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Dr Carl Wieland is on the Wrong Train (NAiG)

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This is a response to the No Answers in Genesis (NAiG) article, "Dr. Carl Wieland is on the Wrong Train". The NAiG article is itself a response to "The evolution train’s a-comin’ (Sorry, a-goin’—in the wrong direction)" by Dr. Carl Wieland, published in the March 2002 edition of Creation.

Critical Analysis

Review

Dr [medical doctor] Carl Wieland, writing in CreationDigest.com once again raises the creationist argument that genetic mutations cannot increase information.

Below Paul A. Poland refutes Dr Wieland's claims. The full text of Dr Wieland's article "The Evolution Train's a-Comin'" can be read here.

Paul A. Poland has a Masters Degree in Biology (West Virginia University 1990) and is currently a Research Specialist, Level IV, at the University of Pittsburgh.

Immediately an emphasis is put on credentials as NAiG emphasizes Dr. Wieland's medical doctor status while expressing Paul A. Poland (who does not possess a PhD) as a highly educated research specialist in the field of Biology. It should be noted that in no way does the education of an individual immediately make that individual's argument any more or less substantial. Instead, what should be seen is the content and substance of the argument.

For example, if a university Professor claims that 2 + 2 = 5, and a child points out that 2 + 2 = 4, the former argument is not made any more substantial.

Why can one say with confidence, concerning the biological changes observable today (man-induced or otherwise) that the train is headed in the wrong direction? Why is it that when evolutionists use this "grandma's train" extrapolation argument, it can be turned around to make the opposite point? Because the real issue in biological change is all about what happens at the DNA level, which concerns information. The information carried on the DNA, the molecule of heredity, is like a recipe, a set of instructions for the manufacture of certain items. (Carl Wieland, The evolution train’s a-comin’)
But, thanks to mutations, the recipes CAN BE CHANGED. (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

Poland is correct and mainstream creation science would agree with this claim. However, it is the hidden assumptions underlying the ultimate conclusions of the words chosen. These recipes can also be diversified through genetic recombination, a creationist theory for predicting changing quantities, orders and mixtures with a specific desired outcome. Creationists also support mutation and natural selection as a natural occurring phenomenon.

Evolutionists teach that one-celled organisms (e.g. protozoa) have given rise to pelicans, pomegranates, people and ponies. In each case, the DNA "recipe" has had to undergo a massive net increase of information during the alleged millions of years. (Carl Wieland, The evolution train’s a-comin’)
And there are MANY ways to do this - duplications (of genomes, groups of genes, genes, exons, control regions), transposable elements (add coding or regulatory regions), exon shuffling (most large modern proteins are modular), mutation/modification (alter a gene's activity or timing of expression - especially useful when regulatory genes are tweaked). (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

A common method used by anti-creationists when debating or criticizing creation theory, is to raise questions or arguments that were not even intended to be addressed in that particular article, and ignore the fact that they have been addressed elsewhere by the same author or organization. For example, CMI has addressed gene duplication, exon shuffling and transposons [1] [2] [3]. And Wieland himself had earlier addressed beneficial but information-losing mutations in Beetle bloopers: Even a defect can be an advantage sometimes

Mr. Poland claims modifications of an organism's DNA, such as duplications, transposable elements, exon shuffling, and mutation, provide "MANY ways to do this" changing of recipes he alluded to earlier. However, the desired research of evolutionists falls short and reliance upon blind extrapolation is needed. What has been shown by these proposed mechanisms of changing organisms DNA is that they usually do not provide a net increase of information but rather a change in the already present DNA of specific species. This change according to creationist predictions will never be seen to produce above the genus or family of the taxonomic hierarchy.

Duplications do not show an outside process adding anything new to the organism's genome; it simply copies what is already there in a specific species DNA makeup.

