Why do you need the intrinsic pathway when you have faster extrinsic pathway?

Why do you need the intrinsic pathway when you have faster extrinsic pathway?

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There are two pathways in blood clot fromation; the extrinsic pathway and the intrinsic pathway.

The extrinsic pathway is faster than intrinsic pathway because it has less number of steps. So, why do we need intrinsic pathway then?

In short: The extrinsic cascade reacts to damages of the blood vessel, the intrinsic pathway reacts to damages of the walls. But as with all things, the long version is ways more complicated:

The extrinsic pathway is activated when you damage tissue and factor VII come in contact with tissue factor (also known as factor III). Tissue factor is located in the membrane of the cells and is only released when the cells are damaged. Then the cascade starts and delivers a very fast large amounts of active thrombin, which then converts fibrinogen to fibrin to build a block of the damaged blood vessel. The step from the thrombin is common between both pathways.

The intric pathway is also called the "contact pathway", which starts when the factor VII comes in contact with collagen or anionic surfaces. The main advantage of this pathway is the strong amplification of the initial signal from the intrinsic pathway by a factor of about 1000 fold. The intrinsic pathway is also co-activated by active thrombin (which stands at the end of the cascade) meaning it is also a powerfull feedback loop to make the initial reaction much stronger. This also overcomes weak activation which where the active thrombin will be inactivated by Tissue Factor Pathway Inhibitor. The coagulation cascade has a pretty nice article in the Wikipedia.

Interestingly it is now believed, that the start of the intrinsic pathway plays no or almost no role in vivo. There are people which "suffer" from a deficiency in factor XII which is necessary to start the intrisic cascade. These people have absolutely no problems with their coagulation, so the first steps are not necessary (any more?). This article presents findings, that it stabilizes a thrombus:"The intrinsic pathway of coagulation is essential for thrombus stability in mice." Here are some further articles about the intrinsic pathway:

The extrinsic pathway is activated by extrinsic trauma , that makes blood escape out from the vascular system , and then after the formation of a small amount of fibrin , a substance called Tissue Factor Pathway Inhibitor ( TFPI ) is released , this inhibitor prevent more activation of factor x , it's thought that TFPI is responsible for preventing more un-needed fibrin , but if the injury need more fibrin to cure , at this point the intrinsic pathway will be activated to form more needed fibrin

SCHC hematology II

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What is the most common hereditary clotting problem?
--Von Willebrand's Dz (factor is absent or abnormal, many varieties)

What do you call an inactive enzyme precursor in the clotting cascade?
--a zymogen

What do you call a coagulation deficiency from to a deficiency of Factor VIII due to an X-linked recessive gene?

--hemophilia A

Which pathway is Factor VIII a part of?
--the INTRINSIC pathway

How long does the intrinsic pathway normally take to form a clot?
--1-6 seconds

Who gets this kind of hemophilia?
--1/2 of the sons of mothers who carry the recessive gene

Which factor is deficient in hemophilia B?
--factor IX

What is the factor that allows platelets to adhere to endothelial basement membranes to begin a clot?
--Von Willebrand's factor (VWF) = large, multimeric circulating proteins which link platelet glycoproteins (Ib/IX/V) to collagen fibrils-->activating the platelets

Where does von Willebrand's factor come from?
--endothelial cells (also make plasminogen activator and possibly factor V)

What syndrome is a lack of platelet glycoproteins receptors for VWF? (also decreases clotting)
--Bernard-Soulier syndrome

Where do platelets come from?
--megakaryocytes in the bone marrow

What do platelets release from their granules once they are activated?
--ADP, serotonin, platelet-activating factor (PAF), vWF, platelet factor 4, and thromboxane A2 (TXA2)

How do those chemicals cause increased clotting?
-->activate a Gq-linked protein receptor cascade-->increased calcium concentration in PLT cytosol-->activates protein kinase C-->activates phospholipase A2 (PLA2)-->modifies integrin membrane glycoprotein IIb/IIIa increasing its affinity for fibrinogen-->activated platelets change shape from spherical to stellate-->fibrinogen cross-links with glycoprotein IIb/IIIa aggregates more platelets

Why does clotting speed increase exponentially once started?
--autoactivation: many of the factors increase activation of themselves or other supporting factors in the cascade

What common drug irreversibly inhibits thromboxane A2 (vasoconstrictor) via the COX pathway?

