Blood Clotting and Irreducible Complexity

irreducable-complexity

√ Image Source: http://www.sciohio.org/PosPaper1_2.htm

1.  This is a good time for us to take a foray into a discussion of “Irreducible Complexity”

  • Michael Behe really championed this concept with his book, Darwin’s Black Box: The Biochemical Challenge to Evolution

√ Source: http://www.talkorigins.org/faqs/behe.html

  • Classic and simple example of this is the mouse trap – 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

√ Source: http://www.sciohio.org/PosPaper1_2.htm

2.  There are tons of examples of biological components that are irreducibly complex. In other words, unless you have all of the parts of the biological component or all of the steps in place for the biological process – the system or process would be entirely useless

  • Blood-clotting in mammals is a good example of a process that is irreducibly complex
  • Clotting involves a complex cascade of reactions involving platelets, enzymes, and structural proteins

√ Source: http://www.biologyreference.com/Bl-Ce/Blood-Clotting.html#b

3.  Blood clotting pathways consist of many factors, and all the factors are necessary for the pathway to function properly. Thus, evolution (which works via the mechanism of small, gradual steps that keep only that which is immediately functional) could not have formed these pathways.

4.  For example, if only three of the blood-clotting enzymes/factors (there are many factors in the complete pathway) were formed in an organism, blood would not clot, and thus the factors would not be kept because they are not currently useful to the organism

  • Evolutionary processes do not allow the organism to keep the three factors in the hopes that one day the rest of the blood-clotting factors will form
  • Evolution is goalless and purposeless; therefore, it does not keep the leftovers

5.  What exactly happens when we cut ourselves? (All of these enzymes, vitamins and processes have to occur in just the right order for blood to clot and each of these factors must be present in the blood at the same time)

  • The right enzymes must be engineered in such a way as to stick to the surface of the cells near the cut
  • The body then has to know when to stop the clotting process
  • It then needs a way of removing the clot once the wound has healed.

√ Source: See Michael Behe’s Darwin’s Black Box: The Biochemical Challenge to Evolution (see chapter entitled “Rube Goldberg in the Blood”)

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.

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.