Experimental
Support for the Design Inference
by
Michael J. Behe
To Darwin, the cell – and every microbiological function
– was an unknowable black box. Now that we can look
into this box, can we apply Darwin’s theory to it? Why
is it that, of the thousands of papers published in science
journals, none ever discuss detailed models for intermediates
in the development of complex biomolecular structures? In
drawing his ground-breaking conclusions, Behe is not inferring
design from what we do not know, but from what we do know.
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Darwinism’s
Prosperity
Within
a short time after Charles Darwin published The Origin of
Species the explanatory power of the theory of evolution was
recognized by the great majority of biologists. The hypothesis
readily resolved the problems of homologous resemblance, rudimentary
organs, species abundance, extinction, and biogeography. The
rival theory of the time, which posited creation of species
by a supernatural being, appeared to most reasonable minds
to be much less plausible, since it would have a putative
Creator attending to details that seemed to be beneath His
dignity.
As
time went on the theory of evolution obliterated the rival
theory of creation, and virtually all working scientists studied
the biological world from a Darwinian perspective. Most educated
people now lived in a world where the wonder and diversity
of the biological kingdom were produced by the simple, elegant
principle of natural selection.
However,
in science a successful theory is not necessarily a correct
theory. In the course of history there have also been other
theories which achieved the triumph that Darwinism achieved,
which brought many experimental and observational facts into
a coherent framework, and which appealed to people’s
intuitions about how the world should work. Those theories
also promised to explain much of the universe with a few simple
principles. But, by and large, those other theories are now
dead.
A
good example of this is the replacement of Newton’s
mechanical view of the universe by Einstein’s relativistic
universe. Although Newton’s model accounted for the
results of many experiments in his time, it failed to explain
aspects of gravitation. Einstein solved that problem and others
by completely rethinking the structure of the universe.
Similarly,
Darwin’s theory of evolution prospered by explaining
much of the data of his time and the first half of the 20th
century, but my article will show that Darwinism has been
unable to account for phenomena uncovered by the efforts of
modern biochemistry during the second half of this century.
I will do this by emphasizing the fact that life at its most
fundamental level is irreducibly complex and that such complexity
is incompatible with undirected evolution.
A Series of Eyes
How
do we see?
In
the 19th century the anatomy of the eye was known in great
detail and the sophisticated mechanisms it employs to deliver
an accurate picture of the outside world astounded everyone
who was familiar with them. Scientists of the 19th century
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.
Thus it was concluded that the eye could only function if
it were nearly intact.
As
Charles Darwin was considering possible objections to his
theory of evolution by natural selection in The Origin of
Species he discussed the problem of the eye in a section of
the book appropriately entitled "Organs of extreme perfection
and complication." He realized that if in one generation
an organ of the complexity of the eye suddenly appeared, the
event would be tantamount to a miracle. Somehow, for Darwinian
evolution to be believable, the difficulty that the public
had in envisioning the gradual formation of complex organs
had to be removed.
Darwin
succeeded brilliantly, not by actually describing a real pathway
that evolution might have used in constructing the eye, but
rather by pointing to a variety of animals that were known
to have eyes of various constructions, ranging from a simple
light sensitive spot to the complex vertebrate camera eye,
and suggesting that the evolution of the human eye might have
involved similar organs as intermediates.
But
the question remains, how do we see? Although Darwin was able
to persuade much of the world that a modern eye could be produced
gradually from a much simpler structure, he did not even attempt
to explain how the simple light sensitive spot that was his
starting point actually worked. When discussing the eye Darwin
dismissed the question of its ultimate mechanism by stating:
"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 to answer the question:
19th century science had not progressed to the point where
the matter could even be approached. The question of how the
eye works–that is, what happens when a photon of light
first impinges on the retina–simply could not be answered
at that time. As a matter of fact, no question about the underlying
mechanism of life could be answered at that time. How do animal
muscles cause movement? How does photosynthesis work? How
is energy extracted from food? How does the body fight infection?
All such questions were unanswerable.
The Calvin and Hobbes Approach
Now,
it appears to be a characteristic of the human mind that when
it is lacks understanding of a process, then it seems easy
to imagine simple steps leading from nonfunction to function.
