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A sequel to Refuting Evolution that refutes the latest arguments to support evolution (as presented by PBS and Scientific American).

Table of Contents

Refuting Evolution 2, revised and expanded edition, 2011



Unit 1

Chapter 1

Argument: Creationism is religion, not science

Chapter 2

Argument: Evolution is compatible with Christian religion

Chapter 3

Argument: Evolution is true science, not ‘just a theory’

Unit 2

Chapter 4

Argument: Natural selection leads to speciation

Chapter 5

Argument: Some mutations are beneficial

Chapter 6

Argument: Common design points to common ancestry

Chapter 7

Argument: ‘Bad design’ is evidence of leftovers from evolution

Chapter 8

Argument: The fossil record supports evolution

Unit 3

Chapter 9

Argument: Probability of evolution

Chapter 10

Argument: ‘Irreducible complexity’

Chapter 11

Argument: Evolution of sex

Chapter 12

Argument: Evolution of mankind

Appendix 1

Common arguments for evolution that have been rejected

Appendix 2

Common arguments for creation that should not be used

Refuting Evolution 2—Chapter 4

A sequel to Refuting Evolution that refutes the latest arguments to support evolution (as presented by PBS and Scientific American).

by with Michael Matthews

Argument: Natural selection leads to speciation

Evolutionists say, ‘Natural selection has been observed to cause profound changes in populations—providing abundant evidence for speciation.’

First published in Refuting Evolution 2, Chapter 4

Galápagos finches—evolution in action?

The opening episode of the PBS Evolution series makes much of the Galápagos finches—considered one of the classic evidences of ‘evolution in action.’ But PBS admits that Darwin didn’t even realize that the birds were finches and he failed to label which island they came from. All the same, he managed to acquire this information, and he eventually concluded that they had descended from mainland finches with modification just as the biblical creation/Fall/Flood/migration model would predict! He correctly realized that finch beak size was the result of adaptation to different food sources.


The problem is that Darwin and the PBS series taught that this adaptation could explain the general theory of evolution (GTE). But the finch beak variation is merely the result of selection of existing genetic information, while the GTE requires new information. Also, an 18-year study by zoologist Peter Grant showed that a new species could arise in only 200 years,1 which is inadvertent support for the biblical model of rapid speciation.2 However, another problem with using these finches is that the variation seems to be cyclic—while a drought resulted in a slight increase in beak size, the change was reversed when the rains returned. So it looks more like built-in adaptability to various climatic conditions than anything to do with the GTE.

PBS also discusses the change in beak length of hummingbirds, to adapt to changes in the lengths of flowers where they obtain nectar. But the same points apply—no evidence was produced that any new information is required for these changes, as opposed to selection of already-existing information.

What is the biblical creationist model?

Perhaps the most frequently repeated mistake that evolutionists make in their attacks on creation is to assert that ‘natural selection’ and ‘speciation’ prove evolution and disprove the biblical account of origins. Their bait-and-switch arguments imply that creationists believe in ‘fixity of species.’ The glossary for the PBS Evolution series Online Course for Teachers: Teaching Evolution explicitly makes this empty allegation:

In creationism, species are described as ‘fixed’ in the sense that they are believed not to change their form, or appearance, through time.

But no reputable creationist denies speciation—in fact, it is an important part of creationist biology. In the previous chapter, I showed that the real issue is whether evolution can explain the increase of genetic information content—enough changes to turn microbes into men, not simple change through time. Before laying to rest the evolutionists’ pointless arguments on this issue, it might be helpful to review the creationist model in detail.

Biblical ‘kinds’ are not modern species

Creationists, starting from the Bible, believe that God created different kinds of organisms, which reproduced ‘after their kinds’ (Gen. 1:11, 12, 21, 24, 25). Thus the biblical kinds would have originally been distinct biological species, i.e., a population of organisms that can interbreed to produce fertile offspring but that cannot so breed with a different biological species.

But creationists point out that the biblical ‘kind’ is larger than one of today’s ‘species.’ Each of the original kinds was created with a vast amount of information. God made sure that the original creatures had enough variety in their genetic information so that their descendants could adapt to a wide variety of environments.

Based on the biblical criterion for kinds, creationists have made several deductions about the modern descendants of the original creations. They deduce, for example, that as long as two modern creatures can hybridize with true fertilization, the two creatures are descended from the same kind.3 Also, if two creatures can hybridize with the same third creature, they are all members of the same kind.4 The hybridization criterion is a valid operational definition, which could in principle enable researchers to list all the kinds. The implication is one-way—hybridization is evidence that two creatures are the same kind, but it does not necessarily follow that if hybridization cannot occur then they are not members of the same kind (failure to hybridize could be due to degenerative mutations). After all, there are couples who can’t have children, and we don’t classify them as a different species, let alone a different kind.

