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One of the “top arguments” against the creation world view is the well-documented development of insect resistance to insecticides. Many Neo- Darwinists claim that the historical development of pesticide resistance in insects is actually one of the strongest evidences of Neo-Darwinian evolution by mutations: “Insects that survived insecticides did so by helpful genetic mutations, and thus they bred a new generation that was not brought down by the farmers’ poison” (Larry Witham. 2002. Where Darwin Meets the Bible. Oxford University Press p. 78)

This article focuses on the common claim that the development of insect resistance to insecticides provides evidence for molecules-to-human evolution theory and, at its foundation, that such resistance is based on mutations.


The development of insecticide resistance is well documented as a major problem today. Some insects are tolerant to so many insecticide families that chemical control has become almost useless. By 1990, over 500 insect species were known to be resistant to one or more insecticides.

The question is, how did this resistance develop? Several reasons exist for this problem. Firstly, all insects possess many inbuilt complex resistance mechanisms that help them withstand a wide variety of toxins. For example, when exposed to insecticides, they can up-regulate a variety of insecticide detoxifying enzymes.

In some cases, mutations are involved in the development of resistance. For instance, mutations can result in the overproduction of detoxification compounds, producing abnormally high resistance levels (Sabourault et al. 2001. Insect Molecular Biology 10 #6: 609-618).

Other cases are due to the disruption of the toxin-receptor binding or a condition that causes “relatively low receptor concentration in midgut cells” (Nielsen-Leroux et al. 2002. Journal of Medical Entomology 39 # 5: 729-735).

The problem is so common that most insects eventually develop resistance to many insecticides, making control difficult. As Francisco Ayala remarked in 1978: “Insect resistance to a pesticide was first reported in 1947 for the housefly (Musca domestica) with respect to DDT. Since then the resistance to one or more pesticides has been reported in at least 225 species of insects and other arthropods. The genetic variants required for resistance to the most diverse kinds of pesticides were apparently present in every one of the populations exposed to these man-made compounds.” (Scientific American 239 #3 p. 65).

A good example of how resistance develops is the situation observed with DDT. This compound functions by binding to a specific matching site on the membrane of the insect’s nerve cells. When a certain level of DDT binds to the nerve cell membrane, the nervous system no longer is able to function properly. As a result, the insect dies. Any mutation that adversely affects the binding of DDT to the nerve cell, if it is not lethal or almost lethal, has the potential of conferring DDT resistance to the insect. The other side is that the mutation also interferes with the ability of the cell to bind to other products, causing it to be less effective. As a result, the DDT-resistant insect is less able to compete in an insecticide-free environment (the normal, natural environment.)

The means by which insects develop DDT resistance is similar to that of bacterial antibiotic resistance; mutations in insects result in a certain “cost of resistance” or tradeoff, as does bacterial resistance (Cooper and Lefevere. 2002. Heredity 88 # 1: 35-38).

Cost of Resistance

Insects that have become resistant to insecticides by mutations have been shown to be less fit in the wild, a phenomenon called the cost of resistance. The reason why this cost is common is because the resistance that results from mutations normally damages a structure so that it works less effectively at what it was designed to do.

As Gazave et al noted in 2001, resistance alters “some components of the basic physiology” and interferes “with fitness-related life history traits” (Heredity 87 p. 441). The result is a “high fitness cost” that can rapidly wipe out the resistant strains in a normal environment.

For example, pesticide resistance can be a consequence of damage to the cell membrane that results in slowing uptake of the pesticide into the cell and thus preventing cells from accumulating toxic concentrations. In an insecticide-free environment,by Jerry Bergman these insects cannot take in needed materials as effectively and, consequently, the resistant insects are less able to compete, and usually die off more rapidly than the wild type.

As Lenski notes in the 2002 Encyclopedia of Evolution: “the same mutation that confers resistance interferes with some other aspect of the organism’s performance. Such multiple effects of the same mutation are termed pleiotropy in genetics” (volume 2 p. 1009). For example, many resistant insects are less active and slower to respond to various stimuli than other insects.

This effect has been researched most extensively, specifically in the case of mosquitoes. Although the DDT-resistant insect is more fit in the environment in which the insecticide is present, the more sluggish nervous system in the resistant insect causes it to be less fit in a normal, insecticide-free environment.

Nonetheless, prolonged use of insecticides can produce large numbers of resistant insects that, even though they are less fit as a whole, are better able to survive in an environment that contains high levels of DDT. As a result, the resistant population becomes larger in spite of its members’ overall less-effective nervous system. As Levine and Miller note: “resistance to poisons is rarely a ‘free ride’ for either insects or other organisms, because the selective tradeoffs imposed by pleiotropy often maintain polymorphism either within or between populations of a species … the same sort of phenomenon has been demonstrated for the alleles that confer resistance to DDT and to dieldrin in mosquitoes” (Biology: Discovering Life. 1994 p. 257).


The sheep blowfly (Lucilia cuprina) is a common insect pest in Australia that was effectively controlled for years by diazinon insecticide. A mutation eventually appeared that conferred resistance to this compound. Nevertheless the resistance had a clear fitness cost. For example, the resistant flies were “noticeably inferior to their sensitive counterparts in certain other respects, such as requiring a longer time to develop from eggs into adults in the absence of the insecticide” (Lenski p. 1009).

In the blowfly and other insects, it was found that resistant forms have a “higher mortality during colder, wetter and windier weather, caused by a direct mortality through freezing and/or an indirect mortality through maladaptive behaviour” (Gazave et al p. 442). Another resistance mechanism in the blowfy involves certain cytochrome p450s and glutathione S-transferases that help to break down and detoxify toxins in all normal insects. In multiresistant strains, the genes for these proteins are constitutively overexpressed, producing very high levels of detoxification enzymes.

A mutation has been implicated in causing overproduction of the cytochrome p450 protein CYPGA1, evidently by release of the transitional repression controlling genes coding for several detoxification enzymes including CYPGA1 (Sabourault et al). This overexpression costs energy and is advantageous only in an environment that contains the toxin.

Probably the most common example of resistance is the mosquito Culex pipiens, which becomes resistant by overproduction of esterase as a result of either gene amplification or gene regulation abnormalities. In one study by Gazave et al, the authors found that a “large fitness cost (42%)” resulted from the development of insecticide resistance (441).

It is evident that the recent development of insect resistance to pesticides does not support Neo- Darwinism. Macroevolution requires information-building that adds new information to the genome and we do not see that here. In all confirmed cases, insect resistance is a result of the exploitation of existing systems or is due to mutations that result in an organism which is less fit except only in an insecticide environment. In the few cases where a mutation is involved, development of resistance involves only a loss mutation, such as one that produces deformed enzymes.

This finding is confirmed by the fact that insect resistance is usually acquired very rapidly, in far too brief a period for the evolutionary emergence of complex biochemical or physiological systems. Mutation-caused resistance results in less viability in the wild, and as a result the resistant insects usually cannot compete effectively with the wild type in an insecticide free environment. None of this is good news for evolution theory.

Dr. Bergman is based in Archbold, Ohio. A detailed bibliography for this article is available upon request.

Jerry Bergman
April 2004

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