A happy example of this is seen in the popular comic strip
Calvin and Hobbes . Little boy Calvin is always having adventures
in the company of his tiger Hobbes by jumping in a box and
traveling back in time, or grabbing a toy ray gun and "transmogrifying"
himself into various animal shapes, or again using a box as
a duplicator and making copies of himself to deal with worldly
powers such as his mom and his teachers. A small child such
as Calvin finds it easy to imagine that a box just might be
able to fly like an airplane (or something), because Calvin
doesn’t know how airplanes work.
A good example from the biological world of complex changes
appearing to be simple is the belief in spontaneous generation.
One of the chief proponents of the theory of spontaneous generation
during the middle of the 19th century was Ernst Haeckel, a
great admirer of Darwin and an eager popularizer of Darwin’s
theory. From the limited view of cells that 19th century microscopes
provided, Haeckel believed that a cell was a "simple
little lump of albuminous combination of carbon", not
much different from a piece of microscopic Jell-O ® .
Thus it seemed to Haeckel that such simple life could easily
be produced from inanimate material.
In 1859, the year of the publication of The Origin of Species,
an exploratory vessel, the H.M.S. Cyclops, dredged up some
curious-looking mud from the sea bottom. Eventually Haeckel
came to observe the mud and thought that it closely resembled
some cells he had seen under a microscope. Excitedly he brought
this to the attention of no less a personage than Thomas Henry
Huxley, Darwin’s great friend and defender, who observed
the mud for himself. Huxley, too, became convinced that it
was Urschleim (that is, protoplasm), the progenitor of life
itself, and Huxley named the mud Bathybius haeckelii after
the eminent proponent of abiogenesis.
The mud failed to grow. In later years, with the development
of new biochemical techniques and improved microscopes, the
complexity of the cell was revealed. The "simple lumps"
were shown to contain thousands of different types of organic
molecules, proteins, and nucleic acids, many discrete subcellular
structures, specialized compartments for specialized processes,
and an extremely complicated architecture. Looking back from
the perspective of our time, the episode of Bathybius haeckelii
seems silly or downright embarrassing, but it shouldn’t.
Haeckel and Huxley were behaving naturally, like Calvin: since
they were unaware of the complexity of cells, they found it
easy to believe that cells could originate from simple mud.
Throughout history there have been many other examples, similar
to that of Haeckel, Huxley, and the cell, where a key piece
of a particular scientific puzzle was beyond the understanding
of the age. In science there is even a whimsical term for
a machine or structure or process that does something, but
the actual mechanism by which it accomplishes its task is
unknown: it is called a "black box." In Darwin’s
time all of biology was a black box: not only the cell, or
the eye, or digestion, or immunity, but every biological structure
and function because, ultimately, no one could explain how
biological processes occurred.
Biology has progressed tremendously due to the model that
Darwin put forth. But the black boxes Darwin accepted are
now being opened, and our view of the world is again being
shaken.
Take our modern understanding of proteins, for example.
Proteins
In
order to understand the molecular basis of life it is necessary
to understand how things called "proteins" work.
Proteins are the machinery of living tissue that builds the
structures and carries out the chemical reactions necessary
for life. For example, the first of many steps necessary for
the conversion of sugar to biologically-usable forms of energy
is carried out by a protein called hexokinase. Skin is made
in large measure of a protein called collagen. When light
impinges on your retina it interacts first with a protein
called rhodopsin. A typical cell contains thousands and thousands
of different types of proteins to perform the many tasks necessary
for life, much like a carpenter’s workshop might contain
many different kinds of tools for various carpentry tasks.
What
do these versatile tools look like? The basic structure of
proteins is quite simple: they are formed by hooking together
in a chain discrete subunits called amino acids. Although
the protein chain can consist of anywhere from about 50 to
about 1,000 amino acid links, each position can only contain
one of 20 different amino acids. In this they are much like
words: words can come in various lengths but they are made
up from a discrete set of 26 letters.
Now,
a protein in a cell does not float around like a floppy chain;
rather, it folds up into a very precise structure which can
be quite different for different types of proteins. Two different
amino acid sequences–two different proteins–can
be folded to structures as specific and different from each
other as a three-eighths inch wrench and a jigsaw. And like
the household tools, if the shape of the proteins is significantly
warped then they fail to do their jobs.
The
Eyesight of Man
In
general, biological processes on the molecular level are performed
by networks of proteins, each member of which carries out
a particular task in a chain.
