One of My Very First “Debate Style” Responses (20-Years Ago)

Imported from my old blog, which was itself imported from a 1999 forum debate. 20-years ago. It is a little rudimentary, but the format then was limited. I link many names of the people referenced for those curious. Almost all are evolutionists.

Enjoy.

Question Posed To Me In A Previous Debate:

  • (Gene90 asked) “Do you deny that some mutations are beneficial? (Such as, antibiotic resistance in a bacterium).”

MY RESPONSE

What about this example of bacteria resisting antibiotics? Actually, some bacteria possess a natural genetic capacity to resist certain antibiotics; mutations are not involved in these. Mutations cause a structural defect in ribosomes – the cellular constituents that antibiotics like streptomycin attach to. Since the antibiotic doesn’t connect with the misshapen ribosome, the bacterium is resistant.

Spetner: “We see then that the mutation reduces the specificity of the ribosome protein, and that means losing genetic information… Rather than say the bacterium gained resistance to the antibiotic, we would be more correct to say it lost its sensitivity to it. It lost information. The NDT [neo-Darwinian theory] is suppose to explain how the information of life has been built up by evolution Information cannot be built up by mutations that lose it. A business can’t make money by losing it a little at a time.” (Dr. Spetner’s book was one of the first intelligent design oriented books I read [1997])

In other cases, some mutant bacteria, because they have defective membranes, don’t absorb nutrients well. Fortuitously for them, that inefficiency also prevents their absorbing antibiotics. And so, in this instance also, they survive better than their normal cousins. But the mutation did not make them stronger or create new information, or “evolve” to a higher state. Likewise, if the world’s light suddenly disappeared, blind people might have an advantage over others, since they were already accustomed to operating in darkness. Nevertheless, we cannot then interpret blindness as positive, or representing new information or evolutionary advance.

C.P. Martin, writing in American Scientist, made a similar point when he compared x-rays’ effects on the body to being kicked and beaten [nice family publication]:

“It is quite possible that violent knocking about might dislocate a man’s shoulder, and that continued knocking about might actually reduce the previous dislocationno sane person would cite such a case as this to prove that the results of knocking a man about are not injuries; nor would anyone refer to the result as evidence that knocking a man about can produce an improvement over the normal man. For a truly progressive or evolutionary-apt mutation must result in an improvement over the normal condition. The truth is that there is no clear evidence of the existence of such helpful mutations. In natural populations endless millions of small and great genic differences exist, but there is no evidence that any arose by mutation.”

A more recent — what would be a “sister post” of sorts — is this: Antibiotic Resistance Evidence of “Devolution”

Second Question Posed

  • (Gene90 asked) “Do you deny that parents pass traits to their offspring?”

SECOND RESPONSE

This statement and the evolutionary implications get into what Darwin himself believed while writing his original manifesto, that is – Lamarckism. Lets see what some evolutionary scientists had to say (excerpted from my vestigial organs post).

  • Two of the most powerful causes of mutation are mustard gas and x-rays. A moments reflection on the horror of Hiroshima children born with deformed limbs and bodies, or blood disorders condemning them to premature deaths, is enough to show that they were unlikely candidates, to say the least, to win the struggle for existence in a life-game where survival of the fittest is the governing rule.” (British science writer Francis Hitching)
  • To postulate, as the positivists of the end of the last century and their followers here have done, that the development and survival of the fittest is entirely a consequence of chance mutations, or even that nature carries out experiments by trial and error through mutations in order to create living systems better fitted to survive, seems to me a hypothesis based on no evidence and irreconcilable with the facts…These classical evolutionary theories are a gross oversimplification of an immensely complex and intricate mass of facts, and it amazes me that they were swallowed so uncritically and readily, and for such a long time, by so many scientists without a murmur of protest.” (Biochemist Ernst Chain, who shared a Nobel Prize for his work on penicillin)
  • Simultaneous appearance of several gene mutations in one individual has never been observed, so far as I know, and any theoretical assertion that this is an important factor in evolution can be dismissed… the probability that five simultaneous mutations would occur in any one individual would be about .0000000000000000000001. This means that if the population averaged 100,000,000 individuals with the average length of generations of only one day, such an event could be expected only once in about 274,000,000,000 years – a period about one hundred times as long as the age of the earth.” (George Gaylord Simpson [R.I.P.], Professor of vertebrate paleontology at Harvard, and, perhaps, the twentieth century’s foremost paleontologist)

