To: Marty Leipzig
From: Michael Hardy
-=> Quoting Marty Leipzig to Michael Hardy <=-
MH> 2. Complexity -- the irreducible complexity of even simple life forms. Even something as primitive as photosynthesis requires up to five hundred steps take place in order and at the proper times.<<<
ML> So? The old numbers game again. How many BILLION steps must be taken to form a Mikey Hardy, complete with ridiculous arguments? Quite a few, but yet you're still here. <<<
Note that I said IRREDUCIBLE complexity. This is complexity which cannot be accounted for by an accumulation of small mutations. It is as if a Mikey Hardy just popped whole into existence, exactly the kind of occurrence you're denying can happen.
Let me offer you an example, from Michael Behe's book Darwin's Black Box, which I highly recommend to you. This is what causes blood to clot.
1. About 2 to 3 percent of the protein in blood plasma is a protein complex called fibrinogen. It is what makes the fibers that form the actual clot. It is made of six protein chains, containing twin pairs of three different proteins.
2. Fibrinogen usually floats around the bloodstream doing nothing. In its whole state, it is useless. When you get cut, a protein called thrombin slices off some pieces of protein from nearby fibrinogen. The trimmed pieces, now called fibrin, have sticky patches that had been covered by the pieces that were cut off. The sticky patches are precisely complementary to other fibrin molecules. The fibrins stick together to form a mesh net that entraps blood cells. The meshwork is an efficent design that covers a maximum area with minimum protein.
3. Thrombin has to be controlled. If it were always active, slicing up fibrinogen all the time, your blood vessels would quickly fill up with clots. A protein called the Stuart factor becomes activated when you get cut, turning on the inactive prothrombin, turning it into thrombin. But that gives rise to the same problem -- the Stuart factor needs a control, or you'll still die of a massive blood clot.
4. Stuart factor, it turns out, can't do the job by itself. It needs another protein, called accelerin, to get the prothrombin going.
5. Accelerin is initially inert. It is activated by -- thrombin! Because Stuart factor alone, without accelerin, can activate small amounts of prothrombin, there is always a little bit of thrombin in the blood.
6. We further add to this Rube Goldberg device by learning that prothrombin cannot be turned into thrombin at all when it is first manufactured in a cell. It must first be modified by having ten specific amino acid residues, called glutamate residues, turned into gamma-carboxyglutamate residues. This allows the prothrombin to bind to the surfaces of cells. Only in this form can prothrombin be turned into thrombin by Stuart factor and acclerin.
7. Converting these amino acid residues requires vitamin K and an enzyme.
8. There are two pathways for activating Stuart factor, the intrinsic and the extrinsic. Behe outlines both, but I'll just do the intrinsic, for simplicity's sake.
9. When an animal is cut, a protein called Hageman factor sticks to cells near the wound.
10. Bound Hageman factor is immediately cleaved by a protein called HMK to yield activated Hageman factor.
11. Immediately the activated Hageman factor converts another protein, called prekallikrein, to its active form, kallikrein. Kallikrein helps HMK speed up the conversion of Hageman factor to its active form.
12. Activated Hageman factor and HMK then together transform another protein, called PTA, to its active form. Activated PTA together with the activated form of another protein called convertin switch a protein called Christmas factor to its active form. Finally, activated Christmas factor, together with antihemphilic factor, change Stuart factor to its active form.
(That's the end of the divergence. Back to common paths now.)
13. Once begun, clotting must be controlled, or the animal will turn into one big blood clot. A protein called antithrombin binds to the actie (but not the inactive) form of most clotting proteins and deactivates them.
14. Antithrombin itself is relatively inactive unless it binds to a substance called heparin. Heparin occurs inside cells and undamaged blood vessels.
15. Another protein, protein C, destroys acclerin and activated antihemophiliac factor.
16. Thrombomodulin lines the surfaces of the cells on the inside of blood vessels. It binds thrombin, slowing down its cutting of fibrogen, and also aiding it in activating protein C.
17. After the clot forms, a protein called FSF ties the fibrin together with chemical cross-links between the molecules. This strengthens the clot so that it's not easily dislodged.
18. Finally, a protein called plasmin comes along to snip the fibrin bonds and remove the clot -- after some times has passed for the wound to heal.
You and Darwin chew on that one for a while.
If you call tell me how THAT system evolved, you might convert me. (Not assure me that it did, but explain to me HOW it could have. Note that while there may be simpler clotting systems, they cannot be physical precursors to this one, because all 18 steps outlined above MUST be in place for this one to work at all.
Behe makes a distinction between a CONCEPTUAL precursor and a PHYSICAL precursor. A bicycle is a conceptual precursor to a motorcycle, but the only physical precursor to a motorcycle is a simpler motorcycle. And if you argue that a motorcycle can be as simple as a bicycle with a motor attached, you've introduced the irreducibly complex motor in one leap.)