Let
us return to the question, how do we see? Although to Darwin
the primary event of vision was a black box, through the efforts
of many biochemists an answer to the question of sight is
at hand. The answer involves a long chain of steps that begin
when light strikes the retina and a photon is absorbed by
an organic molecule called 11-cis-retinal, causing it to rearrange
itself within picoseconds. This causes a corresponding change
to the protein, rhodopsin, which is tightly bound to it, so
that it can react with another protein called transducin,
which in turn causes a molecule called GDP to be exchanged
with a molecule called GTP.
To
make a long story short, this exchange begins a long series
of further bindings between still more specialized molecular
machinery, and scientists now understand a great deal about
the system of gateways, pumps, ion channels, critical concentrations,
and attenuated signals that result in a current to finally
be transmitted down the optic nerve to the brain, interpreted
as vision. Biochemists also understand the many chemical reactions
involved in restoring all these changed or depleted parts
to make a new cycle possible.
To Explain Life
Although
space doesn’t permit me to give the details of the biochemistry
of vision here, I have given the steps in my talks. Biochemists
know what it means to "explain" vision. They know
the level of explanation that biological science eventually
must aim for. In order to say that some function is understood,
every relevant step in the process must be elucidated. The
relevant steps in biological processes occur ultimately at
the molecular level, so a satisfactory explanation of a biological
phenomenon such as sight, or digestion, or immunity, must
include a molecular explanation.
It
is no longer sufficient, now that the black box of vision
has been opened, for an "evolutionary explanation"
of that power to invoke only the anatomical structures of
whole eyes, as Darwin did in the 19th century and as most
popularizers of evolution continue to do today. Anatomy is,
quite simply, irrelevant. So is the fossil record. It does
not matter whether or not the fossil record is consistent
with evolutionary theory, any more than it mattered in physics
that Newton’s theory was consistent with everyday experience.
The fossil record has nothing to tell us about, say, whether
or how the interactions of 11-cis-retinal with rhodopsin,
transducin, and phosphodiesterase could have developed, step
by step.
"How
a nerve comes to be sensitive to light hardly concerns us
more than how life itself originated", said Darwin in
the 19th century. But both phenomena have attracted the interest
of modern biochemistry in the past few decades. The story
of the slow paralysis of research on life’s origin is
quite interesting, but space precludes its retelling here.
Suffice it to say that at present the field of origin-of-life
studies has dissolved into a cacophony of conflicting models,
each unconvincing, seriously incomplete, and incompatible
with competing models. In private even most evolutionary biologists
will admit that science has no explanation for the beginning
of life [especially at the complex level].
The
same problems which beset origin-of-life research also bedevil
efforts to show how virtually any complex biochemical system
came about. Biochemistry has revealed a molecular world which
stoutly resists explanation by the same theory that has long
been applied at the level of the whole organism. Neither of
Darwin’s black boxes–the origin of life or the
origin of vision (or other complex biochemical systems)–has
been accounted for by his theory.
Irreducible Complexity
In
The Origin of Species Darwin stated:
"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."
A
system which meets Darwin’s criterion is one which exhibits
irreducible complexity. By irreducible complexity I mean a
single system which is composed of several interacting parts
that contribute to the basic function, and where the removal
of any one of the parts causes the system to effectively cease
functioning. An irreducibly complex system cannot be produced
directly by slight, successive modifications of a precursor
system, since any precursor to an irreducibly complex system
is by definition nonfunctional.
Since
natural selection requires a function to select, an irreducibly
complex biological system, if there is such a thing, would
have to arise as an integrated unit for natural selection
to have anything to act on. It is almost universally conceded
that such a sudden event would be irreconcilable with the
gradualism Darwin envisioned. At this point, however, "irreducibly
complex" is just a term, whose power resides mostly in
its definition. We must now ask if any real thing is in fact
irreducibly complex, and, if so, then are any irreducibly
complex things also biological systems?
Consider
the humble mousetrap. The mousetraps that my family uses in
our home to deal with unwelcome rodents 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 wire 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 holds the hammer back when
the trap is charged and connects to the catch. There are also
assorted staples and screws to hold the system together.
If
any one of the components of the mousetrap (the base, hammer,
spring, catch, or holding bar) is removed, then the trap does
not function. In other words, the simple little mousetrap
has no ability to trap a mouse until several separate parts
are all assembled.
Because
the mousetrap is necessarily composed of several parts, it
is irreducibly complex. Thus, irreducibly complex systems
exist.
Molecular Machines
Now, are any biochemical systems irreducibly complex? Yes,
it turns out that many are.
