Evidence For Christianity

All over the internet we run into Darwinists who believe that "science" is on the side of the evolutionists.

Now those of us who are truly informed know that is completely wrong, but our efforts to educate those who don't know the truth must never stop.

Below is an excellent article that we found on the irreducible complexity of blood clotting. It is a very, very long article, but we would encourage you to read it all because it makes amazing points about irreducible complexity:

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http://www.doesgodexist.org/NovDec98/IrreducibleComplexityBloodClotting.html

Irreducible Complexity? Blood Clotting!
by Robert Harsh

Editors note: We have had many questions about the concept of irreducible complexity and what it means. The following article is quite technical, but will give a good example of the concept. Robert Harsh is a biology teacher in the Pittsburgh area.

Question: Does your blood clot when you get a cut? Where did the first animal that could make its blood clot get that ability? The crystal clear answer is; it had to have the right DNA. Processes like blood clotting only happen because DNA had the right code.

Darwinian evolution demands that the right mutations happened undirected and by pure chance and one at a time. David Noonan wrote about the blood clotting process, "It is a host defense system that evolved over millions of years. As the earliest living organisms evolved from single cells to more complex forms, they developed circulatory systems to supply oxygen and other vital nutrients to their multicelled bodies. Without a clotting response to protect against injury, these circulatory systems would not have been able to prevent fatal leaks: evolution as we know it would have been impossible; and only the simplest forms of life, such as algae and bacteria, would exist" (D. Noonan, "The Perils of Hemophilia", in Blood-Bearer of Life and Death, 1993).

Creationists appeal to the argument of "design demands a designer". God designed animals with the ability to form effective blood clots. How does blood clot? When you get a cut your body tries to stop the loss of blood in three ways. First, the blood vessels around the cut contract, thus decreasing the flow of blood. At the same time platelets adhere to collagen fibers of the damaged blood vessel's wall. This produces a temporary plug of platelets. Third, damaged cells and platelets activate a series of chemical reactions that are known as the clotting cascade. The final goal of clotting is to produce intertwining threads of fibrin. These threads strain the leaking blood until enough platelets and red and white blood cells accumulate and plug the leaking wound.

Clotting enzymes are proteins called factors. In order to do anything, each enzyme must be turned on or activated. Enzymes are activated by another chemical removing the specific site on the enzyme.

A mouse trap that is set in comparison to one that is not set is a good analogy of non-activated enzymes. A set mouse trap looks an awful lot like one that is not set; but, on the other hand, it can do things the other can not. The same is true of activated enzymes. They can do things that non-activated enzymes can not.

Let us examine next, in some detail, the clotting cascade. I do not personally believe it is important for most of us to know all of these sets. I need to give all of the details so that I can make the case for irreducible complexity. Failure of a single link in this chain of enzymes can cause the whole blood clotting process to fail. I ask you to try your best to follow the flow of the cascade. You may need to read the following section several times until you gain the ability to appreciate its beauty.

The Blood Clotting Cascade

1. A cut occurs and Hageman Factor sticks to the surface of cells near the wound. Bound Hageman Factor reacts with another enzyme called HMK to produce Activated Hageman.

2. Pre Kallikrein reacts with Activated Hageman to produce Kallikrein.

3. Hageman Factor also reacts with HMK and Kallikrein to form Activated Hageman.

4. PTA reacts with Activated Hageman and HMK to produce Activated PTA.

5. Christmas Factor reacts with Activated PTA and Convertin to produce Activated Christmas Factor.

6. Antihemophilic Factor is activated by Thrombin to produce Activated Antihemophilic Factor.

7. Stuart Factor reacts with Activated Christmas Factor and Activated Antihemophilic Factor to produce Activated Stuart Factor.

8. Proconvertin is activated by Activated Hageman Factor to produce Convertin.

9. When a cut occurs, Tissue Factor (which is only found outside of cells) is brought in near the wound where it reacts with Convertin and Stuart Factor to produce Activated Stuart Factor. (Note that step 9 involves an extrinsic process whereas step 7 is an intrinsic process.)

10. Proaccelerin is activated by Thrombin to produce Accelerin.

11a. GLU-Prothrombin reacts with Prothrombin Enzyme and Vitamin K to produce GLA-Prothrombin. (Note that Prothrombin cannot be activated in the GLU form so it must be formed into the GLA form. In this process ten amino acids must be changed from glutamate to gama carboxy glutamate.)