An example of an observable effect of a duplication is in people with Down Syndrome. In this case, they have three instead of two copies of chromosome 21. Transposable elements do not insert new information either, they are merely sequences of already existing DNA that can be moved to different positions within the genome. Exon shuffling again, is merely shuffling genes already present within the organism. Deletions also occur sometimes during the process of genetic mutation. These mutations can and have been observed as having a positive effect on an organism's DNA through the process of decreasing the amount of information.

Mutations are very limited in their ability to produce true Darwinian evolution consisting of not only the creationist supported and observable speciation but also protozoa-to-man, radical ever-more related and complex morphological change driven by mutation and selection. They do not inject unique information into the DNA of an organism producing a net gain without effecting already present DNA. These proposed mutation types, as a creationist prediction will be phenotype expression change within structures or behavioral patterns of individual species or populations of organisms.

A very small percentage of all mutations actually have a positive effect. These mutations lead to new versions of proteins that help an organism and its future generations better adapt to changes in their environment. For example, a specific 32 base pair DELETION in human CCR5 (CCR5-Δ32) confers HIV resistance to homozygotes and delays AIDS onset in heterozygotes.[4] The CCR5 mutation is more common in those of European descent. One theory for the etiology of the relatively high frequency of CCR5-Δ32 in the European population is that it conferred resistance to the bubonic plague in mid-14th century Europe. People who had this mutation were able to survive infection thus its frequency in the population increased.[5] It could also explain why this mutation is not found in Africa where the bubonic plague never reached. Newer theory says the selective pressure on the CCR5 Delta 32 mutation has been caused by smallpox instead of bubonic plague. - Wikipedia (see also CCR5–delta32: a very beneficial mutation)

None of these mechanisms are outside of the organism's genome. They are not natural processes adding new genetic information. While evolutionists claim that they have evidence that new and inserted information has occurred, there has been little observation of chance "MUTATIONS" being the cause of this.

A one-celled organism does not have the instructions for how to manufacture eyes, cars, blood, skin, hooves, brains, etc. which ponies need. So for protozoa to have given rise to ponies, there would have to be some mechanism that gives rise to new information. (Carl Wieland, The evolution train’s a-comin’)
There are SEVERAL mechanisms that can generate novel information. (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

We have discussed all of Paul A. Poland's proposed methods. What does Poland mean by novel information? If he means information altered to change the read-out, we fully agree. If Poland means new information producing a net gain without effecting already present DNA within an organism being responsible for all of evolutionary change throughout history, he is incorrect.

Genetic recombination can change the genome and can even produce new alleles [4]. However, evolutionists refrain from using genetic recombination as a method to produce new information because of the growing understanding of intentional and directed recombination that is carried by the organism with specific purpose, which goes against the evolutionary presumptions of random and accidental changes causing organisms to evolve from one type to another. Genetic recombination can not create new information either. It is limited to the pre-existing information in the genome and can only create variation within specific structures.

Evolutionists hail natural selection as if it were a creative goddess, but the reality (which they invariably concede when pressed) is that selection on its own always gets rid of information, never the opposite. (Carl Wieland, The evolution train’s a-comin’)
And mutation - which creationists always ignore - INCREASES information, by making the population more heterogenous and variable. (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

As this article attests to, creationists do not ignore but in fact embrace mutational load as a prediction rooted in observational science repeatable through experimentation. The amount of diversity possible, or the heterogeneous potential through mutational genetic change and natural selection favoring organisms who adapt fitly is something with which creationists have argument over.

To have a way to add information, the "only game in town" for evolution's true believers is genetic copying mistakes or accidents, i.e. random mutations (which can then be "filtered" by selection). However, the problem is that if mutations are capable of adding the information required, we should see hundreds of examples all around us, considering that there are many thousands of mutations happening continually. But whenever we study mutations, they invariably turn out to have lost or degraded the information. (Carl Wieland, The evolution train’s a-comin’)

Paul A. Poland posts a rather large list of journal references, probably with the intent of showing the readers that the references contradict Dr. Wieland's statements (an unethical debating technique sometimes called "elephant -hurling").