What did Wiggins teach us activates protein C?
--excess thrombin

And what activates prothrombin-->thrombin?

Calcium ions are required for promotion/acceleration of all clotting reactions EXCEPT?
--the first two steps of the intrinsic pathway

Which clotting factors are dependent on Vitamin K?
--synthesis of factors II (prothrombin), VII, IX, X
--also protein C and protein S which form the PCa/PS complex which inhibits factors V and VIII
--factor VII and protein C are MOST SENSITIVE to vit K levels
--if K deficient PT is always prolonged, PTT mb prolonged
--if factors II, VII, IX, X, PC and PS are all deficient-->diagnostic for low K

Where are clotting factors II, VII, IX, X, XI, XII, plasminogen and prothrombin made?
--in the liver
--note: plasminogen also made in kidney
--factor V may be made in liver or by endothelial cells, not sure
What causes vitamin K deficiency?
--malabsorption dt biliary tract dz

Why do you need bile to absorb vitamin K?
--it's fat soluble and won't be digested or absorbed w/o bile salts

What cofactor besides calcium and vitamin K is needed for many clotting reactions?
--platelet phospholipid

What is the most common cause of abnormal bleeding?
--thrombocytopenia, usu PLT below 70,000

What are some of the causes of thrombocytopenia?
--decreased PLT production dt BM damage
--congenital abn ie: Fanconi's aplastic anemia
--nutritional deficiency esp: B12 and folate
--DIC or purpura-->increased destruction of PLTs

What common hemorrhagic syndrome occurs following the uncontrolled activation of clotting factors and fibrinolytic enzymes throughout small blood vessels?
--disseminated intravascular coagulation (DIC)
--involves clotting throughout CV system
--fibrin deposited everywhere
--PLT's and clotting factors consumed
--anticoagulation systems are overwhelmed and worsen process as fibrin degradation products (incl D-dimers) inhibit fibrin polymerization and block PLT fx-->lethal tissue necrosis and bleeding

What triggers DIC?
--acute usudt massive tissue damage such as large severe burns, sepsis, or complication of pregnancy
--chronic dt certain cancers, retained dead fetuses, aneurysms or hemangiomas, insidious onset

What are the new names for the intrinsic and extrinsic coagulation pathways?
--contact activation pathway and tissue factor pathway respectively

What drug acts very quickly to antagonize thrombin in the intrinsic/&common pathway?

What drug slows the extrinsic pathway?
--warfarin/coumarin, use PT lab to monitor

How does coumadin work?
--inhibits vit K utilization by competing with it as a cofactor
--slow acting, onset of action is 2-7 days, the half life of the factors
--usu pts use heparin therapy until coumadin takes effect

Which lab do you use to monitor conversion of X to Xa?
--PT, still

Which pathway is faster?
--the extrinsic one

Which pathway are you testing with the PT lab?

At what factor do the intrinsic and extrinsic pathways merge to form the common one?
--factor Xa (activated)

How long does the intrinsic pathway take to form a clot after trauma to a vessel or blood?
--15 seconds to a minute

What lab test do you use to measure intrinsic pathway function?
--the PTT
--measure heparin therapy

What does plasmin do?
--attacks fibrin at 50 sites to break down tight clots

Where does antithrombin III come from?
--basophils and platelets

How do basophils know to release it?
--I have no idea

What does antithrombin III do?
--inhibits factors IIa, IX, Xa, XI, XII (three in the intrinsic pathway, two in the common)

What drug increases the action of antithrombin III by 1000 times?

