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Author | Topic: why creation "science" isn't science | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
Hi TrueCreation!
I've been following a number of the threads on this board. You have often repeated: quote: I find this an interesting statement. Could you please provide one or two specific examples of this evidence? When I say specific, I don't mean a general statement like "the geologic record" or "irreducible complexity". I hope you can provide an example such as "evaporites in the Toroweap Formation of the Grand Canyon are evidence of Creationism because...", or "the 1300 separate dinosaur trackways of the Purgatoire Valley, erroneously attributed to the Jurassic, are evidence of Creationism because...". Or if you'd prefer biology, how about "the existence of a vestigal pelvis in the rainbow boa, but not in many other snakes, is evidence of Creationism because...", or "the three separate reproductive designs in modern sharks is evidence of Creationism because...". You get the picture. Specifics. Thanks in advance.
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
Hi again, TrueCreation. Thanks for your response. I actually meant those examples I gave as illustrative of the "type" of evidence discussion I was looking for. You didn't have to use those - although I appreciate your effort. If you'd like to use different examples, that's fine. I don't want anyone to think my post was some kind of "set up". Alternatively, we can keep looking at the ones I used. Your call...
quote: Good response. Although Joe stole a lot of my thunder (quote: quote: I guess this was sort of a trick question. The key issue here is that the Purgatoire trackways were imbedded in four distinct rock layers. The Morrison (Purgatoire) formation is one of the most famous megatrackways in the Colorado Plateau/Grand Canyon assembly. Included in these layers are abundant fossils of plants, algae, snails, clams, crustaceans, and fish, indicating the formation occured on the shores of a large lake - not deposited by a flood. Sometimes the tracks contain crushed clam shells and flattened plant stems created perhaps when dinosaurs came to the shore for a drink. Another key problem with your response is that the Morrison Formation is only one of over 400 distinct layers - all containing tracks - in the plateau area. Trackways in the Colorado plateau and their associated fossils are perfectly stratified: small transitional amphibians (such as Stenichnus) and small mammal-like reptiles (pelycosaurs) in the lowest (Permian) layers to the true huge dinos such as brachiosaur in the Morrison (Jurassic) to ornithopod tracks in the upper levels (Cretaceous). In other words, perfectly consistent with evolution and change over 200 million years - but inconsistent with a catastrophic flood and rapid deposition. Remember, we're talking over 5000 feet of sedimentary deposition.
quote: The biblical Garden of Eden explanation only works if ALL snakes had these vestiges - they don't. AFAIK, only three groups retain vestigal limbs and or pelvises. Boas even retain a vestigal claw. If the curse applied to the ancestors of all snakes, it would make sense to that the same vestigals would be present in each species since all snakes were cursed at the same time - a situation which is manifestly NOT the case. Again, we see evidence that is consistent with evolutionary pressures operating differentially on isolated populations, but not biblical interpretation. The same problem with vestigal organs occurs throughout the record and across multiple taxonomic orders. (BTW: there is no such thing as "devolution" - the snakes are evolving toward better adaptation to their particular niche. Slow elimination of unneeded structures - and a case could be made that limbs are actually a hinderance to snakes - is consistent with evolution and is seen throughout the record. c.f. whales, moles, cave fish and arthropods, etc).
quote: Yep, that's what I was referring to. It might be a good idea to table this last question for a bit. I think we might end up arguing how to differentiate "kinds", etc. (For ex, are you proposing that there were three "shark kinds"? What about skates and rays - they are also related to sharks? Are they a different kind? You get the picture.) Anyway, thanks for the responses. Again, we can continue with these examples, or you could pick some others that show evidence for Creationism. Toodles.
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
Hi TrueCreation:
I was wondering if you'd had a chance to look at my response (Message 50) to your explanations (Message 43) - which was itself a response to my Message 41. I thought we had the start of something interesting there - exploring your statement that the evidence for creationism is as valid as that for evolution (and in fact the same evidence can be used for both). I know you're involved in multiple conversations on this thread, but I hope to hear from you. Reminder: you are free to pick other specific examples of evidence for Creationism if you don't like the ones I used.
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
TrueCreation: Take your time. Just didn't want to lose sight of what we were doing. It's an interesting conversation. I'll try and dig up (sorry) good basic references on geology, but to be honest, your best bet would be accessing the library of any decent-sized university. There are also a fair number of references on-line (I'd start with peer-reviewed geology, geographic society, and geophysics pubs).
I look forward to hearing from you when you get a chance.
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
Okay cobra: You wanted a evolution explained in our own words. Please note that I reject utterly your spurious attempt to link evolution with abiogenesis and cosmogenesis. These latter have no place in evolutionary theory, and efforts to include them is a vain try at erecting a strawman. You have been told repeatedly, in many ways by many posters that Darwinian evolution deals ONLY with biology. Biology is where my theory remains.
