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0:00
- How can all the diversity and, sort of, seeming order that's out there in the world emerge from a process dependent upon chance?
0:08
It kind of works like a staircase. Chance invents, and natural selection propagates that chance invention. Our immune system works on the very same principles of mutation and selection as evolution at large does in the big world.
0:25
Cancer is truly an evolutionary disease, meaning that it is a disease that results from the exact same evolutionary process we're describing. So while Darwin's is the most famous figure associated with the theory of evolution, Alfred Russel Wallace played a key part. And in their day, this was referred to as the Darwin-Wallace theory. I'm Sean B. Carroll, evolutionary biologist and author of several books, including my most recent, "A Series of Fortune Events:
0:54
Chance and the Making of Planet, Life, and You."
1:04
- [Narrator] Chapter one, how life works: the staircase of evolution. - So evolution, what it really means is change over time. So we wanna know how that change occurs over time. And there's two dimensions to this process, and it kind of works like a staircase. And one process is mutation, and that's the rise in the staircase. Those occur by chance. If mutation didn't happen, all things would be identical. So you need mutation to make individuals different from one another.
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Those mutations are genetic changes, changes in their DNA.
1:39
If by chance that changes a property that favors reproduction, survival of the individuals, it will spread, and that's the selection process. And that's, sort of, the run in the staircase. Chance invents, and natural selection propagates that chance invention. And once that process has happened, new mutations can then be added on top of that, maybe even changing the character a little bit further. And that's another rise in the staircase. And if that's working better, that's gonna spread.
2:09
And so it's the cumulative set of mutations and the cumulative process of selection that takes us up that staircase. So that staircase could have goodness knows how many stairs, but it has to go through this stepwise process of individual mutations arising, sweeping through the population, new ones arising, sweeping through the populations. It doesn't go from the base of the stairs to the top of the stairs in one jump. And this is hard for people to get their heads around
2:36
because they may think about that first step. And it's, sort of, hard to imagine, you know, how do you get something as complicated, you know, as individual organs like an eye or a wing of a bird or things like that. But time, immense time. The speed with which some new adaptation spreads through a population depends upon the magnitude of the advantage it conveys. If it's about a 3% advantage, meaning that about 103 individuals survive for every 100 that don't have it,
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well, that will take about a thousand generations to spread through the population. Now, I'm saying generations because it depends upon the generation time of the creature. So if the generation time, for example, if humans is 25 years, it'll take 25,000 years for that to spread through the human population. But if the generation time is 20 minutes, you can work it out. It'll take, you know, 20,000 minutes to spread through, which is much shorter. It's a matter of generations because reproduction
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is a generation-by-generation process. It's really important to underscore that these mutations occur at random without any consideration of whether they're good or bad for the organism. It's the external conditions that are gonna sort this out. So some things can be good for one creature and bad for another, okay? So for example, a color change might make a creature more invisible in some settings, more visible in another.
3:59
Some mutation may make it better adapted to warmer climates, less well adapted to colder climates, right? So it depends on these external circumstances. So the mutations arise at random. Well, what about those external circumstances? Well, we'd say it's the abiotic conditions, the physical world that the creature is living in. Well, that's also generated a lot at random. Tectonic plates moving across the earth, vulcanism, all the things that shape the conditions of life
4:29
are often due to physical processes of the earth. Of all the many thousands and millions of things that creatures have come up with, I have a few of my favorites that I think really exemplify this process of adaptation. And one of my favorite sets of creatures, there's some fish called icefish. They live in the southern ocean around the Antarctic. And they live in water that is actually below the freezing temperature of fresh water. They're right around about 29 degrees Fahrenheit,
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is the ocean around the Antarctic. And that's a challenging environment, so challenging, for example, that you may know that there's ice flows around there, and if little ice crystals just get into the bodies of these fish, they'll nucleate freezing. They'll freeze like fish sticks. So they need to have a mechanism that prevents them from freezing at that cold temperature. And what they've done is they've evolved antifreeze. Certain proteins in their bloodstream, made in very large quantities,
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suppress the ability of ice crystals to grow inside their bodies. And so they're able to tolerate that subfreezing water of the Antarctic, and other fish aren't. So what's happened over the last 30 or 40 million years is that a lot of fish that were once swam in those oceans, sharks and rays and all that, they're all gone. They're extinct from those waters. We find them in more temperate waters. But it's the icefish and the antifreeze-bearing relatives that those waters.
