Which explanation is better? Intelligent Design or Natural Processes

Yeah, I think we’re saying the same thing. I find many here, including myself, clinically interesting. Why do we think the way we do? How do we think? What happened to us? The subject matter is irrelevant as it is often incoherent, untransferable, it actually deconstructs to arbitrary subjectivism. Fear is the key. For us all. Including those of us who think we stand. Why are so many of us deranged one way or another?

[Nobody here has any idea : ) Nobody. Nobody anywhere virtually. Nobody is actually able to take it, lead it, lead us in finding a way ahead together. A few academics are trying now, as in my link, but not here. I know of one church in my entire not insignificant country. That’s trying. It tries above all in its praxis. And I do see good praxis here, in the very American bible belt culture war. Ah well.]

[Some young Americans can be lifted out of fundamentalism, empowered, so that’s good.]

You are probably not aware of the work biologists have been doing on de novo genes. Mani and Tlusty recently published a mathematical exploration of de novo gene generation based on several classes of empirical observations (i.e., not based on conjecture). Among their model’s empirical parameters are:

  • distribution of fitness effects
  • fixation rates
  • pervasive transcription
  • pre-adaptation
  • RNA expression

Because these observations are empirical, they already incorporate the constraints of the laws of thermodynamics.

After their computation, Mani and Tlusty make the following conclusion:

Our model supports the idea that de novo gene birth is a widespread and frequent process, and depending on the organism, the process of gene birth should take on the order of 105 – 106 years. Particularly, our results suggest that rare, large-effect mutations that occur in the more long-tailed DFEs play a major role in facilitating gene birth. Also, under the regime of fluctuating DFE, which represents shifts in mutational biases, the likelihood of de novo gene birth increases even further. While large events, such as transposition, are very likely to occur in this time frame, and are known to be associated with de novo gene birth ( Ruiz-Orera et al., 2015 ), our results suggest that smallscale spontaneous mutations, such as substitutions and small indels on their own are capable of pushing non-genic loci towards ‘genehood’.

I do not expect, @SixDays, that you would possess an existing well of knowledge about empirical biology parameters such as:

  • distribution of fitness effects
  • fixation rates
  • pervasive transcription
  • pre-adaptation
  • RNA expression

I would hope, however, that you can recognize that others who have, unlike you, studied this field do in fact have something to contribute to your knowledge, if you are willing to learn.

Best,
Chris Falter

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Hi Chris. I was working and only had time for a quick response but I wanted to follow up with a longer response.

Please explain why it is the Texas Sharpshooter fallacy. The first mutation- the one you want - has a discrete set of follow on mutations required, which sets up the target. You don’t have added function because the system is not integrated, so you don’t get selection. Without the selection, the probability is extremely small as my approximation shows.

The genetic processes of evolution are much more like random walks and annealing searches than like designing aircraft systems and subsystems.

Still you need the precise mutations to get the integrated system. There may be some mutations that have some malleability but I would predict you would find at least 30 that had absolutely none. If you want to connect a new artery to an old one, they have to connect and the morphology has to be conducive for blood flow and containment of the blood.

The genome behaves as a thermodynamic system where the second law applies. The vast number of deleterious mutations versus the small number of beneficial mutations produces the trend of genetic deterioration rather than the evolutionary paradigm.

Here’s a book of one. Here’s another. They’re wrong of course on your ipse dixit. What happened to you Thomas? That you find yourself in the position of saying something so easily refuted? And the… ‘knowledge’ that followed? [The prescient certainty based on nothing at all.] That you cannot acknowledge is utterly and completely wrong?

There’s something else going on here Thomas, obvious to everyone, but you can’t speak of it. What do you need from us that you can? [How can we help? Help us to help you?]

  1. Because there are many, many different ways to achieve a desirable phenotypic function.
  2. Because a stochastic series of changes can result in a desirable function, even if the function is not specified in advance.

I will give empirical evidence for each of these points.

