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Author Topic:   "The Edge of Evolution" by Michael Behe
Colin
Junior Member (Idle past 5245 days)
Posts: 27
From: Adelaide, Australia.
Joined: 10-14-2009


Message 16 of 149 (531086)
10-16-2009 5:01 AM
Reply to: Message 12 by Modulous
10-14-2009 9:18 PM


Re: What Behe's calculations actually mean for human evolution
Hello again, your are right when you say I am citing a specific and asking about a general. Let me discuss for a moment what I think Behe is getting at.
Actually before this, let me discuss the issue of setting targets for evoluiton. I understand the fallacy of such comments like, the probability of humans turning out exactly like we see is x, which is very small, therefore evolution could not have occurred. I have heared this going around, but I do not believe this is the type of argument Behe is making. He has defined a unit of probablility which he calls a CCC, or chloroquine complexity cluster, which is the probability of an oraganism achieving a step with the difficulty of that faced by malaria, in regards to developing a resistance. This is a loaded statement and alone is enough to spark fierce debate. So let me read between the lines and lay it down the way I see it. As I have stated, this unit of probability is referring to observed events. In the thoretical world it is very hard to define. Imagine if we were to try to define this probability theoretically, before the outcome was observed. What is the chances that Darwinian evolution will find a solution in malaria for chloroquine? Well, we have no idea how many solutions there are, or how complex they are. We could call the answer a guess at best. But having ran the experiment we can see what actually does happen in the given time. Remember, malaria was free to try all and any mutations available for any solution, no matter how simple or grand. Including avoiding the problem all together by sourcing a different living. Is this setting a target for evolution? Yes. Absolutely. But is it wrong of me to say that evolution is said to be able to cause a species to survive due to the process of mutation and natural selection? No specifics were applied to this hindisghted test, other than to survive. And survive they did. Had they become extinct, this still would not be a problem for evoluiton. Since evoluton assumes extinction to be a relatively common event.
The question is, can this specific example be used at all to make judgements on evolution in general? It depends on the assumptions we make, and what we believe to be reasonable. We are dealing with probability after all. If you assume that this is a special case, and normally the process of evoluiton would have found many solutions much sooner, then the discussion can not really go much further. If however, the step from suseptible to resistant, is typical in likelyhood to other problems, then evolution has a real problem.
Let me discuss the problems bit, form above. Again, evoluiton has no foresight, no ambition, no plans. But we do believe it tends to develop a species into other species, correct? For example, given a primitave Earth with little variation in species, can we expect evolution to create diverse eco systems? Or is what happened here on Earth just a lucky lottety ticket? Given what we see around us, and assuming evolution to be true, can we conclude that evolution acts not only to develop a species so that at least a small number of brances will continue to reproduce, but that the trend will be upwards evolution, to more complex organisms. If we assume that life on Earth started with simple celled organisms, it cannot exactly go backwards. Like I said, the option of concluding that Earth is just the lucky planet is always available, which, i'll change my mind, will probaly lead to completely different topic of debate rather than end it. So by problem, I mean, from a particular state, a species has many steps set out before it. Some lead to death or deformity, some are neutral, some impede the creature, others benefit the creature. Where I believe we may disagree, is on the issue of how many options are open that will benefit the species? And how likely are they? I dont think the available options are plentiful. If a structure for something or other is partially complete (I know, targets!) there is a limmited number of useful, beneficial ways in which to improve this structure for the species sake. But this is talking about hypothetical machines. A shark didnt need to develop long range sensors, it could have developed a signal generator that lured fish right into its mouth! For example. But how can we possibly imagine all possible scenarios and then decide how likely they are? Maybe some day, but not now.
That is where Behes unit of probability comes in. If, developing an advantage in an environment is on par with the difficulty of malaria developing an advantage in its environment, then we can estimate the likelyhood of it happening. If more solutions are available from that point, the species is more likely to prosper. If the solutions are also more simple, the species is again more likely to prosper. (I know there is much more on this to be said)
The question is, in all the possibilities open before an organism, how many are there that even create a working thing? And how many of these are beneficial to the creature? And how do these options remaining, compare to the task of developing ANY soluiton to a poisonous drug to trillions upon trillions of malaria?
Edited by Colin, : No reason given.