First off, there are some very basic statements that, for evolution to be true, must be true. All provide potential pathways for falsification. All lend themselves to development of testable hypotheses. All have (scientifically) predictive value: 1. If all the offspring that organisms can produce were to survive and reproduce, they would soon overrun the earth. 2. As a consequence, there is competition to survive and reproduce, in which only a few individuals succeed in leaving progeny. 3. Organisms show variation in characteristics or traits that influence their success in this struggle for existence. Individuals within a population vary from one another in many traits. 4. Offspring tend to resemble parents, including in characters that influence success in the struggle to survive and reproduce. 5. Parents possessing certain traits that enable them to survive and reproduce will contribute disproportionately to the offspring that make up the next generation. 6. To the extent that offspring resemble their parents, the population in the next generation will consist of a higher proportion of individuals that possess whatever adaptation enabled their parents to survive and reproduce. Next, you need to understand (and remember) that natural selection leading to evolution is simply the differential reproduction of genotypes. There are two basic assumptions for natural selection to work: 1. There must be heritable variation for some trait. Examples: beak size, color pattern, thickness of skin, fleetness, visual acuity. 2. There must be differential survival and reproduction associated with the possession of that trait. Graphically:
Heritable variation occurs by mutational changes in an organism’s DNA (any change in the hereditary message — base pair substitution or insertion/deletion of new bases) leading to the creation of new genetic material AND/OR creation of new genetic combinations through transposition (changing the position of a gene changes what it does), recombination (through cross-over during meosis), or genetic reshuffling (through sexual reproduction). Without getting too deep into it, selection can only act on the phenotype. A gene can be present, but not expressed (e.g. a recessive allele). Only homozygous recessives will show the trait and be selected for or against. In addition, selection acts on the whole organism (a conspicuously-colored moth, for ex, can have all sorts of wonderful genes, but if a bird nails that moth, its entire genotype is gone). And finally, selection doesn’t have to cause changes. It also can maintain the status quo. Therefore, the general predictions of evolution are: 1. Given heritable variation over time, new species can and do arise.2. Over sufficiently long time periods, due to various mechanisms surviving populations will vary sufficiently from the parent population to constitute new taxa. And that’s my description of evolution. If you are unable to approach this level of discussion on Creationism, then you truly do NOT have a theory beyond goddidit.BTW: There are a couple of interesting corollaries to my definition. Basically, the above means that there is no requirement that evolution proceed in a linear fashion. Nor is it necessary that evolution produce either greater complexity, greater perfection or greater information (LOL) for evolution to be true. This is a creationist fallacy. As an example, it is quite common to have an organism’s DNA contain multiple non-significant (unexpressed) or recessive alleles. Because these alleles serve no immediately useful function for an organism’s individual survival/reproductive success, natural selection simply ignores them. Meaning that if environmental conditions change there are generally individuals in a given population whose traits all of a sudden become important to their survival. This is one of the primary ways bacteria develop resistance to antibiotics: the resistance was already present in the population. All the antibiotics have done is eliminate all the members WHO DID NOT ALREADY HAVE THE TRAIT, increasing the overall frequency of alleles which are resistant within the population. Another marvelous outgrowth of evolution by natural selection is that often different combinations of genes or even macrostructures that are useful for one thing are found to be ultimately useful for something else, as well. These traits are then co-opted by natural selection to other uses. Evolution as I’ve described it only requires a single step at a time AND each step needn’t (in fact shouldn’t) be considered in light of any subsequent step — only in comparison to its predecessor. New genes (hence new traits) do not arise because they are needed, and no organism ever made a living as a transitional — all were sufficiently well adapted for their particular niche and lifestyle to reproduce. Otherwise they would have quickly become extinct.
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
TrueCreation, Retrochrono:
Since cobra hasn't seen fit to respond, I hereby challenge either of you to provide an operationalized theory of Creationism. I refer you to my post #154 in this thread. In that post I provided a succinct, operational definition and explanation for evolution. The explanation provides falsifiable statements, testable hypotheses, a mechanism, even a graphic representation. It also provides a basis for developing predictions. If Creationism can not approach this level of debate, then your contention that it is "scientific" is specious. In other words, time to "put up or shut up".
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
Cobra: Outstanding!! Thanks for your efforts. Your post has to be one of the best attempts at defining (in biological terms, anyway
Okay, now that I’ve congratulated you, let’s discuss your model. I’ll start with your first area of contention: [QUOTE]This is where I start to disagree with you (and indeed some evolutionists do as well). I do not believe that mutations can be the raw material for evolution. First of all, beneficial mutations are extremely rare. Second of all, I've never heard of a beneficial mutation that increased the amount of information. This is where Creation and Evolution go seperate ways. Creationists don't think mutations could ever cause the amount of change required, evolutionists do. If you want to debate further, this would be an excellent area to debate.[/QUOTE] Actually, no evolutionist (do you also say atomist?) disagrees with what I said. There is considerable debate in biology about the relative importance of the mutation factor (c.f. debate between selectionist, mutationist, and neutralist), which has implications for the relative importance of natural selection, evolutionary stable strategies (ESS), gradualism vs PE, etc, but no one to my knowledge denies mutations provide most of the raw material. After all, even Gould’s exaptations had to have arisen by mutation. This is kind of a minor point, and I don’t want to get too far off-track. I personally find the debate fascinating, so would be happy to discuss it further later, if you’d like. Also, I’d be interested in reading one of the evolutionary biologists you say disagree. <b>Beneficial mutations are extremely rare</b>: There are a couple of problems with this statement. In the first place, what does beneficial mean in the context of evolution? Generally, evolution by natural selection implies that an organism will be sufficiently adapted for its <b>current</b> environment to survive long enough to reproduce. A grass species adapted for existence in a certain soil and climatic type obviously implies that the alleles that allow it to do so be beneficial. These adaptational alleles would be either neutral or deleterious in another location. This can be shown quite well in the adaptation of closely related species to different environments. Here’s an example: <i>Lepus arcticus</i> and <i>Lepus townsendi</i>. Both are hares. Both are well adapted to their local environment. However, <i>L. arcticus</i> has thick, multi-layered fur, short limbs and small ears to enable it to retain heat in an extremely cold environment. Its relative <i>L. townsendi</i>, on the other hand, has short fur, very long ears and limbs, in order to better shed heat in its desert environment. Take either of these two species of hares out of their current environment and place them in the other's and they will quickly succumb. Obviously, it’s hard to observe this taking place in slow-generational organisms. Microbiologists have provided substantial experimental evidence for beneficial mutations. Here’s a short list (some on line):
