Darwinian biologist Jerry Coyne denounces Michael Behe’s forthcoming book unread

That didn't last- Jerry booted me and his exit rant proved that he is a clueless dolt:

I’ve missed most of your comments about ID, which show a profound ignorance of both evolution and even ID. You spout nonsense with no backing (“ID is not anti-evolution”–seriously?), and you have no data or calculations showing that the reptile-mammal transition could not occur by “blind and mindless processes.” We’ve seen very rapid evolution in real time depending on those “blind” processes (a 10% change in finch beak size in ONE YEAR), as well as humans using those random mutations to create big changes through artificial selection. You can give no reason why natural selection, an analogue of artificial selection in which nature determines the optimum, couldn’t do the same thing. Your dislike of evolution is based on no data at all, but your ignorance and perhaps your religiosity. I don’t know if you’re religious, but you’re certainly ignorant about the things you speak of.

Yes, Jerry, ID is not anti-evolution. ID is OK with a change in allele frequency over time, ie evolution. ID is OK with descent with modification, ie evolution. It is only if you define evolution as the blind watchmaker thesis that ID is anti-evolution. ID is OK with every textbook definition of evolution I could find. You lose, Jerry The calculations to support my claim are in the peer-reviewed paper titled "Waiting for Two Mutations". It shows the difficulty of getting a mere TWO specified mutations. The change from reptile to mammal requires more than that. You lose, Jerry. Beak size- wow! Too bad beak size means nothing in the grand scheme of things and as far as you know it is all designed in variability. You have nothing that can account for the existence of birds, loser. Natural selection is not an analogue of artificial selection. Ernst Mayr explained the differences in "What Evolution Is":

Page 117: What Darwin called natural selection is actually a process of elimination. Page 118: Do selection and elimination differ in their evolutionary consequences? This question never seems to have been raised in the evolutionary literature. A process of selection would have a concrete objective, the determination of the “best” or “fittest” phenotype. Only a relatively few individuals in a given generation would qualify and survive the selection procedure. That small sample would be only to be able to preserve only a small amount of the whole variance of the parent population. Such survival selection would be highly restrained. By contrast, mere elimination of the less fit might permit the survival of a rather large number of individuals because they have no obvious deficiencies in fitness. Such a large sample would provide, for instance, the needed material for the exercise of sexual selection. This also explains why survival is so uneven from season to season. The percentage of the less fit would depend on the severity of each year’s environmental conditions.

"BY CONTRST" means they are not analogues but dissimilar. So clearly there is no "nature determines the optimum" except in the ignorant and wishful minds of evos, like Jerry Coyne. Natural selection could never do what we can do. It could never produce the different breeds of dogs but take away humans and NS will take away those breeds. NS is good at undoing what we have done. Jerry Coyne is an ignorant loser feeding the Kool Aid to the ignorant minions. ET

Bob, That is what science is for- to answer those questions. What directs transposons? The cellular programming- it's OS. I mentioned telic processes and provided a short list. ET

ET @ 8 - what are these "built-in responses"? As for transposons, what direct them? As far as we know, they integrate into specific sites at random, so what directs them? They also wouldn't explain evolution in bacteria, for obvious reasons. You mention "telic processes", but what were these processes? To put it bluntly: how did the designer do their job? Bob O'H

I just posted the following on Jerry's blog: The mechanisms for ID are telic processes as opposed to your blind and mindless processes, Jerry. ID holds that organisms were not only intelligently designed, but designed with the ability to evolve and adapt. IDists can test the claim that, for example, ATP synthase was the result of intelligent design. Can anyone say how to test the claim it evolved by means of blind and mindless processes? Will he allow it to stay? ET

Bob O'H You and others often ask "... Where is the evidence for ID or creation?” The evidence is as close to you as your own head, so let me present the evidence from the top down, the top being the human head. The human head is an amazing collection of instrumentation, computing power and inventive genius that far surpasses any collection of machines brought about by those same heads. To continue on with this, click this link: https://ayearningforpublius.wordpress.com/2013/07/16/intelligent-design-creation-the-evidence/ And also get my layman's look at the subject: https://www.amazon.com/gp/product/172008193X/ref=dbs_a_def_rwt_bibl_vppi_i5 As my former Marine Corp boss (a general) used to say "This should be obvious even to a sea-going corporal." ayearningforpublius