Note to self:
--intrinsic, heparin, PTT, slow
--extrinsic, tissue factor, warfarin, PT, fast

What's another name for tissue factor?
--factor III

What may trigger idiopathic thrombocytopenic purpura?
--a viral URI in a child

What is the most common hereditary hypercoagulability disorder amongst Eurasians?
--Factor V Leiden
--present in 3-8% of caucasians
--risk of venous thrombosis, OB complications
--increased risk for women on birth control pills (35X).

What is the principle clot eliminator of the body?

What causes the hypercoagulability in Factor V Leiden?
--the Leiden variant of factor V cannot be inactivated by activated protein C

What is a FDP?
--fibrin degradation product (after plasmin breaks fibrin clot to fragments)

Diagnostic testing for venous thromboembolisms & pulmonary embolisms relies on finding what?

What two actions does thrombin take to activate clotting?
--activates factor XIII and converts fibrinogen to fibrin monomers

What two actions does plasmin take to break down clots?
--breaks fibrinogen to FDPs and fibrin clots to D-dimers

What affects PT, prothrombin time?
--extrinsic and common coag pathways
--first effect: vactor VII, later II, IX, and X
--time INCREASED by hepatocellular liver disease, obstructive biliary disease (low vit K), and coumadin

How does coumadin increase PT?
--inhibition of vit K dependent factor depletion

What's INR?
--international normalized ratio = patient protime / normal protime
--a calculation to eliminate variation in PT measurements between labs
--used for monitoring effect of coumadin therapy

What factors can interfere with PT?
--alcohol increases time dt liver damage
--diarrhea prolongs dt vit K malabsorption
--high fat/leafy veg diet may shorten due to high vit K intake

Which factor is activated by the PTT test (partial thromboplastin time)?
--factor XII
--monitor heparin therapy

What can cause increased PTT times?
--congenital (hemophilia, A/classical is factor VIII, B and VWDz act on factor IX)
--liver cirrhosis
--vit K deficiency
--heparin or coumadin therapy

What can decrease PTT times?
--early DIC
--extensive cancer

What screening test for platelet function abnormalities is likely to be on ND boards but barely used anymore?
--bleeding time
--PLT count under 50,000 prolongs BT

What other outdated test was mentioned in lecture and will likely be on boards?
--venous clotting time, 4-10 minutes, heparin monitoring


The anticoagulant system exerts a regulatory role over the procoagulant activity in blood thus localizing the thrombus formation.[13] The main anticoagulant mechanisms naturally present in the body include the following:


Antithrombin (AT), previously known as AT III is the main inhibitor of thrombin. It is a serine protease inhibitor, which binds and inactivates thrombin, factor IXa, Xa, XIa and XIIa. The enzymatic activity of AT is enhanced in the presence of heparin. However, the plasma concentration of heparin is low and does not contribute significantly to the in vivo activation of AT. AT is activated by binding of heparin sulphate present on endothelial cell surface. AT binds coagulation factors in a ratio of 1:1 and this complex is removed by reticuloendothelial cells. Other thrombin inhibitors are heparin cofactor II, 㬒 macroglobulin and 㬑-antitrypsin.[24,25]

Tissue factor plasminogen inhibitor

It is a polypeptide produced by endothelial cells. It acts as a natural inhibitor of the extrinsic pathway by inhibiting TF-VIIa complex.[25,26] Protein S enhances the interaction of factor Xa in the presence of calcium and phospholipids.[27]

Protein C pathway

The propagation phase of the coagulation is inhibited by the Protein C pathway that primarily consist of four key elements:

Protein C is a serine protease with potent anticoagulant, profibrinolytic and anti-inflammatory properties. It is activated by thrombin to form activated protein C (APC) and acts by inhibiting activated factors V and VIII (with Protein S and phospholipids acting as cofactors)

