We all learned the Darwin Double-Step, or "dubstep" for short, as children in school. Oh what fun we had. If you know the lyrics sing along with me:
Neckie the Slightly-Longer-Necked Giraffe
Had a slightly longer neck
And if you ever saw it
You lived a million years ago (like a lightbulb!)
All of the other giraffes
Used to laugh and call him names
They never let poor Neckie
Play in any giraffe games
Then one terrible drought season
All the leaves on the lower branches were eaten
Then Neckie with his neck so long
Ate leaves from the higher branches
Then all the other giraffes
Died horribly of starvation
Neckie never had any kids and the entire species died out
Because there were no females with the same mutation! (you sexist pig!)
Hmmm. Actually I think that may have been the naughty creationist version they were not allowed to teach us in school. Let me try again:
Neckie the Slightly-Longer-Necked Giraffe
Had a slightly longer neck
And if you ever saw it
You lived a million years ago (like a lightbulb!)
All of the other giraffes
Used to laugh and call him names
They never let poor Neckie
Play any giraffe games
Then poor Neckie got thirsty
And traveled to the water hole
He bent his head down to take a drink
And all the blood went straight to his head
Neckie didn't have the special blood valves
That all modern giraffes have in their neck
So the first time he tried to take a drink
He died of a brain aneurysm! (more blood than Kill Bill!)
Okay, I lied. That was another naughty creationist version they never taught you in school. I don't actually remember the real version. The lyrics to the real version don't fit the melody very well and the creationist ones are pretty much right on, so they are easier to remember.
"What does this have to do with the fourth video?" you might be asking. Well, not much to be honest, but since the material here is not very original I thought I'd take the opportunity to discuss Michael Behe's thesis in The Edge of Evolution, which actually is related to the malaria versus sickle cell anemia relationship, which Behe describes as evolutionary "trench warfare". Trench warfare as practiced during World War I was a strategy of attrition: everybody is dying by the millions with no military objectives achieved, but I'm betting that you run out of guys before I do. Evolution operates that way, at least in the real world. Once an organism runs out of genes it can break without killing itself, it's out of options. And anyway it's not a great idea to break genes unless there's a severe selective pressure involved, the kind that kills.
Briefly, malaria is a disease caused by parasitic bacteria that survive by consuming human hemoglobin right inside living human blood vessels. It is both deadly and very common in certain parts of the world. Sickle cell anemia is a human genetic disease caused by a mutation affecting hemoglobin which also confers resistance to malaria. It is caused by a point mutation in one out of two hemoglobin genes. If both genes have the mutation, the person dies very early in development. Sickle cell anemia is clearly the result of a broken gene that has only been passed on because it confers some resistance to malaria. It certainly wasn't passed on because it severely inhibits normal hemoglobin function. It's a pretty nice demonstration of the power of Darwinian evolution to destroy things if there's a fitness benefit involved. In that respect, it's no different than the other examples in these videos and does not require a separate argument.
But Behe's main thesis in the book involves the most common malaria causing bacteria, P. falciparum. Humans have been using an anti-malarial drug called chloroquine for about fifty years, and a certain strain of P. falciparum has evolved a resistance to it. In fact, this resistance required the performance of an extremely rare Darwin Double-Step, and is far more interesting than the single-step sickle cell anemia mutation. Behe calls this specific example of the Darwin Double-Step the "chloroquine complexity cluster" (CCC). It's a double point mutation that appears to cause a leak in a particular organelle where chloroquine would normally concentrate and kill the bug. The leak allows chloroquine to leak out of the organelle into the cytoplasm, drastically reducing its concentration and toxicity. The protein in question appears to be important enough to the bug's survival that it cannot simply be deleted, a job which any number of single mutations could accomplish. The double mutation is required to first cause the leak and then partly compensate for the change in its structure and accompanying loss of function. Simply causing the leak by messing up the protein doesn't appear to work, and the likely explanation is the cell needs the protein in a marginally functional capacity to survive. Like most mutations of this kind, the CCC appears to cause a loss of absolute fitness versus the wild type in a normal environment and only confers a fitness advantage in the presence of the very strong selective pressure of chloroquine.
Now at this point evolutionists would ask what the difference is between a single mutation and a double mutation. No, they haven't forgotten how to count and they still have all their fingers. Their contention is that once a single mutation occurs and provides a benefit, natural selection acts on that benefit and the mutation spreads throughout the entire population. Then the species can start over from a new, higher baseline and the process repeats over and over and over for a very long time, making dramatic changes possible. The problem in this particular case, and as far as we know in most other hypothesized cases, is that a Darwin Double-Step is required before the organism gets any benefit at all. In other words, the first mutation, whichever of the two occurs first, confers no benefit. Therefore natural selection cannot act on it and spread it through the population. In fact, the first mutation appears to be deleterious, causing a significant degradation in fitness and is actually more likely to be selected out completely, much less spread through the population. Yet the trait exists. Why? Most likely, both mutations occurred at the same time in the same individual. Poor Neckie the Slightly-Longer-Necked Giraffe would have been saved by a Darwin Double-Step giving him both a longer neck and special valves in his neck all at once. (I knew there was a connection somewhere!)
