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Evidence
for Intelligent Design from Biochemistry
From a speech
delivered at Discovery Institute's God & Culture Conference
Michael
J. Behe
Discovery
Institute
August 10,
1996
|
A
Series of Eyes
How do we see? In the 19th century the anatomy of the eye was known in
great detail, and its sophisticated features astounded everyone who was
familiar with them. Scientists of the time correctly observed that if a
person were so unfortunate as to be missing one of the eye's many
integrated features, such as the lens, or iris, or ocular muscles, the
inevitable result would be a severe loss of vision or outright
blindness. So it was concluded that the eye could only function if it
were nearly intact.
Charles Darwin knew about the eye too. In the Origin of Species,
Darwin dealt with many objections to his theory of evolution by natural
selection. He discussed the problem of the eye in a section of the book
appropriately entitled "Organs of extreme perfection and
complication." Somehow, for evolution to be believable, Darwin had
to convince the public that complex organs could be formed gradually, in
a step-by-step process.
He succeeded brilliantly. Cleverly, Darwin didn't try to discover a real
pathway that evolution might have used to make the eye. Instead, he
pointed to modern animals with different kinds of eyes, ranging from the
simple to the complex, and suggested that the evolution of the human eye
might have involved similar organs as intermediates.
Here is a paraphrase of Darwin's argument. Although humans have complex
camera-type eyes, many animals get by with less. Some tiny creatures
have just a simple group of pigmented cells, or not much more than a
light sensitive spot. That simple arrangement can hardly be said to
confer vision, but it can sense light and dark, and so it meets the
creature's needs. The light-sensing organ of some starfishes is somewhat
more sophisticated. Their eye is located in a depressed region. This
allows the animal to sense which direction the light is coming from,
since the curvature of the depression blocks off light from some
directions. If the curvature becomes more pronounced, the directional
sense of the eye improves. But more curvature lessens the amount of
light that enters the eye, decreasing its sensitivity. The sensitivity
can be increased by placement of gelatinous material in the cavity to
act as a lens. Some modern animals have eyes with such crude lenses.
Gradual improvements in the lens could then provide an image of
increasing sharpness, as the requirements of the animal's environment
dictated.
Using reasoning like this, Darwin convinced many of his readers that an
evolutionary pathway leads from the simplest light sensitive spot to the
sophisticated camera-eye of man. But the question remains, how did
vision begin? Darwin persuaded much of the world that a modern eye
evolved gradually from a simpler structure, but he did not even try to
explain where his starting point for the simple light sensitive spot
came from. On the contrary, Darwin dismissed the question of the eye's
ultimate origin:
How a nerve comes to be sensitive to light hardly concerns us more than
how life itself originated. He had an excellent reason for declining the
question: it was completely beyond nineteenth century science. How the
eye works; that is, what happens when a photon of light first hits the
retina simply could not be answered at that time. As a matter of fact,
no question about the underlying mechanisms of life could be answered.
How did animal muscles cause movement? How did photosynthesis work? How
was energy extracted from food? How did the body fight infection? No one
knew.
To Darwin vision was a black box, but today, after the hard, cumulative
work of many biochemists, we are approaching answers to the question of
sight. Here is a brief overview of the biochemistry of vision. When
light first strikes the retina, a photon interacts with a molecule
called 11-cis-retinal, which rearranges within picoseconds to
trans-retinal. The change in the shape of retinal forces a change in the
shape of the protein, rhodopsin, to which the retinal is tightly bound.
The protein's metamorphosis alters its behavior, making it stick to
another protein called transducin. Before bumping into activated
rhodopsin, transducin had tightly bound a small molecule called GDP. But
when transducin interacts with activated rhodopsin, the GDP falls off
and a molecule called GTP binds to transducin. (GTP is closely related
to, but critically different from, GDP.)
GTP-transducin-activated rhodopsin now binds to a protein called
phosphodiesterase, located in the inner membrane of the cell. When
attached to activated rhodopsin and its entourage, the phosphodiesterase
acquires the ability to chemically cut a molecule called cGMP (a
chemical relative of both GDP and GTP). Initially there are a lot of
cGMP molecules in the cell, but the phosphodiesterase lowers its
concentration, like a pulled plug lowers the water level in a bathtub.
Another membrane protein that binds cGMP is called an ion channel. It
acts as a gateway that regulates the number of sodium ions in the cell.
