Whale and Human Vestiges (Pelvic Bone | Appendix)

Shun the Non-Believer…

A CLIP FROM CHARLIE THE UNICORN

Before posting what I did on Facebook as part of a response to a conversation regarding the below graphic… I want to say that by showing vestiges…

  • a rudimentary structure in humans corresponding to a functional structureor organ in ancestral animals

…in no way undermines Intelligent Design, or somehow PROVES evolution. Let me explain.

Darwin said he didn’t see an issue with whales evolving from bears, or some bear like creature. In his first edition of Origin of Species, Darwin said this:

  • “I can see no difficulty in a race of bears being rendered, by natural selection, more and more aquatic in their structure and habits, with larger and larger mouths,” Darwin concluded, “till a creature was produced as monstrous as a whale.”

ARCHAEOPTERYX

This does not involve “devolution,” a loss of specificity which the below picture captures… but rather, evolution demands an increase in specificity in gene and DNA specificity in the creation of whole new organs and how they act. Similarly, the Archaeopteryx is proffered as an example of evolution, but evolutionists themselves would say that this is only an example of “devolution,” and not an increase of specificity in a species (a clipping from my post: “Was Archaeopteryx Devolving? Thus Losing It’s Ability to Fly?“):

Since other feathered “birds” have been found around the same time or earlier than Archaeopteryx, causing Alan Feduccia to quip, “You can’t be older than your grandfather” (Creation.com)… NATURE has published an article pointing out that Archaeopteryx is JUST LIKE modern flightless birds. And so it could have been losing its ability for flight (like modern birds have).

“We know Archaeopteryx was living on an archipelago during the Jurassic. And with its feathers and bones looking so much like modern flightless island birds, it just makes me wonder,” says…. Michael Habib, a biologist at the University of Southern California….

[….]

“Just because Archaeopteryx was the first feathered dinosaur found, doesn’t mean it has to play a central role in the actual history of the origins of birds,” says palaeontologist Thomas Holtz of the University of Maryland in College Park. “We have to remember it appears 10 million years or so after the oldest known bird-like dinosaurs and so our famous ‘first bird’ may really be a secondarily flightless one.”…

(Nature Journal)

There is just as much [at best] evidence for this proposition as the next. “Devolution” — a loss of specificity/use, may be a more reasonable position to take via observed evidence. We see this all the time (directly below is an example from Lee Spetner’s new book), and EVOLUTION NEWS says that “looks like Archaeopteryx may have to be reclassified as a different sort of icon — symbolizing evolution by loss of function.” Oops.

So these types of examples ACTUALLY COUNT AGAINST the main idea that neo-Darwinism proposed… that I came from a rock.

I find it interesting that people think this whale bone pictured above is a vestigial organ. Very similar to the list of a 180 vestigial structures said to be in the human body in the late 1800’s dwindling to effectively zero, and the damage and laziness such thinking cost lives and sciences advancement (see more here):

TONSILS

In the 1930’s over half of all children had their tonsils and adenoids removed.  In 1969, 19.5 out of every 1,000 children under the age of nine had undergone a tonsillectomy.  By 1971 the frequency had dropped to only 14.8 per 1,000, with the percentage continuing to decrease in subsequent years. Most medical authorities now actively discourage tonsillectomies.[1] Many agree with Wooley, chairman of the department of pediatrics at Wayne State University, who was quoted in Katz: “If there are one million tonsillectomies done in the United States, there are 999,000 that don’t need doing.”

Among the first medical doctors seriously to question the wisdom of tonsillectomies was Albert Kaiser.  For ten years he kept complete records of the illnesses of 5,000 children. They were divided into two groups – those who had tonsils removed and those who did not.  Kaiser found: “…no significant difference between the two groups in the number of colds, sore throats and other upper respiratory infections.”[2]

Tonsils are important to young people in helping to establish the body’s defense mechanism which produces disease-fighting antibodies.  Once these mechanisms are developed, the tonsils shrink to almost nothing in adults, and other organs take over this function.[3]  In the Medical World News,[4] a story stated that although removal of tonsils at a young age obviously eliminates tonsillitis (the inflammation of the tonsils) it may significantly increase the incidence of strep-throat and even Hodgkin’s disease.  In fact, according to the New York Department of Cancer Control: “…people who have had tonsillectomies are nearly three times as likely to develop Hodgkin’s Disease, a form of cancer that attacks the lymphoid tissue.”[5]

THE POINT

My point is this, the Tonsils were once included in a list of 180 vestigial (“useless, or nearly useless”) organs.[6]  And because the assumption was first made that these were organs left over from a previous genetic ancestor (ape, dog, early-man, whatever), that they were deemed useless – ad hoc – because science did not know at that time what their functions were.

So for many years, doctors and scientists that accepted the evolutionary paradigm did not investigate the possible functionality of these organs.  Many people suffered and died needlessly due to this philosophical assumption that evolution is true.  You will see this assumption play out again and again where medical science and the evolutionary issue intersect.  You see, if you come to the table with an understanding that we were created, then these structures serve a purpose, or are a neutral combination of the possible male/female outcome of the fertilized egg (for instance, male nipples[7]).  If the assumption is made that these structures are designed, then the medical world would strive to investigate and understand the organ in question, not simply state that it is useless.

[1] Robert P Bolande, “Ritualistic Surgery – circumcision and tonsillectomy,” New England Journal of Medicine, March 13 (1969) pp. 591-595; Alvin Eden, “When Should Tonsils and Adenoids be Removed?” Family Weekly, September 25 (1977), p. 24; Lawrence Galton, “All Those Tonsil Operations: Useless? Dangerous?” Parade, May 2 (1976), pp. 26ff; Dolras Katz, “Tonsillectomy: Boom or Boondoggle?” The Detroit Free Press, April 13 (1972), p. 1-C; Samuel Lipton, “On the Psychology of Childhood Tonsillectomy,”  found in: The Psychoanalysis Study of the Child (International Universities Press, New York: 1962).
[2] Galton, p. 26.
[3] Martin L. Gross, The Doctors (Random House, New York: 1966); Simpson Hall, Diseases of the Nose, Throat and Ear (E. and S. Livingston, New York: 1941).
[4] N. J. Vianna, Peter Greenwald, and U. N. Davies,  September 10, 1973, p.10
[5] Galton, p. 26-27.
[6] This is an important issue, for instance, during the famous Scopes trial in 1925 – which allowed evolution to be taught alongside creation – zoologist Horatio Hacket Newman, a defense witness, stated: “There are, according to Wiedersheim, no less than 180 vestigial structures in the human body, sufficient to make of a man a veritable walking museum of antiquities.”
[7] Also, if created by a personal God who has created sex to be pleasurable, then the nipples have a purpose other than the neutral canvas of the fertilized egg.

  • Jerry Bergman and George F. Howe, Vestigial Organs Are Fully Functional (Creation Research Society Books, Kansas City: MO: 1990). 

WHALE TALES

SIMILARLY, the laziness in neo-Darwinian evolutionary propositions in this “example” of a vestigial organ shows the laziness in thought, and, the stalling of advancing science in understanding nature. Now, we know, and even the secular world acknowledges this fact in “discovering” [yet again] that pronouncements made by the evolutionary community of scientists is woefully wrong. Here is an example via THE DAILY MAIL – take note how I and the researches end the article:

Whale Sex Revealed: ‘Useless’ Hips Bones Are Crucial To Reproduction – And Size Really Matters, Study Finds

  • Whales and dolphins have pelvic bones, which are evolutionary remnants from when their ancestors walked on land more than 40 million years ago
  • Scientists from the University of Southern California and the Natural History Museum of Los Angeles County, analysed pelvic bones for four years
  • Muscles that control a cetacean’s penis attach directly to its pelvic bones
  • They found the bigger the animals’ testis, the bigger their pelvic bone
  • Males from more promiscuous species evolve larger penises, so larger pelvic bones are necessary to attach bigger muscles for penis control, they said
  • Study changes the way we think about vestigial structures

[…..]

