In this entry, I will review the history of evolutionary and ecological genetic of research, with the emphasis on the latter. Most investigations have focused on two of the most prominent patterns in nature: (1) adaptation, or the ‘fit’ between organism and environment; or, (2) polymorphism, the maintenance of two or more phenotypic or genetic forms in a single population. The earliest studies attempted to document the action of natural selection in wild populations in support of Darwin. While natural selection is the only evolutionary force that can account for adaptation, several evolutionary forces, acting alone or in combination, can sustain a polymorphism, at least transiently. Thus, assigning causal agency is a much more difficult problem for explanations of polymorphism than it is for adaptation. Conspicuous phenotypic polymorphisms, such as the spotting patterns on butterfly wings or banding patterns of snail shells, were the material of the earliest investigations of natural populations. In these studies, natural selection was ‘privileged’ among the four evolutionary that change gene frequencies as an explanation for the maintenance of polymorphisms. I will show that the continuing emphasis on detecting natural selection is, at least in part, historical with its roots in the works of its founder, E. B. Ford, and his collaborators, notably R. A. Fisher (cf., Ford 1975). In the beginning period (1928-1950), much of the problem of assigning causal agency to the maintenance of genetic polymorphism was resolved by definition rather than by empirical observation (see below: Classical Ecological Genetics and Polymorphism). In the later period (1966-present), molecular ecological genetics attempts to investigate a less biased sample of genetic polymorphisms, such as allozymes and single nucleotide polymorphisms, but still retains the early emphasis on natural selection as the single most important evolutionary force shaping the hereditary material.
Ecological genetics began at a time when the major theoretical aspects of the Modern Synthesis were in place, when the marvels of adaptation were clear, but when few empirical examples of natural selection in action were available. Adaptive perfection by Fisherian gradualism requires long periods of time wherein “… a very slight selective effect acting for a correspondingly long time will be equivalent to a much greater effect acting for a proportionately shorter time” (R. A. Fisher 1921, in correspondence with S. Wright, quoted in Provine , p. 247). Very weak natural selection, however, is an impediment to the goal of ecological genetics to illuminate natural selection in action. Thus, the shift in focus to understanding the role of strong natural selection in maintaining genetic polymorphism is understandable. As put by its founder, E. B. Ford (1975, p.3), “It [ecological genetics] supplies the means, and the only direct means, of investigating the actual process of evolution taking place in the present time.”
The focus of traditional ecological genetic research on the current action of natural selection has been broadened in several ways over the past twenty-five years. First, whereas the early studies tended to focus on evolution in single populations, there is now a significant emphasis in ecological genetics on the population genetic structure of metapopulations and the roles of migration, extinction, and colonization on evolutionary and adaptive processes. Secondly, whereas the earliest studies emphasized chromosomes and their influence, the advent of biochemical genetics in the late 1960s significantly broadened the phenotype, beginning with the application of electrophoretic methods to population studies. These studies revealed abundant ‘hidden polymorphism’ in the new, biochemical phenotype of enzyme mobility. These methods extended the domain of ecological genetics from the classic ‘conspicuous phenotypic polymorphisms’ in color, shape and behavior to the physiological domain of enzyme function. The new emphasis on biochemical phenotype, however, did not change the explanatory or causal framework of the field. Determining the role of natural selection in maintaining enzyme polymorphisms, such as the fast/slow polymorphisms of alcohol dehydrogenase (which detoxifies environmental alcohol), superoxide dismutase (which catalyzes the removal of free oxygen radicals), or the esterases (which are involved in the detoxification of pesticides by many insects), became a primary focus of investigation with the goal of finding a selective basis for the enzyme variants in terms of differences in their physical and kinetic properties. Indeed, the roots of controversy between the selectionist and neutralist schools over the maintenance of ‘balanced’ polymorphisms (cf. Lewontin 1974) lie in the controversy over random genetic drift versus natural selection in early ecological genetic research (see below). Thirdly, the more recent advent of DNA sequencing initiated the growth of molecular phylogenetics and added not only a new phenotype, but also a more pronounced historical dimension to ecological genetic research. Molecular phylogenics and comparative sequence analysis have become the primary modern tools for the investigation of the evolutionary patterns and processes that shape DNA sequences. These methods have strengthened inferences regarding biogeography, speciation, and adaptation, especially in regard to the diversification of taxonomic lineages that attends ecological release and adaptive radiations. They have shifted the focus from polymorphism within species to diversification among clades and permitted the investigation of the history of individual genes. Two new patterns in particular have been recognized by these DNA-based methods. The first is the preponderance of ‘purifying selection’, wherein the conservative power of natural selection is seen as a barrier to diversity. It is this conservative aspect of natural selection acting at the molecular level that lends power to the investigation of the genetic architecture of model organisms vis a vis human genetics. The second pattern is the discovery of the existence of ancient polymorphisms, molecular genetic variation whose duration may be greater than that of the species or taxon in which it was discovered. Natural selection, however, still remains the privileged explanatory force in modern sequence studies. Indeed, the search for and documentation of uniquely molecular patterns, such as codon bias and selective sweeps, has, if anything, elevated the focal explanatory power of natural selection in evolutionary studies.
In this entry, I will first review classical ecological genetics and then discuss the novel kinds of processes and explanations that accompanied the expansion of the field from single populations to genetically structured metapopulations and from phenotypic to biochemical and DNA sequence polymorphisms. I will show that the central early controversy over the roles of random genetic drift and natural selection in evolution has continued to this day, not withstanding the apparent technological refinements afforded by the availability of biochemical and DNA sequence data. That is, finer scale or more reductionistic genetic data has not yet led to a resolution of the original conceptual issues that lie at the foundation of ecological genetics.
2. Classical Ecological Genetics and Polymorphism
Historically, the starting point of ecological genetic research has been the discovery of variation within a natural population, i.e., a phenotypic polymorphism. The subsequent goal is three-fold: (1) determination of whether or not the polymorphism has a genetic component; (2) determination of the frequency of each of the polymorphic types; and, (3) determination of how natural selection maintains the polymorphism, either alone or in combination with other evolutionary forces. Ford (1975 p. 109; and see also Ford 1940) defines genetic polymorphism as “…the occurrence together in the same locality of two or more discontinuous forms of a species in such proportions that the rarest of them cannot be maintained merely by recurrent mutation”. Although recurrent mutation in conjunction with mutation can maintain a polymorphism indefinitely at mutation-selection balance, here Ford is clearly interested in a more active role for natural selection in the maintenance of polymorphism. The first task was facilitated by early developments in population genetic theory, particularly the findings of Fisher (1930), which Ford interpreted to mean that naturally occurring, discontinuous phenotypic variation is “nearly always genetic”. The reasoning stems from the theoretical findings that, in large populations, it is unlikely that the positive and negative effects of an allele (or chromosomal inversion) on fitness will be exactly balanced and that the number of individuals with a rare neutral mutation is proportional to the number of generations since its origin. Furthermore, if truly neutral, such alleles would spread so slowly through a large population by random genetic drift that the ‘delicate equipoise required for their neutrality will have been upset by changes in the environment and in the genetic outfit of the organism’ (Ford 1975, p. 110) before a neutral allele reached appreciable frequency. In addition, recurrent mutation as a cause of persistent polymorphism was considered most unlikely and, in fact, this evolutionary cause is explicitly excluded from the definition of genetic polymorphism by Ford (see above). Hence, neutral genetic polymorphism was considered an exceptionally rare event by the founders of ecological genetics and, consequently, such polymorphisms were the hallmark of strong, active natural selection.
