Microbiologist admits Darwinism’s shortcomings, says we should stick with it for now because …

_{Denyse O'Leary

February 17, 2014

Darwinism, Evolution, News}

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There’s a difference between a theory being wrong and being incomplete. In science, we cling to incomplete theories all the time. Especially when the alternative is complete ignorance.

No really, BigThink’s Kas Thomas actually admits,

Darwin’s landmark work was called The Origin of Species, yet it doesn’t actually explain in detail how speciation happens (and in fact, no one has seen it happen in the laboratory, unless you want to count plant hybridization or certain breeding anomalies in fruit flies). …

Yes, Darwinism is always promoted on faith; you just don’t expect to hear biologists admit that. Hope this guy’s job is safe. Many places have frozen hiring, now limited to career zombies.

Also,

When I was in school, we were taught that mutations in DNA are the driving force behind evolution, an idea that is now thoroughly discredited. The overwhelming majority of non-neutral mutations are deleterious (reducing, not increasing, survival). This is easily demonstrated in the lab.

Yes of course, but those are unspeakable words. Read the rest and note the comments.

Okay. Here’s the problem with his approach, summarized from above: A theory that so consistently misleads as he describes is probably wrong, not just incomplete. It’s like going south when you should be going north. We keep explaining away the discrepancies in landmarks until finally, we just have to stop and ask, “Where exactly are we in relation to our destination?” But then we must begin by acknowledging that “evolution” (Darwinism) is not better than nothing, instead of shutting down online discussion.

Wish the guy luck; he’s into good questions.