[URL=http://www.pnas.org/cgi/content/abstract/98/20/11388] Contribution of individual random mutations to genotype-by-environment interactions in Escherichia coli[/URL]Changes in the substrate specificities of an enzyme during directed evolution of new functions. Hall BG Biochemistry 1981 Jul 7 20:14 4042-9 Predator induced evolution in chemostat culture. Boraas, M. E. 1983. EOS. Transactions of the American Geophysical Union. 64:1102. Functional divergence of the L-Fucose system in Escherichia coli Lin, E.C.C., & Wu, T.T. (1984) John Kimball’s Biology Pages[/URL]. <b>Second of all, I've never heard of a beneficial mutation that increased the amount of information.</b> I really can’t answer this question until you define what you mean by an increase in the amount of information. If you are talking about new bases in the genome, almost anything that increases (from duplication and crossover to retrogene insertion) the number of base pairs will increase information. To be honest, the concept of information in genetics is somewhat misleading in the first place. A gene simply provides a chemical template for a particular protein (or is part of a cascade building a particular protein). Although comparing DNA/RNA to the bits and bytes in a computer makes it easier to conceptualize, the analogy shouldn’t be taken too far. In addition, most changes in genome that permit the organism to live at all are evolutionarily neutral (taken in context of an organism’s survival potential in its current environment). It’s only when the organism’s environment changes — or when some selective advantage accrues — that unexpressed mutated alleles become important. Also, benefit does not imply any increase in the amount of genetic material!!! A mutation can be a change in <i>existing</i> genes that provide the organism some advantage in passing on its genetic inheritance. [Note: I am aware this is simplistic — but unless we want to get in to genetic loading, deleterious/neutral/beneficial allelic fixation rates, etc, I think the above is sufficient for this discussion.] [QUOTE]<b>2. "Over sufficiently long time periods, due to various mechanisms surviving populations will vary sufficiently from the parent population to constitute new taxa."</b> I do not agree with this statement. This is an important area of debate. (Please note that even some evolutionists do not agree with you, so I am not making a bold statement to disagree with you on this particular point.)[/QUOTE] Actually, I figured you wouldn’t agree with this — after all, this is the definition of so-called macroevolution. [IMG] However, I would need to read some literature on evolutionists not agreeing. Could you provide a reference? Anyhow, what do YOU disagree with? What is the barrier that prevents statement 1 (speciation) from eventually having statement 2 be true? At what taxonomic level does this supposed barrier occur? Remember, it isn’t expected to be visible over the lifetime of a human. It takes, by my model, a whole lot longer to see changes in family, for ex, than in genera, but the mechanisms are identical. The only difference is time scale required. One way this idea can be argued is comparison of the relative rates of change of specific proteins. Based on pairwise comparisons between different taxa, different proteins, such as cytochrome-c (an electron transport molecule in cells) evolve at a constant rate. This rate then can be used to determine the degree of relatedness, or time of divergence of different taxa. Here’s a chart showing the divergence of higher taxa based on cytochrome-c comparisons:
[IMG] As you can see, there is solid molecular evidence that taxa diverged in the past. There is substantial fossil evidence (at least for certain lineages) to back up the molecular evidence (or vice versa). http://www.evcforum.net/Images/Smilies/wink.gif[/IMG]-->
The last question on the divergence of higher taxa is how we know they are related. One way is the presence of retrogenes in identical locations on strands of DNA. Retrogenes are molecular remnants of a past parasitic viral infection. The inheritance of a piece of viral DNA is a fairly rare occurrence, as it can only happen if the infection occurs in a germ-line cell (sperm or egg). Finding a retrogene at the identical locus on the same chromosome of two different animals is pretty solid evidence of relatedness. For example, all the small cat kind [IMG] (<i>Felis spp</i>) have just such a retroviral insertion — from domestic kitties to African wildcats to the margay of Latin America. HOWEVER, the large cat lineage that led to both the new and old world large cats (leopard, jaguar, lion, puma, cheetah) do NOT have this retroviral insertion. What does this mean? It means that the speciation event that ultimately led to the large cats diverged from the general cat lineage way before the speciation events that created all the individual species of cats (small or large). Here we have evidence of a divergence of higher taxon in the distant past. I lied. I promise I’ll get to your model in my next post. The above is already too bloody long. [IMG]
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
Hi Cobra, as promised:
quote: Excellent. We’re at least on the same sheet of music. Your assumptions:1. Mutations should almost always cause a bad effect. I guess the first thing to do would be to ask to what extent, or at what scale, mutations have effects which can be unambiguously classified as either beneficial, deleterious, or neutral. IMO, The answer would depend on the particular phenomenon you’re trying to explain. As I pointed out above, the most parsimonious explanation for the different adaptations of hares is that some combination of beneficial traits —based on lagomorph change over time — allowed each of the distinct species to adapt to their environment. Obviously, these traits would be beneficial in the organism’s current context. However, that is the evolutionary paradigm, and shouldn’t be used as a basis for determining the truth or invalidity of your model. Restating your assumption: It has been observed that mutations arise continuously in all populations, and the vast majority of those which effect fitness are deleterious. I would say this could actually be expected, because most organisms are at least sufficiently adapted to survive or they wouldn’t be there, and any mutation that effected the functioning of an organism would tend to be negative. Over time, the net effect of mutations would thus be a continual decline in the correlates of fitness in a population. IOW, over time, if all mutations are negative, the deleterious mutational load on a population will ultimately lead to its extinction. In short, there would be a net decrease in biodiversity over time as populations reached their crash threshold. Is this what is observed? No. The persistence of natural populations at all indicates that there is some other effect in operation. The deleterious mutation/crash effect would be especially evident in spatially isolated populations such as islands. It turns out that the exact opposite occurs: in geographically isolated ecosystems (such as islands), and dependent on the carrying capacity of the particular area, a net increase in species diversity is observed. The most famous example for animalia is the Galapagos Archipelago. On the Galpagos, 34% of plant species (eg the cactus Jasminocerus thousari), 63% of reptile species (eg the land iguana Conolophus subcristus, the marine iguana Ambyrhynchus cristatus and its seven subspecies) and 73% of land bird species (eg the hawk Buteo galapagoensis, the martin Progue modesta and the rail Laterallus spilontus, the penguin Spheniscus mendiculus, plus the finches of course) are endemic, found nowhere else in the world. There are endemic rice rats (Oryzomys), bats (Lasiunis brachyotis), and a flightless cormorant (Nannopetrum harrisi). Lava lizards of the genus Microlophus are found only on the Galpagos. There are seven Microlophus species endemic to the archipelago — and each island that has Microlophus has a different species. This represents a literal explosion of diversity. Galagpagos does not represent a unique case. Every island visited throughout the world shows similar patterns of explosive diversity. In addition, each isolated lake ecosystem contains endemic species: an example are the cichlids of Laguna Xiloa and Lago de Apoyo in Nicaragua. Less than ten miles apart, these two lakes each contain half a dozen species of native cichlids not found anywhere else in the world - and which are not the same species in both lakes! The same holds true for cave systems. It does not appear that this assumption is valid. Assumption:2. Mutations should rarely or never increase the amount of information. I have already noted my problem with the concept of information when discussing biological systems in my previous post. Information is a weak and misleading analogy for genetics. The assumption — taken only at face value — would also presuppose that there is no possibility of increasing the amount of genetic material in an organism. Given the experimental evidence available (some of which I noted previously) showing how new biological pathways can develop, even this assumption falls flat. Assumption:3. Speciation should occur as a product of the great variability programmed into living things, combined with mutations. In the first place, this assumption would seem to directly contradict your assumption one. The consequences of assumption one — that there will be a net decrease in diversity — indicates there should be less variation observable in nature via subtraction of species which have gone extinct. Another implication is that, given similar environmental conditions, the same type of organism will be found where ever these environmental conditions apply (within the limitations imposed by the programmed variability, whatever that is, within species). Again, this is not what is observed. Similar niches are filled with (often radically) different organisms. Australia lacks placental wolves or big cats, for ex, but it did have marsupial equivalents. A woodpecker finch is practical only in the absence of woodpeckers - thus there is a Galpagos woodpecker finch, Cactospiza pallidus. The pattern is always by area, not by environment type. Assumption:4. All living things should be fully formed from the start. (i.e. no reptiles with "half-wings" or "half-feathers.") On the face of it, this is a true statement. No organism ever made a living as a transitional form. There are actually two difficulties with this assumption, however. In the first place, there is an implicit assumption of linearity or purpose in nature that is not borne out by observation. Living organisms are observed to be, in general, sufficiently functional in their current environment to reproduce their species. Again, however, we have a contradiction of assumption one. If assumption one is true, that there is a net increase over time in the deleterious mutational load on a population, unless all organisms’ environments are also deteriorating at a nearly one-to-one ratio, including all abiotic factors, all populations will rapidly become extinct, as there is no possibility of "positive" adaptations to changing conditions in the absence of beneficial or novel alleles. Finally, there are numerous modern examples of organisms caught in the act as it were with partial adaptations. One example is the existence of radically different organisms with various mechanisms for gliding, including lizard, frog, several squirrels, a marsupial, etc. All of these organisms have various types of membranes — some more or less effective — to enable them to glide greater or longer distances. Here are transitional forms between terrestrial/arboreal and flight. In addition, several species of fish seem to be transitional between fish and amphibian (ex, lungfish and mud skippers) with various adaptations to — at least temporarily — breath air rather than relying solely on gills [there are also several species of goby which I have personally witnessed having the ability to jump out of their intertidal zone pool and survive on land for up to ten minutes by gulping air.] Therefore, there exist sufficient examples from nature that tend to falsify this assumption. Assumption:5. Due to the typically negative effect of mutations, speciations should arise primarily as a result of LOSS or CORRUPTION of information, which makes the species less varied. Although primarily a restatement of assumption one, this assumption more explicitly states that no improvement can occur (as such, directly contradicting assumption two, three and four.) The assumption seems to imply that if species change over time, such change would make them less fit for their environment. In addition, this assumption explicitly states that daughter species, if they arose, would have net negative fitness correlation as compared to the parent species. Again, there are numberless examples from nature that show either increased fitness over time or epistasis over time. Even artificial manipulation of populations results in similar improvements, ultimately developing new or improved organisms in accordance with a pre-determined (in this case) normative standard or desired result. "Wild" populations show similar improvements or stability.
quote: 1. Fully formed creatures in the fossil record (no "half-features") True as stated. There can be no such thing as half features, for the simple reason that half features would not allow survival. However, the fossil record is replete with forms — obviously related by morphology — which are different in the aggregate, but share numerous traits in common (such as dentition, number and arrangement of phalanges, etc). In addition, the fossil record shows that there is a distinct stratigraphy associated with these fossils: i.e., fossil type A found in a lower (and hence geologically older) strata with primitive features or traits distinctive of one particular taxonomic order, followed in successively younger strata by fossil type B of obviously related organisms which shares traits with A but which also has traits related to a different taxonomic order. Finally, pure forms of this new order (fossil C) are found which share traits with B but not with A, again in younger geologic strata. Now obviously, there may not be a direct linear relationship between A, B, and C. However, it is possible to estimate degrees of relatedeness fairly accurately based on morphological similarity. It may not always be possible to distinguish a direct ancestor, principally because of the vagaries of fossilization, and the disturbance/destruction of fossils over time — in general, a brother or sister of the missing link is close enough. The prediction is proven false by the available evidence. 2. An increased genetic burden over time as a result of the negative effect of mutations. This prediction is probably true in the absence of beneficial mutations or natural selection. If this prediction were true in nature, there should be a net decrease in overall population fitness of any given population of organisms over time. If this was the case, the survival of a given population over more than a few generations is questionable, and relates strictly to the rate that major deleterious mutations occur. Even with the action of natural selection (in the sense that it can select against negative mutations), the best that a population can hope for is a very tenuous equilibrium — that would be completely upset if the environment changed. Again, the evidence we would see would include rapid population crashes, and given the interrelatedness of populations within a given ecosystem, continuous (rather than episodic) mass extinctions. This is not the pattern we observe.
quote: It was certainly a valiant attempt. quote: Probably not. [Cobra: I will be traveling in Poland next week, so may not have access to the ‘net. I will try and check several times, but you know how that goes I will look for a response to any of your comments next Sunday. It’s been a pleasure.]
