Evidence for Intelligent Design from
Biochemistry
by
Michael J. Behe
(From a speech delivered at Discovery Institute's God & Culture
Conference, August 10,1996)
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.
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"?
The Cilium
Now, are any
biochemical systems irreducibly complex? Yes, it turns out that many are. A good
example is the cilium. Cilia are hairlike 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. Inhumans, 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 (subfiber A) fused to an
assembly of 10 filaments (subfiber B). The filaments of the microtubules are
composedof two proteins called alpha and beta tubulin. The 11 microtubules
forming an axoneme are held together by three types of connectors: subfibers 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 subfiber 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.
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.
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
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.
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.
Although ,western scientist give credit to Copernicus and Galileo; about earth moves around sun ,but it was already discovered in Indian Scriptures and documented. Click here(
SCIENTIFIC VED
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).