Shadowing Practice: How evolution works, in 54 minutes | Sean B. Carroll: Full Interview - Learn English Speaking with Video
Creating lesson...
1
How can all the diversity and sort of seeming order that's out there in the world
2
emerge from a process dependent upon chance?
3
It kind of works like a staircase.
4
Chance invents and natural selection propagates that chance invention.
5
Our immune system works on the very same principles of mutation and selection as evolution at large does in the big world.
6
cancer is truly an evolutionary disease meaning that it is a disease
7
that results from the exact same evolutionary process we're describing so
8
while darwin's is the most famous figure associated with the theory of evolution alfred russell wallace played a key part
9
and in their day this was referred to as the darwin wallace theory i'm sean b carroll evolutionary biologist
10
and author of several books including my most recent a series of fortunate events chance
11
and the making of planet life and you chapter one how life works the staircase of evolution
12
so evolution what it really means is change over time
13
so we want to know how that change occurs over time
14
and there's two dimensions to this process and it kind of works like a staircase
15
and one process is mutation and that's the rise in the staircase those occur by chance
16
if mutation didn't happen all things would be identical
17
so you need mutation to make individuals different from one another those mutations are genetic changes changes in their DNA.
18
If by chance that changes a property that favors reproduction, survival of the individuals, it will spread.
19
And that's the selection process.
20
And that's sort of the run in the staircase.
21
Chance invents and natural selection propagates that chance invention.
22
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.
23
And that's another rise in the staircase.
24
And if that's working better, that's going to spread.
25
And so it's the cumulative set of mutations and the cumulative process of selection that takes us up that staircase.
26
So that staircase could have goodness knows how many stairs, but it has to go through this stepwise process of individual mutations arising,
27
sweeping through the population, new ones arising, sweeping through the populations.
28
It doesn't go from the base of stairs to the top of the stairs in one jump
29
and this is hard for people to get their heads around
30
because they may think about that first step
31
and it's sort of hard to imagine you know how do
32
you get something as complicated you know as individual organs like an eye
33
or a wing of a bird or things like that
34
but time immense time the speed with
35
which some new adaptation spreads through a population depends upon the magnitude of the advantage it conveys
36
if it's about a three percent advantage, meaning that about 103 individuals survive for every hundred that don't have it.
37
Well, that will take about a thousand generations to spread through the population.
38
Now, I'm saying generations because it depends upon the generation time of the creature.
39
So if the generation time, for example, of humans is 25 years, it'll take 25 ,000 years for that to spread through the human population.
40
But if the generation time is 20 minutes, you can work it out.
41
It'll take 20 ,000 minutes to spread through, which is much shorter.
42
It's a matter of generations because its reproduction is a generation -by -generation process.
43
It's really important to underscore
44
that these mutations occur at random without any consideration of whether they're good or bad for the organism.
45
It's the external conditions that are going to sort this out.
46
So some things can be good for one creature and bad for another.
47
So, for example, a color change might make a creature more invisible in some settings, more visible in another.
48
Some mutation may make it better adapted to warmer climates, less well adapted to colder climates, right?
49
So it depends on these external circumstances.
50
So the mutations arise at random.
51
Well, what about those external circumstances?
52
What we'd say is the abiotic conditions, whether the physical world that the creature is living in.
53
Well, that's also generated a lot at random.
54
Tectonic plates moving across the earth,
55
um, you know, volcanism, all the things that shape conditions of life are often due to physical processes of the earth.
56
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.
57
And one of my favorite sets of creatures are some fish called ice fish.
58
They live in the Southern Ocean around the Antarctic
59
and they live in water
60
that is actually below the freezing temperature of fresh water they're
61
right around about 29 degrees Fahrenheit is the ocean around the Antarctic and that's a challenging environment,
62
so challenging, for example, that you may know that there's ice flows around there.
63
And if little ice crystals just get into the bodies of these fish, they'll nucleate freezing.
64
They'll freeze like fish sticks.
65
So they need to have a mechanism that prevents them from freezing at that cold temperature.
66
And what they've done is they've evolved antifreeze.
67
Certain proteins in their bloodstream made in very large quantities suppress the ability of ice crystals to grow inside their bodies.
68
And so they're able to tolerate that sub -freezing water of the Antarctic.
69
And other fish aren't.
70
So what's happened over the last 30 or 40 million years is
71
that a lot of fish that once swam in those oceans, sharks and rays and all that, they're all gone.
72
They're extinct from those waters.
73
We find them in more temperate waters.
74
But it's the ice fish and the antifreeze -bearing relatives that exploit those waters.
75
And the ice fish have also come up with something that's incredibly nifty and shocked naturalists when they first discovered it, which is if you open, which any fish you know,
76
slice it open, you're going to see red blood because that's something
77
that animals with backbones have and have had for almost 500 million years on this planet.
78
But you slice open an ice fish, their blood is colorless because they've gotten rid of red blood cells.
79
So they don't even have a mechanism for carrying oxygen actively in their bloodstream like we do.
80
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.
81
To the ice fish, it was an advantage to get rid of red blood cells.
82
To the rest of us, it's instantly fatal.
83
So it's a good illustration of just how conditional these adaptations are, that to exploit the resources of the Southern Ocean, you've got to make antifreeze
84
and get rid of your red blood cells where the other parts of the world antifreeze would be irrelevant
85
and your red blood cells are necessary for every second of life let's talk about speciation
86
that process of variations helping to adapt that's the process of adaptation
87
but speciation is the generation of two species from one what is what does
88
that take for there to be two to two species to form
89
and we know this is where the island biology of Wallace
90
and Darwin help is that they were seeing species on different islands.
91
Well, islands provide some isolation, and that isolation means that those populations aren't exchanging genes.
92
Over time, each of those populations will accumulate mutations that exist in one population and not the other, vice versa.
93
Well, those can 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.
94
So how long does that take?
95
Well, it's been estimated for big animals like mammals and birds, that works out to roughly be about two million years.
96
But two million years is still a long time.