  1. Lactase persistence alleles - Up to about 30,000 years ago, human bodies did not keep producing lactase past the age of 18 months or so, when weaning occurred. Coinciding with the advent of herding, various peoples across the globe had mutations in their genome that resulted in the persistence of lactase production into adulthood. These changes provided an advantage and were fixed in the populations. Note two key points:
    • There are at least six (6) different alleles for lactase persistence scattered throughout humanity, not just one. In other words, there are many paths to the phenotypic function of lactase persistence.
    • The 6 alleles have varying levels of efficacy. Some yield stronger lactase persistence than others. What this shows is that perfection is not needed for a set of mutations to persist–just some sort of relative advantage. I don’t think you would design a jet engine this way, but the process of evolution (designed by God, IMO) is not producing jet engines.
  2. Drift leading to aerobic citrate metabolism in E. Coli - In the Long-Term Evolution Experiment (LTEE), aerobic citrate metabolism arose in one of the 12 E. Coli populations at about generation 31,000. When Lenski’s team analyzed the set of point mutations leading to the new function, they discovered that the vast majority of the mutations had occurred long previously and had had an approximately neutral selective advantage (i.e., no increase or degradation in phenotypic functionality). The final mutation, however, combined with the previous mutations to produce the new phenotypic function of aerobic citrate metabolism. Thus many mutations were simply drift, accompanied by no significant change in functionality. This is how a large set of mutations can accumulate without any apparent “direction” with regard to functionality. Biologists have in fact incorporated drift into their understanding of evolutionary mechanisms for almost 50 years.

As a non-biologist, you were probably not aware of these points. I hope that you will open your eyes to learn, even though it’s obviously tempting to keep insisting that you know more than an entire scientific community.

While there are a few biological functions whose genetic instructions are highly constrained, the vast majority are not. So I must insist that you kindly supply a citation from the peer-reviewed biology literature, dear friend. You are not a biologist; you don’t carry a card that allows you to just fabricate assertions like this out of whole cloth.

Best,
Chris Falter

EDIT - word-smithery

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No, that’s pretty much perfectly wrong. Biological systems are generally quite tolerant under perturbations, and this also makes them highly tolerant of mutations. Biological systems are also loosely coupled and are highly tolerant under changes to other systems.

Based on your reasoning, a change to the length of a femur, say, would have to be precisely matched to changes to the length of muscles, nerves, and blood vessels, and change would be almost impossible. In the real world, the length of the femur varies a lot, based on both genetics and environment, and everything around it handles the variation without the slightest trouble. Try changing the length of a crucial component of an airplane engine by several inches – it won’t fit and the engine won’t work. Biological systems are not like human-designed mechanical systems, and any conclusions you draw based on that kind of analogy will be wrong.

This is theoretically ungrounded and empirically false.

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Hi Chris,

Let us go through and look at this a little deeper. First, built into your model is the notion that common descent did happen. This is a major assumption and given the fact that it is so easy to generate new genes (105-106 years) as your article claims, one is left wondering how on earth is this even rational. How exactly do you determine this? As Ernst Mayer says in his book, “What is Evolution (pg. 16):

“The study of phylogeny is a study of homologous characters. Since all members of a taxon must consist of the descendants of the nearest common ancestor, this common descent can be inferred only by the study of their homologous character. But how do we determine whether or not the characters of two species or higher taxa are homologous? We say that they are if they conform to the definition of homologous: A feature in two or more taxa is homologous when it is derived from the same (or a corresponding) feature of their nearest common ancestor.”

Now your study that you referenced is based on orphan genes. What is an orphan gene?