11b. GLS-Prothrombin is then able to bind to Calcium. This allows GLA-Prothrombin to stick to surfaces of cells. Only intact modified Calcium-Prothrombin Complex can bind to the cell membrane and be cleaved by Activated Stuart and Accerlerin to produce Thrombin.

12. Prothrombin-Ca (bound to cell surface) is activated by Activated Stuart to produce Thrombin.

13.Prothrombin also reacts with Activated Stuart and Accelerin to produce Thrombin. (Step 13 is much faster than step 12.)

14. Fibrinogin is activated by Thrombin to produce Fibrin. Threads of Fibrin are the final clot. However, it would be more effective if the Fibrin threads could form more cross links with each other.

15. FSF (Fibrin Stabilizing Factor) is activated by Thrombin to form Activated FSF.

16. When Fibrin reacts with Activated FSF many more cross ties are made with other Fibrin filaments to form a more effective clot.

Well now, I am wondering to myself whether you are experiencing frustration or intrigue, weariness, or exctiment. There are a lot of details but let me ask you a leading question. Is this intricate system something that man developed or is it something that man has discovered? Blood clotting is not an invention of man. It is the invention of either God or "Mother Nature" (i.e., it invented itself). Regardless of how you believe the clotting cascade came to be, the fact remains that blood clotting is a clear example of irreducible complexity.

Let us next consider that this irreducibly complex system of blood clotting must have a way to remove the clot once the wound has healed. How is this done?

17a. A blood protein, Plasminogin is activated by + - Pa to produce Plasmin. This acts like tiny chemical scissors which cuts up the Fibrin filaments of the clot.

17b. The rate at which the clot is broken up is controlled by yet another blood protein named Alpha 2 Antiplasm, which in turn inactivates Plasmin. One of the most important parts of this whole blood clotting machine is the ability it has to keep the clotting localized to the area of the wound and to stop the clotting cascade. What is the biggest killer of human beings? That's right, blood clots. Most heart attacks and strokes are caused by blood clots lodging. I believe the way your body shuts down the clotting cascade is a fascinating as the clotting process itself.

18. Antithrombin inactivates Activated Christmas, Activated Stuart and Thrombin.

19. Protein C is activated by Thrombin to produce Activated Protein C.

20. Activated Protein C inactivates Accelerin and Activated Antihemophilic.

21. Finally, Thrombomodulin which lines the inside of your blood vessels prevents Thrombin from activating Fibrinogin. A logical question is : How do we know that we have to be able to produce the whole set of enzymes or factors in the clotting cascade in order to successfully accomplish the procedure?

Probably the best answer is illustrated by the disease hemophilia. Hemophilia A is the form of the disease that 85% of hemophiliacs have and it is caused by a deficiency of Stuart Factor. The 14% that have hemophilia B are deficient in Accelerin. People who have severe hemophilia A are able to produce 2-5% of normal levels while another 15% are mild and are only able to make 5-30% of normal levels of Stuart Factor output.

Like all enzymes, Stuart Factor is produced by protein synthesis. As you know, amino acids are joined together one at a time by this orderly process. The gene for Stuart Factor contains 186,000 base pairs and occupies 0.1% of the X chromosome. Note that this does not translate into Stuart Factor having 62,000 amino acids because only the "exon" portions of the DNA molecule are expressed. The largest portion of the DNA in this gene is found in the "intron" base pair sequences. The gene for Accelerin contains 31,000 base pairs.

Why can a hemophiliac not stop bleeding? They cannot stop because they either do not produce enough Stuart Factor or they produce defective Stuart Factor. And why do they not produce the right amount to type of Stuart Factor? The answer is, because their body does not know how. Their parent passed on defective information on their X chromosome, and incidentally, they will pass on the same defective information on to their offspring.

No one knows how this defective genetic condition got started but it probably got started by a mutation or a change in the DNA. Possibly a deletion, addition, or substitution at the exact site where Stuart Factor protein must be cleaved to become activated. In this case sufferers produce the normal amount of Stuart Factor in their blood but it cannot be activated.

What is our reasonable conclusion? It seems like it is very important to have the proper amount and type of Stuart Factor and I see no reason why we could logically conclude that proper blood clotting would be performed without each step in the clotting cascade.

