A favourite icon of evolutionists, i.e. oft-cited by them as evidence of evolution, is the phenomenon of pesticide resistance.
On the evolution-proclaiming PBS1 website for example, the diminished efficacy of rodent poisons and insecticides is because “we have simply caused pest populations to evolve”.2 And no doubt wanting to prove that evolutionary theory has practical relevance, the PBS Evolution Library paints a grim picture of how this “evolution” is making life harder for us:
Having now got the reader’s attention, and warning that “the problem is getting worse”, the PBS article comfortingly (?) says, “but the pests are only following the rules of evolution”.
However, looking past the evolutionary assertions, the PBS article makes it clear that pesticide resistance is not evidence of evolution at all:
So the mechanisms that allow pests to tolerate pesticides are already present in “a few naturally resistant members of the targeted population”, which survive to reproduce themselves, thus passing the genes conferring pesticide resistance to the next generation.
Thus pests are not “slowly developing genetic shields” because the “genetic shield” already exists, i.e. it has not “evolved” out of thin air. What is happening is that the “genetic shield” becomes more widespread in the population, as an astute reader will discern from the PBS article’s subsequent explanation of what happens when farmers, noting lowered kill rates, increase the dosage:
And the spread of the genetic mechanisms conferring resistance can be very rapid indeed—coming to “dominate the population” in just a few generations, in fact.
For example, when researchers exposed the nematode Caenorhabditis elegans to the widely used nematicide levamisole, they reported that resistance to that pesticide “accumulated within very few generations”.3
The researchers explained that this rapid adaptation was likely due to the “standing genetic variation” of the nematode population, i.e. that the genes conferring resistance were already present in the population, but at low frequency. Exposing the nematodes to levamisole selected for the resistant individuals, “providing a direct demonstration of the speed of this process”. (Emphasis added.) There are numerous other examples of rapid adaptation in the scientific literature.4
Evolutionists are often needlessly surprised at the speed with which a population can adapt to a change in environment, because they are so used to thinking of such changes as being “evolution”, with evolution being inextricably associated with slow-and-gradual-over-millions-of-years processes (see Speedy Species Surprise). The changes are rapid alright, but they are not evolutionary—that is, relevant to the core claim of evolution that primordial microbes changed into mankind and all other living things.
But even the nematode researchers were victims of their evolutionary mindset. Despite not having observed any evolution whatsoever (i.e. the sorts of changes that supposedly resulted in pond scum becoming pesticide scientists), they nevertheless peppered their scientific paper with claims it was rapid “evolution” they had witnessed. “Our results demonstrate that pesticide resistance can evolve at an extremely rapid pace,” they wrote. Their results demonstrated no such thing. Rapid rise in resistance to pesticides—yes; but “evolve”?—no, as individuals with the “genetic shield” conferring nematicide resistance were apparently already in the population.
Mechanisms of pesticide resistance can come at a cost, research has shown. Referred to as “fitness cost”, resistance genes are said to “alter some components of the basic physiology and interfere with fitness-related life history traits”.5
A famous example is that of warfarin resistance in rats, first detected in the late 1950s.6 Rats resistant to that poison have a higher requirement for vitamin K than normal rats (more than 10 times!). When vitamin K is inadequate, warfarin-resistant rats suffer from blood clotting disorders—in fact, many will die from internal bleeding. Consequently, resistant individuals have a lower fitness under most field conditions, hence the proportion of rats having warfarin resistance in Britain was seen to decline when rat populations were no longer exposed to the rodenticide.
So, the genetic makeup conferring warfarin resistance in rats is associated with increased survival when the pesticide is present, but decreased survival when the pesticide is absent.
That “fitness cost” phenomenon occurs in insect pests too. Researchers monitoring Culex pipiens mosquitoes overwintering in a cave in southern France (in an area where organophosphate insecticides are widely used) noted a decline in the overall frequency of insecticide-resistant mosquitoes relative to susceptible ones as the winter progressed, indicating “a large fitness cost”.5 This is understandable in the light of the genetic mechanism conferring resistance in these mosquitoes. Organophosphate insecticides affect the ability of certain enzymes (proteins) called esterases to function properly, thus killing the insect. But the resistance genes “induce an overproduction of esterase, due to either gene amplification or gene regulation”.5 Note that having additional copies of existing genes or having genes that fail to switch off (regulate) production is not evidence for evolution because to change microbes into microbiologists, evolution needs a mechanism for adding new complex functions, not copying existing ones or breaking them (photocopying a chapter of a book or breaking an electric switch does not create new new complex functionality).
