Previously
I have proved that life cannot have evolved. Today I will prove that
life cannot exist.
Let us begin with Samuel Johnson’s response when asked
whether we have free will. He replied that all theory holds that we do not, all
experience that we do. A similar paradox occurs in the realm of Impossibility
Theory. Many things occur in biology that all science says are possible, while
all common sense says that they are not.
Consider the development of a barely-existent zygote into
seven pounds of puzzled and alarmed baby. (“Where the hell is this?”)
Anyone familiar with Murphy’s Law knows that it isn’t possible. Half an hour
with a textbook of embryology will confirm this judgement. It is a case of
phenomenal complexity following phenomenal complexity building on phenomenal
complexity with, almost always, no errors of consequence.
The resulting little science project enters wherever we are
with a squall, the ductus arteriosus closes, the nursing instinct kicks in, and
the interloper eventually grows into, God help us, a teenager (arguably the
only flaw in the process)….
Suspensory ligaments, connecting the lens of the eye to
the ciliary body. Do you really believe these delicate ropes can
form perfectly all by themselves ? If so, I figure somebody must have put
something in your drugs.
Common
sense says that it can’t work. The sciences say that it can, and the fact that
it does lends a certain weight to their argument. Each step in this impossible
process can be shown to follow the laws of chemistry and physics. It all works.
There is no need for spirits or poltergeists to explain it. Except that it
obviously can’t happen.
Sez me,
Something Else has to be involved. You tell me what, and we will split the
Nobel money……
The following simplified description of the
biochemical functioning of the retina is fromDarwin’s
Black Box: The Biochemical Challenge to Evolutionby Michael Behe. The book,
which I recommend, is accessible to the intelligent laymen, for whom it is
written. The author includes the following techno globe on the biochemistry of
the retina to give a flavor of the complexity of things. The sensible
reader will skip most of it.
When light first strikes the
retina a photon interacts with a molecule called 11-cis-retinal, which
rearranges within picoseconds to trans-retinal. (A picosecond is about the time
it takes light to travel the breadth of a single human hair.) The change in the
shape of the retinal molecule forces a change in the shape of the protein,
rhodopsin, to which the retinal is tightly bound. The protein’s metamorphosis
alters its behavior. Now called metarhodopsin II, the protein sticks to another
protein, called transducin. Before bumping into metarhodopsin II, transducin
had tightly bound a small molecule called GDP. But when transducin interacts
with metarhodopsin II, the GDP falls off, and a molecule called GTP binds to
transducin. (GTP is closely related to, but critically different from, GDP.)
GTP-transducin-metarhodopsin
II now binds to a protein called phosphodiesterase, located in the inner
membrane of the cell. When attached to metarhodopsin II and its entourage, the
phosphodiesterase acquires the chemical ability to “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, just
as 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 that, finally,
causes a current to be transmitted down the optic nerve to the brain. The
result, when interpreted by the brain, is vision. If the reactions mentioned
above were the only ones that operated in the cell, the supply of
11-cis-retinal, cGMP, and sodium ions would quickly be depleted. Something has
to turn off the proteins that were turned on and restore the cell to its
original state. Several mechanisms do this. First, in the dark the ion channel
(in addition to sodium ions) also lets calcium ions into the cell. The calcium
is pumped back out by a different protein so that a constant calcium
concentration is maintained. When cGMP levels fall, shutting down the ion
channel, calcium ion concentration decreases, too. The posphodiesterase enzyme,
which destroys cGMP, slows down at lower calcium concentration. Second, a
protein called guanylate cyclase begins to resynthesize cGMP when calcium
levels start to fall. Third, while all of this is going on, metarhodopsin II is
chemically modified by an enzyme called rhodopsin kinase. The modified
rhodopsin then binds to a protein known as arrestin, which prevents the
rhodopsin from activating more transducin. So the cell contains mechanisms to
limit the amplified signal started by a single photon. Trans-retinal eventually
falls off of rhodopsin and must be reconverted to 11-cis-retinal and again
bound by rhodopsin to get back to the starting point for another visual
cycle. To accomplish this, trans-retinal is first chemically modified by an
enzyme to trans-retinol— a form containing two more hydrogen atoms. A second
enzyme then converts the molecule to 11-cis-retinol. Finally, a third enzyme
removes the previously added hydrogen atoms to form 11-cis-retinal, a cycle is
complete.
The
biochemistry is way over my head, but the complexity is clear. The idea that
this came about by accident requires powers of belief beyond mine, and the idea
that it functions flawlessly for seventy years is more so. Ask a biochemist
whether he can construct this system in the laboratory. Ask him whether he can
construct any system of similar complexity that will work,
maintaining itself, for seventy years.
From all of which I conclude
that we are more puzzled than we believe we are. These thoughts will not be
well-received by those more inclined to protect the paradigm than to
examine it. Oh well.