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And the icefish have also come up with something that's incredibly nifty and shocked naturalists when they first discovered it, which is if you open any fish you know, slice it open, you're gonna see red blood because that's something that animals with backbones have and have had for almost 500 million years on this planet. But you slice open an icefish, their blood is colorless 'cause they've gotten rid of red blood cells. So they don't even have a mechanism for carrying oxygen actively
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in their bloodstream like we do. They've ditched red blood cells, and the reason they've ditched red blood cells is that those low temperatures, it makes their blood too viscous. And that's a disadvantage. To the icefish, it was an advantage to get rid of red blood cells. To the rest of us, it's instantly fatal. So it's a good illustration of just how conditional these adaptations are that to exploit the resources of the southern ocean, you gotta make antifreeze
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and get rid of your red blood cells, where the other parts of the world, antifreeze would be irrelevant, and your red blood cells are necessary for every second of life. Let's talk about speciation. That process of variations helping to adapt, that's the process of adaptation. But speciation is the generation of two species from one. What does that take for there to be two species to form? And we know, and this is where in the island biology of Wallace and Darwin help,
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is that they were seeing species on different islands. Well, islands provide some isolation, and that isolation means that those populations aren't exchanging genes. Over time, each of those populations will accumulate mutations that exist in one population and not the other, vice versa. Well, those could become genetically distinct enough that if those things were ever to come back again in contact, they may not be compatible with one another, and they'll be species. So how long does that take?
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Well, it's been estimated for big animals like mammals and birds, that works out to roughly be about 2 million years. But 2 million years is still a long time. And you've probably heard, for example, that there's now very strong evidence that Homo sapiens, our species, mated with Neanderthals a distinct species.
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And what's really happened in the last few decades is that for biologists, that species barrier has become much more porous than we first thought it was. In the old days, in Darwin's day, species were characterized as really distinct things, and we didn't think there was any kinda shenanigans going on between them. But we now understand that it's a much more porous situation, that for some period of time as populations are diverging, they can get back together.
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And things that we humans might call distinct species can often interbreed. Another common question or idea is that, you know, for example, if humans evolve from apes, why are apes still around? Well, important thing is to understand that evolution is a splitting process. So the family trees keep splitting. So the human part of that tree has had now its own separate history from the eight part of that tree. We shared a common ancestor about 6 million years ago.
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But apes have gone on living as they do, for example, in the old world. And there's a great diversity of apes, of course, still here, baboons, orangutans, gorillas, chimpanzees, et cetera, while the human branch has gone on and has its own evolutionary trajectory. It's not that evolution is linear and that everything new replaces the old. It's a splitting process. And so that's why the tree of life has just split into enormous numbers of branches from common ancestors.
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Two of our main records of evolution are the fossil record and the DNA record. The DNA record is largely only accessible to us for living creatures and maybe some creatures that have lived over the past million years. You know, do we have every brick? Do we have every intermediate? No, 'cause, you know, extinction takes away 99.9% of all species. So if there was no extinction, we'd have a perfect record of evolution, right? We don't have the DNA record of dinosaurs, for example,
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but we've got the fossil record of dinosaurs. So we use these two records to, sort of, reconstruct the history of life. That allows us to reconstruct the evolution of things that are fairly complex. Let's take something like a walking limb from a fish fin. This evolutionary process transpired over, eh, 20, 30 million years, about 380, 390 million years ago. To do that, we have to get fossils that represent the various stages of evolution and see, how did all the bones change
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so you went from a swimming fin to a walking limb? And the fossil record, by now, is pretty darn good. Then we can go to creatures that have fins, fish, and we go to creatures like amphibians that have limbs, and we can figure out how do those genetic programs work, and where are the differences? Now, we don't have every detail sorted out, and that would be incredibly time-consuming and expensive to do, but we certainly have the general picture that we understand how the bones changed in history
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and we understand how the development of program changed to generate a limb in the place of a fin. And that's not something Darwin ever had. That's something that we really only had for the last 20 to 25 years. So evolutionary science keeps building on this huge foundation, and what we get is an ever more detailed and ever more confident record of what's happened. But what's at no doubt is that this process, mutation and selection, mutation and selection,
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is the universal, going on in every population of every living thing every day. In fact, this process of mutation and selection seems so universal that we think it must have played a vital role at the origin of life. And that anywhere where life exists in the universe, it's operating. So evolution is this vast and rich process, and you know, we've been trying to understand it for 160 years. And in the course of that, there's some misunderstanding in just how it's communicated,
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where I think there's some conflict between the terms we scientists use and, sort of, their common understanding. And one of those is theory. We talk of scientific theories. Theory is much higher on the hierarchy than, for example, a fact or just an observation. A theory is assembled from lots and lots of facts and independent lines of evidence that, sort of, cohere. So a theory is really, sort of, the top category of scientific idea, where, of course, you know, in the street,
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theory might mean that's my best guess or that's just something that I'm conjecturing. The way we talk about those kind of conjectures, we call those hypotheses. And that when hypotheses have been rigorously tested, that's what can contribute to making a theory. So folks, when we speak of theory, think that we're still very tentative about, you know, the truth of evolution. That's not all the case. The theory of evolution, which has grown enormously in the last 160 years,
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is a huge body of observations, evidence, and facts that are consistent with one another, that come from completely different sources of science. And that's what gives it its power. We, of course, wish that maybe that connotation of theory that's, you know, more of the everyday connotation would be better understood.
