Why would I want my doctor to have studied evolution?

_{scordova
March 12, 2007

Intelligent Design

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Intelligent Design}

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From Dr. Michael Egnor:

No Nobel prize in medicine has ever been awarded for work in evolutionary biology. In fact, I think it’s safe to say that the only contribution evolution has made to modern medicine is to take it down the horrific road of eugenics, which brought forced sterilization and bodily harm to many thousands of Americans in the early 1900s. That’s a contribution which has brought shame — not advance — to the medical field.

So ‘Why would I want my doctor to have studied evolution?’ I wouldn’t. Evolutionary biology isn’t important to modern medicine. That answer won’t win the ‘Alliance for Science’ prize. It’s just the truth.

Comments

"You'd be wrong-ish. Everyone in malaria endemic areas gets infected at some point during their life." --HodorH Point taken; I admittedly know very little about malaria epidemiology. I imagine the reduced probability of being infected at any given time-slice of one's life, over the long-haul, is positively correlated with the probability of not dying from malaria. Although, biologically speaking, the same factors that make a person's cells less likely to support initial infections (i.e. the property of resistance) would likely--if an infection did nevertheless ensue--mitigate just how rampant it could become and thus reduce the chance of mortality. So maybe survival rates among S-allele carriers vs. noncarriers are the main factor here, and the correlation observed between s-allele carriers and low rates of infection is just a by-product of the underlying biology? This could possibly explain the puzzle you pose about the incongruence between mortality rates and transmission rates, but see below, b/c I'm not sure I understood your puzzle exactly. Also, if you could link to a source for those child vs. adult S-allele frequencies, that would be great, as it's difficult to think of a more straightforward way to illustrate natural selection occurring in this case. "Here's another puzzler to think about: Malaria mortality is not stongly corelated with malaria transmission." -HodorH I'm wondering if I properly understand your wording here. Is this correlation you speak of between the number of malaria deaths in a region and the number of verified transmission events between any infected individuals? Or is the correlation between only those individuals that die and the individuals they transmit to? Or are these correlations involving properties of different strains of malaria? Or is it something else?great_ape_{March 16, 2007
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Survival rates would be nice data to have, but I'm going to speculate that the most fool-proof way to avoid death by malaria is to never become infected with malaria in the first place.
You'd be wrong-ish. Everyone in malaria endemic areas gets infected at some point during their life. Adults that grew up in these regions are less susceptible to severe malaria than visitors (don't forget your anti-parasitics!). To send an ace your way, I can tell you that in malaria endemic regions, the freuqency of the S allele is higher in adults than in children. Here's another puzzler to think about: Malaria mortality is not stongly corelated with malaria transmission.HodorH_{March 16, 2007
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"It shouldn't be using infection rates, but malarial survival rates." --PaV Survival rates would be nice data to have, but I'm going to speculate that the most fool-proof way to avoid death by malaria is to never become infected with malaria in the first place. "On the other hand, I noticed the obvious: the S-allele wasn't much of a defense against getting infected." --PaV Who can hope to prevail against reasoning such as this? I've nothing else to say on the matter. Perhaps someone else can provide illumination.great_ape_{March 16, 2007
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great_ape: "Your argument is essentially equivalent to arguing that europeans are not really taller than chinese because, golly gee, how would you explain Yao mingÃ¢â‚¬Â¦" I'm afraid that is not the case at all. Your argument seems to be that, yes, we should look blindly at the data, crunch the numbers, and let the numbers speak for themselves. Are you aware of the highly correlated connection between who wins the Super Bowl and how the Stock Market fares in that same year? That's statistics. Should be conclude from this high correlation that the two phenomena are connected? Now, as the "ace up my sleeve", here's a quote from a PBS story: " A Mutation Story: A gene known as HbS was the center of a medical and evolutionary detective story that began in the middle 1940s in Africa. Doctors noticed that patients who had sickle cell anemia, a serious hereditary blood disease, were more likely to survive malaria, a disease which kills some 1.2 million people every year. What was puzzling was why sickle cell anemia was so prevalent in some African populations." You see, this whole exercise is using the wrong kind of data. It shouldn't be using infection rates, but malarial survival rates. And, do you further see, that it didn't matter to them, and it didn't matter to you. You simply wanted to "crunch the numbers"! (Every student who completed the exercise could then tell their friends: "Yes, indeed, the S-allele does confer 'selective advantage', and I can prove it statistically!") On the other hand, I noticed the obvious: the S-allele wasn't much of a defense against getting infected. With computers, and statistics, it's the same aphorism: "junk in; junk out". A final note: I've looked high and low doing searches for relevant data here, and could find none really. Does data exist? Where is it? I'm hoping someone can answer these questions. This whole thing smells of Kettlewell's moths. P.S. I study statistics when I have to; otherwise its' quite boring.PaV_{March 16, 2007