Ford (1940) further distinguished two types of selective polymorphism, transient polymorphism and balanced polymorphism.Transient polymorphism, caused by a new favorable mutation in the process of displacing its ancestral allele, was considered unlikely, because “…advantageous genes will usually have been already incorporated into the genetic constitution of the species” (Ford 1975, p. 110). This and statements like it reflect the viewpoint that organisms in nature are exquisitely adapted to their environments by the long-acting process of Fisherian gradualism. It is a prelude to the more explicitly adaptationist views found in the current behavioral literature (see review in Shuster and Wade 2003). This view of the evolutionary process as primarily one of refinement of existing organismal adaptation is an essential part of the Fisherian theory of evolutionary genetics (Wade and Goodnight 1998).
The presumptions of a genetic basis for discontinuous phenotypic polymorphism and its maintenance by natural selection are clear from the writings of Ford cited above but these principles also can be found together in a single statement: “In view of these considerations it is clear that if any unifactorial character is at all widespread it must be of some [adaptive] value. Indeed, it is probably true that even if it occurs at as low a frequency as 1 per cent, it must have been favored by selection” (Ford 1975, p. 110). Thus, the primary goal of the ecological geneticist is to discern exactly how natural selection is acting to maintain a balanced polymorphism by the relative strength of opposing fitness effects acting on the different sexes or at different stages in the life history of the organism.
The existence of males and females was discussed by Ford as a prime example of a balanced polymorphism because, “It is obvious that any tendency for the males to increase at the expense of the females, or the reverse, would be opposed by selection” (Ford 1975, p. 111). Fisher (1930) first argued that, because every individual has a mother and a father, the mean fitness of males must be equal to the mean fitness of females multiplied by the sex ratio, expressed as the number of females to males (i.e., the mean number of mates per male; see also Shuster and Wade 2003, Chapter 1). As a result fitness increases with rarity, and, in this circumstance, whenever the population sex ratio deviates from unity, a gene that increases the numbers of the minority sex at birth will have a selective advantage. Thus, a sex ratio of unity is a stable, balanced polymorphism, achieved in many species by chromosomal determination of sex, which Ford referred to as a “‘built-in’ genetic switch-mechanism”, characteristic of other genetic polymorphisms, like Batesian mimicry. In general, the fitnesses of the different types constituting a phenotypic polymorphism must be equal to be maintained within a population by natural selection at a non-zero equilibrium frequency (a point recognized by Darwin 1874, p. 275). However, the balance of selective forces for non-sex related (or even sex-linked) polymorphisms is very different from that required to maintain an equal sex ratio, namely, the necessity that each offspring inherit equally from each sex parent. Using the existence of the separate sexes as an example of a balanced polymorphism is misleading or, at least unrepresentative, of the selective forces necessary to sustain balanced polymorphisms in general.
3. Classical Ecological Genetics, Population Size, and Natural Selection
The founding ecological geneticists dismissed any significant role for random genetic drift in evolution. The theoretical interaction of random genetic drift and natural selection for single genes with constant effects can be seen in Figure 1. Fisher in his evolutionary theory assumed that natural populations achieved or sustained the very large sizes as seen in his in correspondence with S. Wright (cited in Provine 1971) where he stated that “I believe N must usually be the total population on the planet, enumerated at sexual maturity”. Similarly, according to his intellectual biographer W. Ewens (2000, p. 33): “Fisher never paid much attention to the concept [effective population size] as he should have … and used extremely high population sizes (up to 1012) in his analyses, surely far too large in general.” For such extremely large population sizes, the threshold between selection and drift (see Fig. 1), which is determined by the effective population size, Ne, is much lower. As a result, the strength of random genetic drift, which is proportional to (1/2Ne), is very, very weak and even genes with very small values of s have their evolutionary fate determined entirely by selection. This is the essence of “Fisherian gradualism” — very small selective forces given sufficient time can have effects on adaptation similar to those of genes with much larger effects acting over a shorter time period. With very large Ne, the domain of random genetic drift is greatly restricted even as that of natural selection is expanded (see Fig. 1).
Figure 1. The interaction of Random Genetic Drift and Natural Selection. The strength of selection is measured by the selective effect, s, of a single gene and the strength of random genetic drift is indicated by (1/2Ne), where the population has effective size, Ne. When s exceeds (1/2Ne), then the evolutionary fate of a gene is determined primarily by Natural Selection. When s is less than (1/2Ne), then the evolutionary fate of a gene is determined primarily by Random Genetic Drift. Thus, the evolutionary domains of natural selection (upper) and random genetic drift (lower) are separated by the wavy boundary determined by the effective population size.
However, ecological geneticists did not dismiss random genetic drift as a significant evolutionary force for the same reasons that Fisher did. Field observations conducted with the mark-recapture methods developed by ecological geneticists documented generation-to-generation fluctuations in population size up to or exceeding an order of magnitude in most natural populations studied long term. Thus, small local population sizes were not seen as unusual by ecological geneticists. Indeed, Ford believed that “… organisms automatically generate their own cycles of abundance and rarity and that the changes in selection pressure with which these are associated many greatly increase the speed of evolution” (Ford 1975, p. 36). Despite the not infrequent occurrence of small population sizes where drift would be expected to be most efficacious, random genetic drift was considered an irrelevant evolutionary force in ecological genetics because natural selection was viewed as being particularly strong during periods of population decline. The smallest populations showed little phenotypic variation, which was seen as evidence that they were the most fit or most finely adapted populations. The stressful environmental conditions responsible for the decline in numbers also were seen as causing particularly strong natural selection. Thus, the lack of phenotypic variation in small populations was owing to it having been eliminated by natural selection during the immediately prior period of decline. Conversely, under periods of population increase, natural selection was seen as weaker and more permissive of variation. This concept of relaxed selection provided Ford with a cause for the increase in observations of rare phenotypic variants in large and growing natural populations. If selection pressure increases inversely to population size, then the role of random genetic drift in evolution must be greatly restricted.
In addition, Ford (1975, p. 38) considered that ecological genetic research had clearly demonstrated that the selective advantage of a gene in nature ‘… quite commonly exceeds 25 per cent and is frequently far more …” Referring to Figure 1, this means that the range for values of s in natural populations lies significantly above 0.01, placing genes in very small populations firmly in the domain governed by natural selection.
Furthermore, Ford considered that not only the strength but also the nature of selective pressures must frequently change with density because “… an organism has not the same adaptive requirements when abundant as when rare, or when the plant and animal forms which impinge on it are so” (Ford 1975, p. 39). Indeed, he thought that the fluctuating selection pressure caused by variations in abundance ‘invalidates’ Wright's Shifting Balance Theory of Evolution, which he referred to as ‘far-fetched’. Interestingly, Ford and his colleagues believed that genetic subdivision of the sort postulated by Wright would promote rapid evolution but for very different genetic reasons and by different genetic mechanisms (natural selection instead of random genetic drift, local selection, and interdemic selection). Ford (1975, p. 40-44) argued that subdivision of a large, geographically extensive population into relatively small groups promotes rapid evolution because, “… when populations occupy a series of restricted habitats they can adapt themselves independently to the local environment in each of them, while when spread over a larger area they can be adjusted [by natural selection] only to the average of the diverse conditions which obtain there. This, however, requires that the adaptations should not be constantly broken down by a trickle of immigrants from one small colony to another”. Here, he proposes a trade-off between specialized adaptation to local conditions in the absence of migration and generalized adaptation to global conditions in the presence of migration. In modern terms, this is called genotype-by-environment interaction, where the selective effect, s, of a gene changes with change in the environment. A gene might be adaptive in one environmental context (i.e., s > 0) but maladaptive in another (i.e., s < 0). Migration between local environments mixes the adaptive and maladaptive responses to selection and reduces the average magnitude of gene frequency change. In this sense, genotype-by-environment interaction is viewed as an evolutionary constraint because is limits the rate of gene frequency change. The restraint can be removed simply by stopping gene flow or the mixing of genes across different local environments. Thus, the fixed selective effect illustrated in Figure 1, must be considered an average selective effect across environments. Clearly, large local effects of opposite sign must be averaged when there is gene flow among habitats and the averaging tends to reduce the gene's selective effect. Ford also suggests that the genetic mechanism involves “gene complex[es] balanced to fit their own local environment”. That is, he claims interactions among genes, or epistasis, contribute to local adaptation. Thus, Ford invokes genotype-by-environment interactions for fitness as well as gene-gene interactions for fitness in his cases of rapid evolution. Both of these kinds of interactions change the depiction of the threshold separating natural selection from random genetic drift (Figure 1) in important ways (see below). Before turning to interaction effects, I will examine a representative discussion of ecological genetics of random genetic drift using data from a natural population.