The boundaries of the ‘kind’ do not always correspond to any given man-made classification such as ‘species,’ genus, family, etc. But this is not the fault of the biblical term ‘kind’; it is actually due to inconsistencies in the man-made classification system. That is, several organisms classified as different ‘species,’ and even different genera or higher groupings, can produce fertile offspring. This means that they are really the same species that has several varieties, hence a polytypic (many type) species. A good example is Kekaimalu the wholphin, a fertile hybrid between a male false killer whale (Pseudorca crassidens) and a female bottlenose dolphin (Tursiops truncatus), i.e., between two different so-called genera.5 There are more examples in reference 3.

Biologists have identified several ways that a loss of genetic information through mutations (copying mistakes) can lead to new species—e.g., the loss of a protein’s ability to recognize ‘imprinting’ marks, ‘jumping genes,’ natural selection, and genetic drift. When these mutations take place in small populations, they can sometimes result in sterile or nonviable offspring. Or changes in song or color might result in birds that no longer recognize a mate, so they no longer interbreed. Either way, a new ‘species’ is formed. Thus, each created kind may have been the ancestor of several present-day species.

But again, it’s important to stress that speciation has nothing to do with real evolution (GTE), because it involves sorting and loss of genetic information, rather than new information.

The biblical model predicts rapid speciation

The biblical creation/Fall/Flood/migration model would also predict rapid formation of new varieties and even species. This is because all the modern varieties of land vertebrates must have descended from comparatively few animals that disembarked from the ark only around 4,500 years ago. In contrast, Darwin thought that this process would normally take eons. It turns out that the very evidence claimed by evolutionists to support their theory supports the biblical model.

Biologists have identified several instances of rapid adaptation, including guppies on Trinidad, lizards in the Bahamas, daisies on the islands of British Columbia, and house mice on Madeira.6 Another good example is a new ‘species’ of mosquito that can’t interbreed with the parent population, arising in the London Underground train system (the ‘Tube’) in only 100 years. The rapid change has ‘astonished’ evolutionists, but should delight creationists.7 Scientific American admits as much.

These days even most creationists acknowledge that microevolution has been upheld by tests in the laboratory (as in studies of cells, plants and fruit flies) and in the field (as in Grant’s studies of evolving beak shapes among Galápagos finches). [SA 80]

And why should creationists deny such things? All of this so-called microevolution is part of a created and fallen world, but has never been observed to add new genetic information. In fact, the sorts of changes which are observed are the wrong type to drive the evolutionary story.8 Scientific American is forced to make a pointless claim about evidence of ‘profound’ changes:

Natural selection and other mechanisms—such as chromosomal changes, symbiosis, and hybridization—can drive profound changes in populations over time. [SA 80]

Again, do these profound changes increase information? No populations are seen losing information, and adapting within the constraints of the information they already have. In contrast, goo-to-you evolution requires something quite different—the progressive addition of massive amounts of genetic information that is novel not only to that population, but to the entire biosphere.

Straw man 1: Natural selection can’t explain new species

Scientific American falls for the same straw-man argument as PBS, failing to recognize that creationists accept new species arising within the kind. Creationists recognize how reproductive isolation can result from information loss. (See discussion above.)

11. Natural selection might explain micro-evolution, but it cannot explain the origin of new species and higher orders of life.

Evolutionary biologists have written extensively about how natural selection could produce new species. For instance, in the model called allopatry, developed by Ernst Mayr of Harvard University, if a population of organisms were isolated from the rest of its species by geographical boundaries, it might be subjected to different selective pressures. Changes would accumulate in the isolated population. If those changes became so significant that the splinter group could not or routinely would not breed with the original stock, then the splinter group would be reproductively isolated and on its way toward becoming a new species. [SA 82]

Indeed, creationists point out that Mayr’s allopatric model would explain the origin of the different people groups (‘races’) after the confusion of languages at Babel induced small population groups to spread out all over the earth.9 Of course, the modern people groups are not reproductively isolated and are still a single biological species.

Creationists also point out that the mountainous topography of the ark’s landing place would be ideal for geographical isolation. This would allow much post-Flood diversification from comparatively few (~8,000) kinds of land vertebrates, by splitting up the original high genetic variation.

Note that the reproductive isolation is an informationally negative change, even if beneficial, because it blocks the interchange of genetic information between populations.

Evolutionists brag that natural selection is the best studied of the evolutionary mechanisms, but these studies show that it has nothing to do with evolution of more complex life forms! All we observe it doing is removing information, not adding it. Scientific American suggests that there are other feasible mechanisms to explain evolution, but they do not hold up, either.