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"Your analysis just blindly looks at statistics." --PaV That's the idea. Frame the question properly, make a hypothesis, and dispassionately determine if there is a significant effect there that is not expected by chance. There is always some degree of noise in the data. This may manifest itself in the fact that there is less difference between the two allele groups in Nigeria than you might expect. Your argument is essentially equivalent to arguing that europeans are not really taller than chinese because, golly gee, how would you explain Yao ming... I'm guessing you have never had a formal statistics course of any sort. The entire point of developing the science of statistics is to avoid the kind of fuzzy arguments that you're trying to make about your impressions of the numbers when looking at particular data points. That's not how it's done and for good reason. And that has nothing to do with biology; that's not how it's done in *any* field. Twain's quote is funny, yes, but the field of statistics was not abandoned after it was made. The fact of the matter is that, without formal statistics, it's a lot *easier* to lie and also a lot easier to be just plain wrong.great_ape_{March 16, 2007
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great_ape: "Roughly equal heads and tails. I put the numbers in Excel and did it myself just to be sure: in each and every case, infection rate for the AA-group is higher than for the S-group. That's ten heads in a row. That's rather significant. Looking at various ratios in particular populations, as you did, can be misleading when you haven't formally framed the question and decided what your hypothesis is and how you're going to test it vs. chance. The big picture clearly shows a *lower incidence of infection* for the S-allele carrying group. That's the take-home message. But don't take my word for it. I suspect there are a number of folks lurking here that will tell you just the same. " Your analysis just blindly looks at statistics. I won't bother to quote Twain again. Look at the numbers for S. Ghana and Nigeria again. One can explain the significant difference between the two countries this way: in S. Ghana, malaria hasn't been virulent, while in Nigeria, it has. But then in Nigeria we see that there is almost NO difference between the S-carriers and the AA-homozygotes. If, indeed, the S-allele has some advantage, then why in an area that is apparently being ravaged by malaria do we see no difference in infection rates? Do you have an answer for that? And, beware, I have another ace up my sleeve. ;) This whole exploration of sickle-cell anemia and "microevolution" is turning out to be just like my search for a Darwinian explanation for "macroevolution": "Where's the beef?" So far it simply looks like another "just-so" story. Why should I be surprised?PaV_{March 16, 2007
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Ã¢â‚¬Å“BTW Great_Ape any chance of you showing us the scientific data that accounts for the physiological and anatomical differences observed between chimps and humans?Ã¢â‚¬Â Ã¢â‚¬â€œJoseph Great_Ape: Not terribly likely, as I'm not even sure what that question means exactly (i.e. what level of detail you're looking for or what would satisfy you). Give us what you have. IOW what was it that satisfied you that humans and chimps shared a common ancestor? Do we know what, if anything, can account for the rearrangement of toes? (chimps have an opposable big toe) Do we know what, if anything, can account for bipedal, upright walking? (spine attaches differently to the skull, legs are different, rib cage different, etc.) And those are just two examples. The point being without that data all you have is faith inm your imagination. Great_Ape: You claimed that you couldn't imagine how **any** amount of genetic change could account for the physiological/anatomical differences between humans and chimps. Umm That was NOT my claim. My claim was that NO ONE can account for the physiological and anatomical differences observed between chimps and humans. And reality supports that claim. Great_Ape: That was a poorly thought-out claim on the grounds of basic biology aloneÃ¢â‚¬â€œall questions of evolution aside. It is a cliam supported by reality. IOW if anything is faulty it is your responses.Joseph_{March 16, 2007
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I believe Malaria can fix sickle-cell anemia if all other factors are equal. When we observe anti-biotic resistance in a petri dish we have strong selective forces and control in making "all other factors equal". What may be happening with the fixing of sickle-cell anemia in the wild is the issue of the strength of selection and the other factors.
