questions evolutionists can't or won't answer

That it would P, and when I produced public access video's I fully expected that this would be a point for callers in to NOT hang on to and too debate. For I would disagree with JM on if Jimmy Cricket ever came from the torque I subscribed to in the thread on sexual reproduction. It was for this reason that I pointed out in the videos that I thought it was a point won by Gish and not Morowitz (though I appreciated the need to enhance all chemistry education)Becasue a "side chain" is not necessarily and sufficiently a "functional group". I was thinking when in Providence RI of trying to write a book on the math that would be visualized in order to show how torque plus multi-gradients on the sea floor AND a transition from sulfur to oxygen may have been able to get the barrier from a cell to fish solved fancy enough to contain L. Pauling's thought on Euclid thus the chemical bond no matter how the dissipativeness could writ be. But the video was not to be. Maybe here more progress will occur without a simple antipattern being displayed. Call in telephone people were not this smart. Nor was/were the TImeWarner people who faciliated the show airing. I did not explain the first cytoplasm however which would have been requried to debate further.I am nearing this explanation as well as to rejecting some aspect in the behavior of Gottlieb that Lewontin already back peddled the waterfall on but I know acutally nothing on this point.

Percy writes:

---

No matter what label you place on him, were [Kelvin] alive today I suspect you two would agree on very little.

---

John Paul replies:

---

Would you want to live in a world where everyone agreed on everything?

---

You're missing the point, which was that Kepler's views on key points, such as the age of the earth, are in dramatic contradiction to your own. If you're looking for someone to cite in support your position, he seems an odd choice.

xxx writes:

---

What would call him? An anti-Darwinist (but not a Creationist)?

---

First, you can't equate modern Creationist views with those of scientists past (eg, Newton, Pasteur, Pascal, Mendell, Linne, Kepler) who merely accepted the then prevailing view of origins without being actual geologists (some in your list predated the field).Second, this is the fallacy of appeal to authority.Third, many of roughly Newton's time made more flexible Biblical interpretations then do YECs like yourself. They held the Biblical stories to be of actual events, but didn't believe them to be 100% accurate. The inflexible "literally inerrant" view only came about with the "Back to Fundamentals" movement of the early 20th century.Fourth, we don't know what they would think if they had the evidence available to us today.--Percy

quote:

---

Originally posted by Quetzal:
What's left, therefore, are the few mutations that are either mild enough to permit the organism to live long enough to reproduce, OR provide a genuinely beneficial phenotypical change These are the mutations that create the actual heritable novelty in a population. They are not "in the a priori (sic) population’s gene pool". They represent NEW additions

​

Actually, your error is your misunderstanding that mutation = cancer. As I explained, this is not necessarily the case.

---

--Your response does not go unnoticed.--Calling things NEW additions seems rash from the ‘mega’ perspective of the ToE. I observe them as mere DIFFERENT LATENT manifestations, because:
1) They do appear grossly ‘walled in’ by genetic-structural boundaries of the organism. That every organism indeed has its genetic bounds is presently seen and expected.
2) What is new is never ‘significantly’ new: i.e., never beneficial enough to incrementally make a novel complicated biochemical (let alone cellular) labyrinth and/or algarhythm. Recombinant technology splices only in metastatic ways that benefit non-host organisms (e.g., for human exploitation).
3) New isnever enough to incrementally make novel complicated labyrinths and/or algarhythms become another kind of life form. Speciation (even in the form of polyploidy) never forms new complex algarhythms and/or labyrinths, only new latent ‘traits’.
--This aspect of your mechanism must never be over-generalized in science until demonstrated. Else you, too, become religious while inferring polyploid mutations (the raw mechanism of the ToE) to cause of life’s complex labyrinths and algarhythms.
4) The sums of ‘new’ additions never harmonize those exceedingly complex interactions of these labyrinths and algarhythms, which are so unique and ‘set-in’ within every biodiversity.--Metastasis is a term that may be used in genetics. Non-oncologists and laymen may adopt this cancerous term, to express cancerous reproductive aberrations (genetics) in gamete cells.
--Polyploidy is an interesting phenomenon, but again limited to mutation spots else you observe metastasis, decay, etc. No doubt metastasis arises in these [i]hot[/] spots as well. Randomness and decay, thus, are allowed ‘some’ free expression beyond the mainstream norm as in your multi-tiered mechanism of NS involving beneficial mutations.--Note: (Correct me if I’m wrong) You seem to be scientifically underplaying mutations in the mega-ToE. That in my perspective is ‘jumping the boat’. Do you not need to DRASTICALLY ‘play up’ ka-zillions of incremental beneficial mutations (vs mere traits) for the mega-ToE to be viable? (I invite anyone to debate this)--Does not reproductive metastasis (cancer) remain as the only viable mutational mechanism left for the mega-ToE at this point, Quetzel (or any one)?

quote:

---

--Calling things NEW additions seems rash from the ‘mega’ perspective of the ToE. I observe them as mere DIFFERENT LATENT manifestations, because:

---

Why is this rash? Any mutation that causes a change to the DNA code and hence final protein product would be a new addition since the new code sequence didn’t exist in the genome before the mutation. It is certainly not a latent manifestation — implying the new code was already present (as opposed to gene duplication, reshuffling, etc, which could fit under a very generous interpretation of latent). Remember, a mutation is merely a copying error in DNA that isn’t repaired by the cell’s own repair mechanisms. I would argue that any change in the protein product — whether a single-base substitution, a frameshift or even duplication constitutes a NEW addition.

quote:

---

1) They do appear grossly ‘walled in’ by genetic-structural boundaries of the organism. That every organism indeed has its genetic bounds is presently seen and expected.

---

I’m sorry, Philip, but I have no idea what you’re on about here. What are the genetic-structural boundaries of an organism. Could you please provide an example of genetic bounds — since you state they are presently seen?

quote:

---

2) What is new is never ‘significantly’ new: i.e., never beneficial enough to incrementally make a novel complicated biochemical (let alone cellular) labyrinth and/or algarhythm. Recombinant technology splices only in metastatic ways that benefit non-host organisms (e.g., for human exploitation).