Natural selection is the best studied of the evolutionary mechanisms, but biologists are open to other possibilities as well. Biologists are constantly assessing the potential of unusual genetic mechanisms for causing speciation or for producing complex features in organisms. Lynn Margulis of the University of Massachusetts at Amherst and others have persuasively argued that some cellular organelles, such as the energy-generating mitochondria, evolved through the symbiotic merger of ancient organisms. [SA 82]

The endosymbiosis theory has many problems, such as the lack of evidence that prokaryotes are capable of ingesting another cell and keeping it alive, and the large differences in genes between mitochondria and prokaryotes.10 Scientific American admits that it’s open to any other mechanism to explain nature—as long as it excludes God!

Thus, science welcomes the possibility of evolution resulting from forces beyond natural selection. Yet those forces must be natural; they cannot be attributed to the actions of mysterious creative intelligences whose existence, in scientific terms, is unproved. [SA 82]

We have already cited more honest admissions by evolutionists Lewontin and Todd about their a priori rejection of a Designer before even examining the evidence. But evolutionary propaganda for public consumption persists in claiming that evolution is accepted purely on scientific grounds.

Straw man 2: Evolutionists have seen species evolve

Scientific American tries to make hay with this straw man, devoting two points to ‘proving’ natural selection and speciation. Informed creationists don’t teach against these biological processes—even though some ‘day-age’ advocates, like Hugh Ross, do.11

12. Nobody has ever seen a new species evolve.

Speciation is probably fairly rare and in many cases might take centuries. [SA 82]

It might take centuries, but it need not. In fact, speciation can happen much faster than most evolutionists (and ‘day-age’ advocates) realize. Creationists following the biblical creation/Fall/Flood/migration model expect such rapid non-evolutive speciation, as we pointed out earlier.

Furthermore, recognizing a new species during a formative stage can be difficult, because biologists sometimes disagree about how best to define a species. The most widely used definition, Mayr’s Biological Species Concept, recognizes a species as a distinct community of reproductively isolated populations—sets of organisms that normally do not or cannot breed outside their community. In practice, this standard can be difficult to apply to organisms isolated by distance or terrain or to plants (and, of course, fossils do not breed). Biologists therefore usually use organisms’ physical and behavioral traits as clues to their species membership. [SA 82]

We agree. It’s important to note this difficulty in defining ‘species’ whenever evolutionists claim that creationists don’t have a consistent definition of ‘kinds’ (which we do, as discussed before). We also agree with Scientific American’s recognition of recent experiments that have caused artificial speciation.

Nevertheless, the scientific literature does contain reports of apparent speciation events in plants, insects, and worms. In most of these experiments, researchers subjected organisms to various types of selection for anatomical differences, mating behaviors, habitat preferences, and other traits and found that they had created populations of organisms that did not breed with outsiders. For example, William R. Rice of the University of New Mexico and George W. Salt of the University of California at Davis demonstrated that if they sorted a group of fruit flies by their preference for certain environments and bred those flies separately over 35 generations, the resulting flies would refuse to breed with those from a very different environment. [SA 82–83]

None of this is news to informed creationists. Once again, there is no new information, but sorting and loss of already existing information.

Ecology proves evolution?

While evolutionists claim that natural selection is the best-studied mechanism for evolution, they also must explain the real-life processes behind natural selection. Their discussion of ecology is very interesting (and factual), but it tells us nothing about GTE.

Changing populations within healthy forest ecosystems

For example, PBS 3 devotes a whole segment to show how a healthy forest ecosystem has a large carnivore at the top of the food chain, which can cause drastic changes in the population of the forest. It takes 100 pounds of plant to feed 10 pounds of herbivore, which in turn feed 1 pound of carnivore. So the existence of carnivores indicates the health of the supporting animals and plants. Later on in the program, Wildlife Conservation Society biologist Alan Rabinowitz claims that this healthy forest exhibits ‘evolution going on around us,’ but all he means is the replacement of one species with another. Of course, already-existing species replacing other already-existing species has nothing to do with the origin of new species with new genetic information. Once again, ‘evolution’ is a vacuous catch-all term, with any change in population numbers tossed out to the unwary listener as evidence of the goo-to-you theory.

Founder effect

Then the PBS program moves on to isolated habitats and the ‘founder effect.’ This is where a single breeding pair or pregnant female colonizes a new niche, and carries only a fraction of the gene pool. Therefore its descendants also contain a small fraction of the original gene pool, so the new population can be very different from the old. This also offers no comfort or support to the notion of evolution because the new population has less information than the old.