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- [Narrator] Chapter two, how our bodies work: the staircase of self-defense. - Now, here's something about the staircase of evolution that's very little appreciated. It's going on in every one of our bodies every day. It's keeping us alive. And that's because our immune system works on the very same principles of mutation and selection as evolution writ large does in the big world. Every day, we are exposed to all sorts of potential pathogens: bacteria viruses fungi parasites.
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We've gotta fend these off.
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And by the time we're full-grown adults, there are actually more bacterial cells living on and in our bodies than there are our own cells, trillions and trillions of microbes. We've gotta keep these in check, or, of course, we'll suffer and potentially die. And that's the job of our immune system. And our immune system operates on the very same principles as the staircase of evolution. It's a staircase of self-defense. And the most remarkable property, our immune system,
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is it seems to be able to recognize as foreign virtually anything that can come at us out of nature, including entirely new pathogens that didn't even exist in the human population. And how do we do that?
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Well, it involves a process based on mutation and selection. And the way this starts, I'll just describe it starting with a single cell. So you have billions of cells, but these cells have different molecules on their surface that when they are complementary to molecules on the surface of a pathogen, they're activated, they're engaged. And when engaged, they multiply very rapidly such that over a period of about a week, one cell may become billions of cells and start to pump out large quantities
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of chemical weapons known as antibodies that thwart that invader. These billions of cells over our immune system are actually clones, clones that are subtly distinct from each other that have unique ability to recognize something else. Now, that something else could be any variety of things on an invading pathogen, but once they recognize that, that clone gets amplified, can grow to be many, many, many cells in the course of a week or so. That first wave of defense is decent, but not optimized.
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There's actually a mechanism to make those chemical weapons, the antibodies that cell makes, even more potent, even more deadly to essentially the invading pathogen. And that's because there's a specific genetic mechanism that mutates the antibody-encoding genes. Leaves the rest of the genes in the body alone, but just the antibody genes start undergoing a process called hypermutation and, therefore, generating all sorts of antibody variants. And the antibody variants
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that recognize the pathogen better are selected for. So here we go. We're climbing the staircase. So this hypermutation process, we now select antibodies, and this can go through various cycles to make ever better and better antibodies. So we're really zeroing in on this particular pathogen. So late in immune response, say, for example, the second week you're recovering from a flu virus, your immune system is ever more potent,
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ever more powerful in defeating its enemy because it's up that staircase. Eventually, a staircase, sort of, splits, and some cells are set aside as what's called memory cells. They're there to be used when this pathogen is encountered again. Other cells continue to make the antibodies. Now, this is the marvelous thing. Y'all are familiar with a phenomenon where, for example, you don't get measles twice, you don't get chicken pox twice, et cetera. Why is this? Immunological memory.
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That even if 50, 60, whatever number of years ago you might have been exposed to that virus, your immune system is still poised
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to attack it again if you're exposed again so you don't even get the infection. This system is called adaptive immunity, much like the process of evolution of mutation and selection is adaptive. It really only exists in this form, in animals with backbones, long-lived, generally larger animals. And you can see its utility because the longer your lifespan, the greater the chance you're gonna re-encounter a particular pathogen. If you're a short-lived mayfly or something like this,
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you don't live long enough to see the same thing twice. There's not that kind of immunity. So lots of animals including, you know, simpler things like worms and flies and all that, they have what we call innate immunity. They have ways that, sort of, put barriers up against pathogens. But this adaptive immunity only exists in creatures with backbones, with vertebrates. And it's pretty elaborate in us, in mammals, animals with fur, et cetera. But it's pretty well developed
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even in things like fish and sharks. Inside our bodies, the timescale of this process is very, very fast. It's more like what we described with respect to microbes 'cause it starts with cells and cells that can multiply pretty frequently. So a lot of evolution can take place in a short time. Most of us are, sort of, familiar that, you know, most infections don't knock us down for more than about a week. That's when our immune system eventually, sort of, catches up and overtakes the pathogen.
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So that gives you a sense of the timescale it takes to mount the response, expand that response to the point where it overwhelms the pathogen, whereas out there in the world, sort of, a battle between predator and prey or whatever, that may go on for hundreds of thousands of years before there's, sort of, a winner. Same process, much more rapid timescale in your body.
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How is it possible that we can recognize virtually anything that the world will throw at us? And fundamentally, one of the problems there is, sort of, a coding problem. How can one make all the different kinds of antibodies that could recognize all the different possible pathogens that, you know, a species might encounter?