They wrote in the journal Evolution, the muscles that control a cetacean’s highly flexible penis, attach directly to its pelvic bones.

The scientist theorised that the pelvic bones could affect the level of control over the penis that an individual cetacean has, perhaps offering an evolutionary advantage.

To test their idea, they examined hundreds of pelvic bones and used a 3D scanner to make digital models of the curved bones in order to gain an unprecedented level of detail about their shape and size, as well as to compare them.

They then gathered data about testis size relative to the mass of whales. In the natural world, more ‘promiscuous’ species where females mate with many males, create a more competitive mating environment and the males develop larger testes as a way of attracting females.

[…..]

The experts compared the size of pelvic bones to the size of an animal’s testes, relative its body size, and found that the bigger the testes, the bigger the cetacean’s pelvic bone.

Males from more promiscuous species also evolve larger penises, so larger pelvic bones appear necessary to attach larger muscles for penis control, they said.

‘Our research really changes the way we think about the evolution of whale pelvic bones in particular, but more generally about structures we call vestigial,’ Professor Dean said.

‘AS A PARALLEL, WE ARE NOW LEARNING THAT OUR APPENDIX IS ACTUALLY QUITE IMPORTANT IN SEVERAL IMMUNE PROCESSES, NOT A FUNCTIONALLY USELESS STRUCTURE,’ he added….

(emphasis added)

AMBULOCETUS NATANS

In conversation about the above, the person I was speaking with posted a series of evolution from creature-to-creature proving the evolution of the whale.

I have already refuted this clean progression, HERE, but I noted something that this person was not aware of. As most people are not. You see, when you bring your kid to the Natural History Museum, you see this picture of the RED OUTLINED creature in the evidence for whales evolving:

The problem with this evidence is that it is based primarily on an artists rendition. Here is the actual bones all this Ambulocetus Natans is based on — see #3:

I merely commented that his believing and passing along graphics showing full skulls by artists, or the above “skeletal” sequence, reminds me of the movie scene from the Matrix:

In similar fashion, this artistic rendition used in the Scopes “Monkey” Trial was used as evidence proving evolution:

However, this was based off a single tooth. NOT ONLY THAT, but the tooth put forward as hominid, ended up being an extinct pig’s tooth.

APPENDIX

In similar form, many people still think the APPENDIX is a vestigial organ. Here is my response (since updated) to one of my son’s teachers in high school dealing with what was being taught as FACT… that is, that the appendix had no known use:


FULL UPDATED PAPER


Context this short paper was written:

This paper evolved over many years.  It was one of the first subjects I debated at a science discussion board on the Internet many years ago prior to the NetZero days.  Then I updated it to respond in writing to a Discover magazine article (a much larger paper, of which this takes up two pages).

Finally, as my son has been studying science in seventh grade, his science textbook states many “facts” wrongly, this being only one of the many I have since written about (peppered moths, embryos going through stages of a fish, homology, and the like).

I like to think that the teacher’s role is to not just teach what the “state” requires – this reminds me of the novels 1984, or Animal Farm – but to allow updated information into the classroom that will best challenge these students to become that medical doctor, chemist, or physicist.  In other words, I want my son to have the best information that may spark the interest to become, say, a medical doctor.  This is all that I argue for.

As it so happened, the teacher merely regurgitated what the “state” wanted her to (even after reading such a cogent and well laid response to her saying “there is no use for the appendix in the human body”).  Much like when the dog cubs were taken and “educated” in the novel Animal Farm.

Much thought – and enjoy the read – SeanG!

THE APPENDIX

Dr. Kawanishi,[1] showed that human lymphoid cells in the appendix are immunologically functional as T helper cells and antibody-producing B cells, making IgA molecules in response to immunological challenges.  He noted that:

“The human appendix, long considered only an accessory rudimentary organ, could posses a similar antigen uptake role prior to replacement by fibrosed tissue after repeated subclinical infections, or at least in early childhood when it is most prominent.”[2]

The appendix is also rich in argentaffin cells, which can be identified with the use of silver salt staining.  The function of these cells has long been obscure, but the evidence suggests that they may be involved with endocrine gland function.[3]  Many sources (encyclopedias, textbooks, etc.) still erroneously state that the appendix is useless.  Interestingly, the Grolier Multimedia Encyclopedia states in one place: that “In humans the cecum and appendix have no important function,” and in another place that “the appendix is now thought to be one of the sites where immune responses are initiated.”

Dr. Howard R. Bierman… studied several hundred patients with leukemia, Hodgkin’s disease, cancer of the colon and cancer of the ovaries.  He found that 84% [of his sample] had [their] appendix removed….  In a control group without cancer, only 25% had it removed.[4]

Bierman himself had concluded that the appendix may be an immunological organ whose premature removal during its functional period permits leukemia and other related forms of cancer to begin their development.[5]  Bierman and his associates realized that the lymphoid tissue located on the walls of the appendix may secrete antibodies which protect the body against various viral agents.

While high school and college textbooks today will mention the appendix as vestigial, specialists in their field have for many years stated the necessity of the appendix as useful.

  • “There is no longer any justification for regarding the vermiform appendix as a vestigial structure.”[6]
  • For at least 2,000 years, doctors have puzzled over the function of…  the thymus gland…. Modern physicians came to regard it, like the appendix, as a useless vestigial organ which had lost its original purpose, if indeed it ever had one.  In the last few years, however,…  men have proved that, far from being useless, the thymus is really the master gland that regulates the intricate immunity system which protects us against infectious diseases….  Recent experiments have led researchers to believe that the appendix, tonsils, and adenoids may also figure in the antibody responses.[7]
  • The appendix is not generally credited with significant function; however, current evidence tends to involve it in the immunologic mechanism.[8]
  • The mucosa and submucosa of the appendix are dominated by lymphoid nodules, and its primary function is as an organ of the lymphatic system.[9]

The appendix is in fact part of the G.A.L.T. (Gut Associated Lymphoid Tissue) system.  The lymphoid follicles develop in the appendix at around two weeks after birth, which is the time when the large bowel begins to be colonized with the necessary bacteria.  It is likely that its major function peaks in this neonatal period.  Making it anything other than vestigial!

As Dr. Peter Faletra (Ph.D.), who is Senior Science Advisor Office of Science Department of Energy, says in response to a question on an online question-and-answer service for K-12 teachers run by the Argonne National Laboratories:

“As a histologist I see no reason to consider the v. appendix as having no function since it contains numerous lymphoid follicles that produce functional lymphocytes and a rich blood supply to communicate them. The general idea of vestigial organs is to me a measure of ignorance, arrogance and lack of imagination. Ignorance in that we label it as such because we do not know its function; arrogance in that we declare it of no value since we can see none; and lacking in imagination in so far as when we cannot see its function cannot imagine one. I call your attention to that other ‘vestigial organ’ the thymus without which, in early life, we would produce a severely compromised cell-mediated immune system as the ‘nude’ mouse and numerous thymectomized mammalian studies have shown. Although some general reference books still list the v. appendix as ‘vestigial’ most immunologists (I included) would strongly disagree!”[10] (emphises added)

UPDATE

Since the above was removed, I want to embolden the thinking by excerpting a SCIENTIFIC AMERICAN article:[11]

A study in the Journal of Evolutionary Biology finds that many more animals have appendixes than was thought, and that the appendix is not merely a remnant of a digestive organ called the cecum. All of which means that the appendix might not be so useless. Steve Mirsky reports.

Two years ago, Duke University Medical Center researchers said that the supposedly useless appendix is actually where good gut bacteria safely hide out during some unpleasant intestinal conditions. 