Invasion—the leafy spurge

Another ecological topic is biological invaders, the bane of all countries that depend on agriculture and livestock to feed their people and earn export dollars. The invaders are often more mobile and adaptive, so they out-compete native species. Modern technology has vastly increased the rate of hostile invasions, as animals stow away on ships and in the undercarriage of airplanes, although some species have been introduced deliberately. Fordham University paleoecologist David Burney investigated what happened in Hawaii when Polynesians and then Europeans introduced new species. He claimed:

Evolution has now entered a new mode. Something altogether new is happening, and it has to do with what humans do to the evolutionary process. [PBS 3]

Ho hum, this is just another example of replacement of one species with another, which again has nothing to do with showing how particles could have turned into people.

Pioneers introduced a weed called leafy spurge into North Dakota from Russia, and it ‘threatens to kill off all native grasses.’ A cattle rancher claimed on PBS that ‘it is a cancer to the land … it makes the land just totally useless.’ Actually, the first claim is an exaggeration, and the second is a matter of perspective—sheep and goat farmers would have no problems.

But the rancher said that herbicides were very expensive, so the narrator asks:

… what’s left? … The solution may be another invader—discovered when scientists learned what kept leafy spurge in check in its native Russia. It’s the flea beetle—a case of fighting evolutionary fire with fire. [PBS 3]

Canisters of flea beetles are dropped from airplanes, then the narrator says:

So now we’re in a race most of us don’t even know we’re running—to learn as much as possible about evolution before it’s too late. [PBS 3]

Huh? Using already-existing enemies of the leafy spurge requires ‘evolution’? This must be the nadir of the contentless nature of this word, even by the pathetic standards of the PBS series. Farmers have used such common-sense biological controls for centuries, well before Darwin. Interestingly, one of the classic cases of successful biological control was the defeat of Australia’s cactus invader, the prickly pear, through the introduction of the Cactoblastis organism. John Mann, the scientist responsible for saving Australia from ecological and economic ruin in this way, was heaped with accolades and honors for his feat. Mann was a convinced biblical creationist, who was interviewed by Creation before his death.12


PBS 3 also describes the leaf-cutting ants of Brazil. They form colonies containing eight million insects, and they cut leaves into pieces and bring them to the nest, but they don’t eat them. Rather, other leafcutter ants mulch them and use the mulch to grow a fungus ‘garden.’ This fungus is used as food for the young leafcutters, which thus depend on the fungus for survival, but the fungus depends on the ants to provide the mulch.

But this fungus garden has a ‘weed,’ a virulent mold that badly hinders the fungal growth. To combat this, some ants have a white waxy coating that is now known to be tangled mats of bacteria that produce antibiotics that kill the mold.

Presumably, by this stage in the series, the producers hope that viewers are so indoctrinated in evolution that they don’t even need to try to produce evidence. To the diehard evolutionist, any phenomenon at all can be adduced as ‘evidence’ for evolution. In this case, they don’t bother to explain how such a complex symbiosis could have evolved, but merely assert that the bacteria and mold are products of an arms race lasting 50 million years.

Predator–prey, driving force of evolution?

While evolutionists discuss natural selection and speciation, they like to emphasize the bloodshed and violence that drives these biological changes. They see ‘Nature, red in tooth and claw,’ in the memorable phrase from the very long 1850 poem In Memoriam, A.H.H. by Alfred Lord Tennyson (1809–1892). In debates they love to pull out this as ‘knock-down’ evidence against Christians, believing it disproves the possibility of a benevolent, wise Creator—following Darwin. The fact that Tennyson’s poem predated Darwin’s Origin indicates that Darwin was greatly influenced by philosophical ideas of his day.

But their viewpoint overlooks an obvious incident in biblical history—Adam’s sin and God’s subsequent curse on the whole creation, as I will explain further on. Unfortunately, many in the ‘intelligent design movement’ refuse to invoke the Bible, which provides the only plausible answer, so they are stumped by this argument.13 So, upon closer inspection, the predator–prey paradigm testifies to the accuracy of the biblical account and offers nothing to resolve the fundamental flaw of the general theory of evolution: where does new genetic information come from?

Episode 4 of the PBS Evolution series aims to show that these violent biological forces, rather than the environmental ones, drive evolution most strongly, based largely on extensive interviews with the atheistic sociobiologist Edward O. Wilson. The title of PBS 4, ‘The Evolutionary Arms Race!’ reflects the struggle between predator and prey: as a prey evolves stronger defense mechanisms, an attacker must evolve stronger mechanisms to survive, and vice versa. Of course, evolutionary biologists think there is no design behind this: the only prey that survive have chance copying mistakes in their genes that confer a strong defense, and they pass on these genes to their offspring. Faced with these stronger defense mechanisms, only those predators that happen to have mutations conferring better attacking power will be able to eat the prey, while the others starve and fail to pass on their genes.

