Introducing Geremy (and Behe)

Please justify this division you have created between “direct, indirect and theoretical evidence.” Is it a principle of science that indirect evidence is weaker than direct? What differentiates “indirect” from “theoretical” evidence? We need to be on the same page on these basic issues before you go and elaborate at length on the basis of these assertions of yours. If it turns out these assertions are unjustified, then it will save a lot of time, yours included.

Also, are you under the impression that the evidence for common descent is limited to inter-fertility, introgression and homology? Have you not overlooked some other very important evidences? This might help you answer that:


Without a basis in observable phenomena what would be the difference between science and philosophy? So let’s take the theory of a static universe for example. Much like, evolutionary theory the idea of an eternal universe is one that is rooted in the philosophy of the ancient Greeks. Since it eliminated a priori any need to explain the origin of the universe, it was a favorite theory of those who believe that the philosophy of materialism is the only logical basis for science. However, its plausibility was based on ignorance about how the physics of the universe worked. Despite being based on false presuppositions the static universe model was able to accommodate most evidences from modern physics including relativity all that was needed were a few post hoc adjustments to it such the universal constant. Similarly common descent can explain everything so long as one is willing to make few post hoc adjustments to align ones results to the “known” phylogenies.

So sticking with my comparison between cosmology and biology, inter fertility is equivalent to trigonometric parallax, both are examples of direct measurement, or observations, and without any scientific theory having an empirical basis either direct measurements or observations then we are discussing philosophy not science. Similarly, much as astronomers and astrophysicists were able to create by directly measuring nearby Cepheid variables and using those measurements to create brightness scales by using red shift to indirectly measure how far away nearby galaxies are, biologists are able to use evidence of past genetic introgressions to indirectly demonstrate common descent in organisms where there is currently no known active gene exchange.

Beyond the point of direct and indirect measurement the accuracy of any theory is dependent on the how close the presuppositions that it is based on accurately reflect reality. Since presuppositions are by definition philosophical, they are speculative and maybe overturned by contrary data at any time, so we should not have confidence in their accuracy, only in their explanatory power or lack thereof. Just as the null theory of the static universe was Big Bang cosmology, the null theory of universal common decent, is limited common descent.

Even if evolutionary biologists reject such a null theory in practice and decide to call it something else such as convergent evolution, the inability of evolutionary theory to falsify the null theory that something other than common descent is responsible for certain aspects of biology still, weakens the premise that the theory is based on because it raises the possibility that other aspects of biology currently attributed to common descent are in fact caused by something else as well. So in my humble opinion, the goal of ID should not be to replace one speculative philosophy of science with another one, but rather to discover what causes the appearance to some of common descent where there is none.

Thanks for writing a bunch of words that did not answer my questions. I hope you had more fun writing them than I did reading them.

I suggest you stop trying to convince the members of this forum that you are a brilliant unschooled genius regarding evolutionary biology, and just pay attention to the corrections and explanations you are receiving from people who actually understand this subject.


Cart before horse. You haven’t established that there is none. You haven’t even presented an alternative to common descent, though you may think you have. Perhaps you might try clearly articulating this alternative, and you might also articulate where you think common descent ends. What parts of the tree of life are not actually due to descent?


Actually, just the opposite. The proposed universal common ancestor would have existed well after the first life emerged.

Where do the authors state that universal common ancestry can not be tested at all? The authors are arguing that it is difficult to impossible to determine if protein sequences are convergent or inherited.

Common descent among vertebrates would seem to be rather easy to demonstrate.

No scientists are claiming that any living ape is a human ancestor. You are using ladder thinking instead of tree thinking.

You should also realize that chimps share more DNA with humans than they do any other ape species.

