Pesticide resistance is not evidence of evolution


Published: 20 August 2009 (GMT+10) An aeroplane crop-dusting
Since aerial application of pesticides (“crop dusting”) first began in the 1920s, there have been tremendous improvements in knowledge, technology and safety. However, irrespective of the application method used, farmers must face the phenomenon of pesticide resistance.

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:

“It has the menacing sound of an Alfred Hitchcock movie: Millions of rats aren’t even getting sick from pesticide doses that once killed them. In one county in England, these ‘super rats’ have built up such resistance to certain toxins that they can consume five times as much poison as rats in other counties before dying. From insect larvae that keep munching on pesticide-laden cotton in the US to head lice that won’t wash out of children’s hair, pests are slowly developing genetic shields that enable them to survive whatever poisons humans give them.”2 (Emphasis added.)

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:

“Every time chemicals are sprayed on a lawn to kill weeds or ants for example, a few naturally resistant members of the targeted population survive and create a new generation of pests that are poison-resistant.”2 (Emphasis added.)

And again:

“Individuals with a higher tolerance for our poisons survive and breed, and soon resistant individuals outnumber the ones we can control.”2

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:

“Farmers spray higher doses of pesticide if the traditional dose doesn’t kill, so genetic mechanisms that enable the pests to survive the stronger doses rapidly become widespread as the offspring of resistant individuals come to dominate the population.”2 (Added emphasis.)

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.

Rapid resistance in nematodes

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.

The price of resistance

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.

Photo stock.xchng A rat
Warfarin is an anti-coagulant (stops blood clotting) drug, used both in the treatment of human thromboses (unwanted blood clots) and as a poison for rats and mice. Obviously the amounts administered to people are carefully controlled, whereas the aim in giving it to rats is to kill them. It works by interfering with the normal blood-clotting mechanism, such that the normal rapid repair of small blood vessel leakages does not occur. The rat then dies from internal bleeding. Warfarin was first used in Britain in 1953, and was at first extremely effective at killing rodents. But colonies of resistant rats were first noticed in 1959 in Welshpool, then in the United States and continental Europe.

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

Right in line with the Bible

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.

A worm in an apple
The old joke about “What’s worse than finding a worm in your apple?” [Answer: Half a worm!] is no joke for apple producers. The FAO has estimated that pests cost horticultural and agricultural producers thousands of millions of dollars annually in lost production. At least 520 insects and mites, 150 plant diseases and 113 weeds have become resistant to pesticides meant to control them.

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

Not an “arms race”

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

Implications for (rather, from!) effective pest control in today’s world

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:

  • An individual rat or insect or other pest does not develop resistance over time. What changes over time is the susceptibility of a population to a pesticide.
  • Resistance may be present in a population even before being exposed to a new pesticide—but in very low numbers. The resistance mechanism might affect the pest adversely in certain ways. But upon exposure to pesticide, those individuals that have the ability to break down a pesticide molecule that kills most other individuals in the population survive.
  • Individuals surviving a pesticide application pass the genetic mechanisms conferring resistance to that particular pesticide on to the next generation. Thus the resistant genes make up a greater proportion of the total gene pool than they did before.
  • At first, a farmer might not notice a pest population’s increasing resistance to a pesticide. However, with the passage of (pest) generations, there comes a point where the farmer is confronted by “control failure”. But the resistance hasn’t “suddenly appeared”, but rather built up steadily since first exposure to the pesticide.17

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.