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
Cobra: You've now had over a week to respond. I answered your post in good faith. Seems you've decided that my effort was unworthy or something. Please advise whether you intend to continue our discussion or not.
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
Hey Cobra, thanks for your response.
quote: If you restate this as natural selection cannot operate on neutral mutations unless expressed (and delete the reference to progress), then I would agree with you. However, your assumption was mutations should almost always cause a bad effect. The vast majority of mutations are actually neutral in terms of their effect on survival. Also, you can’t seem to get away from comparing the two theories, which was not our intent. I merely worked through the implications of your assumption: if all (or nearly all) mutations are bad, populations will quite rapidly come to a situation of error catastrophe or mutational meltdown (I love that term). Your assumption, at least as stated, doesn’t even permit epistasis (equilibrium). Either the assumption is invalid, or it needs to be re-examined and modified. It simply cannot stand as a necessary assumption for creationism because both the evidence (of the majority of mutations being either neutral or beneficial) and the implications of the assumption make it invalid as stated. Note: given continually increasing deleterious mutational load, even with natural selection weeding out negative mutations at 100% efficiency — which is not observed — any change in the environment will wipe out the population because they are in a very tenuous situation.
quote: (a) Agreed. It is readily observed in nature that a small, isolated population is much more rapidly effected by changes in allelic frequency. However, and this is a key concept, changes in allelic frequency ONLY occur in relation to the marginal fitness of the alleles. (This is defined as the average fitness, weighted by frequency, of genotypes containing the allele of interest.) Any direct fitness effects of the allele translate directly into an effect on its marginal fitness. If there is linkage disequilibrium between the allele of interest and other selected alleles, this will also affect the marginal fitness. IOW, if all you have are negative mutations, even if partially offset by natural selection, your population rapidly goes bye-bye because of the net reduction of marginal fitness. A genetic death spiral. I’d appreciate your comments on what I wrote originally about mutational load==>crash vs the persistence of natural populations, which you failed to address. (b) Correct, they do not provide evidence against creationism. However, changes in allelic frequency based on your assumption #1, because of what I noted in (a), and the existence of beneficial mutations (which is how natural populations survive in the first place) DO invalidate your first assumption — which you have stated is a necessary pre-condition for creationism to be valid (the definition of a scientific assumption in a theory).
quote: All very nice. However, once again I need to point out the error in a too-strict application of your idea information to genetics, especially when we’re talking about mutation. I didn’t really want to get this deep into it, but it looks like I’ll have to. In the first place, you are misunderstanding what a mutation is. DNA in living organisms undergoes frequent chemical changes, especially during replication. Although most of these changes are quickly repaired, the ones that don’t are called mutations. A mutation, then, can be considered a failure of DNA repair. Your mathematical model is overly simplistic, as it assumes only insertion or deletion of a codon (if I understand what the numbers represent — although what is 0 supposed to be?). Another problem is most mutations occur in non-coding areas of the DNA string (introns). These mutations are, by definition, neutral — information can be added, subtracted, multiplied or divided on an intron with absolutely no effect on anything. There are quite a number of different types of mutation. Just to go into the most common:a) Single base substitution: A single base, say an A, becomes replaced by another. Single base substitutions are also called point mutations. This can take the form of: - missense mutation: the new nucleotide alters the codon so as to produce an altered amino acid in the protein - nonsense mutation: the new nucleotide changes a codon that specified an amino acid to one of the STOP codons. Therefore, translation of the messenger RNA transcribed from this mutant gene will stop prematurely. The earlier in the gene that this occurs, the more truncated the protein product and the more likely that it will be unable to function. - silent mutations: Most amino acids are encoded by several different codons. For example, if the third base in the TCT codon for serine is changed to any one of the other three bases, serine will still be encoded. Such mutations are said to be silent because they cause no change in their product. - splice site mutation: The removal of intron sequences, as pre-mRNA is being processed to form mRNA, must be done with great precision. Nucleotide signals at the splice sites guide the enzymatic machinery. If a mutation alters one of these signals, then the intron is not removed and remains as part of the final RNA molecule. The translation of its sequence alters the sequence of the protein product. b) Frameshift mutations: extra base pairs can be added or removed. The number can be from one to thousands. Frameshifts really mess things up if they occur in an exon in multiples of one or two. In multiples of three, there’s less problem (because the reading frame is shifted one full frame, rather than partially.) c) Duplications are a doubling of a section of the genome. During meiosis, crossing over between sister chromatids that are out of alignment can produce one chromatid with a duplicated gene and the other having two genes with deletions. This is also one way for both new information and novel genes to be produced. d) Translocations are the transfer of a piece of one chromosome to a nonhomologous chromosome. Translocations are often reciprocal; that is, the two nonhomologues swap segments. The break may occur within a gene destroying its function, the new genes may come under the influence of different promoters and enhancers so that their expression is altered, or the breakpoint may occur within a gene creating a hybrid gene (novel function). Every single one of these mutation types has the capability of either changing or increasing information, if you insist on looking at it that way.
quote: As stated, this makes no sense to me. You seem to be confusing biodiversity with inherited variability. These are two completely different concepts. Biodiversity refers to the relative numbers of different species within an ecosystem. We often talk about the richness of biodiversity. For example, a tropical rainforest is richer in biodiversity than a temperate pine forest, because there are simply more, different species for the same size geographical area. Variability refers to the relative frequency of different traits (alleles) within a species. For example, among butterflies there is huge variation in coloration and patterning within a single species — so much so that often only an expert with time on their hands can tell whether a particular specimen is the same or a different species. Speciation occurs by natural selection (which you apparently accept) operating on inheritable variability. IOW, variability causes (or permits, anyway) biodiversity. I guess my question is: how does an increase in biodiversity translate into a decrease in inheritable variability. By observation, it appears the opposite is true: more species yields more opportunities for mutation to create novel alleles for natural selection to operate on. It isn’t a zero-sum game. The parent species in the Galapagos example gave rise to 13 new daughter species — the parent species is still living in Ecuador. In point of fact, there’s a fourteenth daughter species living on Cocos Island (about 850 km from the Galapagos). Simply because they are different species and can’t inter-breed does not mean there is any loss of variability within species.