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Comments

wd400 funny how no one really understands evolution except you and your Darwinian cohorts! As well, since you quoted it, do you have a problem with this claim?
"The overwhelming majority of non-neutral mutations are deleterious (reducing, not increasing, survival). This is easily demonstrated in the lab."
Because that is exactly what we find!:
“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/
and:
Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 - May 2013 Excerpt: It is almost universally acknowledged that beneficial mutations are rare compared to deleterious mutations [1–10].,, It appears that beneficial mutations may be too rare to actually allow the accurate measurement of how rare they are [11]. 1. Kibota T, Lynch M (1996) Estimate of the genomic mutation rate deleterious to overall fitness in E. coli . Nature 381:694–696. 2. Charlesworth B, Charlesworth D (1998) Some evolutionary consequences of deleterious mutations. Genetica 103: 3–19. 3. Elena S, et al (1998) Distribution of fitness effects caused by random insertion mutations in Escherichia coli. Genetica 102/103: 349–358. 4. Gerrish P, Lenski R N (1998) The fate of competing beneficial mutations in an asexual population. Genetica 102/103:127–144. 5. Crow J (2000) The origins, patterns, and implications of human spontaneous mutation. Nature Reviews 1:40–47. 6. Bataillon T (2000) Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? Heredity 84:497–501. 7. Imhof M, Schlotterer C (2001) Fitness effects of advantageous mutations in evolving Escherichia coli populations. Proc Natl Acad Sci USA 98:1113–1117. 8. Orr H (2003) The distribution of fitness effects among beneficial mutations. Genetics 163: 1519–1526. 9. Keightley P, Lynch M (2003) Toward a realistic model of mutations affecting fitness. Evolution 57:683–685. 10. Barrett R, et al (2006) The distribution of beneficial mutation effects under strong selection. Genetics 174:2071–2079. 11. Bataillon T (2000) Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? Heredity 84:497–501. http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0006 Response to John Wise - October 2010 Excerpt: A technique called "saturation mutagenesis"1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans--because none of the observed developmental mutations benefit the organism. http://www.evolutionnews.org/2010/10/response_to_john_wise038811.html Mutations and Darwinism - Dr Jerry Bergman - June 2013 - video http://www.youtube.com/watch?v=pfgiAWBluxE
In fact the top five supposedly 'beneficial' mutations of Lenski's LTEE, after 50,000 generations were combined and found to negative epistasis. This is NOT what you need to have your preferred hypothesis be true wd400! The reason why mutations are overwhelmingly detrimental, and we have such a hard time finding any truly beneficial mutations on there way to building things up wd400, is because of the 'poly-constraint' imposed by the poly-functionality' inherent within an organism. The following article is about the genome but the principle of poly-constraint due to poly-functionality is also extended to proteins:
Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 - published online May 2013 Excerpt: In the last decade, we have discovered still another aspect of the multi- dimensional genome. We now know that DNA sequences are typically “ poly-functional” [38]. Trifanov previously had described at least 12 genetic codes that any given nucleotide can contribute to [39,40], and showed that a given base-pair can contribute to multiple overlapping codes simultaneously. The first evidence of overlapping protein-coding sequences in viruses caused quite a stir, but since then it has become recognized as typical. According to Kapronov et al., “it is not unusual that a single base-pair can be part of an intricate network of multiple isoforms of overlapping sense and antisense transcripts, the majority of which are unannotated” [41]. The ENCODE project [42] has confirmed that this phenomenon is ubiquitous in higher genomes, wherein a given DNA sequence routinely encodes multiple overlapping messages, meaning that a single nucleotide can contribute to two or more genetic codes. Most recently, Itzkovitz et al. analyzed protein coding regions of 700 species, and showed that virtually all forms of life have extensive overlapping information in their genomes [43]. 38. Sanford J (2008) Genetic Entropy and the Mystery of the Genome. FMS Publications, NY. Pages 131–142. 39. Trifonov EN (1989) Multiple codes of nucleotide sequences. Bull of Mathematical Biology 51:417–432. 40. Trifanov EN (1997) Genetic sequences as products of compression by inclusive superposition of many codes. Mol Biol 31:647–654. 41. Kapranov P, et al (2005) Examples of complex architecture of the human transcriptome revealed by RACE and high density tiling arrays. Genome Res 15:987–997. 42. Birney E, et al (2007) Encode Project Consortium: Identification and analysis of functional elements in 1% of the human genome by the ENCODE pilot project. Nature 447:799–816. 43. Itzkovitz S, Hodis E, Sega E (2010) Overlapping codes within protein-coding sequences. Genome Res. 20:1582–1589. http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0006
The primary problem that poly-functional complexity presents for neo-Darwinism is this: To put it plainly, the finding of a severely poly-functional/polyconstrained genome by the ENCODE study, and many other studies, has put the odds, of what was already astronomically impossible, to what can only be termed fantastically astronomically impossible. To illustrate the monumental brick wall any evolutionary scenario (no matter what “fitness landscape”) must face when I say genomes are poly-constrained by poly-functionality, I will use a puzzle: If we were to actually get a proper “beneficial mutation’ in a polyfunctional genome, then instead of the infamous “Methinks it is like a weasel” single element of functional information that Darwinists pretend they are facing in any evolutionary search, with their now falsified genetic reductionism scenario I might add (Shapiro, Nobel), we would actually be encountering something more akin to this illustration found on page 141 of Genetic Entropy by Dr. Sanford.
S A T O R A R E P O T E N E T O P E R A R O T A S Sator Square http://en.wikipedia.org/wiki/Sator_Square