97
And you've probably heard, for example, that there's now very strong evidence that Homo sapiens, our species, mated with Neanderthals,
98
a distinct species and what's really happened in the last few decades is
99
that for biologists
100
that species barrier has become much more porous than we first
101
thought it was in the old days in darwin's day species were characterized as really distinct things
102
and we didn't think there was any kind of
103
shenanigans going on between them but we now understand
104
that it's a it's a much more porous situation
105
that for some period of time as populations are diverging they can get back together
106
and things that we humans might call distinct species can often interbreed another common question
107
or idea is is that you know for example
108
if humans evolved from apes why are apes still around well the important thing is understand
109
that evolution is a splitting process so the family trees keep splitting
110
so the human part of
111
that tree has had now its own separate history from the eight part of
112
that tree we shared a common ancestor about six million years ago but apes have gone on living as they do, for example, in the old world.
113
And there's a great diversity of apes, of course, still here, baboons, orangutans, gorillas, chimpanzees, et cetera,
114
while the human branch has gone on and has its own evolutionary trajectory.
115
It's not that evolution is linear and that everything new replaces the old.
116
It's a splitting process.
117
And so that's why the tree of life has just split into enormous numbers of branches from common ancestors.
118
Two of our main records of evolution are the fossil record and the DNA record.
119
The DNA record is largely only accessible to us for living creatures
120
and maybe some creatures that have lived over the past million years you know, do we have every brick?
121
Do we have every intermediate?
122
No, because extinction takes away 99 .9 % of all species.
123
So if there was no extinction, we'd have a perfect record of evolution, right?
124
We don't have the DNA record of dinosaurs, for example, but we've got the fossil record of dinosaurs.
125
So we use these two records to sort of reconstruct the history of life.
126
That allows us to reconstruct the evolution of things that are fairly complex.
127
Let's take something like a walking limb from a fish fin.
128
This evolutionary process transpired over 20, 30 million years, about 380, 390 million years ago.
129
To do that, we have to get fossils
130
that represent the various stages of evolution
131
and see how did all the bones change so you went from a swimming fin to a walking limb.
132
And the fossil record by now is pretty darn good.
133
Then we can go to creatures that have fins, fish, and we go to creatures like amphibians that have limbs,
134
and we can figure out how do those genetic programs work and where are the differences.
135
Now, we don't have every detail sorted out, and that would be incredibly time -consuming and expensive to do,
136
but we certainly have the general picture that we understand how the bones changed in history,
137
and we understand how the development of program changed to generate a limb in the place of a fin.
138
And that's not something Darwin ever had.
139
That's something that we really only had for the last 20 to 25 years.
140
So evolutionary science keeps building on this huge foundation.
141
And what we get is an ever more detailed and ever more confident record of what's happened.
142
But what's it no doubt is that this process,
143
mutation and selection, mutation and selection is the universal going on in every population of every living thing
144
every day in fact this process of mutation and selection seems
145
so universal that we think it must have played a vital role at the origin of life
146
and that anywhere where life exists in the universe it's operating
147
so evolution is this vast and rich process
148
and you know we've been trying to understand it for 160 years
149
and in the course of that there's some misunderstanding and just how it's communicated,
150
where I think there's some conflict between the terms we scientists use and sort of their common understanding.
151
And one of those is theory.
152
We talk of scientific theories.
153
Theory is much higher on the hierarchy than, for example, a fact or just an observation.
154
A theory is assembled from lots and lots of facts
155
and independent lines of evidence that sort of cohere
156
so a theory is really sort of the top category of
157
scientific idea of course you know in the street theory might mean that's my best guess
158
or that's just something that i'm conjecturing
159
the way we talk about those kind of conjectures we call those hypotheses
160
and that when hypotheses have been rigorously tested that's what can contribute to making
161
a theory so folks when we speak of theory think that we're still very tentative about the truth of evolution.
162
That's not all the case.
163
The theory of evolution, which has grown enormously in the last 160 years, is a huge body of observations,
164
evidence, and facts that are consistent with one another, that come from completely different sources of science.
165
And that's what gives it its power.
166
We, of course, wish that maybe that connotation of theory that's you know, more of the everyday connotation would be better understood.
167
Chapter Two, How Our Bodies Work, The Staircase of Self -Defense.
168
Now here's something about the staircase of evolution that's very little appreciated.
169
It's going on in every one of our bodies every day.
170
It's keeping us alive.
171
and that's because our immune system works on the very same principles of mutation and selection
172
as evolution writ large does in the big world every day
173
we are exposed to all sorts of potential pathogens bacteria viruses fungi parasites we've got to fend these off
174
and by the time we're full grown adults,
175
there are actually more bacterial cells living on and in our bodies than there are our own cells.
176
Trillions and trillions of microbes.
177
We've got to keep these in check or of course we'll suffer and potentially die.
178
And that's the job of our immune system.
179
And our immune system operates on the very same principles as the staircase of evolution it's a staircase of self -defense.
180
And the most remarkable property of our immune system is it
181
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.
182
in the human population.
183
And how do we do that?
184
Well, it involves a process based on mutation and selection.
185
And the way this starts, I'll just describe it starting with a single cell.
186
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,
187
they're activated, they're engaged.
188
And when engaged, they multiply very rapidly such that over a period of about a week, one cell may become billions of cells
189
and start to pump out large quantities of chemical weapons known as antibodies that thwart that invader.
190
These billions of cells of our immune system are actually clones, clones that are subtly distinct from each other,
191
that have unique ability to recognize something else.
192
Now, that something else could be any variety of things on an invading pathogen.
193
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.
194
That first wave of defense is decent, but not optimized.
195
There's actually a mechanism to make those chemical weapons, the antibodies that cell makes even more potent,
196
even more deadly to essentially the invading pathogen.
197
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.
198
Just the antibody genes start undergoing a process called hypermutation
199
and therefore generating all sorts of antibody variants and the antibody variants that recognize the pathogen better are selected for.
200
So here we go.
201
We're climbing the staircase.
