Developing College-Level ID/Creation Courses

LOL! Says the guy who didn’t bother even reading the quote he was bellyaching about. :rofl:

I have to say your knee-jerk defenses of anything even remotely connected to your Creationist beliefs can be damn funny sometimes. :slightly_smiling_face:

It would be no less likely than any other combination that came up on a single toss of all 500 at once. So why should “design” only apply if they all come up heads? Think carefully about this. It is a very crucial and pervasive error made by ID Creationists all the time.

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It would be no less likely than any other permutation. There’s a big difference between permutation and combination. There are 500! / (250!)(250!) => (~10150) combinations for tossing exactly 250 heads with 500 coins, for example.


Of course I am. It’s just that neither science nor Scripture tells us abiogenesis was a direct act of God.

Yes I do.

Well, Scripture tells us that Jesus rose from the dead by a direct act of God. That is different than abiogenesis.

Believing God created the first cell is certainly not outrageous. Maybe he did.

The disagreement is, rather, about the validity of the arguments being marshaled to make your case. Even if you are ultimately right, and God did create the first cell, I don’t think your argument is valid. That is the crux of the issue.


What is the weakness of his argument?

Hi @stcordova -

Thanks for sharing your 2 slide decks. Here’s my feedback:

  1. The Law of Large Numbers is not violated by zinc finger proteins as far as I can tell, and I have no idea how you arrived at the conclusion they violate the law. Without some mathematical explanation on your part, I don’t know how to provide a counterpoint.
  2. The article representing the supposedly inactive research area ("Evolution of protein domain promiscuity in eukaryotes - Basu, et al., 2008) has been cited 161 times in the past decade according to Google Scholar.
  3. Contrary to your assertion, promiscuous protein domains are not a problem for evolution. Basu’s abstract explains why:

The set of promiscuous domains is enriched for domains mediating protein–protein interactions that are involved in various forms of signal transduction, especially in the ubiquitin system and in chromatin. Thus, a limited repertoire of promiscuous domains makes a major contribution to the diversity and evolvability of eukaryotic proteomes and signaling networks.

  1. My analogy from chess positions applies quite directly to your assertions on slides 37-40 of part 2. I.e., disparate functional architectures could still have a common ancestor. Of course, Art Hunt’s argument is also a strong refutation and has the imprimatur of a biology Ph.D, to boot.
  2. You cite Ewert’s ideas on modularity as if they have withstood critical examination. They have not. See Winston Ewert: The Dependency Graph of Life for an extended examination of why not. Several contributions explain the problems in Ewert’s analysis. I found the contributions by @glipsnort to be especially incisive.
  3. Likewise with Doug Axe’s 2004 paper. See the contributions from biologists on this thread: How Does Tokuriki 2009 Affect Conclusions from Axe 2004?
  4. I’m not sure what publication by Behe in 2008 you are referring to. Perhaps I overlooked something in your slides. Can you point me to what I missed? Or, alternatively, tell me what reference could be added?
  5. The notion that zinc finger proteins cast suspicion on MLE or parsimony methods for finding most probable trees does not begin to make sense to me. Those methods aim to minimize a loss function measured by homoplasy, and you have not provided any rationale for why analyses of zinc finger proteins cannot proceed along these lines. I don’t know how to provide a rebuttal because I don’t understand how you reached the conclusion. I certainly don’t see the math in the slides.
  6. Unless you can show that LUCA’s biology used only a single protein, there is no reason to think that the lack of PUCA somehow refutes LUCA.
  7. Contrary to your assertion, CTVT does not contain a canine genome. It contains a tiny portion of a canid genome. Moreover, it has nothing to say about ERVs, whose provenance is well-established.
  8. The idea that much of the genome has the “function” of adding length to a DNA strand to make transcription work effectively does not imply that the theory of evolution is wrong. This argument against evolution is furthered weakened by the fact that the sequence of the “lengthening” sequences often matters not–they are not under selection.
  9. I don’t know enough about racemization to offer a critique of that specific argument for life being no more than 10k years old. However, you do students no favors if you deliberately omit discussion of the dozens of methods and tens of thousands of confirming observations that reach a different conclusion. It is millions of times easier to believe that Cordova’s understanding of racemization is incorrect than to believe that the standard scientific understanding is incorrect for
    A. Geologic dating methods of the layers surrounding fossils
    B. The patterns of fossils with respect to dates and locations
    C. C14 dating of archeological finds.
    D. Lenski’s LTEE
    E. ERV-derived trees of primate ancestry
    F. etc., etc., etc., etc., etc., etc., etc.

As a general critique, I would offer that by omitting any mention of major classes of data that support the theory of evolution, you have built one of the feeblest straw-man versions of evolutionary theory I have ever read. You owe it to your students to give them the complete picture, and I have no doubt that your desire to give them the complete picture is genuine. However, your slides that you linked to above show that you are far, far from achieving that desire, and give no evidence that you have a plan to achieve it.

I hope you find these observations useful.