Thrombomodulin - A transmembrane receptor on the endothelial cells, it prevents the formation of the clot in the undamaged endothelium by binding to the thrombin

Endothelial protein C receptor is another transmembrane receptor that helps in the activation of Protein C

Protein S is a vitamin K-dependent glycoprotein, synthesised by endothelial cells and hepatocytes. It exists in plasma as both free (40%) and bound (60%) forms (bound to C4b-binding protein). The anticoagulant activity is by virtue of free form while the bound form acts as an inhibitor of the complement system and is up regulated in the inflammatory states, which reduce the Protein S levels thus resulting in procoagulant state. It functions as a cofactor to APC in the inactivation of FVa and FVIIIa. It also causes direct reversible inhibition of the prothrombinase (FVa𠄿Xa) complex.[28]

Protein Z dependent protease inhibitor/protein Z (PZI)

It is a recently described component of the anticoagulant system that is produced in the liver. It inhibits Factor Xa in reaction requiring PZ and calcium.[29]

How does the clotting cascade work, and why is it so complicated.

There are two big starting points in clotting "intrinsic" and "extrinsic" (though I believe this is outdated language). "Intrinsic" clotting is essentially a cascade of factors being activated which in turn activate other factors, down the line until Tissue Factor (from the "extrinsic" pathway and a protein that is released when cells are damaged) is released, leading to the production of Thrombin (the clotting factor that initiates the creation of fibrin and creates the fibrous net that platelets stick to to create the clot).

What I don't get is what causes clots to be generated "spontaneously" - isn't TF needed in order to finish the cascade? Also, why do things like DVT happen without injury: it seems that essentially "slow blood" can clot without some external factor causing the clot. Is this true, or is there always an underlying injury that starts the reaction?

Regarding DVT - the classic description of what predisposes to thrombus is called Virchow's Triad, and the components are stasis of blood flow, endothelial injury, and hypercoagulability.

Stasis: Yes, "slow blood" can clot, as can turbulent or otherwise abnormal blood flow. Two good examples are deep venous thrombosis in patients immobilized for a prolonged period of time and stroke risk in atrial fibrillation. In atrial fibrillation, instead of a nice synchronized contraction of the atria of the heart followed by the ventricles, you have the atria quivering relatively uselessly and the ventricles beating in an irregular manner. The resulting abnormal blood flow creates a huge risk of blood clotting in the atrium. A nice clot in the left atrium is two valves and one ventricle away from being shot out into your aorta where it may happily go up to your brain and cause a stroke. The presence of other factors makes the risk worse - if someone's a chronic vasculopath with tons of atherosclerotic vessel damage (endothelial injury), stasis is especially dangerous, but stasis is bad news on its own. This is why most everyone in the hospital ends up getting anticoagulation for DVT prophylaxis.

Endothelial injury: Damage to the lining of a vessel exposes subendothelial collagen, to which von Willebrand Factor can bind and start promoting thrombus formation. A nasty example here is rupture of an atherosclerotic plaque in a blood vessel, leading to thrombus formation which can either further occlude a vessel or break off and travel as an embolus.

Hypercoagulability: This is your pick of any of the potential causes of genetic or acquired defects that promote coagulation. To give an example, Factor V Leiden is a common one where Factor V is mutated and thus unable to be normally destroyed by activated protein C (an anti-coagulant)

Why Is It Important?

To understand the importance of intrinsic factor, it’s necessary to understand the importance of B12. Vitamin B12 is involved in the metabolism of every cell in the human body. It plays a key role in DNA synthesis and formation, red blood cell creation, and brain function. The human body does not create vitamin B12 on its own, so it must be consumed from the diet. The human digestive tract may have bacteria that produce B12 however, dietary B12 is the best way to ensure adequate nutrition.