This message is a reply to:
 Message 12 by Modulous, posted 10-14-2009 9:18 PM Modulous has replied

Replies to this message:
 Message 18 by Modulous, posted 10-16-2009 8:51 AM Colin has replied

  
Colin
Junior Member (Idle past 5245 days)
Posts: 27
From: Adelaide, Australia.
Joined: 10-14-2009


Message 17 of 149 (531088)
10-16-2009 5:06 AM
Reply to: Message 14 by bluegenes
10-15-2009 5:57 AM


Re: Targets are for creationists.
Hi, "targets" is a big topic in its self, and i know iv'e left myself open. I have responded a little about this to modulus's comment. But i am not avoiding the issue. I will go into more detail a bit later.

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Modulous
Member
Posts: 7801
From: Manchester, UK
Joined: 05-01-2005


Message 18 of 149 (531122)
10-16-2009 8:51 AM
Reply to: Message 16 by Colin
10-16-2009 5:01 AM


Re: What Behe's calculations actually mean for human evolution
Hi - I trust this place is growing on you!
If, developing an advantage in an environment is on par with the difficulty of malaria developing an advantage in its environment, then we can estimate the likelyhood of it happening
That's a big if, and there is no evidence to suggest it is true and plenty of evidence to suggest that it is not true. Malaria had a very significant and highly specific problem to adapt to which presented a huge selection pressure. Humans as a species, for example, would not survive such a selective pressure. My post did go into this. What do you have to say about what I already said so I don't repeat myself needlessly?
Edited by Modulous, : No reason given.

This message is a reply to:
 Message 16 by Colin, posted 10-16-2009 5:01 AM Colin has replied

Replies to this message:
 Message 21 by Colin, posted 10-16-2009 10:05 PM Modulous has replied

  
Dr Adequate
Member (Idle past 284 days)
Posts: 16113
Joined: 07-20-2006


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Message 19 of 149 (531124)
10-16-2009 8:54 AM
Reply to: Message 5 by Colin
10-14-2009 5:27 PM


Re: Needs more information
Consider the Malarial parasite as a real life case study for evolution. since an anti malarial drug "chloroquine" was first mass produced sometime during WW2, it is thought that malaria developed resistance to the drug about 4 times independently. Behe is happy to call this less than 10, to be safe. All of the known resistant malarial strains have common changes in 2 amino acids, located in a section of DNA which encodes for a protein pump.
Other later drugs, put up much less of a fight, and became ineffective much quicker, sometimes just weeks. These drugs could be overcome by a mutation of just one of several amino acids.
By taking the estimated number of chloroquine resistant strains (10) over the past half century, the approximate number of malarial parasites in each infected host (1 trillion), and the estimated number of infected hosts in the same time 10 million, the chances of malaria developing a resistance to chloroquine is approximately 1 in 10^20.
But the fallacy here seems obvious. The fact that resistance "only" evolved four times is not an indictment of the failure of mutation to produce the necessary alleles, but rather a testament to the efficiency of natural selection in spreading it. Indeed, if the areas where malaria existed were contiguous, and chloroquine was used throughout that area, we might well have expected resistance to have evolved only once.
Indeed, if you think about the random nature of mutations, it is obvious that the mutations in question must have arisen literally millions and millions of times in the past --- they just never got spread by natural selection, because we hadn't invented chloroquine at that point. But once we did, and they were spread by natural selection, they could no longer arise. Because they were already present.
Edited by Dr Adequate, : No reason given.
Edited by Dr Adequate, : No reason given.

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Replies to this message:
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 Message 55 by Kaichos Man, posted 10-20-2009 8:38 PM Dr Adequate has replied

  
traderdrew
Member (Idle past 5153 days)
Posts: 379
From: Palm Beach, Florida
Joined: 04-27-2009


Message 20 of 149 (531170)
10-16-2009 11:26 AM
Reply to: Message 19 by Dr Adequate
10-16-2009 8:54 AM


Re: Needs more information
But the fallacy here seems obvious.
There is no fallacy. What colin posted was under the chapter of "What Evolution Can Do." Everything else in your post I agree with.