Chris Falter


Several people on the thread have been explaining the weaknesses.

Sometimes he is arguing against a strawman version of evolutionary theory at times (e.g. no one thinks all proteins must have a common ancestor).

Other times his conclusions do not logically follow (e.g. see comments by @Chris_Falter on the chess board).

Other times he is unaware of the evidence for common descent (e.g. see when I asked for an alternate quantitative explanation).

This has been a far ranging conversation. I have not yet seen evidence to make the case strong against abiogenesis or common descent. To be clear, I don’t think we know how the first cell arose. Maybe God did create the first cell. As @John_Harshman rightly puts it, there is


I agree.

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To this point I agree. There is too much data for anyone to focus and help. Chris was trying but to get into detail on all the arguments which is next to impossible. The Zip finger argument is nuanced and very technical. The homochirality argument (500 heads) was not understood. So lack of focus leads to us talking over each other. That why you try to split threads when focus is not adhered to.

Those who deliberately ignore the incredibly broad and deep amount of physical evidence for the 4.5 billion year age of the Earth and the 3.8+ billion year history of life on the planet automatically disqualify themselves from any serious scientific discussion IMHO.


Just because the evidence went over your head doesn’t mean others couldn’t understand it Bill.

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@stcordova asked for no splits.

It is understood what he was saying. However, he seems unaware of the many natural processes we know of that can produce homochirality: How Homochirality Arises. @Timothy_Horton gave a helpful analogy:


It isn’t that he’s unaware. He’s been told about it often enough, just as Bill has. He just refuses to believe it, and he thinks that if evolution doesn’t or can’t happen solely through natural causes, then the preferable alternative is separate creation, not guided evolution. Neither Sal nor Bill has ever been able to explain why that is. Or why natural causes can be known to be inadequate either.

You might ask about Sal’s flower.


Yes, my error. Thanks for the correction.

My point remains: If we were somehow able to keep track of each coin and whether it came up heads or tails, then all heads is no less probable than any other permutation.

A more pertinent analogy is probably one involving tossing a single coin and having it come up heads 500 times in a row. There, we are only dealing with permutations.


So is a tornado.

Think about it. Countless bajillions of water molecules and other constituents can each have many, many different orientations and relationships with other molecules, but somehow they end up working with the other bajillions of molecules to form a large, organized, irreducible complex system. The total number of possible interactions of all these molecules exceed the capabilities of most calculators, but somehow they find the precise combination to create these unique systems. Like the DNA in Tan’s “lesson”, tornadoes are statistical miracles.


I very much want to thank Dr. Swamidass for not splitting my threads! Please don’t split my thread. Thank you.

Natural selection in the Darwinian sense doesn’t operate in most hypothetical pre-biotic environments for the major compounds involved because of chemistry.

Borrowing terms from statistical mechanics, the macrostate of homochiral amino acids in a polypeptide/protein is critical for the formation of alpha helices and beta sheets. This is basic biochemistry 301, like the first few classes on Protein Secondary Structure. The following protein secondary structure, the alpha helix for example, will absolutely fail if there is no homochirality, and without alphahelix, there are no proteins, and without proteins, there is no protein-based life, and with no life there is no replication, and with no replication there is no Darwinian selection!

Not every amino acid is the L-AA (L-amino acid) form in life. Many organisms metabolize or utilize the D-AA form for certain applications, but for the vast majority of proteins, the homochirality is crucial because of the crucial role of secondary structures like alpha helices and betasheets.

However, chemically, the Gibbs free energy favors the heterochiral state, and in over time, even if the homochiral amino acid state was the starting state, it won’t last for long relative to geological time as spontaneous isomeraization will happen.

The NATURAL tendency is toward heterochirality (the term for amino acids is racemic, I don’t know if there is a term for nucleotides) over time, and it will reach the racemic state naturally. What Tim Horton described is fantasy, it is Darwinian fantasy, it is not chemistry, it is not physical chemistry, it is not physics, it is not science.

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Living organisms require rapid production of chiral amino acids. This is critical for protein folding. I read thorough the post and there is no credible explanation there on how life originated with chiral amino acids.

Different question. That’s a change of topic.

This video connects the importance of the Law of Large Numbers with Statistical Mechanics. With some thought, one ought to see why the Texas Sharshooter fallacy is not in play for critical macroproperties such as homochirality and “homo-linkage” (like alpha peptide bonds, and the problems Dr. Tan pointed out) and why violations of the law of large numbers is required for protein/DNA based life.

The law of large numbers is like really basic probability and statistics. I used it a lot in my Casino days before I got kicked out.

So, how do you explain the cases where homochirality arises by normal chemical processes?

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You are using catalysts to get consistent chirality. Where are these catalysts at OOL?

What we are observing in minimum living cells are enzymes that can manufacture homo chiral AA’s rapidly allowing for enough protein production to sustain life.

A critical component for life to get started is the rapid production of reliable catalysts that in turn can rapidly produce amino acids. Without this you don’t have self replication.