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And the solution to that required understanding how antibody genes are encoded in DNA, something we weren't able to do until the 1970s or so. And what that's revealed is that we mix and match pieces of antibodies in a way that we can generate millions of combinations of antibodies. And it's now estimated that we may be able to make about 10 billion different antibodies. And you might go, "Well, that sounds, sort of, impressive, but okay." Well, here's the thing:
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In our entire genome, all of our DNA, we only have about 20,000 genes. So how do you make 10 billion antibodies when there's only 20,000 genes to begin with? And this is the brilliant trick of the immune system. It makes antibodies from short little gene segments that it mixes and matches in millions, if not billions, of combinations. So the trick of combinations is that it's just like in a, you know, if you can take a deck of cards, right,
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and you have, you know, five cards you draw from a deck, there's lots and lots of different combinations you can, even if you have only 52 different cards. And so from a modest number of antibody genes on the order of a few hundred, by mixing and matching them in pieces, we can generate enormous numbers of antibodies. So the immune system, even with all its powers, can still be, sort of, beat to the punch. There's still pathogens that can kill us. And this is why we vaccinate.
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And we understand, in vaccines, generally what we're giving is a little component, usually a non-living component, not the virus itself, not the pathogen itself, but maybe just a molecule that represents that pathogen. And we're using that to prime the immune system. So we're activating the immune system so it goes through some of those steps on the staircase, establishes memory, and is poised to respond, should we encounter that pathogen. And by being vaccinated, by being immunized,
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that can save lives, certainly save the suffering of a particular disease, shorten its course, save us days off work, whatever it might be. But this is why we have these vaccine strategies and we seek ways to give our immune system a head start 'cause if we don't vaccinate, then we're at risk of suffering the damage that pathogen causes unless or until our immune system catches up, feeling lousy, or in some cases, there's lots of morbidity with these infections. One of the most notorious ones
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in human history is the smallpox virus, which killed hundreds of millions of people in human history and even tens of millions of people in the 20th century until we came up with a vaccine. And there was a global effort to vaccinate virtually every human on the planet. And that eradicated smallpox from the world so that now we don't even vaccinate for smallpox. But that was a virus that moved faster and caused greater pathology than our bodies could keep up with.
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- [Narrator] Chapter three, how cancer works: the staircase of mutation.
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- So we understand this evolutionary process is what drives our adaptive immune system and protects us against enemies from without. But it turns that sometimes the enemy is coming from within the house. And I'm speaking specifically of cancer. And cancer is truly an evolutionary disease, meaning that it is a disease that results from the exact same evolutionary process we're describing of the evolutionary process in the external world, of the evolutionary process in the immune system.
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Cancer forms in the same way, and that is mutations take place in individual cells that if they convey some growth advantage to those cells,
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those cells may outgrow their neighbors, and additional mutations may happen so they outgrow their neighbors further. And that's what we define as a tumor, a population of cells that is now growing unregulated relative to its normal neighbors. And that's a threat because that unregulated growth can lead to spread throughout the body, can lead to organ involvement, et cetera, and death. But the other concern is, is that cancer gets larger,
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some of those cells are gonna get yet additional mutations, and some of those cells are gonna get yet additional mutations. And so as cancer progresses over time, that tumor is less and less like the cell it started from, and the tumor itself is more genetically diverse. And that's giving us a real challenge therapeutically. So there is a staircase of cancer, and the way to understand that is that our risk of cancer is really age-dependent. The incidence of cancer goes up really significantly
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as we get older. And think for a moment why that might be. And what that is is it takes time to climb that whole staircase. So later in life, individual cells have gone through more divisions, they've had more chances to accumulate mutations, mutations that give them some growth advantage over other cells. And so our risk of cancer grows really significantly as we get into our 40s, 50s, 60s, and 70s.
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So that tells us not only is it an evolutionary disease, it's a genetic disease. It's mutations taking place in genes that somehow disrupt the normal process of controlling cell growth. So a huge interest has been, what are those genes? How do we find them? How does this all work? We first got a hint that cancer was a genetic phenomenon when scientists first started seeing chromosomal changes in cancers, chromosomes that were broken and fused and things like this and that all the tumor cells
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would have those broken chromosomes or tumors that arose independently in different people would have those rearranged chromosomes. And that gave us a hint, okay, something genetically is going on. But the crucial thing was to identify, well, what genes? Well, thanks to genomics, thanks to gene cloning, we now know that there are about 20,000 genes that essentially run the human body. And we've identified 150 of those that, when mutated, can contribute in some way to cancer.
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We'll call those drivers, and those drivers split into two classes.
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One class we'll call accelerators because when they're mutated, they really accelerate cell multiplication. They also have the name oncogenes, promoting cancer. Another class of genes, they serve as brakes, they hold back proliferation, But if they're disrupted by mutation and we no longer have their braking function, then the cells can grow out of control. So just like an out-of-control car, out-of-control self-proliferation can even be due to a stuck accelerator or a broken brake.
