Saturday, April 22, 2006

The evolution of clots #5

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 ... Continued from part #4.

[Graphic: "Thrombus Formation I - Platelet Activation," Internet Stroke Center.]

Again, keep in mind what genetics professor Steve Jones (my namesake) claimed, that "the machinery of blood clotting, can be explained by Darwinism," that is the natural selection of random micromutations (NSRM).

To give a feel for the complexity of the blood clotting cascade, and therefore the difficulty facing a `blind watchmaker' in constructing it, step-by-tiny-step, here are quotes from my biology and molecular textbooks:

"Blood Clotting Blood must be a free-flowing liquid if it is to circulate easily through blood vessels, but this liquidity can also cause serious problems. Any injury that breaks a large blood vessel can quickly lead to a serious loss of blood. This is countered by a complex clotting (coagulation) mechanism. Clots form temporary barriers to blood loss until a vessel's walls have healed. When a blood vessel is injured, blood platelets begin to congregate near the cut or injury, forming a barrier known as the platelet plug. There are 200 to 400 platelets per mm3 of blood. Platelets are fragments of large bone marrow cells, called megakaryocytes, that disintegrate and discharge them into the bloodstream. When platelets come into contact with an injured vascular wall, they swell up, become sticky, and release certain, chemicals. Some of these chemicals stimulate the blood vessel to constrict; some increase the tendency of platelets to form a plug; and some help initiate the process of blood clotting. Blood clotting requires a complex and precise series of reactions that satisfy the requirement for a delicate balance between quick and efficient clot formation as a response to significant blood vessel damage and prevention of accidental formation of clots that interfere with normal circulation. Since blood clotting is so complex, we will consider only the major events involved ... Prothrombin and fibrinogen are two proteins manufactured by the liver that are always present in the plasma. Injured tissues and platelets release prothrombin activator and this along with calcium ions (Ca++) convert prothrombin into the enzyme thrombin. Thrombin in turn, acts as an enzyme that severs two short amino acid chains from each fibrinogen molecule. These activated fragments then join end to end, forming long threads of fibrin. Fibrin threads wind around the platelet plug in the damaged area of the blood vessel and provide the framework for the clot." (Mader S.S., "Biology," [1985], Wm. C. Brown Co: Dubuque IA, Third Edition, 1990, pp.524-525. Emphasis original)

I like the `Rube Goldberg' touch above, that "Platelets are fragments of large bone marrow cells, called megakaryocytes, that disintegrate and discharge them into the bloodstream"! See also below that "Platelets are formed from bits of cytoplasm that are pinched off from very large cells (megakaryocytes) in the bone marrow. Thus, a platelet is not a whole cell but a fragment of cytoplasm enclosed by a membrane."

"Platelets Function in Blood Clotting In most vertebrates other than mammals, the blood contains small, oval cells called thrombocytes, which have nuclei. In mammals thrombocytes are tiny spherical or disc-shaped bits of cytoplasm that lack a nucleus. They are usually referred to as blood platelets. About 300,000 platelets per microliter are present in human blood. Platelets are formed from bits of cytoplasm that are pinched off from very large cells (megakaryocytes) in the bone marrow. Thus, a platelet is not a whole cell but a fragment of cytoplasm enclosed by a membrane. Platelets play an important role in hemostasis (the control of bleeding). When a blood vessel is cut, it constricts, reducing loss of blood. Platelets stick to the rough, cut edges of the vessel, physically patching the break in the wall. As platelets begin to gather, they release ADP, which attracts other platelets. Within about 5 minutes after injury a complete platelet patch, or temporary clot, has formed. At the same time that the temporary clot forms, a stronger, more permanent clot begins to develop. More than 30 different chemical substances interact in this very complex process. The series of reactions that leads to clotting is triggered when one of the clotting factors in the blood is activated by contact with the injured tissue. ... Prothrombin, a plasma protein manufactured in the liver, requires vitamin K for its production. In the presence of clotting factors, calcium ions, and compounds released from platelets, prothrombin is converted to thrombin. Then thrombin catalyzes the conversion of the soluble plasma protein fibrinogen to an insoluble protein, fibrin. Once formed, fibrin polymerizes, producing long threads that stick to the damaged surface of the blood vessel and form the webbing of the clot. These threads trap blood cells and platelets, which help to strengthen the clot." (Solomon E.P., Berg L.R., Martin D.W. & Villee C.A., "Biology," [1985], Harcourt Brace: Orlando FL, Third Edition, 1993, pp.885-886. Emphasis original).

Note: More than 30 different chemical substances interact in this very complex process (my emphasis)!

"HOW DOES BLOOD CLOT? The hypotheses suggested by the various experiments outlined here have been corroborated: both damaged tissues and disintegrating platelets release a complex substance, called thromboplastin, that initiates blood clotting. For reasons not well understood, however, thromboplastin is not effective unless calcium ions are present. ... Two substances essential for normal blood clotting, then, are thromboplastin and calcium ions; a third is the plasma protein fibrinogen. But if we mix these three substances in a dish, no clotting occurs. Clearly, something else must be involved. That something else seems to be one of the globulin proteins of the plasma, known as prothrombin. If prothrombin is added to the mixture of fibrinogen, thromboplastin, and calcium ions, a clot will form. It can be demonstrated, however, that prothrombin itself has no effect on clotting; it must first be converted into thrombin, the substance that converts fibrinogen into its crystalized form, fibrin, of which the clot is made. Now we have identified the main ingredients in the clotting process. Thromboplastin, produced by disintegrating platelets or damaged tissue, converts the plasma protein prothrombin into thrombin; this is the reaction in which the calcium ions participate. The thrombin then converts another plasma protein, fibrinogen, into fibrin. The fibrin fibers form a meshwork, which begins to shrink; finally, the fluid blood serum is squeezed out, and a hardened clot is left in place. ... Actually, numerous other substances-accelerators, inhibitors, and the like-also play roles in the clotting process. A reaction series of this sort in which the first step releases another, which then triggers yet another, and so on, is referred to as a cascade reaction." (Keeton W.T., Gould J.L. & Gould C.G., "Biological Science," [1967], W.W. Norton & Co: New York NY, Fourth Edition, 1986, p.343. Emphasis original)

This is also a neat touch, that prothrombin is inactive but ready to be converted to its active form, thrombin, which then converts the inactive fibrogen into the active fibrin! Isn't the `blind watchmaker' so clever and so far-sighted! ;-)

"Blood clotting When blood is exposed to air, even in a test tube, it forms a clot, thrombus, within a few minutes. The yellowish fluid outside the clot is serum, which is plasma minus some of the protein constituents that help form the clot. The reactions leading to clot formation are extremely complex. They involve a cascade of perhaps 12 sequential enzymatic reactions, with 'failsafe thresholds' at each stage to prevent accidental triggering of clot formation. Each reaction converts an inactive form of an enzyme into an active form, which is capable of catalysing the next reaction of the cascade and producing hundreds of active products. Thus, the number of products is multiplied at each step. The final reaction involves the enzyme thrombin, which converts soluble plasma protein, fibrinogen, into fine strands of insoluble fibrin. These fibres form a meshwork that traps erythrocytes and platelets to form a clot ... When a vessel is broken, the endothelial layer is breached, exposing collagen fibres in the deeper layers. Platelets immediately attach to the collagen and each other. Thrombin, which forms as outlined above, has three effects on platelets. It causes them to: * become sticky and attach to fibrinogen; * become fragile and release ADP, which enhances linking with fibrinogen; * form long pseudopod-like processes, which attach to adjacent platelets. Thrombin converts fibrinogen to fibrin, which further strengthens the clot. The gap in the vessel quickly fills with a mat of fibrin and aggregated platelets. Thrombin apparently stimulates platelets to contract, squeezing serum from the clot and drawing the broken edges of the vessel together. Platelets also release a substance that makes the surrounding blood vessels contract, further reducing the blood flow to the area. " (Knox B., Ladiges P. & Evans B., eds., "Biology," [1994], McGraw-Hill: Sydney, Australia, 1995, reprint, pp.466-467. Emphasis original).