"Evolution of anti-freeze glycoprotein from a trypsinogen gene in Antarctic notothenioid fish" Chen L, DeVries AL, Cheng CC, Proceedings of the National Academy of Science 94:3811-16, April 1997

"Tandem sequence duplications functionally complement deletions in the D1 protein of Photosystem II", Kless H, Vermaas W, J Biol Chem 270(28): 16536-165451, July 1995

"Transposable elements are found in a large number of human protein-coding genes", Nekrutenko A, Li W-H, Trends in Genetics 17(11):619-621 Nov '01

"Evolution of biological information", Schneider TD, Nucleic Acids Research 28(14): 2794-99, July '00

"Positive Darwinian selection after gene duplication in primate ribonuclease genes", Zhang J, Rosenberg HF, Nei M, PNAS 95: 3708-3713, Mar '98

"Adaptive evolution of a duplicated pancreatic ribonuclease gene in a leaf-eating monkey", Zhang J, Zhang Y-P, Rosenberg HF, Nature Genetics 30:411-415, April '02

"Origin of new genes and source for N-terminal domain of the chimerical gene, jingwei, in Drosophila", Long M, Wang W, Zhang J, Gene 238: 135-141, Sep 99

"Origin of sphinx, a young chimeric RNA gene in Drosophila melanogaster", Wang W, Brunet FG, Nevo E, Long M, PNAS 99(7):4448-44532, April '02

"Selective sweep of a newly evolved sperm-specific gene in Drosophila", Nurminsky DI, Nurminskaya MV, De Aguiar D, Hartl DL, Nature 396: 572-575, Dec '98

"A gene network model accounting for development and evolution of mammalian teeth", Salazar-Cuidad I, Jervall J, PNAS 99(12):8116-8120, Jun '02

"Adaptive evolution of a DUPLICATED pancreatic ribonuclease gene in a leaf-eating monkey", J Zhang, Y-P Zhang, HF Rosenberg, Nature (Genetics) 30:April 2002, pg 411-415 - ONLY colombine monkeys have RNAse1B and RNAse1; all other primates have ONLY RNAse1.

"Natural selection and the ORIGIN of jingwei, a chimeric processed functional gene in Drosophila", M Long, CH Ling, Science 260: 2 April 1993, pg 91-95; this gene exists ONLY in sister species D. yakuba and D. teisseri (formed from parts of other genes). (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

Unfortunately, Mr. Poland does not elaborate on these references, what they are supposed to prove, or give an explanation of how Wieland's statement is wrong. He also gives no indication as to how mutations have caused specific new data to be added to an organism's already existing DNA. It can be hypothesized, however, that Mr. Poland is trying to provide us with examples where it appears that mutations have caused "brand new" genes in organisms. Under examination, the references prove interesting and extensively researched information about mere adaptations, but still fail to provide "proof" of new genetic information, a net gain causing true evolutionary transformation. Mr. Poland is merely quoting research that has been conducted by scientists with evolutionary presuppositions.

For example Michael Behe's book The Edge of Evolution discusses antifreeze proteins (pp. 77–83, 2007). They are nothing like the complex interacting proteins that comprise molecular machines, but rather just gum up ice crystal seeds and prevent them from expanding. Repeated sequences of DNA were duplicated, making them more effective at gumming up ice crystal growth. Behe compares molecular machines with engineered dams that block water, while the antifreeze proteins are more like the gunk that jams his kitchen drain—anything will do: food, paper, large or small. Duplication events for the antifreeze protein are more akin to more of the same type of, "jamming gunk." The antifreeze protein certainly shows what mutation and selection can achieve, but it offers no comfort to true believers in the evolution of from simple to vastly more complex biological machinery.