The probabilities involved for two successive single mutations versus a Darwin Double-Step are quite different. In the first case the second mutation can occur anywhere in the entire population as long as the first mutation has taken over. The second mutation then has the same probability as the first mutation, just minus the amount of time it took the first one to take hold. For a Darwin-Double Step, however, both mutations happening at the same time in the same organism multiplies the probabilities together, increasing the difficulty by many, many orders of magnitude. The same principle is at work in the Powerball lottery. The probability of matching one ball is much, much higher than the probability of matching all six in one draw. A Darwin Double-Step is a very rare occurrence, but one appears to have occurred in P. falciparum within the last fifty years. Behe estimates the total number of bugs that have lived and died in that time to be around 10^20, and assigns the probability of 10^-20 to the CCC. He then estimates the total number of organisms that have lived in the entire history of life to be around 10^40, and concludes the maximum number of steps we should rationally expect Darwinian evolution to be capable of achieving at one time with those probabilistic resources is a double-CCC corresponding to a probability of 10^-40, or a Darwin Four-Step. (Not quite the same ring to that one.) Behe equates a CCC to the difficulty of finding a new protein-protein binding site, and a double-CCC to finding via Darwinian processes two novel protein-protein binding sites. In doing so, he makes very generous assumptions, since even a single protein-protein binding site has been experimentally found to require five or six mutations, none of which are independently beneficial nor selectable, and the CCC required only two mutations. He concludes that just two novel binding sites appearing together is beyond the edge of evolution, which corresponds to complexes of three or more proteins. Most proteins operate in complexes of six or more, far beyond the edge.
Initially most public critics argued that Behe had gotten the probabilities wrong because the CCC was most likely two successive single mutations, which is hilarious because that actually hurts their case. Here Behe went to all the trouble of finding a double mutation that was actually, empirically, observed to occur and using it to propose a limit, or edge, to evolution, and the immediate response of the critics was to restrict his edge of evolution even further, without realizing that's what they were doing! "You're wrong about something, even if it hurts our position," was the response. It was all quite entertaining, especially considering that Behe referenced everything to the scientific literature. After having examined much of it myself, his case that chloroquine resistance is caused by a double mutation of the type he describes is very strong. There really are quite a lot of very stupid but well-educated and well-credentialed people in the world who think they are really smart.
The main problem seems to be that evolutionists believe there is always a pathway of single step mutations from one protein function to another, different function. Behe was trying to give the benefit of the doubt and suggest that a Darwin Double-Step, despite its rarity, was allowable as a regular evolutionary mechanism in the search for mutational pathways between functions and got reamed by a bunch of idiots who didn't understand he was being generous. As usual, he was operating several steps ahead of his critics and only failed in his overestimation of their intelligence. Behe, and most biochemists with their heads on straight, knows that there simply cannot be an unlimited supply of single-step pathways between functional proteins. Yet this is a fundamental assumption of neo-Darwinism. Evolutionists do not respond well to the contention that single step pathways may not exist in the required number because they probably know that the theory cannot explain all of biological diversity without them. The observable, empirical, scientific evidence suggests rather strongly that a very high proportion of mutations are either neutral or deleterious to the protein's function. Natural selection either doesn't favor it over the wild-type in the case of a neutral mutation or actually works against it in the case of a deleterious mutation, selecting it out of the population because it's harmful to fitness. Evolution cannot advance neutral mutations in a Darwinian fashion and must depend on luck, otherwise known as "genetic drift", in order for the mutation to spread through the population, which doesn't really help the probabilities like natural selection does. In the case of deleterious mutations it's back to square one for the population rather quickly, since the organism with the mutation gets pwned by natural selection.
Evolutionists cannot simply assume that single or even double step pathways exist. They must demonstrate such pathways exist empirically. If neo-Darwinian evolution is true then there must be an awful lot of these pathways within the protein shape space and it should not be hard to find them. They must specify which specific mutations are incrementally beneficial to fitness and also lead to novel protein functions and prove it through experimentation, otherwise no one is under any obligation to believe their cute little fables. That's how science works. Until then, they have less than nothing. They have fairy tales and a belief in something they have not observed. Last I checked, that's precisely their oft-repeated criticism of religion.