Note: The reactions leading to clot formation are extremely complex. They involve a cascade of perhaps 12 sequential enzymatic reactions, with 'failsafe thresholds' at each stage to prevent accidental triggering of clot formation! Maybe it wasn't a `blind watchmaker' who designed this after all? ;-) Keep this in mind when in the next part we see Jones in the next part #6 dismissing this as, "the rickety apparatus that stops us from bleeding was assembled from random bits that just happened to be hanging around."

"How does blood clot? Step 1 A blood clot is initiated by the binding of a membrane receptor by a circulating protein factor. Step 2 The complex of protein receptor and protein factor then binds with factor 10, changing it to the active form, factor 10a. Step 3 Each molecule of 10a binds to another protein factor, and this complex catalyzes the conversion of prothrombin to thrombin. Step 4 Thrombin interacts with fibrinogen, promoting its conversion to fibrin. Finally fibrin traps blood cells that seal the wound. ... Platelets Help Blood to Clot. Certain large cells within the bone marrow, called megakaryocytes, regularly pinch off bits of their cytoplasm. These cell fragments, called platelets, contain no nuclei; they enter the bloodstream, where they play an important role in controlling blood clotting. A blood clot is a seal of a ruptured blood vessel. The ruptured vessel seals itself by generating a matrix of long fibers and trapped cells that fills the gap from components present in the plasma. In a clot the gluey substance is a protein called fibrin (derived from fibrinogen), which sticks platelets together to form a tight, strong seal. Recently scientists have discovered that the fibrin that forms blood clots is generated in a spreading cascade of molecular events ... The clotting process is initiated by injury to blood vessel cells attracting platelets, which releases a protein factor that starts the cascade. At each stage in the cascade that follows, proteins from cells and blood combine in fast-rising waves, involving many more molecules in the progressive steps of the process. Billions of molecules of fibrin can be formed from a single clot-initiating event." (Raven P.H. & Johnson G.B., "Biology," [1986], Wm. C. Brown: Dubuque IA, Third Edition, 1995, p.1064. Emphasis original)

Note: "At each stage in the cascade that follows, proteins from cells and blood combine in fast-rising waves, involving many more molecules in the progressive steps of the process. Also keep this amplification function of the cascade when in the next part #6 consider Jones' dismissal of this as "the rickety apparatus that stops us from bleeding ..."

"Blood Clotting We all get cuts and scrapes from time to time, yet we do not bleed to death because blood contains a self-sealing material that plugs leaks in our vessels. The sealant is always present in our blood in an inactive form called fibrinogen. A clot forms only when this plasma protein is converted to its active form, fibrin, which aggregates into threads that form the fabric at the clot. The clotting mechanism usually begins with the release of clotting factors from platelets and involves a complex chain of reactions that ultimately transforms fibrinogen to fibrin .... More than a dozen clotting factors, have been discovered, and the mechanism is still not fully understood. ... The clotting process begins when the endothelium of a vessel is damaged and connective tissue in the vessel wall is exposed to blood. Platelets adhere to collagen fibers in the connective tissue and release a substance that makes nearby platelets sticky. (2) The platelets form a plug that provides emergency protection against blood loss. (3) This seal is reinforced by a clot of fibrin when vessel damage is more severe. Fibrin is formed via a multistep process: Clotting factors released from the clumped platelets or damaged cells mix with clotting factors in the plasma, forming an activator that converts a plasma protein called prothrombin to its active form, thrombin. Calcium and vitamin K are among the plasma factors required for this step. Thrombin itself is an enzyme that catalyzes the final step of the clotting process, the conversion of fibrinogen to fibrin. Thus, in a cascade of reactions, injury activates prothrombin to thrombin, which then activates fibrinogen to fibrin. The threads of fibrin become interwoven into a patch." (Campbell N.A., Reece J.B. & Mitchell L.G., "Biology," [1987], Benjamin/Cummings: Menlo Park CA, Fifth Edition, 1999, pp.824-825. Emphasis original)

Note: "The clotting mechanism involves a complex chain of reactions .... More than a dozen clotting factors, have been discovered, and the mechanism is still not fully understood"!

Finally, here are two quotes from one of my molecular biology textbooks:

"An example of how prostaglandins function in paracrine signaling is seen in the activation of blood platelets. Platelets are essential components of the blood-clotting mechanism that plug sites where blood vessels are ruptured. Platelets are not true cells; they have no nucleus, and are produced by the fragmentation of certain bone marrow cells. Clotting is a complex cascade of enzymatic events that is triggered by injury and leads rapidly to the formation of a clot, a tangled mass of red blood cells, platelets, and fibers of a protein called fibrin. The clotting mechanism must be carefully regulated, because inappropriate blood clots lead quickly to life-threatening situations. The coronary arteries of the heart are only 1 millimeter or so in diameter, and most heart attacks result from a small blood clot that blocks coronary circulation. Similarly, clots in the venous system can produce phlebitis (inflammation of the veins) in the lower limbs and embolisms (obstructions) in the lungs. Thus, clot formation is essential, but it must be confined to the area where the damage occurs. Platelets have many different receptors that sense when a tissue is damaged. Most relevant to our discussion of paracrine regulation, platelets can be activated by members of the prostaglandin family such as thromboxane A2, as well as by extracellular adenosine diphosphate. These substances are released by activated platelets and then function as paracrine hormones to activate other platelets. ... Most of the known platelet activators act through G protein-linked receptors to activate phospholipase C, which triggers the release of calcium from a calcium-storing tubular network known as the dense tubular system; this results in the release of arachidonic acid. An enzymatic pathway starting with cyclooxygenase then converts the arachidonic acid to thromboxane A2. Thromboxane A2 diffuses out of the platelet and acts on G protein-linked thromboxane receptors of neighboring platelets. The thromboxane receptors in turn activate phospholipase C, triggering the activation of nearby platelets. As a result, platelets in the area are recruited to the site of injury." (Becker W.M., Kleinsmith L.J. & Hardin J., "The World of the Cell," [1986], Benjamin/Cummings: San Francisco CA, Fourth edition, 2000, p.294. Emphasis original)

See above and previous (here and here) about the `Rube Goldberg' touch! See also an excerpt from Behe's "Darwin's Black Box" section, "Rube Goldberg In The Blood."

"The Process of Platelet Activation. (a) Platelets are activated by several substances and aggregate upon activation, forming a blood clot. (1) Collagen exposed in a damaged blood vessel wall stimulates platelet activation and adherence. (2) Activated platelets release the platelet factors ADP and thromboxane A2 (TA2), which (3) stimulate the activation and aggregation of more platelets -the vicinity. The release of A2 and ADP is an example of paracrine signaling. (b) Paracrine signaling by platelets uses some of the same classes of receptors and signal transduction pathways described for the endocrine hormones. The receptors for thrombin, TA2, and collagen all appear to be G protein-linked receptors that activate phospholipase C. However, the activation of the thrombin receptor is unusual in that it depends on the protease thrombin removing a portion of the receptor protein. When newly exposed collagen in a damaged blood vessel wall binds to a G protein-linked collagen receptor, membrane phospholipase C is activated, causing the production of InsP3 and DAG, and ultimately the release of calcium from the dense tubular system. Increased calcium concentration inside the platelet stimulates the secretion of granules that contain growth factors and ADP. Phospholipase A is thought to be simultaneously activated by a G protein. The activation of phospholipase A2 releases arachidonic acid, which is converted to TA2. TA2 binds to the TA2 receptors on nearby platelets, causing elevated calcium levels, whereas ADP binds to what is probably a ligand-gated calcium channel. Both messengers stimulate platelets to aggregate." (Becker, Ibid., 2000, p.295)

There is also a nice graphic demonstration of blood clotting at McGraw-Hill's "Essential Study Partner" site.