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It can be due to oncogenes that promote cancer or tumor suppressors that would normally suppress that cancer, but they've been disrupted by mutation. So scientists have banded together across the world to build this, sort of, catalog of driver genes. And so they study the state of these genes in all sorts of cancers. And there's some really, really clear insights from doing this. And the first is, well, it's a multi-hit process. Usually, any cancer has disruptions to multiple genes,
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might be three, four or five, even seven of these driver genes. And if we look at cancers that arrive in kids and compare that with cancers that arise in adults, there's a really profound distinction. When we look in kids, we see there are very few mutations overall in the DNA of the cancer cell, but they'll be in driver genes. And you don't see many other mutations that have taken place that are different, say, from Mom and Dad's DNA. And that's because a young child,
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its cells have not gone through that many divisions. It's not accumulated very many other mutations. It just so happens the mutations that occurred were in these critical driver genes. It's horrible, heartbreaking, bad luck.
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But the longer we live, all of our cells, whenever DNA is copied, mutations occur. Now, most of those mutations have no effect. They're sprinkled among the billions of bases that we have. But every now and then, one of these driver genes gets hit. Well, the longer we live and the more divisions our cells have gone through, the greater the chance that there have accumulated mutations
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and eventually hit one or more driver genes. And once they hit a driver gene, if that cell starts to out-proliferate its neighbors, well, then those cells in turn may be going through more rounds of division, more mutations. And so now, essentially the snowball is rolling
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such that by later in life, we have cells that have accumulated a number of driver mutations, and many of our cells at least have one driver mutation. It may not be pathogenic whatsoever, but a lot of our cells will have mutations in them, some of which could eventually be a problem. So understanding that cancer is this, sort of, disease, this interplay of mutation and selection, there's really three factors that can contribute to the formation of cancer.
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First is just bad luck, that the small number of mutations that are gonna happen anyway just happen to hit driver genes. Really, that's the explanation of pediatric cancer. And the kindest thing you can do to any parent whose child is struck is to reassure them that there was nothing they did to cause it and nothing they could have done to prevent it. Then there are lifestyle issues, like tobacco use and sun exposure. They'll increase the risk of particular cancers,
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lungs because that's where the smoke goes, and of course, the skin 'cause that's what's being exposed to the sunlight. And the third is just age. It's time. The longer we live, the more divisions our cells have gone through, the more mutations have happened, and the more all the environmental things that we've been exposed to have had chance to work on us so that later in life, our cells are carrying loss of mutations, and we just hope that none of those cells
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have, sort of, that unlucky combination of mutations that will make it an uncontrollable tumor. So I think there's a few pillars of how we're combating cancer now that's really different from how we did it before. Now, for prevention, we're looking for these mutations. So you've seen, for example, a product like Cologuard where a stool sample can be sent to a company. Well, they're looking for mutations characteristic of gastrointestinal cancers in that fecal sample, okay?
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So that's early detection. And we know that the earlier you can detect cancer, the better shot you have of counteracting it.
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The second pillar is to know those cancers and to realize that different driver genes are mutated in different cancers. So instead of treating breast cancer as a monolith, we now subtype breast cancer according to the mutations that exist in an individual's tumor. So it's really important that the genotype, meaning the genetic makeup of a tumor, is analyzed when that is first diagnosed. That will shape the treatment course because the other thing that oncologists are doing
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is they use different drugs, different regimens to go after these cancers is to study which things work against which genotypes of cancer. So we're now, I think, classifying and categorizing cancers with much greater degree of sophistication. And then there is the specific therapy side. All sorts of drugs have been designed to go after those mutated genes,
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so to specifically target what has gone wrong in an individual cancer because of the mutation of a particular gene. Some of these drugs have been spectacular success. Some are doing a good job at, let's just say buying time in the hope that the cancer be contained and, you know, managed over the longer period of time and treated more as like a chronic disease, not necessarily eliminated, but at least managed. Only in the last about 25 years has this really been possible, but the practice of this
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has really grown enormously in the last about 15 years. And there's all sorts of new drugs under clinical trials at any given moment, again, trying to give a much more specific therapy to the particular alterations that had happened in a given individual's tumors. Better prevention, better diagnosis, better therapy, this is driving cancer rates down, certainly for certain types of cancers, and hopefully going to drive survival rates up over the long term.
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These parallels in how life evolves, how the immune system works, how cancer arises, at one level, they're startling because the connections aren't so obvious, but fundamentally, they're operating on the same process, this mutation and selection. But of course, mutation is a random process, and it's really hard to get our heads around, how can all the diversity and, sort of, seeming order that's out there in the world
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emerge from a process dependent upon chance? Yet there you have it. Whenever you have variation and you have competition, natural selection operates and gives us the variety of life. In the immune system, chance is being exploited. You think, "Well, we can't leave the defense of our bodies against chance," but here we're exploiting chance. Now, of course, cancer has its root in chance, the unlucky mutation that hits a gene that could throw a cell out of balance with a body.