This message is a reply to:
 Message 19 by Dr Adequate, posted 10-16-2009 8:54 AM Dr Adequate has replied

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Colin
Junior Member (Idle past 5245 days)
Posts: 27
From: Adelaide, Australia.
Joined: 10-14-2009


Message 21 of 149 (531299)
10-16-2009 10:05 PM
Reply to: Message 18 by Modulous
10-16-2009 8:51 AM


Re: What Behe's calculations actually mean for human evolution
Yes, this place is definitely growing on me! About the big "if." It is a big if, but not totally necessary. I don't think for a moment he is suggesting that all advantages are as complex, he is just making an arbitrary benchmark for comparison. But i think he is assuming it is not all that special either, in terms of developing new body plans in general, in one of MANY directions.
There surely must be a limited number of the potential advantageous mutations in mammals for example, that you refer to. In trying to compare this situation with malaria, you are correct in saying that firstly malaria had a very specific problem and the solution was highly selective. This is true, but necessary in order to be able to make any reasonably defined calculations on the observations. It would be very hard to judge or even keep track of general advantageous changes. But also keep in mind that the type of solution or mutations were not limited for the example. So, getting back to comparing this example to the potential mammal examples you talk about. Under no specific selective pressure, a whole new diverse range of options are open, making the event more likely. However, the number of trials are greatly reduced, even considering our macro bodies, to the comparative number of malaria, reducing the probability. Also, I believe Behe would have probably had in mind the fact that if an advantage requires a string of changes, even accounting for the range of multiple possible paths along the way, the event of finding any advantage becomes more unlikely. Again, I think we have different perceptions or expectations about how many legitimate paths of advantage are actually open. Dawkin's if i remember rightly, refers to this as "animal space" or something similar. It could be imagined as three dimensions, but in fact would have many dimensions. Legitimate paths would consist of small beneficial steps, connected by reasonable possibility of achieving those steps, leading to more complex structures that also give advantage. From an engineering perspective, i imagine these paths would be very tight. In the last comments, i realize i am again attributing goals of some sort to the process of evolution, but only in the light of observing our world, and assuming that this must be the trend.

This message is a reply to:
 Message 18 by Modulous, posted 10-16-2009 8:51 AM Modulous has replied

Replies to this message:
 Message 25 by Modulous, posted 10-17-2009 6:48 AM Colin has replied

  
Dr Adequate
Member (Idle past 284 days)
Posts: 16113
Joined: 07-20-2006


(1)
Message 22 of 149 (531317)
10-17-2009 12:11 AM
Reply to: Message 20 by traderdrew
10-16-2009 11:26 AM


Fallacy
There is no fallacy.
I think there is. Behe is apparently trying to estimate the difficulty or improbability of malaria parasites evolving chloroquine resistance by counting the number of times it happened.
I think my post makes it clear that why that's not a legitimate procedure.
Edited by Dr Adequate, : No reason given.

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Colin
Junior Member (Idle past 5245 days)
Posts: 27
From: Adelaide, Australia.
Joined: 10-14-2009


Message 23 of 149 (531333)
10-17-2009 4:39 AM
Reply to: Message 22 by Dr Adequate
10-17-2009 12:11 AM


Re: Fallacy (+ new argument of sickle gene)
I must admit, I had misunderstood your first argument. The section where Behe is talking about this, he mentions things such as the time taken for the first resistant strain to show, the fact that when the drug is removed the resistant strains decrease, and uses the words "spontaneous resistance" to describe new cases of resistance. Reading between the lines, I suspect that the sources he cites for this information were able to tell the difference between inherited resistance and spontaneous resistance, and would have the common sense to not include malaria carriers of resistant strains in a region as "trials" to find an already present resistance. Of course this is an assumption, i wonder if Behe himself would be willing to comment on this by email. It's worth a try. It is clear that the history of chloroquine use is not as simple as assuming continued widespread use in regions despite a known resistance being present. Will have to do some research and come back to this. (in the interest of thoroughness)
--- Major New Line of Argument --- No sidestep intended
I had forgotten, but another post reminded me that Behe makes a point about another resistance that has yet to be overcome at all, based on our current knowledge. And that is the sickle gene. Apparently thousands of years old, the trait gives a person resistance to malaria, and to date, malaria has found no solution. This is highlighted by Behe as an example of something evolution cannot seem do (at least yet). Again considering the vast numbers of malaria available to crunch the numbers, such a case suggests that if a step of similar complexity stood between our ancestors and a particular beneficial mutation, it would not happen. Even giving that at any one time, not one, but many such opportunities for developing an advantage may exist. The number of potential (and theoretical) paths to advantage, could not reasonably offset the population size of malaria.
Again, the obsession with malaria here, is that it is a real example of evolution causing an organism to adapt to its environment, and the efficiency at which it does so. You may suggest that with such deep time on our hands efficiency is not really an issue. But if organisms are said to crack the code to successful body plans with "brute force," then even with deep time, efficiency remains an issue.