Sources of B12 include fish, shellfish, meat, liver, eggs, poultry, and dairy products. Batabata-cha, a Japanese fermented black tea, contains large amounts of B12 which may be bioavailable to humans. [1] This tea is considered to be a vegan source of vitamin B12. Kombucha is also reported to contain varying amounts of B12. Without this essential nutrient, neurologic concerns result and, if left untreated, death follows. But B12 has a concern — it cannot survive the trip through the stomach due to the stomach’s high acid content. Fortunately for us, that’s where intrinsic factor comes to save the day.

Evidence for God from Science

Before we begin this discussion we need to first understand the cascade system.

And point out why is a cascade with so many steps the best design?
Why not fewer or more or more straightforward?

Also contrary to KMart's claims this argument has been successfully refuted before, however I will take a completely novel approach.

would anyone care to take a shot at answering the questions?

Post by August » Wed Sep 21, 2005 12:56 pm

Acts 17:24-25 (NIV)
"The God who made the world and everything in it is the Lord of heaven and earth and does not live in temples built by hands. [25] And he is not served by human hands, as if he needed anything, because he himself gives all men life and breath and everything else."

Post by Byblos » Wed Sep 21, 2005 1:24 pm

^ and at what stage on the evolutionary ladder did it go wrong so as to become a not so ideal design.

It seems that you're looking for a perfect design or lack thereof, to disprove ID. Your intent will backfire my friend as it is precisely the imperfection of the design that goes to the heart of ID. For without it there can be no free will and, by extension, you would not have the freedom to disagree with it.

Post by AttentionKMartShoppers » Wed Sep 21, 2005 1:27 pm

"My actions prove that God takes care of idiots."

He occasionally stumbled over the truth, but hastily picked himself up and hurried on as if nothing had happened.
- On Stanley Baldwin

An atheist can't find God for the same reason a criminal can't find a police officer.

You need to start asking out girls so that you can get used to the rejections.

Post by BGoodForGoodSake » Wed Sep 21, 2005 1:45 pm

Post by BGoodForGoodSake » Wed Sep 21, 2005 1:48 pm

I am assuming that everyone has read the background material and has a general understaning of the cascading clotting mechanism of vertabrates.

First question which needs to be asked is what is the advantage of having so many different proteins involved in the cascading sequence?

And which proteins are really essential for the clotting mechanism to work.

Post by BGoodForGoodSake » Wed Sep 21, 2005 2:32 pm

Well the cascade is very complex indeed as the many factors interact with those down the line and also with those before them in the cascade. This seems very complex until you realize that many of the factors are very similar in build. Perhaps they are the result of duplicate genes which have diverged? No matter lets continue.

The only required protein is of course fibrinogen and the protease which works on it. In this case its thrombin. The thrombin breaks the fibrinogen apart and allows the resulting proteins to stick together.

Another thing to keep in mind is that there are two pathways the extrinsic and the intrinsic pathway. However the extrinsic pathway is much faster compared to the reaction time of the intrinsic pathway. So why have the intrinsic pathway in the first place? Well the intrinsic system responds to damage to cell surfaces as in a cut. While the extrinsic system responds to proteins only found in the bodies tissues not in the bloodstream. This pathway would be activated in the case lets say that your kidney is hemorrhaging.

The intrinsic pathway also creates in the cascading enzymatic action, an anti-thrombin which ceases the action of the protease thrombin (ie. stops clotting). This gives us a clue into why there are so many steps in the intrinsic pathway.

Now we need an analogy to simplify this discussion. Don't worry we will always refer back to the actual chemistry and not depend on the analogy so much. It is only to help us get a picture in our minds to work with.

Lets use a management ladder for the intrinsic pathway, and for the extrinsic one we will use, the emergency response system, like a firehouse.

Now before we go into the next section we need a basic understanding of what a protease is.

It is an enzyme which acts on proteins.

Ok cool, now we can continue. Imagine that each protease can convert 4 molecules a minute.