Well, Bob, Dr. Spetner (Not By Chance) proposed "built-in responses to environmental cues", which clearly has the environment as the cause and those built-in responses as a mechanism. Epigenetics has helped confirm it. He also has transposons as mechanisms for directed change- Perry Marshall is also a proponent of transposons for directed change. Then there are all the changes discussed by Shapiro in "Evolution: a view from the 21st century". Organisms were designed to evolve and evolved by design, Bob- they were designed with the ability to adapt. Telic processes took place to produce all of the biological codes and systems (physical components) needed to carry them out. Telic processes take place to run all of the codes and systems to keep cells functioning. Telic processes take place in proof reading, error correction, editing, splicing, transcribing and translating. It takes place with chaperones helping the polypeptides find their shape and ferrying them to their destination. That is for starters, Bob. The alternative, Bob, is changes just happen (just because). Those which make it past the error correcting (which also just happened) will either be eliminated or allowed to accumulate. And when the "right" changes just happen to happen, well you know, here we are! ET

Well, ET, what specific process have design theorists proposed? What are the specific causes? What is the reason or mechanism? What telic processes took place? Bob O'H

I will note that Bob O'H's ignorance is not an argument. ID is not anti-evolution, Bob, so clearly ID does not try to show what evolution can't do. The debate is all about what blind and mindless processes can do vs what it takes telic processes to produce. So yes, ID has proposed telic processes as the mechanism as opposed to blind and mindless processes. "Not By Chance" was published in 1997. That's 21 years ago. It does exactly what Bob says doesn't exist. Then there's John Davison's "Prescribed Evolutionary Hypothesis"- again it does what Bob says doesn't exist. ET

Cotnes highlights this from the publishers' blurb:

But Intelligent Design goes a step further asking, what caused such astounding changes to take place? What is the reason or mechanism for evolution? For Behe, this is what makes Intelligent Design so important.

This is baffling - if there's one thing ID has failed to do it is to ask these questions. It's all about trying to show what evolution can't do. (to be fair, I should mention Mike Gene's front-loading as about the only exception to my criticism) Bob O'H

I own and have read 2 of Dr. Behe's books and find them fascinating, and VERY convincing. If he's written another book, I'll buy it (and read it) as soon as it's available. I especially like the way he has overviews in the main text for us non-Biology majors and then MUCH more detailed explanations in appendices. That is, he knows how to be instructive without being condescending. vmahuna

Of course such pervasive negative interactions between supposedly 'selfish' and/or individualistic genes is completely devastating to the materialistic presuppositions of Darwinian evolution. (Which more or less hold genes to be fairly individualistic in their actions) Whereas, on the other hand, for the Christian Theist who presupposes life to have an 'author', and since every book is dominated by a holistic 'context' in which 'the whole (book) is required to give meaning to the part (sentence)'.,,,

A Meaningful World: How the Arts and Sciences Reveal the Genius of Nature – Book Review Excerpt: They focus instead on what “Methinks it is like a weasel” really means. In isolation, in fact, it means almost nothing. Who said it? Why? What does the “it” refer to? What does it reveal about the characters? How does it advance the plot? In the context of the entire play, and of Elizabethan culture, this brief line takes on significance of surprising depth. The whole is required to give meaning to the part. http://www.thinkingchristian.net/C228303755/E20060821202417/

,,, then such pervasive mutual interdependence among genes is exactly what we would expect to see beforehand. And indeed that is exactly what we find over and over again. As Dr. Wells states, "It's the organism controlling the DNA, not the DNA controlling the organism."

Ask an Embryologist: Genomic Mosaicism - Jonathan Wells - February 23, 2015 Excerpt: humans have a "few thousand" different cell types. Here is my simple question: Does the DNA sequence in one cell type differ from the sequence in another cell type in the same person?,,, The simple answer is: We now know that there is considerable variation in DNA sequences among tissues, and even among cells in the same tissue. It's called genomic mosaicism. In the early days of developmental genetics, some people thought that parts of the embryo became different from each other because they acquired different pieces of the DNA from the fertilized egg. That theory was abandoned,,, ,,,(then) "genomic equivalence" -- the idea that all the cells of an organism (with a few exceptions, such as cells of the immune system) contain the same DNA -- became the accepted view. I taught genomic equivalence for many years. A few years ago, however, everything changed. With the development of more sophisticated techniques and the sampling of more tissues and cells, it became clear that genetic mosaicism is common. I now know as an embryologist,,,Tissues and cells, as they differentiate, modify their DNA to suit their needs. It's the organism controlling the DNA, not the DNA controlling the organism. http://www.evolutionnews.org/2015/02/ask_an_embryolo093851.html

Supplemental note: The unifying 'form', i.e. 'context', of an organism is found to forever be beyond the grasp of 'bottom up' Darwinian explanations:

Darwinism vs Biological Form – video https://www.youtube.com/watch?v=JyNzNPgjM4w

Verse:

Acts 3:15 You killed the author of life, but God raised him from the dead. We are witnesses of this.

bornagain77

This negative effect on the 'holistic' network of genes within a organism has been revealed by what is termed negative and/or antagonistic epistasis between mutations

Response from Ralph Seelke to David Hillis Regarding Testimony on Bacterial Evolution Before Texas State Board of Education, January 21, 2009 Excerpt: He has done excellent work showing the capabilities of evolution when it can take one step at a time. I have used a different approach to show the difficulties that evolution encounters when it must take two steps at a time. So while similar, our work has important differences, and Dr. Bull’s research has not contradicted or refuted my own. http://www.discovery.org/a/9951 Mutations : when benefits level off - June 2011 - (Lenski's e-coli after 50,000 generations) Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually. http://www2.cnrs.fr/en/1867.htm?theme1=7 Epistasis between Beneficial Mutations - July 2011 Excerpt: We found that epistatic interactions between beneficial mutations were all antagonistic—the effects of the double mutations were less than the sums of the effects of their component single mutations. We found a number of cases of decompensatory interactions, an extreme form of antagonistic epistasis in which the second mutation is actually deleterious in the presence of the first. In the vast majority of cases, recombination uniting two beneficial mutations into the same genome would not be favored by selection, as the recombinant could not outcompete its constituent single mutations. https://uncommondesc.wpengine.com/epigenetics/darwins-beneficial-mutations-do-not-benefit-each-other/ Beneficial mutations that aren’t? -June 2011 Three recent papers in Science: In Evolution, the Sum Is Less than Its Parts; Diminishing Returns Epistasis Among Beneficial Mutations Decelerates Adaptation; Negative Epistasis Between Beneficial Mutations in an Evolving Bacterial Population https://uncommondesc.wpengine.com/intelligent-design/beneficial-mutations-that-aren%E2%80%99t/ The diminishing returns of beneficial mutations - July 2011 Excerpt: Evolution thus has three strikes against it: most mutations are not beneficial, practically all mutations destroy specified complexity, and, now, even ‘beneficial’ mutations work against each other. While mutations may be of limited benefit to a single organism in a limited context (e.g., sickle cell anemia can protect against malaria even though the sickle cell trait is harmful), mutations seem to be no benefit whatsoever for microbes-to-man evolution, whether individually or together. http://creation.com/antagonistic-epistasis New Research on Epistatic Interactions Shows "Overwhelmingly Negative" Fitness Costs and Limits to Evolution - Casey Luskin June 8, 2011 Excerpt: In essence, these studies found that there is a fitness cost to becoming more fit. As mutations increase, bacteria faced barriers to the amount they could continue to evolve. If this kind of evidence doesn't run counter to claims that neo-Darwinian evolution can evolve fundamentally new types of organisms and produce the astonishing diversity we observe in life, what does? http://www.evolutionnews.org/2011/06/new_research_on_epistatic_inte047151.html A Serious Problem for Darwinists: Epistasis Decreases Chances of Beneficial Mutations - November 8, 2012 Excerpt: A recent paper in Nature finds that epistasis (interactions between genetic changes) is much more pervasive than previously assumed. This strongly limits the ability of beneficial mutations to confer fitness on organisms. https://evolutionnews.org/2012/11/epistasis_decr/

bornagain77

What both Behe and Sanford prove,,,

Darwin Devolves — Preorder Behe’s New Book; Plus Video Course on Intelligent Design! – Nov. 14, 2018 https://evolutionnews.org/2018/11/darwin-devolves-preorder-behes-new-book-plus-video-course-on-intelligent-design/ John Sanford gives lecture at NIH on mutations and human health - November 15, 2018 https://www.youtube.com/watch?time_continue=10&v=eqIjnol9uh8

,,, is that the overwhelming majority of mutations, even supposedly beneficial mutations, are detrimental.

“The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain - Michael Behe - December 2010 Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain. http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/

One of the main reasons why mutations will, for all practical purposes, always be detrimental is because genes, (contrary to the ‘selfish gene’ concept, that is more of less directly based on Darwin’s own ‘survival of the fittest’ thinking), genes are instead best thought of as existing in a holistic web of mutual interdependence and cooperation.