---

I’m not going to argue with your jargon — although I’ve never heard the terms labyrinth and algorithm used in this context in biology (you wouldn’t be inventing terms just to confuse me, would you? You can point to some mainstream literature that uses the terms in this fashion, yes?). You are simply incorrect that novel biochemical structures are never created naturally.The classic example is the evolution of an anti-freeze glycoprotein derived from a pancreatic gene that normally codes for trypsinogen in Antarctic fish. A reading error or frameshift mutation occurred in a small region spanning the boundary between the first intron and second exon of the trypsinogen gene plus amplification of a 9-nt Thr-Ala-Ala coding element from the trypsinogen progenitor to create a new protein coding region for the repetitive tripeptide backbone of the antifreeze protein. (The full article, Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish.) This is by no means the only example.

quote:

---

3) New isnever enough to incrementally make novel complicated labyrinths and/or algarhythms become another kind of life form. Speciation (even in the form of polyploidy) never forms new complex algarhythms and/or labyrinths, only new latent ‘traits’.

---

Again, I’m not entirely clear what you are trying to say. If you are attempting to argue against speciation in toto, I’m afraid I’m going to have to ask you to explain away a lot of very compelling evidence to the contrary, including ring species, rodent speciation (check out Madeiras Island studies on Mus musculus — six different species on one island — and they’ve only been there for 250 years!), the observed evolution of sticklebacks, the entire science of developmental genetics and molecular phylogeny, etc.

quote:

---

--This aspect of your mechanism must never be over-generalized in science until demonstrated. Else you, too, become religious while inferring polyploid mutations (the raw mechanism of the ToE) to cause of life’s complex labyrinths and algarhythms.

---

Once again, I have absolutely no idea what you’re on about. What aspect? You seem to be arguing that polyploidy — which is a whole ‘nother mechanism of speciation unrelated to anything we’ve discussed so far — is the ONLY mechanism. Wrong again. Polyploidy — chromosome multiplication. It’s very common in plant speciation, but relatively rare in animals. It is NOT a mutation.

quote:

---

4) The sums of ‘new’ additions never harmonize those exceedingly complex interactions of these labyrinths and algarhythms, which are so unique and ‘set-in’ within every biodiversity.

---

Sorry, once again you’ve gone over my head. Could you possibly explain what you’re talking about in layman’s terms, without jargon? Thanks.

quote:

---

--Metastasis is a term that may be used in genetics. Non-oncologists and laymen may adopt this cancerous term, to express cancerous reproductive aberrations (genetics) in gamete cells.

---

Uhhh, okay. However, you’re back to insisting mutation = cancer. This is not the case. [QUOTE]--Polyploidy is an interesting phenomenon, but again limited to mutation spots else you observe metastasis, decay, etc. No doubt metastasis arises in these [i]hot[/] spots as well. Randomness and decay, thus, are allowed ‘some’ free expression beyond the mainstream norm as in your multi-tiered mechanism of NS involving beneficial mutations. [/QUOTE]Once again you’re confusing mutation and polyploidy. Not the same thing.

quote:

---

--Note: (Correct me if I’m wrong) You seem to be scientifically underplaying mutations in the mega-ToE. That in my perspective is ‘jumping the boat’.

---

Err, nope. That’s pretty straightforward neo-Darwinian evolution. Mutation is how novel genetic material is produced. Variation is only the first step — after that you start working with natural selection and all its various complex mechanisms.

quote:

---

Do you not need to DRASTICALLY ‘play up’ ka-zillions of incremental beneficial mutations (vs mere traits) for the mega-ToE to be viable? (I invite anyone to debate this)

---

Nope. Just a few beneficial mutations or genetic reshuffling of existing genes, plus natural selection (especially directional selection: try this website Examples of Beneficial Mutations and Natural Selection for some nice abstracts of recent articles. Here’s a good article on evolution of novel proteins in mammals, Positive Darwinian selection drives the evolution of several female reproductive proteins in mammals. Here’s a really good article on the genetic basis for evolution, Morphological innovation and developmental genetics. I like this one because it shows that a small number of genes may be responsible for major morphological changes.

quote:

---

--Does not reproductive metastasis (cancer) remain as the only viable mutational mechanism left for the mega-ToE at this point, Quetzel (or any one)?

---

Since cancer is a negative survival pressure, I’d say 1. There’s no such thing as reproductive metastasis, and 2. It’s not even ONE of the mechanisms for ToE, let alone the only viable one.Philip, I say this with all due respect, you really need to read some basic biology — I’m not sure you even understand what you’re arguing against.

[QUOTE]Originally posted by Quetzal:
1. There’s no such thing as reproductive metastasis:
[/B][/QUOTE]DORLAND’S DEFINITION of metastasis: The transfer of disease from one organ or part to another not directly connected with it.
WEBSTER’S:
1. (Theol.) A spiritual change, as during baptism.
2. (Med.) A change in the location of a disease, as from one part to another. Dunglison.I’ve used the term metastasis, perhaps too loosely from your restricted ‘book’ perspective, I admit I can not find a better term at present to verbally express transfer of detrimental DNA to ‘non-direct’ parts of reproductive chromosomes: i.e., in gametes, diploid individuals, or other microbiological reproductive components of species. Perhaps you can suggest a better term.And the term labyrinth (Websters):
1 a : a place constructed of or full of intricate passageways and blind alleys
b : a maze (as in a garden) formed by paths separated by high hedges
2 : something extremely complex or tortuous in structure, arrangement, or character :
3 : a tortuous anatomical structure; especially : the internal ear or its bony or membranous partExamples are too numerous: ears, eyes, olfactory senses, sympathetics, reproductive systems, and the ka-zillions of biochemical labyrinths associated with each.The term algorithm= a step-by-step procedure for solving a problem or accomplishing some endExamples are too numerous: ears, eyes, olfactory senses, sympathetics, reproductive systems, numerous other systems and the ka-zillions of biochemical algorithms associated with each: Positive and negative eedback loops of harmones, enzymes, etc. on the biomechanical level. Cascading events in blood coagulation, healing, inflammation, etc. etc. Time would fail to go into algorithms of the immune system(s), botanical and environmental algorithms [QUOTE]Originally posted by Quetzal:
2. It’s not even ONE of the mechanisms for ToE, let alone the only viable one.
[/B][/QUOTE]Ah but it is the only viable one that I can conclude under the mutationalist scheme. [QUOTE]Originally posted by Quetzal:
Philip, I say this with all due respect, you really need to read some basic biology — I’m not sure you even understand what you’re arguing against.
[/B][/QUOTE]I’ve had too much biology (M.S.B.S), tutored and/or taught it on H.S., college, graduate, and post-graduate levels. Currently I have an applied working knowledge of it as a podiatric surgeon, etc. I admit my language is more crude compared to your scientific rhetoric (which I appreciate), but I believe I know what I’m arguing against:
1) A ToE that ‘forgets’ ‘beneficial mutations’ alone are the foundation of the mega-ToE.
2) The impossibility of such incrementally complex mutations forming labyrinths/ algorithms seen and expected to be seen everywhere in nature (without excuse).
3) Respectfully, human error and self-deception regarding ‘cause-effect’ relationships in biology.
4) My own misconceptions as well, in this field (which is why I enjoy discussing/arguing with you). That I may mature in my science as a physician, and in my ‘spiritual’ well-being, too.
5) The fraudulent and 'bigoted' study of our origins (both camps).--Philip