To try to even imagine this being put together, step-by-tiny-step, by a `blind watchmaker', who is nothing but "the blind forces of physics," "Natural selection, the blind, unconscious, automatic process," which "has no purpose in mind. It has no mind and no mind's eye. It does not plan for the future. It has no vision, no foresight, no sight at all":

"All appearances to the contrary, the only watchmaker in nature is the blind forces of physics, albeit deployed in a very special way. A true watchmaker has foresight: he designs his cogs and springs, and plans their interconnections, with a future purpose in his mind's eye. Natural selection, the blind, unconscious, automatic process which Darwin discovered, and which we now know is the explanation for the existence and apparently purposeful form of all life, has no purpose in mind. It has no mind and no mind's eye. It does not plan for the future. It has no vision, no foresight, no sight at all. If it can be said to play the role of watchmaker in nature, it is the blind watchmaker."(Dawkins R., "The Blind Watchmaker: Why the Evidence of Evolution Reveals a Universe Without Design," W.W Norton & Co: New York NY, 1986, p.5)

It just occurred to me (although I have a vague idea I said before), that if the Darwinists really thought that "the machinery of blood clotting, can be explained by Darwinism" then why 1) : did they never mention it until Behe brought it up? and; 2) do they waste their time on comparatively trivial examples like peppered moths and finch beaks?

[Continued in part #6]

Stephen E. Jones, BSc (Biol).
"Problems of Evolution"

Friday, April 21, 2006

The evolution of clots #4

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," [1978], 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," [1975], 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! ]

Stephen E. Jones, BSc (Biol).
"Problems of Evolution"


"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)

Tuesday, April 18, 2006

Movement of chromosome in nucleus visualized

Movement of chromosome in nucleus visualized, EurekAlert, 17-Apr-2006, Jeanne Galatzer-Levy, University of Illinois at Chicago [Graphic: San Diego State University College of Sciences, "Actin Myosin Crossbridge 3D Animation." Note: This is not a model of the cell nucleus actin- myosin motor referred to in the article, but presumably the principle is the same.] The cell is understood to be highly organized, with specialized areas for different functions and molecular motors shuttling components around. Researchers from the University of Illinois' Chicago and Urbana-Champaign campuses now offer the first imaging evidence from live cells of ongoing organization and transport within the cell nucleus. ... But scientists have had no way to track chromosome movement inside the nucleus or to determine whether the location of the chromosomes was the result of random diffusion or if they are moved around by molecular motors. In a study published in the April 17 issue of Current Biology, UIC and UIUC researchers show that chromosomes in the cell nucleus are capable of directed, long-range movement that depends on actin and myosin, the major molecular motor complex in the cytoplasm. Chien-Hui Chuang studied a chromosome that is normally found in an inactive state near the nuclear periphery and moves to the interior of the nucleus when it receives an activating signal. "The movement following activation was radically different from the rapid, but short-range, diffuse movement previously observed in these nuclei," said Dr. Andrew Belmont .... It was clear that this was directed movement that required a motor, Belmont said, because the chromosome was moving in a nearly straight line perpendicular to the nuclear envelope. .... "It looked nothing like the random, but localized, bouncing around that had been previously observed," he said. Belmont's group collaborated with Primal de Lanerolle who had discovered a type of myosin in the nucleus. Most myosin molecules are found in the cytoplasm, where they interact with actin filaments to do physical work. Because these molecules can contract muscles or move things around, they are called molecular motors. .... When the researchers introduced a mutant form of myosin protein to the nucleus, the movement slowed. Introducing a mutant actin that does not form filaments stopped the movement, while the introduction of an actin mutant that enhances filament formation accelerated the movement. In addition, when a drug that inhibits actin/myosin interactions was added to the cells, the chromosome movement was stopped completely. These experiments conclusively established that actin and myosin are involved in this chromosome movement. "While we have known for a long time that actin is present in the nucleus and we had shown that myosin is also present in the nucleus, nobody really knew if they worked together," said de Lanerolle. "There has been tantalizing evidence of organization in the nucleus--active genes found in the central region associated with nucleus complexes of transcription machinery necessary for gene expression, while inactive genes are found at the periphery," Belmont said. "For the first time, we have been able to observe an active mechanism for directed long-range chromosome movements that depend directly or indirectly on actin and myosin." ... [Also at ScienceDaily. Yet another vital function of the cell under the control of molecular machines! How could (and why would) a `blind watchmaker' be so far-sighted? And so clever?]

Stephen E. Jones, BSc (Biol).
"Problems of Evolution"


"Hunt Morgan and other geneticists have shown that certain variations can be brought about by the action of heat and electricity, radium and X-rays, and that these variations are inherited-at least for some generations. And here it appeared that Nature had something tangible to select, and thus produce new species. No doubt in Nature lightning is common, and cosmic rays are apparently raining on the earth all the time, but there is no evidence whatever that such agencies have ever produced a new species. In fact, it seems that even if such mutations are selected by man, they only last for a few generations, and gradually the animals revert to the normal." (Broom R., "Finding the Missing Link," [1950], Greenwood Press: Westport CT, Second edition, 1951, Reprinted, 1975, pp.98-99)

The evolution of clots #3

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 [Continued from part #2]

Source: Berg, J.M., et al., "Biochemistry," W.H. Freeman, Fifth edition, 2002.

[I will hold my namesake to his claim that "the machinery of blood clotting, can be explained by Darwinism", that is the natural selection of random micromutations (NSRM). The great French zoologist Pierre Grasse, independently of Mike Behe, came to the conclusion that the machinery of blood clotting, cannot be explained by Darwinism:

"The genesis of control systems with no intervention by the organism is difficult to imagine and postulates Himalayas of chance occurrences that, moreover, could not have happened for lack of time and a sufficient number of generations. Take, for example, regulation of the coagulation of blood, a highly complex phenomenon to which biologists seem to have given little thought. Its normal cause is the opening of a vein, artery, or capillaries; the blood brought into contact with the lip of the wound (damaged tissues) becomes the site of chain reactions ending in the formation of a clot. This is only possible because there preexist in the blood reaction agents or their precursors whose end effect is to coagulate certain proteins of the blood plasma. The organism, ready for all eventualities, bears within itself in the latent state its own protective system. Genes control the elaboration of coagulants, proteins, and enzymes. Such a process forms a single whole; a lack of a substance arises, an enzyme is affected, and the system will not work. One does not see how it can have been formed by successive chance effects supplying a protein or an enzyme in any random order. Besides, we know that the effects of mutations on the system are disastrous and form the lengthiest chapter in blood pathology. The system has become functional only when all its components have come together and adjusted themselves to one another. The Darwinian hypothesis compels us to postulate a preparatory period during which selection acts upon something that does not, physiologically speaking, yet exist. Under the necessary conditions of the postulate, the action can only have been prophetic!" (Grasse P.-P., "Evolution of Living Organisms: Evidence for a New Theory of Transformation," Academic Press: New York NY, 1977, pp.151-152. Emphasis in original)]

Queen Victoria, in an early tilt towards evolution, saw orang-utans as "frightful, and painfully and disagreeably human". She herself had the misfortune to inherit a flaw in a body system much appealed to by the ID crew, for several of her descendants had haemophilia and bled freely after a cut. [This too is false. IDists have not "appealed to haemophilia." ID theorist Mike Behe appeals to the blood-clotting cascade as an example of an irreducibly complex system that could not plausibly arise by the Darwinian mechanism of the natural selection of random micromutations (see long quote of Behe in my "Pierre Grasse and the `irreducible complexity' of the blood-clotting cascade"). Remember that is Behe's mainpoint:

"Darwin knew that his theory of gradual evolution by natural selection carried a heavy burden: `If it could be demonstrated that any complex organ existed which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.' [Darwin C., 1872, "Origin of Species", 6th ed., 1988, New York University Press: New York, p.154]. It is safe to say that most of the scientific skepticism about Darwinism in the past century has centered on this requirement. From Mivart's concern over the incipient stages of new structures to Margulis's dismissal of gradual evolution, critics of Darwin have suspected that his criterion of failure had been met. But how can we be confident? What type of biological system could not be formed by `numerous, successive, slight modifications'? Well, for starters, a system that is irreducibly complex. By irreducibly complex, I mean a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning. An irreducibly complex system cannot be produced directly (that is, by continuously improving the initial function, which continues to work by the same mechanism) by slight, successive modifications of a precursor system, because any precursor to an irreducibly complex system that is missing a part is by definition nonfunctional. An irreducibly complex biological system, if there is such a thing, would be a powerful challenge to Darwinian evolution. Since natural selection can only choose systems that are already working then if a biological system cannot be produced gradually it would have to arise as an integrated unit, in one fell swoop, for natural selection to have anything to act on." (Behe M.J., "Darwin's Black Box: The Biochemical Challenge to Evolution," Free Press: New York NY, 1996, p.38. Emphasis original)

This was made even more explicit by Behe in his paper specifically in defence of the blood-clotting cascade, where he revised his definition of "irreducibly complex" to focus on "unselected steps" so that Darwinists cannot (like Jones does here) propose "just-so stories that leap over many steps without comment":

"In Darwin's Black Box I defined the concept of irreducible complexity (IC) in the following way. `By irreducibly complex I mean a single system which is composed of several well-matched, interacting parts that contribute to the basic function, and where the removal of any one of the parts causes the system to effectively cease functioning. (Behe 1996, 39)' While I think that’s a reasonable definition of IC, and it gets across the idea to a general audience, it has some drawbacks. Envisioning IC in terms of selected or unselected steps thus puts the focus on the process of trying to build the system. A big advantage, I think, is that it encourages people to pay attention to details; hopefully it would encourage really detailed scenarios by proponents of Darwinism (ones that might be checked experimentally) and discourage just-so stories that leap over many steps without comment. So with those thoughts in mind, I offer the following tentative `evolutionary' definition of irreducible complexity: An irreducibly complex evolutionary pathway is one that contains one or more unselected steps (that is, one or more necessary-but-unselected mutations). The degree of irreducible complexity is the number of unselected steps in the pathway. That definition has the advantage of promoting research: to state clear, detailed evolutionary pathways; to measure probabilistic resources; to estimate mutation rates; to determine if a given step is selected or not. It allows for the proposal of any evolutionary scenario a Darwinist (or others) may wish to submit, asking only that it be detailed enough so that relevant parameters might be estimated. If the improbability of the pathway exceeds the available probabilistic resources (roughly the number of organisms over the relevant time in the relevant phylogenetic branch) then Darwinism is deemed an unlikely explanation and intelligent design a likely one." (Behe M.J., "In Defense of the Irreducibility of the Blood Clotting Cascade: Response to Russell Doolittle, Ken Miller and Keith Robison," Discovery Institute, Seattle WA, July 31, 2000)

So if a Darwinist (like Jones) comes up with a non-Darwinian explanation of the blood-clotting cascade (including one that "leap[s] over many steps without comment"), then he has conceded Behe's main point!]

The clotting machinery is an icon of just how complex life may be. [Indeed, Jones gives it as an example in one of his books, noting that "From cut to clot involves several steps. Different proteins are arranged in a cascade which responds to the damage ... A dozen or more different genes scattered all over the DNA co-operate in the production line" (my emphasis):

"Now whole sections of DNA from normal and haemophiliac families can be compared to show exactly what has happened and, just like the genetic map itself, things have got much more complicated. Haemophilia shows how molecular biology has made geneticists' lives more difficult. First, uncontrollable bleeding is not a single disease, but several. This is because clotting itself is a complicated business. From cut to clot involves several steps. Different proteins are arranged in a cascade which responds to the damage, produces and then mobilises the material which makes up the clot and finally assembles it into a tough protective barrier. A dozen or more different genes scattered all over the DNA co-operate in the production line." (Jones J.S., "The Language of the Genes: Biology, History and the Evolutionary Future," [1993], Flamingo: London, 1994, reprint, pp.81-82)

So how did the Darwinian `blind watchmaker' set up a "production line" involving "A dozen or more different genes scattered all over the DNA"? ]

Designers love it: for to staunch the flow needs a cascade of a dozen or more enzymes that work like a row of toppling dominoes. [Great analogy! In fact Jones himself in his "Almost Like a Whale" (aka "Darwin's Ghost" in the USA) gives the blood clotting cascade as a prime example of a system that does not "vary most" because it is "least important," i.e. it varies least because it is so important:

"Perhaps, some say, most of the DNA is an organ of small importance, whose presence is not noticed by Darwin's machine. If so, much of life is neutral ground upon which natural selection enacts its few rare struggles. That view is supported by a surprising fact: that the parts of the body that vary most are those that appear to be least important. Blood clots are made when small proteins link together in response to damage. For much of the time each unit floats in the plasma, its ability to bind checked by a short piece that blocks the crucial site. After a cut, the plug is snipped out, the molecules link up and the clot forms. Most of the protein does not vary at all, but the stopper, with its simple job, is filled with diversity. Natural selection surely cannot act to retain differences in the part of the molecule with the least exacting task. Most of the changes in the stopper probably have no effect on how it works and merely accumulate with time. In the same way, in DNA as a whole, the parts that make no protein vary more than those that do, and the more embedded in the machinery of the cell any protein may be, the less variable its gene. Diversity, it seems, builds up where it does no harm, but is excluded from places where it might cause trouble. The champions of Darwinism find it painful to admit that most variation under Nature is a spectator at the evolutionary play. " (Jones J.S., "Almost Like a Whale: The Origin of Species Updated," Doubleday: London, 1999, pp.142-143) ]

Two interacting pathways meet at a crucial junction point. One is set off by a change in acidity after a cut, while the other acts when it picks up chemical cues from damaged cells. An injury sets off a chain reaction until the job is done and, if any step goes wrong, the whole system collapses. [Indeed. So Darwinism has to explain not just one pathway, but two, and which moreover "meet at a crucial junction point". And how could such a system that "collapses" "if any step goes wrong", be assembled by a Darwinian "step"-by-tiny-"step" mechanism?]

How could such a complicated machine evolve from simple beginnings? [Note how Jones now changes the question. The issue is not how did the blood clotting cascade "evolve from simple beginnings," since both Behe (and I) accept universal common ancestry:

"For the record, I have no reason to doubt that the universe is the billions of years old that physicists say it is. Further, I find the idea of common descent (that all organisms share a common ancestor) fairly convincing, and have no particular reason to doubt it." (Behe, Ibid, 1996, pp.5-6)

and so I (and I presume Behe) expect that the existing system was built on the foundations of a previous system (or systems). The question that Jones needs to answer is: how did the blood clotting cascade "evolve" by the Darwinian natural selection of random micromutations "from simple beginnings"?]

What use is part of a clot? Much better, in fact, than no clot at all. [This also is an attempt to change the question. The issue is not "part of a clot" but part of a blood clotting system. An animal that had blood but "no" clotting system "at all" would not be viable and so would be eliminated by natural selection. And as for "part of a" clotting system, Jones does not specify how much a part. A 99% "part" of a clotting system might be viable but a 1% "part" of a blood clotting system would not be any better than "no" clotting system "at all". In fact, Jones' own quote above about, "parts of the body that vary most are those that appear to be least important" and for "Blood clots ... Most of the protein does not vary at all" is evidence that, apart from the "plug", even a 99% "part" of the existing blood clotting system is not better than "no" clotting system "at all"!