" We estimated nucleotide divergence in unique gap-free sequence, indicated at each node, from the alignment of rhesus macaque (yellow), gibbon (purple), orang-utan (orange), gorilla (aqua), chimpanzee (green) and human (blue) whole genome shotgun reads to the human reference (Hs.35; Supplementary Information section 3). Note that the Bornean ( P. pygmaeus ) and Sumatran ( P. abelii ) orang-utan species showed nucleotide identity comparable to that of bonobo ( Pan paniscus ) and chimpanzee ( Pan troglodytes ). Estimates of divergence time based on sequence identity are indicated at each node, ∼1 Myr implies approximately 1 Myr or less. Values taken from refs 29 and 30 where indicated."

The phylogenetic relationships are based on DNA sequence which isn’t speculative at all.


Then how is it that you have been able to find so many reports by people who study mechanical forces?


Why would it imply that? It just says all known life is genealogically related, which by itself says nothing about the relationship between what life is and the origins of cells.

Also, leaving aside the subject of universal common descent, the relationship between the origin of life and the origin of cells appears to be a matter of definition. If you simply define life such that it would have to be cellular(if you were to say that in your view, if itsn’t cellular then it doesn’t count as a form of life), then life originated at the origin of the first cell regardless of how that occurred exactly.

By insisting on such a definition of life you do not really argue that life could not originate by some sort of evolutionary process, as it is entirely possible there was a substantial period of pre-cellular evolution (a sort of chemical evolution) that eventually gave rise to the first cells.

Non-life —> chemical evolution —> origin of cellular life —> more evolution —> last universal common ancestor —> diversification of all known cellular life into it’s extant forms.


See this new paper:


I think that it is safe to say that there isn’t any evidence that spontaneously occurring abiogenesis is actually possible. Even if one discounts the possibility of intelligent design the organization of proteins into cells is dependent on at least two different types of information.

  1. The physicochemical properties of the molecules.
  2. The sequence in which molecules are arranged.

Most OOL research is focused solely on the first type of information, as they diligently look for evidence that complex chemistry of cells can form in plausible abiotic conditions, such as proteins, sugars and other chemical substances that the cell uses to function, faster than the environment can decompose them. Which has a sort of reductionist logic to it because only this part of the process of building a cell is reducible to blind physicochemical processes. At present there is no evidence that any environment can spontaneously achieve even that bench mark nor any evidence based reason to believe such an environment has ever existed, as is well explained by James Tour here:

As far as the other type of information I think that the situation is much worse. Here is how one Davies explains the relationship between life and information:

Explaining the chemical substrate of life and claiming it as a solution to life’s origin is like pointing to silicon and copper as an explanation for the goings-on inside a computer… Rather, the puzzle lies with something fundamentally different, a problem of causal organization having to do with the separation of informational and mechanical aspects into parallel causal narratives. The real challenge of life’s origin is thus to explain how instructional information control systems emerge naturally and spontaneously from mere molecular dynamics.

As it is I am unaware of any evidence that such processes actually exist, so what the OOL community needs here is a proof of concept, something that I know can be very difficult because that is a big part of what I do.

As I mentioned earlier I design mostly simple machines, whenever I respond to a company’s request for a proposal, they require I make what is called a proof of concept video. Here’s an old example of such a video that I made some years ago:

Now as simple as this device is, it makes use of at least three types of information.

  1. The inherent properties of materials (battery chemistry, fiber optics, diodes, electromagnets, etc).
  2. The sequence in which these components are organized, as detailed in schematic diagrams I haven’t shown you.
  3. The logical processes of a (hopefully intelligent) mind.

Now when we look throughout the natural world we do not find any cells without molecular machine Evolutionary theory demands that we search for strong evidence that the molecular machines evolved, while the theory of Intelligent Design posits that much like the only a machine produces narrow band radio waves that SETI searches for, only intelligent agents make such machines. The reality is that the only known cause of the creation of machines is a mind, so it is a legitimate scientific interpretation of the evidence to consider the above machines as evidence of deliberate design as well. The earliest evolutionary theorists understood this concept very well, for example Ernst Haeckel wrote 115 years ago the following:

The familiar comparison of an organism to a machine has given rise to very serious errors in regard to the former, and has, of late, been made the base of false dualistic principles. The modern “machine-theory of[30] life” which is raised thereon demands an intelligent design and a deliberate constructing engineer for the origin of the organism, just as we find in the case of the machine…

The whole of this favorite machine-theory of life, and the far-reaching dualistic conclusions drawn from it, tumble to pieces when we study the simplest organisms known to us, the monera; for these are really organisms without organs—and without organization!