4. The Sewall Wright Effect
Several wing coloration variants segregating in a small natural population of the moth, Panaxia dominula (Fisher and Ford 1947), were investigated using mark-recapture in one of the longest continuous studies of a single population in evolutionary research. The goal of Fisher and Ford was to determine whether year-to-year fluctuations in the frequency of the variants (medionigra, a heterozygote, and bimaculata, a homozygote) were better explained by natural selection or by random genetic drift. They inferred from their analysis
“The conclusion that natural populations in general, like that to which this study is devoted, are affected by selective action, varying from time to time in direction and intensity and of sufficient magnitude to cause fluctuating variations in all gene frequencies is in good accordance with other studies of observable frequencies in wild populations. We do not think, however, that it has been sufficiently emphasized that this fact is fatal to the theory which ascribes particular evolutionary importance to such fluctuations in gene ratios as may occur by chance in very small isolated populations… Thus our analysis, the first in which the relative parts played by random survival and selection in a wild population can be tested, does not support the view that chance fluctuations can be of any significance in evolution.”
With this paper, Fisher and Ford moved the long-standing debate between Wright and Fisher over the relative roles of natural selection and random genetic drift in evolution from theory to nature. It is remarkable that, in the first such study with only eight years of observations on a single locus with alternative alleles, they are confident in rejecting Wright's theory and random genetic drift in its entirety. In his response (Wright 1948), Wright pointed out, first, that his theory of evolution explicitly involved the simultaneous action of several forces (selection, drift, mutation, and migration) and he emphatically rejected the paradigm of Fisher and Ford that either selection or drift alone had to be responsible for all of the observed fluctuation in gene frequencies. Wright noted that, in order to reach their statistical conclusion, Ford and Fisher had to include gene frequency data from a decade before the more careful study, notably a period without any estimates of population size. Without this earlier data point, the average fluctuations were much smaller and not significant. He pointed out that, like the mark-recapture estimates of population numbers, the gene frequencies themselves were estimates whose variation, based on the reported sample sizes, accounted for more than half (55.2%) of the observed variance that Fisher and Ford were trying to explain. He then showed that, if one assumed only the unitary explanation of natural selection, then the observed gene frequency fluctuations were so large even without the sampling variance that the temporal variations in the allelic selection coefficients must range from near lethality (or sterility) to tremendous advantage (i.e., -0.50 to +0.50). However, Fisher and Ford (1947) provided no indication of comparable levels of temporal variation in any environmental factor acting as a selective agent. Wright argued that the effective population sizes used in the analysis were almost certainly too large, possibly by an order of magnitude, and that Fisher and Ford had made no attempt to estimate the factors expected to reduce effective size, like temporal variation in breeding numbers, non-random mortality among larvae (mortality clustered within families as might affect a species which experiences > 85% pupal mortality owing to viral infection), or other causes of the variance in offspring numbers (such as variation among females in egg numbers or variation among males in mate numbers). In an unyielding reply, Fisher and Ford (1950) labeled chance or random fluctuations in gene frequency, the Sewall Wright Effect, a term which has endured to the present day as a synonym for random genetic drift.
With a larger data set covering several more years, Ford (1975, p. 146) revisited this exchange and argued that Wright remained wrong on each count. Ford also showed that the selective advantage for the rarer of the genes varied widely, from -0.10 to +0.20, and that there was no evidence of heterozygote advantage. He did not find, however, the expected negative correlation between strength of selection and population size in these data. In the intervening decades, data from a variety of other organisms and natural population had become available and its review led Ford (1975, p. 389) to conclude: “As a result, it is no longer possible to attribute to random genetic drift or to mutation any significant part in the control of evolution.” Thus, throughout its founding period, ecological genetics was relentlessly supportive of natural selection as unitary explanation for evolutionary change. (Later laboratory research has shown that the expression of the color patterns is sensitive to the thermal environment during development and thus the gene frequency estimates may be subject to significant measurement error, owing to the misclassification of genotypes. This is yet another source of variation, not accounted for in the Ford analyses. In addition, empirical evidence has found, as Wright expected, that temporal fluctuations in population size, large variance among females in fecundity, and sexual selection reduce the effective number to less than half the Fisher-Ford estimate. In addition, more careful studies have reduced Ford's estimates of the magnitude of the average genic selection coefficient by about two thirds [cf. Cook and Jones 1996].)
5. Interactions and their Effect on the Threshold between Natural Selection and Random Drift
The existence of either genotype-by-environment interaction (G × E) or gene-by-gene interaction (epistasis or G × G) greatly complicates the estimation of selection coefficients. Ecological geneticists like Ford postulated interactions of the sort that could change the sign of genic selection coefficients with changes in the environment (including density) or in the genetic background. This kind of reversal of selective effect requires what is known as a ‘crossing-type’ norm of reaction for G × E or additive-by-additive epistasis for G × G (Wade 2002). The simplest model of crossing-type G × E, consists of additive selection (i.e., genotypic fitnesses of 1 + 2s, 1 + s, and 1 for genotypes AA, Aa, and aa, in one environment and the opposite order in the second environment) in each of two alternative environments, E1 and E2, with frequencies, fE1 and fE2, respectively. As the two environments fluctuate in frequency, spatially or temporally, the selective effect of an A allele changes in both magnitude and sign (see Figure 2). Depending upon the relative frequencies of the alternative environments and the amount of gene flow or migration between them, the A allele on average can be a ‘good’ gene or a ‘bad’ gene, a gene of major effect or minor effect, or even a neutral gene if the two environments are equally abundant. The smaller the amount of migration between the environments, the greater is the degree of local adaptation to each as Ford suggested (see above). However, the average selective effect of the gene in the sense of Fisher's theory must be smaller than the average observation in a particular locality at a particular time because the long-term average contains both positive and negative values of s. Furthermore, to the extent that the local value of s changes sign owing to continuous fluctuations in local environmental conditions, the A allele will also move from the domain of selection to the domain of drift as Wright suggested. Thus, the very kind of population subdivision imagined by Ford, with selection acting in every locality albeit in different directions, creates, rather than eliminates, the opportunity for random genetic drift.
Figure 2. The interaction of Random Genetic Drift and Natural Selection, when there is either genotype-by-environment interaction or additive-by-additive epistasis (see text). The selective effect, s, of a single gene changes magnitude as the frequency of the alternative environments, fE1 and fE2, connected by gene flow, changes or as the frequency of alternative alleles, pB and pb, change at an interacting locus. Thus, neither the selective effect of a gene nor the effective population size remains constant. As a result, relative to Figure 1, the threshold boundary between the domains of Natural Selection and Random Genetic Drift is greatly widened, meaning that both forces play more or less equal evolutionary roles over a broad range of values of s and Ne. Furthermore, interactions of this sort open the possibility that changes in the relative frequencies of alternative environments or alternative alleles at other loci can move a gene's selective effect from the domain of selection that of drift or vice versa during the course of its evolution.