quote:

---

Originally posted by Quetzal:
1. There’s no such thing as reproductive metastasis:

---

quote:

---

DORLAND’S DEFINITION of metastasis: The transfer of disease from one organ or part to another not directly connected with it.
WEBSTER’S:
1. (Theol.) A spiritual change, as during baptism.
2. (Med.) A change in the location of a disease, as from one part to another. Dunglison.

​

I’ve used the term metastasis, perhaps too loosely from your restricted ‘book’ perspective, I admit I can not find a better term at present to verbally express transfer of detrimental DNA to ‘non-direct’ parts of reproductive chromosomes: i.e., in gametes, diploid individuals, or other microbiological reproductive components of species. Perhaps you can suggest a better term.

---

Actually, my objection is that I don’t think there’s any reason to bring in a new term. It’s not a question of perspective — book or not, the way I use the terminology is pretty much the way every biologist uses it. As to your specific use of metastasis, I appreciate the clarification, but submit that mutation covers any change in DNA code sequence either pre- or post-zygote. Once again, mutation does NOT equate necessarily to disease. Your use of metastasis in this context is misleading, at best. Beneficial mutations DO exist (see the articles I referenced in my previous post for several examples). The fact is, most mutations of any stripe are simply neutral as far as the individual organism is concerned.Although I accept the fact that you have a degree in biology, once again you bring in elements that are very non-standard, or at least used incorrectly, in the discipline. What do you mean by non-direct parts of reproductive chromosomes? The phrase doesn’t seem to make sense to me. Perhaps you could explain what you mean.In addition, all sexually reproducing organisms are diploid. One copy of the chromosomes is received from each parent. This is one of the reasons that even germline mutations may not have any effect on the organism — they may have received a fully functioning copy from the other parent (c.f, heterozygous recessives.)

quote:

---

And the term labyrinth (Websters):
1 a : a place constructed of or full of intricate passageways and blind alleys
b : a maze (as in a garden) formed by paths separated by high hedges
2 : something extremely complex or tortuous in structure, arrangement, or character :
3 : a tortuous anatomical structure; especially : the internal ear or its bony or membranous part
Examples are too numerous: ears, eyes, olfactory senses, sympathetics, reproductive systems, and the ka-zillions of biochemical labyrinths associated with each.

---

I understand what labyrinth means. If you are referring to anatomical structures in the sense that they are irreducibly complex (a la Behe), then your use in the context of definition 2 above is at least slightly justified — although in this case you’re going to have to show that the examples you gave are, in fact, irreducibly complex — something Behe himself has failed to do. I’m not going to argue definitions with you, but I would like to point out that definition 3 is merely a reference to the shape — a labyrinth can be used as a descriptive metaphor for the convolutions and maze-like structure of the inner ear. I don’t suppose there’s any point in drawing your attention to the varieties of suture patterns in foraminifera (you’d love ‘em, they’re an almost classic example of the golden mean in action in nature) as an illustration of how convoluted — labyrinthine — structures can be formed quite easily in nature? My point is you are not justified in using the term as a falsification.As for how complicated systems such as protein cascades can be formed (evolved ) naturally, that’s a subject a whole lot more complicated than can be realistically covered in an Internet forum post. With cooption, recruitment, exon shuffling, and a dozen other observed mechanisms that can be involved, my only suggestion here is for you to check out a recent book on evolutionary developmental biology. Alternatively, you can probably find this article in a good university library: Thornhill RH, Ussery DW 2000, A classification of possible routes of Darwinian evolution, published in The Journal of Theoretical Biology, 203: 111-116, 2000. Once you’ve caught up on some of the recent advances in evolutionary biology and microbiology, anatomy, etc, you may find the evidence more compelling. Happy reading!

quote:

---

The term algorithm= a step-by-step procedure for solving a problem or accomplishing some end
Examples are too numerous: ears, eyes, olfactory senses, sympathetics, reproductive systems, numerous other systems and the ka-zillions of biochemical algorithms associated with each: Positive and negative eedback loops of harmones, enzymes, etc. on the biomechanical level. Cascading events in blood coagulation, healing, inflammation, etc. etc. Time would fail to go into algorithms of the immune system(s), botanical and environmental algorithms

---

I’m aware what the term algorithm means. My question was how you were using it. Would you care to try an algorithmic approach to refute the evidence provided in the antifreeze glycoprotein article I referenced? The authors certainly don’t see an evolutionary problem in the development of this protein. Considering that in Algorithm Information Theory (at least as proposed by Kolmogorov-Chaitan) the amount of information is an abstract thing, not a concrete fact about the world, it applies only to a description of things, not to the things themselves. If DNA is information bearing, it is because we can make a sequence of abstract symbols out of it and apply AIT to that. Even so, we keep finding features of DNA that the simple code does not capture (eg, histone and methylation patterns). I bid you, Good luck in your refutation.

quote:

---

Originally posted by Quetzal:
2. It’s not even ONE of the mechanisms for ToE, let alone the only viable one.

---

quote:

---

Ah but it is the only viable one that I can conclude under the mutationalist scheme.