202
So this hypermutation process, you now select antibodies, and this can go through various cycles to make ever better and better antibodies.
203
So we're really zeroing in on this particular pathogen.
204
So late in immune response, say for example, the second week you're recovering from a flu virus,
205
your immune system is ever more potent ever more ever more powerful in defeating its enemy
206
because it's up that staircase eventually a staircase sort of splits
207
and some cells are set aside so it's called memory cells
208
they're there to be used
209
when this pathogen is encountered again other cells continue to make
210
the antibodies now this is the marvelous thing y 'all are familiar with a phenomenon where for For example, you don't get measles twice.
211
You don't get chicken pox twice, et cetera.
212
Why is this immunological memory?
213
That even if 50, 60, whatever number of years ago you might have been exposed to that virus,
214
your immune system is still poised to attack it again if you're exposed again, so you don't even get the infection.
215
This system is called adaptive immunity, much like the process of evolution of mutation and selection is adaptive.
216
It really only exists in this form in animals with backbones, long -lived, generally larger animals.
217
And you can see its utility because the longer your lifespan, the greater the chance you're going to re -encounter a particular pathogen.
218
If you're a short -lived mayfly or something like this.
219
You don't live long enough to see the same thing twice.
220
There's not that kind of immunity.
221
So lots of animals, including simpler things like worms and flies and all that, they have what we call innate immunity.
222
They have ways that sort of put barriers up against pathogens.
223
But this adaptive immunity only exists in creatures with backbones,
224
with vertebrates and it's pretty elaborate in in us in in mammals animals with fur etc
225
but it's pretty well developed even in things like fish
226
and sharks inside our bodies the time scale of this process
227
is very very fast it's more like what we described with respect to microbes
228
because it starts with cells and cells that can multiply pretty frequently
229
so a lot of evolution can take place in a short time most of us are sort of familiar
230
that you know most infections don't knock us down for more than about a week that's
231
when our immune system eventually sort of catches up
232
and overtakes the pathogen so
233
that gives you a sense of the time scale it takes to mount the response expand
234
that response to the point where it overwhelms the pathogen whereas
235
out there in the world sort of a battle between predator
236
and prey or whatever
237
that may go on for hundreds of thousands of years before
238
there's sort of a winner same process much more rapid time scale in your body how is it possible
239
that we can recognize virtually anything that the world will throw at us.
240
And fundamentally, one of the problems there is sort of a coding problem.
241
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?
242
And the solution to that required understanding how antibody genes are encoded in DNA,
243
something we weren't able to do until the 1970s or so.
244
And what that's revealed is that we mix
245
and match pieces of antibodies in a way that we can generate millions of combinations of antibodies.
246
And it's now estimated that we may be able to make about 10 billion different antibodies.
247
And you might go, well, that sounds sort of impressive, but okay.
248
Well, here's the thing.
249
In our entire genome, all of our DNA, we only have about 20 ,000 genes.
250
So how do you make 10 billion antibodies when there's only 20 ,000 genes to begin with.
251
And this is the brilliant trick of the immune system.
252
It makes antibodies from short little gene segments that it mixes and matches in millions, if not billions, of combinations.
253
So the trick of combinations is that it's just like in a, you know, if you can take a deck of cards, right?
254
And you have five cards you draw from a deck.
255
there's lots and lots of different combinations you can, even if you have only 52 different cards.
256
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.
257
So the immune system, even with all its powers, can still be sort of beat to the punch.
258
There's still pathogens that can kill us.
259
And this is why we vaccinate.
260
And we understand in vaccines, generally what we're giving is a little component usually a non
261
-living component not the virus itself not the pathogen itself
262
but maybe just a molecule that represents that pathogen and we're using
263
that to prime the immune system so we're activating the immune system
264
so it goes through some of those steps on the staircase establishes memory
265
and is poised to respond should we encounter that pathogen and by being vaccinated by being immunized that can save lives
266
certainly save the suffering of any of a particular disease you
267
know shorten its course save us days off work whatever it might be
268
but this is why we have these vaccine strategies and we seek ways
269
to give our immune system a head start because
270
if we don't vaccinate then we're at risk of suffering the damage
271
that pathogen causes unless or until our immune system catches up feeling lousy
272
or in some cases there's lots of morbidity with these infections
273
one of the most notorious ones in human history is the smallpox virus
274
which killed hundreds of millions of people in human history
275
and even tens of millions of people in the 20th century until we came up with a vaccine.
276
And there was a global effort to vaccinate virtually every human on the planet.
277
And that eradicated smallpox from the world so that now we don't even vaccinate for smallpox.
278
But that was a virus that moved faster and caused greater pathology than our bodies could keep up with.
279
So we understand this evolutionary process is what drives our adaptive immune system and protects us against enemies from without.
280
But it turns out that sometimes the enemy is coming from within the house.
281
And I'm speaking specifically of cancer.
282
And cancer is truly an evolutionary disease, meaning that it is a disease
283
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.
284
Cancer forms in the same way and that is mutations take place in individual cells
285
that if they convey some growth advantage to those cells,
286
those cells may outgrow their neighbors and additional mutations may happen so they outgrow their neighbors further.
287
And that's what we define as a tumor, a population of cells that is now growing unregulated relative to its normal neighbors.
288
And that's a threat because that unregulated growth can lead to spread throughout the body, can lead to organ involvement, etc., and death.
289
But the other concern is, as that cancer gets larger, some of those cells are going to get yet additional mutations.
290
And some of those cells are going to get yet additional mutations.
291
And so as cancer progresses over time,
292
that tumor is less and less like the cell it started from and the tumor itself is more genetically diverse.
293
And that's giving us a real challenge therapeutically.
294
So there is a staircase of cancer.
295
And the way to understand that is that our risk of cancer is really age -dependent.
296
The incidence of cancer goes up really significantly as we get older.
297
And think for a moment why that might be.
298
And what that is, is it takes time to climb that whole staircase.
299
So, later in life, individual cells have gone through more divisions, they've had more chances to accumulate mutations,
300
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.