[Continued in part #4]

Stephen E. Jones, BSc (Biol).
"Problems of Evolution"

Monday, April 17, 2006

Re: Do they expect that naturalistic methods will be able to explain a pathway to a minimum life form with 1000 genes?

AN (copy to CED minus your personal identifying information)

Thanks for your message and apologies for the delay in replying.


----- Original Message -----
From: AN
To: Stephen E. Jones
Sent: Tuesday, April 11, 2006 8:50 PM
Subject: 'More genes' needed to make life

AN>Hello,
>Regrading your last post in your blog I need to ask something. When we look at abiogenesis researchers we see two distinct type of researchs that are totally conflicting in my view. On one side we have researchers who claim that life can be reduced to structures as simple as RNAs and self-replicators, on the other side there are results showing that minimum requirements for something that we can call minimum life can't be less than 500-1000 genes as you mentioned in your last post. For example here we have a paper with various claims for first protocells and RNAs leading to more complex life.

This is a good point, but those who claim that "life can be reduced to structures as simple as RNAs and self-replicators" are, quite frankly, deluding themselves. There are no such things as "simple ... self-replicators." All replication takes place in a cell, by a coordinated system of ~50 molecular machines. The creationist chemist and early ID theorist Wilder-Smith makes this point, that "the synthesis of life has little to do with the clever synthesis of just one super molecule which self-replicates ... A real synthesis of life will more probably lie in the synthesis and ordering or arranging of the many component parts (i.e. molecules) of the von Neumann machine":

"To return to the technique required for abiogenetic in vitro synthesis: In the first place, there are probably no such things as single self-replicating molecules-although one speaks a great deal about them today. To achieve self-replication in general, one needs more than single molecules, the interaction of several different types of molecules with one another is mandatory. Maybe a DNA or RNA molecule might be able to replicate itself but it will be in the presence of certain other molecules - such as enzymes or replicases. Maybe the one molecule can act in several roles, of course. In this sense there have been reports, that some nucleic acids can act as their own catalysts. But it is usually the interaction of several molecules with one another that brings self-replication into play. The interacting molecules need not be all of varying analyses - as in the case of the molecules which act as their own catalysts. Varying roles are required for replication. We keep. then. in mind that the replication of one molecule entirely by itself is not yet known. Several molecules interact with one another to give the replication we ascertain in the von Neumann machine known as the biological cell. This interaction reminds us again of the machine nature of the self-replicating von Neumann machine, for the latter consists of an interacting multitude of component parts to achieve self-replication. The many different molecules correspond to the many different components of the replicating von Neumann machine. The above being the case, the synthesis of life has little to do with the clever synthesis of just one super molecule which self-replicates and hides the secret of life even though the literature speaks often of a primeval self-reproducing molecule arising. A real synthesis of life will more probably lie in the synthesis and ordering or arranging of the many component parts (i.e. molecules) of the von Neumann machine. By interacting with one another these components will produce the dynamic metabolic machine. Obviously the synthesis of a machine consisting of a multitude of mutually reacting component parts is an entirely different project to that which was formerly envisaged - the synthesis of one large macromolecule. It is for this reason that, although the DNA molecule is vital for biology in that it is life's information storage and retrieval system, yet it itself has to provide somehow the various different molecules with which it can react, as life starts to develop from the zygote. In the synthesis of the cell or the virus it is, then a question, not so much of the synthesis of any single macromolecule (although that will come into the solution of the problem) but the synthesis of a whole hierarchy of interacting molecules, that is, of a dynamically metabolizing, functioning machine." (Wilder-Smith A.E., "The Scientific Alternative to Neo-Darwinian Evolutionary Theory," T.W.F.T. Publishers: Costa Mesa CA, 1987, pp.94-95)

And as Von Neumann showed mathematically in the 1950's before the cell's replication mechanism was known in detail (and even then his was an oversimplification) that a minimum self-replication system (not just the one we have here on Earth but anywhere) is enormously complex (See my The Minimal Cell: A Problem of Evolution 2/2). As Cairns-Smith notes, "Von Neumann himself ... found the origin of life to be utterly perplexing'":

"So please respect the humble bacterium that is playing this game. It can reproduce, it can evolve. E. coli must have some sort of long-term memory about how to make itself that can outlast its substance. That means that an E. coli must be an automatic factory containing something analogous to control tapes and automatic manufacturing equipment. And that is only part of it. All the equipment must be contained, organised, fed. Pieces for it to work on, energy to drive it, must be provided by the E. coli cell. Apart from the manufacturing machinery that can follow instructions, there has also to be another kind of machinery that instead reprints them - something analogous to a Xerox machine or a tape copier. All these things have to be contrived through the manufacturing machinery duly instructed by appropriate bits of the Library tape. It may seem hardly surprising that no one has ever actually made a self-reproducing machine, even though Von Neumann laid down the design principles more than 40 years ago. You can imagine a clanking robot moving around a stock-room of raw components (wire, metal plates, blank tapes and so on) choosing the pieces to make another robot like itself. You can show that there is nothing logically impossible about such an idea: that tomorrow morning there could be two clanking robots in the stock-room... (I leave it as a reader' home project to make the detailed engineering drawings.) There is nothing clanking about E. coli; yet it is such a robot, and it can operate in a stock-room that is furnished with only the simples raw components. Is it any wonder that E. coli's message tape is long? (... about 10 kilometres long.) Is it any wonder that no free-living organisms have been discovered with message tapes below '2 kilometres'? Is it any wonder that Von Neumann himself, and many others, have found the origin of life to be utterly perplexing?'" (Cairns-Smith A.G., "Seven Clues to the Origin of Life: A Scientific Detective Story," Cambridge University Press: Cambridge UK, 1993 reprint, pp.14-15. Emphasis in original).

By the way, the above, "Is it any wonder that no free-living organisms have been discovered with message tapes" (DNA molecules) "below '2 kilometres'" is another way of saying that the minimum DNA molecule for a free-living organism is the equivalent of a 2 kilometre computer paper tape (p.11). So how can non-living chemicals get from zero length to 2 kilometres computer paper tape equivalent before they can even begin self-replication (assuming they also have the tape feeder, tape reader and convertor of the 2-D digital instructions into a 3-D machine, which can then repeat the process)?


AN>Now I want to ask, can't they see that there is a vast sea of conflictions between these two claims? Do they expect that naturalistic methods somehow will be able to explain a magical pathway from self-replicators and RNA to a minimum life form with 1000 genes which is much much more complex than a hypothetical protocell?

It is all decided at the metaphysical level. If 1) naturalism is true (which it isn't); and 2) we are here; then there simply must have been a naturalistic pathway from non-living chemicals to the first living cell. Actually finding that naturalistic pathway is not necessary. The Harvard chemist George Wald expressed this naturalist faith (actually I presume to the convinced naturalist it is more than a faith, it is a necessity - like 2 + 2 = 4 does not require faith):

"Organic molecules therefore form a large and formidable array, endless in variety and of the most bewildering complexity. One cannot think of having organisms without them. This is precisely the trouble, for to understand how organisms originated we must first of all explain how such complicated molecules could come into being. And that is only the beginning. To make an organism requires not only a tremendous variety of these substances, in adequate amounts and proper proportions, but also just the right arrangement of them. Structure here is as important as composition-and what a complication of structure! The most complex machine man has devised-say an electronic brain-is child's play compared with the simplest of living organisms. The especially trying thing is that complexity here involves such small dimensions. It is on the molecular level; it consists of a detailed fitting of molecule to molecule such as no chemist can attempt. ... One has only to contemplate the magnitude of this task to concede that the spontaneous generation of a living organism is impossible. Yet here we are, as a result, I believe, of spontaneous generation." (Wald G., "The origin of life," Scientific American, Vol. 191, No. 2, August 1954, pp.45-53, p.46)

Note that Wald can, because of "the magnitude of this task", "concede that the spontaneous generation of a living organism is impossible." Yet nevertheless he assumes it must have happened because: 1) "here we are"; and 2) naturalism is true.