Now the research team has looked at the appendix over evolutionary history. They found that animals have had appendixes for about 80 million years. And the organ has evolved separately at least twice, once among the weird Australian marsupials and another time in the regular old mammal lineage that we belong to. 

Darwin thought that only a few animals have an appendix and that the human version was what was left of a digestive organ called the cecum. But the new study found that 70 percent of rodent and primate groups have species with an appendix….

While Scientific American still tries to relegate it to evolution, they do so by supposition. Almost by metaphysical statements. William Parker, Ph.D., assistant professor of experimental surgery, who conducted the analysis in collaboration with R. Randal Bollinger, M.D., Ph.D., Duke professor emeritus in general surgery – said this:

  • “While there is no smoking gun, the abundance of circumstantial evidence makes a strong case for the role of the appendix as a place where the good bacteria can live safe and undisturbed until they are needed”[12]

WIKIPEDIA has a decent section on the appendix’s function as well.[13]

PS – (from the original letter)
This P.S. was to the teacher after she responded to my e-mail, I corrected her on something that any science teacher who isn’t guided by a presupposed philosophy – namely Naturalism – would have correctly defined.

Oh, I forgot, as I was falling asleep last night and running through the day in my head, something occurred to me.  You mentioned that theories are, quote:

  • “Theories are well tested concepts scientists use to help explain something based on repeated findings.”

Yes, a great quick explanation of a proper theory.  However, when the appendix was placed on the vestigial organ list along with 180 other organs by Ernst Haekel in the late 1800‘s – where it has stayed since – no repeatable tests were ever done to confirm the hypothesis that it was useless.  In fact, every medical test done of the type of tissue found (argentaffin cells, and lymphoid cells) in the appendix shows that it has a use.

So I would say that the theory that it is useful is quite sound, where as the hypothesis that it is useless is waning and ill founded ~ un-scientific in other words.


FOOTNOTES


[1] H. Kawanishi, “Immunocompetence of Normal Appendiceal Lymphoid cells: in vitro studies,” Immunology, 60(1) (1987), 19-28.

[2] Ibid., 19.

[3] Marti-Ibanez (editor), “Tuber of Life,” M. D. Magazine (1970) #14, p. 240; William J. Banks, Applied Veterinary Histology (Williams and Wilkins, Baltimore: 1981), 390.

[4]  Richard G. Culp, Remember thy Creator (Baker Book House, Grand Rapids,; MI: 1975).

[5]  Howard R. Bierman, “Human Appendix and Neoplasia,” Cancer 21 (1) (1968), 109-118.

[6] William Straus, Quarterly Review of Biology (1947), 149.

[7] “The Useless Gland that Guards Our Health,” in Reader’s Digest, November (1966), 229, 235.

[8] Henry L. Bockus, Gastroenterology, 2:1134-1148 [chapter The Appendix, by Gordon McHardy], (W.B. Saunders Company, Philadelphia, Pennslyvania: 1976).

[9] Frederic H. Martini, Ph.D., Fundamentals of Anatomy and Physiology, (Prentice Hall, Englewood Cliffs, New Jersey: 1995), 916

[10] (Since removed) From the site Newton, which is an electronic community for Science, Math, and Computer Science K-12 Educators.  Argonne National Laboratory, Division of Educational Programs, Harold Myron, Ph.D., Division Director.  Quote: http://www.newton.dep.anl.gov/askasci/mole00/mole00225.htm   Home page: http://www.newton.dep.anl.gov/

[11] “That’s No Vestigial Organ, That’s My Appendix,” Scientific American (8-24-2009), found at: http://tinyurl.com/ycb9dcnv

[12] Duke University Medical Center, “Appendix isn’t useless at all: It’s a safe house for bacteria,” EurekaAlert! (AAAS | 10-08-2008); found at: http://tinyurl.com/yadgop2l

[13] Appendix, Functions – found at: http://tinyurl.com/k245vmb

 

Antibiotic Resistance Evidence of “Devolution”

Updated near the bottom.

The issue involved in the above video is not evolution, but in fact, DEVOLUTION. In other words, “no newly evolved complex information has been demonstrated,” EVOLUTION NEWS AND VIEWS continues with a quote and then some commentarry [I am working on getting the graphic mentioned]:

A key aspect of bacterial survival is the ability to evolve while migrating across spatially varying environmental challenges. Laboratory experiments, however, often study evolution in well-mixed systems. Here, we introduce an experimental device, the microbial evolution and growth arena (MEGA)-plate, in which bacteria spread and evolved on a large antibiotic landscape (120 × 60 centimeters) that allowed visual observation of mutation and selection in a migrating bacterial front. While resistance increased consistently, multiple coexisting lineages diversified both phenotypically and genotypically. Analyzing mutants at and behind the propagating front, we found that evolution is not always led by the most resistant mutants; highly resistant mutants may be trapped behind more sensitive lineages. The MEGA-plate provides a versatile platform for studying microbial adaption and directly visualizing evolutionary dynamics.

The key to understanding the paper is its Figure 3C. There it shows the genes that have undergone more than one mutation across tested bacteria. They break the mutations down into silent changes, changes of amino acids (point mutations), and insertion-deletion or nonsense mutations, which almost certainly are loss of function (LOF). Over half of genes contain such LOF mutations, along with some point mutations, which likely also degrade or destroy function. In other words, devolution….

In another post over at EVOLUTION NEWS AND VIEWS, it is mentioned that “Evolutionists often speak in generalities about beneficial mutations. They may be rare, we are assured, but they happen.” But is this the case? Continuing we read:

…when they do [happen], “natural selection is daily and hourly scrutinising, throughout the world, every variation, even the slightest; rejecting that which is bad, preserving and adding up all that is good; silently and insensibly working, whenever and wherever opportunity offers, at the improvement of each organic being in relation to its organic and inorganic conditions of life” (Darwin, Origin of Species). All right, we have some data to look at. We can put a number to the frequency of beneficial mutations in a large sample. The number is zero.

Genome sequencing technology has progressed very rapidly in only the last few years. NATURE just published results of the Exome Aggregation Consortium (ExAC), the largest survey of human genes to date. (An “exome” is the portion of the genome that codes for proteins.) The exomes from 60,706 individuals from a variety of ethnic groups have been collected and analyzed. If we multiply 60,000 people by the 20,000 genes in the human genome (the lowest estimate), we get a minimum of 1.2 billion genes that have been examined by ExAC for variants. That sounds like a pretty good sample size for scrutinizing some of those beneficial variations that Darwin said his law of natural selection could add up and preserve.

Large-scale reference data sets of human genetic variation are critical for the medical and functional interpretation of DNAsequence changes. Here we describe the aggregation and analysis of high-quality exome (protein-coding region) DNA sequence data for 60,706 individuals of diverse ancestries generated as part of the Exome Aggregation Consortium (ExAC). This catalogue of human genetic diversity contains an average of one variant every eight bases of the exome, and provides direct evidence for the presence of widespread mutational recurrence. We have used this catalogue to calculate objective metrics of pathogenicity for sequence variants, and to identify genes subject to strong selection against various classes of mutation; identifying 3,230 genes with near-complete depletion of predicted protein-truncating variants, with 72% of these genes having no currently established human disease phenotype. Finally, we demonstrate that these data can be used for the efficient filtering of candidate disease-causing variants, and for the discovery of human ‘knockout’ variants in protein-coding genes. [Emphasis added.]

Out of this high ratio of variants (one in eight bases shows variation, they said), there should be some proportion, even if small, that improves fitness. But we search the paper in vain for any mention of beneficial mutations. There’s plenty of talk about disease. The authors only mention “neutral” variants twice. But there are no mentions of beneficial mutations. You can’t find one instance of any of these words: benefit, beneficial, fitness, advantage (in terms of mutation),improvement, innovation, invention, or positive selection.