301
So that tells us, not only is it an evolutionary disease, it's a genetic disease.
302
It's mutations taking place in genes that somehow disrupt the normal process of controlling
303
cell growth
304
so a huge interest has been what are those genes how
305
do we find them how does this all work we first got a hint
306
that cancer was a genetic phenomenon
307
when scientists first started seeing chromosomal changes in cancers chromosomes
308
that were broken infused and things like this and
309
that all the tumor cells would have those broken chromosomes
310
or tumors that arose independently in different people would have those rearranged chromosomes
311
and that gave us a hint okay something genetically is going on
312
but the crucial thing was to identify well what genes well thanks to
313
genomics thanks to gene cloning we now know
314
that there are about 20 000 genes that essentially run the human body
315
and we've identified about 150 of those that
316
when mutated can contribute in some way to cancer we'll call those drivers
317
and those drivers split into two classes one class
318
we'll call accelerators because when they're mutated they really accelerate cell multiplication
319
they also have the name oncogenes promoting cancer another class of genes they serve as brakes they hold back proliferation
320
but if they're disrupted by mutation and we no longer have their braking function
321
and the cells can grow out of control
322
so just like an out of control car out control cell proliferation can be due to a stuck accelerator or broken brake.
323
It can be due to oncogenes that promote cancer or tumor suppressors would normally suppress that cancer, but they've been disrupted by mutation.
324
So scientists have banded together across the world to build this sort of catalog of driver genes.
325
And so they study the state of these genes and all sorts of cancers.
326
And there's some really, really clear insights from doing this.
327
And the first is, well, it's a multi -hit process.
328
Usually any cancer has disruptions to multiple genes, might be three, four, five, even seven of these driver genes.
329
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.
330
when we look in kids we see there are very few mutations overall in the dna of the cancer cell
331
but they'll be in driver genes you don't see many other mutations
332
that have taken place that are different say from mom
333
and dad's dna and that's because a young child its cells have not gone through
334
that many divisions it's not accumulated very many other mutations it just
335
so happens the mutations that occurred were in these critical driver genes it's horrible heartbreaking bad luck But the longer we live,
336
all of our cells, whenever DNA is copied, mutations occur.
337
Now, most of those mutations have no effect.
338
They're sprinkled among the billions of bases that we have.
339
But every now and then, one of these driver genes gets hit.
340
Well, the longer we live and the more divisions our cells have gone through,
341
the greater the chance that there have accumulated mutations and eventually hit one or more driver genes.
342
And once they hit a driver gene, if that cell starts to outproliferate its neighbors,
343
well then those cells in turn may be going through more rounds of division, more mutations.
344
And so now essentially the snowball is rolling such that by later in life,
345
we have cells that have accumulated a number of driver mutations.
346
And many of our cells at least have one driver mutation.
347
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.
348
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.
349
First is just bad luck, that the small number of mutations that are going to happen anyway just happen to hit driver genes.
350
Really, that's the explanation of pediatric cancer and
351
And the kindest thing you can do to any parent whose child is struck is to reassure them
352
that there was nothing they did to cause it and nothing they could have done to prevent it.
353
Then there are lifestyle issues like tobacco use and sun exposure.
354
They'll increase the risk of particular cancers.
355
Lungs, because that's where the smoke goes.
356
And of course, the skin, because that's what's being exposed to the sunlight.
357
And the third is just age.
358
It's time.
359
The longer we live, the more divisions our cells have gone through, the more mutations have happened.
360
And the more all the environmental things that we've been exposed to have had a chance to work on us.
361
So that later in life, our cells are carrying lots of mutations And we just hope
362
that none of those cells have sort of that unlucky combination of mutations that will make it an uncontrollable tumor.
363
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.
364
Now, for prevention, we're looking for these mutations.
365
So you've seen, for example, a product like Cologuard, where a stool sample can be sent to a company.
366
Well, they're looking for mutations characteristic of gastrointestinal cancers in that fecal sample.
367
Okay, so that's early detection.
368
And we know that the earlier you can detect cancer, the better shot you have of counteracting it.
369
The second pillar is to know those cancers and to realize that different driver genes are mutated in different cancers.
370
So instead of treating breast cancer as a monolith,
371
we now subtype breast cancer according to the mutations that exist in an individual's tumor.
372
So it's really important that the genotype, meaning the genetic makeup of a tumor, is analyzed when that is first diagnosed.
373
That will shape the treatment course, because the other thing that oncologists are doing is they use different drugs,
374
different regimens to go after these cancers is to study which things work against which genotypes of cancer.
375
So we're now, I think, classifying and categorizing cancers with much greater degree of sophistication.
376
Then there is the specific therapy side.
377
All sorts of drugs have been designed to go after those mutated genes.
378
So to specifically target what has gone wrong in an individual cancer because of the mutation of a particular gene.
379
Some of these drugs have been spectacular success, some are doing a good job at let's just say buying time in the hope
380
that the cancer can be contained
381
and you know managed over a longer period of time and treated more as like a chronic disease, not necessarily eliminated, but at least managed.
382
Only in the last about 25 years has this really been possible, but the practice of this has really grown enormously in the last about 15 years.
383
And there's all sorts of new drugs under clinical trials at any given moment.
384
Again, trying to give a much more specific therapy to the particular alterations that have happened in a given individual's tumors.
385
Better prevention, better diagnosis, better therapy.
386
This is driving cancer rates down, certainly for certain types of cancers, and hopefully going to drive survival rates up over the long term.
387
These parallels in how life evolves, how the immune system works,
388
how cancer arises, they're, at one level, they're startling because the connections aren't so obvious,
389
but fundamentally they're operating on the same process, this mutation and selection.
390
But of course, mutation is a random process.
391
And it's really hard to get our heads around how can all the diversity
392
and sort of seeming order that's out there in the world emerge from a process dependent upon chance.
393
Yet, there you have it.
394
Whenever you have variation and you have competition,
395
natural selection operates and gives us the variety of life.
396
In the immune system, chance is being exploited.