Specifically regarding, "Adaptive evolution of a DUPLICATED pancreatic ribonuclease gene in a leaf-eating monkey," if RNAse1B is unique of RNAse1, in that it contains different information and not just re-arranged information, RNAse1B was probably present in all monkeys at one time. Only colobine monkeys have retained RNAse1B while all other variants have lost this gene. However, this is highly unlikely because most of the evidence points to duplication and then divergence. There are several amino acid differences between the two genes doing the same thing in different ways. While RNAse1 served two specific functions, RNAse1B now excels at one while failing at the other. Because RNAse1 and RNAse1B are both present in the genome, there is no negative effect on the monkeys because both genes successfully serve their purposes.

Functional assays revealed that the colobine-specific RNASE1B achieves maximal efficiency at pH 6, which is within the pH range of the colobine foregut. This is in contrast to RNASE1, which functions optimally at the pH 7.4 characteristic of the human small intestine. Thus, the preponderance of negative substitutions in the evolution of RNASE1B seems directly related to the enzyme's role in the low-pH colobine foregut. By contrast, site-directed mutagenesis revealed that seven of the nine substitutions that distinguish the sequence of RNASE1B from that of RNASE1 reduce its efficiency in degrading double-stranded RNA, a task of the ancestral enzyme. It appears that the evolutionarily innovative features of RNASE1B arose at the direct expense of efficiency in its ancestral function. [5]

A mutation has probably occurred that has created a different gene. However, while this gene increases the efficiency of one function, it loses its ancestral function. Normally, this type of mutation would be harmful to the organism, but in the case of the Colobine, a copy of RNAse1 is still present. The extent of the research also fails to conclude how this information was not present in the genome of the Colobine and because Poland did not draw his own conclusions about what this information means, there is nothing to rebut.

This is so even in those rare instances when the mutational defect gives a survival advantage, e.g. the loss of wings on beetles on windy islands.

As creatures diversify, gene pools become increasingly thinned out. The more organisms adapt to their surroundings by selection, i.e. the mere specialized they become, the smaller the fraction they carry of the original storehouse of created information for their kind. (Carl Wieland, The evolution train’s a-comin’)

Too bad that 1) mutations RESTOCK variation, and 2) 'kind' has NEVER been defined in any meaningful way. (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

Wieland points out that the information in a gene pool increasingly thins out as creatures diversify. This is absolutely correct and observable. However, genetic recombination provides restocking of variations to a certain degree. Mr. Poland is also correct when he states that mutations, "RESTOCK variation," however not at a high enough rate to allow for steady increase of genetic diversity and complexity, or net gains in genetic information within a specific species. Another problem with mutations as a mechanism for evolutionary genetic diversity is that time does not favor positive mutations and allows for negative mutational load.

Poland makes the claim that the created kind has never been defined in any meaningful way. This is untrue and is telling of his research rigor. When the word "kind" is invoked by creationists they are referring to the biblical references of a creation act by God. This act, similar to that of abiogenesis within an evolutionary framework produced life. This life was represented in original kinds or representatives, such as Adam and Eve for humanity as well as many creatures that have now diversified into what we see today within the animal kingdom.

It can be compared to that of the evolutionary tree of life however it isn't just one single-celled organism but many representatives of each kind of life we see today.

Thus, there is less information available on which natural selection can act in the future to "readapt" the population should circumstances change. Less flexible, less adaptable populations are obviously heading closer to extinction, not evolving. (Carl Wieland, The evolution train’s a-comin’)
Again, mutations restock variation - there is a LOT of variation in populations, it's just that most of it is masked ("Hsp90 as a capacitor for morphological evolution", Rutherford SL, Lindquist S, Nature 396: 336-341, Jun '02). (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

Finally Mr. Poland expands on what a peer-reviewed journal article states and his conclusions. However his ultimate conclusions of protozoa-to-man evolutionary change is severely lacking credibility even with his referenced paper. The paper's abstract states;