The latter to Wald is an unquestioned ultimate premise. And as Johnson pointed out, "A system's ultimate premise is always beyond question; that is what it means to say that it is an ultimate premise":

"What Leff said is fascinating, but what he failed to say is more fascinating still. If there is no ultimate evaluator, then there is no real distinction between good and evil. It follows that if evil is nonetheless real, then atheism-i.e., the idea of the nonexistence of that evaluator or standard of evaluation-is not only an extraordinarily unappetizing prospect, it is also fundamentally untrue. Because the reality of evil implies the reality of the evaluator who alone has the authority to establish the standard by which evil can deserve to be damned. When impeccable logic leads to self-contradiction, there must be a faulty premise. In this case the premise is that because God is dead, `it looks as if we are all we have.' Why not reexamine the premise? Why not at least explain why you refuse to reexamine the premise? By not asking that last question, Leff in effect placed the death of God in the place of God. In his system, the absence of a supernatural evaluator was a premise so far beyond question that it could not be doubted even when it pointed to a conclusion Leff desperately wanted to escape, even a conclusion he acknowledged to be false. If we know that totalitarian mass murder is evil, and that those who acquiesced in it deserve damnation, then we know something about that absolute evaluator as well. Leff offered no reason for protecting modernism's founding premise from the brilliant skeptical analysis that he directed at everything else. To a theist this must seem indefensible, but Leff could not have done otherwise without ceasing to be a modernist. A system's ultimate premise is always beyond question; that is what it means to say that it is an ultimate premise." (Johnson P.E., "Nihilism and the End of Law," First Things, Vol. 31, March 1993, pp.19-25. Emphasis original)

AN>Regards,
AN

Stephen E. Jones, BSc (Biol).
"Problems of Evolution"

Saturday, April 15, 2006

Re: What is your view of the Noahacian flood? #3

AN

----- Original Message -----
From: AN
To: Stephen E. Jones

Sent: Tuesday, April 11, 2006 3:25 AM
Subject: Hi; Question re: Your Site

[Continued from part #2]

[c] "fully local" This has the least problems. A local Flood would avoid all the difficulties of a global (part #1) and anthropologically universal (part #2) Flood. For example, the water could drain away from a high local area like the plateau at the foothills of the Ararat range, and there would be no reason why there would be a lot of sediment (since sediment accumulates downstream on the flats where water slows):

"Arguments for a local flood. Although many Christians still believe in the universal flood, most of the recent conservative scholarship of the church defends a local flood. Those who defend a local flood believe that the time of the flood was some time prior to 4000 B.C. The waters were supplied by the rains from above and the ocean waters beneath. Some sort of geological phenomenon is indicated by the expression `and the fountains of the deep were broken up.' This caused the ocean waters to creep up the Mesopotamian valley. The waters carried the ark up to the Ararat range. The Hebrew text does not mean that the ark was deposited on the 17,000 foot summit of the peak, but that the ark rested somewhere on the Ararat range. It would have taken a special miracle to get Noah and his family down from such dizzy mountain heights where the cold would have been extreme. By the reversal of the geological phenomenon, the water is drained back from the valley. ... The purpose of the flood was to blot out the wicked civilization of Mesopotamia, and being a local flood of a short duration we would not expect to find any specific evidence for it, especially after the minimum of another six thousand years of weathering." (Ramm B.L., "The Christian View of Science and Scripture," [1955], Paternoster: Exeter, Devon UK, 1967, reprint, p.162).

By comparing scripture with scripture, it can be readily seen that (just as in our everyday conversation) universal-sounding language does not necesarily mean literally that:

"It cannot demonstrate that totality of language necessitates a universal flood. Fifteen minutes with a Bible concordance will reveal many instances in which universality of language is used but only a partial quantity is meant. All does not mean every last one in all of its usages. Psa. 22:17 reads: `I may tell all my bones,' and hardly means that every single bone of the skeleton stood out prominently. John 4:39 cannot mean that Jesus completely recited the woman's biography. Matt. 3:5 cannot mean that every single individual from Judea and Jordan came to John the Baptist. There are cases where all means all, and every means every, but the context tells us where this is intended. ... The universality of the flood simply means the universality of the experience of the man who reported it. When God tells the Israelites He will put the fear of them upon the people under the whole heaven, it refers to all the peoples known to the Israelites (Deut. 2:25). When Gen. 41:57 states that all countries came to Egypt to buy grain, it can only mean all peoples known to the Egyptians. Ahab certainly did not look for Elijah in every country of the earth even though the text says he looked for Elijah so thoroughly that he skipped no nation or kingdom (1 Kings 18:10). From the vantage point of the observer of the flood all mountains were covered, and all flesh died. We must concur that: `The language of the sacred historian by no means necessarily implies that the flood overspread the whole earth. Universal terms are frequently used in a partial and restricted sense in Scripture.' ["JFB Bible Commentary," 1870, Vol. I, p.98]" (Ramm, Ibid, p.164. Emphasis in original)

There remains one problem with the local Flood interpretation, Gen 7:19-20; 8:3-5, which says that "The waters ... covered the mountains [Heb. hills] to a depth of more than twenty feet" towards the end of the Flood, "the tops of the mountains became visible" clearly implying the mountains had been completely covered:

"19They rose greatly on the earth, and all the high mountains under the entire heavens were covered. 20The waters rose and covered the mountains to a depth of more than twenty feet. ? 3The water receded steadily from the earth. At the end of the hundred and fifty days the water had gone down, 4and on the seventeenth day of the seventh month the ark came to rest on the mountains of Ararat. 5The waters continued to recede until the tenth month, and on the first day of the tenth month the tops of the mountains became visible."

Personally, I consider that the interpretation that this is from Noah's perspective looking out of the Ark:

"Genesis 7:19,20: `And the waters prevailed exceedingly upon the earth; and all the high hills, that were under the whole heaven, were covered. Fifteen cubits upward did the waters prevail; and the mountains were covered.' Some Genesis commentators have seized on these passages to assert that the high mountains of the whole earth were covered to a depth of fifteen cubits (about 22 feet). Where the water would have come from is problematical, as well as what became of it. Measuring any depth at all raises a question. How would the passengers from inside the ark have any idea what the depths were? ... Again, the word for `mountains' and `hills' is the same in Hebrew. If the flooding was restricted to the region of the Mesopotamian valley, then the `mountains' submerged by the flood could have been the lower mountains of the region surrounding the valley, or it may signify the lower foothills at the beginning of a mountain range. As to the language used to describe the flood, it would make no difference whether the flood, in fact, was global or local. From the standpoint of the passengers on the ark, the description is entirely true and accurate in either case. These verses do not oblige us to ponder whether the Rockies, or the Andes, or the Urals, or the Himalayas were under water. Considering that mountains were not inundated by the flood, as the evidence indicates, in no way should that impugn the accuracy or inerrancy of Scripture. From Noah's and Shem's view point, the text describes their situation and surroundings in terms we might have used had we been passengers on the ark ourselves." (Fischer D., "The Origins Solution: An Answer in the Creation-Evolution Debate," Fairway Press: Lima OH, 1996, pp.283-284)

is perfectly adequate. Particularly when the Flood account (Genesis 6-9) is either on "Tablet 3 ... The histories of Noah" or on "Tablet 4 ... The histories of the sons of Noah" :