---

Perhaps it is the only viable one you can conclude. However, in this case, you’re pretty much a minority of one. You certainly have failed to show that disease metastasis even has any bearing on this discussion — let alone that evolutionary biologists are basing their theories on it as such.

quote:

---

Originally posted by Quetzal:
Philip, I say this with all due respect, you really need to read some basic biology — I’m not sure you even understand what you’re arguing against.

---

quote:

---

I’ve had too much biology (M.S.B.S), tutored and/or taught it on H.S., college, graduate, and post-graduate levels. Currently I have an applied working knowledge of it as a podiatric surgeon, etc. I admit my language is more crude compared to your scientific rhetoric (which I appreciate), but I believe I know what I’m arguing against:

---

No insult intended. My apologies if you took it that way. However, with your stated background I’m having difficulty comprehending why you consistently misunderstand basic biological concepts. Your genetics, developmental biology, microbiology, and biochemistry assertions are often simply wrong. I’m having a hard time reconciling the two.

quote:

---

1) A ToE that ‘forgets’ ‘beneficial mutations’ alone are the foundation of the mega-ToE.

---

This is YOUR assertion — and I have to say it’s becoming a rather obvious strawman. I have argued consistently (and repetitiously, I’m afraid) that beneficial mutations are only ONE aspect of the ToE. Selection pressures operating on the phenotypical variations occurring in a given population of organisms — whether arising through mutation or the normal recombination/reshuffling of genetic material that occurs during gametogenesis — provide the foundation of the ToE. Your assertion is wrong, and ignores almost all of biology. You don’t even have to accept evolution to be aware of variation in populations and the statistical processes that change the relative frequency of expressed alleles. Just look in the mirror: unless you are a clone of your parents, you differ from them in many traits. Your cousin is even more different. In the wild, given that some of these traits can have an effect on the survival of an organism (an herbivore that runs very fast or jumps very high has a better chance of surviving a predator’s attack than one that runs slowly or doesn’t jump high enough), the variation that provides at least some survival advantage to an organism is the one that gets passed on. This is the type of variation that drives evolution. The origin of that variation is what I’ve been discussing in the last several posts.

quote:

---

2) The impossibility of such incrementally complex mutations forming labyrinths/ algorithms seen and expected to be seen everywhere in nature (without excuse).

---

Why is it impossible? For just one example, Bandyopdhyay PK, Garrett JE, Shetty RP, Keate T, Walker CS, and Olivera BM, 2001, Glutamyl carboxylation: An extracellular posttranslational modification that antedates the divergence of molluscs, arthropods, and chordates. In this article, the authors report the discovery that one of the key essential elements in the mammalian blood clotting cascade, carboxylglutamate (Gla), is a modification of much older protein found in simpler organisms.

quote:

---

In 1984, Gla was shown to be present in a highly specialized invertebrate system, venom peptides of the marine cone snails (Conus). It was found that a neuroactive Conus peptide, conantokin-G, which is a 17-aa peptide ligand produced in the venom of the fish-hunting cone snail, Conus geographus, contained five residues of Gla. This peptide targets a subtype of the glutamate receptor, the N-methyl-D-aspartate receptor. A variety of other Conus venom peptides, some in the conantokin family related to conantokin-G, but others with completely unrelated amino acid sequences, also proved to have Gla residues. These discoveries provided initial evidence suggesting that the role of this posttranslational modification in blood clotting might be only a small part of the total biological picture. Not only was Gla present in invertebrates (which was totally unexpected), but it was found in several entirely different structural and functional contexts. Biochemical experiments established that the posttranslational conversion of glutamate to Gla in Conus peptides had the same general requirements as had been established for mammalian -carboxylation, i.e., reduced vitamin K, carbon dioxide, molecular oxygen, and a recognition signal sequence. (emphasis added, references removed for clarity)

---

Impossible? Apparently not

quote:

---

3) Respectfully, human error and self-deception regarding ‘cause-effect’ relationships in biology.

---

This certainly occurs. However, I think you need to provide specific examples showing how widespread the problem is, as well as how this refutes the ToE. This isn’t biblical inerrancy, after all. It’s science.

quote:

---

4) My own misconceptions as well, in this field (which is why I enjoy discussing/arguing with you). That I may mature in my science as a physician, and in my ‘spiritual’ well-being, too.

---

Okay, glad you’re enjoying the discussion. I obviously don’t expect to change your mind, but from my perspective it’s useful to get the actual science on the table. Viva los lurkers! [QUOTE] Hmm, not sure I understand this. If you’re arguing that the biochemical origins of life are not proven, I agree with you. However, since every OTHER phenomenon in nature IS understandable using natural laws without recourse to the supernatural, I have to say that I’m relatively confident that abiogenesis will ultimately be understood the same way. I’m content to wait. Fraudulent it certainly isn’t — nobody’s setting out to deceive anyone. The only true a priori bias I’ve ever encountered is from the religious side. After all, since you don’t profess a belief in the Egyptian or Norse pantheon alongside your particular flavor of the Christian god, I’d have to say that the only difference between us is that I believe in one less deity than you do

quote:

---

Originally posted by Quetzal:
I have argued consistently (and repetitiously, I’m afraid) that beneficial mutations are only ONE aspect of the ToE.
Selection pressures operating on the phenotypical variations occurring in a given population of organisms — whether arising through mutation or the normal recombination/reshuffling of genetic material that occurs during gametogenesis — provide the foundation of the ToE.

---

(Note, before commencing, I appreciate your quoting Bandyopdhyay PK, et al, as I do not actually look up most Internet references; your own sequential logic seems to supercede theirs, however--no flattery intended)--Your quoted statement above is all that is necessary to refute. You just inferred normal recombination/reshuffling of genetic material and played-out all the freak mutations, rhetorically. You can’t do that Quetzel, not within the framework of the mega-ToE (supposed high level trans-taxonomic ‘speciation’) ... because:--Incrementally, Mega-ToE mutations/recombination/reshuffling must become abnormal, albeit beneficial to be viable: That is innumerable incremental mutations must be eventually become uncanny to be 'selected':--There can be nothing ‘normal’ about incrementally uncanny variations of ‘set in’ and highly interdependent complexities (not merely ICs )of organs, the higher-level organs, especially. Thus the mega-ToE of origins becomes increasingly impossible, the more interdependent the biological complexities become (see my foot example under the thread listed below).--At least call your theory of origins by its correct name: the Mega-ToM (the ‘M’ for ‘Mutants’ since ‘Metastasis’ is an unacceptable biological term at present)--The perpetrated fraud, self-deception, obstinacy, and/or delusion here is maxed-out, precisely here ... by numerous 'scientists'. Why, exactly, I won't sermonize here. (Note: Your keenness in this subject is nonetheless appreciated)--Now knowing you will perceive all this ‘Brad-like’, hypocritical, etc., I invite you to rebuke me here, but then, continue a logical rebuttal on the thread entitled: Has human evolution stopped. There, I logically explained why mega-evolution of the human foot has indeed stopped (and never started).