This message is a reply to:
 Message 22 by Dr Adequate, posted 10-17-2009 12:11 AM Dr Adequate has replied

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 Message 26 by Dr Jack, posted 10-17-2009 6:57 AM Colin has not replied

  
Dr Adequate
Member (Idle past 284 days)
Posts: 16113
Joined: 07-20-2006


(1)
Message 24 of 149 (531341)
10-17-2009 6:06 AM
Reply to: Message 23 by Colin
10-17-2009 4:39 AM


Sickle Cell
I had forgotten, but another post reminded me that Behe makes a point about another resistance that has yet to be overcome at all, based on our current knowledge. And that is the sickle gene. Apparently thousands of years old, the trait gives a person resistance to malaria, and to date, malaria has found no solution. This is highlighted by Behe as an example of something evolution cannot seem do (at least yet).
Human malaria itself may be as little as 3000 years old.
You don't say where you got the figure for the age of sickle cell. But I don't actually think it's time that's been the problem for Plasmodium. We know that almost inevitably, to become better adapted to one environment is to become worse adapted to the original environment. And people with the sickle-cell allele are in a minority. It is possible that some parasite, or many of them, have come up with just the right mutations to live in the red blood cells of people with the sickle-cell allele (we may note in this connection that sometimes malaria does successfully infect people with the sickle-cell allele). But it is not at all clear that such a variation would ever be favored by natural selection.
Again considering the vast numbers of malaria available to crunch the numbers, such a case suggests that if a step of similar complexity stood between our ancestors and a particular beneficial mutation, it would not happen.
Any particular beneficial mutation? I suppose not. Evolution produces adaptation, not perfection. I guess that's why we're not all immune to all diseases. And why all diseases aren't able to overcome all our mechanisms of immunity. Oh look, evolution fails twice!
Meanwhile, that ol' Intelligent Designer is so smart that all of his creations are perfect. I wonder why we never see any of 'em.
Again, the obsession with malaria here, is that it is a real example of evolution causing an organism to adapt to its environment, and the efficiency at which it does so.
And, fortuitously, a case where it would be downright immoral to perform pretty much any relevant experiment one can think of.
Edited by Dr Adequate, : No reason given.
Edited by Dr Adequate, : No reason given.

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Modulous
Member
Posts: 7801
From: Manchester, UK
Joined: 05-01-2005


(1)
Message 25 of 149 (531342)
10-17-2009 6:48 AM
Reply to: Message 21 by Colin
10-16-2009 10:05 PM


Re: What Behe's calculations actually mean for human evolution
There surely must be a limited number of the potential advantageous mutations in mammals for example, that you refer to.
Undoubtedly limited - and probably incalculable. Without it being calculable you have no idea what the probability of any given population striking them within whatever time period we are discussing.
However, the number of trials are greatly reduced, even considering our macro bodies, to the comparative number of malaria, reducing the probability.
Yes. But don't forget we are also talking about time periods like 500,000 times greater. So we still have many many billions of trials (as described earlier), and an open-ended set of problems rather than the highly specific problem of a specific poisonous environment to adapt to.
Also, I believe Behe would have probably had in mind the fact that if an advantage requires a string of changes, even accounting for the range of multiple possible paths along the way, the event of finding any advantage becomes more unlikely.
Indeed - but we have to take into account neutral mutations too of which there are very many - increasing the probability.
Dawkin's if i remember rightly, refers to this as "animal space" or something similar. It could be imagined as three dimensions, but in fact would have many dimensions.
Yes - in Dawkins' metaphor each gene represents one dimension.
Legitimate paths would consist of small beneficial steps, connected by reasonable possibility of achieving those steps, leading to more complex structures that also give advantage. From an engineering perspective, i imagine these paths would be very tight.
For an animal well adapted to its environment - you are probably right. However, if the environment changes or the population finds itself in a new environment or what have you - then there are more disadvantages and advantages possible. If you change the environment to include a lot of poison - then suddenly any mutation that renders one immune to that poison increases its reproductive success even if that same mutation was once neutral or harmful.
With 6 billion people all having on average 1 child that survives to reproduce each (conservative since our population is increasing) - each one with about 100 mutations of their own...there are a lot of genetic mutations out there. The paths to tread might be tight - but the net is cast wide.