But as explained earlier, real evolution requires changes that increase genetic information, while non-information-increasing changes are part of the creation model. None of the examples presented in episode 4 prove that information has increased, so they provide no support for evolution or against creation.

Poison newt

PBS takes viewers to Oregon, where there were mysterious deaths of campers, but it turned out that newts were found boiled in the coffee pot. These rough-skinned newts (Taricha granulosa) secrete a deadly toxin from their skin glands so powerful that even a pinhead-sized amount can kill an adult human. They are the deadliest salamanders on earth. So scientists investigated why this newt should have such a deadly toxin.

They theorized that a predator was driving this ‘evolution,’ and they found that the common garter snake (Thamnophis sirtalis) was the newt’s only predator. Most snakes will be killed by the newt’s toxin, but the common garter snake just loses muscle control for a few hours, which could of course have serious consequences. But the newts were also driving the ‘evolution’ of the snakes—they also had various degrees of resistance to the newt toxin.

Are these conclusions correct? Yes, it is probably correct that the predators and prey are driving each other’s changes, and that they are the result of mutations and natural selection. Although it might surprise the ill-informed anti-creationist that creationists accept mutations and selection, it shouldn’t be so surprising to anyone who understands the biblical creation/Fall model (see What is the biblical creationist model?, above).

So is this proof of particles-to-people evolution? Not at all. There is no proof that the changes increase genetic information. In fact, the reverse seems to be true.

The snakes with greater resistance have a cost—they move more slowly. Since PBS provided no explanation of the poison’s activity, it’s fair to propose possible scenarios to explain the phenomenon under a biblical framework (it would be hypocritical for evolutionists to object, since they often produce hypothetical ‘just-so’ stories to explain what they cannot see).

Suppose the newt’s poison normally reacts with a particular neurotransmitter in its victims to produce something that halts all nerve impulses, resulting in death. But if the snake had a mutation which reduced the production of this neurotransmitter, then the newt’s poison would have fewer targets to act upon. Another possibility is a mutation in the snake altering the neurotransmitter’s precise structure so that its shape no longer matches the protein. Either way, the poison would be less effective. But at the same time, either mutation would slow nerve impulses, making the snake’s muscle movement slower.

So either of these would be an information loss in the snake that happens to confer an advantage. This is far from the only example. The best known is sickle-cell anemia, a common blood disorder in which a mutation causes the sufferer’s hemoglobin to form the wrong shape and fail to carry oxygen. People who carry two copies of the sickle-cell gene (homozygous) often develop fatal anemia. But this misshapen hemoglobin also resists the malaria parasite (Plasmodium). So humans who are heterozygous (have both a normal and abnormal gene) have some advantage in areas where malaria is prevalent, even though half their hemoglobin is less effective at its job of carrying oxygen. Another example is wingless beetles, which survive on windy islands because they won’t fly and be blown into the sea.14

As for the newt, likewise, increased secretion of poison can result without any new information. One possibility is an information-losing mutation that disables a gene controlling the production of the poison. Then it would be over-produced, which would be an advantage in defending against the snake, but a wasteful use of resources otherwise.

There are other related examples, e.g., one way that the Staphylococcus bacteria becomes resistant to penicillin is via a mutation that disables a control gene for production of penicillinase, an enzyme that destroys penicillin. When it has this mutation, the bacterium over-produces this enzyme, which means it is resistant to huge amounts of penicillin. But in the wild, this mutant bacterium is less fit, because it squanders resources by producing unnecessary penicillinase.

Another example is a cattle breed called the Belgian Blue. This is very valuable to beef farmers because it has 20–30% more muscle than average cattle, and its meat is lower in fat. Normally, muscle growth is regulated by a number of proteins, such as myostatin. However, Belgian Blues have a mutation that deactivates the myostatin gene, so the muscles grow uncontrolled and become very large. This mutation has a cost, in reduced fertility.15 A different mutation of the same gene is also responsible for the very muscular Piedmontese cattle. Genetic engineers have bred muscular mice by the same principle.

In all these cases, a mutation causes information loss, even though it might be considered ‘beneficial.’ Therefore it is in the opposite direction required for particles-to-people evolution, which requires the generation of new information.

Did God create carnivory?