They mention all kinds of harmful effects from most variants: missense and nonsense variants, frameshift mutations, proteins that get truncated on translation, and a multitude of insertions and deletions. Quite a few are known to cause diseases. There are probably many more mutations that never survive to birth. As for natural selection, the authors do speak of “negative selection” and “purifying selection” weeding out the harmful mutations, but nowhere do they mention anything worthwhile that positive selection appears to be preserving…

Yep. I note this “devolution” in a conversation with a biology graduate student in regards to evidences for the GENERAL THEORY OF EVOLUTION (GTE).

▼ It has been proven that resistance to many modern antibiotics was present decades before their [the antibiotics] discovery. In 1845, sailors on an ill-fated Arctic expedition were buried in the permafrost and remained deeply frozen until their bodies were exhumed in 1986. Preservation was so complete that six strains of nineteenth-century bacteria found dormant in the contents of the sailors’ intestines were able to be revived! When tested, these bacteria were found to possess resistance to several modern-day antibiotics, including penicillin. Such traits were obviously present prior to penicillin’s discovery, and thus could not be an evolutionary development. (Medical Tribune, December 29, 1988, p. 1, 23.)

In 1998, the National Academy of Sciences published and distributed a book to public schools and other institutions entitled Teaching About Evolution and the Nature of Science. Jonathan Sarfati, Ph.D., F.M., wrote a book, Refuting Evolution, which is a topic by topic rebuttal to this Academy of Sciences publication. Under the evidence for evolution in the evolutionist text is the following quote:

▼ Similar episodes of rapid evolution are occurring in many different organisms. Rats have developed resistance to the poison warfain. Many hundreds of insect species and other agricultural pests have evolved resistance to the pesticides used to combat them – even to chemical defenses genetically engineered into plants.

(Sarfati’s reply – any words in the [boxes] are mine):

▼ However, what has this to do with the evolution of new kinds with new genetic information? Precisely nothing. What has happened in many cases is that some bacteria already had the genes for resistance to the antibiotics. In fact, some bacteria obtained by thawing sources which had been frozen before man developed antibiotics have shown to be antibiotic-resistant [6 different antibiotics in fact, penicillin in modern doses – which is way beyond the strength of natural penicillin found in nature]. When antibiotics are applied to a population of bacteria, those lacking resistance are killed, and any genetic information they carry is eliminated. The survivors carry less information [or specificity], but they are all resistant. The same principle applies to rats and insects “evolving” resistance to pesticides. Again, the resistance was already there, and creatures without resistance are eliminated.

[Much like if we killed all dogs (including Canis Domesticus and Canis Lupus) except for Chihuahuas, we would permanently lose the information of the parent population. You could then breed Chihuahuas for a millennium and not get an Irish Wolfhound]

▼ …In other cases, antibiotic resistance is the result of a mutation, but in all known cases, this mutation has destroyed information. It may seem surprising that destruction of information can sometimes help. But one example is resistance to the antibiotic penicillin. Bacteria normally produce an enzyme, penicillinase, which destroys penicillin. The amount of penicillinase is controlled by a gene. There is normally enough produced to handle any penicillin encountered in the wild, but the bacterium is overwhelmed by the amount given to patients. A mutation disabling this controlling gene results in much more penicillinase being produced.

[Thus, the bacteria found frozen in 1845 already had the mutation to overcome modern medical doses of penicillin. So the mutation wasn’t the result of the penicillin in modern doses, thus seemingly becoming resistant… it already had the resistant mutation – informational or specificity losing – in the population. In other words, no new information was added to the parent population!]

(See more in this entire chapter discussing the issue: “VARIATION AND NATURAL SELECTION VERSUS EVOLUTION“)

Updated info with a h-t to ‎TOMI AALTO’S site‎ and it comes by way of PHYS.ORG:

Excerpt: “Pioneering work being carried out in a cave in New Mexico by researchers at McMaster University and The University of Akron, Ohio, is changing the understanding of how antibiotic resistance may have emerged and how doctors can combat it in the future.

In research published in Nature Communications today, the scientists examined one bacterium found 1,000 feet underground (called Paenibacillus) that demonstrated resistance to most antibiotics used today, including so-called ‘drugs of last resort’ such as daptomycin. These microorganisms have been isolated from the outside world for more than four million years within the cave.

The results show the bacterium is resistant to 18 different antibiotics and uses identical methods of defense as similar species found in soils.

Among the different ways that the bacteria could be resistant to antibiotics, the scientists identified five novel pathways that were of potential clinical concern. Finding these new pathways is particularly valuable, as it gives researchers time to develop new drugs to combat this type of resistance, potentially decades before it will become a problem for doctors and their patients.

“The diversity of antibiotic resistance and it’s its prevalence in microbes across the globe should be humbling to everyone who uses these lifesaving drugs,” said Gerry Wright, an author of the paper and scientific director of McMaster’s Michael G. DeGroote Institute for Infectious Disease Research.

“It reflects the fact that we must understand that antibiotic use and resistance go hand in hand.”

My [Tomi’s] comment: How could anyone talk about bacterium evolution after this finding? We can’t observe evolution, we can only observe reaction and adaptation. We can also see strong evolutionary stasis here. Bacteria have not experienced changes in assumed millions of years. They have not evolved the ability to rapidly adapt to modern medicines. Instead, they already have all necessary genomic information and capabilities for ecological adaptation. These features are built in by Intelligent source and the Creator. The evolutionary theory is a dangerous heresy.

Was Archaeopteryx Devolving? Thus Losing It’s Ability to Fly?

The below is a response to a conversation elsewhere on the WWW.

ARCHAEOPTERYX

I have a digital edition of Science Magazine and they allow me to read all the past articles (like this one, Archaeopteryx: Early Bird Catches a Can of Worms). In the article a wild eyed creationist… er… I mean, a respected evolutionist discusses how Archaeopteryx is more bird like, not the missing link between dino and bird.

In the article we find this:

✦ feathers are 100% bird feathers;

✦ hollow bones like birds;

✦ It’s claws were perching claws (similar to the Bowerbird)…

✦ doubts connected with dico/bird progression

…even the father of the modern “bird/dino” theory, John Ostrom, says this of recent revelations about Archaeopteryx:

✦ “I’m just having a ball,” he said with a chuckle. “It sounds to me as if Alan [Feduccia] has presented a very good argument; I’m not sure he’s absolutely right, but I’m sure he’s on solid ground.”

Since the writing of the linked article at Science, more evidence (I will repeat, e-v-i-d-e-n-c-e) has come to light supporting the articles authored (Alan Feduccia) and curator of birds at the Smithsonian Institute, Storrs Olson:

✦ bumps in the bone where feathers were connected (just like birds);

✦ the avian lung was present in Archaeopteryx [pneumatized vertebrae and pelvis];

✦ Cat Scans of the skull shows that the brain was birdlike, not dino-like (“Axial and appendicular pneumaticity in Archaeopteryx,” Proceedings of the Royal Society of London, Series B. 267:2501–2505, 2000);

✦ similar inner ear findings (“The avian nature of the brain and inner ear of Archaeopteryx,” Nature 430(7000):666–669, 5 August 2004; Witmer, L.M, “Inside the oldest bird brain, perspective,” same issue, pp. 619–620);

✦ In 2011, “the Royal Society’s Biology Letters, the researchers wrote that Archaeopteryx’s assignment to a dinosaur group earlier this year ‘was acknowledged to be weakly supported’, They constructed new cladograms that pictured Archaeopteryx with birds, and not with any dinosaurs, with a caption that reads, ‘Archaeopteryx robustly reinstated as the most basal bird’.” (“Likelihood reinstates Archaeopteryx as a primitive bird,” Biology Letters. Published online before print October 26, 2011).