397
You think, well, we can't leave the defense of our bodies against chance, but here we're exploiting chance.
398
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 the body.
399
That evolutionary process we've been discussing is one of error and trial, whereas humans sort of think like engineers,
400
that we think of what we want as an outcome and how we can get there sort of in the shortest distance.
401
And we may use some trial and error, but we really try to minimize the error, whereas really these evolutionary processes start with error.
402
They start with a random change and then try those things out.
403
and it's i think it's just been hard for us to get our heads around
404
that yet the more we understand this and all of us manifestations, and the immune system and cancer are two later realizations,
405
we see that this process is a fundamental biological process,
406
random genetic variation and the sorting of that variation through natural selection.
407
Chapter four, the untold story of Alfred Russell Wallace.
408
so about 15 years ago on a visit to the university
409
of cambridge i happened to visit the archives there where they hold a lot of original materials from darwin
410
and to my astonishment they brought out
411
and placed into these sweaty hands a copy of one of the early manuscripts
412
that many many many years later would be modified into the origin of species after darwin got back from his voyage
413
He was pondering these ideas, and he decided to write them down in essay form.
414
And by 1844, he completed a 230 -page essay that fleshed out a lot of his basic ideas.
415
He wouldn't publish anything on evolution for 15 years.
416
That essay, I think, was lost for decades and found under the steps of his house.
417
So when it was presented to me, all over the manuscript, including on the back pages, there were drawings by Darwin's kids.
418
They had been using it like scrap paper.
419
It was a spine -tingling moment for me
420
because this was really the birth of one of the biggest ideas humans have ever had.
421
And I'm grateful that they found it under the stairway at Darwin's house.
422
So while Darwin's is the most famous figure associated with the theory of evolution, Alfred Russell Wallace played a key part and deserves huge credit,
423
both for his ideas and for his enormous effort.
424
So really important to understand that the prevailing idea at the time to
425
which Darwin subscribed and most British scientists subscribed was what we'll call special creation or the theory of special creation.
426
And that was the idea that every species was specially created by God and sort of placed,
427
or at least emerged, in the habitat or in the place on the globe that best suited it.
428
Now, what started to shake that theory in Darwin's mind and in Wallace's mind was in the course of their journeys,
429
particularly when they visited archipelagos, strings of islands.
430
Each of them observed species on different islands that were slightly different from one another.
431
Now, Darwin, this is just a twist of his story.
432
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.
433
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.
434
And Darwin was at first just crestfallen that he wasn't headed home, but he needed to make good use of that time.
435
And he started to take his notebooks out and review what he had seen, but also sort of annotate them.
436
And he thought back to the Galapagos Islands, and he thought back to these mockingbirds that had seen on different islands.
437
And he saw that on different islands, the mockingbirds were slightly different from one another in their feather patterns and things like that.
438
And he thought these islands were within sight of one another, just 50 or 60 miles away from one another.
439
If a creator was placing species sort of perfectly adapted to each place, why would these mockingbirds be just slightly different from one another?
440
Now Wallace's story is almost is more dramatic because Wallace, after four years in the Amazon,
441
really at the breaking point, decided to return to England with specimens and whatever ideas he had collected.
442
And on his way home, his ship caught fire.
443
He had to get into a lifeboat.
444
The ship sank right in front of him with all of his specimens.
445
And he was in an open lifeboat for 10 days, hoping to be picked up.
446
And he was picked up, eventually made his way back to England.
447
You'd think after that experience, he would have sworn off all voyaging.
448
But two years later, he goes back out
449
and does an eight -year voyage across the Malay archipelago and collects tens of thousands of more specimens.
450
He noticed, for example, the bird -winged butterflies.
451
These beautiful, incredibly brilliantly colored large butterflies were slightly different from island to island.
452
They both thought, in the theory of special creation, these islands all looked alike.
453
Why would there be just slightly different species island to island?
454
And it struck both of them because species could change.
455
Species weren't stable.
456
They weren't immutable, as the theory of special creation argued.
457
They, in fact, changed.
458
And this opened up the big question then, or at least the daring question, of...
459
are species the product of natural processes or divinely created
460
and they thought this was strong evidence
461
that species change naturally they change according to the conditions they encounter in different places
462
and the islands were crucial sort of laboratories for understanding this because
463
the volcanic islands of the galapagos look very similar to one another
464
but the creatures were a bit different the islands of the melee archipelago very similar foliage
465
and all that but the creatures were a little bit different.
466
And the only way they could sort of reconcile that was to say, well, the species were changing.
467
They weren't fixed.
468
They weren't immutable.
469
And as they worked further, they thought about some other patterns.
470
They knew about fossils.
471
In fact, Darwin discovered some really interesting fossils on the coast of Argentina.
472
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.
473
So he found, for example, giant ground sloths, huge, like eight feet tall ground sloths, much larger than the living ones.
474
But he realized, hmm, those are extinct creatures.
475
What's the relationship between the extinct and the living?
476
He's starting to think about that genealogy between the extinct and the living.
477
And Wallace is also becoming aware of these fossils
478
because he's reading now what's coming out from the first studies
479
of fossils in Britain in the first part of the 19th century.
480
They had also each read this work by an economist, Thomas Malthus.
481
And Malthus emphasized that there were limits on populations.
482
He thought about the growth of populations.
483
And Malthus said that disease and famine, that limited, for example, the growth of populations.
484
Well, Darwin and Wallace, being out of nature, they understood that life was very tough.
485
They understood that really life was a battlefield, a contest, and that far more young are produced than can survive to adulthood.
486
And what's uncanny is when you look at the writings of each of these individuals, Darwin's notebooks, Wallace's draft manuscript,
487
they use the same language.
488
They describe life as, quote, quote, a struggle for existence.
489
Exactly the same words, unbeknownst to each other.
490
And they talk about variations, however slight, and that they could be favored.
491
And that led Darwin to coin the word natural selection.
492
They'll be selected for in nature.
493
And the things that are disadvantaged will be selected against.
