EXAMPLES OF INTELLIGENT DESIGN -BLOOD CLOTTING
The Perfect Enzyme Chain in Blood Clotting
The blood-clotting system is an extraordinary phenomenon that operates so flawlessly that when you cut yourself, you can be sure that the flow of blood will soon stop and the injury will seal itself up. That certainty stems from the way the enzymes in your body work in a flawless, systematic manner.
A wound sends the entire body into alarm. The intervention will take place at the site of the cut. When bleeding starts anywhere in the body, all available means are mobilized and flow in the direction of the injury. At this point, certain molecules traveling through the bloodstream suddenly become active, at enormous speed.
First aid is delivered by blood platelets known as thrombocytes. These travel dispersed throughout the bloodstream, so that wherever bleeding may occur, a thrombocyte will always be patrolling nearby.
The blood clotting system is an extraordinary phenomenon that occurs through the activity of a series of enzymes. Each enzyme must be in the right place and go into action at the right time. Countless enzymes work just as if they knew where they had to be, and when.
A protein known as von Willebrand factor works like a policeman calling for backup assistance by indicating the site of an accident. It halts thrombocytes when it detects them and ensures that they remain at the site. The first thrombocyte to arrive signals others by releasing a special substance, just as if it were summoning assistance over the radio.
Once the first intervention has occurred, enzymes take over the work. Up to this point, in fact, a large number of enzymes have already become involved, but we shall concentrate on those that complete the coagulation process. The body always stores inactive enzymes for later use, coding them to go into action only when they receive the signal that their presence is required.
Fibrinogen is a non-active enzyme that travels freely through the body and is found dissolved in blood plasma. It circulates at random until the body suffers a cut anywhere, and then it suddenly goes into action. This protein that serves no function in the plasma heads towards the region of the injury. When a state of alarm develops, another enzyme called thrombin cuts two of the three links in fibrinogen's protein chain, thus converting fibrinogen into fibrin. In other words, a previously non-active enzyme assumes an active role. Small, adhesive parts have now appeared on the injured surface. These allow fibrin to bond to other fibrin molecules. The result is a long chain, and the proteins quickly combine and interlace with one another. This is the primary clot that forms. Subsequently, this fibrin mesh will continue to cover the wound just like a tightly-woven fishing net.
At the same time, thrombin turns the enzyme factor XIII into factor XIIIa, which strengthens the fibrin clot.85
The thrombin that activates fibrinogen also exists in the blood in an inactive state known as prothrombin. This is vital, because if thrombin constantly coursed through the bloodstream, it would sever all the fibrinogens. Uncontrolled clotting would occur in the body constantly. In order to avoid any such danger, prothrombin too must be activated by another enzyme.
That enzyme, called the Stuart factor, cleaves and activates prothrombin. But what applies to thrombin also applies to Stuart factor. Were it to be moving actively in the blood right from the outset, then in that case, the Stuart factor would constantly initiate the clotting mechanism and uncontrolled clotting would also begin. For that reason, Stuart factor also exists in an active state while circulating in the blood. However, Stuart factor by itself is not enough for prothrombin to be set into action. Still another enzyme, accelerin, works with it to convert prothrombin into thrombin.
The enzymes that enable blood clotting literally know what needs to happen when, where they must concentrate, which gap in the body they need to close, and what sequence they need to follow. This immaculate system is too complex for any of its stages to have come about by chance.
We might therefore assume that accelerin is also initially not in an active state. However, its activation system involves a puzzle reminiscent of the riddle of "the chicken and the egg"â€â€because it is thrombin that activates accelerin! How do we explain the fact that accelerin is activated by the very enzyme that it itself activates?
The reason is that Stuart factor cleaves the prothrombin at a very low rate. The result is that as a precautionary measure, a certain amount of thrombin is always ready in the body. The whole phenomenon begins with this significant precaution and as the Stuart factor goes into action, the clotting system also goes into action at high speed.
This system of various factors enables blood clotting to take place. The enzymes must know which have to go into action when, where they need to concentrate, and what gap in the body they have to cover over. They also need to know when to stop their work. If the clotting process that begins over a wound does not stop at the proper stage, this will constitute a serious danger for the body. Uncontrolled clotting will mean blood vessel congestion, and vital organs will fail to function. It is therefore essential to halt the activities of these enzymes that consecutively activate one another. Yet other enzymes inform them of this.
Once the wound has healed, the blood clot also needs to be removed. The molecules that arrive on the scene for this task are, again, enzymes. The one known as plasmin works like a pair of scissors to cut the fibrin clots. Plasmin works on fibrin, but not on fibrinogen, the latter's inactive state. Were that not so, it would cause a serious difficulty for future clotting. Plasmin cannot act too quickly, which is actually an advantage: Otherwise, the wound would not heal before plasmin, which is activated when the wound appears, had severed the fibrin, breaking down clots as soon as they formed. ; olur.
Were it not for the blood-clotting system, we would be defenseless against all kinds of injuries to our bodies. Beginning in infancy, the smallest cut would lead to a severe loss of blood.
There are numerous other enzymes involved in the blood clotting system. Each is necessary to carry out or complete a particular process, and all are parts of an irreducibly complex system from which not a single component can be removed.
The formation of a blood clot is a complex, multi-step process that utilizes numerous proteins, many with no other function besides clotting. Each protein depends on an enzyme to activate it. So to paraphrase Behe very simply: What evolved firstâ€â€the protein or enzyme? Not the protein; it cannot function without the enzyme to switch it on. But why would nature evolve the activating enzyme first? Without the protein, it serves no purpose. Furthermore, if blood clotting had evolved step-by-step over eons, creatures would have bled to death before it was ever perfected. The system is irreducibly complex.