Normally the ion channel allows sodium ions to flow into the cell, while
a separate protein actively pumps them out again. The dual action of the
ion channel and pump keeps the level of sodium ions in the cell within a
narrow range. When the amount of cGMP is reduced because of cleavage by
the phosphodiesterase, the ion channel closes, causing the cellular
concentration of positively charged sodium ions to be reduced. This
causes an imbalance of charge across the cell membrane which, finally,
causes a current to be transmitted down the optic nerve to the brain.
The result, when interpreted by the brain, is vision.
My explanation is just a sketchy overview of the biochemistry of vision.
Ultimately, though, this is what it means to "explain" vision.
This is the level of explanation for which biological science must aim.
In order to truly understand a function, one must understand in detail
every relevant step in the process. The relevant steps in biological
processes occur ultimately at the molecular level, so a satisfactory
explanation of a biological phenomenon such as vision, or digestion, or
immunity must include its molecular explanation.
Now that the black box of vision has been opened it is no longer enough
for an "evolutionary explanation" of that power to consider
only the anatomical structures of whole eyes, as Darwin did in the
nineteenth century, and as popularizers of evolution continue to do
today. Each of the anatomical steps and structures that Darwin thought
were so simple actually involves staggeringly complicated biochemical
processes that cannot be papered over with rhetoric. Darwin's simple
steps are now revealed to be huge leaps between carefully tailored
machines. Thus biochemistry offers a Lilliputian challenge to Darwin.
Now the black box of the cell has been opened and a Lilliputian world of
staggering complexity stands revealed. It must be explained.
Irreducible Complexity
How can we decide if Darwin's theory can account for the complexity of
molecular life? It turns out that Darwin himself set the standard. He
acknowledged that:
If it could be demonstrated that any complex organ existed which could
not possibly have been formed by numerous, successive, slight
modifications, my theory would absolutely break down. But what type of
biological system could not be formed by "numerous, successive,
slight modifications"?
Well, for starters, a system that is irreducibly complex. Irreducible
complexity is just a fancy phrase I use to mean a single system which is
composed of several interacting parts, and where the removal of any one
of the parts causes the system to cease functioning.
Let's consider an everyday example of irreducible complexity: the humble
mousetrap. The mousetraps that my family uses consist of a number of
parts. There are: 1) a flat wooden platform to act as a base; 2) a metal
hammer, which does the actual job of crushing the little mouse; 3) a
spring with extended ends to press against the platform and the hammer
when the trap is charged; 4) a sensitive catch which releases when
slight pressure is applied, and 5) a metal bar which connects to the
catch and holds the hammer back when the trap is charged. Now you can't
catch a few mice with just a platform, add a spring and catch a few more
mice, add a holding bar and catch a few more. All the pieces of the
mousetrap have to be in place before you catch any mice. Therefore the
mousetrap is irreducibly complex.
An irreducibly complex system cannot be produced directly by numerous,
successive, slight modifications of a precursor system, because any
precursor to an irreducibly complex system that is missing a part is by
definition nonfunctional. An irreducibly complex biological system, if
there is such a thing, would be a powerful challenge to Darwinian
evolution. Since natural selection can only choose systems that are
already working, then if a biological system cannot be produced
gradually it would have to arise as an integrated unit, in one fell
swoop, for natural selection to have anything to act on.
Demonstration that a system is irreducibly complex is not a proof that
there is absolutely no gradual route to its production. Although an
irreducibly complex system can't be produced directly, one can't
definitively rule out the possibility of an indirect, circuitous route.
However, as the complexity of an interacting system increases, the
likelihood of such an indirect route drops precipitously. And as the
number of unexplained, irreducibly complex biological systems increases,
our confidence that Darwin's criterion of failure has been met
skyrockets toward the maximum that science allows.
The Cilium
Now, are any biochemical systems irreducibly complex? Yes, it turns out
that many are. A good example is the cilium. Cilia are hair-like
structures on the surfaces of many animal and lower plant cells that can
move fluid over the cell's surface or "row" single cells
through a fluid. In humans, for example, cells lining the respiratory
tract each have about 200 cilia that beat in synchrony to sweep mucus
towards the throat for elimination. What is the structure of a cilium? A
cilium consists of bundle of fibers called an axoneme. An axoneme
contains a ring of 9 double "microtubules" surrounding two
central single microtubules. Each outer doublet consists of a ring of 13
filaments (sub-fiber A) fused to an assembly of 10 filaments (sub-fiber
B). The filaments of the microtubules are composed of two proteins called
alpha and beta tubulin. The 11 microtubules forming an axoneme are held
together by three types of connectors: sub-fibers A are joined to the
central microtubules by radial spokes; adjacent outer doublets are
joined by linkers of a highly elastic protein called nexin; and the
central microtubules are joined by a connecting bridge. Finally, every
sub-fiber A bears two arms, an inner arm and an outer arm, both
containing a protein called dynein.
