this idea, I think, the fall back hypothesis that, of course, when these swings of climate happen they put pressure on all animal population. And what most animals tend to do is that they fall back on the one thing they are good at. So that, for instance the [robust australopithecenes] who have these massive jaws, they get bigger jaws and they concentrate on the one way they know that they can get food which is crushing up the roots and things like that. What is interesting about the human case is that it seems that the response in our line of evolution was to grow bigger brains, which gave us the capacity to adapt to these swings. So rather than focusing in on one behavioral trait and one little ecological niche and hanging on to that through these periods of climate [variability], our ancestors sort of went with them and developed bigger brains, which will allow them to come up with new behaviors and adapt to these things. So it is really, I [found] these a [fascinating set] of ideas. The idea, I [guess] is really that a, sort of, rather than adapting to any one specific environment, we adapted to variation itself.
Steve: And that would be a really key thing for making a species incredibly successful. And, hey, look at us: We are everywhere in huge numbers.
Townsley: It is so true, and for the first time in the seven million years since we slipped from that apes, there is only one hominid species on earth, and I think that is another interesting thing that we all discovered in this process. The norms through most of the last seven million years is that there were many different hominid species on earth at the same time. And it is only in the last 30,000 years since the last Neandertals disappeared that [there's] only be[en] one—us. So that was a very surprising thing to me, and I think that it would be the most [people.]
Steve: I mean, we have seen it in the Planet of the Apes movie, if you will, but it is a fascinating idea to contemplate a world in which there are multiple species within our Homo genus and try to imagine how they might all interact.
Townsley: It really is and, of course, we have no real way of knowing, and I guess the nearest examples we would take would be from the ape world. And we think of different, you know, chimps and bonobos or different species of gorilla in similar environments—would they interact or not? It is a fascinating idea. Then the other great question is, why did all the others die out? Why were we so successful and all the others not? And it seems to be something to do with this remarkable intelligence that we evolved and this capacity to adapt to so many environments. The Neandertals, sort of did one thing and just kept doing it—they were top-level carnivores and they were hunters living off the herds at the edge of the ice sheet; and it couldn't adapt. And suddenly [along comes this] species which seems to be able to live everywhere and have this very adaptable and flexible technology and learns so fast and keeps developing things.
Steve: And not only learns but is able to then pass on that new knowledge to the next generation, which does not have to reinvent the wheel.
Townsley: Exactly, exactly, because one of the other things that really interested in me—and my background is in cultural anthropology more—is this whole phenomenon of culture. And again of course that doesn't leave much in the archaeological record going back, you know, [a] very long way. But it is just very interesting to think about. At what point do our ancestors stop being the ape-like creatures and develop culture; when [does] language emerge? When do all the social impulses emerge? When exactly does a culture start to exist outside of their brains that can get passed on from generation to generation?
Steve: One of the other subjects, based on the press materials I have had a chance to see, that is going to come up is, the possible importance that, you know—sorry to you vegetarians, who are listening—but that meat might have played in our physical and the mental evolution.
Townsley: Yes. It seems that that's huge. It has a lot to do, I think, with our brains and the fact that our big brains are such energy-hungry organs. In our resting stage our brain consumes 25 percent of our body's energy, and it is very difficult to, sort of, fuel the energy budget that this brain has without eating meat. And it seems that meat eating came in with the emergence of our genus, the Homo genus, you know with Homo erectus and Homo habilis the first members of that, and one of their key novel adaptation[s] was meat eating, and it was that that allowed them to go on to, you know, develop these larger brains.
Steve: These are very energy rich concentrated packages; it is like the, you know, the fast food of its time.
Townsley: Exactly, that is exactly right and I was fascinated by this and; although of course you know we can become vegetarians, and we can live quite happily, but it is very hard to imagine our evolution ever happening without meat eating.
Steve: Right. This should not be construed as any kind of a value judgment on people's personal choices today.
Steve: So give us a quick summary of each episode—when it is going to air in and what people could expect.
