Owen Strachan offers some thoughts on Craig’s book on the historical Adam

Belfast @4 You seem to be obsessed about my obsessions........ :-) chuckdarwin

Chuck, do you enjoy repeating yourself? Have you ever considered you may have an obsession? Belfast

And keep in mind that this is just one novel 10^20 protein/protein binding site that is leaving the Darwinian mechanism dead in the water. Yet in order to explain the origin of humanity, the Darwinian Mechanism would have to account for far, far, more than just one novel protein/.protein binding site being generated. First off it is important to note that “alternative splicing patterns are very different even between humans and chimpanzees,”

Evolution by Splicing – Comparing gene transcripts from different species reveals surprising splicing diversity. – Ruth Williams – December 20, 2012 Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,, A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species.?On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,, http://www.the-scientist.com/?articles.view%2FarticleNo%2F33782%2Ftitle%2FEvolution-by-Splicing%2F?

And it is also important to note that, "Alternatively spliced isoforms of proteins exhibit strikingly different interaction profiles and thus, in the context of global interactome networks, appear to behave as if encoded by distinct genes rather than as minor variants of each other.,,, and that "As many as 100,000 distinct isoform transcripts could be produced from the 20,000 human protein-coding genes (Pan et al., 2008), collectively leading to perhaps over a million distinct polypeptides obtained by post-translational modification of products of all possible transcript isoforms",,,

Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing - 2016 In Brief Alternatively spliced isoforms of proteins exhibit strikingly different interaction profiles and thus, in the context of global interactome networks, appear to behave as if encoded by distinct genes rather than as minor variants of each other.,,, Page 806 excerpt: As many as 100,000 distinct isoform transcripts could be produced from the 20,000 human protein-coding genes (Pan et al., 2008), collectively leading to perhaps over a million distinct polypeptides obtained by post-translational modification of products of all possible transcript isoforms (Smith and Kelleher, 2013). http://iakouchevalab.ucsd.edu/publications/Yang_Cell_OMIM_2016.pdf

Thus since alternative splicing and post-translational modification leads "to perhaps over a million distinct polypeptides" existing in humans that are not present in chimpanzees, (and all these 'million distinct' proteins would obviously have to interact with each other in new and meaningful ways), yet the Darwinian mechanism requires 10^20 trials to find even one novel protein/protein binding site, then that, obviously, leaves the Darwinian mechanism of RM/NS as being grossly inadequate as to 'scientifically' explaining how humans originated. Verses:

Genesis 1: 27 So God created humankind in his image, in the image of God he created them; male and female he created them. Genesis 2:7, "And the LORD God formed man of the dust of the ground, and breathed into his nostrils the breath of life; and man became a living soul."

Of supplemental note as the 'distinctness' of the human genome:

THE UNIQUENESS OF HUMANS IS CLEARLY DEMONSTRATED BY THE GENE-CONTENT,, METHOD - 2019 Excerpt page 137: The humans included in the next cluster (p = 1.91 x 10^-30) are remarkably similar in expressed proteins among themselves and strikingly different from all other animals. This supports the humanity of Neanderthals and Denisovans, as much as it contradicts evolutionary narratives about common descent between humans and apes. In conjunction with other lines of evidence of human morphological, cognitive, and genetic (including non protein coding regions) distinctiveness, it clearly demonstrates that the evolutionary ideas on the origin of man have no plausible scientific foundation (Tomkins, 2012, 2014, 2016, 2018). https://www.creationresearch.org/crsq-2019-ekinds/ 3-D Human Genome Radically Different from Chimp - Jeffrey Tomkins, PH.D. - Jan. 7, 2021 Excerpt: Now a new study published in Trends in Genetics evaluates research in this emerging field that shows the human 3-D genome is distinctly unique to humans, confirming previous research that showed it is as different compared to chimp as it is to mouse.1,,, One important aspect of 3-D genome structure has to do with the epigenetic modification of proteins called histones that the DNA is wrapped around. A 2011 study showed that a specific type of histone modification had only about a 70% overlap or similarity between humans and chimps.4 Remarkably, another study in 2012 showed that humans had about a 70% similarity for the same feature with mice.5 In other words, humans were as different to mice as they were to chimps for this particular genome conformation metric. In the Trends in Genetics study, scientists wanted to take a closer look at this evolutionary anomaly to see if it held true for one of the most important features of genome conformation—TAD similarity. They found that in comparing humans and chimps, “only ~43% of TADs conserved [similar] between these species, but across many different parameters (e.g., resolution, window size, genome assembly) and different downstream analysis decisions, no more than 78% of domains and 83% of TAD boundaries were found to be shared between humans and chimpanzees.” This huge evolutionary discrepancy led them to conclude, “In our mind, there is no strong basis for the common and often unchallenged notion that TADs are highly conserved.”1 ,,, https://www.icr.org/article/human-genome-radically-different-from-chimp