Earlier
we discussed proteins. In many biological structures proteins
are simply components of larger molecular machines. Like the
picture tube, wires, metal bolts and screws that comprise
a television set, many proteins are part of structures that
only function when virtually all of the components have been
assembled.
A
good example of this is a cilium. Cilia are hairlike organelles
on the surfaces of many animal and lower plant cells that
serve to move fluid over the cell’s surface or to "row"
single cells through a fluid. In humans, for example, epithelial
cells lining the respiratory tract each have about 200 cilia
that beat in synchrony to sweep mucus towards the throat for
elimination.
A
cilium consists of a membrane-coated 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 composed of 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 that consist 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 the protein
dynein.
But
how does a cilium work? Experiments have indicated that ciliary
motion results from the chemically-powered "walking"
of the dynein arms on one microtubule up the neighboring subfiber
B of a second microtubule so that the two microtubules slide
past each other. However, the protein cross-links between
microtubules in an intact 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 sit back, review the workings of the cilium, and consider
what it implies. Cilia are composed of at least a half dozen
proteins: alpha-tubulin, beta-tubulin, dynein, nexin, spoke
protein, and a central bridge protein. These combine to perform
one task, ciliary motion, and all of these proteins must be
present for the cilium to function. If the tubulins are absent,
then there are no filaments to slide; if the dynein is missing,
then the cilium remains rigid and motionless; if nexin or
the other connecting proteins are missing, then the axoneme
falls apart when the filaments slide.
What
we see in the cilium, then, is not just profound complexity,
but it is also irreducible complexity on the molecular scale.
Recall that by "irreducible complexity" we mean
an apparatus that requires several distinct components for
the whole to work. My mousetrap must have a base, hammer,
spring, catch, and holding bar, all working together, in order
to function. Similarly, the cilium, as it is constituted,
must have the sliding filaments, connecting proteins, and
motor proteins for function to occur. In the absence of any
one of those components, the apparatus is useless.
The
components of cilia are single molecules. This means that
there are no more black boxes to invoke; the complexity of
the cilium is final, fundamental. And just as scientists,
when they began to learn the complexities of the cell, realized
how silly it was to think that life arose spontaneously in
a single step or a few steps from ocean mud, so too we now
realize that the complex cilium can not be reached in a single
step or a few steps.
But
since the complexity of the cilium is irreducible, then it
can not have functional precursors. Since the irreducibly
complex cilium can not have functional precursors it can not
be produced by natural selection, which requires a continuum
of function to work. Natural selection is powerless when there
is no function to select. We can go further and say that,
if the cilium can not be produced by natural selection, then
the cilium was designed.
A Non-Mechanical Example
A
non-mechanical example of irreducible complexity can be seen
in the system that targets proteins for delivery to subcellular
compartments. In order to find their way to the compartments
where they are needed to perform specialized tasks, certain
proteins contain a special amino acid sequence near the beginning
called a "signal sequence."
As
the proteins are being synthesized by ribosomes, a complex
molecular assemblage called the signal recognition particle
or SRP, binds to the signal sequence. This causes synthesis
of the protein to halt temporarily. During the pause in protein
synthesis the SRP is bound by the trans-membrane SRP receptor,
which causes protein synthesis to resume and which allows
passage of the protein into the interior of the endoplasmic
reticulum (ER). As the protein passes into the ER the signal
sequence is cut off.
For
many proteins the ER is just a way station on their travels
to their final destinations. Proteins which will end up in
a lysosome are enzymatically "tagged" with a carbohydrate
residue called mannose-6-phosphate while still in the ER.
An area of the ER membrane then begins to concentrate several
proteins; one protein, clathrin, forms a sort of geodesic
dome called a coated vesicle which buds off from the ER. In
the dome there is also a receptor protein which binds to both
the clathrin and to the mannose-6-phosphate group of the protein
which is being transported. The coated vesicle then leaves
the ER, travels through the cytoplasm, and binds to the lysosome
through another specific receptor protein. Finally, in a maneuver
involving several more proteins, the vesicle fuses with the
lysosome and the protein arrives at its destination.
During
its travels our protein interacted with dozens of macromolecules
to achieve one purpose: its arrival in the lysosome. Virtually
all components of the transport system are necessary for the
system to operate, and therefore the system is irreducible.