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That evolutionary process we've been discussing is one of error and trial,
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whereas humans, sort of, think like engineers. We think of what we want as an outcome and how we can get there, sort of, in the shortest distance. And we may use some trial and error, but we really try to minimize the error, whereas really these evolutionary processes start with error. They start with a random change and then try those things out.
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And I think it's just been hard for us to get our heads around that, yet the more we understand this and all of its manifestations and the immune system and cancer are too later realizations, we see that this process is a fundamental biological process, random genetic variation and the sorting of that variation through natural selection.
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- [Narrator] Chapter four: The untold story of Alfred Russel Wallace.
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- So about 15 years ago on a visit to the University of Cambridge, I happened to visit the archives there where they hold a lot of original materials from Darwin.
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And to my astonishment, they brought out and placed into these sweaty hands a copy of one of the early manuscripts that, many, many, many years later, would be modified into the origin of species.
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After Darwin got back from his voyage, he was pondering these ideas, and he decided to write them down in essay form. And by 1844, he completed a 230-page essay that's fleshed out a lot of his basic ideas. He wouldn't publish anything on evolution for 15 years. That essay, I think, was lost for decades and found under the steps of his house. So when it was presented to me, all over the manuscript, including on the back pages, there were drawings by Darwin's kids,
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they had been using it like scrap paper.
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It was a spine-tingling moment for me because this was really the birth of one of the biggest ideas humans have ever had. And I'm grateful that they found it under the stairway at Darwin's house. So while Darwin's is the most famous figure associated with the theory of evolution, Alfred Russel Wallace played a key part and deserves huge credit, both for his ideas and for his enormous effort. So really important to understand that the prevailing idea at the time to which Darwin subscribed
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and most British scientists subscribed was, we'll call special creation or the theory of special creation. And that was the idea that every species was specially created by God and, sort of, placed, or at least emerged in the habitat or in the place on the globe that best suited it. Now, what started to shake that theory in Darwin's mind and in Wallace's mind was in the course of their journeys, particularly when they visited archipelagos, strings of islands,
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each of them observed species on different islands that were slightly different from one another. Now, Darwin, and this is just a twist of his story, after nearly five years at sea and having made a full voyage around the world, they were about to turn from the southern tip of Africa back up to Europe. But his captain, who was, sort of, obsessive, decided he wanted to do some more measurements in South America, so he went back across the Atlantic. And Darwin was, at first, just crestfallen
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that he wasn't headed home, but he needed to make good use of that time. And he started to take his notebooks out and review what he had seen, but also, sort of, annotate them. And he thought back to the Galapagos Islands, and he thought back to these mockingbirds that he had seen on different islands. And he saw that on different islands, the Mockingbird were slightly different from one another in their feather patterns and things like that. And he thought,
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these islands were within sight of one another, just 50 or 60 miles away from one another. If a creator was placing species, sort of, perfectly adapted to each place, why would these mockingbirds be just slightly different from one another? Now, Wallace's story is more dramatic because Wallace, after four years in the Amazon, really at the breaking point, decided to return to England with specimens and whatever ideas he had collected. And on his way home, his ship caught fire.
39:07
He had to get into a lifeboat. The ship sank right in front of him with all of his specimens. And he was in an open lifeboat for 10 days, hoping to be picked up.
39:17
And he was picked up, eventually made his way back to England. You'd think after that experience, he would've sworn off all voyaging. But two years later, he goes back out and does an eight-year voyage across the Malay Archipelago and collects tens of thousands of more specimens. He noticed, for example, that birdwing butterflies, these beautiful, incredibly brilliantly-colored, large butterflies were slightly different from island to island. They both thought in the theory of special creation,
39:45
these islands all looked alike. Why would there be just slightly different species, island to island? And it struck both of them: because species could change. Species weren't stable, they weren't immutable, as the theory of special creation argued. They in fact changed. And this opened up the big question then, or at least the daring question, of, are species the product of natural processes or divinely created? And they thought this was strong evidence that species change naturally.
40:20
They change according to the conditions they encounter in different places. And the islands were crucial, sort of, laboratories for understanding this because the volcanic islands of the Galapagos look very similar to one another, but the creatures were a bit of different. The islands of the Malay Archipelago, very similar foliage and all that, but the creatures were a little bit different. And the only way they could, sort of, reconcile that was to say, well, the species were changing.