​

[This message has been edited by Philip, 06-03-2002]

I'm a bit unhappy, after the last two lengthy posts I provided, that this is the best you can come up with. Philip, it appears you are studiously ignoring my specific points. If this discussion is to continue, I would ask that you take a little more time and address or rebut the points I've made. Especially since the examples and discussion I have laboriously provided are direct refutations of many of your assertions. Thanks. [QUOTE]Originally posted by Philip:
Quetzal: I have argued consistently (and repetitiously, I’m afraid) that beneficial mutations are only ONE aspect of the ToE.
Selection pressures operating on the phenotypical variations occurring in a given population of organisms — whether arising through mutation or the normal recombination/reshuffling of genetic material that occurs during gametogenesis — provide [b]the foundation of the ToEPhilip: --Your quoted statement above is all that is necessary to refute. You just inferred normal recombination/reshuffling of genetic material and played-out all the freak mutations, rhetorically. You can’t do that Quetzel, not within the framework of the mega-ToE (supposed high level trans-taxonomic ‘speciation’) ... because:[/QUOTE]This is getting a tad surreal. I'm not quite sure why you keep insisting that I subscribe to your (erroneous) version and/or misunderstanding of evolution. Nothing I have posted so far on this thread or any other is in any way controversial or unaccepted in the context of mainstream evolutionary biology and genetics. I'm quite sure that if I had posted anything incorrectly, one of the experts on this board would have been all over it with hob-nailed boots.I haven't "inferred" anything when I talk about "normal" recombination during gametogenesis. This is such fundamentally basic biology - it's not even evolution!!! - that I'm surprised you would even question it. EVEN IN THE ABSENCE OF MUTATION, the process of meiosis in sexually reproducing organisms produces variation upon which natural selection can operate.Cross-over: In prophase I, two non-sister chromatids aligned together swap sections while synapsed together. The process is called crossing over. It is reciprocal - the segments exchanged by each non-sister chromatid are identical (but often carry different alleles).Each chromatid contains a single molecule of DNA. So crossing over is really just the swapping of portions of adjacent DNA molecules. It must be done with great precision so that neither chromatid gains or loses any genes. In fact, crossing over has to be sufficiently precise that not a single nucleotide is lost or added at the crossover point if it occurs within a gene. OTHERWISE YOU GET A MUTATION! This form of recombination can create new alleles in the recipient gamete. THIS IS NOT MUTATION!!!! It is a basic property of meiosis.Random assortment: In meiosis I, the orientation of paternal and maternal homologous chromosomes during metaphase is random - hence during anaphase I each homologue separates and moves to its respective pole. The poles are separated in meiosis II. Therefore, although each cell produced by meiosis contains one of each homologue, the number of possible combinations of maternal and paternal homologues is 2^n, where n = the haploid number of chromosomes. In humans this translates to 2^23, or 8,388,608 possible combinations of chromosomes FOR EACH GAMETE!!!!!Fertilization: If the parents differ genetically - each providing one of the 8 million possible combinations - new combinations of genes occur in their offspring.This is one of the primary ways variation occurs within a population: the recombination of existing genetic material. Natural selection operating on the individual expression of this variety leads to changes in the frequency of alleles in the population. This is utterly uncontroversial and so basic that I'm aware the idea is presented in Jr High School biology texts. You must have slept through that part of all those biology courses you supposedly took.

quote:

---

--Incrementally, Mega-ToE mutations/recombination/reshuffling must become abnormal, albeit beneficial to be viable: That is innumerable incremental mutations must be eventually become uncanny to be 'selected':

---

This is your assertion. If you are going to continue to argue this point, you need to present evidence that meiosis in the absence of mutation is abnormal. Then you can present evidence that all mutations are themselves "abnormal". Mutations, as I've continually pointed out, are the source of novel genetic material. When the selection pressures on a population change, it is the presence (or absence) of these novel traits that determines the survival or extinction of the population. A very conservative estimate is about one non-lethal mutation in any given locus per 100,000 gametes. That means that a human baby, for instance, will be born with 1-3 mutations. Combine these mutations (most of which are neutral in terms of survival) with the recombination during meiosis, and voila, you have literally staggering amounts of potential variation upon which natural selection can operate.

quote:

---

--There can be nothing ‘normal’ about incrementally uncanny variations of ‘set in’ and highly interdependent complexities (not merely ICs )of organs, the higher-level organs, especially. Thus the mega-ToE of origins becomes increasingly impossible, the more interdependent the biological complexities become (see my foot example under the thread listed below).

---

Ah, the old argument from incredulity raises its head. Pure assertion - care to take a stab at providing evidence of "uncanny variation", and what you mean by "set in"?

quote:

---

--At least call your theory of origins by its correct name: the Mega-ToM (the ‘M’ for ‘Mutants’ since ‘Metastasis’ is an unacceptable biological term at present)

---

You can call it anything you want - and as often as you want. Your insistence on this point when I have patiently provided the actual scientific terms and mechanisms is becoming redundant. "My theory", as you put it, is absolutely, positively, wholly neo-Darwinian synthesis. I'm probably about as orthodox in this science as you can get.

quote:

---

--The perpetrated fraud, self-deception, obstinacy, and/or delusion here is maxed-out, precisely here ... by numerous 'scientists'. Why, exactly, I won't sermonize here. (Note: Your keenness in this subject is nonetheless appreciated)

---

Again, you should - as I asked previously - provide evidence that any biologist has deliberately "perpetrated fraud", indulged in "self deception", or is somehow deluded because they find that nearly every observation they make in nature adds more to the strength of the evolutionary edifice. The only obstinancy I see is yours.

quote:

---

--Now knowing you will perceive all this ‘Brad-like’, hypocritical, etc., I invite you to rebuke me here, but then, continue a logical rebuttal on the thread entitled: Has human evolution stopped. There, I logically explained why mega-evolution of the human foot has indeed stopped (and never started).

