Blind Evolution or Intelligent Design?
Michael Behe The following is from an address I gave
at the American Museum of Natural History.
Talk delivered at the American Museum
of Natural History, 23 April 2002 at a discussion titled ¡°Blind Evolution or
Intelligent Design?¡± The participants included ID proponents William A. Dembski
and Michael J. Behe as well as evolutionists Kenneth R. Miller and Robert T.
Pennock. Eugenie C. Scott moderated the discussion. An introduction was given
by National History Editor, Richard Milner.
Thanks very much, Dr. Scott! It¡¯s great to be
back in New York City. I taught at Queens College and City University for three
years in the early nineteen-eighties; my wife grew up on Cambreleng Avenue near
187th Street in the Bronx and our first child was born here, so New York holds
many happy memories for our family.
My talk will be divided into four parts: first,
a sketch of the argument for design; second, common misconceptions about the
mode of design; third, misconceptions about biochemical design; and finally,
discussion of the future prospects of design. Before I begin, however, I¡¯d
like to emphasize that the focus of my argument will not be descent with modification,
with which I agree. Rather, the focus will be the mechanism of evolution?how
did all this happen, by natural selection or intelligent design? My conclusion
will not be that natural selection doesn¡¯t explain anything; Rather, the conclusion
will be that natural selection doesn¡¯t explain everything.
So, let¡¯s begin with a sketch of the design
argument. In the Origin of Species, Darwin emphasized that his was a very gradual
theory; natural selection had to work by ¡°numerous, successive, slight modifications¡±
to pre-existing structures. However, ¡°irreducibly complex¡± systems seem quite
difficult to explain in gradual terms. What is irreducible complexity? I¡¯ve
defined the term in various places, but it¡¯s easier to illustrate what I mean
with the following example: the common mousetrap. A common mechanical mousetrap
has a number of interacting parts that all contribute to its function, and if
any parts are taken away, the mousetrap doesn¡¯t work half as well as it used
to, or a quarter as well?the mousetrap is broken. Thus it is irreducibly complex.
Suppose we wanted to evolve a mousetrap by something
like a Darwinian process. What would we start with? Would we start with a wooden
platform and hope to catch mice inefficiently? Perhaps tripping them? And then
add, say, the holding bar, hoping to improve efficiency? No, of course not,
because irreducibly complex systems only acquire their function when the system
is essentially completed. Thus irreducibly complex systems are real headaches
for natural selection because it is very difficult to envision how they could
be put together? that is, without the help of a directing intelligence ?by the
¡°numerous, successive, slight modifications¡± that Darwin insisted upon. Irreducibly
complex biological systems would thus be real challenges to Darwinian evolution.
Yet modern science has discovered irreducibly
complex systems in the cell. An excellent example is the bacterial flagellum
which is literally an outboard motor that bacteria use to swim. The flagellum
has a large number of parts that are necessary for its function?a propeller,
hook, drive shaft, and more. Thorough studies shows it requires 30-40 protein
parts. And in the absence of virtually any of those parts, the flagellum doesn¡¯t
work, or doesn¡¯t even get built in the cell. Its gradual evolution by unguided
natural selection therefore is a real headache for Darwinian theory. I like
to show audiences this picture of the flagellum from a biochemistry textbook
because, when they see it, they quickly grasp that this is a machine. It is
not like a machine, it is a real molecular machine. Perhaps that will help us
think about its origin.
I have written that not only is the flagellum
a problem for Darwinism, but that it is better explained as the result of design
? deliberate design by an intelligent agent. Some of my critics have said that
design is a religious conclusion, but I disagree. I think it is wholely empirical,
that is, the conclusion of design is based on the physical evidence along with
an appreciation for how we come to a conclusion of design. To illustrate how
we come to a conclusion of design, let¡¯s look at the following. This is a Far
Side cartoon by Gary Larson showing a troop of jungle explorers, and the lead
explorer has been strung up and skewered. Now, everyone in this room looks at
this cartoon and you immediately realize that the trap was designed. But how
do you know that? How do you know the trap was designed? Is it a religious conclusion?
Probably not. You know it¡¯s designed because you see a number of very specific
parts acting together to perform a function; you see something like irreducible
co
mplexity or specified complexity.
Now I will address common misconceptions about
the mode of design, that is, how design may have happened.