494
And Wallace said essentially the same thing, that one could imagine if there's a slight advantage
495
that slight advantage will be passed on generation after generation
496
so darwin for 20 years is back home in england he's well known
497
because right after he did the voyage on the beagle he wrote a book
498
that we call today the voyage of the beagle
499
and it was a popular read it's a great read it's still a great read today about his travels
500
and he was an eminent naturalist.
501
Wallace was an unknown.
502
He was from far more modest upbringing
503
and he was really paying his way on his voyages by selling a fraction of the specimens that he was collecting.
504
So he was thousands and thousands of miles away from the center of science in England
505
and he wasn't connected really at all.
506
So Wallace by 1858 has a pretty good idea that life changes, life evolves.
507
And he writes up a very short account of his thinking about how that works.
508
And he decides to send it to the one naturalist with whom he struck up a correspondence who thinks might appreciate it.
509
He sends it to Charles Darwin.
510
Well, this event rocks Darwin because Darwin has not gone public with his theory of evolution.
511
And now here's this far away correspondent, 7 ,000 miles away from England, who in just a few pages has essentially the same idea that Darwin has,
512
that Darwin's labored on for about 20 years.
513
Well, Darwin's friends rally and decide
514
that the best thing to do would be to read Wallace's paper
515
and an excerpt from Darwin's work in front of a British
516
scientific society to sort of put both of these ideas out in the public.
517
Darwin wasn't there.
518
It turns out Darwin had suffered tragedy.
519
He was burying his Charles Jr., one of his sons, on the day this paper was read.
520
And Wallace was 7 ,000 miles away, didn't even know it was going on.
521
It really didn't make much of a splash.
522
Not much attention was paid.
523
But the next year is when Darwin published on The Origin of Species, and that's when everyone paid attention.
524
The response and acceptance or rejection, particularly.
525
to Darwin's Origin of Species because that's the book everybody could put their hands on.
526
It sold out in its first printing.
527
It was reprinted quickly.
528
It was translated into other languages.
529
American versions were made.
530
So people who are interested in science, biology, natural history around the world could get their hands on Darwin's ideas.
531
So the reactions were a very wide spectrum.
532
Thomas Huxley, who was one of Darwin's close confidants, sort of thought, you know, wow, why didn't I think of that?
533
He thought it was, you know, compelling and sort of obvious.
534
But I think one thing to appreciate with Darwin is that his book is extraordinary in that he also
535
presents and analyzes the critiques of his own theory.
536
I mean, imagine that this is just something that human beings don't generally do.
537
If they've got an idea, they're going to put out all the evidence in favor of their idea,
538
and they're usually not going to present to the opposition all the evidence either against it or all the evidence that's missing.
539
But Darwin did this in a masterful way and basically often saying things like, you know, if something, if a particular thing was found, it could crush my theory.
540
Or if my theory is true, this would be true, but there wouldn't necessarily be any evidence weighing on that.
541
So it was a masterful presentation.
542
And I think that gave, it made it very accessible to people.
543
They understood the strengths and weaknesses of the theory.
544
And then new discoveries could be interpreted in light of that theory.
545
And as some new discoveries, particularly from the fossil record, came to light, well that gave a lot of power to Darwin.
546
Because Darwin at the time Origin of Species was published, the fossil record was pretty skimpy.
547
But Darwin made some really strong predictions about what should be found, for example, in the fossil record.
548
And one of those was transitional forms.
549
If the tree of life has evolved in the way that he said, there should be forms that are intermediate between existing forms today.
550
And two years after the origin of species, a fossil called Archaeopteryx, which has got mixed characteristics of both birds and reptiles, was discovered.
551
And I mean, you couldn't have drawn anything better than that fossil for supporting Darwin's theory.
552
So I think the reception of the scientific community, some of it at first was, you know, positive, but there were long, long holdouts.
553
There were career -long holdouts against Darwin among even very eminent natural historians, biologists, and scientists.
554
And that holdout was really for reasons we'd all recognize today.
555
While Darwin didn't, in 1859 didn't comment directly on the evolution of humans.
556
He did later in 1871.
557
Everyone knew that humans were going to be a touchy subject because for at least a couple millennia,
558
the thinking was that man was created in God's image, not descended from some previous animal forms.
559
But clearly Darwin's theory would be interpreted to say that no, humans, just like every other animal,
560
evolved their anatomy and their physiology from pre -existing forms.
561
And some scientists held out on that point, both perhaps from their own viewpoint of faith,
562
but also, I think, because of some pressures in the academy.
563
Darwin was on the short list to be knighted.
564
When the origin of species came out, well, he never got that knighthood.
565
So, you know, This was an idea that many people found repulsive.
566
They were really worried about the societal implications to sort of
567
take the creator out of the immediate picture of sort of tending to human affairs.
568
And that's, of course, still a struggle that exists today.
569
And scientists being part of society, it was not universally accepted,
570
far from it where Wallace really finally grasped the scope of what Darwin had been working and thinking
571
was in 1859 when The Origin of Species was published
572
and he got he received a copy of The Origin of Species
573
and he read it
574
and re -read it in fact Wallace's own copy is in the Natural History Museum in London
575
so we can understand sort of his reactions in real time
576
But I think one of the most poignant things I know in the history of science
577
was Wallace's put his thoughts and reactions in a letter to his close friend and confidant, Henry Walter Bates, with whom he had first traveled to the Amazon.
578
And Wallace is just gushing with admiration for Darwin.
579
And he says, I never, given any amount of time, I could have never come up with something as massive and compelling as Darwin.
580
And he said, I don't think any branch of science has ever been created by an individual such as this, such as Darwin.
581
So, Wallace was in awe of Darwin's synthesis, which was the origin of species.
582
But they were mutually generous to each other.
583
Darwin, right off on page one, acknowledges Wallace and Wallace's ideas.
584
And Wallace later, for example, when he writes his first major book, he dedicates it to Darwin.
585
They are mutual admirers to the point where, for example, Wallace is going to be a pallbearer at Darwin's funeral.