Orphan genes are protein-coding regions that have no recognizable homolog in distantly related species. A substantial fraction of coding regions in any genome sequenced consists of orphan genes, but the evolutionary and functional significance of orphan genes is not understood.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC403679/

We and others have shown that every newly sequenced genome contains a significant number of ORFans (4–6), although the percentages of ORFans vary considerably (5) in different species.

https://journals.asm.org/doi/10.1128/mSystems.00290-18

Orphan genes that lack detectable homologues in other lineages could contribute to a variety of biological functions. However, their origination and function mechanisms remain largely unknown.

https://link.springer.com/article/10.1007/s11427-019-9482-0

From these quotes we realize there are many orphan genes, we have no idea how they came about from an evolutionary perspective, and we don’t understand their function. At heart of the matter, these genes are an obstacle which evolutionists need to explain for common decent to make any sense so they develop models to explain them away. Here is the process that evolutionist goes through:

A) We assume that common decent took place.

B) We examine the DNA looking for homologues in distant related species which is assumed to be evidence for common decent.

C) We find many orphan genes which counters the notion of common decent.

D) We make models assuming common decent basing it on empirical parameters such as:

  • distribution of fitness effects
  • fixation rates
  • pervasive transcription
  • pre-adaptation
  • RNA expression

E) We run those models to determine how long it would take for de novo gene birth to occur based on the orphan genes and find very short time distances.

F) We declare victory that new genes can arise and that common descent is indeed a fact.

Does this even make sense on a logical level? Essentially, your assumptions are driving your conclusions. You say common decent happened so there must be an evolutionary explanation to explain orphan genes. Your model is based on the assumption of common decent, so why wouldn’t your results give you what you assume.

A creationist looks at what you have done and questions your foundational assumption of common decent (A). We would question if (B, searching for homologues) is even a worthwhile activity. We would look at (C) and say that it is the death knell of common decent. Your model (D) is based on junk and doesn’t represent reality because it is based on something that never happened. It is empirically based on the smart programming found in life - it is not just purposeless mutations! Life has to be robust or it would just die out. It has to endure many environments and just like systems that have to do this, we know the design is more complex and difficult. Now in part (E) you have a faulty model to begin with so why do you suppose that it will give you any valid results? In fact given the short time frame (about a 100 years) that a de novo gene develops, why do you even suppose this is true given the volume of information that is in a gene?

And note, others also take issue with your methods and conclusions.

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The laws of thermodynamics can be found explained at Flanders & Swann - 'First And Second Law' - YouTube

Saying that the laws of thermodynamics do not apply to open systems is sloppy terminology. They do apply, but they do not apply the way that antievolutionary claims assert. On the other hand, the laws of thermodynamics do show that quite a lot of young-earth and global flood models do not work, because the waste heat generated by the scenario would quickly vaporize the earth.

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Hello Thomas,

You are viewing this issue in quite the binary way, as if all genes must be either ORFANs or homologous, leaving evolutionary biologists on the horns of a dilemma. This is quite contrary to the evidence biologists have published, and reflects a grave misunderstanding of how biologists think about this issue. You have also missed important advances in the articles you cited. All in all, you have not portrayed evolutionary theory or evidence accurately.

A tangent: I am not a biologist, but I have been reading mainstream biologists and ID biologists for about 20 years. I typically ask biologists such as @glipsnort to correct me if I have misunderstood something, and have learned much from the corrections they have given me. Given your background in the biological literature, I would heartily recommend that you follow a similar practice.

Back from the tangent. Roughly 90% of genes are homologous across species and 10% are ORFans, although this ratio can vary. The homologous genes are not sequence-identical; in fact, they almost invariably exhibit a pattern of nested hierarchy. Moreover, those nested hierarchies are almost invariably aligned with nested hierarchies based on other factors such as ERVs, amino acids, biological characters, and fossil characters. The existence of the nested hierarchies and their consilience provide powerful evidence of common descent. So biologists are not just starting with an assumption; common descent flows from the strong mathematical evidence provided by nested hierarchy studies.

But evolutionary theory has not until very recently shed much light on the other 10%, the ORFans, as Anne Gauger noted in 2019. Of course, the incompleteness of a theory does not imply that what a theory has explained and predicted is necessarily wrong. To take an example from another scientific field, the inability so far of astrophysicists to fully explain the nature of dark matter does not imply that it does not exist, and most certainly does not imply that the Big Bang did not occur.