But how does a cilium work? Experiments have shown that ciliary motion
results from the chemically-powered "walking" of the dynein
arms on one microtubule up a second microtubule so that the two
microtubules slide past each other. The protein cross-links between
microtubules in a cilium prevent neighboring microtubules from sliding
past each other by more than a short distance. These cross-links,
therefore, convert the dynein-induced sliding motion to a bending motion
of the entire axoneme.
Now, let us consider what this implies. What components are needed for a
cilium to work? Ciliary motion certainly requires microtubules;
otherwise, there would be no strands to slide. Additionally we require a
motor, or else the microtubules of the cilium would lie stiff and
motionless. Furthermore, we require linkers to tug on neighboring
strands, converting the sliding motion into a bending motion, and
preventing the structure from falling apart. All of these parts are
required to perform one function: ciliary motion. Just as a mousetrap
does not work unless all of its constituent parts are present, ciliary
motion simply does not exist in the absence of microtubules, connectors,
and motors. Therefore, we can conclude that the cilium is irreducibly
complex; an enormous monkey wrench thrown into its presumed gradual,
Darwinian evolution.
Blood Clotting
Now let's talk about a different biochemical system of blood clotting.
Amusingly, the way in which the blood clotting system works is
reminiscent of a Rube Goldberg machine.
The name of Rube Goldberg; the great cartoonist who entertained America
with his silly machines, lives on in our culture, but the man himself
has pretty much faded from view. Here's a typical example of his humor.
In this cartoon Goldberg imagined a system where water from a drain-pipe
fills a flask, causing a cork with attached needle to rise and puncture
a paper cup containing beer, which sprinkles on a bird. The intoxicated
bird falls onto a spring, bounces up to a platform, and pulls a string
thinking it's a worm. The string triggers a cannon which frightens a
dog. The dog flips over, and his rapid breathing raises and lowers a
scratcher over a mosquito bite, causing no embarrassment while talking
to a lady.
When you think about it for a moment you realize that the Rube Goldberg
machine is irreducibly complex. It is a single system which is composed
of several interacting parts, and where the removal of any one of the
parts causes the system to break down. If the dog is missing the machine
doesn't work; if the needle hasn't been put on the cork, the whole
system is useless.
It turns out that we all have Rube Goldberg in our blood. Here's a
picture of a cell trapped in a clot. The meshwork is formed from a
protein called fibrin. But what controls blood clotting? Why does blood
clot when you cut yourself, but not at other times when a clot would
cause a stroke or heart attack? Here's a diagram of what's called the
blood clotting cascade. Let's go through just some of the reactions of
clotting.
When an animal is cut a protein called Hageman factor sticks to the
surface of cells near the wound. Bound Hageman factor is then cleaved by
a protein called HMK to yield activated Hageman factor. Immediately the
activated Hageman factor converts another protein, called prekallikrein,
to its active form, kallikrein. Kallikrein helps HMK speed up the
conversion of more Hageman factor to its active form. Activated Hageman
factor and HMK then together transform another protein, called PTA, to
its active form. Activated PTA in turn, together with the activated form
of another protein (discussed below) called convertin, switch a protein
called Christmas factor to its active form. Activated Christmas factor,
together with antihemophilic factor (which is itself activated by
thrombin in a manner similar to that of proaccelerin) changes Stuart
factor to its active form. Stuart factor,working with accelerin,
converts prothrombin to thrombin. Finally thrombin cuts fibrinogen to
give fibrin, which aggregates with other fibrin molecules to form the
meshwork clot you saw in the last picture.
Blood clotting requires extreme precision. When a pressurized blood
circulation system is punctured, a clot must form quickly or the animal
will bleed to death. On the other hand, if blood congeals at the wrong
time or place, then the clot may block circulation as it does in heart
attacks and strokes. Furthermore, a clot has to stop bleeding all along
the length of the cut, sealing it completely. Yet blood clotting must be
confined to the cut or the entire blood system of the animal might
solidify, killing it. Consequently, clotting requires this enormously
complex system so that the clot forms only when and only where it is
required. Blood clotting is the ultimate Rube Goldberg machine.