The Project Gutenberg eBook of The Woders of Life, by Ernst Haeckel. pages 29- 31

Haeckel’s argument that intelligent design was absurd because bacteria have no mechanical parts, unlike the real intelligently designed machines, was due to his limited knowledge of how they function. I think that the entire field of OOL research is based on speculations that seemed much more plausible decades ago when most biologists still thought Haeckel was right. Such thinking only was overcome in the past few decades as explained here:

You need to define “machine”. Are all proteins to be considered machines? You also need to define “evolved”. Is guided evolution still evolution? If not, then it can never be shown that any molecular machine evolved, since it’s impossible to distinguish guided evolution from unguided evolution, even if we see it happening in real time. On the other hand, we can convincingly show the evolution of many proteins (or more accurately the genes from which they are transcribed and translated) from ancestral sequences. Was a “mind” involved? How would you know?

Now of course the only known cause of the creation of machines, in the usual sense that doesn’t include organisms, would be not “a mind” but human beings. Your proper conclusion, then, would be that human beings designed life. Generalizing from human manufacture to disembodied deities isn’t really valid.


Wow what a great paper! You know it reminds me of another paper that I read about how the ZEB2 transcription is upregulated in cardiac fibroblasts after a heart attack. It explains:

Myofibroblasts have a characteristic contractile property that helps in the process of wound closure. Myofibroblasts maintain the matrix in the wound area under tension, which helps reduce wound size and ensures rapid healing [37]. Myofibroblasts synthesize large amounts of contractile proteins such as α-SMA and SMemb, which generate tension by actively contracting to generate force [33,38]. There are also other pathways that can contribute in inducing contractile property of myofibroblasts, for example, Ca2+ signaling and Rho/ROCK signaling [39]. We have demonstrated that Zeb2 overexpression in myofibroblasts leads to increased contractility as compared to the Ad-LacZ control (Figure 5). Thus, the finding of increasing myofibroblast marker expression (α-SMA and SMemb) reflects the induction of a more contractile mature cardiac myofibroblast phenotype.

Thanks to this paper I will now refine my hypothesis to be that increased contractive force, causes ZEB2 to be unregulated which fixates the more contractive phenotype in a positive feedback loop during cell migration.

You appear to be unfamiliar with metabolism-first hypotheses.


How do believe it is determined whether something is “actually possible”?


Sorry that’s just wrong. Living creatures are full of simple machines - levers, ball-and-socket joints, screws, molecular flagella “motors”, even bumps that function as gears which are known to have evolved. You’re making the fallacy of assuming your conclusion.


That’s actually not true. There is some evidence that life’s origin, or at the very least the protein constituents of extant cells, ultimately derive from some sort of abiotic chemistry.

Inferences of ancestral nodes in the phylogenetic trees of the oldest (most widely conserved) protein sequences increasingly mirror the abiotic distribution of amino acids produced by nonbiological chemical reactions, as we go further and further back in time. That’s evidence right there that the earliest proteins were synthesized from amino acids that were produced by nonbiological processes, and that the biosynthetic pathways for their synthesis subsequently evolved. The “modern” distribution of amino acids we see in extant proteins increasingly gives way to the nonbiological distribution the further back we go, and larger and more complex amino acids like Tryptophan become less frequent, while the simpler amino acids like glycine, alanine, valine and so on become more and more frequent. This trend increasingly mirrors the distribution expected from chemical thermodynamic calculations of the ease of their synthesis, the distribution observed in various carbonaceous chondrites, and mirrors the distribution also seen in various experiments in abiotic organic chemistry, such as simulated hydrothermal conditions, volcanic and atmospheric spark-discharge experiments, and so on.