But significant progress on ORFans has been made quite recently. One of the findings was in an article you cited, but somehow you missed it:

Our results presented the first systematic evidence on the evolution of orphan genes and de novo origin of genes in nematodes and their impacts on the functional and phenotypic evolution, and thus could shed new light on our appreciation of the importance of these new genes.

In bacteria, a class of ORFans seems to play a role in pathogenicity, as explained in another passage you missed in a different cited article:

All of these findings suggest the greater importance of PS-ORFans for bacterial pathogenicity.

The contribution of the 2021 article I cited was its demonstration of the likelihood (indeed, the inevitability) of the evolution of ORFan genes from non-coding sequences. This does not contradict anything about homologous genes; it is simply another evolutionary mechanism that biologists are understanding more and more.

The reason I cited that article was that it shows that your mathematical analysis of genetic evolution is indeed based on the Texas Sharpshooter Fallacy.

You do not seem to want to learn from the community of biologists, Thomas. Here’s an analogy: If you are determined to take ivermectin as COVID prophylaxis and you’re willing to look hard enough, you can find a doctor to prescribe it for you. (I would strongly discourage it, because the best reviews based on random controlled studies show that ivermectin has no positive effect on COVID prevention or treatment.) Similarly, if you look hard enough, you can find a biologist who rejects the consensus of the other 99.9% of biologists.

Here’s a sincere question for you, though: Have you considered learning what the other 99.9% really say? So far, you have manifested no understanding of either the theory or the evidence of evolutionary biology. I do not say this as a criticism of your intellect or sincerity, Thomas. To use yet another analogy, I know nothing about click languages and couldn’t understand a single statement by a speaker of such a language, but I do not consequently feel stupid. However, it would be quite infelicitous of me to assert that an African who was clicking or whistling was not communicating complex thoughts simply because speakers of the languages I happen to know do not use clicks or whistles to communicate complex thoughts.

Are you interested in spending a few months to acquire a reasonable background in evolutionary biology? If so, folks around here (including me) would be happy to suggest some resources.

Best regards,
Chris Falter

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this is perhaps the oddest argument that evolutionary creationist leaning skeptics of ID ever proffer.

firstly, it is exceedingly unsound logically as a rebuttal against something’s design. if i find a clearly functional and exceedingly complex computer program on my hard drive, which does not function to the degree that i would like to see and i wonder why the programmer “didn’t do a better job”… this is somehow a serious argument that said program wasn’t designed?

Secondly, if this is to be a real argument, it must claim that my individual judgment on “optimal design” is the standard by which all things must be judged, including anything God may or may not have designed? If God in fact does something, but i could imagine a way i would have made it that was "better… poof! unassailable proof God could not have made it?? it is not possible that he has purposes beyond my understanding for why he designed things to operate in certain ways?

Thirdly, it belies the idea that evolutionary creationists do believe that we are the product of God’s intentional design as is so often claimed, but rather confirms to me that what is embraced is essentially creationary deism. using this kind of argument “shows the hand” for those who make it that they really believe God was not directly involved, or was not intentionally guiding the universe to make us, since the “real” cause of our being designed as we are was the blind natural process that produced a sub-par job, not God’s intent or purpose that would of course produced something optimal.

And fourthly, is everyone who makes this argument seriously that ignorant of the biblical doctrine of the fall… that God, after creating things perfectly for his purposes, in response to human sin, actually cursed his creation, introduced death, decay, and pain into the world that previously knew none of these things?

That analogy completely fails because of the categories. It’s purely fallacious. Upon fallacy, upon epicyclic fallacy. If God had anything to do with evolution beyond grounding eternal infinite nature, it would be obvious that He’d done any job at all, let alo[n]e a better one. Intervening above the ground of being and then wiping out all traces makes Him a creation denialist. So those who are in denial of rationality are in exalted company indeed.