Now in a thromin fibrinogen system the only enzymatic activity is the thrombin cutting the fibrinogen.
In an organism such as this, like the modern lobster the thrombin material is stored intracellularly. The thrombin is realeased and the process is very slow. So we have
Minute 1 4 fibrinogens cut
Minute 2 4 fibrinogens cut
Minute 3 4 fibrinogens cut
Minute 4 4 fibrinogens cut
Result 16 fibrinogens cut. In a vertebrate with a high pressure vascular system I would have bled to death.

Now lets add a cascade level.
We now have prothrombin in the blood and factor X to cut it is now residing intracellularly. The cell is now damaged releasing factor X. Each factor X cuts 4 molecules a minute, and what is it cutting? Prothrombin.
Each Prothrombin becomes a Thrombin protease which in turn cuts 4 Fibrinogen's a minute. So we have
Minute 1 4 prothrombins cut
Minute 1 4 prothrombins cut 16 fibrinogens cut
Minute 1 4 prothrombins cut 32 fibrinogens cut
Minute 1 4 prothrombins cut 48 fibrinogens cut
Result 96 fibrinogens cut. Increddible I add one step and the process is now 6 times faster!

Now lets take a look at the intrinsic system where there is only one protease acting on factor X. In this system factor X is in an inactive form and requires an enzyme to activate it. Lets call this enzyme factor IX.
When a cell is damaged there are proteins on the surface of a cell which will activate factor IX. So we have.
Minute 1 4 factor IX cut
Minute 2 4 factor IX cut 16 Factor X cut
Minute 3 4 factor IX cut 32 Factor X cut 64 prothrombins cut
Minute 4 4 factor IX cut 48 Factor X cut 128 prothrombins cut 256 fibrinogens cut

So now we can see why there is an advantage to having multiple steps. A small stimulus gets amplified greatly!

One should note that adding more cascading steps will delay the point where actual Thrombine is active. but at this point it will be a large amount of proteins working.

Ok great we have answered the innitial questions. What now?
Well next we will examine the factors more closely and see how they interact.
And we will answer this question, why not add one more step to make the process even faster?

Post by AttentionKMartShoppers » Wed Sep 21, 2005 2:54 pm

You keep on saying that. "it's been done". but you want us to take this on BLIND FAITH? Uh, no thank you.

And, you've. told a lovely story backing up Behe-instead of saying "well, there used to be a simpler path. " you instead say "wow, look at the great advantages of two blood clotting pathways! Are you on our side or are you trying to prove us wrong and showing that IR biological machines can in fact be put together via evolution?

"My actions prove that God takes care of idiots."

He occasionally stumbled over the truth, but hastily picked himself up and hurried on as if nothing had happened.
- On Stanley Baldwin

An atheist can't find God for the same reason a criminal can't find a police officer.

You need to start asking out girls so that you can get used to the rejections.

Post by BGoodForGoodSake » Wed Sep 21, 2005 3:02 pm

You keep on saying that. "it's been done". but you want us to take this on BLIND FAITH? Uh, no thank you.

And, you've. told a lovely story backing up Behe-instead of saying "well, there used to be a simpler path. " you instead say "wow, look at the great advantages of two blood clotting pathways! Are you on our side or are you trying to prove us wrong and showing that IR biological machines can in fact be put together via evolution?

I'm getting there, I thought you would be able to appreciate that I am laying the framework for a discussion. Who cares if its been done before or not, I wanted to use a novel approach, read the first post.
Please read posts before responding.

I will give you a link to an example of rebuttal but only after we have finished this discussion, because I know that it will take away from our discussion and take things off topic. Please, I am putting alot of effort and time into this discussion, if you are going to persist in sabataging the effort, I am going to have to beg you to stop.

Post by AttentionKMartShoppers » Wed Sep 21, 2005 5:35 pm

"My actions prove that God takes care of idiots."

He occasionally stumbled over the truth, but hastily picked himself up and hurried on as if nothing had happened.
- On Stanley Baldwin

An atheist can't find God for the same reason a criminal can't find a police officer.