quote: Besides defining kind so that it can be used in discussion, you would need to show me some evidence that there were unoccupied niches lying around. Because of the exceptional diversity and apparent plasticity of life, even the most counter-intuitive niches are already filled: there are organisms found on the tops of the Himalayas and at the bottom of the Marianas Trench. There are organisms that live in petroleum and others which don’t even use the same chemistry we do that thrive on submarine thermal vents and metabolize sulfur.
quote: Agreed. Complex organisms, or even complex parts of organisms, are formed by natural selection operating on many mutations over very long periods of time. It appears, however, that you are falling into the trap of linearity. To wit, you are assuming the result was known in advance, and that what we see in nature today is some kind of epitome of life. This idea contradicts your earlier assumptions that life is going downhill in a handbasket. The apparent implication of your statement is if wings were fully formed from the start, and all change is negative, then over time birds would no longer be able to fly. That may be an oversimplification, but you do need to take all of the implications of your arguments into consideration when formulating a theory like this.
quote: Careful, you’re slipping away from defense/support of your theory to attacking ToE. I thought we’d agreed not to do that (I think I’ve been a very good boy in that respect thus far). Remember, you can’t validate a theory by trying to disprove another one. You can only validate a theory by providing positive evidence or inference. It’s fair to argue with, refute, or explain my counter-arguments directed at your assumption, but only by using evidence that I’ve ignored or misinterpreted — not by constructing a strawman to knock down. Who is they by the way?
quote: Actually, it isn’t all that complex. If you’ve got skin webbing between grasping members or loose skin between limbs (like the potto), and happen to be a tasty arboreal potential dinner, it is certainly within your interest to be able to jump from limb to limb, tree to tree, or cushion your way to the ground. Natural selection alone (which I remind you you accept) would tend to reinforce this adaptation by increasing the area of skin available as a gliding surface over the generations — he who jumps furthest safely lives longer to reproduce and pass on his jumping ability. BTW: the animals I referred to are living organisms. As such, the gliding frog would not be transitional to birds (which already exist). It could, however, be transitional to a flying frog down the roadquote: Wow, there’s a bunch of stuff here. Let’s see: 1. You need to define improvement and loss of information and then show with an example from nature of what this means. I can’t really follow your argument. 2. You are still back on the assumption of some kind of zero-sum game involved with heritable variation as it relates to biodiversity. I think at this point I would be justified in asking for some positive evidence (i.e., an example from nature) of what you mean.
quote: Ummm, what do you mean the difficulty of evolving dumbed down versions of traits? I think I missed that reference. If I did, I apologize and perhaps you could point it out. OTOH, a lot of eyes are complex. I wasn’t aware that trilobite eyes were much more than a pinhole camera — one of the simplest eye types beyond simple photophores. However, I’ll wait until you answer the geology question (or we can table it for now, suspending this prediction pending further review).
quote: I think you need to provide some evidence for the assertion that negative mutations are generally recessive traits. This is not borne out by the evidence. Just a few examples: a missense mutation causes sickle cell anemia, a nonsense (actually 200 different) mutation causes cystic fibrosis, etc. These are certainly not recessive (see below for further amplification).
quote: Actually, we have two problems here. In the first place, you are confusing somatic mutations (which are the most common) with germline mutation (which are the only ones inherited). Also, you don’t take into account inherited sex-linked mutations (which invalidate your oversimplified model). Finally, the model does not apply to asexually reproducing species. IOW, your explanation doesn’t work.
quote: See my response about marginal fitness waaaaay up above. Your assumptions, without being substantially reworked, do not appear to allow this final conclusion. Maybe it might be useful at this point for you to select a few concrete examples from nature that would provide, if not evidence, at least a point of discussion, for your model.
quote: You’re very welcome. I enjoy this level of discussion. Even if I disagree with you, the obvious effort you’ve put in to it and the depth of discussion is quite refreshing. Not to be snide, but have you considered fleshing out your model, adding a bit more detail, and trying to get ICR or AiG to publish it? Even if it’s wrong (
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
*Bump*
I don't want Cobra to forget about my and Mark's last posts. Giving him another chance to respond...
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
Cobra: Excellent post. I'll get to a substantive response hopefully today or tomorrow. Just wanted to say I've seen it, and thank you for responding.
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
quote: Way to go, Cobra!
quote: Not because they are insignificant (which I’m not sure means what you think it means in this context), rather because the vast majority of all mutations are neutral. By definition, even if thousands of base pairs were effected, if the mutation didn’t change the final product, there would be no effect on the organism’s survival one way or the other.
quote: Remember your statement of this assumption: 1. Mutations should almost always cause a bad effect. It really doesn’t matter for the sake of this part of the discussion how old life is. Error catastrophe as a direct result of mutational load depends on population size, relative susceptibility, the generation rate of the particular species, and a host of environmental factors. In other words, as I’ve argued elsewhere, without examining the particular organism in context, the part about bad effect is mostly meaningless. An example of this was a small fish studied in Mexico (I don’t have the actual study under my hand, but I can try and look it up if you want). Under certain conditions, the species reproduced asexually. Under other conditions, it used sexual reproduction (the study wanted to see which was a better bet for the species). The species was found asexually reproducing in one lake, while conditions favored sexual reproduction in a nearby lake. Cutting to the chase, in the asexually reproducing population there was a substantial increase in deleterious mutation load, observable by a decrease in population density, smaller average size, increased susceptibility to disease, etc. All observed in a very few years. Error catastrophe would have occurred relatively quickly in this population. In another study, this time on sexually reproducing European barn swallows (Ellegren H, Lindgren G, Primmer CR, Moller AP. 1997. Fitness loss and germline mutations in barn swallows breeding in Chernobyl. Nature 389:593-596) in a high-mutation environment (in and around the destroyed Chernobyl Nuclear Power Plant in Ukraine), there has been a substantial increase in deleterious mutational load observed in an isolated population. Albinism (a rare occurrence normally in this species), 70% reduction in population density, etc. All occurred in less than 10 years. The population of this species living in the highly radioactive exclusion zone around the plant is rapidly approaching crash. Both of these examples fit the pattern you have predicted for your assumption #1. I use these examples to illustrate that if we extrapolate these results to all of life, in a relatively short period of time we have all species heading the way of our Mexican fish and Ukrainian swallows. In larger, less isolated populations the effect would take longer — but not that much longer. The fact that these populations are exceptions rather than the rule — in other words, we don’t see this pattern commonly — disproves your first assumption.