Townsley: Well, there are three episodes, and they start to air on November the 3rd, and then there is the second one on the 10th and then the third one a week later on [the] 17th. We organize them—there is [only] really one good way, I think, to tell a long historical story and that [is] sequentially. So it will start at the beginning and work through to the end, which is us. So the first show is about the very early members of our evolutionary line, the upright walking apes, who first, sort of, descended from the trees, we imagine 6 or 7 million years ago; creatures like Lucy, like Dikika child, Australopithecus and others. And that really goes in[to this] very exciting idea about climate. Can we think about, I mean, what was it that first of all encouraged our ancestors to develop into these upright-walking bipedal apes and then secondly propelled them on into the later evolution towards [our genus], Homo. And we look into these ideas about climate variability. So there is a quite a lot in that series with fascinating stuff with paleoclimatologists and trying to bring together, you know, their work with the work of paleoanthropologists about, you know, these ancient hominid species. So the first show will take us from seven million years ago up to about two million years ago which is this huge span of time when there is all these different species of all upright walking small brain apes around in Africa. The second show is really about the emergence of our genus, Homo, and concentrates on Homo erectus which is probably the most, certainly the most successful hominid species of all kind, and they were around for almost 2 million years, they colonized the whole planet. And we really go into what was different about them, what was special about them; and this seems to be the species that pioneer[ed] what it means to be human. And we have a lot of very interesting ideas about the origins of fire; about exactly hunting and meat eating, how they might have organized that, the brain growth; and all the things that has set the stage for us. And then the final show brings us up to us, and that is really about the last half million years of our evolution. It looks into the amazing finds at Atapuerca in Spain, [the] just unprecedented the discovery of 30 complete skeletons of a species called Homo heidelbergensis, half a million years ago, which gave us an amazing insight into that world. And these were the precursors of the Neandertals, so we follow that line of evolution into the world of the Neandertals. And finally [we] consider the emergence of our species, Homo sapiens, and what were the things that really made us different from all the others and why exactly are we now the only hominid on earth after so many millions of years when lots of hominids lived side by side on the planet. And so there you have it—it's sort of the grand arc of our human story.
Steve: How many years you have been working on this?
Townsley: Two years. I mean it seems like five to tell [the truth]. It is almost two years now. It was an amazing process, because I had a, sort of, a background, I [had a doctorate] in cultural anthropology, but I didn't really know this evolutionary stuff; and so I feel like I got a crash course in human evolution, which is, of course, now a huge field. And then there was just a challenge of making the films, trying to find some way to bring these stories alive, because in visual terms you don't have much to look at. You know we filmed with most of the important characters in the field and authentic sites in Africa and elsewhere but it was a struggle to make them work, just come alive with films and so make it [a] sort of watchable, entertaining story.
Steve: And are all the episodes going to be archived on the PBS site once they have aired.
Townsley: I am sure they will, you will be able to get them through the NOVA PBS Web site.
Steve: But if you can catch it on your HDTV, I am sure that is the most rewarding visual experience.
Townsley: Absolutely, absolutely and they look great, they really look stunning. We actually ended up getting a huge variety of different visual materials, plus some really high-end graphics which will bring these creatures alive, bring some of the early hominids alive, and Homo erectus alive; and so they are really quite, they are quite entertaining. We have characters, we made characters out of some of these finds, and they really tell us stories.
Steve: Now it's time to play TOTALLY....... Y BOGUS. Here are four science stories; only three are true. See if you know which story is TOTALL....... Y BOGUS.
Story number 1: Idling vehicles in New York City turn out as much pollution as 9 million diesel trucks driving between the Bronx and Staten Island.
Story Number 2: Pro golfers who slept less than four hours before the final round of a major European tournament actually scored better than those who got a full seven to eight hours of sleep.
Story Number 3: Necco Wafers are going all natural; no more artificial colors or flavors, which means sacrificing the lime flavored Necco Wafers because the green color could not be produced naturally.
And Story Number 4: Minivans are just 7 percent of the vehicles visiting your Yosemite Park but 29 percent of the ones vandalized by bears.
Time is up.
Story number 4 is true. Bears preferentially break into minivans in your Yosemite. That is according to a study in the Journal of Mammalogy. Researchers think it is because minivans are more likely to have kids [who are] more likely to leave remnants of cereals, juice boxes and other sweets that the bears like to snack on. The study looked at 908 vehicles broken into by bears between 2001 and 2007.
Story number 1 is true. Idling cars, trucks and buses put out 9 million diesel trucks driving between the Bronx and Staten Island worth of pollution in New York City. That is according to an article in Environmental Health News, bad news in a city with lots of asthmatic children. By law vehicles are not allowed to idle for more than one minute but the law is rarely enforced and vehicles sit there with the engines running for extended periods, including school buses right in front of schools filled with asthmatic kids.
And story number 3 is true. Necco Wafers will now be made with ingredients like beet juice and purple cabbage, but they couldn't find a good way to make green wafers so the lime-flavored ones are being scrapped.
All of which means that story number 2 about sleep-deprived pro golfers scoring better is TOTALL....... Y BOGUS. But what is true is that amateur golfers with sleep apnea were able to shave up to three strokes off their game by getting nasal positive airway pressure treatment, or NPAP. For more, check out the November 2nd episode of the daily Scientific American podcast, 60-Second Science. Because [televised] golf may be great to sleep to on a Sunday afternoon, but when you are actually playing golf it is good to stay awake.
Well that's it for this episode of Science Talk. Check out www.ScientificAmerican.com for the latest science news and George Musser's blog, "Solar at Home" about his attempts to power his house with solar energy. And follow us on Twitter as SciAm, S-C-I-A-M, and Steve Mirsky. For Science Talk, the podcast of Scientific American, I am Steve Mirsky. Thanks for clicking on us.