40:44
They weren't fixed. They weren't immutable. And as they worked further, they thought about some other patterns. They knew about fossils. In fact, Darwin discovered some really interesting fossils on the coast of Argentina. And through correspondence back home while he was at sea, he realized these were, sort of, larger versions of animals that lived in South America at the time. So he found, for example, giant ground sloths. You know, huge, like, eight-feet-tall ground sloths,
41:12
much larger than the living ones. But he realized, hmm, those are extinct creatures. What's the relationship between the extinct and the living? And he's starting to think about that genealogy between the extinct and the living. And Wallace is also becoming aware of these fossils 'cause he's reading now what's coming out from the first studies fossils in Britain in the first part of the 19th century. They had also each read this work by an economist Thomas Malthus. And Malthus emphasized
41:46
that there were limits on populations. He thought about the growth of populations. And Malthus said that, you know, disease and famine, that limited, for example, the growth of populations. Well, Darwin and Wallace being out in nature, they understood that life was very tough. They understood that, really, life was a battlefield, a contest, and that far more young are produced than can survive to adulthood. And what's uncanny is when you look at the writings
42:15
of each of these individuals, Darwin's notebooks, Wallace's draft manuscript, they use the same language. They describe life as, quote, "A struggle for existence," exactly the same words, unbeknownst to each other. And they talk about variations, however slight, and that they could be favored. And that led Darwin to coin the word natural selection. They'll be selected for in nature. And the things that are disadvantaged will be selected against. And Wallace said essentially the same thing,
42:51
that one could imagine if there's a slight advantage, that slight advantage will be passed on, generation after generation. So Darwin, for 20 years, is back home in England. He's well-known because right after he did the voyage on the Beagle, he wrote a book that we call today, "The Voyage of the Beagle." And it was a popular read. It's a great read. It's still a great read today about his travels. And he was an eminent naturalist. Wallace was an unknown. He was from far more modest upbringing,
43:24
and he was really paying his way on his voyages by selling a fraction of the specimens that he was collecting. So he was thousands and thousands of miles away from the center of science in England, and he wasn't connected really at all. So Wallace, by 1858, has a pretty good idea that life changes, life evolves. And he writes up a very short account of his thinking about how that works. And he decides to send it to the one naturalist with whom he struck up a correspondence
43:57
who thinks might appreciate it. He sends it to Charles Darwin.
44:02
Well, this event rocks Darwin, because Darwin has not gone public with his theory of evolution. And now here's this far-away correspondent, 7,000 miles away from England, who, in just a few pages, essentially the same idea that Darwin has, that Darwin's labored on for about 20 years. Well, Darwin's friends rally and decide that the best thing to do would be to read Wallace's paper and an excerpt from Darwin's work in front of a British scientific society
44:30
to, sort of, put both of these ideas out in the public. Darwin wasn't there. It turns out Darwin had suffered tragedy. He was burying Charles Jr., one of his sons, on the day this paper was read. And Wallace was 7,000 miles away, didn't even know it was going on.
44:47
It really didn't make much of a splash, not much attention was paid. But the next year is when Darwin published "On the Origin of Species," and that's when everyone paid attention. The response and acceptance or rejection, particularly to Darwin's "Origin of Species," 'cause that's the book everybody could put their hands on. It sold out in its first printing, it was reprinted quickly, it was translated into other languages, American versions were made.
45:14
So people who are interested in science, biology, natural history around the world could get their hands on Darwin's ideas. So the reactions were a very wide spectrum. Thomas Huxley, who was one of Darwin's close confidants, sort of, thought, "You know, wow, why didn't I think of that?" He thought it was, you know, compelling and sort of obvious. But I think one thing to appreciate with Darwin is that his book is extraordinary in that he also presents
45:45
and analyzes the critiques of his own theory. I mean, imagine that. This is just something that human beings don't generally do. If they've got an idea, they're gonna put out all the evidence in favor of their idea and they're usually not going to present to the opposition all the evidence either against it or all the evidence that's missing. But Darwin did this in a masterful way and basically often saying things like, you know, if a particular thing was found, it could crush my theory.