The heat-shock protein Hsp90 supports diverse but specific signal transducers and lies at the interface of several developmental pathways. We report here that when Drosophila Hsp90 is mutant or pharmacologically impaired, phenotypic variation affecting nearly any adult structure is produced, with specific variants depending on the genetic background and occurring both in laboratory strains and in wild populations. Multiple, previously silent, genetic determinants produced these variants and, when enriched by selection, they rapidly became independent of the Hsp90 mutation. Therefore, widespread variation affecting morphogenic pathways exists in nature, but is usually silent; Hsp90 buffers this variation, allowing it to accumulate under neutral conditions. When Hsp90 buffering is compromised, for example by temperature, cryptic variants are expressed and selection can lead to the continued expression of these traits, even when Hsp90 function is restored. This provides a plausible mechanism for promoting evolutionary change in otherwise entrenched developmental processes. (Hsp90 as a capacitor for morphological evolution, Rutherford SL, Lindquist S, Nature 396: 336-341, Jun '02 [6])

Hsp90 is a heat-stock protein and has been called a molecular chaperon machine in that it helps other proteins find their ultimate shapes. In that way it is considered a controlling morphological factor that determines phenotype expression of an organism.

The abstract of this very interesting article merely points to Hsp90 being a protein very essential to developmental pathways of a given species' various traits that make up the many segments of a fruit fly's overall physical structure. What is important to note is that changes in these fruit flies was induced through drugs.

All of the affected fies in line HV2 expressed mild to moderate defects, whereas most of the affected fies from lines HV1 and HV3 expressed severe defects. This partitioning of the wing-vein phenotype between lines confirmed that more than one genetic determinant affected the trait. (Hsp90 as a capacitor for morphological evolution, Rutherford SL, Lindquist S, Nature 396: 336-341, Jun '02 [7])

There is no observational science within this paper implying that these drug-induced Hsp90 determined pathway variants produce anything regarding massive, cascading morphological change from one kind of animal to another. For true neo-Darwinian evolution to have been observed, it would include drastic related mutations of the fruit fly, turning it into a honey bee or something completely different other than simple differences between fruit fly wing-vein segments. In saying that, this is clear-cut evidence of what can be called phenotype diversity within species or an originally created kind and can be classified under another prediction observed within creation biology.

Somehow this program had to be written. New information had to arise that did not previously exist, anywhere. (Carl Wieland, The evolution train’s a-comin’)
It's fortunate there are MANY ways to generate new info. (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

Paul A. Poland has thus far been unsuccessful in showing how these, "MANY ways" bring in "NEW information" that actually produces the totality of evolution.

Later, there were lungs, but no feathers anywhere in the world, thus no genetic information for feathers. (Carl Wieland, The evolution train’s a-comin’)
Pardon? Feathers are just very modified scales. (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

Poland tries to imply that feathers are just very modified scales. This is simply an unwarranted and unproven evolutionary extrapolation that stems from a presupposition that birds evolved from reptiles. While it is possible for this to be true, it is equally possible for these fossil transitions from reptile to bird are actually the history of long extinct distinct species of their own, completely unrelated to the fossil found higher up in the geological column.

Real world observation has overwhelming shown mutation to be totally unable to feed the required new information into the system. (Carl Wieland, The evolution train’s a-comin’)
Bullcrap - see the above articles. (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

At this point, Poland is trying to use intense language to imply to the reader that Wieland's statements are clearly and obviously incorrect. However, this article has thus far demonstrated how Poland's arguments are far more nuanced and clarification of limits of his examples need to be shown.

In fact, mutations overall hasten the downward trend by adding genetic load in the form of harmful mutations. of which we have all accumulated hundreds over the generations of our ancestry.

In other words, populations can change and adapt because they lave a lot of information (variety) in their DNA "recipe." But unless mutations can feed in new information, each time their is variation/adaptation, the total information decreases (as selection gets rid of the unadapted portions of the populations some information is lost in that population). Thus, given a fixed amount of information, the more adaptation we see the less the potential for future adaptation. The train is definitely header downhill, destined to fall oft the jetty of extinction. (Carl Wieland, The evolution train’s a-comin’)

Only in your deluded dreams. "Information" can be gained - since "fittest" is dependent upon many factors, a mutation that is harmful in one context may be neutral or beneficial in another. This fact is what Dembski and the other Misinformation Theorists like to ignore - there are no fixed "predetermining filters". Creationists use some sort of hybrid info theory - see this TalkOrigins article for the reason the creationists' Misinformation Theory is bunk. (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

While it could be argued that genetic recombination could contribute to restoring lost information and changing pre-existing information (such as gene expression, quantities, etc.) it can not provide brand new information producing truly unique structures from its previous form. The point of evolution is not to devolve in one context but in another evolve, it is complete upward momentum of complex morphological change from a protozoa-to-man.