According to the Bible, the original diet of both humans and animals was vegetarian (Gen. 1:29–30). So how do creationists explain today’s carnivory? Episode 4 of the PBS Evolution series showed many examples of animals killing other animals, which doesn’t seem like a ‘very good’ creation (Gen. 1:31). According to the Bible, death was introduced with Adam’s sin (Gen. 2:17; Gen. 3:17–19; Rom. 5:12; 1 Cor. 15:21–22). While these verses refer explicitly to human death, Genesis 3 is clear that Adam’s sin had further unpleasant effects because Adam was the federal head of creation. The reformer John Calvin commented on Genesis 3:19:

Therefore, we may know, that whatever unwholesome things may be produced, are not natural fruits of the earth, but are corruptions which originate from sin.16

This is supported by Paul’s teaching of Romans 8:20–22, that God subjected the whole creation to futility, and many commentators believe Paul was alluding to Genesis 3. Further support comes from the fact that the restored creation will have no carnivory (Isa. 65:25).

The Bible doesn’t specifically explain how carnivory originated, but since creation was finished after day 6 (Gen. 2:1–3), there is no possibility that God created new carnivorous animals. Instead, creationists have three explanations in general, although the specific explanation depends on the particular case.17

  1. The Bible appears not to regard insects as living in the same sense as humans and vertebrate animals the Hebrew never refers to them as nephesh chayyah (‘living soul/creature’), unlike humans and even fish (Gen. 1:20, 2:7).

  2. Before the Fall, many attack/defense structures could have been used in a vegetarian lifestyle. For example, even today, some baby spiders use their webs to trap pollen for food,18 and there was the case of a lion that wouldn’t eat meat.19 Many poisons actually have beneficial purposes in small amounts.20 Even PBS pointed out that microbes ‘help prime the immune system’ and that many allergies might be due to a society that’s too clean.

  3. God foreknew the Fall, so He programmed creatures with the information for design features for attack and defense that they would need in a cursed world. This information was ‘switched on’ at the Fall.

For the poisonous newt, it seems that #3 is the best explanation for the molecular structure of the deadly toxin itself and the poison glands on the skin. In general, I believe #3 is the best explanation for structures that seem specifically designed for attack and defense.

Evolution of pathogens

If evolutionists hope to find evidence of modern-day evolution, they have a perfect opportunity with pathogens. In just a few months, bacteria can go through hundreds of thousands of generations, equivalent to ‘millions of years’ in vertebrates. Yet in spite of this rapid change, the bacteria that we see today are essentially the same as the bacteria retrieved from the tombs of the pharaohs, and even with those discovered in salt crystals ‘dated’ millions of years old.21

HIV resistance to drugs

PBS 1 claims that Darwin didn’t really see evolution in action, but now we do. Supposedly HIV, the cause of AIDS, evolves resistance to drugs faster than we can make them. Because the virus can produce billions of copies per day, it can ‘evolve’ in minutes to hours. One researcher said that this rapid change would be a ‘surprise’ if we didn’t have the concept of evolution. PBS also attempted to tug heartstrings, by portraying AIDS patients as ‘victims of evolution.’

First, we see the equivocation—HIV producing HIV is supposed to show that particles could turn into people; but they’re still HIV—they haven’t changed into something else.

Second, in PBS 4, it’s made clear that the related phenomenon of antibiotic resistance in bacteria took the medical community by surprise—this means that it wasn’t a prediction of evolution, except after the fact.

Third, they fail to demonstrate that new information is involved, and in fact the next segment of the program showed that the opposite is true. Veronica Miller of Goethe University in Germany experimented by ceasing all antiviral drug treatments to a patient. Without the drugs, the few surviving original (‘wild’) types that had infected the patient could grow more easily. It turned out that they easily out-competed the vast numbers of resistant forms that had developed in the hospital. She said this was a risk because the wild types were also more dangerous—more efficient than the new strains that had survived the earlier drug treatments. The superior efficiency and reproductive success of the wild type implies that the other ‘evolved’ strains acquired resistance due to a loss of information somewhere.

This should not be surprising, because the same is true of many examples of antibiotic resistance in bacteria. For example, some bacteria (see Poison newt, above) have an enzyme that usually has a useful purpose, but it also turns an antibiotic into a poison. That is, it’s not the antibiotic per se that’s damaging, but its chemical byproduct from the bacterium’s metabolism. So a mutation disabling this enzyme would render the antibiotic harmless. But this bacterium is still disabled, because the enzyme is now hindered, so the bacterium would be unable to compete in the wild with non-resistant ones. The information loss in both HIV and the bacterium is the opposite of what evolution requires.22

Tuberculosis and antibiotic resistance

PBS describes the microbe as a ‘predator’ of humans, although ‘parasite’ would be more accurate. Mummies show that the tuberculosis bacillus (TB) affected Egyptians 4,000 years ago. The Black Death wiped out one-third of Europe’s population in 1347–1351, and the influenza pandemic of 1918–1919 killed 20 million people—more than World War 1 that had just ended.