---

I have never accused you of Brad-like behavior. I have stated, and will continue to do so, that in many cases your use of non-standard terms is confusing. As far as the human foot goes, since I know sod-all about it, I'll take a look at the thread but doubt I'll have anything to do with the discussion.Meanwhile, you can try your hand at refuting any of the evidence I've provided in this thread. More handwaving or ignoring my posts will ultimately get you on my ignore list.

quote:

---

Originally posted by Quetzal:
I'm a bit unhappy, after the last two lengthy posts I provided, that this is the best you can come up with. Philip, it appears you are studiously ignoring my specific points. If this discussion is to continue, I would ask that you take a little more time and address or rebut the points I've made. Especially since the examples and discussion I have laboriously provided are direct refutations of many of your assertions. Thanks.

​

Meanwhile, you can try your hand at refuting any of the evidence I've provided in this thread. More handwaving or ignoring my posts will ultimately get you on my ignore list.

---

--When have I ignored any of your posts! I fished out info from your last post because many of your specific points there, I’ve already ‘dismissed’ from my perspective; that is, they are no longer dissonant to my scientific and/or ethical conscience. I’ve focused on the dissonant ones in order to cut to the chase. I, too, have spent hours of laborious time (probably exceeding yours) addressing your keen points, marveling at your rhetoric.--But enough!--You’ve got me convinced that meiosis is highly variable and even mutable (may I use that term) to allow much beneficial adaptation within the confines of the gene-pool
1)--Without arguing on terms, even a so-called ‘non-mutational’ meiotic mega-ToE mechanism appears to me as mutational or mutation-like, since eventually diploidy, recombinance, deletion, or other mutational (-like) phenomenon will have to occur in the chromosomes, right? That brings us back to mutations as being foundational in the ToE, Quetzel.
2)--Also, numerous Drosophilae studies seem to infer high taxonomic genetic limitations and restrictions don’t you think? Do you currently uphold that non-mutational mechanisms are foundational for fruit flies (or a more mutable pre-cursor) to ‘evolve’ into humans as such?
3)--Gross--not minute--mutations are necessary. I don’t see how anyone can conclude meiosis (that is ‘micro-mutational’) in NS is ever powerful enough (Dawkin’s word) to make sophisticated gross high taxonomic changes, due to the innumerable delicately balanced interdependent bio-complexities that must be negotiated with such changes.
--Thus, mutational/mutation-like changes is all I see for the mega-ToE to be viable. The necessary gross mutational/mutation-like changes (normal or abnormal) that are not neutral are almost always adverse, i.e., catastrophic to the delicately balanced interdependent bio-complexities of the organism. Extinction invariably follows such a course.
--The alternative, minute non-mutational micro-evolution fails in the mega-ToE as explained in 1. and 2. (above).If you don’t like my ‘hand-waving’, then I respect you if you put me on your taboo list.
--I can’t argue what is already clear to me, scientifically.
--It’s nearly impossible to win with a creationist at my age (45).
--My time is as valuable as yours. I’m not trying to cheapen your discussion. Forgive me if it appears that way, or if I have offended in any way.
--Now, I thoroughly appreciate your evo-stance, your coherence per se, your patience with me, and your very excellent discourse of Meiosis as a strong mechanism of genetic variation sans mutation. (I wish the others patiently laid it out and spelled it all out as you did. Note: The books, the experts on this panel, etc. do not (in my meager opinion) coherently nor mechanistically express the ToE to the same degree as you do.)

quote:

---

Originally posted by degreed:

​

One of my Favorite Flaws
--Even crude mathematical models can demonstrate (and can be field-tested) that any species wishing to evolve significantly (into another species) would require a time period of at least one quadrillion years, a body length of one or fewer centimeters, and a generation cycle of no more than three months. Biology is more fun than math (to me), but it leaves excess room for debate (which is also fun).

---

Wow. I have read some doosies in my time, but this one is a mind-bender.Perhaps you could provide some references for this, degreed?

JP posted his opener verbatim on the Baptist Board, got some replies, and engaged in his usual rhetoric. Here is my last response there, dated 6/17, as yet unanswered:

quote:

---

:

​

Scott Page:
The time constraint issue is a flim-flam

​

John Paul:
Things take time that much is for sure. Science is NOT in the habit of producing instant results. Surely a person in your position would understand this. The only flim-flam is the passing of the ToE as science.

---

Science does take time. But as you just admitted, creation had been the reigning paradigm since well before the ToE. Regardless of your personal distaste for and inexperience in the sciences, the ToE is, in fact, scientific and it has in its support data from numerous fields of science. These repeated charges of the ToE not being science and such smack of desperation and an ignorance of the available data.

quote:

---

:

​

Scott Page:
As for the ‘questions’ posed to evolutionists, they are largely of the type that there will probably be no answers for, as they seem to be in the realm of the origin and very early diversification of life. Not coincidentally, I’m sure, an area that there is very little physical evidence for.

​

John Paul:
Thank you. Then the ToE is out of the realm of science and out of reach of scientific method.

---

Now THAT is a non-sequitur. Please produce documentation that abiogenesis is the pillar of the ToE that you seem to be making out to be. If this one tangential issue is inaccessible to the normal routes of investigation, I fail to see any logic or rationale in proclaiming that the ToE is therefore not scientific. A dearth of physical evidence means simply that any given hypothesis will benefit from only a small amount of evidence. Your ‘conclusion’, therefore, is quite unwarranted.

quote:

---

:

​

​

Scott Page:
The questions have little to do with evolution as such.

​

John Paul:
They show the grand sweep of the ToE can’t be objectively tested.