Higgs PG, Pudritz RE. A thermodynamic basis for prebiotic amino acid synthesis
and the nature of the first genetic code. Astrobiology. 2009 Jun;9(5):483-90.
DOI: 10.1089/ast.2008.0280

Brooks DJ, Fresco JR, Lesk AM, Singh M. Evolution of amino acid frequencies in
proteins over deep time: inferred order of introduction of amino acids into the
genetic code. Mol Biol Evol. 2002 Oct;19(10):1645-55. DOI: 10.1093/oxfordjournals.molbev.a003988

Jordan IK, Kondrashov FA, Adzhubei IA, Wolf YI, Koonin EV, Kondrashov AS,
Sunyaev S. A universal trend of amino acid gain and loss in protein evolution.
Nature. 2005 Feb 10;433(7026):633-8. Epub 2005 Jan 19. Erratum in: Nature. 2005
May 26;435(7041):528. DOI: 10.1038/nature03306

This ultimately chemical origin of the first proteins is clearly an outcome that is much more expected on the hypothesis that life began through some process of abiotic geochemistry and physics.

Meanwhile in reality there isn’t any evidence that’s impossible.

Even if one discounts the possibility of intelligent design the organization of proteins into cells is dependent on at least two different types of information.

  1. The physicochemical properties of the molecules.
  2. The sequence in which molecules are arranged.

Most OOL research is focused solely on the first type of information, as they diligently look for evidence that complex chemistry of cells can form in plausible abiotic conditions, such as proteins, sugars and other chemical substances that the cell uses to function, faster than the environment can decompose them. Which has a sort of reductionist logic to it because only this part of the process of building a cell is reducible to blind physicochemical processes. At present there is no evidence that any environment can spontaneously achieve even that bench mark nor any evidence based reason to believe such an environment has ever existed, as is well explained by James Tour here:
Animadversions of a Synthetic Chemist | Articles | Inference: International Review of Science

All of this is based on the unsubstantiated assumption that life has to begin with a sort of spontaneous self-assembly of a cellular-life form more or less “all at once”, or that there was never any kind of chemical or pre-cellular evolution occurring by which something like extant cells gradually developed from simpler precursors.

Of course, the only way to find evidence that some hypothesized environment existed is to look for it, or try to recreate it in the laboratory and see whether it behaves as expected.

Of course that’s always the case before new and unexpected discoveries are made. Before the process of evolution was discovered, nobody knew it existed. Same goes with things like fission and fusion of atomic nuclei, stellar nucleosynthesis, convection, thermophoresis, and thousands of other processes that we didn’t know existed at various points in history, and for a long time never even dreamt of.

Now of course given what we know of the history of the universe, life must have somehow originated from non-life because if we go back far enough, the elemental constituents of life didn’t even exist.

Going back far enough if you assume life couldn’t somehow arise through processes of mere physics and chemistry, but instead requires some long series of extraterrestrial alien biochemists to create each other, you’re going to run out of time for alien biochemists to exist because at some point the universe was just some hot and dense plasma in which no chemistry was possible. So now your premise runs into a historical problem which presents you with a trilemma:
A) Your assumption that life couldn’t possibly arise by just physical and chemical processes is wrong.
B) Magical wishing made life arise.
C) We’ve got the history of the universe wrong and the history of life stretches infinitely and unendingly far into the past.

Supposing you refuse to budge on A, consider C preposterous, and go for option B, you’re back to the very problem you asserted with abiogenesis to begin with:
I think that it is safe to say that there isn’t any evidence that magically wishing for matter to assemble into life is actually possible.


I wonder what evidence you have that such machines are not the product of design?

You’re the one claiming they’re designed. You produce your positive evidence for such design. Meanwhile we have 160+ years of empirical observations of evolutionary processes producing incredibly complex features and not a single instance of external “design” seen anywhere, save for the trivial cases of humans manipulating genomes.


What evidence could there possibly be?

I notice that you consistently ignore everything I post, by the way. Why?



I have a question for you.

Is the tail of the spider tailed horned viper designed?