586
And in their day, this was referred to as the Darwin -Wallace theory.
587
It's only later that biologists and historians just started kind of forgetting about Wallace and crediting Darwin.
588
Now, there might be reasons for that.
589
Darwin came from a wealthy family.
590
The University of Cambridge did a great job at sort of amassing Darwin's collections and Darwin's writings.
591
And so we just have a better historical record of everything that Darwin did.
592
But at the time, it was the Darwin -Wallace theory.
593
And I think by today's scientific standards, given the genesis of this theory, the theory certainly of natural selection by the two individuals, we would be crediting both of them.
594
And it's just, you know, it's just the unfortunate sort of,
595
you know, accidents of time that people kept talking about Darwin and Wallace sort of faded to the background.
596
But I really feel in the last 25 years or so
597
that Wallace has seen sort of a renaissance and that people are much more aware of Wallace's huge contributions.
598
And then Wallace outlived Darwin by 30 years.
599
So he was a really important figure in the discussion of evolution because, you know, this was a brand new science.
600
It had relatively few advocates at the beginning, certainly people that really understood it well.
601
And so Wallace played a a huge role in getting people to help understand these ideas.
602
I think if Darwin and Wallace were alive today,
603
they would be so overjoyed by the detail with which we understand the process that they first figured out.
604
They knew variation was important.
605
They knew variation was the fuel of the evolutionary process, had no idea how that variation arose.
606
Now, any biologist can point right to the DNA in a newly hatched creature and say, there's the mutation.
607
That's what's going to make the difference.
608
So our understanding of the material basis of evolution is phenomenally strong.
609
And I think that would be extremely gratifying to them.
610
But these other manifestations, the role it plays in health and disease were nowhere in Darwin and Wallace's minds.
611
So I think that would,
612
again, further astound them that this process they figured out had such widespread ramifications beyond just the natural world.
613
What we've seen are striking parallels in how life evolves, how our immune system works,
614
and even how cancer arises this process of mutation and selection, this staircase.
615
So really the process that Darwin and Wallace had that first insight into is a universal process.
616
Wherever there's variation, wherever there's competition, selection will operate.
617
For me personally, as an evolutionary biologist,
618
this just underscores the explanatory power of evolutionary theory and the importance of understanding the evolutionary process.
619
You might think, well, the evolutionary process, let's just leave it to the scientists to worry about it.
620
But I think in our daily lives, you understand that this is why we vaccinate.
621
This is why we are now developing these strategies against cancer that we, of course, hope everybody will be able to benefit from.
622
That's a long way from the Beagle voyage of 160 years ago.
623
But that's fundamentally where Darwin and Wallace have brought us.
📺 Same Channel
C113
Why successful people set habits, not just goals | Wendy Wood
Business EnglishUniversity StudentsWorking Adults
C167
What science can’t answer, according to physicist Jim Al-Khalili | Big Think
IELTS PrepTOEFL PrepUniversity Students
C15
Your genes affect your education. Here’s why that’s controversial. | Kathryn Paige Harden
IELTS PrepTOEFL PrepUniversity Students
C14
Hit peak performance with the power of habit | Wendy Wood
Business EnglishUniversity StudentsWorking Adults
C11
What happens to your brain when you’re dreaming
Daily ConversationUniversity StudentsWorking Adults
C11
Cornel West: How Intellectuals Betrayed the Poor | Big Think
IELTS PrepTOEFL PrepUniversity Students
C13
A mind-blowing explanation of symmetry | Frank Wilczek for Big Think
IELTS PrepTOEFL PrepUniversity Students
B23
How do elite performers automate their habits? | Wendy Wood
Business EnglishUniversity StudentsWorking Adults
C13
What if quantum physics could eradicate illness? | Jim Al-Khalili for Big Think
IELTS PrepTOEFL PrepUniversity Students
B21
Why softness beats stress | Giulia Enders
Business EnglishUniversity StudentsWorking Adults
C13
Your brain wasn't built to hold this much information | Richard Cytowic
Daily ConversationUniversity StudentsWorking Adults
B23
Who decides what is socially “normal”? | Christine Emba
Daily ConversationUniversity StudentsWorking Adults
C120
Harvard negotiator explains how to argue | Dan Shapiro
Business EnglishUniversity StudentsWorking Adults
B23
Curiosity Is a Superpower — If You Have the Courage to Use It | Big Think
Business EnglishDaily ConversationUniversity Students
C17
Einstein’s beef with quantum physics, explained | Jim Al-Khalili for Big Think
IELTS PrepTOEFL PrepUniversity Students
C12
Physicist Brian Cox explains quantum physics in 22 minutes
Business EnglishUniversity StudentsWorking Adults
C19
Keep your brain from declining after age 30
Business EnglishUniversity StudentsWorking Adults
C14
A neuroscientist’s guide to reclaiming your brain | Nicole Vignola
Business EnglishUniversity StudentsWorking Adults
C16
Expand your perception. Change your life. | Dr. Jill Bolte Taylor
Business EnglishUniversity StudentsWorking Adults
B22
How Apple and Nike have branded your brain | Your Brain on Money | Big Think
Business EnglishUniversity StudentsWorking Adults
✨ Recommend Video
C1113
15 sentences
Could Humans Evolve Flight?
IELTS PrepTOEFL PrepUniversity Students
C12
33 sentences
1 8 What is Causation
IELTS PrepTOEFL PrepUniversity Students
C11
26 sentences
How do vaccines work?
IELTS PrepTOEFL PrepUniversity Students
C11
146 sentences
The Most Complex Language in the World
IELTS PrepTOEFL PrepUniversity Students
C1552 sentences
The Professor Who Taught People How To Think (1962)
IELTS PrepTOEFL PrepUniversity Students
C1114
14 sentences
Arguments for God: The Fine Tuning Argument
British AccentIELTS PrepTOEFL PrepUniversity Students
C14
131 sentences
The medicine myth | Denis Noble, Nessa Carey, Guy Brown
IELTS PrepTOEFL PrepUniversity Students
C11
135 sentences
The Most Overlooked Qur'anic Verse About Human Origins!