After the world wars, antibiotics were considered the ‘magic bullet,’ and there were optimistic claims even as late as 1969 that ‘infectious diseases were a thing of the past.’ But they failed to anticipate the development of resistance. This shows that bacterial resistance was hardly a ‘prediction’ of evolution, but is really a phenomenon they try to explain ‘after the fact’ as due to evolution. As will be shown, there is nothing to support molecules-to-man evolution; rather, a properly understood creation model makes good sense of the evidence.

PBS 4 discussed a new strain of TB that had arisen in the overcrowded Russian prison system, containing malnourished prisoners with weakened immune systems. One inmate, ‘Sasha’ (Alexandr), had failed to complete his course of antibiotics. This meant that a few bacteria survived because they had some resistance to the antibiotic, and then proliferated once the treatment stopped. But the program itself makes it clear that the resistance was already present, so this is not evolution, although it is natural selection.

These resistant bacteria are not confined to the prison, but have spread because of travel. One 19-year-old Russian student, ‘Anna,’ has a strain resistant to five antibiotics. Immunologists predict that TB could soon claim 2–3 million lives per year.

But as shown, there is no proof that any antibiotic resistance is due to increased genetic information. The above example shows that the information was already present, and I previously explained how a loss of information could confer resistance. Sometimes bacteria can pass genes to each other by exchanging plasmids, and sometimes these genes confer resistance. But of course, these examples involve no new information produced in the biosphere.

Evolution of less harmful bacteria?

Paul Ewald of Amherst College claimed on PBS 4 that ‘evolution’ may not only be a problem, but could also be harnessed to ‘evolve’ less harmful bacteria. If a pathogen spreads by close contact between people, then it’s in its best interest not to make people so sick that they can’t move around. But those pathogens spread by water and insects tend to be deadly.

In the 1991 cholera epidemic in South America, a million people were infected, and 10,000 died. The bacterium (Vibrio cholerae) was spread by contaminated water, so ‘evolved’ high levels of toxicity. The solution was to clean the water supply, so that only healthier people could spread the germ. So the germ ‘evolved’ mildness, and many infected people didn’t even develop symptoms.

But here again, there is indeed natural selection, but the result is that Vibrio cholerae turn into Vibrio cholerae! There is no proof that any new information was produced, but rather, selection of existing genetic variation.

PBS 4 compared this phenomenon to breeding domestic dogs from wolves, but again this involved loss of information.

Pathogens and creation

Some people wonder where disease germs fit into the biblical framework, if God created everything ‘very good.’ Under this framework, obviously the Fall was responsible for disease, but how, if God had finished creating at the end of creation week? The phenomenon described in the previous section can provide some insights. It clearly shows that even something usually known as a deadly germ can have a mild variant that causes no illness. Presumably something like this was created during creation week—even today, Vibrio cholerae has a role in the ecosystems of brackish waters and estuaries, and the original may have had a role living symbiotically with some people. Even its toxin probably has a beneficial function in small amounts, like most poisons. The virulence arose after the Fall, by natural selection of varieties producing more and more toxin as contaminated water became more plentiful. No new information would be needed for this process. Recent evidence shows that the loss of chemotaxis—the ability to move in response to changes in chemical concentrations—will markedly increase infectivity in an infant mouse model of cholera.23

Another factor is that the bacterium itself doesn’t carry the gene for the cholera toxin that attacks the intestine. This is coded by a temperate bacteriophage called CTXφ, which inserts itself into the bacterial genome. Other bacteria that are normally non-virulent but become virulent upon infection by a phage that contains genes for toxins include those that cause diphtheria, shigellosis dysentery, and botulism.

Another likely example of virulence arising by information loss is the mycoplasmas, the smallest known self-reproducing organisms (parasitic bacteria with no cell walls and fewer than 1,000 genes, found in the respiratory system and urogenital tracts of humans). Loss of genetic information, e.g., for amino acid synthesis, could have resulted in the mycoplasmas becoming increasingly dependent on their hosts for survival.24 Some clues to possible benign pre-Fall roles for viruses can be gleaned from functions they have even today. Viruses are non-living entities, which function like seeds and spores, transporting genes among plants and animals. They also help keep soil fertile, keep water clean, and regulate gases in the atmosphere.25 So once again, some alleged evidence for evolution actually provides support for the creation/Fall model.

Has immunity evolved?

In PBS 4, Stephen O’Brien of the National Cancer Institute wondered why the big cats have ‘evolved’ resistance to a disease deadly to humans. There is a Feline Immunodeficiency Virus (FIV) that should cause AIDS-like symptoms. Supposedly the cats’ ancestors were almost wiped out by the virus, but some had resistant genes. Supposedly, the FIV evolved to mildness.