Gene Pleiotropy Roadblocks Evolution by Jeffrey P. Tomkins, Ph.D. – Dec. 8, 2016 Excerpt: Before the advent of modern molecular biology, scientists defined a gene as a single unit of inheritance. If a gene was found to influence multiple externally visible traits, it was said to be pleiotropic—a term first used in 1910.2 During this early period of genetic discovery, pleiotropy was considered to be quite rare because scientists assumed most genes only possessed a single function—a simplistic idea that remained popular throughout most of the 20th century. However, as our understanding of genetics grew through DNA science, it became clear that genes operate in complex interconnected networks. Furthermore, individual genes produce multiple variants of end products with different effects through a variety of intricate mechanisms.2,3 Taken together, these discoveries show that pleiotropy is a common feature of nearly every gene.,,, The pleiotropy evolution problem is widely known among secular geneticists, but rarely discussed in the popular media. In this new research report, the authors state, “Many studies have provided evidence for the ability of pleiotropy to constrain gene evolution.”,,, “Our study provided supportive evidence that pleiotropy constraints the evolution of transcription factors (Tfs).”,,, The authors state, “We showed that highly pleiotropic genes are more likely to be associated with a disease phenotype.”,,, http://www.icr.org/article/9747 What If (Almost) Every Gene Affects (Almost) Everything? – JUN 16, 2017 Excerpt: If you told a modern geneticist that a complex trait—whether a physical characteristic like height or weight, or the risk of a disease like cancer or schizophrenia—was the work of just 15 genes, they’d probably laugh. It’s now thought that such traits are the work of thousands of genetic variants, working in concert. The vast majority of them have only tiny effects, but together, they can dramatically shape our bodies and our health. They’re weak individually, but powerful en masse. https://www.theatlantic.com/science/archive/2017/06/its-like-all-connected-man/530532/ Theory Suggests That All Genes Affect Every Complex Trait – June 20, 2018 Excerpt: Mutations of a single gene are behind sickle cell anemia, for instance, and mutations in another are behind cystic fibrosis. But unfortunately for those who like things simple, these conditions are the exceptions. The roots of many traits, from how tall you are to your susceptibility to schizophrenia, are far more tangled. In fact, they may be so complex that almost the entire genome may be involved in some way,,, One very early genetic mapping study in 1999 suggested that “a large number of loci (perhaps > than 15)” might contribute to autism risk, recalled Jonathan Pritchard, now a geneticist at Stanford University. “That’s a lot!” he remembered thinking when the paper came out. Over the years, however, what scientists might consider “a lot” in this context has quietly inflated. Last June, Pritchard and his Stanford colleagues Evan Boyle and Yang Li (now at the University of Chicago) published a paper about this in Cell that immediately sparked controversy, although it also had many people nodding in cautious agreement. The authors described what they called the “omnigenic” model of complex traits. Drawing on GWAS analyses of three diseases, they concluded that in the cell types that are relevant to a disease, it appears that not 15, not 100, but essentially all genes contribute to the condition. The authors suggested that for some traits, “multiple” loci could mean more than 100,000. https://www.quantamagazine.org/omnigenic-model-suggests-that-all-genes-affect-every-complex-trait-20180620/ Why the ‘Gene’ Concept Holds Back Evolutionary Thinking – James Shapiro – 11/30/2012 Excerpt: The Century of the Gene. In a 1948 Scientific American article, soon-to-be Nobel Laureate George Beadle wrote: “genes are the basic units of all living things.”,,, This notion of the genome as a collection of discrete gene units prevailed when the neo-Darwinian “Modern Synthesis” emerged in the pre-DNA 1940s. Some prominent theorists even proposed that evolution could be defined simply as a change over time in the frequencies of different gene forms in a population.,,, The basic issue is that molecular genetics has made it impossible to provide a consistent, or even useful, definition of the term “gene.” In March 2009, I attended a workshop at the Santa Fe Institute entitled “Complexity of the Gene Concept.” Although we had a lot of smart people around the table, we failed as a group to agree on a clear meaning for the term. The modern concept of the genome has no basic units. It has literally become “systems all the way down.” There are piecemeal coding sequences, expression signals, splicing signals, regulatory signals, epigenetic formatting signals, and many other “DNA elements” (to use the neutral ENCODE terminology) that participate in the multiple functions involved in genome expression, replication, transmission, repair and evolution.,,, Conventional thinkers may claim that molecular data only add details to a well-established evolutionary paradigm. But the diehard defenders of orthodoxy in evolutionary biology are grievously mistaken in their stubbornness. DNA and molecular genetics have brought us to a fundamentally new conceptual understanding of genomes, how they are organized and how they function. http://www.huffingtonpost.com/james-a-shapiro/why-the-gene-concept-hold_b_2207245.html

The fairly obvious result of genes existing in a holistic web of mutual interdependence is that mutations to one element of the web will, in fairly quick order, detrimentally effect the whole holistic web that comprises the genome of an organism. bornagain77