IELTS PrepTOEFL PrepUniversity Students
C14
34 sentences
The Evolution of Human Skin Colour | BBC Earth Science
IELTS PrepTOEFL PrepUniversity Students
C1121
29 sentences
The Neuroscience of Creativity
IELTS PrepTOEFL PrepUniversity Students
Vocabulary and speaking notes for this lesson
This speaking lesson is built on the video “How evolution works, in 54 minutes”. The speaker keeps coming back to these words: mutation, cell, cancer, Darwin, process. This video has 455 sentences and 8516 words to shadow. The speech runs for 54:32. The speaker talks at a natural 156 words per minute, close to everyday conversation. 82% of the words are among the 3,000 most common in English; the rest is worth studying before you start.
Key vocabulary in this video
15 words from the video worth learning, with pronunciation and meaning:
| Word | Pronunciation | Meaning |
|---|---|---|
| mutation noun | /mjuˈteɪʃən/ | Any alteration or change. |
| gene noun | /d͡ʒiːn/ | A theoretical unit of heredity of living organisms which may take several values and (in principle) predetermines a precise trait of an organism's form… |
| evolution noun | /ˌiːvəˈluːʃ(ə)n/ | A manoeuvre of troops or ships. |
| immune adjective | /ɪˈmjuːn/ | Exempt; not subject to. |
| staircase noun | /ˈstɛɹˌkeɪs/ | A flight of stairs; a stairway. |
| evolutionary adjective | /ˌiː.vəˈluː.ʃən.ɛɹ.i/ | Of or relating to the biological theory of evolution. |
| fossil noun | /ˈfɑsl̩/ | The mineralized remains of an animal or plant. |
| tumor noun | /tuː.məɹ/ | An abnormal growth; differential diagnosis includes abscess, metaplasia, and neoplasia. |
| variation noun | /ˌvɛəɹiˈeɪʃn̩/ | The act of varying; a partial change in the form, position, state, or qualities of a thing. |
| arise verb | /əˈɹaɪz/ | To come up from a lower to a higher position. |
| genetic adjective | /d͡ʒəˈnɛt.ɪk/ | Relating to genetics or genes. |
| evolve verb | /ɪˈvɑlv/ | To move (something) in regular procession through a system. |
| voyage noun | /ˈvɔɪ.ɪd͡ʒ/ | A long journey, especially by ship. |
| essentially adverb | /ɪˈsɛnʃəli/ | In essence: by nature. |
| virus noun | /ˈvaɪ.ɹəs/ | A submicroscopic, non-cellular structure that consists of a core of DNA or RNA surrounded by a protein coat, that requires a living host cell to replicate, and… |
Phrasal verbs you will hear
| Word | Pronunciation | Meaning |
|---|---|---|
| go through verb | To travel from one end of something to the other. | |
| come up with verb | To manage to produce, deliver, or present (something) by inventing, creating, thinking of, or obtaining it. | |
| figure out verb | To come to understand; to discover or find a solution; to deduce. | |
| catch up verb | To pick up suddenly. | |
| pick up verb | To lift; to grasp and raise. | |
| bring out verb | To elicit, evoke, or emphasize (a particular quality). | |
| come back verb | To return to a place. | |
| come out verb | /ˌkʌm ˈaʊt/ | To be discovered; to be revealed. |
Sentences worth repeating
Short, complete lines from the video that you can reuse in everyday conversation:
- To the rest of us, it's instantly fatal.
- You know, do we have every brick?
- Do we have every intermediate?
- We've gotta fend these off.
- How do we find them?
Grammar in this video
The structures the speaker uses most, with the exact words from the video:
| Structure | In the video |
|---|---|
| Conditional sentences if + clause, will/would + verb — a condition and its result | if mutation didn't happen all things would be · if there was no extinction, we'd have · if my theory is true, this would be |
| Present perfect continuous have/has been + -ing — an action that started earlier and is still going on | we've been trying · we've been discussing |
| Present perfect have/has + past participle — a past action that still matters now | has happened · have come · they've done |
| Passive voice be + past participle — the focus is on what happens, not who does it | was referred · be added · been estimated |
Pronunciation to watch
The speaker uses 131 contractions and reduced forms, such as they're, don't, we're. Say them the short way, as you hear them.
- The “th” sounds: hypothesis /haɪˈpɒθɪsɪs/, pathogen /ˈpæθəd͡ʒn̩/, sloth /slɔθ/
- The “sh” and “zh” sounds: mutation /mjuˈteɪʃən/, evolution /ˌiːvəˈluːʃ(ə)n/, evolutionary /ˌiː.vəˈluː.ʃən.ɛɹ.i/, variation /ˌvɛəɹiˈeɪʃn̩/, essentially /ɪˈsɛnʃəli/
- Long words — get the stress right: evolution /ˌiːvəˈluːʃ(ə)n/, evolutionary /ˌiː.vəˈluː.ʃən.ɛɹ.i/, essentially /ɪˈsɛnʃəli/, mechanism /ˈmɛk.ə.nɪ.zəm/, immunity /ɪˈmjuːnəti/
How to practise with this video
- Listen to the whole video once without speaking and note the words you do not know.
- Start at 0.75× speed, shadow it sentence by sentence, then go back to normal speed once it feels easy.
- Record yourself and compare with the original, paying attention to words like mutation, gene, evolution.
What is the Shadowing Technique?
Shadowing is a science-backed language learning technique originally developed for professional interpreter training and popularized by polyglot Dr. Alexander Arguelles. The method is simple but powerful: you listen to native English audio and immediately repeat it out loud — like a shadow following the speaker with just a 1–2 second delay. Unlike passive listening or grammar drills, shadowing forces your brain and mouth muscles to simultaneously process and reproduce real speech patterns. Research shows it significantly improves pronunciation accuracy, intonation, rhythm, connected speech, listening comprehension, and speaking fluency — making it one of the most effective methods for IELTS Speaking preparation and real-world English communication.