As a further consequence, even alleles with smallish selective benefits will proceed (pretty much) deterministically to fixation. Kimura showed probability of fixation is approximated by: p(fixation) = (1 - exp(-4Nsq) / (1 -exp(-4Ns))
There was the "no selection box" in Sanford's book. At some point, if the selection force is so dilute, it can not be a factor, the trait will be appropriately modeled as neutral. It's like trying to listen to someone whispering to you across a crowded noisy room. There were many conceptions sketched out in Sanford's book that would be worth exploring theoreticaly and empricially. I think it's pre-mature to be making certain conclusions.... Somewhat off topic, but for what it's worth, here is a monkey wrench article: Remote Sheep Population Resists Genetic Drift Science Daily Stories like this suggest Solexa technolgy will reveal the fact our conceptions of even evolution today are probably more off the mark than we are will to admit. Until then, it might be advisable to be cautious in our conclusions.scordova_{March 15, 2007
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"Sanford rightly argues that advantages can be drowned out by noise (i.e. random bad luck)." -Sal This is correct... but just for the record, people should know that this idea of "drowning out" was not a novel insight on Sanford's part. This is part of basic population genetics. The beauty of sampling statistics, though, is that even modest (e.g. mammalian) breeding population sizes yield fairly good approximations of the total allele frequency in the entire population. As a result, wild fluctuations in allele frequencies from "random bad luck" are not generally expected. As a further consequence, even alleles with smallish selective benefits will proceed (pretty much) deterministically to fixation. Kimura showed probability of fixation is approximated by: p(fixation) = (1 - exp(-4Nsq) / (1 -exp(-4Ns)) Where q is the initial allele frequency, N the breeding population size, and s the selection coefficient (roughly, relative benefit). This includes "random bad luck," whose influence is inversely proportional to population size. Try some numbers out and you'll see that the initial frequency is critical. Once an allele reaches 1% frequency, even in a population as small as 10000 individuals, an allele conferring 0.5% advantage has a probability of fixing of over 98%.great_ape_{March 15, 2007
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Considering the topic, perhaps it would have been more appropriate to bold
Indeed, after 50 years of investigation, we can't convincingly demonstrate selection for most of the red-blood-cell diseases, other than sickle-cell anaemia, that are probably coevolving with the strong selective force of malaria. Other best-case scenarios for human genetic adaptation, such as adult lactase persistence and skin colour, are also incomplete.
HodorH_{March 15, 2007
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See: Darwinist chastised for spinning Ã¢â‚¬Å“just soÃ¢â‚¬Â stories, but he still brings home the bacon
Indeed, after 50 years of investigation, we can't convincingly demonstrate selection for most of the red-blood-cell diseases, other than sickle-cell anaemia, that are probably coevolving with the strong selective force of malaria. Other best-case scenarios for human genetic adaptation, such as adult lactase persistence and skin colour, are also incomplete.
Selection happens, but there are numerous problems in it's efficacy in mammalian populations, not the least of which are those outlined in Sanford's GeneticEntropy. Sanford rightly argues that advantages can be drowned out by noise (i.e. random bad luck).scordova_{March 15, 2007
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"Yet what do we see in the data? Roughly equal heads and tails." --me Oops; the second sentence quoted should have gone before the first in my statistics post. Makes much more sense that way. Don't know how I managed that one...great_ape_{March 15, 2007
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PaV, Read through the entire tutorial (linked above) in which you found these numbers carefully . I does a fairly good job of illustrating one way to calculate statistics for the malaria data, and discusses the logic behind the calculation. Pay particular attention to the part about coin flipping. In short, you first need to set up a null hypothesis. In this case the null hypothesis is that there is no effect of the S-allele on incidence of infection (probability of a given individual being infected with malaria). What is the expectation under this hypothesis? You allele status (S/*) or (A/A)) will *not* be related the frequency of infection in a subpopulation. Restated, assuming an appropriately random sample, in any given population examined (Nigeria, Ghana, etc), the sub-group that has the S-allele and the sub-group that doesn't have the S-allele should have an equal chance of being infected with malaria. Just like there is an equal chance of getting heads or tails when flipping a coin. Here, they've looked at ten populations. In each population, you need to calculate the frequency of infection of those people with the S-allele and the frequency of infection among those without it. [note: this is, in each subpopulation and in each allelic subgroup (i.e. calculate separately S/* and A/A), the number of infected individuals divided by the sum of both the infected and uninfected individuals) Under our null hypothesis (no effect of S-allele) the S-allele group's infection frequency should sometimes be higher than the AA-allele group and