Now that's whack.
Neckie the Slightly-Longer-Necked Giraffe
Had a slightly longer neck
And if you ever saw it
You lived a million years ago (like a lightbulb!)
All of the other giraffes
Used to laugh and call him names
They never let poor Neckie
Play in any giraffe games
Then one terrible drought season
All the leaves on the lower branches were eaten
Then Neckie with his neck so long
Ate leaves from the higher branches
Then all the other giraffes
Died horribly of starvation
Neckie never had any kids and the entire species died out
Because there were no females with the same mutation! (you sexist pig!)
Hmmm. Actually I think that may have been the naughty creationist version they were not allowed to teach us in school. Let me try again:
Neckie the Slightly-Longer-Necked Giraffe
Had a slightly longer neck
And if you ever saw it
You lived a million years ago (like a lightbulb!)
All of the other giraffes
Used to laugh and call him names
They never let poor Neckie
Play any giraffe games
Then poor Neckie got thirsty
And traveled to the water hole
He bent his head down to take a drink
And all the blood went straight to his head
Neckie didn't have the special blood valves
That all modern giraffes have in their neck
So the first time he tried to take a drink
He died of a brain aneurysm! (more blood than Kill Bill!)
Okay, I lied. That was another naughty creationist version they never taught you in school. I don't actually remember the real version. The lyrics to the real version don't fit the melody very well and the creationist ones are pretty much right on, so they are easier to remember.
"What does this have to do with the fourth video?" you might be asking. Well, not much to be honest, but since the material here is not very original I thought I'd take the opportunity to discuss Michael Behe's thesis in The Edge of Evolution, which actually is related to the malaria versus sickle cell anemia relationship, which Behe describes as evolutionary "trench warfare". Trench warfare as practiced during World War I was a strategy of attrition: everybody is dying by the millions with no military objectives achieved, but I'm betting that you run out of guys before I do. Evolution operates that way, at least in the real world. Once an organism runs out of genes it can break without killing itself, it's out of options. And anyway it's not a great idea to break genes unless there's a severe selective pressure involved, the kind that kills.
Briefly, malaria is a disease caused by parasitic bacteria that survive by consuming human hemoglobin right inside living human blood vessels. It is both deadly and very common in certain parts of the world. Sickle cell anemia is a human genetic disease caused by a mutation affecting hemoglobin which also confers resistance to malaria. It is caused by a point mutation in one out of two hemoglobin genes. If both genes have the mutation, the person dies very early in development. Sickle cell anemia is clearly the result of a broken gene that has only been passed on because it confers some resistance to malaria. It certainly wasn't passed on because it severely inhibits normal hemoglobin function. It's a pretty nice demonstration of the power of Darwinian evolution to destroy things if there's a fitness benefit involved. In that respect, it's no different than the other examples in these videos and does not require a separate argument.
But Behe's main thesis in the book involves the most common malaria causing bacteria, P. falciparum. Humans have been using an anti-malarial drug called chloroquine for about fifty years, and a certain strain of P. falciparum has evolved a resistance to it. In fact, this resistance required the performance of an extremely rare Darwin Double-Step, and is far more interesting than the single-step sickle cell anemia mutation. Behe calls this specific example of the Darwin Double-Step the "chloroquine complexity cluster" (CCC). It's a double point mutation that appears to cause a leak in a particular organelle where chloroquine would normally concentrate and kill the bug. The leak allows chloroquine to leak out of the organelle into the cytoplasm, drastically reducing its concentration and toxicity. The protein in question appears to be important enough to the bug's survival that it cannot simply be deleted, a job which any number of single mutations could accomplish. The double mutation is required to first cause the leak and then partly compensate for the change in its structure and accompanying loss of function. Simply causing the leak by messing up the protein doesn't appear to work, and the likely explanation is the cell needs the protein in a marginally functional capacity to survive. Like most mutations of this kind, the CCC appears to cause a loss of absolute fitness versus the wild type in a normal environment and only confers a fitness advantage in the presence of the very strong selective pressure of chloroquine.
Now at this point evolutionists would ask what the difference is between a single mutation and a double mutation. No, they haven't forgotten how to count and they still have all their fingers. Their contention is that once a single mutation occurs and provides a benefit, natural selection acts on that benefit and the mutation spreads throughout the entire population. Then the species can start over from a new, higher baseline and the process repeats over and over and over for a very long time, making dramatic changes possible. The problem in this particular case, and as far as we know in most other hypothesized cases, is that a Darwin Double-Step is required before the organism gets any benefit at all. In other words, the first mutation, whichever of the two occurs first, confers no benefit. Therefore natural selection cannot act on it and spread it through the population. In fact, the first mutation appears to be deleterious, causing a significant degradation in fitness and is actually more likely to be selected out completely, much less spread through the population. Yet the trait exists. Why? Most likely, both mutations occurred at the same time in the same individual. Poor Neckie the Slightly-Longer-Necked Giraffe would have been saved by a Darwin Double-Step giving him both a longer neck and special valves in his neck all at once. (I knew there was a connection somewhere!)