We see that just like with the train pulling out from Miami and headed south, if the sorts of changes we see today are extrapolated over time, they lead to extinction, not onwards evolution.

Remember. evolutionary belief teaches that once upon a time, there were living things but no lungs - lungs had not evolved yet, so there was no DNA information coding for lung manufacture. (Carl Wieland, The evolution train’s a-comin’)

You are making the rather simple minded assumption that a single gene could do this. There are salamanders LIVING TODAY that have a wide range of lung types - simple lungs, simple sacs, to none at all. Structures like this are built by gene interactions.

Salamanders are very special and unique creatures and could be compared to butterflies and frogs in that they go through metamorphosis. The method of which salamanders grow and develop varies between groups and is highly influenced by environmental stresses. One could argue that all salamanders have the genetic ability to develop in a variety of ways and that the process of metamorphosis is clearly directed by the organism. It is not mutations that cause different lung types in salamanders, but environmental stress and metamorphosis processes.

Dr. Wieland's statement is not simple minded because it is clear that protozoa do not have the required information required for lung manufacturing, while all salamanders do or at one point did making the creature more fit.

The supreme irony is that, of all the examples lauded by Dr. Coyne as "evolution", whether antibiotic resistance or changes in fish growth rates, not one single one supports his "train" analogy, but rather the reverse. Not one involves a gain of information; all show the opposite, a net loss. Pondering all this, l feel a sense of the same sort of frustration (only in reverse) that my evolutionist opponent was airing all those years ago, which he could have paraphrased as: "Why can't they see it? It's obvious, isn't it?" (Carl Wieland, The evolution train’s a-comin’)
Yes, it is QUITE obvious that creationists don't have a clue. (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

Apparently, creationists are somehow not putting together the puzzle. Of course, evolutionists would like us to ignore the rest of "their" puzzle.

Who knows, perhaps somehow this article will get into Dr. Coyne's hands. Maybe it will give him, and some other evolutionist apologists food for thought the next time they put one of their grandmothers on a train. (Carl Wieland, The evolution train’s a-comin’)
Let's see - we have the simpering reference to "evolutionist BELIEF" and "evolutionist apologist", inferring the standard lie that evolution is a religion. If this "article" were read by Dr Coyne, he'd probably conclude that you are at best misrepresenting genetic science or at worst ignorant of genetic science. Perhaps REALITY will give creationists food for thought. But I suspect not. (Paul A. Poland, Dr Carl Wieland is on the Wrong Train)

This is a typical response. Creationists only point out the philosophical not scientific underpinnings of the ultimate unobserved conclusions that evolution posits as fact. It requires faith to believe in the unobserved and this is chiefly accomplished by relying upon materialism and naturalism.

Conclusion

This article has critically analyzed statements by both Dr. Carl Wieland and Paul. A. Poland, in an attempt to draw an informative conclusion of both views and arguments.

While both parties have many good points, it is clear through peer-review that Mr. Poland is unwarranted in his criticism of Dr. Wieland and in his attempts to discredit Dr. Wieland's article. Mr. Poland's evolutionary bias has drastically impaired his understanding of genetic change. Neo-Darwinism fails largely to provide evolutionary evidence because mutations do not provide a viable mechanism for cascading morphological change. Mr. Poland's bias against creation and intelligent design forces him to reject much of the evidence that has been provided for genetic recombination and for negative mutational load, which are increasingly casting shadows over Neo-Darwinism.

References


See Also