sometimes lower. Let's call cases where S-group is higher "tails" and cases where S-group incidence of infection is lower "heads." Under the null hypothesis, the system should behave just like a coin flip. Yet what do we see in the data? Roughly equal heads and tails. I put the numbers in Excel and did it myself just to be sure: in each and every case, infection rate for the AA-group is higher than for the S-group. That's ten heads in a row. That's rather significant. Looking at various ratios in particular populations, as you did, can be misleading when you haven't formally framed the question and decided what your hypothesis is and how you're going to test it vs. chance. The big picture clearly shows a *lower incidence of infection* for the S-allele carrying group. That's the take-home message. But don't take my word for it. I suspect there are a number of folks lurking here that will tell you just the same.great_ape_{March 15, 2007
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I've quickly looked over the numbers, and, yes, in the case of Nigeria the numbers speak otherwise. In any event, it was only meant to rub it in some. Nonetheless, my point is still made: Africans carrying the S-allele in Nigeria are infected in a 3 to 1 ratio, while those in S. Ghana are infected in a 1 to 3 ratio. If, indeed, the S-allele has a selective value in making people less prone to malarial infection, then how do you propose to explain these results? I haven't the foggiest notion of how these numbers support the notion that sickle-cell anemia confers resistance to carriers.PaV_{March 15, 2007
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"But, of course, you can do the calculation, and then tell everyone how sickle-cell anemia confirms Darwinism!" -PaV Someone in you guys' camp should probably spell this one out for PaV. I fear I lack the necessary restraint this evening.great_ape_{March 15, 2007
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great_ape: What precisely do you mean by Ã¢â‚¬Å“look closelyÃ¢â‚¬Â? Is that your general impression of the numbers or did you calculate the statistics? There is the implication, if you you read further down the article, that the statistics come out as showing a positive advantage for the S allele (it only has to be a modest advantage to be propped up and not lost to negative selection or drift) But I haven't done the stats myself either so I can't say. Looking at the statistics, I was quite surprised. I expected to see ratio of infected (I) to uninfected (U) that would be radically different between the S-allele carriers and the AA-homozygotes. But what you see is that the ratios are generally not that far away from each other (except when the test size was small), and you never saw instances where, e.g., one ratio was above 1 and the othe below 1. Similarly, the data show populations where the ratio of I/U is greater than 1 (#s 2,5,6,8,&9). That's half of the ten populations they studied. So, does the S-allele help at all? The only "help" comes from the fact that the AA populations has a higher ratio. But then there's this--which is easily observable from the data: some of these ratios are quite equal between the S-carriers and the AA's. Notice: Pop.#4: S. Ghana: S-allele I/U= 0.32; AA-homozyg: I/U= 0.47 and, then, Pop. #10 S. Ghana: S-allele I/U= 0.38; AA-homozyg: I/U= 0.42. But, here's the whopper!!! Pop. #6 Nigeria: S-allele: I/U= 3.17; AA-homozyg: I/U= 3.23!!!!! Yes, that's right, the AA-homozygotes had a "slight" advantage, i.e., 3.23/3.17= 0.02 selective advantage. Well, there you have it: in the LARGEST SAMPLE SIZE of all the given populations, the AA-homozygotes statistically have a selective advantage over the S-allele carriers. [[great-ape: (from above) "(it only has to be a modest advantage to be propped up and not lost to negative selection or drift)"]] You see, just more Darwinian garbage. Haldane speculates, scientists investigate, and then (WRONGLY) interpret the data to fit their preconceived Darwinian idea!! I'm forced to add that you, as well, have fallen for it. As Twain said, "There's lies, damn lies, and statistics". Look at the numbers: Population #4: S-allele: I/U= 0.32; Population #6: S-allele: I/U= 3.17. Do you see how far off the numbers are?!?!! It is obvious to anyone who spends more than five minutes time on these numbers, and, more importantly doesn't come at them with a Darwinian bias, that the numbers---for the purpose of calculating "selective advantage"--- are simply MEANINGLESS! Something far different is afoot in these numbers. Why is Nigeria so different from Ghana? Is it hospitialization? Is it food supply? I don't know what causes the difference, but when ratios become that skewed, then it is obvious that an "S-allele selective advantage" has NOTHING to do with it. But, of course, you can do the calculation, and then tell everyone how sickle-cell anemia confirms Darwinism!PaV_{March 15, 2007
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In first and second year medicine, we had to do a number of courses to indoctrinate us into Darwinism. I am sure that this was done to counter the obvious design inference that we inevitably gathered from everything else we learned in anatomy, physiology, embriology, biochemistry, pharmacology ... the list goes on and on. I was glad to hear the best Darwinists had to serve up to us. Unlike Richard Dawkins who found out at the aga of 9, I was not convinced in my twenties that the most powerful idea in history was more than the most powerful delusion in history. I am sure my patients do not suffer from my non conformity.idnet.com.au_{March 15, 2007