Recommended Resources


  1. PBS broadcast the infamous TV series Evolution in 2001, which CMI has rebutted. Return to text.
  2. WGBH Educational Foundation, Evolution Library: Pesticide Resistance, <>, 22 June 2009. Return to text.
  3. Lopes, P., Sucena, E., Santos, M., Magalhaes, S., Rapid experimental evolution of pesticide resistance in C. elegans entails no costs and affects the mating system, PLoS ONE 3(11):e3741, November 2008. Return to text.
  4. E.g., Asser-Kaiser, S., Fritsch, E., Undorf-Spahn, K., et al., Rapid emergence of baculovirus resistance in codling moth due to dominant sex-linked inheritance, Science 317(5846): 1916–1918, 2007. Return to text.
  5. Gazave, E., Chevillon, C., Lenormand, T., Marquine, M., Raymond, M., Dissecting the cost of insecticide resistance genes during the overwintering period of the mosquito Culex pipiens, Heredity 87:441–448, 2001. Return to text.
  6. Hoffmann, A., and Parsons, P., Extreme Environmental Change and Evolution, Cambridge University Press, Cambridge, 1997, p. 100. Return to text.
  7. Chiu, T.-L., Wen, Z., Rupasinghe, S., and Schuler, M., Comparative molecular modelling of Anopheles gambiae CYP6Z1, a mosquito P450 capable of metabolizing DDT, Proceedings of the National Academy of Sciences USA 105(26):8855–8860, July 2008. Return to text.
  8. Yates, D., Team finds key mechanism of DDT resistance in malarial mosquitoes, University of Illinois News Bureau, <>, 16 June 2008. Return to text.
  9. Daborn, P., Yen, J., Bogwitz, M., Le Goff, G., Feil, E., Jeffers, S., Tijet, N., Perry, T., Heckel, D., Batterham, P., Feyereisen, R., Wilson, T., ffrench-Constant, R., A single P450 allele associated with insecticide resistance in Drosophila, Science 297(5590):2253–2256, 2002. Return to text.
  10. Sometimes researchers have stated that resistance mechanisms have “little or no fitness cost” in light of studies where pesticide resistant genes persist in the absence of pesticide selection. (E.g. refs 3 and 7.) However, it is likely that moving resistant individuals into a harsher environment (e.g. beyond the nutrient-rich agar base of a laboratory Petri dish) would reveal a fitness cost in most, if not all, instances. Return to text.
  11. Pesticide resistance has clear parallels with resistance to penicillin in Staphylococcus bacteria (see Superbugs not so super after all and Has evolution really been observed?), where overproduction of penicillinase increases resistance to penicillin. But in the wild, away from artificial (e.g. hospital) environments swamped with penicillin, the Staphylococcus with the “genetic shield” for penicillin resistance would be less “fit” because it wastes energy and resources producing heaps of unnecessary protein. Return to text.
  12. For further explanation on this in relation to warfarin resistance in rats, see: More, E., Rats! Another case of sickle-cell anemia, Creation 17(2):44–45, 1995, <>. Return to text.
  13. This concept was very cleverly expounded by Michael Behe in his 2007 book The Edge of Evolution, Free Press, New York, USA. For a review see Batten, D., Clarity and confusion, Journal of Creation 22(1):28–33, 2008; <>. Return to text.
  14. It is now generally recognized that “resistance genes need not arise de novo to cause problems in a particular region. Through natural migration or human-mediated transport, resistant pests have the capacity to disperse and transfer genes over large areas in very short periods of time.” Denholm, I., Devine, G., and Williamson, M., Insecticide resistance on the move, Science 297(5590):2222–2223, 27 September 2002. Return to text.
  15. E.g., McFadden-Smith, W., Pesticide Resistance—How it happens and how you can delay it, OMAFRA, <>, 2 December 2008; and Murphy, G., Managing Fungicide Resistance, OMAFRA, <>, 1 March 2006. Return to text.
  16. A classic example of this is Philip Batterham (ref. 9), Professor of Genetics at the University of Melbourne, Australia. He said recently, “I work on insecticide resistance and it is probably one of the very best examples of evolution in short time frames”, and yet his qualifying remarks, when asked how insects could change in such a rapid time, indicate no molecules-to-man-type evolution in evidence at all: “They have a lot of genetic diversity. They have genes that sit there and are primed to provide resistance with minor modifications, … ”. ABC Radio National The Science Show segment entitled ‘Darwin Year—2009’, , broadcast 29 November 2008. It’s also worth noting that Professor Batterham spoke at a church service at St Paul’s Cathedral Melbourne (Australia) on 8th February 2009 as part of a celebration of “Evolution—The Festival”; see—the-intersection (last accessed 20 July 2009).  Return to text.
  17. Murphy, G., Pesticide Resistance 101, OMAFRA,, 1 November 2005. Return to text.
  18. Murphy, G., Resistance Management—Pesticide Rotation, OMAFRA,, 1 December 2005. Return to text.
  19. Carter, N., Rotation helps prevent resistance, OMAFRA,, 1 December 2002. Return to text.

Helpful Resources

Refuting Evolution
by Jonathan Sarfati
US $10.00