quote: Yep, but that’s not what your assumption #1 predicts — that’s what we actually observe. See the difference?
quote: I think you’re confusing several issues here. In the first place, you have agreed that most mutations are neutral, neither negative nor positive. Second, I have shown that, in populations where your assumption is true, the populations are rapidly approaching meltdown. Basically, as I stated before, your assumption #1 is invalid. You have attempted to wiggle out from under this conclusion by agreeing that there are such things as neutral and beneficial mutations — but this very agreement violates your assumption.
quote: You’re dragging in a whole different animal. In fact, you’re dragging in several different animals. Could you please explain to me how this paragraph refers to 1. Mutations should almost always cause a bad effect. ? (I’m not avoiding the issue — we’ll be discussing it below.)
quote: There’s a problem here. As I’ve argued elsewhere, I don’t accept that genetics can be described as information in the context of this kind of discussion. Information can be a useful analogy, but as with any analogy too strict a reliance on it is hopelessly misleading. A lot of people take the analogy too far. Dawkins called it bad poetry (from Unweaving the Rainbow), and I agree. Remember that all RNA/DNA is is a chemical template for the construction of proteins. It manifestly NOT information. In the first place, you have not yet defined which type of information you’re referring to: 1. Shannon-Weaver Information: this is pure communications theory - defined as the probability that a given sequence will be received as sent. Information entropy changes depending on the probability you assign to a given sequence. This obviously doesn’t apply to biology, and certainly not to genetics — especially since, to make even an approximate measure of the Shannon information in a biological system you would have to include how influential the environmental factors are that effect the fitness of a particular trait. In short, the more descriptive you are about the system itself (including environmental variables), the more information the system contains. This, of course, has absolutely nothing to do with the number of base pairs on a chromosome or any mutational changes. 2. Kolmogorov-Chaitin Information: The Algorithm Information Theory (AIT) basically refers to the shortest possible program or string that describes the thing that contains information. IOW, it’s an abstract — a description of a thing — not the concrete thing itself. As such, not only doesn’t AIT apply to RNA/DNA, but it doesn’t even take into consideration things like methylation patterns, histones, etc. 3. Semantic Information: Again, purely a description, not a concrete thing. This describes the function, role, purpose, task, etc of a thing. IOW, besides being almost teleological when ascribed to a living system, it is again an abstract with no real relationship to an actual thing. I’m going to have to be somewhat dogmatic about this. Look, all these information concepts are abstract properties of abstract symbols. Information neither causes anything nor prevents anything. Information lies in our heads or in the way our heads relate to the rest of the world. It is trivially easy to change the information content of the genetics of an organism - just describe more or less detail. Information is an analytic property. Information theory can be a very useful tool, but insisting that there is some real-world relationship between information theory and genetics is like saying two round tree-grown fruits containing vitamin C are the same simply because one can be used to describe the other by analogy (i.e., apples=oranges, rather than apples resemble oranges in some ways). If you want to use information in this discussion, you’re going to have to convince me that it is relevant and actually represents a concrete reality — not an abstract analytical construct. (With thanks to Dr. John Wilkins).
quote: No! The two concepts are UTTERLY UNRELATED. Comparing them makes no sense whatsoever. [Takes deep breath.] Alright, one more time. 1. Species diversity, aka biodiversity, simply refers to the total number of different species within a given ecosystem. It does NOT refer to or even have anything to do with variability. A North American pine forest ecosystem contains about 20-30 species of birds. A tropical rainforest ecosystem can contain as many as 650. Hence, a tropical rainforest is higher in biodiversity. It has nothing to do with relatedness between species, and everything to do with the relative abundance of niches. Period. 2. Variability in biology ONLY refers to relative frequency of alleles within a particular species OR differences between parent and offspring within a sexually reproducing species. One example of the former is the mimicry found in many butterflies — there are innumerable species (and even whole genera) of tasty butterflies which resemble species of noxious butterflies. (I’ll forward some examples later — I don’t have my Butterflies of Costa Rica handy). For an example of the latter — just look in a mirror: the fact that you look different than your parents is an example of inherited variability.
quote: However, the basic idea of natural selection, which you have said you accept, is that Finch B will not directly produce Finch C, but rather some intermediate like Finch B2. In fact, Finch B wouldn’t exist if it hadn’t come originally, again via gradual mutations allowing adaptational change in a population of Finch A’s. Islands are really cool because that’s where we see the most striking examples of adaptive radiation (founder effect). There’s an island off Brazil called Quemada Grande where a single species of Bothrops was able to establish itself. Now, our good fer-de-lance is relatively common in the rainforests of Central and South America. Each of the Bothrops species and subspecies is poisonous, some more, some less. However the golden fer-de-lance of Quemada Grande is one of the most poisonous snakes in the world — and found nowhere else. Why? Oddly enough, because there aren’t any mammals on the island!!! (the snake’s normal prey). Hunh? The reason is because the snake has adapted to killing birds! A Bothrops on the mainland will normally bite, then follow its prey until it dies by scent. Guess what happens when you try that with a bird? It flies away. So the golden fer-de-lance species has, through natural selection, increased the virulence of its poison so the bird dies relatively immediately! Our golden killer is a distinct species — antivenin designed for a mainland Bothrops won’t save you from the bite of the ones on Quemada Grande. There’s heritable variation for you. In an even more relevant example: the rough-backed newt of the western US also displays a huge variation in skin toxicity depending on the local environment. In areas without heavy predation, it’s practically benign (well, not exactly). In areas where there are a lot of predators, specimens have been found that contain enough nerve toxin in their skin secretions to kill 17 fully-grown humans. This is variability within a single species — environmentally dependent adaptation. Take the toxic one’s out to a place where there’s no predation, and within a very few generations their skin is less toxic. I guess what I’m trying to say is you need to show me a) what programmed variability is and how it differs from Darwinian natural selection and b) how this provides evidence for creationism.