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"BTW Great_Ape any chance of you showing us the scientific data that accounts for the physiological and anatomical differences observed between chimps and humans?" --Joseph Not terribly likely, as I'm not even sure what that question means exactly (i.e. what level of detail you're looking for or what would satisfy you). "On another site you were so sure of yourself but you never supported your assertions." Joseph We were discussing a slightly different issue. You claimed that you couldn't imagine how **any** amount of genetic change could account for the physiological/anatomical differences between humans and chimps. That was a poorly thought-out claim on the grounds of basic biology alone--all questions of evolution aside. I explained to you why it was faulty. My position hasn't changed.great_ape_{March 14, 2007
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Look closely at the statistics for Africa, with Ã¢â‚¬Å“SÃ¢â‚¬Â allele and Ã¢â‚¬Å“AAÃ¢â‚¬Â homozygotes" --PaV What precisely do you mean by "look closely"? Is that your general impression of the numbers or did you calculate the statistics? There is the implication, if you you read further down the article, that the statistics come out as showing a positive advantage for the S allele (it only has to be a modest advantage to be propped up and not lost to negative selection or drift) But I haven't done the stats myself either so I can't say. "In it, one of the world's foremost authorities on malaria debunks GW claims that GW will spread malaria to more northern climates by noting that the worst outbreak of malaria occurred in Russia; in fact, in a very cold region of Russia." --PaV Isolated instances of malaria outbreaks in northern climes do not refute or even detract from the natural selection hypothesis for S-allele malaria resistance for multiple reasons: #1) just because the mutation *might* prove advantageous in a Russian population or elsewhere in the Northern region doesn't mean that they will (a)possess the appropriate S-alleles or b)experience a new (de novo) S-allele mutation. There are any number of mutations that undoubtedly *would* prove beneficial to members of a population, but that does not imply that those individuals would actually *possess* or *acquire* them. #2) even ignoring #1, which can't be ignored, it would require a relatively constant selective pressure (relatively constant malaria exposure) to maintain the S-alleles. I did not see this film, but I suspect it is not the case that malaria outbreaks in these Northern regions are common and/or continual. That is different from a tropical climate or subtropical climate where it is a persistent aspect of existence.great_ape_{March 14, 2007
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Thank you bFast. That was an excellent explanation. It all comes back to "designed to evolve" vs."evolved via culled genetic accidents". IOW JMCD, if the organisms had the information for variation already in their genomes all it would take is some new niches to bring it out. And this would be especially so if on Noah's Ark (for example) each pair was as gentically different (high degree of heterozygosity) as successful reproduction could allow. This is discussed in "Noah's Ark: A Feasibility Study". NOTE: I am NOT arguing for YEC or Noah's Ark. All I am doing is to show that the accpeted definition of macroevolution just adds more confusion to the debate than it does to show what is being debated.Joseph_{March 14, 2007
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jmcd, with the line between macro and micro set at the species level, the YEC crowd must accept some macroevolution. Noah's ark was by no means capable of holding all species. If it only had to hold all families, for instance, it would be a lot easier. But that would mean that there was only one species of cat represented on the ark. With lions, tigers, cheetahs, leopards, house cats and all, the species boundary must have been crossed many times. That said, I find it a bit silly to have the line between macro and micro on the species level. To me the great challenge for evolution is the development of new structures -- knee joints, etc., and new organs -- lungs, etc. It is at this level that I most expect that ID will prove to provide the only explanation.bFast_{March 14, 2007
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Quick question: How can someone that believes the Earth has only been around for ten thousand years believe in macro evolution? That would entail so many inconsistencies and contradictions as to render the belief a bit absurd.jmcd_{March 14, 2007
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When most people talk about evolution they do so in the context of Common Descent linked to "culled genetic accidents". However when some people then say they disagree with evolution (in that sense) some whacko will, always and without fail, bring up variations within a population in an attempt to discredit that "denier". And before we start talking about micro vs. macro we need a good definition of both. Because as it stands today even YECs accept macroevolution and have since at least the time of Linneaus. macroevolution
In evolutionary biology today, macroevolution is used to refer to any evolutionary change at or above the level of species. It means at least the splitting of a species into two (speciation, or cladogenesis, from the Greek meaning "the origin of a branch", see Fig. 1) or the change of a species over time into another (anagenetic speciation, not nowadays generally accepted [note 1]).