More interesting was the claim that about 10 percent of humans have a ‘whopping mutation’ that confers resistance to HIV. This turns out to be the loss of certain receptors on the immune cells preventing the HIV from docking on them. Again, this change is in the opposite direction required to change particles into people.

From mycoplasmas to big cats, from TB to poison newts, there’s not a shred of evidence that might explain the evolution of new genetic information, but the loss that we see fits nicely with the biblical creationist model.

References and notes

  1. P.R. Grant, Natural Selection and Darwin’s Finches, Scientific American 265(4):60–65 (October 1991). Return to text.
  2. See Carl Wieland, Darwin’s Finches: Evidence supporting rapid post-Flood adaptation, Creation 14(3):22–23 (June–August 1992). Return to text.
  3. F.L. Marsh, Variation and Fixity in Nature (Mountain View, CA: Pacific Press, 1976), p. 37. Return to text.
  4. Wm. A. Dembski, Mere Creation: Science, Faith and Intelligent Design, Basic Types of Life, by S. Scherer (Downers Grove, IL: InterVarsity Press, 1998), p. 197. Return to text.
  5. Donald Batten, Ligers and wholphins? What next? Creation 22(3):28–33 (June–August 2000). Return to text.
  6. David Catchpoole and C. Wieland, Speedy species surprise, Creation 23(2):13–15 (March–May 2001). Return to text.
  7. See C. Wieland, Brisk biters, Creation 21(2):41 (March–May 1999). Return to text.
  8. See C. Wieland, The evolution train’s a-coming, Creation 24(2):16–19 (March–May 2002). Return to text.
  9. The human ‘races’ issue is covered more fully in chapter 18 of D. Batten, D. Catchpoole, J. Sarfati, and C. Wieland, The Creation Answers Book (Creation Book Publishers, Brisbane, Australia: CMI, 2006). Return to text.
  10. See D. Batten, Did Cells Acquire Organelles Such as Mitochondria by Gobbling Up Other Cells? Return to text.
  11. See Ten major differences and similarities between Calendar-Day and Day-Age Creationists. Return to text.
  12. Interview with creationist biological control expert, Dr John Mann, M.B.E., Creation 5(2):20–21, October 1982. Return to text.
  13. See C. Wieland, CMI’s views on the intelligent design movement, 30 August 2002. Return to text.
  14. See C. Wieland, Beetle bloopers: Even a defect can be an advantage sometimes, Creation 19(3):30 (June–August 1997). Return to text.
  15. J. Travis, Muscle-bound Cattle Reveal Meaty Mutation, Science News 152(21):325 (22 November 1997). Return to text.
  16. J. Calvin, Genesis, 1554 (Edinburgh, UK: Banner of Truth, 1984), p. 180. Return to text.
  17. This topic is covered more fully in chapter 6 of D. Batten, D. Catchpoole, J. Sarfati, and C. Wieland, The Creation Answers Book (Creation Book Publishers, Brisbane, Australia: CMI, 2006). Return to text.
  18. See Pollen-eating spiders, Creation 22(3):5–7 (June–August 2000); Nature Australia (Summer 1999–2000): p. 5. Return to text.
  19. D. Catchpoole, The lion that wouldn’t eat meat, Creation 22(2):22–23 (March–May 2000). Return to text.
  20. See J. Bergman, Understanding Poisons from a Creationist Perspective, Journal of Creation 11(3):353–360, 1997. Return to text.
  21. D. Batten, Frankenstein foods? Creation 24(4):10–13 (September–November 2002). Return to text.
  22. For more information on bacterial and viral resistance to drugs see C. Wieland, Superbugs not super after all, Creation 20(1):10–13 (Dec. 1997–Feb. 1998)
    C. Wieland, Has AIDS Evolved? Creation 12(3):29–32 (June–August 1990)
    J. Sarfati, Anthrax and antibiotics: Is evolution relevant? 15 November 2001. Return to text.
  23. D.S. Merrell et al., Host-induced Epidemic Spread of the Cholera Bacterium, Nature 417(6889):642–644 (6 June 2002). Return to text.
  24. T.C. Wood, Genome Decay in the Mycoplasmas, Impact 340, October 2001; icr.org/article/genome-decay-mycoplasmas.
    C. Wieland, Diseases on the Ark (Answering the Critics), Journal of Creation 8(1):16–18, 1994, explains important related concepts. Return to text.
  25. J. Bergman, Did God make pathogenic viruses? Journal of Creation 13(1):115–125, 1999. Return to text.

Note about citations: Quotations from the Scientific American article by John Rennie will be labeled ‘SA,’ followed by the page number. Quotations from, and other mentions of, the PBS-TV series ‘Evolution,’ will be labeled ‘PBS,’ followed by the episode number, e.g. ‘PBS 6’ refers to Episode 6. Return to article. 

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