quote: How else? Again, we go back to the meaning of programmed variability. How is it defined? How is it detected? How do you differentiate this programming from RM&NS?
quote: See above inre Finches. Also see above inre Information.
quote: quote: I’ll allow a retraction of this statement. I was merely responding to your assertion. Not really relevant, anyway.
quote: Okay, how does your model explain inter-species competition? There are numerous examples — modern examples — of one species supplanting another because it is better adapted to a particular niche. How does special creation — and programmed variability — explain why this occurs (preferably without reference to the Fall quote: Actually, not really. You need to understand two things: 1) No step on the road can be considered in light of any subsequent step, only its predecessor. IOW, whereas I quite agree that a giant leap from scales to the seven complex forms of feathers used in flight is probably impossible (for all practical purposes), a change from scale to a slightly better insulating scale is quite possible. And from thence to increasing ability to insulate a poorly-homeothermic saurian body; to a small, well-insulated theropod that lived in trees and discovered (sorry about the anthropomorphism) that feathers were useful for gliding as well as insulation — and in fact permitted a radiation into a whole new, three-dimensional ecosystem. 2) No organism ever made a living as a transitional form. IOW, there isn’t a single complex structure possessed by any organism in nature, be it blood clotting or wings or the vertebrate eye, that was not fully functional and useful for its possessor AT THE TIME. Changes that allowed a net fitness advantage for the particular organism (not even the species as a whole), would be selected for. The definition of RM&NS.
quote: There’s evidence that arthropods pulled off the trick twice. Nonetheless, I think you’re basing your disagreement on an argument from incredulity, rather than evidence. There are a lot of radically different animals (I mentioned placentals and marsupials a while back), who’ve developed similar responses to particular environmental problems or opportunities. How does your model explain vastly dissimilar organisms filling nearly identical niches, separated only by geography (I’ve got a list as long as my arm from living organisms and fossils if you’d like to discuss specifics)? Also, how does the model explain symbiotic relationships between entirely different phyla (again, I have a list as long as my arm)?
quote: This assertion is not borne out by the evidence from nature. Examples of perfectly adapted flightless birds, for ex, abound. These were all positive adaptations - they lost their wings because they were no longer needed, and the birds were much more effective without them. (Sort of like snakes and whales losing legs, no?) Admittedly, many of these flightless birds are now extinct — but only because of a new factor in the natural selection equation: Man.
quote: Two things: I was talking about living gliders — and how examination of their current adaptations show at least one possible route towards flight. How does your model explain the potto or the other gliders I mentioned? Some of these critters are very close morphologically to their nearest, non-gliding, relatives — with the obvious exception that they can (almost) fly. Second, the statement about the designer is borderline argument from incredulity. Your assertion is not evidence. You would have to show positive evidence that a designer was required, or positive evidence of its existence for the statement to be valid.
quote: I’d say it already is — don’t look now but flight ain’t the only thing we can see in nature that could be on the road to something else we see in nature — lungfish and mudskippers come to mind (fish with transitional legs and an ability to breath air!) Your model needs to explain this apparent illusion.
quote: So you ARE using Kolmogorov-Chaitan AIT? I think I responded to that above — it is an invalid definition. You even admit it’s descriptive rather than functional. Next
quote: I’ll go along with a strict definition of improvement as you stated. However, you need to be careful that you don’t use it to imply there is some kind of purpose or ultimate end-state defined by improvement. As long as we keep this restricted to survival of a particular organism in its specific environment, then we’re in agreement. Remember, there’s no guarantee that an improvement will not be deleterious in the long run if things change. After all, the dinosaurs were improving their fitness for their particular ecosystem(s) for 120 million years. One piece of cosmic bad luck and bye-bye. The same problem occurs on the local as well as giant-cataclysm level.
quote: You didn’t really answer my question. Anti-bacterial resistance doesn’t reflect on biodiversity. I also recommend you reconsider playing the information card — I think I’ve shown it’s the wrong suit, and I won’t accept it until you show me otherwise. How does your model account for both antibiotic resistance AND biodiversity?
quote: See similar argument above.
quote: That’s not entirely accurate. However, I’ll be addressing that on Moose’s PE thread whenever I get around to it. Suggest we stick to the massive amount we’ve already got on the table here
quote: Cool by me. Outstanding response, Cobra. I think we’re finally starting to get somewhere. Thanks for the level of debate. Even if I (totally
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Quetzal Member (Idle past 5872 days) Posts: 3228 Joined: |
Cobra: You're doing great. You're going through, on a smaller (and certainly less acrimonious), scale what any scientist goes through when they propose a theory. Moreover, your responses are reasoned and well-thought-out. You're thinking through your model while we're discussing it. You even seem to be realizing that there may be implications to your model that you hadn't had a chance to consider. In addition - and for this I personally thank you - you have not resorted to spurious debate point-scoring tactics, ad homs, and specious quotations. In other words, you're doing better than 99.9% of the creationists I've either debated or read - including many of those who have impressive credentials and work at creationist organizations.
I look forward to your next response. It's a pleasure discussing this with you... [Edited to fix formatting.] [This message has been edited by Quetzal, 03-07-2002]
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