The Professional Literature
Other examples of irreducible complexity abound in the cell, including
aspects of protein transport, the bacterial flagellum, electron
transport, telomeres, photosynthesis, transcription regulation, and much
more. Examples of irreducible complexity can be found on virtually every
page of a biochemistry textbook. But if these things cannot be explained
by Darwinian evolution, how has the scientific community regarded these
phenomena of the past forty years? A good place to look for an answer to
that question is in the Journal of Molecular Evolution. JME is a
journal that was begun specifically to deal with the topic of how
evolution occurs on the molecular level. It has high scientific
standards, and is edited by prominent figures in the field. In a recent
issue of JME there were published eleven articles; of these, all eleven
were concerned simply with the comparison of protein or DNA sequences. A
sequence comparison is an amino acid-by-amino acid comparison of two
different proteins, or a nucleotide-by-nucleotide comparison of two
different pieces of DNA, noting the positions at which they are
identical or similar, and the places where they are not. Although useful
for determining possible lines of descent, which is an interesting
question in its own right, comparing sequences cannot show how a complex
biochemical system achieved its function; the question that most
concerns us here. By way of analogy, the instruction manuals for two
different models of computer putout by the same company might have many
identical words, sentences, and even paragraphs, suggesting a common
ancestry (perhaps the same author wrote both manuals), but comparing the
sequences of letters in the instruction manuals will never tell us if a
computer can be produced step by step starting from a typewriter.
None of the papers discussed detailed models for intermediates in the
development of complex biomolecular structures. In the past ten years
JME has published over a thousand papers. Of these, about one hundred
discussed the chemical synthesis of molecules thought to be necessary
for the origin of life, about 50 proposed mathematical models to improve
sequence analysis, and about 800 were analyses of sequences. There were
ZERO papers discussing detailed models for intermediates in the
development of complex biomolecular structures. This is not a
peculiarity of JME. No papers are to be found that discuss detailed
models for intermediates in the development of complex biomolecular
structures in the Proceedings of the National Academy of Science,
Nature, Science, the Journal of Molecular Biology
or, to my knowledge, any science journal whatsoever.
"Publish or perish" is a proverb that academicians take
seriously. If you do not publish your work for the rest of the community
to evaluate, then you have no business in academia and, if you don't
already have tenure, you will be banished. But the saying can be applied
to theories as well. If a theory claims to be able to explain some
phenomenon but does not generate even an attempt at an explanation, then
it should be banished. Despite comparing sequences, molecular evolution
has never addressed the question of how complex structures came to be.
In effect, the theory of Darwinian molecular evolution has not
published, and so it should perish.
Detection of Design
What's going on? Imagine a room in which a body lies crushed, flat as a
pancake. A dozen detectives crawl around, examining the floor with
magnifying glasses for any clue to the identity of the perpetrator. In
the middle of the room next to the body stands a large, gray elephant.
The detectives carefully avoid bumping into the pachyderm's legs as they
crawl, and never even glance at it. Over time the detectives get
frustrated with their lack of progress but resolutely press on, looking
even more closely at the floor. You see, textbooks say detectives must
"get their man," so they never consider elephants.
There is an elephant in the roomful of scientists who are trying to
explain the development of life. The elephant is labeled
"intelligent design." To a person who does not feel obliged to
restrict his search to unintelligent causes, the straightforward
conclusion is that many biochemical systems were designed. They were
designed not by the laws of nature, not by chance and necessity. Rather,
they were planned. The designer knew what the systems would look like
when they were completed; the designer took steps to bring the systems
about. Life on earth at its most fundamental level, in its most critical
components, is the product of intelligent activity.
The conclusion of intelligent design flows naturally from the data
itself, not from sacred books or sectarian beliefs. Inferring that
biochemical systems were designed by an intelligent agent is a humdrum
process that requires no new principles of logic or science. It comes
simply from the hard work that biochemistry has done over the past forty
years, combined with consideration of the way in which we reach
conclusions of design every day.
What is "design"? Design is simply the purposeful arrangement
of parts. The scientific question is how we detect design. This can be
done in various ways, but design can most easily be inferred for
mechanical objects. While walking through a junkyard you might observe
separated bolts and screws and bits of plastic and glass, most
scattered, some piled on top of each other, some wedged together.
