The evolution of clots, Daily Telegraph, April 4, 2006 ... Intelligent Design is the logic of ignorance - complex life, such as the machinery of blood clotting, can be explained by Darwinism, says Steve Jones
[Graphic: "Disorders of coagulation and haemostasis," Surgical-tutor.org.uk]
[Continued from part #3. Again, remember what my namesake, genetics professor Steve Jones, claimed: that "the machinery of blood clotting, can be explained by Darwinism", that is the natural selection of random (i.e. undirected) micromutations (NSRM).]
Plenty of animals manage with just a few parts of the machinery. [Note that Jones does not give details of: 1) which "animals" and 2) what "parts of the machinery" they don't have. Later in the article (which I will deal with in part #6, i.e. after the next part #5) he mentions "turtles" and "flies" but that is fallacious, as we shall see.
In fact we will start to see right now! Wikipedia says that "Coagulation" (blood clotting) "is extremely similar in all mammals" and the nearest "nonmammalian animal that uses serine proteases for blood coagulation is the Horseshoe Crab" (my emphasis):
"Coagulation The coagulation of blood is a complex process during which blood forms solid clots. It is an important part of haemostasis, whereby a damaged blood vessel wall is covered by a fibrin clot to stop hemorrhage and aid repair of the damaged vessel. Disorders in coagulation can lead to increased hemorrhage and/or thrombosis and embolism. Coagulation is extremely similar in all mammals, with all mammals using a combined cellular and serine protease mechanism. The system in humans is the most extensively researched and therefore the best known. This article focuses on human blood coagulation. All mammals have an extremely closely related blood coagulation process, using a combined cellular and serine protease process. In fact, it is possible for any mammalian coagulation factor to "cleave" its equivalent target in any other mammal. The only nonmammalian animal that uses serine proteases for blood coagulation is the Horseshoe Crab."
Also, here is what my two Animal Physiology textbooks say about blood-clotting, which confirm Behe's description of its description as a "cascade", where the output of one step is the input of the next step:
"Coagulation of the blood involves a cascade of events in which many factors normally found in the blood are activated in sequence, leading eventually to the formation of thrombin and activated factor XIII. Thrombin converts fibrinogen to fibrin, which then polymerizes into an insoluble fibrin clot. Sticky platelets have exposed fibrin receptors to which fibrin adheres, and the resulting fibrin-platelet mesh traps red blood cells and plasma. The sticky platelets contract, pull on the fibrin, and squeeze out serum (plasma minus fibrinogen), and the clot shrinks. The platelets also release phospholipid PF3, which is involved in activating one of the factors in the clotting cascade. There are two different pathways that may lead to this reaction. Tissue damage, which results in the release of thromboplastin, activates the so-called extrinsic cascade. The exposure of collagen, or exposure to glass or other surfaces, activates the intrinsic pathway. The extrinsic and intrinsic pathways converge on the activation of factor X, which along with a number of other cofactors catalyzes the cleavage of prothrombin to thrombin. Calcium is required for the activation of many factors in both the extrinsic and intrinsic pathways. Removal of Ca2+ prevents clotting. An inappropriate clot that forms in the circulation, called a thrombus, can block blood flow. Animals produce a number of anticoagulants to prevent clotting and remove blood clots once they form. The anticoagulant heparin is found on the surfaces of endothelial cells, especially in the lungs, and inhibits platelet adhesion. Cell surfaces also have a protein, thrombomodulin, that binds thrombin. The complex thus formed activates protein C, which inhibits clotting by degrading factor V and catalyzing the production of plasmin from plasminogen. Plasmin dissolves fibrin and, therefore, blood clots. Thus thrombin has two major actions: first to initiate clot formation and then to promote clot dissolution." (Randall D.J., Burggren W.W. & French K., "Eckert Animal Physiology: Mechanisms and Adaptations," , W. H. Freeman and Company: New York NY, 2001, Fifth edition, 2002, Second printing, pp. 522. Emphasis original)
and the system is a delicate balancing act between not enough, and too much, clotting:
"The clotting or coagulation mechanism has been well studied in mammals, particularly humans, because blood clotting is of great medical importance. To be effective, a clotting mechanism must act rapidly; yet blood must not clot within the vascular system. Blood must therefore have the inherent ability to clot, and the clotting mechanism should be ready to be turned on when needed. On the other hand, this mechanism must not go off inadvertently. In vertebrates the blood clot consists of the protein fibrin, an insoluble fibrous protein formed from fibrinogen, a soluble protein present in normal plasma in an amount of about 0.3%. The transformation of fibrinogen to fibrin is catalyzed by the enzyme thrombin, and the reason blood does not clot in the vascular system is that thrombin is absent from the circulating blood. Thrombin, however, can be formed rapidly because its precursor, prothrombin, is already present in the plasma. What is necessary to initiate coagulation is the formation of thrombin from prothrombin. This is only the final step in a complex sequence of biochemical events that has been slowly unraveled in studies of human patients with various deficiencies in the clotting mechanism (e.g., hemophilia). A total of 12 clotting factors have been identified, numbered I through XIII (factor VI is a term no longer used)." (Schmidt-Nielsen K., "Animal Physiology: Adaptation and Environment," , Cambridge University Press: Cambridge UK, Fifth edition, 1997, reprint, 1998, p.121. Emphasis original)]
I will quote more from this last book in part #6.
Working through these above two quotes, brought to mind Behe's quote below, that the blood clotting cascade is like a Rube Goldberg machine, and paradoxically (Paley makes this point too - see `tagline' quote to this post) it is precisely Rube Goldberg machines, with their contrivances that are the best evidence of design!]
To be continued in part #5, which is this post split into two because of its length. It will be mainly quotes from my biology and molecular biology textbooks, to give a feel for the extreme complexity of the blood clotting cascade and therefore the difficulty facing a `blind watchmaker' in constructing it, step-by-tiny-step, by the natural selection of random (i.e. undirected) micromutations! ]
"Rube Goldberg systems always get a good laugh; the audience enjoys watching the contraption work and appreciates the humor in applying great gobs of ingenuity to a silly purpose. But sometimes a complicated system is used for a serious purpose. In this case the humor fades, but admiration for the delicate interactions of the component remains. Modern biochemists have discovered a number of Rube Goldberg-like systems as they probe the workings of life on the molecular scale. In the biochemical systems the string, stick, ball, seesaw, rock, sandpaper, match, fuse, cannon, cannonball, funnel, saw, rope, and telephone pole of the cartoon are replaced by proteins with eyeglazing names such as `plasma thromboplastin antecedent' or `high-molecular-weight kininogen.' The inner balance and crisp functioning, however, are the same. ... Like some ultimate Rube Goldberg machine, the clotting cascade is a breathtaking balancing act in which a menagerie of biochemicals sporting various decorations and rearrangements conferred by modifying enzymes-bounce off one another at precise angles in a meticulously ordered sequence until, at the denouement, Foghorn Leghorn pushes off the telephone pole and gets up from the ground, the bleeding from his wounds stopped. The audience rises to its feet in sustained applause." (Behe M.J., "Darwin's Black Box: The Biochemical Challenge to Evolution," Free Press: New York NY, 1996, pp.77,97)