(Referring to a previous statement about the Panda) – were you there to see the Panda’s thumb change? Is there fossil proof for it (that could pass the Smithsonian Institutes tests [referring to the virulent rejection by the Smithsonian of the recent “feathered dinosaur” published by Natural Geographic])? Do genetic mutations back up the hypothesis?

I could equally say that an alien race came to earth and “tinkered” with rat till they got a Panda. I would have just as much proof as do evolutionists for the Panda evolving from a lower species, or higher (i.e. fish left the water to eventually become a cow, who, eventually went back to the water to become a whale – this is what evolutionary textbooks teach). I see all this as crazy! I say that I came from a cause greater than the universe and myself. Evolutionists say I came from a rock.

  • It is easy to make up stories of how one form gave rise to another, and to find reasons why the stages should be favored by natural selection. But such stories are not part of science, for there is no way of putting them to the test.” (Colin Patterson of the British NaturalHistory Museum)
  • Paleontologists (and evolutionary biologists in general) are famous for their facility in devising plausible stories; but they often forget that plausible stories need not be true.” (Stephen Jay Gould, Harvard’s famed paleontologist and probably evolution’s leading spokesperson today)

Take the human body, as a total system, is irreducibly complex. It is difficult to change one part without influencing others. The liver for example: it manufactures bile; detoxifies poisons and wastes; regulates storage and use of glucose, proteins, fats and vitamins; synthesizes blood clotting and immune system factors; and processes breakdown products of old blood cells. Or take the kidneys: they remove wastes through urine production; regulate the body’s water content and electrolytes (sodium, calcium, etc.); and support the adrenal glands, which secrete hormones such as adrenaline. Or the human heart: blood is pumped to from the right side of the heart to the lungs, where it receives oxygen; then back to the heart’s left side, which propels it to the rest of the body through more than 60,000 miles of vessels. The heart has four chambers; a system of valves prevents backflow into any of these; electrical impulses from a pacemaker control the hearts rhythm.

Rarely, babies are born with congenital heart disorders, making blood shunt to the wrong place. There is no known case of mutations improving circulation!Hemoglobin – the blood’s oxygen-carrying component – has over 40 mutant variants. NOT ONE transports oxygen as well as normal hemoglobin! Theodosius Dobzhansky, one of the twentieth centuries leading Darwinists, acknowledged this:

  • “And yet, a majority of mutations, both those arising in laboratories and those stored in natural populations, produce deteriorations of viability, hereditary diseases, and monstrosities. Such changes, it would seem, can hardly serve as evolutionary building blocks.” 
  • British science writer Frances Hitching says this: “On the face of it, then, the prime function of the genetic system would seem to be to resist change: to perpetuate the species in a minimally adapted form of response to altered conditions, and if at all possible to get things back to normal. The role of natural selection is usually a negative one; to destroy the few mutant individuals that threaten the stability of the species.”
  • Richard Goldschmidt, well known American geneticist said this: “It is true that nobody thus far has produced a new species or genus, etc., by macromutation. It is equally true that nobody has ever produced even a species by selection of micromutaions.”

Dr. Goldschmidt would have known – he bread gypsy moths for twenty years and a million generations in various environments. All he ever got was more gypsy moths. Anyone who thinks that an accumulation of mutations (information-losing processes) can lead to Macroevolution (a massive net gain of information) “is like the merchant who lost a little money on every sale but thought he could make it up on volume.” (Spetner, 1997)

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.