Similar overproduction of proteins occurred in DDT-resistant strains of Anopheles mosquitoes, too.7 The proteins metabolize DDT (an organochlorine-based insecticide). In the researchers’ words, “the transcripts and their proteins are over-expressed in the resistant strains and, as a consequence, are allowing them to exhibit this resistance.”8 Similarly, in Drosophila fruit flies, insecticide resistance is associated with “overtranscription” of a particular gene, resulting in 10 to 100 times as much mRNA in resistant strains as in susceptible strains.9 Given the extra energy and resources needed for such overproduction, it’s hardly surprising then that pesticide resistance carries a fitness cost.10,11
In all of the above examples, we’re not seeing the genes, the information, for complex new functions appearing out of nowhere, i.e. by evolution. Instead we’re seeing either possible “amplification” of genes (i.e. additional copies of existing genes) or, more usually, a loss-of-control over regulation of genes. In other words, the mechanisms for pesticide resistance are not from new genes but from existing genes—and especially from damaged versions of existing genes. There has been no increase in meaningful genetic information but rather a loss of information.
Thus the pesticide resistance “icon” of evolution actually gives no support to molecules-to-man evolution whatsoever. It is however right in line with the Bible’s account of origins, beautifully consistent with an originally “very good” creation (Genesis 1:31) now in “bondage to decay” (Romans 8:19–22) as a consequence of the Fall (Genesis 3). We’re not seeing improvement in the genes, we see brokenness, for that is what mutations do—they break genes, not create brand new ones. In today’s world sometimes it’s beneficial to have “broken” genes (e.g. if you’re a rat and there’s warfarin around), but the genes are nevertheless broken—undeniably degraded genetic information. No evolution is in evidence.12
Evolutionists love to portray the development of pesticide resistance as a grim “arms race”, no doubt leaving many people with the perception that pests are evolving new features all the time. But now that we’ve seen that pesticide resistance is due to breaking things, not creating new complex features, we can see that “arms race” is a misnomer. Rather, the struggle is better likened to trench warfare,13 where the defending forces will destroy their own bridge, or blow up their own road, to impede the enemy’s advance. An arms race implies that the defending forces are inventing new weapons, but the processes of selection and mutation operating in pests facing a pesticide are not inventing new weapons. So the phenomenon of resistance to nematicides, rodenticides, insecticides, etc., cannot be construed in any way as giving support to evolution’s Grand Idea that today’s life forms evolved from some single-celled organism billions of years ago.
Rather, the “broken” genes conferring pesticide resistance have arisen in the time since the Fall (about 6,000 years ago). And as surveys have shown, in a world where pesticides are used widely, it doesn’t take long for a genetic mutation conferring resistance to rapidly spread around the world.14
What are the practical implications for pest control programs today—i.e. how should pesticide strategies be changed?
In fact, pesticide advisers15 at the pest control frontline are mostly already operating practically as if with a creationist perspective (even though as individuals they might not realize it, i.e. they might still accept evolution as being true16). They recognize:
Notice that this has no relevance to microbes-to-mankind evolution. This is simply a human-imposed selection process (the same principles are at work with “natural selection”—i.e. no evolution at all).
So what do the pest control experts advise growers to do when faced with loss of pesticide effectiveness? A key resistance management strategy that most farmers are aware of and practice as much as possible, is pesticide rotation.18,19 That is, alternating the use of pesticides that have different modes of action. (I.e., that affect different essential life functions of the pest, e.g. respiration, transmission of nerve signals, etc.) Pesticide rotation works on the principle that when resistance to, say, an organophosphate-based insecticide is beginning to build up in the population, the farmer switches to using, say, a pyrethroid insecticide. Then, as resistance builds up to that pesticide, he switches to a pesticide with a different chemical mode of action again, if one is legally available (e.g. a carbamate).
There have been some instances where “multiple resistance” has developed—the worst case scenario for farmers. However, in no way does this represent evolution, as it involved the same processes as discussed above. The fitness cost of such multiple resistance becomes evident when pesticides are withheld for a period, and non-resistant individuals generally come to dominate the population once more. Thus effective pesticide rotation strategies can begin again.
What are the implications from the day-to-day reality of pest responses to pesticides? Evolution is not in evidence, nor does evolutionary theory have any practical relevance to operational science or farming practise.