A very similar effect on the ‘gene's eye view’ of selection is caused by additive-by-additive epistasis (Goodnight and Wade 2000; Wade 2001, 2002). The simplest model of this kind of G × G, with interaction between loci A and B, each with alternative alleles, results in an average genic selection coefficient acting on the A allele of s(pB − pb). The relative frequencies of the alternative alleles at the B locus, determine whether the A allele is a ‘good’ gene or a ‘bad’ gene, a gene of major effect or minor effect, or even a neutral gene when the alleles are equally abundant (i.e., pB = pb). Whenever allele frequencies of its epistatic partner change, either by drift or selection, the A allele's selective effect also changes and, like the case of G × E, it moves between the domains of natural selection and random drift (Figure 2).
6. Allozyme Variation and the Drift vs Selection Controversy
The central problem with using conspicuous polymorphisms for investigating the relative roles of the variety of different evolutionary forces is that it is not an unbiased sample of genetic diversity with respect to either degree of adaptive function or amount of genetic variation. Indeed, the definition of genetic polymorphism adopted by Ford (see above) incorporates the essence of both of these biases. For a period, it was believed that “The solution to our dilemma lies in the development of molecular genetics” (Lewontin 1974, p. 99). With the advent of electrophoresis, the amino acid sequence of a random sample of proteins from almost any organism could be studied and, for the first time, the level of genetic diversity, in the form of amino acid substitutions, across the genome could be quantified.
Two measures of genetic diversity were possible using electrophoresis: (1) the number of loci polymorphic; and, (2) the average heterozygosity per an individual. From studies across a number of species, it was estimated that 15-40% of all loci were polymorphic and the average individual was heterozygous at 5-15% of its genome. Since this technique measured primarily amino acid substitutions resulting in charge changes, i.e., only one third of all possible amino acid substitutions, one could infer that these were minimal levels of genetic diversity. The conclusion that genetic variation was ubiquitous, with most genes being polymorphic, was inescapable. The search for the adaptive function of allozyme variants and balancing selection at the physiological level ensued.
However, these levels of genetic polymorphism appeared to be much too large to be explained by the type of balancing selection observed by Ford and his colleagues for conspicuous phenotypic polymorphisms in natural populations. The basic problem was that the numbers of selective deaths necessary to account for the observed levels of allozyme polymorphism exceeded the reproductive excess of almost all species. Haldane (1957) called this the “cost of natural selection” and it is also referred to as the substitutional load. Differently put, the mortality of homozygous genotypes, if independently selected, (also known as the ‘segregation load’) would exceed the total numbers of offspring produced by a popualtion. For this reason, Kimura (1983) proposed his neutral theory of molecular evolution, founded on the theoretical observation that the probability of fixation of a novel mutant allele with selective coefficient, s >0, was approximately 2s. Thus, the probability of loss of even a favored mutation was, for small s, only slightly smaller than the probability of loss by chance for a truly neutral allele. Studies of protein structure also revealed that the functional sites of a protein, which constitute the minority of its amino acids, evolved several times more slowly than the non-functional or structural sites. The view that much, if not most, of evolutionary change at the molecular level was determined by random genetic drift and not natural selection was highly controversial. As Kimura noted (1983, p. 22), “…if a certain doctrine is constantly being spoken of favorably by the majority, endorsed by top authorities in their books and taught in classes, then a belief is gradually built up in one's mind, eventually becoming the guiding principle and the basis of value judgment. At any rate, this was the time when the panselectionist or ‘neo-Darwinian’ position was most secure in the history of biology: the heyday of the traditional ‘synthetic theory’ of evolution.”
It was soon recognized that a more reductionistic approach (DNA sequence studies) might help to resolve the issue of whether or not every amino acid was of some functional value because the redundant positions in the code of life were assumed to provide an estimate of the true ‘neutral’ rate of evolution, owing to random genetic drift acting in the absence of selection.
7. Sequence Variation and the Drift vs Selection Controversy
The neutral theory of evolution is the antithesis of ecological genetics. It states that random genetic drift, rather than natural selection, governs most evolutionary change at the level of the DNA and proteins, while admitting that natural selection predominates in shaping the morphological and physiological traits that manifest an adaptive fit with the environment. This is a paradox because most of the DNA appears to be non-functional while most of the externally observable phenotype appears to have adaptive function.
Tests of the theory using DNA sequence data consist of comparisons of the relative evolutionary rates of different kinds of sites (base pairs) within codons and take advantage of the redundancy in the genetic code. The rate of neutral evolution is estimated from levels of polymorphism or numbers of segregating sites within species or the divergence between species in silent or redundant site substitutions. Silent sites are those that do not result in an amino acid change in the protein and, hence, are non-functional in the usual sense. In contrast, the rate of selective change or selective constraint is evaluated relative to the neutral rate using replacement sites, those base pair changes that result in amino acid changes. If the rate of substitution or polymorphism is lower than neutral, it is evidence of selective constraint or purifying natural selection acting to prevent change and preserve function in the face of mutational damage. If the rate of substitution is higher than neutral, then it is evidence of adaptive substitution.
Molecular evolutionary studies also revealed the existence of pseudogenes, non-coding stretches of DNA derived by the tandem duplication and subsequent inactivation by mutation of single copy genes. The lack of function of the pseudogene makes all of its codons effectively neutral and provides another estimate of the rate of neutral evolution. Importantly, ‘replacement’ sites that evolve slowly in the functional gene have been shown to evolve more rapidly in the nonfunctional tandem duplicate pseudogene.
Changes in the pattern of neutral variation in the vicinity of a selected site(s) are also informative because, during an adaptive substitution, neutral variants linked to the piece of selected DNA are carried or ‘swept’ to fixation along with it. This ‘selective sweep’ temporarily reduces the level of neutral variation in the vicinity of selected sites until it can be replaced by mutation. The degree of reduction in neutral variation or the ‘footprint of selection’ depends upon the strength of selection, the frequency of recombination during selection, and the time since the initiation of selection. The footprint is most conspicuous when a selective sweep is initiated by the advent of a single, novel favorable mutation. To the extent that novel selection results from a change of environment and begins to act on existing or standing variation already in the population, the impact on neutral polymorphisms may be quite minimal. Balancing selection of the sort observed by Ford leaves its own unique ‘reverse’ footprint on neutral diversity. Because the segments of DNA constituting the balanced polymorphism are held in the population by selection much longer than expected based on random drift, these segments have a higher effective population size (owing to lower variation in offspring numbers than random) and tend to accumulate mutational variation at nearby neutral sites. Thus, levels of neutral diversity are expected to be enhanced in the vicinity of a molecular balanced polymorphism. When the mating system restricts recombination (e.g., in selfing or inbreeding species), the region of elevated neutral diversity in the vicinity of a balanced polymorphism can be extensive.
Kimura predicted that silent substitutions would evolve more rapidly than replacement substitutions before sequence data were available to test his neutral theory of molecular evolution. Molecular genetic studies have confirmed his prediction: silent sites evolve several times faster than replacement sites. These studies clearly show that the primary mode of action of natural selection at the level of the DNA sequence is purifying selection. It is this highly conservative aspect of natural selection that permits comparative molecular evolutionary studies of developmental processes across species as diverse as humans and flies. At the molecular level, most genes, though polymorphic in sequence, do not display evidence of balancing selection and instead manifest patterns of variation that accord well with neutral theory.