"Accordingly the present writer feels justified in following Wiseman [Wiseman P.J., "New Discoveries in Babylonia About Genesis," 1958, pp.53ff] in the assertion that Genesis contains in the first thirty-six chapters a series of tablets whose contents were linked together to form a roughly chronological account of primeval and patriarchal life written from the standpoint of a Mesopotamian cultural milieu. ... The tablets that may be isolated will be seen to have a title, a residuum of textual matter, and a colophon, along with certain additional features .... The sources can be described briefly as follows:
Tablet 1: Gen. 1:1-2:4. The origins of the cosmos
Tablet 2: Gen. 2 :5-5:2. The origins of mankind
Tablet 3: Gen. 5: 3-6:9a. The histories of Noah
Tablet 4: Gen. 6:9b-10:1. The histories of the sons of Noah
Tablet 5: Gen. 10:2-11:10a. The histories of Shem
Tablet 6: Gen. 11:10b-11:27a. The histories of Terah
Tablet 7: Gen. 11 :27b-25:12. The histories of Ishmael
Tablet 8: Gen. 25:13-25:19a. The histories of Isaac
Tablet 9: Gen. 25:19b-36:1. The histories of Esau
Tablet 10: Gen. 36:2-36:9. The histories of Esau
Tablet 11: Gen. 36:10-37:2. The histories of Jacob
.... The present writer is of the opinion that the foregoing classification of material represents the genuine literary sources underlying the first thirty-six chapters of Genesis." (Harrison R.K., "Introduction to the Old Testament," [1969], Tyndale Press: London, 1970, p.548)

depending on whether the colophon "these are the generations" (KJV) is the header or footer of the tablet. But either way, the Bible itself indicates that the Flood account was based on an eyewitness testimony.

However, John H. Walton (whose argument is that "If we are to reach an understanding of an ancient text such as Genesis 1 [and presumably also Genesis 6-9], we have to be able to think about the issues the way the ancients would have") provides an interesting alternative explanation, namely that to Noah's "an ancient Near Eastern mindset", "the mountains of Ararat" were not regarded as mountains but as the pillars of "the heavens":

"[Genesis 8:3-5] Tops of the mountains visible. This is the most difficult statement to explain for those arguing that the text does not require a global flood. In saying that the tops of the mountains became visible, this verse conveys that the tops, not just the flanks of the mountains, had been obscured. ... If it were not for 8:3-5, an interpreter can easily claim that the face value of the text does not demand a geographically global flood. All of the other statements are compatible with a flood of the known populated world. ... We must still consider whether 8:3-5 strikes us the way it does because we are thinking in terms of our understanding of the world. Would this text have meant something different if we could read it with an ancient Near Eastern mindset? ... In the Mesopotamian worldview the known world was comprised of a single continent fringed with mountains (such as the Zagros mountains in the east and the mountains of Ararat in the north) and ringed by the cosmic sea. The fringe mountains were believed to hold up the heavens and have roots in the netherworld. In the east, the mountain primarily associated with this role is Mount Masu. ... What happens if we try to read the Flood narrative against the background of this sort of worldview? ... Is it possible that the ancient writers did not count the mountains at the fringes of the world among the `high mountains' that the water covered? Cosmic mountains were places of the gods and would be impervious to flood waters sent by the gods. In this scenario, the ark drifts to the edge of the known world and rests against the mountains of Ararat (or perhaps on the foothills of Ararat). Noah views this as the edge of the world, just as some before Columbus's day believed they could reach the edge of the world. There the ark sits while the water recedes and the tops of the mountains in the occupied portion of the continent become visible. This means that when the waters totally dissipate, the ark is at the foot of the Ararat chain. The logic of not including the fringe mountains is that they were believed to support the heavens, and the waters are not seen as encroaching on or encountering the heavens. This way of thinking yields a flood of the then- known world (with boundaries as described, for instance, in the Sargon Geography and in the list of Noah's descendants in Gen. 10); it covered all the elevated places that were within eyesight of the occupants of the ark. Though this would be a geographically limited flood, it could still be anthropologically universal if people had not yet spread beyond this region. One of the advantages of seeking out views such as this is that they allow us to affirm the truth of the text without getting tied up in complicated logistical and scientific discussions." (Walton J.H., "Genesis," The NIV Application Commentary, Zondervan: Grand Rapids MI, 2001, pp.326-328) .

Finally, I wish to add a fourth position (mine), [d] "geographically and anthropologically local but theologically universal." That is, I think that both the YEC global Floodists and the OEC local Floodists are half-right and half-wrong. The OEC local Floodists are right about the Flood being geographically and anthropologically local, and the YEC global Floodists are right that the language is universal. My proposal is that the Flood story started off as a factual, eye-witness account by Noah or one of his sons, but was later recast by Moses (or even Noah) in the literary form of a re-creation epic, to teach universal theological lessons of sin, judgment, mercy, salvation, etc. The evidence is is the deliberate "series of parallels between the events of [Genesis] chs. 8-9 and those of ch. 1 in their literary order ... Ch. 1 describes the original beginning, while chs. 8-9 describe a new beginning after the flood":

"[Gen ]8:1 ? wind. The Hebrew word translated `Spirit' in 1:2 is here rendered `wind,' and introduces a series of parallels between the events of chs. 8-9 and those of ch. 1 in their literary order: Compare 8:2 with 1:7; 8:5 with 1:9; 8:7 with 1:20; 8:17 with 1:25; 9:1 with 1:28a; 9:2 with 1:28b; 9:3 with 1:30. Ch. 1 describes the original beginning, while chs. 8-9 describe a new beginning after the flood." (Barker K., ed., "The NIV Study Bible," Zondervan: Grand Rapids MI, 1985, p.16).

I hope this has been of some help. As I said at the start, my policy is not to get involved in private discussions of creation/evolution/design issues. I try to `kill two birds with one stone' by converting my answers into blog posts, so that others can benefit and I have an additional incentive to be far more comprehensive than I would normally be in a private post. Once again, thanks for your question.

Stephen E. Jones, BSc (Biol).
"Problems of Evolution"

Friday, April 14, 2006

Re: What is your view of the Noahacian flood? #2

AN

----- Original Message -----
From: AN
To: Stephen E. Jones
Sent: Tuesday, April 11, 2006 3:25 AM
Subject: Hi; Question re: Your Site

[Continued from part #1]

5. Now finally to your question: "the Noahacian flood" was it "[a] global, [b] local but anthro- pological universal, or [c] fully local"? As you rightly say, each of these positions "has problems." Since we know from 3. in part #1 that there was a Noah, an Ark and a Flood (or else Jesus was wrong in which case He is not God and Christianity is false and there is no point even bothering about Noah's Flood), it is a case of eliminating those positions which have the most problems.

[a] "Global." This has the most problems:

"The problems in connexion with a universal flood are enormous. .... One point must be dearly understood before we commence these criticisms: the flood is recorded as a natural-supernatural occurrence. It does not appear as a pure and stupendous miracle. The natural and the supernatural work side by side and hand in hand. If one wishes to retain a universal flood, it must be understood that a series of stupendous miracles is required. Further, one cannot beg off with pious statements that God can do anything. We concur enthusiastically with Smith when he wrote: `That the Omnipotent could effect such a work [a universal flood], none can doubt; but we are not at liberty thus to invent miracles, and the narrative in the Book of Genesis plainly assigns two natural causes for the production of the diluvial waters.' [Smith J.P., "On the Relation Between the Holy Scriptures and some parts of Geological Science," Appleton: New York, 1840, p.132]... There is the problem of the amount of water required by a universal flood. All the waters of the heavens, poured all over the earth, would amount to a sheath seven inches thick. If the earth were a perfect sphere so that all the waters of the ocean covered it, the depth of the ocean would be two and one-half to three miles. To cover the highest mountains would require eight times more water than we now have. It would have involved a great creation of water to have covered the entire globe, but no such creative is hinted at in the Scriptures. The mixing of the waters and the pressure of the waters would have been devastating. Many of the salt-water fish and marine life would die in fresh water; and many of the fresh-Water fish and marine life would die in salt water. An entire marine creation would have been necessary if the waters of the earth were mixed, yet no such hint is given in the account. Furthermore, the pressure of the water six miles high (to cover the Himalayas) would crush death the vast bulk of marine life. Ninety per cent of marine life is within the first fifty fathoms. The enormous pressure of six miles of water on top of these forms (most of which cannot migrate, or migrate any distance) would have mashed them. The result on plant life would have been equally devastating. Practically the entire world of plants would have perished under enormous pressure, the presence of salt water, and a year's soaking. Innumerable life cycles of plants and insects would have been interrupted and would have required a creative work almost as extensive as the original creation to restore the earth. No such destruction and no such re-creation is hinted at in the Scriptures. ... Getting rid of such a vast amount of water would have been as miraculous as providing it. If the entire world were under six miles of water, there would be no place for the water to drain off. Yet the record states that the water drained off with the help of the wind (Gen. 8:1). A local flood would readily account for this, but there is no answer if the entire world were under water." (Ramm, ., "The Christian View of Science and Scripture," [1955] Paternoster: Exeter, Devon UK, 1967, reprint, pp.165-166. Emphasis original).