Suppose you saw a pile that seemed particularly compact, and when you
picked up a bar sticking out of the pile, the whole pile came along with
it. When you pushed on the bar it slid smoothly to one side of the pile
and pulled an attached chain along with it. The chain in turn yanked a
gear which turned three other gears which turned a red-and-white striped
rod, spinning it like a barber pole. You quickly conclude that the pile
was not a chance accumulation of junk, but was designed, was put
together in that order by an intelligent agent, because you see that the
components of the system interact with great specificity to do
something.
It is not only artificial mechanical systems for which design can easily
be concluded. Systems made entirely from natural components can also
evince design. For example, suppose you are walking with a friend in the
woods. All of a sudden your friend is pulled high in the air and left
dangling by his foot from a vine attached to a tree branch. After
cutting him down you reconstruct the trap. You see that the vine was
wrapped around the tree branch, and the end pulled tightly down to the
ground. It was securely anchored to the ground by a forked branch. The
branch was attached to another vine, hidden by leaves so that, when the
trigger-vine was disturbed, it would pull down the forked stick,
releasing the spring-vine. The end of the vine formed a loop with a
slipknot to grab an appendage and snap it up into the air. Even though
the trap was made completely of natural materials you would quickly
conclude that it was the product of intelligent design.
A Complicated World
A word of caution; intelligent design theory has to be seen in context:
it does not try to explain everything. We live in a complex world where
lots of different things can happen. When deciding how various rocks
came to be shaped the way they are a geologist might consider a whole
range of factors: rain, wind, the movement of glaciers, the activity of
moss and lichens, volcanic action, nuclear explosions, asteroid impact,
or the hand of a sculptor. The shape of one rock might have been
determined primarily by one mechanism, the shape of another rock by
another mechanism. The possibility of a meteor's impact does not mean
that volcanos can be ignored; the existence of sculptors does not mean
that many rocks are not shaped by weather. Similarly, evolutionary
biologists have recognized that a number of factors might have affected
the development of life: common descent, natural selection, migration,
population size, founder effects (effects that may be due to the limited
number of organisms that begin a new species), genetic drift (spread of
neutral, nonselective mutations), gene flow (the incorporation of genes
into a population from a separate population), linkage (occurrence of
two genes on the same chromosome), meiotic drive (the preferential
selection during sex cell production of one of the two copies of a gene
inherited from an organism's parents), transposition (the transfer of a
gene between widely separated species by non-sexual means), and much
more. The fact that some biochemical systems were designed by an
intelligent agent does not mean that any of the other factors are not
operative, common, or important.
Curiouser and Curiouser
So as this talk concludes we are left with what many people feel to be a
strange conclusion: that life was designed by an intelligent agent. In a
way, though, all of the progress of science over the last several
hundred years has been a steady march toward the strange. People up
until the middle ages lived in a natural world. The stable earth was at
the center of things; the sun, moon, and stars circled endlessly to give
light by day and night; the same plants and animals had been known since
antiquity. Surprises were few.
Then it was proposed, absurdly, that the earth itself moved, spinning
while it circled the sun. No one could feel the earth spinning; no one
could see it. But spin it did. From our modern vantage it's hard to
realize what an assault on the senses was perpetrated by Copernicus and
Galileo; they said in effect that people could no longer rely on even
the evidence of their eyes.
Things got steadily worse over the years. With the discovery of fossils
it became apparent that the familiar animals of field and forest had not
always been on earth; the world had once been inhabited by huge, alien
creatures who were now gone. Sometime later Darwin shook the world by
arguing that the familiar biota was derived from the bizarre, vanished
life over lengths of time incomprehensible to human minds. Einstein told
us that space is curved and time is relative. Modern physics says that
solid objects are mostly space, that sub atomic particles have no
definite position, that the universe had a beginning.
Now it's the turn of the fundamental science of life, modern
biochemistry, to disturb. The simplicity that was once expected to be
the foundation of life has proven to be a phantom. Instead, systems of
horrendous, irreducible complexity inhabit the cell. The resulting
realization that life was designed by an intelligence is a shock to us
in the twentieth century who have gotten used to thinking of life as the
result of simple natural laws. But other centuries have had their shocks
and there is no reason to suppose that we should escape them. Humanity
has endured as the center of the heavens moved from the earth to beyond
the sun, as the history of life expanded to encompass long-dead
reptiles, as the eternal universe proved mortal. We will endure the
opening of Darwin's black box.
Michael J. Behe is Associate Professor of Chemistry at Lehigh University
in Pennsylvania and a Fellow of the Discovery Institute’s Center for
Renewal of Science & Culture.
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