Linneaus put the Created Kind at the level of Genus. BTW Great_Ape any chance of you showing us the scientific data that accounts for the physiological and anatomical differences observed between chimps and humans? On another site you were so sure of yourself but you never supported your assertions. Is that how you discuss things?Joseph_{March 14, 2007
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http://wps.prenhall.com/esm_freeman_evol_3/0,8018,849182-,00.html It was Haldane. And he was guessing. Look closely at the statistics for Africa, with "S" allele and "AA" homozygotes. The data seems to indicate no real advantage/disadvantage to the "S"/"AA" carriers.PaV_{March 13, 2007
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This is also consistent with the fact that the sickle cell allele is found in geographic regions where malaria is common. Well, here's my ace up my sleeve. I just finished watching "The Great Global Warming Swindle" video. In it, one of the world's foremost authorities on malaria debunks GW claims that GW will spread malaria to more northern climates by noting that the worst outbreak of malaria occurred in Russia; in fact, in a very cold region of Russia. This, in turn, throws a damper on the conventional Darwinian wisdom for why sickle-cell anemia exists, which is that is confers a "fitness" advantage. Now, if malaria can occur anywhere on the globe, even colder regions, then maybe the only reason that it is found in certain populations is simply because of the in-breeeding of those populations, and no more. And perhaps the only reason it still is found anywhere is simply because it is only the homozygous form that is deadly. IOW, it exists in the heterozygous form simply because it's not lethal enough to eliminate it--NOT because it confers any advantage. It would be interesting to research how the common, Darwinian understanding of sickle-cell anemia came to be.PaV_{March 13, 2007
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"I pose a question for you, great ape: why does sickle-cell anemia exist? (Watch out, I may have an ace up my sleeve" --PaV And here I was, about to leave when you dangle this morsel in front of me. I presume you know the classic explanation for the sickle-cell allele persistence. I can't recall anything major developing lately in that area--although admittedly things sneak by from time to time. Alright, I'll bite. Sickle cell persists because, in its heterozygous state, the recessive allele that is responsible for it confers partial resistance to malaria. Something about the shape of the blood cell is unpalatable for the parasite in a certain stage of its development. (a bit hazy here) This is also consistent with the fact that the sickle cell allele is found in geographic regions where malaria is common. That's the standard story last I checked. Tell me something interesting. (Preferably something that doesn't entail punishing the evil-doers.)great_ape_{March 13, 2007
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"I understand there are many here who may not agree with this but I wonder if any of the major players would actually disagree." --jerry I'd also be interested to know. "I blame many who espouse NDE as the main source for this when they go far beyond what the data allows in order to make unwarranted scientific conclusions as well as metaphysical conclusions." -jerry You have a point. Those that over-extend what is factually known about NDE's role in biological history vs. what is only inferred (with varying degrees of confidence) share in the blame. No matter how many times or how loud certain things are shouted, many evolutionary "facts" remain inferences and not raw facts per se. Some inferences are simply much better grounded than others. More to blame, IMO, are those who are on personal crusades against religion, spirituality, etc. The frustrating part is that this is ultimately only a small, albeit very vocal, part of the community. Yet they stir many folks in religious circles into thinking a Jihad is required. There is no agenda to undermine religion in evolutionary biology. Or again, if there is, nobody sent me the memo.great_ape_{March 13, 2007
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I think Jerry is right, the real issue in contention is not microevolution, but deeper macroevolution issues. (Although I do think that Jerry's perhaps a bit too optimistic about how many folks on the ground in ID find even microevolution acceptable.) Several years ago, I would have grudgingly conceded microevolution to NDEists, mostly because of Denton's acceptance of it. Grudgingly, because to concede it makes arguing against the unlikelihood of RM+NS that much more difficult. But that admitted, I now find that the more literature I read, the more I think through its implications, RM+NS even at the "micro" level seems questionable. Bacterial SOS responses can hardly be called "random", for example. And is "breeding" really RM+AS? So, I have questions. But it's not simply to deny Darwin his due, but because science seems to be telling me something different. I pose a question for you, great ape: why does sickle-cell anemia exist? (Watch out, I may have an ace up my sleeve).PaV_{March 13, 2007