It is also the least likely, Biblically. That is, Moses and his hearers in ~1,500 BC would not have known that the Earth was a globe, and would have understood by "earth" (Heb. 'eres "land") a local or regional area:

"Noah's Ark and the Flood. As to the Great Deluge of Genesis 6-8 ... the comparative lack of geologic evidence for a world-wide cataclysm has given rise to doubts as to the universality of the Flood. No characteristic or uniform flood-type deposits have been discovered in the sites excavated in the Mesopotamian Valley. The thick flood stratum found by Leonard Woolley at Ur dates from early fourth millennium (ca. 3800 B.C.), but only one other flood stratum from that period has thus far been discovered, that found by Stephen Langdon at Kish (a much shallower deposit, incidentally). The other flood deposits, discovered at Kish, Shuruppak, Uruk and (possibly) Lagash, represent an inundation of a thousand years later, judging from the archaeological remains and stratigraphical sequence. While the excavations may not in all cases have penetrated low enough to reach the 3800 B.C. level in some of the above mentioned, in Kish, at least, the dig went down to apparently undisturbed virgin soil right below the 2800 B.C. level. It is of course true that these few deep excavations are insufficient for any firm conclusions. But they have led most archaeologists to question the possibility of a general deluge over a more than local area-at least within the period investigated in the excavations themselves-and even staunch conservative apologists ... have defended the theory of a flood restricted to the cradle of the human race in Mesopotamia (or possibly extending up to the Caspian basin). ... The Jamieson, Fausset and Brown Commentary (Vol. I, p.98) indicates that the Hebrew text does not necessarily imply a universal flood. .... In explanation of this assertion, it needs to be pointed out that the Hebrew 'eres, translated consistently as `earth' in our English Bibles, is also the word for `land' (e.g., `the land of Israel,' `the land of Egypt'). There is another term tebel, which means the whole expanse of the earth, or the world as a whole. Nowhere does tebel occur in this account, but only 'eres, in all the statements which sound quite universal in the English Bible (e.g., 7:4, 10, 17, 18, 19). Thus, Genesis 6:17c can be rendered: `...everything that is in the land shall die'-that is, in whatever geographical region is involved in the context and situation." (Archer G.L., "A Survey of Old Testament Introduction," Moody Press: Chicago IL, 1964, pp.192-194)

It is ironic that Young Earth Creationists (YECs) who criticise Old Earth Creationists (OECs) like me for reading modern scientific concepts into the Bible, do just that themselves when they read their comparatively modern scientific concept of the Earth as a globe, into an ancient document (Genesis) when the Earth was not known to be a globe!

[b] "local but anthropological universal." This has the problems that: 1) there is evidence of "men ... found outside the Mesopotamian area long before the flood":

"There are three views of the local flood: (i) Some assert that man never spread beyond the Mesopotamian valley. This is impossible to defend in that it is so well proven that men were to be found outside the Mesopotamian area long before the flood. (ii) G.F. Wright believes that the ice-age drove man into the Mesopotamian valley. (iii) A third view, and the one which we hold, is that the entire record must be interpreted phenomenally. If the flood is local though spoken of in universal terms, so the destruction of man is local though spoken of in universal terms. The record neither affirms nor denies that man existed beyond the Mesopotamian valley. Noah certainly was not a preacher of righteousness to the peoples of Africa, of India, of China or of America-places where there is evidence for the existence of man many thousands of years before the flood (10,000 to 15,000 years in America). The emphasis in Genesis is upon that group of cultures from which Abraham [and the Messiah] eventually came." (Ramm, Ibid, p.163. Words in square brackets mine)

Ramm wrote the above over 50 years ago, and today there is evidence of Homo sapiens in Australia ~40,000 years ago:

"Australia's oldest human remains, found at Lake Mungo, include the world's oldest ritual ochre burial (Mungo III) and the first recorded cremation (Mungo I). Until now, the importance of these finds has been constrained by limited chronologies and palaeoenvironmental information. Mungo III, the source of the world's oldest human mitochondrial DNA, has been variously estimated at 30 thousand years (kyr) old, 42-45 kyr old and 62 ±6 kyr old, while radiocarbon estimates placed the Mungo I cremation near 20-26 kyr ago. Here we report a new series of 25 optical ages showing that both burials occurred at 40±2 kyr ago and that humans were present at Lake Mungo by 50-46 kyr ago, synchronously with, or soon after, initial occupation of northern and western Australia. Stratigraphic evidence indicates fluctuations between lake-full and drier conditions from 50 to 40 kyr ago, simultaneously with increased dust deposition, human arrival and continent-wide extinction of the megafauna. This was followed by sustained aridity between 40 and 30 kyr ago. This new chronology corrects previous estimates for human burials at this important site and provides a new picture of Homo sapiens adapting to deteriorating climate in the world's driest inhabited continent." (Bowler J. M., Johnston H., Olley J.M., Prescott J.R., Roberts R.G., Shawcross W. & Spooner N.A., "New ages for human occupation and climatic change at Lake Mungo, Australia," Nature, 421, 20 February 2003, pp.837-840).

And (2), the Bible itself tells us how extensive the Flood was. At the end of the Flood, in Gen 9:18-19, it says that the earth (Heb. land) was repopulated by the descendants of the sons of Noah:

"18The sons of Noah who came out of the ark were Shem, Ham and Japheth. (Ham was the father of Canaan.) 19These were the three sons of Noah, and from them came the people who were scattered over the earth. ? "

and in the next chapter, immediately after the Table of Nations (Gen 10:1-31) in Gen 10:32, it says that from them these "nations spread out over the earth [Heb. land] after the flood":

"32These are the clans of Noah's sons, according to their lines of descent, within their nations. From these the nations spread out over the earth [Heb. land] after the flood."

However, as Ramm points out, "An examination of the Table of Nations of Gen. 10 discloses that no mention of the Mongoloid or Negroid races is made. .... The sons of Noah were all Caucasian as far as can be determined, and so were all of their descendants:"

"An examination of the Table of Nations of Gen. 10 discloses that no mention of the Mongoloid or Negroid races is made. Some anthropologists believe that it is impossible to make any racial distinctions among humans, others make two main divisions, but most accept with modifications and qualifications and exceptions the triadic division of Negroid, Mongoloid, and Caucasoid. As far as can be determined the early chapters of Genesis centre around that stream of humanity (part of the Caucasoid race) which produced the Semitic family of nations of which the Hebrews were a member. The sons of Noah were all Caucasian as far as can be determined, and so were all of their descendants. The Table of Nations gives no hint of any Negroid or Mongoloid peoples." (Ramm, Ibid, p.234).

Genesis itself (and therefore God Himself) is telling us that the Flood was neither global, nor anthropologically universal.

[Continued in part #3]

Stephen E. Jones, BSc (Biol).
"Problems of Evolution"