This message is a reply to:
 Message 21 by Colin, posted 10-16-2009 10:05 PM Colin has replied

Replies to this message:
 Message 33 by Colin, posted 10-18-2009 1:31 AM Modulous has replied

  
Dr Jack
Member
Posts: 3514
From: Immigrant in the land of Deutsch
Joined: 07-14-2003
Member Rating: 8.7


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Message 26 of 149 (531344)
10-17-2009 6:57 AM
Reply to: Message 23 by Colin
10-17-2009 4:39 AM


Sickle cell vs. antimalarials
And that is the sickle gene. Apparently thousands of years old, the trait gives a person resistance to malaria, and to date, malaria has found no solution
Heterozygous sickle cell carriers make up around 10% of the population, they are not completely immune to Plasmodium*, and the mechanism of resistance is that infected blood cells are destroyed before the parasite has time to complete it's life cycle meaning that most resistance strategies would require a remodelling of the parasites life cycle.
In contrast, chloroquine was introduced into the vast majority of the population, induced near 100% Plasmodium mortality in already present populations and the mechanism of resistance have taken the form of simple alterations to existing intergral membrane proteins to export chloroquine from the cell** and no major lifecycle changes.
So, you see, there's a pretty sharp distinction between the two cases. In one you have a mild selective pressure, and no apparent simple means of resistance; in the other you have extreme selection pressure and a simple means of resistance.
I say 'apparent' because there's a big flaw in Behe's argument anyway: the assumption that there have been no adaptions in Plasmodium in response to Sickle Cell. We don't know this. For all we know Sickle Cell used to be much more effective against Plasmodium but changes to the parasite now make it more effectively able to infect such hosts.
* - in fact, the resistance of Sickle Cell heterozygotes to Plasmodium may not be disadvantageous to the parasite at all. Often reduced mortality among hosts is of benefit to parasites.
** - please note that while the mechanism I describe here is the current preferred model of how anti-chloroquine resistance works it has not yet been conclusively demonstrated.

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Dr Adequate
Member (Idle past 284 days)
Posts: 16113
Joined: 07-20-2006


(1)
Message 27 of 149 (531345)
10-17-2009 7:05 AM
Reply to: Message 26 by Dr Jack
10-17-2009 6:57 AM


Re: Sickle cell vs. antimalarials
* - in fact, the resistance of Sickle Cell heterozygotes to Plasmodium may not be disadvantageous to the parasite at all. Often reduced mortality among hosts is of benefit to parasites.
Yes, but surely in this case it's not just reduced mortality, it's reduced probability of becoming infected in the first place. Apart from that, good points.

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 Message 26 by Dr Jack, posted 10-17-2009 6:57 AM Dr Jack has replied

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Dr Jack
Member
Posts: 3514
From: Immigrant in the land of Deutsch
Joined: 07-14-2003
Member Rating: 8.7


(1)
Message 28 of 149 (531348)
10-17-2009 7:28 AM
Reply to: Message 27 by Dr Adequate
10-17-2009 7:05 AM


Re: Sickle cell vs. antimalarials
Yes, but surely in this case it's not just reduced mortality, it's reduced probability of becoming infected in the first place. Apart from that, good points.
As I understand it, malarial infection of sickle cell trait individuals does occur but the levels of infection are sufficently low as to be largely asymptomatic in most cases.
But thinking about it, it is considerably more likely to be disadvantageous.

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Modulous
Member
Posts: 7801
From: Manchester, UK
Joined: 05-01-2005