You need to start asking out girls so that you can get used to the rejections.

That there deal that clots blood

Post by Jbuza » Wed Sep 21, 2005 5:38 pm

And point out why is a cascade with so many steps the best design?

Why not fewer or more or more straightforward?

What is the point of these questions? Are you asking if happenstance could have created a more streamlined design? I don't understand what you are looking for here. How about lets design a working alternative that is more simple. From a strictly scientific approach the most simple system to answer the need should be in place. IF there is in fact a cascade mechanism with "fewer or more straightforward steps" that would answer the need than it would only point to design. REdudant failsafes, complex interactions, these aren't the realm of science they are the realm of design.

Post by AttentionKMartShoppers » Wed Sep 21, 2005 5:43 pm

"My actions prove that God takes care of idiots."

He occasionally stumbled over the truth, but hastily picked himself up and hurried on as if nothing had happened.
- On Stanley Baldwin

An atheist can't find God for the same reason a criminal can't find a police officer.

You need to start asking out girls so that you can get used to the rejections.

Post by Jbuza » Wed Sep 21, 2005 5:47 pm

And we will answer this question, why not add one more step to make the process even faster?

People already have problems with clot formations, wouldn't speeding up or improving the clotting factor of blood lead to more stroked and heart attacks. It is not possible to improve on the clotting factor of blood. Because an intelligence far beyond ours created it.

Post by Kurieuo » Wed Sep 21, 2005 6:20 pm

I've been following to some extent these many design discussions. Quite frankly, I don't feel the issue raised is being dealt with. Both sides seem focused on two entirely different topics. Kmart appears more focused on "irreducible complexity," which is the topic I believe this all begun with. And BGood appears focused on the whodunnit factor (i.e., God) judging by the original questions of this thread. When I saw that KMart was introducing the blood clotting system, I saw it being presented as a case of an "irreducibly complex" system devoid of whodunnit.

The questions of "why is a cascade with so many steps the best design?" or "Why not fewer or more or more straightforward?" is simply irrelevent to what I see KMart has been trying emphasise—that irreducibily complex systems exist within biology. Yet such questions are also irrelevant for different reasons when put forward against Christian theism (not ID—note the difference), because in the end no matter what an all-powerful God would design, one can always say "well why didn't he do it better?" Of course unless God creates God which is logically impossible (for anything created wouldn't have been eternal), it can always be asked why didn't God make something better. Therefore a fallacy is committed within such questions, because 1) they rig standards logically unattainable in any system if such a system was indeed designed by an all-powerful God and 2) they beg the question in assuming God's purpose in creating was to create the most perfect world.

Getting off the topic of "theism" now, and somewhat back to ID and its "irredicible complexity," it is no good to simply say, "such a system has been described" (that is, how the blood clotting system gradually arose has been described), and then want to leave it at that. Isn't this point one of the main points of focus throughout all these discussions? If I began a discussion that sets out to prove God exists, non-theists respond, and then I declare that God does exist because he has been experienced by people. Surely, I am not in some way being intellectually unfair in proclaiming I'm right without really getting into the discussion? So if how blood clotting arose can be described in a step-by-step evolutionary manner (which would show it isn't "irreducibly complex"), then please provide the relevant scientific articles.

Additional note: In relation to this last paragraph, I just noticed the post I was referring to has now been edited, so to some extent it doesn't apply anymore, although articles describing how the blood clotting process gradually came about would be still appropriate to refuting that such a system is irreducibily complex.

Watch the video: 04 Μπερτ: από ξαπλωτή θέση σε καθιστή με τη βοήθεια κουπαστής κρεβατιού GR (May 2022).


  1. Akikree

    Complete bad taste

  2. Dorian

    Straight to the bull's eye

  3. Nilrajas

    I think this is the brilliant idea

  4. Dureau

    the answer Competent, it's entertaining ...

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