Very critical observation…l i would be curious if i may, to ask if when you discuss something like this as an obstacle for common descent, if you mean it was not derived from a predecessor in any means whatsoever, even conceptually? I agree that such orphans pose an insurmountable problem to the idea of blind modification via mutation/natural selection via small unguided descent with modification, but as regards the raw science involved, I am at least open to the idea of an intelligently guided process that chose to keep the earlier design to large extent intact but then add significant entirely novel design and function, de novo. either in practice, or even “on the drawing board”, so to speak?

i can use the following analogy…

If i found two computer programs that were 90% homologous (even if the homologous sections included various small modifications that demonstrated the “nested hierarchy” that conceivably could have arisen by unintelligent/unguided processes), and 10% of the program was entirely new, novel, completely unique, entirely functional, adding new function, and perfectly integrated into the function of the overall program

I agree it would be utterly absurd to ascribe this additional large, intricate, functional, and integrated code to some kind of blind, materialistic, near-magically fortuitous natural unintelligent process.

But on the other hand, the 90% which is homologous would communicate to me that the two programs were also not utterly independent, either. there would have been “descent with modification” in some sense, no? even if it were only in the mind of the programmer, who re-typed his previous code in toto and then added the new orphan code?

thoughts?

Not exactly. But it’s a serious argument that the program wasn’t designed by God. God is supposed to be competent and wise and not under time and budget constraints. Even human programmers will eventually throw out old code and go back to the drawing board, developing new computer languages and programs. If God is a designer he should be capable of going back to the drawing board also. But what we see in nature is that evolution works by tinkering with existing stuff. Look at the recurrent laryngeal nerve. And there are plenty of examples of things no designer would do. Look at rabbits. They can’t digest their food in one pass, so they are force to eat their own poops to extract nutrition from them.

There are good reasons to believe in God but intelligent design is not one of them.

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So what are they?

For me they are:

The fact that this world exists.
The life of Jesus.
The improbable survival of the Jews.

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No. 2 only for me.

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Hi Daniel,

In this thread we have discussed how a realistic model of ORFan gene generation published by Mani and Tlusty demonstrates the overwhelming likelihood of their generation in large numbers. We have also discussed research showing how ORFan genes play specific roles in nematodes and in eubacteria.

I therefore do not understand how your belief about ORFan genes is compatible with belief in the modern scientific process. Perhaps you would care to elaborate?

This is a really, really good point: We humans do not have the ability to understand, much less predict, how God’s design might play out in any particular situation.

The corollary of this really, really good point is that discernment of God’s involvement in design lies entirely outside of the realm of science, which can only make sense of repeatable processes with knowable outcomes that are at least probabilistic if not deterministic.

Thanks for your contributions to the discussion today.

Best,
Chris Falter

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We can’t discern what isn’t there. If anything God grounds being from eternity, it does the rest.

And if God is an omnipotent designer then he should similarly be capable of tinkering with existing stuff rather than starting from complete scratch should that be his intent and desire. So i’m still not following your reasoning… Are you suggesting…

God could not tinker with existing stuff?

Or

God would not tinker with existing stuff?

The first is obviously illogical as i see no reason an omnipotent being could not do so should he choose to do so. For the second, it depends on the “if I were God, I wouldn’t have done it that way, therefore God would not have, either” reasoning, which i trust you could see the problem there?

Yes, and it’s the same problem that every scientist faces: No one can credibly distinguish between God’s design and the ordinary course of nature.

Michael Behe, Ken Ham, Todd Wood, Stephen Meyer… none of them can pull off this feat.

The implication, then, is that there is no method within the realm of biology, geology, computer science, information science, or paleontology that can help us distinguish divine intervention (i.e., special creation) from day-to-day biological processes. As you point out so aptly and so insistently, Daniel, it simply cannot be done.

Thanks again for your contributions to the forum.

Best,
Chris Falter

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“Let your conversation be always full of grace, seasoned with salt, so that you may know how to answer everyone.” -Colossians 4:6

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