(1)
Message 29 of 149 (531354)
10-17-2009 8:27 AM


Joe Thornton
Joe Thornton,
Associate Professor,
Howard Hughes Medical Institute,
Center for Ecology and Evolutionary Biology
It looks like Behe has attempted to use this same line of reasoning in regards to the work of Thornton. Thornton's response looks hautingly familiar:
quote:
Thanks for asking for my reaction to Behe’s post on our recent paper in Nature. His interpretation of our work is incorrect. He confuses contingent or unlikely with impossible. He ignores the key role of genetic drift in evolution. And he erroneously concludes that because the probability is low that some specific biological form will evolve, it must be impossible for ANY form to evolve.
Behe contends that our findings support his argument that adaptations requiring more than one mutation cannot evolve by Darwinian processes. The many errors in Behe’s Edge of Evolution the book in which he makes this argument have been discussed in numerous publications.
In his posts about our paper, Behe’s first error is to ignore the fact that adaptive combinations of mutations can and do evolve by pathways involving neutral intermediates. Behe says that if it takes more than one mutation to produce even a crude version of the new protein function, then selection cannot drive acquisition of the adaptive combination.
This does not mean, however, that the evolutionary path to the new function is blocked or that evolution runs into a brick wall, as Behe alleges. If the initial mutations have no negative effect on the ancestral function, they can arise and hang around in populations for substantial periods of time due to genetic drift, creating the background in which an additional mutation can then yield the new function and be subject to selection. This is precisely what we observed in our studies of the evolution of the glucocorticoid receptor (GR).
You can read the rest here - I recommend it. The concluding paragraphs:
quote:
I considered hard whether I should address Behe’s argument or ignore it. I am well aware that Behe and his supporters might portray my response as an indication that there is scientific debate over the possibility of adaptive protein evolution: Look, an evolutionary biologist who actually does scientific research is arguing with me; let’s teach this controversy in public schools! Because Behe has grossly misinterpreted the results of my research to support his position, however, I feel some responsibility to set the record straight.
Behe’s argument has no scientific merit. It is based on a misunderstanding of the fundamental processes of molecular evolution and a failure to appreciate the nature of probability itself. There is no scientific controversy about whether natural processes can drive the evolution of complex proteins. The work of my research group should not be misintepreted by those who would like to pretend that there is.

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bluegenes
Member (Idle past 2477 days)
Posts: 3119
From: U.K.
Joined: 01-24-2007


(1)
Message 30 of 149 (531357)
10-17-2009 9:05 AM
Reply to: Message 29 by Modulous
10-17-2009 8:27 AM


Re: Joe Thornton (and creationist targets).
Modulous writes:
It looks like Behe has attempted to use this same line of reasoning in regards to the work of Thornton. Thornton's response looks hautingly familiar:
Small world! I read that late yesterday, and was going to put it in a post today, knowing it would interest participants on this thread. Thornton's work might make an interesting thread on its own (I think Wounded King made a links post on an article about it recently).
I'd have quoted this, which struck me as being so close to what we've been saying in this thread, and which sums up Behe's built in misunderstanding of probabilities whenever he tries to attack naturalistic evolution.
quote:
Finally, Behe erroneously equates evolving non-deterministically with impossible to evolve. He supposes that if each of a set of specific evolutionary outcomes has a low probability, then none will evolve. This is like saying that, because the probability was vanishingly small that the 1996 Yankees would finish 92-70 with 871 runs scored and 787 allowed and then win the World Series in six games over Atlanta, the fact that all this occurred means it must have been willed by God.
Consider the future: there are countless possible [outcomes]* that could emerge from our present state, making the probability of the one that actually does evolve extraordinarily low. Does this mean that the future state that will ultimately emerge is impossible? Obviously not. To say that our present biology did not evolve deterministically means simply that other states could have evolved instead; it does not imply that it did not evolve.
Consider your own life history as an analogy. We can all look back at the road we have traveled and identify chance events that had profound effects on how our lives turned out. If the movie I wanted to see that night when I was 25 hadn’t been sold out, I never would have gone to that party at my friend’s house, where I met my future spouse. Everyone can tell a story like this. The probability of the life we actually lead is extraordinarily small. That obviously doesn’t mean that its historical unfolding was impossible.
That we inhabit an improbably reality requires a divine explanation only if we, like Behe, take the teleological view that this is the only reality that could exist. But if we recognize that the present is one of many possibilities, then there is no difficulty reconciling the nature of evolutionary processes with the complexity of biological forms. As history unfolds, potential pathways to different futures are constantly opening and closing. Darwinian processes are entirely adequate to move living forms along these pathways to a remarkable realization — but just one realization out of many others that could have, but didn’t, take place.
*My brackets due to a misprint/word omission in the article.
Hence the "targets are for creationists" subtitle I put in earlier. It's important, because this is a basic mistake that's often made by critics of evolutionary theory. If one gives evolution a retrospective target, the end results always appear unlikely.
Perhaps I can ask Colin what he thinks of the probability of his own particular unique genome, and therefore himself, existing.
If we assume a possible million siblings who could have been born instead, then apply the same to his 2 parents, 4 grandparents, 8 great grandparents, etc., we'll find that the probability of his existence would seem to be negligible even taken from a point just 200 years ago. Something like 1 in 10^500.
But nature without targets doesn't have to face such apparent improbabilities, and Colin, I'm happy to say, is with us.

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