bornagain77

William Lane Craig, and apparently a lot of other smart' people, give far more credence to the human evolution narrative that is put forth by Darwinists than is scientifically warranted and/or justified. I covered several of these fatal scientific weaknesses within the Darwinian narrative for human evolution earlier,

November 2021 - Human evolution? - the evidence from the fossil record refutes Darwinian evolution https://uncommondescent.com/intelligent-design/evangelical-scientists-getting-it-wrong/#comment-740239 November 2021 - Human evolution? - the evidence from genetics, (as well as the mathematics of population genetics itself), when viewed in its entirety, instead of just piecemeal as Darwinists are prone to do, actually falsifies, instead of supports, the Darwinian claim that humans evolved some chimp-like ancestor. https://uncommondescent.com/intelligent-design/evangelical-scientists-getting-it-wrong/#comment-740245 November 2021 - Human exceptionalism refutes Darwinian evolution https://uncommondescent.com/intelligent-design/evangelical-scientists-getting-it-wrong/#comment-740249 Human evolution? the mathematics itself within population genetics falsifies Darwinian evolution. https://uncommondescent.com/intelligent-design/christian-darwinists-must-now-backtrack-re-adam-and-eve/#comment-741335 Dr. John Sanford, whose credentials in genetics are impeccable, has analyzed the mathematics of population genetic inside and out, and, time and time again, Dr. Sanford and company have found that the mathematics of population genetics, (coupled with real time empirical evidence), falsifies Darwin’s theory rather than confirming it.

Since I covered these other fatal scientific weaknesses within the Darwinian narrative for human evolution earlier, today I would like to focus in on the failure of the Darwinian mechanism of RM/NS (Random Mutation/Natural Selection) to account for the origin of even a single novel protein from a preexisting protein, and also the failure of the Darwinian mechanism to account for the plethora of new protein/protein binding sites, (and/or protein 'interaction profiles'), that would have been required to explain the origin of the human form. Doug Axe, (as well as Dan Tawfik). have shown that the origination of a truly novel protein or fold, (from a preexisting protein or fold), as “something like close to a miracle.”

Right of Reply: Our Response to Jerry Coyne - September 29, 2019 by Günter Bechly, Brian Miller and David Berlinski Excerpt: Not so, Coyne argued. Proteins do not evolve from random sequences. They evolve by means of gene duplication. By starting from an established protein structure, protein evolution had a head start. This is not an irrational position, but it is anachronistic. Indeed, Harvard mathematical biologist Martin Nowak has shown that random searches in sequence space that start from known functional sequences are no more likely to enter regions in sequence space with new protein folds than searches that start from random sequences. The reason for this is clear: random searches are overwhelmingly more likely to go off into a non-folding, non-functional abyss than they are to find a novel protein fold. Why? Because such novel folds are so extraordinarily rare in sequence space. Moreover, as Meyer explained in Darwin’s Doubt, as mutations accumulate in functional sequences, they will inevitably destroy function long before they stumble across a new protein fold. Again, this follows from the extreme rarity (as well as the isolation) of protein folds in sequence space. Recent work by Weizmann Institute protein scientist Dan Tawfik has reinforced this conclusion. Tawfik’s work shows that as mutations to functional protein sequences accumulate, the folds of those proteins become progressively more thermodynamically and structurally unstable. Typically, 15 or fewer mutations will completely destroy the stability of known protein folds of average size. Yet, generating (or finding) a new protein fold requires far more amino acid sequence changes than that. Finally, calculations based on Tawfik’s work confirm and extend the applicability of Axe’s original measure of the rarity of protein folds. These calculations confirm that the measure of rarity that Axe determined for the protein he studied is actually representative of the rarity for large classes of other globular proteins. Not surprisingly, Dan Tawfik has described the origination of a truly novel protein or fold as “something like close to a miracle.” Tawfik is on Coyne’s side: He is mainstream. https://quillette.com/2019/09/29/right-of-reply-our-response-to-jerry-coyne/