The rat poison called Warfain works by substituting itself for Vitamin K. You will recall (step 11a above) that in order to be activated, Prothrombin must be changed from the GLU form to the GLA form. Without Vitamin K, Prothrombin cannot be activated into Thrombin. Without Thrombin, Fibrinogin cannot be transformed in Fibrin and the animal will bleed to death. This again illustrates the fact that none of the steps in the clotting cascade can be eliminated and still have a functional system.

But how did this intricate system get its start? Did one step get a foothold and then step by step the whole system evolved by pure, undirected, chance mutations in which these complicated enzymes were captured for posterity by the influence of natural selection? Or is this process so irreducibly complex that it had to come as a package deal created by God?

What is the state of the art explanation offered by evolutionists for the development of blood clotting? Russell Doolittle is a professor of biochemistry at the Center for Molecular Genetics at the University of California at San Diego. He is one of the most prominent people who is interested in discovering how blood clotting evolved. Professor Doolittle wrote an article in Thrombosis and Homeostasis in which he attempted to answer the question, "How in the world did this complex and delicately balanced process evolve?"

In his article, meant for other professionals, Dr. Doolittle used the following phrases in his explanation: "Tissue Factor appeared...", "Prothrombin appears...", "Fibrinogin is born...", "Antithrombin appears...", "Plasminogin is generated...", "Antiplasmin arises...", "TPA springs forth...". "Proconvertin is duplicated from Stuart Factor." If you duplicate this sentence do you get anything different?

"Protein C is genetically derived from Prothrombin." Unless Dr. Doolittle has Lamarkian evolution in mind, proteins like Prothrombin cannot influence the animal's DNA to produce a different enzyme known as Protein C. "Prothrombin engages in an exchange (of gene pieces)." Prothrombin is a protein and as such it cannot influence any specific "gene exchange."

Michael Behe, author of Darwin's Black Box, has the following observations about Dr. Doolittle's explanation of clotting evolution: "At no step--not even one--does Dr. Doolittle give a model that includes numbers or quantities; without numbers there is no science. When a merely verbal picture is painted of the development of such a complex system there is absolutely no way to know if it would actually work. When such crucial questions are ignored we leave science and enter the world of Calvin and Hobbes" (Behe, p. 95). Dr. Behe's major objection to the "state of the art" evolutionary models is his concern for irreducible complexity. Darwinian evolution is theorized to be directed by "natural selection." Natural selection only selects from the structures and biochemistry that are present and cannot work on some kind of future structure.

The engine of Darwinian evolution 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, however, 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 with nothing to do. In the next step (prothrombin popping up already endowed with the ability to bind tissue factor, which somehow activates it) the poor proto-prothrombin would also be twiddling its thumbs with nothing to do until, at last, a hypothetical thrombin receptor appears at the third step and fibrinogin falls from heaven at step four. Plasminogin appears in one step, but its activator (TPA) does not appear until two steps later. Stuart factor is introduced in one step and somehow tissue factor decided that this is the complex it wants to bind. Virtually every step of the suggested pathway faces similar problems" (Behe, p. 95). In order to have a controlled clotting mechanism you have to have two proteins for each step. Both the pro enzyme (non-activated) and its activator are required. Dr. Behe calculated that the odds of getting factor TPA and its activator to be 1/10 to the thirty-sixth power! To compound the problem, if "...a protein appeared in one step with nothing to do, then mutation and natural selection would tend to eliminate it." To prevent this from happening, evolutionists are forced to imagine large clusters of proteins evolving all at once. This reminds one of Goldschmitt's hope monster in which a reptile laid an egg and a bird hatched out.

Is it not much more satisfying to simply believe that God created the whole mechanism fully functional and ready to go? It does not go against reason to believe that intricate design, especially when irreducible complexity is involved, demands an intelligent Designer. On the other hand, it does go against reason to "believe" that natural, pure chance changes in DNA (mutations) are capable of producing a process that is so irreducibly complex such as "simple" blood clotting.

The first mousetrap was not invented by assembling many parts, each part capable of, at least, almost catching mice. No, a person (an intelligent designer) conceived the notion of the entire mouse trap in his mind. The first mousetrap that could indeed catch mice was a full blown trap with at least eight distinct parts. If a Darwinian type of evolution (punctuated equilibrium included), invented blood clotting, physical precursors to each step were required. Each step had to actually work in order for natural selection to have any positive effects. If any organism is to thrive, all of its parts must at least be minimally functional.

An animal that is missing even one of the sixteen steps to a functional clot will not survive. If it does not survive it cannot contribute its genes to the gene pool to be selected from, no matter how much they are needed.