Some more resources for the above bullet points:

  1. Archaeopteryx (unlike Archaeoraptor) is NOT a hoax—it is a true bird, not a “missing link”
  2. Archaeopteryx Is a Bird… Again
  3. Dinosaurs vs. Birds: The Fossils Don’t Lie

AND FINALLY

Since other feathered “birds” have been found around the same time or earlier than Archaeopteryx, causing Alan Feduccia to quip, “You can’t be older than your grandfather” (Creation.com)… Nature has published an article pointing out that Archaeopteryx is JUST LIKE modern flightless birds. And so it could have been losing its ability for flight (like modern birds have).

“We know Archaeopteryx was living on an archipelago during the Jurassic. And with its feathers and bones looking so much like modern flightless island birds, it just makes me wonder,” says…. Michael Habib, a biologist at the University of Southern California….

[….]

“Just because Archaeopteryx was the first feathered dinosaur found, doesn’t mean it has to play a central role in the actual history of the origins of birds,” says palaeontologist Thomas Holtz of the University of Maryland in College Park. “We have to remember it appears 10 million years or so after the oldest known bird-like dinosaurs and so our famous ‘first bird’ may really be a secondarily flightless one.”…

(Nature Journal)

There is just as much [at best] evidence for this proposition as the next. “Devolution” — a loss of specificity, may be a more reasonable position to take via observed evidence. We see this all the time (directly below is an example from Lee Spetner’s new book), and Evolution News says that “looks like Archaeopteryx may have to be reclassified as a different sort of icon — symbolizing evolution by loss of function.” Oops.

Antibiotic Resistance

The evolution of antibiotic resistance has been for some time the Dar­winists’ favorite example for “demonstrating” evolution (Common De­scent). Superficially their case looks good. Antibiotics date only from about 1930 with the discovery of penicillin (Fleming 1929), followed by the development of a method to produce it with high yield (Chain et al. 1940). Antibiotics were first introduced to the public in 1942 to cure bacterial infection (Levy 1992, 4), and by the mid 1940s the first strains appeared of Staphylococcus resistant to penicillin (Fisher 1994, 15). Just a few years after antibiotics were introduced, resistant strains of the pathogens were found to have already evolved. As each new an­tibiotic was discovered and put into use against pathogenic bacteria, resistant strains soon followed. The argument then goes, with a wave of the hand, like this: If a small but significant evolutionary change like antibiotic resistance can evolve in only a few years, then surely in a mil­lion years huge evolutionary changes must occur. Darwinists expect this argument to support Common Descent.

An examination of the phenomenon of antibiotic resistance, however, shows it lends no support at all to Common Descent (Spetner 1997, 138­143). Antibiotics are natural molecules produced by some microorgan­isms for the purpose of killing other hostile microorganisms. A microor­ganism that makes an antibiotic must, itself, be resistant to the antibiotic it makes. For this purpose it is typically endowed with a battery of genes that code for a resistance mechanism. Most useful antibiotics have come from soil bacteria (D’Costa et al. 2006). How bacteria have acquired this resistance initially is not known, nor can neo-Darwinian theory shed any light on it. Antibiotic resistance genes have been found to predate the use of antibiotics by at least many thousands of years (D’Costa et al. 2011). Moreover, bacteria are known to be able to transfer genetic ma­terial to other bacteria through HGT (see above). On occasion, copies of the genes for resistance can find their way from a type of bacterium that is normally resistant to a type that is not normally resistant. When that happens, the recipient bacterium becomes resistant. This is indeed evolution, but it is a limited evolution of the population-change type. It is not the Common-Descent type of evolution.

The resistance genes already exist in the biosphere. No new informa­tion has appeared in the biosphere through this type of evolution of an­tibiotic resistance. Common-Descent evolution cannot be achieved by this procedure even if it were repeated innumerable times in succession, because no new information would be built up. This method of evolving antibiotic resistance therefore lends no support for Common Descent.

Sometimes, however, antibiotic resistance can indeed appear through a random mutation — a DNA copying error, which would bring something new to the biosphere. This kind of change looks like it might satisfy the requirements for Common Descent, so I shall give a brief description of it here, although I have already dealt with it in my previous book.

As an example, let us look at how a bacterium acquires resistance to streptomycin through a random mutation. All cells, whether of bacteria or of plants or animals, contain organelles called ribosomes, whose function it is to make protein according to instructions from the DNA of a gene. Proteins are large molecules, consisting of long chains of small molecules called amino acids, and are essential to all living things. They function as enzymes, which catalyze all the chemical reactions in a cell — each chemical reaction catalyzed by a specific enzyme. Proteins can also serve as structural elements. Of­ten, and maybe even always, a structural protein functions also as an enzyme. For an enzyme to perform its function, it must have a specif­ic sequence of amino acids.

A ribosome is an organelle within a cell that manufactures protein. It makes a protein by putting together a chain of amino acids according to the instructions in the DNA. A segment of the DNA is transcribed into an RNA molecule that matches the DNA nucleotide by nucleo­tide. This RNA is called messenger RNA because it carries the DNA message to the ribosome. The ribosome translates the message in the DNA into amino acids according to the genetic code. Three nucleotides translate into one amino acid. Accordingly, the ribosome constructs a chain of amino acids to form a protein.

The antibiotic streptomycin, for example, acts on a bacterial cell by attaching to a ribosome at a site to which it matches, the way a key fits into a lock. When the streptomycin molecule attaches to this site, it in­terferes with the ribosome function and causes it to make mistakes lead­ing to incorrect, dysfunctional or nonfunctional, protein. The errors it causes prevent the cell from growing, reproducing, and eventually from living. The important feature of streptomycin, and indeed of all other antibiotics, is that it kills bacteria but does not harm the mammalian host. Streptomycin kills the bacterial cells that are infecting you without killing your own cells. It discriminates between the cells of the bacteria and the cells of the host by its specific attachment to a matching site on the bacterial ribosome, a site not found on the host’s ribosomes.

A bacterium will gain resistance to streptomycin if a point mutation occurs in the gene coding for the protein in the ribosome, ruining the matching site, destroying the specificity of the protein, and preventing a streptomycin molecule from attaching. If the streptomycin cannot at­tach to the matching site, the bacterium is resistant. Just one mutation in the portion of the DNA coding for the matching site can mess up the site so the streptomycin cannot attach. It turns out that any one of several mutations in that portion of the DNA will grant the bacterium resistance (Gartner and Orias 1966). Note that this type of resistance is caused by a single random point mutation, but it cannot serve as an example of mutations that can support Common Descent. One cannot expect mutations destroying specificity, no matter how many of them there are, to build information and lead to Common Descent. Destruc­tion of specificity does not add information — it destroys it. One can­not add information by destroying it, no matter how many times one repeats the process. I have previously (Spetner 1997) compared trying to build up information in this manner to the merchant who was losing a little money on each sale but thought he could make it up on volume. The acquisition of antibiotic resistance is indeed evolution, but only a limited form of it. It cannot lead to Common Descent.

No example of antibiotic resistance in bacteria adds information to the biosphere. To become resistant, the bacteria either pick up ready-made resistance genes from other bacteria or they undergo a mu­tation that destroys information. Antibiotic resistance cannot therefore be an evolutionary example that could support Common Descent be­cause a chain of such mutations, no matter how long, does not add in­formation and thus cannot lead to Common Descent. The Darwinists’ favorite example of evolution fails to pass muster.

End Notes

Chain, E. et al. (1940) Penicillin as a Chemotherapeutic Agent. Lancet 239: 226-228.

D’Costa, Vanessa M., Katherine M. McGrann, Donald W. Hughes, and Gerard D. Wright. (2006) Sampling the antibiotic resistome. Science 311: 374-377.

D’Costa, Vanessa M. et. al. (2011) Antibiotic Resistance is Ancient. Nature 477:457-461.