The interaction of selection and random drift across linked regions of DNA sequence is one of the most active current areas of theoretical and empirical research in molecular evolution. Theory shows that it can be difficult to separate cleanly the action of the evolutionary forces of selection and drift except for certain regions of parameter space, whose generality remains unknown and subject to much debate. Like the study by Fisher and Ford (1947), most empirical studies interpret all deviations away from strictly the neutral expectation as evidence of natural selection without addressing the issue of agency. Thus, nonrandom or biased use of redundant codons in some regions of DNA sequence has been documented. Codon bias is seen as evidence that, although they have no effect on amino acid sequence, redundant codons are not all functionally equivalent. This is taken as evidence that natural selection is all powerful, reaching down into the genome to affect even the smallest and least significant components of the hereditary material. Thus, the original ecological genetic view that natural selection is the only significant evolutionary force characterizes much of molecular evolution, despite progress in theory and the availability of much more reductionistic genetic methods. The parallels between the summary statement of Ford (1975, p. 389; see above) and that of the molecular evolutionary geneticist, E. Nevo (2001, p. 6223), twenty-five years later are remarkable: “Biodiversity evolution, even in small isolated populations, is primarily driven by natural selection, including diversifying, balancing, cyclical, and purifying selective regimes, interacting with, but ultimately overriding, the effects of mutation, migration, and stochasticity.”
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- Huxley, J. 1942. Evolution the modern synthesis. Harper & Brothers, New York.
- Kimura, M. 1983. The neutral theory of molecular evolution. Cambridge: Cambridge University Press.
- Lewontin, R. C. 1974. The genetic basis of evolutionary change. New York: Columbia University Press.
- Nevo, E. 2001. "Evolution of genome-phenome diversity under environmental stress." Proc. Natl. Acad. Sci. (USA), 98:6233-6240.
- Provine, W. B. 1971. The origins of theoretical population genetics. Chicago: University of Chicago Press.
- Provine, W. B. 1986. Sewall Wright and evolutionary biology. Chicago: University of Chicago Press.
- Shuster, S. M. and M. J. Wade. 2003. Mating systems and strategies. Princeton: Princeton University Press.
- Wade, M. J. 2001. "Epistasis, complex traits, and rates of evolution." Genetica, 112: 59-69.
- Wade, M. J. 2002. "A gene's eye view of epistasis, selection, and speciation." J. Evol. Biology, 15:337-346.
- Wade, M. J., and C. J. Goodnight. 1998. "Genetics and adaptation in metapopulations: When nature does many small experiments." Evolution, 52:1537-1553.
- Wright, S. 1948. "On the roles of directed and random changes in gene frequency in the genetics of populations." Evolution, 2:279-294.
As our understanding of genetics has improved, it has become increasingly clear that mutations + time + chance do not equal evolution.
We have no acceptable theory of evolution at the present time. There is none; and I cannot accept the theory that I teach to my students each year. Let me explain. I teach the synthetic theory known as the neo-Darwinian one, for one reason only; not because it’s good, we know it is bad, but because there isn’t any other. Whilst waiting to find something better you are taught something which is known to be inexact, which is a first approximation …
–Professor Jerome Lejeune, in a lecture given in Paris
on March 17, 1985, translated by Peter Wilders
What You Will Learn
Textbooks present evolution in two different ways—small, observable changes (natural selection, speciation, adaptation) and large, unobservable changes (molecules-to-man evolution). They show evidence for the former and then conclude that this proves that the latter took place as well.
As our understanding of genetics has improved, it has become increasingly clear that mutations + time + chance do not equal evolution. All observed mutations demonstrate a loss of genetic information from the genetic code, or they are neutral. Evolution claims that the process has no direction or goal. If you look at the complexity of the “first” organism, it must be accepted that a massive amount of information has been produced to explain the variety of life we see today. Mutations cannot generate new genetic information; so they cannot be used to explain how evolution has proceeded from a cell with less information than is present in modern cells.
Despite the claims of evolution, the appearance of new species, antibiotic resistance in bacteria, pesticide resistance, and sickle-cell anemia are not evidence in favor of evolution. They do, however, demonstrate the principle of natural selection acting on existing traits—a concept that creationists and evolutionists agree on. The creationist model of how life spread across the globe after the Flood of Genesis uses many of the same principles of natural selection and adaptive radiation that are used in the evolution model. One of the main differences is that the biblical creation model recognizes that one kind cannot change into another and that the changes are a result of variation within the created kinds—not descent from a single common ancestor. As a result of the Curse, genetic mutations, representing a loss of information, have been accumulating, but these do not cause new kinds to emerge. Accepting the idea of a single common ancestor denies the authority of God’s Word.
What Your Textbook Says about Natural Selection and Evolution
|Evolution is believed by most scientists and is the unifying theory of biology.||9–10, 392–393||T290, T343||T366–367, 367, 369, 386, 410||T6, 9, 276, 283, T410– 411||3:1, 3:7|
|Evolution is not observable on a human timescale.||396–397||—||447||—||3:2, 3:7, 3:11, 3:13, 3:19, 3:24, 3:27, 3:28|
|Origin of Species provided a unifying explanation for the history of life on earth.||396||39, 297||374–375, T374, 378–379||277– 280||3:1, 3:3, 3:4, 3:13, 3:24|
|Genetic drift in isolated populations||280||327–329||T371, 372, 400, 404– 405, T405, 406–409, T407–T409, 439||281, 292, 328||3:5, 3:10, 3:11, 3:12, 3:13, 3:15, 3:22|
|All life has a single common ancestor.||—||304||369||283||3:6, 3:7, 3:8, 3:13, 3:19|
|Mutation is the raw material for evolution.||—||310, 314, 243||17, 308, 392, 394– 395, T406, 406–409||147, T160, 281, 416||3:1, 3:10, 3:13, 3:15, 3:16, 3:19, 3:21, 3:22, 3:23, 3:28|
|Mechanisms of evolution||—||—||T262, 376, T376, 393, 401||326, 329, T330||3:10, 3:11, 3:12, 3:13, 3:15, 3:16, 3:19, 3:22, 3:23, 3:27, 3:28, 3:35|
|Rapid adaptation/ natural selection||—||316||435, 439||290||3:1, 3:5, 3:11, 3:12, 3:13, 3:27|
|Macroevolution and microevolution||—||311, 324–325||435||—||3:1, 3:12, 3:13, 3:27|
|Coevolution in symbiotic relationships||—||—||441||362– 364, T362, 447||3:7, 3:14|
|Mendelian genetics||253||206, 310||263–266, 393||162– 169||3:10, 3:13, 3:15, 3:21|
|Polyploidy generally causes death in animals.||273||250||321||—||3:16|
|Evolution has no purpose or direction.||—||T295||T748||T307||3:4, 3:17, 3:18, 3:19|
|Evidence is correlated from many areas to support evolution.||403||299–300, 344||386||283, 287||3:7|
|Natural selection recycles functions of traits.||—||331–333||—||—||3:19|
|Intelligent design of eyes is not necessary.||—||331–332, 334||—||—||3:2, 3:4, 3:19|
|Types of mutations||280||—||302, 307– 308, T310, T394||124, T123, 180, 219, 327, 216||3:10, 3:13, 3:16|
|DNA requires proteins to produce proteins.||293||125, 238–241||300–301||208– 210||3:20|
|DNA has evolved to maintain its integrity.||296||—||297||—||3:6, 3:15, 3:21|
|Beneficial mutations are evidence for evolution.||296–297||314||308||291, 332||3:10, 3:13, 3:15, 3:22, 3:28|
|Definitions of natural selection, adaptation, and evolution||297||17–18, T16||T2, 16, 381||279, 288– 291, 825||1:3, 3:1, 3:13|
|Definition of evolution||10||298||20, 369||825||1:3, 3:2, 3:4, 3:13, 3:23|
|Process of evolution||392||290, 305||125, 377, 394, 397, 435, T439, 878–882||—||1:3, 3:13, 3:23, 3:28, 3:35|
|Natural selection drives evolution.||392||17–18||380, 386, 397–398, T399, 872, 878||—||1:3, 3:1, 3:10, 3:11, 3:12, 3:13, 3:22, 3:23, 3:27|
|Uniformitarian geology is the basis of the timescale needed for biological evolution.||393, 466–469||295, 356||374–375||277||3:13, 3:25, 3:29|