If you can come up with a credible evolutionary pathway for this system, BTW, you might be eligible for a Nobel. No one else has been able to. Behe examines one argument, put forth by Russell Doolittle of the U. of California, San Diego. I won't reproduce it in detail -- it's in Behe's book -- but in summary, he simply postulates that the necessary proteins and enzymes just kind of accidentally showed up, and then one day, voila, they began interacting as described. (Presumably all creatures were hemophilacs until that moment, and most remained so for some time after.)
I will quote Behe, though:
The first thing to notice is that no causitive factors are cited. Thus tissue factor "appears," fibrinogen "is born," antiplasmin "arises," TPA "springs forth," a cross-linking protein "is unleashed," and so forth. What exactly, we might ask, is causing all of this springing and unleashing? Doolittle appears to have in mind a step-by-step Darwinian scenario involving the undirected, random duplication and recombination of gene pieces. But consider the enormous amount of luck needed to get the right genes in the right places. ... Making a new blood coagulation protein by gene-shuffling is like picking a dozen sentences randomly from an encyclopedia in the hope of making a coherent paragraph. ...
To illustrate the problem, let's do our own quick calculation. Consider that animals have roughly 10,000 genes, each of which is divided into an average of three pieces. This gives a total of about 30,000 gene pieces. TPA has four different types of domains. By "variously shuffling" [Doolittle's phrase], the odds of getting those four domains together is 30,000 to the fourth power, which is approximately one-tenth to the eighteenth power. Now, if the Irish Sweepstakes had odds of winning of one-tenth to the eighteenth power, and if a million people played the lottery each year, it would take an average of about a thousand billion years before *anyone* (not just a particular person) won the lottery. A thousand billion years is roughly a hundred times the current estimate of the age of the universe. Doolittle's casual language ("spring forth," etc.) conceals enormous difficulties.
[Footnote: This calculation is exceedingly generous. It only assumes that the four types of domains would have to be in the correct linear order in order to work; however, the combination would have to be located in an active area of the genome, the correct signals for splicing together the parts would have to be in place, the amino acid sequences of the four domains would have to be compatible with each other, and other considerations would affect the outcome. These further considerations only make the event much more improbable.]
The second question to consider is the implicit assumption that a protein made from a duplicated gene would immediately have the new, necessary properties. ... A gene for a protein might be duplicated by a random mutation, but does not just "happen" to also have sophisticated new properties. Since a duplicated gene is simply a copy of the old gene, an explanation for the appearance of tissue factor must include the putative route it took to acquire a new function. This problem is discreetly avoided. Doolittle's scheme runs into the same problem in the production of prothrombin, a thrombin receptor, antithrombin, plasminogen, antiplasmin, proaccelerin, Stuart factor, proconertin, Christmas factor, antihemophilic factor and protein C -- virtually every protein of the system!
Yet the objections raised so far are not the most serious. The most serious, and perhaps the most obvious, concerns irreducible complexity. Natural selection ... only works if there is something to select -- something that is useful right now, not in the future.
Even if we accept his scenario for purposes of discussion, by Doolittle's own account no blood clotting appears until at least the third step. The formation of tissue factor at the first step is unexplained, since it would then be sitting around with nothing to do. In the next step (prothrombin popping up already endowed with the ability to bind to tissue factor, which somehow activates it) the poor proto-prothrombin would also be twiddling its thumbs until, at last, a hypothetical thrombin receptor appears at the third step and fibrinogen falls from heaven at step four. Plasminogen appears in one step, but its activator (TPA) doesn't appear until two steps later. Stuart factor is introduced in one step, but whiles away its time doing nothing until its activator (proconvertin) appears in the next step and somehow tissue factor decides that this is the complex it wants to bind. ...
Simple words like "the activator doesn't appear until two steps later" may not seem impressive until you ponder the implications. Since two proteins -- the proenzyme and its activator -- are both required for one step in the pathway, then the odds of getting both the proteins together are roughly the square of the odds of getting one protein. We calculated the odds of getting TPA alone to be aboout one-tenth to the eighteenth power; the odds of getting TPA and its activator together would be about one-tenth to the thirty-sixth power. That is a horrendously large number. Such an event would not be expected to happen if the universe's ten-billion year life were compressed into a single second and relived every second for ten billion years.
But the situation is actually much worse: if a protein appeared in one step with nothing to do, then mutation and natural selection would tend to eliminate it. Since it is doing nothing critical, its loss would not be detrimental, and the production of the gene and protein would cost energy that other animals aren't spending. So producing the useless protein would, at least to some marginal degree, be detrimental.
==END BEHE QUOTE==
Can you refute that without appealing to blind faith in evolution?
Without mumbling "Well, it musta happened, however improbable."
The evidence of God is staring you in the face, Marty. This level of complexity is found constantly, from the balance of physical constants in the universe to the cascade of events that make your blood clot.
Natural forces without intelligent design simply cannot explain it.
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