Fisher, Jeffrey A. (1994) The Plague Makers: How we are creating catastrophic new epidemics — and what we must do to avert them. New York: Simon & Schuster.

Fleming, A. (1929) On the antibacterial action of cultures of a Penicillium, with special reference to their use in the isolation of B. influenzae. British Journal of Experimental Pathology 10: 226-238.

Gartner, T. K. and E. Orias, (1966) Effects of mutations to streptomycin resistance on the rate of translation of mutant genetic information. Journal of Bacteriology 91: 1021-1028.

Levy, Stuart B. (1992) The Antibiotic paradox: How Miracle Drugs are Destroying the Miracle. New York: Plenum Press.

Spetner. L. M. (1997) Not by chance! Shattering the Modern Theory of Evolution. Brooklyn: Judaica Press.

Lee Spetner, The Evolution Revolution: Why Thinking People Are Rethinking the Theory of Evolution (Brooklyn, NY: Judaica Press, 2014), 119-120.

A friend comments about the newer position on his Creation/Evolution Headlines saying one “paleontologist remarked, ‘We really need an improved understanding of how anatomy relates to these diverse behaviours, so we can better interpret the fossil record’.” Continuing he adds his thinking to the matter:

No one called Archaeopteryx a “feathered dinosaur” back then, because the phrase only came into vogue with the Chinese fossil discoveries.  From Darwin’s day till recently, it was argued to be a transitional form between reptiles and birds.  Evolutionists emphasized the reptilian traits (teeth, claws on the wings), and creationists emphasized the flight feathers and anatomy that seemed to show it capable of powered flight. They also pointed out that some living birds, like the hoatzin, have claws on their wings as juveniles.  People saw what their biases wanted to see.  Astronomer Fred Hoyle tried to prove it was a forgery.  Today’s evolutionists use the “feathered dinosaur” label, but there is no guarantee that today’s consensus will not shift again.  The new proposal it was secondarily flightless implies a win for creationists – it devolved from a fully-functional flying bird, just like some living birds with stunted wings have on the Galapagos Islands.  Loss of function is not what Darwin needs!

Let’s think about Nature’s comment that the suggestion Archaeopteryx was losing the ability to fly “might have been considered madness” back in 1861 (actually, all the way from 1861 to just a few years ago).  This tells us that if evolutionists consider something madness now, it might be considered sanity later.  It further means that the sane ones could be the skeptics of the consensus, and the mad ones in the majority.  Don’t be deterred, therefore, if you feel you have good evidence and arguments for your position when it runs counter to the consensus.  It’s entirely possible for the intellectual majority to be suffering from delusions.  “We really need an improved understanding … so we can better interpret the fossil record” – good advice, but it implies that understanding is lacking and interpretation is flawed.  If they haven’t gotten it down after 152 years, don’t expect major improvements any time soon.  They might just be secondarily clueless.

The Vitamin C Pseudogene Argument Crumbles… Slowly

See also: Pseudogenes Predicted To Fail by Creationists (Vestigial Response Added)

Bottom Line:

The failure to recognize the full implications of [non-protein–coding DNA] may well go down as one of the biggest mistakes in the history of molecular biology.

(cited in: Gibbs, W.W., The unseen genome: gems among the junk, Scientific American 289[5]:26–33, November 2003.)

…even the staunchest critics of creation theory recognize that “[i]t is impossible to prove absence of function for any region of DNA.”

Edward E. Max, “Plagiarized Errors and Molecular Genetics,” Sec. 5.4 . From: A Critique of “29 Evidences for Macroevolution”

Talk Origins in its 29+ Evidences for Macroevolution (written between 199 and 2004) quotes a 1999 study that purportedly proves their stance:

Furthermore, all of these genes have accumulated mutations at the exact rate predicted (the background rate of mutation for neutral DNA regions like pseudogenes) (Ohta and Nishikimi 1999).


Well, the tables have turned on neo-Darminian claims yet once again and science (not “scientism”) advances:

It is worth mentioning that this supposed truth for evolutionary theory is further along the wrong prediction mark than the proof of “Junk DNA” was along this path when I was debating in 97′ with people over at the Discover site.  (In fact, this “proof” is connected to the “junk DNA” position.) In 1997 people — in debate situation — said that evolution predicts junk DNA and that they have known of junk DNA for quite some time, thus proving evolutionary explanatory power. IN 2003, one of the first articles to hit the mainstream scientific press that this long held assumption was in jeopardy hit Discover and Scientific American magazines, two subscriptions I receive out of the many mags I get. Pictured is the first Discover magazine (yes, I have kept them) ruminations that this “proof” was disintegrating, like the vestigial organs “proof” did, cytochrome C differences, bacterial evolution, etc.

So debating a topic like this supposed proof is funny because it is much further along the scientific path than it was when I first debated the issue. Not to mention all the “evolutionary tree” models that are supposed to be factual when in fact their order is a topic of much debate. For instance, I posted a bit earlier a layman’s article on the argument within the evolutionary camp about mankind coming from orangutans rather than a chimpanzee split in the family tree… (this earlier post mentions the belief within the evolutionary camp that man came from some aquatic ancestor rather than orangutans). A few people likewise believe that apes (Gorillas) are descended from mankind in some way. For instance, Dr. Aaron G. Filler:

Dr. Aaron G. Filler, M.D., Ph.D. studied evolutionary theory under some of the leading biologists and anthropologists of our time: Ernst Mayr, Stephen J. Gould, David Pilbeam, and Irven DeVore. A neurosurgeon at the Institute for Spinal Disorders at Cedars Sinai Medical Center and past associate director of the Comprehensive Spine Center at UCLA, Dr. Filler has been a leading innovator in medical imaging and neuroscience. He is the author of Do You Really Need Back Surgery? (Oxford University Press), as well as numerous scientific articles and patents.

He wrote a book entitled The Upright Ape: A New Origin of the Species, in which he follows the footsteps of another well respected scientist showing that apes are most likely a breakaway group from mankind. The other scientist I mention is Dr. Geoffrey H. Bourne:

He was Director of Yerkes Regional Primate Research Center at Emory University, England. Dr. Bourne is Oxford educated, and is an American cell biologist/anatomist who was considered by most to be the worlds leading primatologist.

He said that apes are descended from man. Why would men of science believe such a thing? Because science has never seen any information being added to the evolutionary upward “slant” that is required by its theory (Darwinism, e.g., “scientism”). So since apes are less than us, Dr. Bourne says that science [not “scientism”] proves his theory due to observable facts. (SEE APPENDIX) All this though, junk DNA being disproved and a differing order of our family tree are other impediments to the Vitamin C Pseudogene argument. In order for this argument to work (and the subsequent predictions made to be coherent), he [the evolutionist] has to have all his ducks in order, this is something he does not have the luxury of (see image at top). One of the papers linked above (GULO pseudogenes have been intensively investigated) and its in-depth research led it two authors to say the following:

When examined in detail, the full pseudogene dataset we collected does not lend itself to a reasonable neo-Darwinian interpretation. Using standard bioinformatics tools and principles, we present alternative designs for at least the exon X portion of the GULO gene. These may be plausible due to nucleotide patterns being relevant as regulatory signals or the favouring of some codons for various possible reasons. We do accept that some mutations have occurred in this exon. But these novel proposals imply that the ancestors of the organisms studied may well never have had the exact same GULO sequence.

That last sentence really shows the assumptions made in this “proof” that steps away from true science and into the realm of historical science. And the historical sciences are fraught with bickering, changing branches of human lineage, and naturalistic philosophies that make the vitamin C pseudogene argument pretty vacuous.