|People used to believe the earth was less than 10,000 years old.||367||292||373||277||3:26|
|Peppered moth and coloration as evolution||397||T296||—||—||3:15, 3:13, 3:27|
|Pesticide resistance is an example of evolution.||—||307–308||T367, 410||T289, 332, 688||3:13, 3:28|
|Antibiotic resistance and information in DNA||399, 498||18, 266, 268, 317–319, 364, 370||T367, T386, 403, 410, 487||T279, 289, 449||3:13, 3:22, 3:28|
|Whales evolved from a wolf-like, hoofed ancestor.||400||300, 344||—||T267, 284– 285, T308, 814||3:9, 3:29|
|Camel and horse evolution series based on fossil record.||400||—||439||—||3:29, 3:30|
|Homology is evidence of common ancestor.||400, 450||301, 304, 343||384–385||286, 307, 594||3:6, 3:7, 3:33|
|Vestigial organs demonstrate evolution.||401–402||302||384, T384||T285, 286||3:7, 3:8|
|Whale pelvis is vestigial.||402||302||—||286||3:8, 3:9|
|Embryonic recapitulation demonstrates descent from a common ancestor.||402||302–303||384–385, T385||286||3:7, 3:31|
|Hox genes demonstrate evolutionary relationships.||—||285, 333–334||312, 440, T440||—||3:7, 3:32|
|Amino acid sequence of proteins determines evolutionary relationships.||403||303–304||865||287, T308||3:6, 3:7|
|Speciation and adaptive radiation (divergent evolution) demonstrate evolution.||395–397, 404–413||305–306, 568–569||436||—||3:1, 3:5, 3:6, 3:11, 3:12, 3:13, 3:28|
|Punctuated equilibrium describes gaps in fossil record.||411||329–330||439, T439||282||3:35|
|Convergent evolution demonstrates evolution of two organisms to look like one another.||413||33, 39, T101, 343, T383, T391, T572||383, T383, 436–437, T436, 828, 832||307||3:6, 3:7, 3:33|
|Malaria and sickle-cell anemia are evidence of evolution.||508–509||317||347–348, T402||8, T180, 180, 329||3:23, 3:28, 3:34|
|Diet can be inferred from tooth structure.||843, 844||—||—||—||3:30, 3:36|
|Genetic engineering shows how humans can interfere with or accelerate evolution.||1076– 1079||274–277||322–333, 360||228– 243||3:37|
|Brain complexity is evidence of evolution.||1090– 1091||—||—||3:4, 3:6|
|Viral evolution affects humans.||—||—||T367, 483||934||3:38|
Note: Page numbers preceded by “T” indicate items from the teacher notes found in the margins of the Teacher’s Edition.
What We Really Know about Natural Selection and Evolution
The ideas of natural selection, speciation, adaptation, and evolution are often used interchangeably by secular scientists. All three of the textbooks reviewed use the terms in this way. When scientists and authors use evolution to mean both “change in features over time” and “the history of life on earth,” it is difficult to know which definition is being used in each instance. This is often used as a bait-and-switch technique (equivocation). When small changes that arise as a result of the loss of information are used as evidence for molecules-to-man evolution, the switch has occurred. Let’s define the terms and see where the switch is happening.
Natural Selection: the process by which individuals possessing a set of traits that confer a survival advantage in a given environment tend to leave more offspring on average that survive to reproduce in the next generation.
Natural selection is an observable process that falls into the category of operational science.
Natural selection is an observable process that falls into the category of operational science. We have observed mosquitoes, birds, and many microorganisms undergoing change in relatively short periods of time. New species have been observed to arise. Biblical creationists agree with evolutionists on most of the ideas associated with natural selection, except the idea that natural selection leads to molecules-to-man evolution.
Speciation: the process of change in a population that produces distinct populations which rarely naturally interbreed due to geographic isolation or other factors.
Speciation is observable and fits into the category of operational science. Speciation has never been observed to turn one kind of animal into another. Lions (Panthera leo) and tigers (Panthera tigris) are both members of the cat kind, but they are considered different species primarily due to their geographic isolation. However, it is possible to mate the two. Ligers (male lion and female tiger) and tigons (male tigers and female lions) are produced (with varying degrees of fertility). These two species came from the original cat kind that would have been present on Noah’s Ark.
Adaptation: a physical trait or behavior due to inherited characteristics that gives an organism the ability to survive in a given environment.
Evolutionists often look at a characteristic of an organism and assume that it was produced through a gradual series of changes and call it an adaptation to a given environment. To an evolutionist, legs on tetrapods are an adaptation that arose as a fish’s fins became adapted to crawling in a shallow stream, providing some form of advantage. The fins with more bones were better adapted to a life partially lived on the land. Fins that developed bones attached to a pectoral girdle (another set of bones that had to develop) gave an advantage to those individuals that wandered onto land to find food or avoid predators. The problems with this scenario are in the amount of time such a change would require and the lack of a mechanism to cause the change.
Evolutionary biologists assume, based on geologic interpretations, that there have been billions of years for this process to occur. But if long ages did not exist, the hypothesis cannot be true.
The other requirement, a mechanism for change, is also assumed to exist—even though it has never been observed. We mentioned earlier that natural selection tends to delete information from the population. If natural selection is the mechanism that explains the successive adaptations in the fish fin example above, it must provide new genetic information. To produce the new bones in the fins requires an elaborate orchestration of biologic processes. The bones don’t just have to be present; they must develop at the right time in the embryo, have their shape and size predetermined by the DNA sequence, be attached to the correct tendons, ligaments, and blood vessels, attach to the bones of the pectoral girdle, and so on. The amount of information required for this seemingly simple transformation cannot be provided by a process that generally deletes information from the genome.
Biblical creationists consider major structures to be part of the original design provided by God. Modifications to those structures, adaptations, occur due to genetic recombination, random mutations, and natural selection. These structures do not arise from the modification of similar structures of another kind of animal. The beak of the woodpecker, for example, did not arise from the beak of a theropod dinosaur ancestor; it was an originally designed structure. The difference in beak shapes among woodpeckers fits with the idea of natural selection leading to changes within a population of woodpeckers—within the created kind.
Consider a woodpecker pair getting off the Ark. The pair may contain genes (information) for long and short beaks. As the birds spread out into the lush new world growing in the newly deposited soil, they produce offspring that contain both long-beak and shortbeak genes. (Although the actual control of beak growth is complex, we will assume that long is dominant over short for this simplistic example.) Areas populated by trees with thick, soft bark would tend to select for woodpeckers with longer beaks. Areas where the bark was thinner and harder would tend to be populated by woodpeckers with shorter beaks. Two new species, with slightly different adaptations, could arise if the two populations were geographically separated. The population of short-beaked woodpeckers would have lost the information for long beaks. No more long-beaked woodpeckers would be produced without a significant addition of genetic information affecting the beak length. The long-beaked woodpeckers would still have the ability to produce short-beaked offspring, but they would be less able to compete, and those genes would tend to decrease in frequency in the population. Due to their isolation, two new species of woodpecker would develop, but within their kind. Observational science supports this type of subtle change within a kind but not molecules-to-man evolution, as we will see in the next section.
Evolution: all life on earth has come about through descent with modification from a single common ancestor (a hypothetical, primitive, single-celled organism).