---

No, they show that you have latched onto an area of research for which there is very little physical evidence and have proclaimed it the most important such area, and that if none of the handful of lurkers or participants on this discussion board can answer the ‘questions’ to your satisfaction — and I doubt you would accept any answer as valid regardless of the source or the amount of documentation — that, therefore, evolution must be wrong/unscientific/etc.

quote:

---

:

​

John Paul:
No it doesn’t. The EVIDENCE when applied objectively indicates a shared (i. e. Common) Creator. We have different number of chromosomes. That, taken objectively, would say we didn’t share a common ancestor unless chromosomal fusion could be objectively tested.

---

What do you mean chromosomal fusion could be objectively tested? Again, it appears that you believe that chromosomal fusion was the linchpin of the descent of humanity from an ape-like ancestral stock. While such a line of reasoning might seem to have merit to the underinformed, in reality, it is a non-starter.
For example, the chromosome numbers in the Primate superfamily Cercopithecoidea vary from 2n=46 and 2n=72 (Primate Anatomy, An Introduction, 2nd Ed. 2000.)This guenon (C. mona) has 2n=66.
http://www.primate.wisc.edu/pin/images/img4697.gifThis one (C. mitis) has 2n=72.
http://www.primate.wisc.edu/pin/images/img4284.gifShould we conclude:1. That chromosomal fusions/splittings/rearrangements are paramount in the microevolution of these guenons?
2. That if we cannot objectively test whether or not such events can explain the descent of these guenons from an ancestral stock that they were independently created?2a. If yes to #2, how then can any karyotypic evidence be used as evidence of any type of descent?

quote:

---

:

​

Scott Page:
Even creation science confirms this - see http://creationresearch.org/crsq/abstracts/sum34_4.html
wherein the objective (molecular) data indicates a human-ape ancestry, but this is rejected in favor of SUBJECTIVE (morphological and ecological) data, even though the same data they rejected had been used as a ‘reliable’ indicator for other groups. I had some personal communication with one of the authors of the linked study, and made some disturbing discoveries regarding their use of morphological data as well, that I will expand on if necessary

​

John Paul:
As I have stated several times now, Baraminology is a relatively new research venue. The current molecular data can easily point to a Common Creator. I am confident that once we decipher the genome, that premise will be borne out.

---

What does that have to do with Baraminology’s inability to apply criteria in an unbiased and arbitrary manner? These are supposed to be the ‘rising/shining stars’ of creation science. ReMine and Wise were consulted and/or used as references in these papers. I am confident that the more we learn about genome evolution, the more descent will be indicated. My confidence is being borne out on nearly a daily basis. Yours first needs to be filtered through the lenses of creationists who discard and wildly extrapolate what evidence there is to fit their preconceived notions.

quote:

---

:

​

Scott Page: What are the objective criteria upon which the exception for humans is premised?

​

John Paul: Baraminology is relatively new. But, unlike the ToE, I would hope it could be objectively tested before its conclusions are considered to be scientific dogma.

Scott Page:
So you have no answer then, fine. The methods employed by those using ToE-based hypotheses of descent have been tested on knowns.

​

Science 1991 Oct 25;254(5031):554-8
Gene trees and the origins of inbred strains of mice.

​

Atchley WR, Fitch WM
Phylogenetic analyses of 144 separate loci reproduce almost exactly the known genealogical relationships among these 24 strains.

​

John Paul:
Wow, mice evolving into mice. Producing a genealogy tree? That’s what you are offering? Are you saying that because this appears to work on knowns that it is OK to extrapolate to unknowns? This is the crux of the debate- extrapolating from knowns. It is hardly a given.

---

You failed to grasp the significance of the results I cited. It is not a question of mice evolving into mice — it is an issue of the testing of the methodology employed examining hypotheses of descent. The methods employed in molecular phylogenetic analyses were used on a known geneaology of inbred mouse strains to see whether or not these methods would reproduce the known relationships. Pretty straightforward.
I am saying that when a methodology works on knowns, that it is standard procedure to then be confident that the conclusions based on these methods, when applied to unknowns, is valid. That is how science — and even, I would hope, engineering — works. Or do you, in designing software, have to continually re-invent the various methods of writing software?

quote:

---

:

​

Scott Page:
One example of many.

​

John Paul:
That’s great. So far it looks like evidence for variations within a Created Kind.

---

Please then explain how one would test a methodology on a ‘known’ set of evolutionarily related non-intraKind creatures to your satisfaction. All I see here is the common creationist tactic of setting up no-win situations for the ToE. Were I to cite a study in which a methodology had been tested on, say, whales and hippos, doubtless the authors would be accused of circular reasoning and the whole issue hand-waved out of existence. There is simply no way to meet the ever-changing, arbitrary, biased ‘demands’ of the non-scientifically oriented ideologue.

quote:

---

:

​

John Paul: Do you have a reference? [re:whale legs]

Scott Page:
I do . Here is one, though not on Minke whales specifically:

​

http://www.ucmp.berkeley.edu/mammal/cetacea/cetacean.html

​

John Paul:
It doesn’t mention a femur. The alleged hind limbs are actually only that in the view of evolutionists.

---

The pelvis is discussed a bit. What do you suggest a long bone associated with a pelvis be called?

quote:

---

:

​

Do we have any genetic evidence that would show that legs can be erased like that?

​

Let me explain: If these bones were at one time femurs that did form hind limbs, then what happened to the rest of the leg? For example, can we, with genetic engineering, alter some organism’s (with legs) genome and see if we can get an organism with only femurs for hind limbs? Or maybe take a whale and using genetic engineering splice the necessary sequence into the whale’s genome (or whatever was necessary) to see if fully formed legs appear?

---

What is this ‘genetic engineering’ all about? There are plenty of genetic conditions that result in the formation of stunted limbs (or no limbs at all). Meromelia is a condition in humans that results in limb malformations. Caudal dysgenesis results in the absence of the coccyx and in some cases the sacrum in humans. It is no real surprise that such anomalies exist. In the case of terrestial bipeds, these conditions are of course non-adaptive. So, yes, there is evidence that limbs or parts of limbs can be un-developed.

quote:

---

:

​

Wouldn’t they only be femurs if they belonged to legs? So by calling these femurs it is being assumed they are legs or were from legs.

​

Scott Page:
Grin They are called femurs because they are attached to or associated with pelvi which are attached to or associated with the sacral portion of the skeleton, just like in us and mice and other mammals.