The following is a good round-up of the problems seen in this line of argument, by Sean D. Pitman MD:

…in 2003, the same Japanese group published the complete sequence of the guinea pig GLO pseudogene, which is thought to have evolved independently, and compared it to that of humans [Inai et al, 2003]. 21 Surprisingly, they reported many shared mutations (deletions and substitutions) present in both humans and guinea pigs. Remember now that humans and guinea pigs are thought to have diverged at the time of the common ancestor with rodents. Therefore, a mutational difference between a guinea pig and a rat should not be shared by humans with better than random odds. But, this was not what was observed. Many mutational differences were shared by humans, including the one at position 97. According to Inai et al, this indicated some form of non-random bias that was independent of common descent or evolutionary ancestry. The probability of the same substitutions in both humans and guinea pigs occurring at the observed number of positions was calculated, by Inai et al, to be 1.84×10-12 – consistent with mutational hotspots.

What is interesting here is that the mutational hot spots found in guinea pigs and humans exactly match the mutations that set humans and primates apart from the rat (see figure below). 21,22 This particular feature has given rise to the obvious argument that Inai et al got it wrong. Reed Cartwright, a population geneticist, has noted a methodological flaw in the Inai paper:

“However, the sections quoted from Inai et al. (2003) suffer from a major methodological error; they failed to consider that substitutions could have occurred in the rat lineage after the splits from the other two. The researchers actually clustered substitutions that are specific to the rat lineage with separate substitutions shared by guinea pigs and humans. . .

If I performed the same analysis as Inai et al. (2003), I would conclude that there are ten positions where humans and guinea pigs experienced separate substitutions of the same nucleotide, otherwise known as shared, derived traits. These positions are 1, 22, 31, 58, 79, 81, 97, 100, 109, 157. However, most of these are shown to be substitutions in the rat lineage when we look at larger samples of species.

When we look at this larger data table, only one position of the ten, 81, stands out as a possible case of a shared derived trait, one position, 97, is inconclusive, and the other eight positions are more than likely shared ancestral sites. With this additional phylogenetic information, I have shown that the “hot spots” Inai et al. (2003) found are not well supported.” (see Link)

It does indeed seems like a number of the sequence differences noted by Cartwright are fairly unique to the rat – especially when one includes several other species in the comparison. However, I do have a question regarding this point.  It seems to me that there simply are too many loci where the rat is the only odd sequence out in Exon X (i.e., there are seven and arguably eight of these loci).  Given the published estimate on mutation rates (Drake) of about 2 x 10-10 per loci per generation, one should expect to see only 1 or 2 mutations in the 164 nucleotide exon in question (Exon X) over the course of the assumed time of some 30 Ma (million years).  Therefore, the argument of the mutational differences being due to mutations in the rat lineage pre-supposes a much greater mutation rate in the rat than in the guinea pig.  The same thing is true if one compares the rat with the mouse (i.e., the rat’s evident mutation rate is much higher than that of the mouse).

This is especially interesting since many of the DNA mutations are synonymous.  Why should essentially neutral mutations become fixed to a much greater extent in the rat gene pool as compared to the other gene pools? Wouldn’t this significant mutation rate difference, by itself, seem to suggest a mutationally “hot” region – at least in the rat?

Beyond this, several loci differences are not exclusive to the rat/mouse gene pools and therefore suggest mutational hotspots beyond the general overall “hotness” or propensity for mutations in this particular genetic sequence.

Some have noted that although the shared mutations may be the result of hotspots, there are many more mutational differences between humans and rats/guinea pigs as compared to apes.  Therefore, regardless of hotspots, humans and apes are clearly more closely related than are humans and rats/guinea pigs.

The problem with this argument is that the rate at which mutations occur is related to the average generation time.  Those creatures that have a shorter generation time have a correspondingly higher mutation rate over the same absolute period of time – like 100 years.  Therefore, it is only to be expected that those creatures with relatively long generation times, like humans and apes, would have fewer mutational differences relative to each other over the same period of time relative to those creatures with much shorter generation times, like rats and guinea pigs.

What is interesting about many of these mutational losses is that they often share the same mutational changes.  It is at least reasonably plausible then that the GULO mutation could also be the result of a similar genetic instability that is shared by similar creatures (such as humans and the great apes).

This same sort of thing is seen to a fairly significant degree in the GULO region.  Many of the same regional mutations are shared between humans and guinea pigs.  Consider the following illustration yet again:

Why would both humans and guinea pigs share major deletions of exons I, V and VI as well as four stop codons if these mutations were truly random?  In addition to this, a mutant group of Danish pigs have also been found to show a loss of GULO functionality.  And, guess what, the key mutation in these pigs was a loss of a sizable portion of exon VIII.  This loss also matches the loss of primate exon VIII.  In addition, there is a frame shift in intron 8 which results in a loss of correct coding for exons 9-12.  This also reflects a very similar loss in this region in primates (see Link).  That’s quite a few key similarities that were clearly not the result of common ancestry for the GULO region.  This seems to be very good evidence that many if not all of the mutations of the GULO region are indeed the result of similar genetic instabilities and that are prone to similar mutations – especially in similar animals.

As an aside, many other genetic mutations that result in functional losses are known to commonly affect the same genetic loci in the same or similar manner outside of common descent.  For example, achondroplasia is a spontaneous mutation in humans in about 85% of the cases. In humans achondroplasia is due to mutations in the FGFR2 gene. A remarkable observation on the FGFR2 gene is that the major part of the mutations are introduced at the same two spots (755 C->G and 755-757 CGC->TCT) independent of common descent. The short legs of the Dachshund are also due to the same mutation(s). The same allelic mutation has occurred in sheep as well.

(SOURCE)

All this is to say, yet again, that this “evidence” is anything but!

Wiki Section:

By definition, pseudogenes lack a function. However, the classification of pseudogenes generally relies on computational analysis of genomic sequences using complex algorithms.[17] This has led to the incorrect identification of pseudogenes. For example the functional, chimeric gene jingwei in Drosophila was once thought to be a processed pseudogene. [18]

It has been established that quite a few pseudogenes can go through the process of transcription, either if their own promoter is still intact or in some cases using the promoter of a nearby gene; this expression of pseudogenes also appears to be tissue-specific.[4] In 2003, Hirotsune et al. identified a retrotransposed pseudogene whose transcript purportedly plays a trans-regulatory role in the expression of its homologous gene, Makorin1 (MKRN1) (see also RING finger domainubiquitin ligases), and suggested this as a general model under which pseudogenes may play an important biological role.[19] Other researchers have since hypothesized similar roles for other pseudogenes.[20] A bioinformatics analysis has shown that processed pseudogenes can be inserted into introns of annotated genes and be incorporated into alternatively spliced transcripts. [10] Hirotsune’s report prompted two molecular biologists to carefully review scientific literature on the subject of pseudogenes. To the surprise of many, they found a number of examples in which pseudogenes play a role in gene regulation and expression,[21] forcing Hirotsune’s group to rescind their claim that they were the first to identify pseudogene function.[22] Furthermore, the original findings of Hirotsune et al. concerning Makorin1 have recently been strongly contested;[23] thus, the possibility that some pseudogenes could have important biological functions was disputed. Additionally, University of Chicago and University of Cincinnati scientists reported in 2002 that a processed pseudogene called phosphoglycerate mutase 3 (PGAM3P) actually produces a functional protein.[24] and Two 2008 publications in Nature discusses that some endogenous siRNAs are derived from pseudogenes, and thus some pseudogenes play a role in regulating protein-coding transcripts.[25][26]

AIG & PDF Sources [PDF source near top]:

….Many of those mammals found unable to synthesize ascorbic acid have regions of their genome that are believed to correspond to parts of the functional GULO gene that is found in those mammals found capable to synthesizing GULO, and thus vitamin C. Evolutionists have cited these apparently vestigial remnants of GULO to make dysteleological arguments against an Intelligent Designer. In addition, they have argued that lesions found in common between the orthologous GULO pseudogenes of simian primates (‘shared mistakes’) argue strongly for their origins from a common ancestor, and all but rule out an independent inactivation of the GULO gene among different simian primates (including humans).