John I do not mean to ignore your questions, it’s just a matter of neglect not intent. There so may of you to respond to and only one of me. As I see it evolutionary theory is designed to be a general theory of biology, but it is not. I think that population genetics still is limited to explaining current and recent genetic conditions, and that the coalescent theory is limited to species that share genes. My goal isn’t to make a speculative theory of everything, but rather to show that biological systems are too interconnected and the genetic mechanism of evolution are to limited to paint an accurate picture of biological history. These are the reasons that evolutionary explanations are limited.

Chromosomal changes are not driven by random chance mutations, but the shortened telomeres of old age.
Since chromosome configuration and number vary from species to species, I decided to look into what the known causes of chromosome change are, and this is how I learned about the role of telomere shortening. Here is how one paper explains this connection:

In the well-established tumorigenesis model, telomeres in human somatic cells gradually become shortened with each cell division. After 50 to 60 cell cycles, cells with shortened telomeres provoke replicative senescence by chromosomal instability and p53 activation, which is induced by the DNA damage response according to telomere shortening [76,77,78]. However, some cells that can overcome senescence by the acquisition of genetic mutations in p53 or other checkpoint proteins continue to proliferate; thus, telomeres become critically short, and apoptosis is subsequently induced (crisis) [79,80]. At this point, a minor population of the cells that activate telomerase (or ALT pathway) acquires immortality and proceeds to carcinogenesis [79]…
Given that telomerase-mediated telomere elongation is important for the infinite proliferation of TERT-positive cancer cells, genetic or pharmacological inhibition of telomerase activity in cancer cells induces gradual shortening of telomeres and eventual cell senescence or apoptosis [109,110,111]. Theoretically, the anticancer effect of telomerase inhibition would emerge earlier in cancer cells with shorter telomeres. In fact, short telomere length could be a predictive biomarker of telomerase inhibitors [[112]

To explain the differences in in chromosomal arrangements evolutionary theorists often claim that these changes are due to random mutations, followed by evolutionary bottle necks. There are two problems with this claim. One easiest problem with this model to demonstrate are the claimed bottlenecks need to fixate the number of changes. After reading about the long chain of chance events, followed by a severe population bottleneck needed to claim that human chromosome 2 fusion happened just by chance. I wondered how many bottlenecks would it take to explain the chromosomal differences between humans and gibbons. Which is how I learned about the research of one oncologist who asked the same question. He writes:

How many bottlenecks are required to generate this kind of karyotypical mess between closely related species? a Gibbon (Hylobates lar) karyotype in comparison to b human karyotype based on correspond- ing color code. Every sporadic chromosomal aberration reduces fertility of heterozygotes due to loss of genetically unbalanced offspring.

The above researcher then develops his own hypothesis of convergent evolution based on progressive telomere erosion while I am not endorsing his hypothesis, I think that the if one wants to claim that chromosome differences are all due to chance driven mutations there would need to be some explanation other than countless low probability mutations, which would cause countless population bottlenecks. The researcher above is aware of the second problem of telomere shortening due to his research in cancer, as I read the profiles of evolutionary biologists who think that there broader theory of evolution is not explained by the current theory I noticed that many of theses biologist are cancer researchers, and physiologists. The reason that I think that this is the case is because cancer researchers get to see the causes and effects of evolution up close in humans, and since different organisms have different genetic toolkits they can see that the sort of model organism based evolutionary explanations that are used to structure evolutionary theory, are not actually universal but confined to the species that have those abilities.

I think the true extent of common descent is unknowable from a scientific standpoint.

This is an interesting consequence of intelligent design, designers make choices even today, a human synthetic biologist might decide to print out functional gene sequences made from scratch, or she/ he may decide to modify existing organisms using guided evolution or both. Without knowing what the designer was thinking, one can not use science alone to demonstrate the limits of common decent, because intelligent agents can do things that chance alone can not. This fact is best explained by of all people Richard Dawkins with his Meme theory, a idea can be reproduced, and adapted to many situations just like a gene can be. So from the standpoint of intelligent design proteins, genomes, lipid structures are ideas, that we can best understand in the terms of mathematics and physics.