Evolution is generally assumed to happen as a natural consequence of natural selection. However, no direct observational evidence supports the concept of a fish turning, however gradually, into an amphibian. Evolutionists will argue that there has simply not been enough time to observe such changes. Man has only been recording information that would be useful for a short period of time relative to the immense amounts of time required by evolutionary theory. This raises the question, “Is evolution a valid scientific idea since it cannot be observed in experiments and repeated to show that the conclusions are valid?”
The fact that evolutionary processes, on the scale of millions of years, cannot be observed, tested, repeated, or falsified places them in the category of historical science. In secular science, evaluating historical events is considered just as acceptable as conducting laboratory experiments when it comes to developing scientific theories. Since scientific theories are subject to change, it is acceptable to work within an admittedly deficient framework until a better or more reasonable framework can be found.
A major problem for evolution, as mentioned above, is the huge increase in information content of organisms through time. Evolutionary theory accepts additions and deletions of information as evidence of evolution of a population. The problem is that through the imagined history of life on earth, the information content of the genomes of organisms must have increased dramatically. Beginning with the most primitive form of life, we have a relatively simple genome compared to the genomes that we see today. Mutations are said to provide the fuel for the evolutionary engine. Virtually all observed mutations result in a loss in the information content of a genome. There would need to be some way to consistently add information to the genome to arrive at palm trees and people from a simple single-celled organism—the hypothetical common ancestor of all life on earth. Evolutionists have failed to answer the question, “Where did all the new information come from since mutations are known to reduce information?” You cannot expect evolution, which requires a net gain in information over millions of years, to occur as a result of mutation and natural selection. Natural selection, evolution’s supposed mechanism, causes a loss of information and can only act on traits that are already present! (The origin of the information is discussed in chapter 5.)
Creationists agree with the idea of “descent with modification” but not with the notion of a single common ancestor. To accept a common ancestor for all life on earth requires a rejection of the biblical account of creation recorded in Genesis and corroborated by many other Scriptures. The order of events of evolutionary history cannot be reconciled with the account recorded in Genesis 1, without compromising one or the other. The philosophies of evolution and biblical Christianity are not compatible. The examples from the texts below and the articles and books will demonstrate this from a biblical creationist perspective.
3:1 Natural selection and speciation, Ham, Wieland, and Batten, The True Origin of the Species
Evolutionists often set up straw man arguments which suggest that creationists believe life was created just as it is seen today. Evolutionists demonstrate that there are many examples of change over time in species and suggest they have disproved creationism. This is an inaccurate description of the biblical creationist model of life on earth. Creationists accept change in animals over time—God didn’t create poodles—but within the boundaries of the created kinds according to Genesis 1.
Using the dog kind as an example, we can see the amazing variety that was programmed into the DNA from creation. Using basic genetic principles and operational science, we can understand how the great diversity seen in the dogs of the present world could have come from one pair of dogs on Noah’s Ark. Using the genes A, B, and C as examples of recessive/dominant traits in dogs, if an AaBbCc male were to mate with an AaBbCc female, there are 27 different combinations (AABBCC … aabbcc) possible in the offspring. If these three genes coded for fur characteristics, we would get dogs with many types of fur—from long and thick to short and thin. As these dogs migrated around the globe after the Flood, they encountered different climates. Those that were better suited to the environment of the cold North survived and passed on the genes for long, thick fur. The opposite was true in the warmer climates. Natural selection is a key component of the explanation of events following the Flood that led to the world we now see.
This type of speciation has been observed to happen very rapidly and involves mixing and expression of the preexisting genetic variability. Not only does natural selection select from already existing information, it causes a loss of information since unfavorable genes are removed from the population. Mutations are not able to add new information to the genome. Not a single mutation has been observed to cause an increase in the amount of information in a genome. The differences in groups of similar organisms that are isolated from one another may eventually become great enough so that the populations no longer interbreed in the wild. This is how new species have formed since the Flood and why the straw man argument set up at the beginning is a false representation of creationist interpretations.
No matter how hard evolutionists try, they cannot explain where the new information that is necessary to turn a reptile into a bird comes from. The typical neo-Darwinian mechanism of mutation, chance, and time cannot generate new information. The failure of evolutionary models to explain how a single cell could have evolved more complex information by additive mutations challenges the entire concept. If we start from the Bible, we begin with the idea of specially created organisms possessing large amounts of genetic variability. These original kinds have undergone mutations—which cause a loss of information—and have been changed into new species by natural selection. In this biblical framework, the history of life makes sense.
3:2 Is evolution a “fact” of science? Thompson, www.apologeticspress.org/articles/1985
In the media, textbooks, and scientific literature the occurrence of evolution has become a “fact.” The definition of the word evolution has also taken on two different meanings that are not equal. Evolution can be used in the sense of change in a species by natural selection. This is often referred to as microevolution and is accepted by evolutionists and creationists alike as good observational science. This type of evolution allows change within groups but not between groups. The other meaning of evolution involves the idea that all organisms on earth share a common ancestor by descent with modification. This idea is commonly referred to as macroevolution. (AiG does not endorse using the terms “microevolution” and “macroevolution.” It is not the amount of change that is different, but the type and direction of change that is different. These terms do not clarify that difference.) The two definitions are often used interchangeably. Typically, textbooks show that new species can form—evolution has occurred—so they argue that it is obvious that evolution, in the molecules-to-man sense, must have occurred. The problem is that just because natural selection and speciation have occurred (and there is strong evidence to support such claims) the claim that all life has evolved from a common ancestor is based on many assumptions that cannot be ultimately proven.
People believe the ideas of the evolutionary development of life on earth for many reasons: it is all that they have been taught and exposed to, they believe the evidence supports evolution, they do not want to be lumped with people who do not believe in evolution and are often considered to be less intelligent or “backward,” evolution has the stamp of approval from real scientists, and evolutionary history allows people to reject the idea of God and legitimize their own immorality. Evaluating the presuppositions behind belief in evolution makes for a much more productive discussion. Two intelligent people can arrive at different conclusions using the same evidence; so their starting assumptions is the most important issue in discussing historical science.
When we deal with the issue of origins, we must realize that no people were there to observe and record the events. When scientists discuss the origins of the universe, the earth, or life on earth, we must realize that the discussion is based on assumptions. These fallible assumptions make the conclusions of the discussion less valid than if the discussion were based on actual observation. Almost all biology books and textbooks written in the last two generations have been written as if these presuppositions were true.
Proponents of the evolutionary worldview expect everyone to accept evolution as fact. This is a difficult case to make when the how, why, when, and where of evolutionary history are sharply contested or unknown by the scientists who insist evolution is a fact.
Evolutionists often claim that creation is not scientific because of the unprovable assumptions that it is based on. The fact that evolution is based on its own set of unprovable, untestable, and unfalsifiable assumptions is recognized by many in the scientific community.
Within the scientific literature, the mathematical and chemical impossibilities of the origin of the universe and life on earth are recognized. Many notable scientists, including Sir Fred Hoyle and Sir Francis Crick, have gone so far as to suggest that life originated on other planets or was brought to earth by an intelligent being. These ideas are no less testable than special creation but avoid invoking God as our Creator.
3:3 Darwin’s illegitimate brainchild, Grigg, Creation 26(2):39–41, 2004
The idea of natural selection was published well before Darwin wrote Origin of Species. Darwin was most likely exposed to the idea in his days as a student in Edinburgh, and those ideas were integrated with the information gathered on his Beagle voyage. Several scholars have suggested that Darwin borrowed ideas from the works of many of his predecessors and contemporaries. It is suggested that Darwin failed to give credit to Edward Blyth for seminal ideas because Blyth was a “special creationist” who viewed natural selection in light of selecting among preexisting Darwin developed traits. Darwin is credited with the idea of evolution by natural selection, but it remains impotent in light of modern genetic concepts of information.