Previous studies of the orthologous primate GULO gene and pseudogene have focused on those parts of a few exons that appear to correspond between humans and rats. A more recent study1 is much more comprehensive. It is now believed that, relative to the 12 exons that comprise the functional rat GULO gene, the human GULO pseudogene is limited to counterparts of exons 4, 7, 9, 10, and 12. Owing to the fact that the guinea pig and the simian primates are obviously not sister groups [see figure near top], it is impossible for the guinea pig GULO pseudogene and the human GULO pseudogene to have both originated from the same ancestral pseudogene. Furthermore, not only are the inactivations of GULO in the guinea pig and primates clearly independent events based on phylogenetic analysis [see figure near top], but also on inferred evolutionistically believed times of inactivation….

Inai, Y., Ohta, Y. and Nishikimi, M., The whole structure of the human non-functional L-gulono-γ-lactone oxidase gene—the gene responsible for scurvy—and the evolution of repetitive sequences thereon, J. Nutritional Science and Vitaminology (Tokyo)49(5):315–319, 2003.

UPDATE:

The “pseudogene” argument (of which Vitamin C Pseudogene is part of) is being shown to not be a “vestige” as claimed and “predicted” by Darwinian theory. Much like the Haeckel’s list of over 100 vestigial organs, science shows that predictions made like this fail. If the predictions of design were assumed, more lives would have been saved and true science would have flourished. JBS Haldane however, said (predicted) that “natural selection cannot possibly select for millions of new mutations over the course of human evolution, Kimura developed the idea of “Neutral Evolution.” If “Haldane’s Dilemma”  was correct, the majority of DNA must be non-functional. Hence, the pseudogene argument. This is an argument that has failed due to recent science, no predictive power left in it. Which is no small issue, since, it is this “predictive value” that makes this argument valid.

Faulkner (in 2009) worked with mice and humans and showed clearly that this RNA/Retrotranposons relationship were not random, and thus transcription is shown to be influenced wholly or partly by this “junk DNA.” — “Therefore, more than one third of the mouse and human genomes, previously thought to be non-functional, may play some role in the regulation of gene expression” (scientists from Jackson Maine, USA laboratories). Creationists have long figured this “junk DNA” to be functional… making design predictions more accurate.

Thankfully, not everyone bought this idea. In the late 1980s, New Zealand–born Australian immunologist Malcolm Simons recognized patterns, or order, in the non-coding DNA that indicated to him that the code must have a function, but others ridiculed the idea. In the mid-1990s, he patented the non-coding DNA (95%) of all organisms on Earth. The company he founded, Genetic Technologies, now reaps license fees from all technologies being developed to cure disease that involve the non-coding DNA. It’s quite controversial, of course, paying such license fees. And since factors involved in all sorts of diseases, such as breast cancer, Crohn’s disease, Alzheimer’s, heart disease, ovarian and skin cancer, are being found in the ‘junk’, Genetic Technologies is doing quite well.

The “vitamin C gene” in question here (L-gulano-g-lactone oxidase gene) is only a valid argument if:

a) a non-functional version of the gene was shown to be functional at some point in our human lineage, it says nothing about ancestors (kinds, or species) who could have been created with an active gene.

b) If the lineage of man can truly be traced through evolutionary ancestors, which it cannot.

c) The same gene could have been inactivated by the same mutation occurring independently is said to be too improbable by strict neo-Darwinists. (Ironic) However, if there is, or was, a mechanism of mutation that favors certain locations in the gene (a hot spot), the odds against an independent occurrence of the mutation drop according to the strength of that bias. This, by-the-way, is more probable considering the fall of the pseudogene argument. In other words, this prediction would now be of a higher order and is an example of loss of function and a disordering of optimum ability. Something the creation model predicts, it is the opposite of what Darwinism requires.

d) Likewise, in order for this line of reasoning to work, a human genome must be compared to an organism with a functioning gene for synthesizing vitamin C. Of course we know they found it in rats (Nishikimi, 1994). Four of the 12 exons (Science Dictionary: A segment of a gene that contains information used in coding for protein synthesis; exons are the modular coding regions of the gene). Here is the downfall, two-thirds of the homologous rat gene is completely missing. Which is to say: “This DNA sequence, labeled as a pseudogene, might have an entirely different function than the rat gene.” This would be — with recent peer reviewed articles in Discover, Scientific American, Nature, Science Weekly, and other pubvlications — be of a higher order than merely saying it is a pseudogene. In other words, the previous predictions are mute and shows that the argument is from silence, or non-science.

Stating that only the last enzyme is missing for the pathway to convert glucose to vitamin C might imply to the untrained individual that there is a biochemical pathway that leads to a dead end. Actually, the biochemical pathway that leads to the synthesis of vitamin C in rats also leads to the formation of five-carbon sugars in the pentose phosphate pathway present in virtually all animals (Linster and Van Schaftingen 2007). There are several metabolic intermediates in this pathway illustrating that these substances can be used as precursors for many compounds in the cell. In the pentose phosphate pathway, five-carbon sugars are made from glucose (a six-carbon sugar) to be used in the synthesis of DNA, RNA, and many energy producing substances such as ATP and NADPH (Garrett 1999). Animals that synthesize vitamin C can use both pathways illustrated in the simplified diagram below. Humans and the other animals “less fortunate” than rats only use the pentose phosphate pathway.

There is no dead end or wasted metabolic intermediates, and there is no need to have the enzyme to make vitamin C since humans are able to get all of the vitamin C they need from food substances. Thousands of human pseudogenes have been catalogued, but in spite of the similarities to functional genes, the exact role of pseudogene sequences in the genome are not known by any scientist. It is not necessary to assume that pseudogenes are remnants of once functioning genes that have been lost and now clutter the genome like junk in a rubbish heap.

Criswell, D. 2007. Adam and Eve, Vitamin C, and Pseudogenes. Acts & Facts. 36 (5).

Conclusion Then

As was said before the known factors of the pentose phosphate pathways:

  • The failure to recognize the full implications of [non-protein–coding DNA] may well go down as one of the biggest mistakes in the history of molecular biology. (cited in: Gibbs, W.W., The unseen genome: gems among the junk, Scientific American 289[5]:26–33, November 2003.)
  • …even the staunchest critics of creation theory recognize that “[i]t is impossible to prove absence of function for any region of DNA.” (Edward E. Max, “Plagiarized Errors and Molecular Genetics,” Sec. 5.4 . From: A Critique of “29 Evidences for Macroevolution”)

So, to sum up, at best this could be viewed as a theological argument: “what should have God done if he did create ‘A’.” At worst it is an argument that has not evolved with science correcting itself and is stuck in the 90’s science and not the mid-to-late part of the first decade of the beginning of the 21st century — science. Science has evolved, have the evolutionists?

This is an excerpt from the much hated book, Of Pandas and People, pp 34-40 (click to enlarge):

Here is the continuation of the devolving of primates:


APPENDIX


1. It takes 6 million years for one mutation to arise in a DNA binding site.
2. 6 million years is how long, historically, one has to get from primates to humans.
3. Humans differ from primates in hundreds of ways, requiring probably thousands of different gene mutations.
4. What’s more, many of the differences between primates and humans would require coordinated mutations. For example, the correct legs, feet, pelvis, spine, and neck to walk upright are differences which individually are useless by themselves.
5. Experiments with bacteria (i.e. with population sizes and mutation rates much higher than primates and humans) suggest that a single protein cannot mutate six or more times in a coordinated fashion in a timespan less than the known age of the universe.
6. Given these numbers, it is impossible for humans to have evolved from primates.