My book, Darwin¡¯s Black Box, in which I flesh
out the design argument, has been widely discussed in many publications. What
have other scientists said about it? Well, they¡¯ve said many things?not all
flattering?but the general reaction is well summarized in a recent book The
Way of the Cell, published last year by Oxford University Press, and authored
by Colorado State University biochemist Franklin Harold, who writes, ¡°We should
reject, as a matter of principle, the substitution of intelligent design for
the dialogue of chance and necessity (Behe 1996); but we must concede that there
are presently no detailed Darwinian accounts of the evolution of any biochemical
system, only a variety of wishful speculations.¡± Let me take a moment to emphasize
Harold¡¯s two points. First, he acknowledges that Darwinists have no real explanations
for the enormous complexity of the cell, only hand-waving speculations, more
colloquially known as ¡°Just-So stories.¡±?how the rhinoceros got its horn;
how the bac
terium got its flagellum. I find this an astonishing
admission for a theory that has dominated biology for so long. Second, apparently
he thinks that there is some principle that forbids us from investigating the
idea of intelligent design, even though design is an obvious idea that quickly
pops into your mind when you see a drawing of the flagellum or other complex
biochemical systems. But what principle is that?
I think the principle boils down to this: ?Design
appears to point strongly beyond nature. It has philosophical and theological
implications, and that makes many people uncomfortable. But any theory that
purports to explain how life occurred will have philosophical and theological
implications. For example, the Oxford biologist Richard Dawkins has famously
said that ¡°Darwin made it possible to be an intellectually-fulfilled atheist.¡±
Ken Miller has written that ¡°[God] used evolution as the tool to set us free.¡±
Stuart Kauffman, a leading complexity theorist, thinks Darwinism cannot explain
all of biology, and thinks that his theory will somehow show that we are ¡°at
home in the universe.¡± So all theories of origins carry philosophical and theological
implications.
But how could biochemical systems have been designed?
Did they have to be created from scratch in a puff of smoke? No. The design
process may have been much more subtle. It may have involved no contravening
of natural laws. Let¡¯s consider just one possibility. Suppose the designer
is God, as most people would suspect. Well, then, as Ken Miller points out in
his book, Finding Darwin¡¯s God, a subtle God could cause mutations by influencing
quantum events such as radioactive decay, something that I would call guided
evolution. That seems perfectly possible to me. I would only add, however, that
that process would amount to intelligent design, not Darwinian evolution.
Now let¡¯s look at common misconceptions about
biochemical design.
Some Darwinists have proposed that a way around
the problem of irreducible complexity could be found if the individual components
of a system first had other functions in the cell. For example, consider a hypothetical
example such as pictured here, where all of the parts are supposed to be necessary
for the function of the system. Might the system have been put together from
individual components that originally worked on their own? Unfortunately this
picture greatly oversimplifies the difficulty, as I discussed in my book, Darwin¡¯s
Black Box. Here analogies to mousetraps break down somewhat, because the parts
of the system have to automatically find each other in the cell. They can¡¯t
be arranged by an intelligent agent, as a mousetrap is. To find each other in
the cell, interacting parts have to have their surfaces shaped so that they
are very closely matched to each other. Originally, however, the individually-acting
components would not have had complementary surfaces. So all of the int
eracting surfaces of all of the components would
first have to be adjusted before they could function together. And only then
would the new function of the composite system appear. Thus the problem of irreducibility
remains, even if individual components separately have their own functions.
Another area where one has to be careful is in
noticing that some systems with extra or redundant components may have an irreducibly
complex core. For example, a car with four spark plugs might get by with three
or two, but it certainly can¡¯t get by with none. Rat traps often have two springs,
to give them extra strength. They can still work if one spring is removed, but
they can¡¯t work if both springs are removed. Thus in trying to imagine the
origin of a rat trap by Darwinian means, we still have all the problems we had
with a mousetrap. A cellular example of redundancy is the hugely-complex eukaryotic
cilium, shown here in cross-section, which has multiple copies of a number of
components, yet needs at least one copy of each to work, as I pictured in my
book.
Many other criticisms have been made against
intelligent design. I have responded to a number of them at the following locations.
I will now discuss how I view the future prospects
of a theory of intelligent design. I see them as very bright indeed. Why? Because
the idea of intelligent design has advanced, not primarily because of anything
I or any individual has done. Rather, it¡¯s been the very progress of science
itself that has made intelligent design plausible. Fifty years ago much less
was known about the cell, and it was much easier then to think that Darwinian
evolution was true. But with the discovery of more and more complexity at the
foundation of life, the idea of intelligent design has gained strength. That
trend is continuing. As science pushes on, the complexity of the cell is not
getting any less; on the contrary, it is getting much greater. For example,
a recent issue of the journal Nature carried the most detailed analysis yet
of the total protein complement of yeast?the so-called yeast ¡°proteome¡±. The
authors point out that most proteins they investigated in the cell function
as multiprotein complex
es?not as solitary proteins as scientists had
long thought. In fact they showed that almost fifty pecent of the proteins in
the cell function as complexes of a half dozen or more, such as the polyadenylation
machinery shown in this figure from the paper. To me, this implies that irreducible
molecular machinery is very likely going to be the rule in the cell, not the
exception. We will probably not have to wait too long to see.