As should be needless to say, and as Ann Gauger bluntly stated, "If enzymes can't be recruited to genuinely new functions by unguided means, no matter how similar they are, the evolutionary story is false.,,,"

"Enzyme Families -- Shared Evolutionary History or Shared Design?" - Ann Gauger - December 4, 2014 Excerpt: If enzymes can't be recruited to genuinely new functions by unguided means, no matter how similar they are, the evolutionary story is false.,,, Taken together, since we found no enzyme that was within one mutation of cooption, the total number of mutations needed is at least four: one for duplication, one for over-production, and two or more single base changes. The waiting time required to achieve four mutations is 10^15 years. That's longer than the age of the universe. The real waiting time is likely to be much greater, since the two most likely candidate enzymes failed to be coopted by double mutations. We have now addressed two objections raised by our critics: that we didn't test the right mutation(s), and that we didn't use the right starting point. We tested all possible single base changes in nine different enzymes, Those nine enzymes are the most structurally similar of BioF's entire family We also tested 70 percent of double mutations in the two closest enzymes of those nine. Finally, some have said we should have used the ancestral enzyme as our starting point, because they believe modern enzymes are somehow different from ancient ones. Why do they think that? It's because modern enzymes can't be coopted to anything except trivial changes in function. In other words, they don't evolve! That is precisely the point we are making. http://www.evolutionnews.org/2014/12/a_new_paper_fro091701.html

And that is just the insurmountable difficulty that the Darwinian mechanism of RM/NS encounters for generating, (and/or 'evolving'), just a single novel protein from a preexisting protein. In answering the question of how hard it would be for the Darwinian mechanism of RM/NS to account for novel proteins actually interacting with other proteins, Michael Behe has, via empirical evidence, found that "The likelihood of developing two binding sites in a protein complex would be the square of the probability of developing one: a double CCC (chloroquine complexity cluster), 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the entire world in the past 4 billion years, so the odds are against a single event of this variety (just 2 binding sites being generated by accident) in the history of life. It is biologically unreasonable."

"The likelihood of developing two binding sites in a protein complex would be the square of the probability of developing one: a double CCC (chloroquine complexity cluster), 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the entire world in the past 4 billion years, so the odds are against a single event of this variety (just 2 binding sites being generated by accident) in the history of life. It is biologically unreasonable." - Michael J. Behe PhD. (from page 146 of his book "Edge of Evolution")

And as Michael further explains in the following article, 'for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years' (1 quadrillion years)(Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans)."

Waiting Longer for Two Mutations - Michael J. Behe Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that 'for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years' (1 quadrillion years)(Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘is 5 million times larger than the calculation we have just given’ using their model (which nonetheless "using their model" gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model. Generally, when the results of a simple model disagree with observational data, it is an indication that the model is inadequate.,,, The difficulty with models such as Durrett and Schmidt’s is that their biological relevance is often uncertain, and unknown factors that are quite important to cellular evolution may be unintentionally left out of the model. That is why experimental or observational data on the evolution of microbes such as P. falciparum are invaluable,,, http://www.discovery.org/a/9461

bornagain77

If WLC is confused, then the rest of us are truly lost. What of this obsession to "prove" Adam and Eve were real people by stretching genealogy, genetics, anthropology and history to the breaking point? Trying to explain how Methuselah managed to live 969 years? Why not simply accept the creation myth for what it is and move on? The origin of all religion is myth and storytelling. chuckdarwin