46:10
Or if my theory is true, this would be true, but there wouldn't necessarily be any evidence weighing on that. So it was a masterful presentation. And I think it made it very accessible to people. They understood the strengths and weaknesses of the theory, and then new discoveries could be interpreted in light of that theory. And as some new discoveries, particularly from the fossil record, came to light, well, that gave a lot of power to Darwin, 'cause Darwin,
46:37
at the time "Origin of Species" was published, the fossil record was pretty skimpy,
46:43
but Darwin made some really strong predictions about what should be found, for example, in the fossil record. And one of those was transitional forms. If the tree of life has evolved in the way that he said, there should be forms that are intermediate between existing forms today. And two years after the "Origin of Species," a fossil called Archaeopteryx, which has got mixed characteristics of both birds and reptiles, was discovered. And I mean,
47:12
you couldn't have drawn anything better than that fossil for supporting Darwin's theory. So I think the reception of the scientific community, some of it, at first, was, you know, positive, but there were long, long holdouts. There were career long holdouts against Darwin among even very eminent natural historians, biologists, and scientists. And that holdout was really for reasons we'd all recognize today. While Darwin didn't, in 1859, didn't comment directly on the evolution of humans,
47:48
he did later in 1871. Everyone knew that humans were gonna be a touchy subject, because for at least a couple millennia, the thinking was that, you know, man was created in God's image, not descended from some previous animal forms. But clearly Darwin's theory would be interpreted to say that, no, humans, just like every other animal, evolve their anatomy and their physiology from preexisting forms. And some scientists held out on that point, both perhaps from their own viewpoint of faith,
48:25
but also, I think, because of some pressures in the academy. Darwin was on the short list to be knighted when the origin of species came out. Well, he never got that knighthood. So, you know, this was an idea that many people found repulsive. They were really worried about the societal implications to, sort of, take the creator out of the immediate picture of sort of, you know, tending to human affairs. And that's, of course, still a struggle that exists to today.
48:57
And, you know, scientists, you know, being part of society, it was not universally, you know, accepted, far from it. Where Wallace really finally grasped the scope of what Darwin had been working and thinking
49:13
was in 1859 when "The Origin of Species" was published. And he received a copy of "The Origin of Species." And he read it and reread it. In fact, Wallace's own copy is in the Natural History Museum in London. So we can understand, sort of, his reactions in real time. But I think one of the most poignant things I know in the history of science was Wallace's put his thoughts in reactions in a letter to his close friend in confidant, Henry Walter Bates,
49:42
with whom he had first traveled to the Amazon. And Wallace is just gushing with admiration for Darwin. And he says, "I never, given any amount of time, I could have never come up with something as massive and compelling as Darwin." And he said, "I don't think any branch of science has ever been created by an individual such as this, such as Darwin." So Wallace was in awe of Darwin's synthesis, which was "The Origin of Species," but they were mutually generous to each other.
50:15
Darwin, right off on page one, acknowledges Wallace and Wallace's ideas. And Wallace later, for example, when he writes his first major book, he dedicates it to Darwin. They are, you know, mutual admirers to the point where, for example, Wallace is gonna be a pallbearer at Darwin's funeral.
50:35
And in their day, this was referred to as the Darwin-Wallace theory.
50:41
It's only later that biologists and historians just started kind of forgetting about Wallace and crediting Darwin. Now, there might be reasons for that. Darwin came from a wealthy family. The University of Cambridge did a great job at, sort of, amassing Darwin's collections and Darwin's writings. And so we just have a better historical record of everything that Darwin did. But at the time, it was the Darwin-Wallace theory. And I think by today's scientific standards,
51:11
given the genesis of this theory, the theory certainly of natural selection by the two individuals, we would be crediting both of them. And you know, it's just the unfortunate sort of, you know, accidents of time that people kept talking about Darwin and Wallace, sort of, faded to the background. But I really feel in the last 25 years or so that Wallace has seen, sort of, a renaissance and that people are much more aware of Wallace's huge contributions.
51:40
And then Wallace outlived Darwin by 30 years. So he was a really important figure in the discussion of evolution 'cause, you know, this was a brand new science. It had relatively few advocates at the beginning, certainly people that really understood it well. And so Wallace played a huge role in getting people to help understand these ideas. I think if Darwin and Wallace were alive today, they would be so overjoyed
52:07
by the detail with which we understand the process that they first figured out. They knew variation was important, they knew variation was the fuel of the evolutionary process, had no idea how that variation arose. Now any biologist can point right to the DNA in a newly hatched creature and say, "There's the mutation. That's what's gonna make the difference." So our understanding of the material basis of evolution is phenomenally strong. And I think that would be extremely gratifying to them.
52:44
But these other manifestations, the role it plays in health and disease were nowhere in Darwin and Wallace's minds. So I think that would, again, further astound them that this process they figured out had such widespread ramifications beyond just the natural world. What we've seen are striking parallels in how life evolves, how our immune system works, and even how cancer arises, this process of mutation and selection, the staircase. So really, the process
53:24
that Darwin and Wallace had that first insight into is a universal process. Wherever there's variation, wherever there's competition, selection will operate. For me personally as an evolutionary biologist, this just underscores the explanatory power of evolutionary theory
53:43
and the importance of understanding the evolutionary process. You might think, "Well, the evolutionary process, let's just leave it to the scientists to worry about it." But I think in our daily lives, you understand that this is why we vaccinate. This is why we are now developing these strategies against cancer that we, of course, hope everybody will be able to benefit from. That's a long way from the Beagle voyage of 160 years ago. But that's fundamentally where Darwin
54:14
and Wallace have brought us.
54:26
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