The Perfect Enzyme Chain in Blood Clotting
The blood-clotting system is an extraordinary phenomenon that operates so flawlessly that when you cut yourself, you can be sure that the flow of blood will soon stop and the injury will seal itself up. That certainty stems from the way the enzymes in your body work in a flawless, systematic manner.
A wound sends the entire body into alarm. The intervention will take place at the site of the cut. When bleeding starts anywhere in the body, all available means are mobilized and flow in the direction of the injury. At this point, certain molecules traveling through the bloodstream suddenly become active, at enormous speed.
First aid is delivered by blood platelets known as thrombocytes. These travel dispersed throughout the bloodstream, so that wherever bleeding may occur, a thrombocyte will always be patrolling nearby.
The blood clotting system is an extraordinary phenomenon that occurs through the activity of a series of enzymes. Each enzyme must be in the right place and go into action at the right time. Countless enzymes work just as if they knew where they had to be, and when.
A protein known as von Willebrand factor works like a policeman calling for backup assistance by indicating the site of an accident. It halts thrombocytes when it detects them and ensures that they remain at the site. The first thrombocyte to arrive signals others by releasing a special substance, just as if it were summoning assistance over the radio.
Once the first intervention has occurred, enzymes take over the work. Up to this point, in fact, a large number of enzymes have already become involved, but we shall concentrate on those that complete the coagulation process. The body always stores inactive enzymes for later use, coding them to go into action only when they receive the signal that their presence is required.
Fibrinogen is a non-active enzyme that travels freely through the body and is found dissolved in blood plasma. It circulates at random until the body suffers a cut anywhere, and then it suddenly goes into action. This protein that serves no function in the plasma heads towards the region of the injury. When a state of alarm develops, another enzyme called thrombin cuts two of the three links in fibrinogen's protein chain, thus converting fibrinogen into fibrin. In other words, a previously non-active enzyme assumes an active role. Small, adhesive parts have now appeared on the injured surface. These allow fibrin to bond to other fibrin molecules. The result is a long chain, and the proteins quickly combine and interlace with one another. This is the primary clot that forms. Subsequently, this fibrin mesh will continue to cover the wound just like a tightly-woven fishing net.
At the same time, thrombin turns the enzyme factor XIII into factor XIIIa, which strengthens the fibrin clot.85
The thrombin that activates fibrinogen also exists in the blood in an inactive state known as prothrombin. This is vital, because if thrombin constantly coursed through the bloodstream, it would sever all the fibrinogens. Uncontrolled clotting would occur in the body constantly. In order to avoid any such danger, prothrombin too must be activated by another enzyme.
That enzyme, called the Stuart factor, cleaves and activates prothrombin. But what applies to thrombin also applies to Stuart factor. Were it to be moving actively in the blood right from the outset, then in that case, the Stuart factor would constantly initiate the clotting mechanism and uncontrolled clotting would also begin. For that reason, Stuart factor also exists in an active state while circulating in the blood. However, Stuart factor by itself is not enough for prothrombin to be set into action. Still another enzyme, accelerin, works with it to convert prothrombin into thrombin.
The enzymes that enable blood clotting literally know what needs to happen when, where they must concentrate, which gap in the body they need to close, and what sequence they need to follow. This immaculate system is too complex for any of its stages to have come about by chance.
We might therefore assume that accelerin is also initially not in an active state. However, its activation system involves a puzzle reminiscent of the riddle of "the chicken and the egg"â€â€because it is thrombin that activates accelerin! How do we explain the fact that accelerin is activated by the very enzyme that it itself activates?
The reason is that Stuart factor cleaves the prothrombin at a very low rate. The result is that as a precautionary measure, a certain amount of thrombin is always ready in the body. The whole phenomenon begins with this significant precaution and as the Stuart factor goes into action, the clotting system also goes into action at high speed.
This system of various factors enables blood clotting to take place. The enzymes must know which have to go into action when, where they need to concentrate, and what gap in the body they have to cover over. They also need to know when to stop their work. If the clotting process that begins over a wound does not stop at the proper stage, this will constitute a serious danger for the body. Uncontrolled clotting will mean blood vessel congestion, and vital organs will fail to function. It is therefore essential to halt the activities of these enzymes that consecutively activate one another. Yet other enzymes inform them of this.
Once the wound has healed, the blood clot also needs to be removed. The molecules that arrive on the scene for this task are, again, enzymes. The one known as plasmin works like a pair of scissors to cut the fibrin clots. Plasmin works on fibrin, but not on fibrinogen, the latter's inactive state. Were that not so, it would cause a serious difficulty for future clotting. Plasmin cannot act too quickly, which is actually an advantage: Otherwise, the wound would not heal before plasmin, which is activated when the wound appears, had severed the fibrin, breaking down clots as soon as they formed. ; olur.
Were it not for the blood-clotting system, we would be defenseless against all kinds of injuries to our bodies. Beginning in infancy, the smallest cut would lead to a severe loss of blood.
There are numerous other enzymes involved in the blood clotting system. Each is necessary to carry out or complete a particular process, and all are parts of an irreducibly complex system from which not a single component can be removed.
The formation of a blood clot is a complex, multi-step process that utilizes numerous proteins, many with no other function besides clotting. Each protein depends on an enzyme to activate it. So to paraphrase Behe very simply: What evolved firstâ€â€the protein or enzyme? Not the protein; it cannot function without the enzyme to switch it on. But why would nature evolve the activating enzyme first? Without the protein, it serves no purpose. Furthermore, if blood clotting had evolved step-by-step over eons, creatures would have bled to death before it was ever perfected. The system is irreducibly complex.