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great_ape. I often make the claim that ID subsumes NDE in the sense that nothing in the science or the findings of NDE is antithetical to ID. Those in ID may object rather strenuously to some of the conclusions that specific researchers make but not necessarily to their findings or methodology. They may also object to some of their philosophy of science too. In other words, ID just extends NDE by assuming that the origin for some new alleles or life forms is not due to random events or lawful processes of nature. No one objects to natural selection which is one of the most over hyped processes in the history of science. I wonder which of the fellows of CSC if any would object to the position that ID subsumes NDE. I know from Behe's comments that he is in agreement with this. I understand there are many here who may not agree with this but I wonder if any of the major players would actually disagree. Many people here routinely bash NDE without really separating out what is perfectly fine from what is seen as objectionable. I blame many who espouse NDE as the main source for this when they go far beyond what the data allows in order to make unwarranted scientific conclusions as well as metaphysical conclusions. It is not hard to find this both in the history of Darwinism or its current offshoots, in the textbooks and with present day advocates of the theory. Starting with Darwin himself, they all saw this theory as a means for undermining traditional religion and they did not hesitate to state it and use it to reduce or eliminate the influence of religion.jerry_{March 13, 2007
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"If you take evolutionary biology, subtract Ã¢â‚¬Å“Genetics is very important, as are population biology and microbiologyÃ¢â‚¬Â, in the remainder you will find the portion of evolutionary biology that Dr. Engor rejects." --bfast I was aware of that particular quote from Egnor. Your paraphrase of it, which I believe is precisely what he intended to say, is just what I take issue with. That sort of subtraction is unwarranted in my opinion and can serve no other purpose than a rhetorical one. If say "evolution is useless to medicine...although X,Y,Z are not.." The implication is that X,Y,and Z are not part of evolution proper. That's false. And I suspect if you backed Egnor in a corner, he'd admit it. But of course, his rhetorical aim is to score a point and be dismissive of evolution as a whole by saying the first part of the statement..."evolution is useless.." ...never mind that his latter qualifications render the statement fairly empty. I think Jerry is right, the real issue in contention is not microevolution, but deeper macroevolution issues. (Although I do think that Jerry's perhaps a bit too optimistic about how many folks on the ground in ID find even microevolution acceptable.) When folks--even if their target is ultimately (RM+NS => information)-- lambast evolutionary biology as a whole, and when in doing so they convey erroneous ideas and are overly dismissive of important concepts, then they need to be responded to according to their statements' face value. We can't just assume "oh, he's just attacking the idea of the increase of information via RM+NS so take anything he says about "evolution" as such with a grain of salt." "So when the words are brought up in a contentious discussion that and that alone is the topic that is really being discussed." --jerry I think it is dangerous to not be explicit about precisely what is debated in these contexts. Whatever the intentions of the speaker, it can only serve to confuse and mislead those who aren't "in the know." And I suspect, from some of the comments that I read, that there are far less people "in the know" than you and I would like to believe. And they don't make any nuanced distinction between macro and micro-evolution. Every negative statement against evolution is another score for the team. Would PZ and company be satisfied if ID supporters, as a group, officially endorsed micro-evolution? I seriously doubt it. But it would go a long way towards clarifying the debate and finding some common ground for reasonable folks to work from. As I see it now, the YECs thrive on the current confusion and that leads to no good for anyone.great_ape_{March 13, 2007
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