Which is translated ; THE SOWER NAMED AREPO HOLDS THE WORKING OF THE WHEELS. This ancient puzzle, which dates back to 79 AD, reads the same four different ways, Thus, If we change (mutate) any letter we may get a new meaning for a single reading read any one way, as in Dawkins weasel program, but we will consistently destroy the other 3 readings of the message with the new mutation (save for the center). This is what is meant when it is said a poly-functional genome is poly-constrained to any random mutations.
Second, third, fourth… genetic codes - One spectacular case of code crowding - Edward N. Trifonov - video https://vimeo.com/81930637
In the preceding video, Trifonov elucidates codes that are, simultaneously, in the same sequence, coding for DNA curvature, Chromatin Code, Amphipathic helices, and NF kappaB. In fact, at the 58:00 minute mark he states, "Reading only one message, one gets three more, practically GRATIS!". And please note that this was just an introductory lecture in which Trifinov just covered the very basics and left many of the other codes out of the lecture. In fact, at the 7:55 mark of the video, there are 13 codes that are listed on a powerpoint, although the writing was too small for me to read. Concluding powerpoint of the lecture (at the 1 hour mark):
"Not only are there many different codes in the sequences, but they overlap, so that the same letters in a sequence may take part simultaneously in several different messages." Edward N. Trifonov - 2010
Supplemental note:
Not Junk After All: Non-Protein-Coding DNA Carries Extensive Biological Information - Jonathan Wells - published online May 2013 Conclusion:,, Recent discoveries of multiple overlapping functions in non-protein-coding DNA show that the biological information in the genome far exceeds that in the protein-coding regions alone. Yet biological information is not limited to the genome. Even at the level of gene expression - transcription and translation — the cell must access information that is not encoded in DNA. Many different RNAs can be generated from a single piece of DNA by alternative splicing, and although some splicing codes occur in intronic DNA there is no empirical justification for assuming that all of the information for tissue- and developmental-stage-specific alternative splicing resides in DNA.,, even after RNA has specified the amino acid sequence of a protein, additional information is needed: Protein function depends on three-dimensional shape, and the same sequence of amino acids can be folded differently to produce proteins with different three-dimensional shapes [144–147]. Conversely, proteins with different amino acid sequences can be folded to produce similar shapes and functions [148,149]. Many scientists have pointed out that the relationship between the genome and the organism - the genotype-phenotype mapping = cannot be reduced to a genetic program encoded in DNA sequences. Atlan and Koppel wrote in 1990 that advances in artificial intelligence showed that cellular operations are not controlled by a linear sequence of instructions in DNA but by a “distributed multilayer network” [150]. According to Denton and his co-workers, protein folding appears to involve formal causes that transcend material mechanisms [151], and according to Sternberg this is even more evident at higher levels of the genotype-phenotype mapping [152]. So non-protein-coding regions of DNA that some previously regarded as “junk” turn out to encode biological information that greatly increases the known information-carrying capacity of DNA. At the same time, DNA as a whole turns out to encode only part of the biological information needed for life. http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0009
bornagain77_{February 17, 2014
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I disagree with the entire quoted text (which is why I quoted all of it). i.e. the argument that because most non-neutral mutations are deleterious, mutations can't be the source of adaptation. There aren't multiple definitions of speciation, and the species probldm is not about speciation but human's ability to delimit species. I'm not sure what you are trying to prove by quoting Moran, who confirms the falsity of Thomas' claim that "almost everything in evolutionary theory is based on 'survival of the fittest'".wd400_{February 17, 2014
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In this case, it’s clear the author’s education has taught them almost nothing about evolutionary biology.
Really? The fact that he has doubts about the extent of what we know via evolutionary biology is enough to indicate that? He seemed to mostly bluntly say what is all too obvious when reading up about the field.
The overwhelming majority of non-neutral mutations are deleterious (reducing, not increasing, survival). This is easily demonstrated in the lab.
Which part of this do you even disagree with? Are you saying most non-neutral mutations are beneficial? Via Nature: Mutational effects can be beneficial, harmful, or neutral, depending on their context or location. Most non-neutral mutations are deleterious.
Or someoe who doesn’t seem to know what speciation is
He does seem to know what speciation is. The fact that the word has multiple meanings doesn't really speak against him.
or thinks ” Almost everything in evolutionary theory is based on “survival of the fittest,”?
Insofar as he means it's historically been selectionist, Larry Moran seems to agree. Sayeth ID-hating Larry: The revolution is over and strict Darwinism lost. We now know that random genetic drift is an important mechanism of evolution and there's more to evolution than natural selection. Unfortunately, this blatantly obvious fact is not understood by the vast majority of people and teachers. There are even many scientists who don't understand evolution. Maybe it's not Kaz Thomas who doesn't know much about evolutionary theory, but his critics.nullasalus_{February 17, 2014
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wd400- evolutionary biology is mostly just a glossy narrative void of scientific rigor and detail. And truthfully it reads like Lamarkism- just look at the narrative of how the vision system allegedly evolved. It is all Lamarkism- all of it physical changes to the vision system that get passed down. Nothing on the molecular level wrt its evolution.Joe_{February 17, 2014