Another example comes from a paper published
in the Journal of Molecular Biology two years ago, which showed that some enzymes
have only a limited ability to undergo multiple changes in their amino acid
sequence, even when the enzymes function alone, as single proteins, and even
when the changes are very conservative ones. This led the author to caution
that ¡°homologues sharing less than about two-thirds sequence identity should
probably be viewed as distinctive designs with their own optimizing features.¡±
The author pictured such proteins as near-islands of function, virtually isolated
from neighboring protein sequences. This may mean that even individual proteins
from separate species that are similar but not identical in their amino acid
sequence might not have been produced by a Darwinian processes, as most scientists
thought, and as even I was willing to concede. Perhaps even I give too much
unearned credit to Darwinian theory.
Finally, to show what research questions might
be asked by a theory of intelligent design, I¡¯d like to briefly describe some
of my own recent work. This is the title slide of a seminar I gave six weeks
ago to the biotechnology group at Sandia National Laboratory. The title, ¡°Modeling
the evolution of protein binding sites: probing the dividing line between natural
selection and intelligent design,¡± points to a question I¡¯m very interested
in exploring. If you are someone like myself who thinks that some things in
biology are indeed purposely designed, but that not all things are designed,
then a question which quickly arises is, where is the broad dividing line between
design and unintelligent processes? I think that question has to be answered
at the molecular level, particularly in terms of protein structure.
Drawings of the bacterial flagellum picture proteins
as bland spheres or ovals, but each protein in the cell is actually very complex.
This ribbon drawing of bovine pancreatic trypsin inhibitor gives a little taste
of that complexity. Now, proteins are polymers of amino acid residues, and some
structural features of proteins require the participation of multiple residues.
For example, this yellow link is called a disulfide bond. A disulfide bond requires
two cysteine residues ? just one cysteine residue can¡¯t form such a bond. Thus,
in order for a protein that did not have a disulfide bond to evolve one, several
changes in the same gene first have to occur. Thus in a real sense the disulfide
bond is irreducibly complex, although not nearly to the same degree of complexity
as systems made of multiple proteins.
The problem of irreducibility in protein features
is a general one. Whenever a protein interacts with another molecule, as all
proteins do, it does so through a binding site, whose shape and chemical properties
closely match the other molecule. Binding sites, however, are composed of perhaps
a dozen amino acid residues, and binding is generally lost if any of the positions
are changed. One can then ask the question, how long would it take for two proteins,
that originally did not interact, to evolve the ability to bind each other by
random mutation and natural selection, if binding only occurs when all positions
have the correct residue in place?
Although it would be difficult to experimentally
investigate this question, the process can be simulated on a computer. Here
is a sample of the data I have generated over the past year or so. The filled
circles are data points from a number of simulations which were all fit by the
following equation, the details of which I will not bother you with here. These
results were presented at the meeting of the Protein Society last summer in
Philadelphia.
In the next slide the log of the expected time
to generate what I call ¡°irreducibly complex¡± protein features is shown as
a function of the log of the population size and the log of the probability
of the feature. The yellow dot is the time expected to generate a new disulfide
bond in a protein that did not have one if the population size is a hundred
million organisms. The expected time is roughly a million generations. The red
dot shows that the expected time needed to generate a new protein binding site
would be a hundred million generations. Using data from these simulations as
well as Bill Dembski¡¯s concept of probabilistic resources, we can come to several
broad, tentative conclusions: 1) that undirected irreducibly complex mutations
cannot have been regularly involved in the evolution of large animals?the time
frame would be too long; and 2) that undirected IC systems of the complexity
of two or more protein binding sites cannot have been regularly involved in
the evolution of verte
brates. This work assumed that all mutations
were neutral. Future work could investigate such questions as, what if intermediate
mutations are selected against? and what happens if there is competition between
IC mutations and single-site mutations?
The broad motivation behind this work is to start
getting some good numbers to plug into Bill Dembski¡¯s explanatory filter, to
try to come to a reasoned conclusion about where in nature design leaves off.
In summary, I want to leave you with four take-home
points: 1) that the question is open: no other scientific theory has yet explained
the data; 2) that intelligent design is an empirical hypothesis that flows easily
from the data, as you can tell by looking at a drawing of the flagellum; 3)
that there is no ¡°principle¡± that forbids our considering design; and best
of all, 4) that there are exciting research questions that can be asked within
a design framework.