​

John Paul:
From Britannica:
FEMUR: limb or appendage of an animal, used to support the body, provide locomotion, and, in modified form, assist in capturing and eating prey (as in certain shellfish, spiders, and insects). In four-limbed vertebrates all four appendages are commonly called legs, but in bipedal animals, including humans, only the posterior or lower two are so called.
Are you changing the definition of femur to suit your needs? Do you have a definition of femur other than the one Britannica offers?

---

I wasn’t aware that
1. Brittanica is the ultimate authority on scientific terminology
2.That shellfish, spiders, and insects have femurs (they have exoskeletons).
3. that a femur is a limb or appendage
Looking into point 2 above should make it clear what I think of my point 1.I prefer to use ‘definitions’ that are relevant to the discussion at hand and that are produced in the proper context. From Kardong’s Vertebrates, 2nd Ed., 1998. In the section on the basic parts of the appendicular skeleton:
The limb region closest to the body is the stylopodium, with a single element: humerus of the upper arm, femur of the thigh.
A few pages later, there is some detail on the anatomy of living and fossil tetrapods and bony fish. On p. 314, Fig. 9.13 has drawings of the limb (fin) structure of some living sarcopterygians. In particular, the Neoceratodus fin/limb structure has a femur explicitly indicated. It is a single bone that connects the pelvic fin to the pelvic girdle (with a ball and socket joint, no less). I would dare say that such an arrangement — the presence of a femur in this fin/limb assemblage — has nothing to do with a leg. Of course, you should have paid more attention to your preferred Britannica definition (emphasis mine):
FEMUR: limb or appendage of an animal, used to support the body, provide locomotion, and, in modified form, assist in capturing and eating prey (as in certain shellfish, spiders, and insects). In four-limbed vertebrates all four appendages are commonly called legs, but in bipedal animals, including humans, only the posterior or lower two are so called.

quote:

---

:

​

Scott Page:
You responded with the above. It is a non-sequitur because it is clear in your quote (I assume this hasn’t or isn’t being tried because of politics. With our genetic engineering we should be able to duplicate that.) that you think that the chromosomal fusion event was pivotal, indeed, perhaps caused the speciation event in question.

​

John Paul:
Not so. I think chromosomal fusion is part of it and a part we should be able to duplicate.

---

Duplicate what? What would we perform this fusion in? I was unaware that the ape-like ancestor from which humans and apes descended had been identified, much less that it is still alive and available for us to perform chromosomal fusion experiments on (please re-read the demolition of this premise above).

quote:

---

:

​

Alleged chromosomal fusion also just happens to be evidence used by evolutionists to claim humans and the great apes share a common ancestor.

---

It is but a small aspect, and it is certainly not used in the way that you seem to be implying. See my example of the guenons above. Are you going to claim that these Old world monkeys cannot possibly be related via descent because of the difference in chromosome number?

quote:

---

:

​

Even IF I did think what you said I think it still wouldn’t make it non sequitur as it still would follow the question. Do you have any information that the alleged chromosomal fusion was NOT pivotal or didn’t cause the speciation event in question?

​

I guess the only way to get around this issue is to do the experiment.

---

I have good reason to believe, based on the observations of obviously closely related species, that such a fusion was not pivotal nor did it cause any speciation event in the human historical lineage.
I, of course, would like to see some experiments that verify NREH in multicellular eukaryotes - and NOT anecdotes, phenotypic plasticity extrapolations, etc.

quote:

---

:

​

Scott Page: There is no reason whatsoever to suspect that the chromosomal fusion event caused and speciation event.

​

John Paul:
Chromosomal fusion would be a start. We have to start somewhere, don’t we?

Scott Page:
See my last response above.

​

John Paul:
See mine. It is obvious when one sets out to show something there has to be a starting point in the process (to test the hypothesis). If you want to start out by genetically engineering all the other differences in the genomes first, fine.

---

I believe that you do not understand how scientific experimentation — especially in the realm of evolutionary biology — is undertaken. From my previous readings of creationists, were someone to undertake the very experiments you now seem to want, and recreate the evolution of some species in a lab, I have absolutely no doubt at all that you would simply declare the results to be supportive not of evolution but of Intelligent Design. It is a no-win situation for the evolutionist, a win-win for the creationist. What you apparently see — or at least want others to see — as some sort of ‘objective test’ of evolution is nothing more than a rhetorical ploy.As I can see little coming form continuing exchanges in this thread, and also due to the fact that I have additional responsibilities at my job, I doubt that I will be able to respond in any sort of depth on this forum in the foreseeable future.*******************************************************************In Helen’s response, she wrote that chromosome number is no big deal. I replied to her:And I suggest that you hook up with John Paul and the two of you decide which side of your mouths the creationism angle is going to be argued from. You see, he says that chromosome numbers are a big deal, you say they are not. It is easy to ‘win’ an argument when you argue both sides of the same coin, no?

How about questions creationists won't answer?What would it take to falsify the creationist theory?If the design is intelligent, why is so much of it bad?Why is their explanation any better than the creationism of the hindus or Austrailian Aboriginies?

Is this the same Scott Page that doesn't even know what organisms have a femur? I responded to your diatribe on the Baptist Board.If anyone is interested in seeing (ahem) professor page getting his lunch handed to him please go to the following link: http://www.baptistboard.com/ubb/ultimatebb.php?ubb=get_topic;f=36;t=000158;p=3------------------
John Paul

[QUOTE]Originally posted by John Paul:
[b]Is this the same Scott Page that doesn't even know what organisms have a femur?[/QUOTE][/b]You seem to be the one off track on this.

quote:

---

If anyone is interested in seeing (ahem) professor page getting his lunch handed to him please go to the following link:

​

http://www.baptistboard.com/ubb/ultimatebb.php?ubb=get_topic;f=36;t=000158;p=3

​

---

I don't get it. Scott ate your lunch.------------------
www.hells-handmaiden.com

John:
I don't get it. Scott ate your lunch.John Paul:
Yes, but only after it passed through my digestive system. Thanks for playing!The fact remains there isn't any way to objectively test the grand sweep of the theory of evolution- from some unknown populations of genetically unknowable organisms to the extinct (fossil evidence) & extant diversity we observe today.If you would like we could focus on one of the alleged "great transformations" such as the alleged evolution of cetaceans from terrestial mammals.------------------
John Paul