Jonathan Sarfati

CMI’s response to PBS-TV series Evolution

Episode 4: The Evolutionary Arms Race!


This program aims to show that biological forces rather than the environmental ones drive evolution most strongly, interviewing the atheistic sociobiologist Edward O. Wilson extensively. The title reflects the struggle between predator and prey: as a prey species evolves stronger defense mechanisms, an attacker must evolve stronger mechanisms to survive, and vice versa. Of course, they think there is no design behind this: of all the individual prey animals, only those with copying mistakes in their genes that confer a strong defense will avoid being eaten, so pass on these genes to their offspring, so the next generations are more strongly defended overall. And faced with these stronger defense mechanisms, only those predatory individuals that have mutations conferring sufficiently strong attacking power will be able to eat the prey, while the others starve and fail to pass on their genes.

But as shown in the rebuttal to Episode 1, 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 provide no support of evolution over creation.

Poison newt

The program moves to Oregon, where there were mysterious deaths of campers, but it turned out that newts were found boiled in the coffee pot. It turns out that 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. (The toxin is tetrodotoxin—the same toxin is found in the blue-ringed octopus and pufferfish.)

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 their conclusions correct? Yes, they are 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 CMI accepts mutations and selection, it shouldn’t be so surprising to anyone who understands the Biblical Creation/Fall/Dispersion model.

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 the PBS episode provides no explanation of the poison’s activity, it’s fair to propose a possible scenario (it would be hypocritical to object, since evolutionists often produce far more hypothetical ‘just-so’ stories): suppose the poison normally reacts with a particular neurotransmitter 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 poison would have fewer targets to act upon. Another possibility is a mutation altering its precise structure so that its shape no longer matches the protein. Either way, the poison would be less effective. But either reduced production of the neurotransmitter or a less precise shape, would slow nerve impulses, meaning that muscle movement is slower.

So this is an information loss that happens to confer an advantage. This is far from the only example. The best known is sickle-cell anemia, where a mutation causes the 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—see Beetle bloopers. Even a defect can be an advantage sometimes.

As for the newt, a possible way that an information-losing mutation can result in increasing amounts of secretion is a mutation disabling a control gene, allowing overproduction.

There are other related examples, e.g. one way for Staphylococcus to become resistant to penicillin is via a mutation that disables a control gene for production of penicillinase, an enzyme that destroys penicillin. Then the bacterium over-produces this enzyme, which means it is resistant to huge amounts of penicillin. But in the wild, this mutant bacterium would be less fit, because it would squander 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 and very tender. 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. A different mutation of the same gene is also responsible for the very muscular Piedmontese cattle, and has also been responsible for a ‘superbaby’. 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, as this requires the generation of new information.

Did God create carnivory?

According to the Bible, the original diet of both humans and animals was vegetarian (Genesis 1:29–30). So how do creationists explain carnivory today? This episode 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 is ‘the last enemy’ (1 Cor. 15:26) and was introduced with Adam’s sin (Genesis 2:17, Gen. 3:17–19, Rom. 5:12, 1 Cor. 15:21–22). While these refer explicitly to human death, Adam’s sin affected the whole creation (Rom. 8:20–22), and this is further supported by the fact that the restored creation will have no carnivory (Isaiah 65:25) [update: see The Fall: a cosmic catastrophe]. How this occurred is not specifically stated, 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. This is explained further in the The Creation Answers Book, Ch. 6:

  1. The Bible appears not to regard insects as living in the same sense as humans and vertebrate animals—they are never referred to as nephesh chayyah (Hebrew נֶפֶשׁ חַיָּה), unlike humans and even fish.

  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 (see Pollen-Eating Spiders), and there was the case of The lion that wouldn’t eat meat. Even many poisons actually have beneficial purposes in small amounts—see Understanding Poisons from a Creationist Perspective. Even this PBS episode 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, as opposed to the possibility of increasing its production rate by information-losing mutations and natural selection. #3 is the best explanation for structures that seem specifically designed for attack and defense.

Tuberculosis and antibiotic resistance

Microbes were described as a ‘predator’ of humans, although ‘parasite’ would be more accurate. Mummies show that Tuberculosis Bacillus (TB) affected Egyptians 4000 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.

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 this 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.

This episode 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. TB could 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 there will be genes conferring resistance. But of course, these examples involve no new information produced in the biosphere. For more information, see Superbugs: Not super after all.

[Note added 26 October: a critic, while actually criticising the section on the poison newt, claimed that there have been examples of information-increasing mutations conferring antibiotic resistance. But it turned out that these mutations actually reduced the specificity of the enzymes, thus they decreased the information content. See critic’s letter plus my response for a detailed explanation.]

Evolution of less harmful bacteria?

Paul Ewald of Amherst College claimed 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 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.

This episode compared this phenomenon with 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—see again Understanding Poisons from a Creationist Perspective. 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. [More recent evidence shows that 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.’ D. Scott Merrell et al., Host-induced epidemic spread of the cholera bacterium, Nature 417(6889):642–644, 6 June 2002]

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. As shown in the article Genome decay in the Mycoplasmas, loss of genetic information, e.g. for amino acid synthesis, could have resulted in the mycoplasmas’ becoming increasingly dependent on their hosts for survival. The article Diseases on the Ark (Answering the Critics) explains important related concepts, and some possible benign pre-Fall roles for viruses are presented in Did God make pathogenic viruses?. So once again some alleged evidence for evolution actually provides support for the Creation/Fall model.

Has immunity evolved?

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. This concept was dealt with in the previous two sections.

More interesting was the claim that about 10% 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.


The program describes the leaf-cutting ants of Brazil. They form colonies containing 8 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 used 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 mould that badly hinders the fungal growth. To combat this, some ants have a white waxy coating that turned out to be tangled mats of bacteria that produce antibiotics that kill the mould.

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 mould are products of an arms race lasting 50 million years.

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