The probabilities involved for two successive single mutations versus a Darwin Double-Step are quite different. In the first case the second mutation can occur anywhere in the entire population as long as the first mutation has taken over. The second mutation then has the same probability as the first mutation, just minus the amount of time it took the first one to take hold. For a Darwin-Double Step, however, both mutations happening at the same time in the same organism multiplies the probabilities together, increasing the difficulty by many, many orders of magnitude. The same principle is at work in the Powerball lottery. The probability of matching one ball is much, much higher than the probability of matching all six in one draw. A Darwin Double-Step is a very rare occurrence, but one appears to have occurred in P. falciparum within the last fifty years. Behe estimates the total number of bugs that have lived and died in that time to be around 10^20, and assigns the probability of 10^-20 to the CCC. He then estimates the total number of organisms that have lived in the entire history of life to be around 10^40, and concludes the maximum number of steps we should rationally expect Darwinian evolution to be capable of achieving at one time with those probabilistic resources is a double-CCC corresponding to a probability of 10^-40, or a Darwin Four-Step. (Not quite the same ring to that one.) Behe equates a CCC to the difficulty of finding a new protein-protein binding site, and a double-CCC to finding via Darwinian processes two novel protein-protein binding sites. In doing so, he makes very generous assumptions, since even a single protein-protein binding site has been experimentally found to require five or six mutations, none of which are independently beneficial nor selectable, and the CCC required only two mutations. He concludes that just two novel binding sites appearing together is beyond the edge of evolution, which corresponds to complexes of three or more proteins. Most proteins operate in complexes of six or more, far beyond the edge.
Initially most public critics argued that Behe had gotten the probabilities wrong because the CCC was most likely two successive single mutations, which is hilarious because that actually hurts their case. Here Behe went to all the trouble of finding a double mutation that was actually, empirically, observed to occur and using it to propose a limit, or edge, to evolution, and the immediate response of the critics was to restrict his edge of evolution even further, without realizing that's what they were doing! "You're wrong about something, even if it hurts our position," was the response. It was all quite entertaining, especially considering that Behe referenced everything to the scientific literature. After having examined much of it myself, his case that chloroquine resistance is caused by a double mutation of the type he describes is very strong. There really are quite a lot of very stupid but well-educated and well-credentialed people in the world who think they are really smart.
The main problem seems to be that evolutionists believe there is always a pathway of single step mutations from one protein function to another, different function. Behe was trying to give the benefit of the doubt and suggest that a Darwin Double-Step, despite its rarity, was allowable as a regular evolutionary mechanism in the search for mutational pathways between functions and got reamed by a bunch of idiots who didn't understand he was being generous. As usual, he was operating several steps ahead of his critics and only failed in his overestimation of their intelligence. Behe, and most biochemists with their heads on straight, knows that there simply cannot be an unlimited supply of single-step pathways between functional proteins. Yet this is a fundamental assumption of neo-Darwinism. Evolutionists do not respond well to the contention that single step pathways may not exist in the required number because they probably know that the theory cannot explain all of biological diversity without them. The observable, empirical, scientific evidence suggests rather strongly that a very high proportion of mutations are either neutral or deleterious to the protein's function. Natural selection either doesn't favor it over the wild-type in the case of a neutral mutation or actually works against it in the case of a deleterious mutation, selecting it out of the population because it's harmful to fitness. Evolution cannot advance neutral mutations in a Darwinian fashion and must depend on luck, otherwise known as "genetic drift", in order for the mutation to spread through the population, which doesn't really help the probabilities like natural selection does. In the case of deleterious mutations it's back to square one for the population rather quickly, since the organism with the mutation gets pwned by natural selection.
Evolutionists cannot simply assume that single or even double step pathways exist. They must demonstrate such pathways exist empirically. If neo-Darwinian evolution is true then there must be an awful lot of these pathways within the protein shape space and it should not be hard to find them. They must specify which specific mutations are incrementally beneficial to fitness and also lead to novel protein functions and prove it through experimentation, otherwise no one is under any obligation to believe their cute little fables. That's how science works. Until then, they have less than nothing. They have fairy tales and a belief in something they have not observed. Last I checked, that's precisely their oft-repeated criticism of religion.
Now that's whack.