And since all of the components of the system are comprised
of single or several molecules, there are no black boxes to
invoke. The consequences of even a single gap in the transport
chain can be seen in the hereditary defect known as I-cell
disease. It results from a deficiency of the enzyme that places
the mannose-6-phosphate on proteins to be targeted to the
lysosomes. I-cell disease is characterized by progressive
retardation, skeletal deformities, and early death.
The Study of "Molecular Evolution"
Other
examples of irreducible complexity abound, including aspects
of protein transport, blood clotting, closed circular DNA,
electron transport, the bacterial flagellum, 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 analysis of protein
or DNA sequences. None of the papers discussed detailed models
for intermediates in the development of complex biomolecular
structures.
In
the past ten years JME has published 886 papers. Of these,
95 discussed the chemical synthesis of molecules thought to
be necessary for the origin of life, 44 proposed mathematical
models to improve sequence analysis, 20 concerned the evolutionary
implications of current structures, and 719 were analyses
of protein or polynucleotide sequences. However, there weren’t
any 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 journal whatsoever.
Sequence
comparisons overwhelmingly dominate the literature of molecular
evolution. But sequence comparisons simply can’t account
for the development of complex biochemical systems any more
than Darwin’s comparison of simple and complex eyes
told him how vision worked. Thus in this area science is mute.
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.
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.
Intelligent
design is a good explanation for a number of biochemical systems,
but I should insert 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.
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), 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.
Conclusion
It
is often said that science must avoid any conclusions which
smack of the supernatural. But this seems to me to be both
bad logic and bad science. Science is not a game in which
arbitrary rules are used to decide what explanations are to
be permitted. Rather, it is an effort to make true statements
about physical reality. It was only about sixty years ago
that the expansion of the universe was first observed. This
fact immediately suggested a singular event–that at
some time in the distant past the universe began expanding
from an extremely small size.
To
many people this inference was loaded with overtones of a
supernatural event–the creation, the beginning of the
universe. The prominent physicist A.S. Eddington probably
spoke for many physicists in voicing his disgust with such
a notion:
"Philosophically,
the notion of an abrupt beginning to the present order of
Nature is repugnant to me, as I think it must be to most;
and even those who would welcome a proof of the intervention
of a Creator will probably consider that a single winding-up
at some remote epoch is not really the kind of relation between
God and his world that brings satisfaction to the mind."
Nonetheless,
the big bang hypothesis was embraced by physics and over the
years has proven to be a very fruitful paradigm. The point
here is that physics followed the data where it seemed to
lead, even though some thought the model gave aid and comfort
to religion. In the present day, as biochemistry multiplies
examples of fantastically complex molecular systems, systems
which discourage even an attempt to explain how they may have
arisen, we should take a lesson from physics. The conclusion
of design flows naturally from the data; we should not shrink
from it; we should embrace it and build on it.
In
concluding, it is important to realize that we are not inferring
design from what we do not know, but from what we do know.
We are not inferring design to account for a black box, but
to account for an open box. A man from a primitive culture
who sees an automobile might guess that it was powered by
the wind or by an antelope hidden under the car, but when
he opens up the hood and sees the engine he immediately realizes
that it was designed. In the same way biochemistry has opened
up the cell to examine what makes it run and we see that it,
too, was designed.
It
was a shock to the people of the 19th century when they discovered,
from observations science had made, that many features of
the biological world could be ascribed to the elegant principle
of natural selection. It is a shock to us in the twenty-first
century to discover, from observations science has made, that
the fundamental mechanisms of life cannot be ascribed to natural
selection, and therefore were designed. But we must deal with
our shock as best we can and go on. The theory of undirected
evolution is already dead, but the work of science continues [not theistic evolution, which is totally possible].
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Associate
Professor in the Department of Biological Sciences at Lehigh
University, Michael Behe is author of the best-selling Darwin’s
Black Box: The Biochemical Challenge to Evolution (The Free
Press, 1996), which discusses the implications for biology
of what he calls "irreducibly complex" biochemical
systems. Dr. Behe is provoking widespread comment in publications
ranging from The New York Times to Science . Dr. Behe received
his Ph.D. in Biochemistry from the University of Pennsylvania
in 1978. His current research involves delineation of design
and natural selection in discrete sub-systems of DNA replication.
Be
Sure to Read the following articles:
The
Bible and the Big Bang
How
far back in time can we actually see?
How
Big is the Universe?
To read an excellent booklet that covers the entire subject of Creation verse Evolution, log onto: http://www.ucg.org/booklet/creation-or-evolution-does-it-really-matter-what-you-believe/
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