To illustrate this point let’s look at the theory of endosymbiosis, which explains that both chloroplasts and mitochondria are remarkably similar to bacteria, and so hypothesizes that their ancestors were bacteria. From an ID perspective bacteria, archaea and eukaryotes all began as ideas in a mind, so the hypothesis that an intelligent agent could combine elements of each to make something new is simple and easy to understand from an engineering standpoint. Now lets look at it from a blind chance perspective. A eukaryotic cell is much more than a just an archaeal cell with mitochondria, so even assuming that an ancient eukaryote engulfed bacteria long ago wouldn’t in itself explain the origins of eukaryotes. So the more common speculation is that an ancient archaea host cell engulfed a bacterial cell and developed a symbiotic relationship. Of course there is one huge problem neither archaean nor bacteria are capable of phagocytosis, so how did this happen in the past? Despite the claims of some researchers there are no demonstrably transitional organisms between archaean and eukaryotes, the claims about Lokiarchaea such claims are contradicted by available data, such as the paper that I linked below:

As I mentioned in an earlier post mutations are caused by physics, so some genetic sequences are simply more stable than others. As explained in Koonin’s common descent paper that I mentioned earlier it would absurd to credit all of this similarity to convergent evolution, however it is not absurd to think that an intelligent agent would use the most stable genetic sequences over and over again to prevent the destruction of these sequences by evolution. This is why I do not agree that phylogenetic trees are genealogical unless common ancestry can be demonstrated by other evidence.

Genome interconnectivity makes gene driven evolution impossible
As I mentioned in an earlier paper most complex traits are spread throughout the entire genome, this design feature is a good way of inhibiting the impact of gene evolution. Another way would be to place the global regulation of genes outside of the reach of physics driven gene evolution. I think that mechanobiologists who think that gene regulation is regulated by mechanical pressures have it right, and that the biologist here who don’t see how such a system of mechanical pressure regulation of the genome can inherited across the theoretical evolutionary tree of life, see the exact same problem that I see and if the above can be demonstrated to be true, the only real solution will be ID, because it is simply a brute fact that intelligent agents can do things that blind natural forces cannot.

So how could mechanobiology regulate gene transcription? This is a long conversation already so I will only provide one example taken from a mechanobiology paper, it explains:

Like twist, tension in the substrate DNA can be critical to this sort of long-range regulatory function. DNA loop formation is driven by thermal fluctuations and intracellular interactions that randomly bend and twist the DNA. When two binding sites come in close proximity to one another, a regulatory protein may form a bridge between the operators to generate a loop in the intervening DNA. The force associated with thermal fluctuations, needed to form such a loop, can be estimated from the persistence length of the DNA at around 0.1 pN—only a fraction of the scale of forces exerted on the DNA during normal cell functioning, like those discussed in §1. It was, therefore, predicted that forces as small as a few hundred femtonewtons could supersede the thermal fluctuations and easily suppress the rate of formation of protein-mediated DNA loops [43,44], effectively preventing all loop formation and, in turn, dramatically altering transcription levels…

In a separate experiment, Chen et al . [46] found that by applying a fluctuating level of tension to the DNA they could greatly enhance the rate of loop formation. The experiment was meant to simulate the fluctuating micromechanical environment of the cellular interior, where fluctuating forces arise from a wide range of intracellular processes. The introduced fluctuations were formally equivalent to increasing the effective temperature of the system and it was found that the loop formation rate could be more than doubled by adding an effective temperature of only 10 per cent of the thermal background. This rate enhancement, owing to force fluctuations, might explain why DNA loops result in a several 100-fold level of repression in vivo [47] despite the observation of equal lifetimes in the looped and unloooped states in vitro . Moreover, the sensitivity of the loop formation rate to the additive fluctuations was shown to be independent of the baseline static tension in the substrate DNA. This led the authors to suggest that schemes which employ mechanical tension as a regulatory switch can be surprisingly robust even in a mechanically noisy environment.

So this is why I consider evolutionary tree of life to be speculative.