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I just read Coyne's "rebuttal"- what a joke. Coyne sez the BF came from the TTSS yet he doesn't say how the TTSS arose. He actually references Pallen and Matzke as if they demonstrated how a BF evolved via natural selection and/ or drift. The best part is Coyne's examples of natural selection in no way indicative of NS being a designer mimic nor creating something like a bacterial flagellum. Too funny...Joe_{February 17, 2014
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Seems like he has a bachelors degree in microbiology, then started a PhD and dropped it. So, not a microbiologists but not without trianing. Of course, we should judge articles but the quality of their arguments, not the credentials on their authors. In this case, it's clear the author's education has taught them almost nothing about evolutionary biology. Does teh ID movement really want to throw it's support by someone who can say something as uninformed at teh quoted text When I was in school, we were taught that mutations in DNA are the driving force behind evolution, an idea that is now thoroughly discredited. The overwhelming majority of non-neutral mutations are deleterious (reducing, not increasing, survival). This is easily demonstrated in the lab. Or someoe who doesn't seem to know what speciation is, or thinks " Almost everything in evolutionary theory is based on "survival of the fittest,"?wd400_{February 17, 2014
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selvaRajan,
Kaz Thomas seems to be a technical writer and a software documentation professional.
According to his bio page at the OP's linked site: A graduate of the University of California at Irvine and Davis (with degrees in biology and microbiology) and a former University of California Regents Fellow, Thomas has taught biology, bacteriology, and laboratory physics at the college level. He was on the Inventions Committee at Novell, Inc. and is the holder of seven U.S. software patents. He has a long and varied background in technical writing (most recently serving as a Technology Evangelist for Adobe Systems) and is in love with the word heterodoxy. He seems to have about as much claim to be a microbiologist as Dawkins has to claim he's a scientist. If we're judging by current professions, Dawkins and Kas Thomas are both writers. And PZ Myers is a blogger who sometimes teaches.nullasalus_{February 17, 2014
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It looks like Kas was formerly a microbiologist. From his blog:
I guess I should have made clear, up front, that I have two degrees in biology: a B.S. from UCI and a master's in microbiology (summa cum laude) from UC Davis, where I was a Regents' Fellow. I took (and passed) qualifying exams for a Ph.D. One of the specialty areas I was examined in was molecular genetics.
Maybe being a microbiologist is like learning to ride a bike?JoeCoder_{February 17, 2014
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News, Kaz Thomas seems to be a technical writer and a software documentation professional. He is not a Microbiologist. Please check http://www.linkedin.com/in/kasthomasselvaRajan_{February 17, 2014
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I see that Jerry Coyne is the self-appointed chief inquisitor of all heresies against the Church of Darwin.Mapou_{February 17, 2014
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Now Darwin's followers are saying Thomas should be stripped of his degrees or should ask for his money back. Guy's got guts. Anyone know him?News_{February 17, 2014
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Boy, this article has Jerry Coyne and fellow Darwinian trolls having a fit in the comment section. :) As well they should be. The points that Dr. Thomas honestly admits to are all severe problems for Darwinism that have all been hammered away at for years by ID proponents:
The Trouble with Darwin by Kas Thomas - February 16, 2014 Excerpt: Darwin's landmark work was called The Origin of Species, yet it doesn't actually explain in detail how speciation happens (and in fact, no one has seen it happen in the laboratory, unless you want to count plant hybridization or certain breeding anomalies in fruit flies). Almost everything in evolutionary theory is based on "survival of the fittest," a tautology that explains nothing. ("Fittest" means most able to survive. Survival of the fittest means survival of those who survive.) The means by which new survival skills emerge is, at best, murky. Of course, we can't expect Darwin himself to have proposed detailed genetic or epigenetic causes for speciation, given that he was unaware of the work of Mendel, but the fact is, even today we have a hard time figuring out how things like a bacterial flagellum first appeared. When I was in school, we were taught that mutations in DNA are the driving force behind evolution, an idea that is now thoroughly discredited. The overwhelming majority of non-neutral mutations are deleterious (reducing, not increasing, survival). This is easily demonstrated in the lab. Most mutations lead to loss of function, not gain of function. Evolutionary theory, it turns out, is great at explaining things like the loss of eyesight, over time, by cave-dwelling creatures. It's terrible at explaining gain of function. It's also terrible at explaining the speed at which speciation occurs. (Of course, The Origin of Species is entirely silent on the subject of how life arose from abiotic conditions in the first place.) It doesn't explain the Cambrian Explosion, for example, or the sudden appearance of intelligence in hominids, http://bigthink.com/devil-in-the-data/the-trouble-with-darwin
Kas Thomas is a graduate of the University of California at Irvine and Davis (with degrees in biology and microbiology) and a former University of California Regents Fellow, Thomas has taught biology, bacteriology, and laboratory physics at the college level.bornagain77_{February 17, 2014
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Why it is an absolute disaster that the ~~incomplete~~ wrong theory of Darwin is allowed to continue as if it has no problems. Because finding God leads to a wonderful life.JDH_{February 17, 2014
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