3:4 Design without a designer, Parker, 2.1 Design Without a Designer
Darwin grew up in an England that acknowledged a biblical worldview. When he wrote On the Origin of Species by Means of Natural Selection, or The Preservation of Favoured Races in the Struggle for Life, he had witnessed a world full of death and disease. How could this be the world created by the God of the Bible? Evolutionary ideas offered people an alternative to a supernatural Creator. Life may appear to be designed, but it is just a product of random changes over millions of years of earth history. This offered people a “scientific” means to reject God and believe in a naturalistic view of the universe. Michael Denton suggests that the chief impact of Darwin’s ideas was to make atheism possible and respectable in light of the evidence for a Designer. Darwin’s ideas fostered an environment where God was no longer needed—nature was all that was necessary. Darwin’s ideas ushered in a pagan era that is now reaching a critical point. The idea that the appearance of design suggests a designer became an invalid argument in the eyes of evolutionists.
3:5 Did God create poodles? Ham, Did God Create Poodles?
Poodles and all other current breeds of dogs are descended from a dog kind that was created on Day 6 and was present on the Ark. The varieties of dogs that we see today, from wolves to coyotes to poodles, are all descendants of the dog kind that came off Noah’s Ark. As populations of wild dogs were spreading across the globe, the environment shaped their characteristics through natural selection. As humans began to domesticate dogs, they artificially selected the traits that they desired in populations. The breeds of modern domestic dogs are a result of the diversity that was programmed into the DNA of the original dog kind. All domestic dogs belong to the same species Canis familiaris and can interbreed.
Purebred dogs have many genetic problems that result from close breeding of individuals over time to concentrate desirable traits. Many breeds have hip dysplaysia, vision problems, and blood disorders. We know that these dogs could not have been in the Garden of Eden because God called His creation “very good” and He would not have included these genetic mutations in that description. We do know that all of the breeds did come from a very narrow gene pool, and this is confirmed by secular scientists. In the journal Science, November 22, 2002, researchers reported, “The origin of the domestic dog from wolves has been established… . We examined the mitochondrial DNA (mtDNA) sequence variation among 654 domestic dogs representing all major dog populations worldwide, … suggesting a common origin from a single gene pool for all dog populations.” It is still important to remember that no new information exists in these mutant forms, only a loss of information from the population, resulting in distinct traits.
3:6 Comparative similarities: homology, Parker, 1.4 Comparative Similarities: Homology
Evolutionists use the idea of “descent from a common ancestor” to explain why the forearm bones of a penguin, bat, and human are so similar. This explanation works for traits in your family, but can it be applied to the history of life on earth? The fact that we use such characteristics to classify organisms into groups does not mean that they are related to a common ancestor. The equally valid alternative is that all of these organisms were created by a common Designer who used the same design principles to accomplish similar functions. Although either explanation may appear equally valid, some instances make the case for a Creator clear.
When structures that appear to be similar to one another develop under the control of genes that are not related, the common ancestor idea fails. Evolution would predict that the structures would be formed from a derived gene that has undergone modification through mutation and natural selection. Frogs and humans supposedly share a common ancestor that would account for the similarity of the limb structures. The problem is that when a frog’s digits develop, they grow out from buds in the embryonic hand. In humans, the digits begin as a solid plate and then tissue is removed to form the digits. These entirely different mechanisms produce the same result, but they are not the result of the same genes.
Another challenge to evolutionary explanations is when two structures appear to be homologous but evolutionists know they don’t share a common ancestor. Such cases are called “convergent evolution.” The eyes of squids and vertebrates are an example where the eyes would be called homologous, but there is no common ancestor to account for the similarities. The common designer argument can once again be used to more easily explain the similarities.
The opposite occurs in “divergent” structures where organisms that appear to be evolutionary cousins have drastically different mechanisms that cannot be explained by a common ancestor. Different light-focusing methods in shrimp provide an example. These systems accomplish the same goal with different and intricate design features— more evidence of their Creator.
Abandoning proof of evolution based on the similarities in large structures, many now look to the similarity in molecular and genetic structure to support evolution. The sporadic presence of hemoglobin in the evolutionary branches of invertebrates is one example. If evolution had occurred, we would expect a predictable pattern—that pattern does not exist. The hemoglobin must have evolved, despite its intricacies, in each of these groups independently. The facts confirm the creationist model of created kinds with great genetic variety and deny evolution from a common ancestor.
The alleged 98% similarity of human and chimp DNA, for example, is often touted as proof of the evolutionary closeness of the two. The 2% difference actually translates into about 60 million base pair differences. The small differences in the genes are actually turned into a large difference in the proteins produced.
The evidence supports the idea of a matrix of specially created organisms with traits occurring where and when they are needed. Discovering the details of this predictive pattern may someday strengthen the validity of the creationist perspective in the minds of skeptics.
3:7 Does homology provide evidence of evolutionary naturalism? Bergman, www.answersingenesis.org/tj/v15/i1/homology.asp
Evolutionists commonly point to the amazing similarity of muscle, bone, and cell structure and function among living things as evidence that all life on earth evolved from a common protocell ancestor some 3.5 billion years ago. Connecting existing animals to the fossil record extends the comparison back to the alleged beginning of time. The idea of homology as proof for evolution is present in almost every high-school or college text on the subject. Evolutionists argue that the only naturalistic explanation for homology is that all of the organisms evolved from a common ancestor. Design arguments are dismissed in naturalistic/ materialistic scientific explanations—even though a common designer can explain the similarities as well.
Before Darwin, creationists used the idea of “ideal archetypes” as evidence for a common designer. The features of comparative anatomy were later reinterpreted by evolutionary biologists to argue for descent from a common ancestor. The real question is: “Does the similarity prove that one structure evolved into another?” Since the requirements are similar for living things, homologous structures would be predicted based on a common designer—structures appear similar because they were designed to accomplish the same task. Tires on bicycles look like tires on motorcycles, with design modifications. Kidneys in a skunk look similar to kidneys in a human because they perform the same task and were designed by a common Designer. Evolutionists tend to accept homologies that fit within the evolutionary framework and set aside those that do not support their predictions; supporting structures are called “homologous,” while those that don’t fit the theory are called “analogous.” The existence of similar body plans in organisms that are not considered to be closely related in evolutionary terms is said to demonstrate convergent evolution. The body plan works, so it evolved independently in the two organisms. There are also many exceptions and there is no way to trace many components back to their alleged ancestors due to the incomplete nature of the fossil evidence. Homologous structures cannot exclude the idea of design.
The idea of convergent evolution of analogous structures has trouble explaining exactly how these structures have evolved at different times to be analogous. Wings are supposed to have evolved in at least four different groups as analogous structures. Another example of convergent evolution is the striking similarity between dogs and the Tasmanian tiger (a marsupial). Evolutionists must say that the two evolved independently of one another even though the homology indicates otherwise. Convergent evolution is used as a way to explain away homologies that appear in organisms that aren’t supposed to be closely related.
Evolutionists use embryological development, the presence of vestigial organs, and biochemical and genetic homologies to argue for descent from a common ancestor. Yet the patterns expected from the Darwinian model of evolution are not seen in most instances. On the other hand, homologies confirm the creationist model of a common Designer, the Creator God of the Bible.
3:8 Cutting out a useless vestigial argument, Wilkinson, www.answersingenesis.org/creation/v26/i3/vestigial.asp
The idea of vestigial organs has been passed on for over 100 years. Vestigial organs are said to be remnants of organs that were used by an organism’s ancestors but are no longer needed, or they function in a reduced capacity in the modern organism. The human appendix is one of the most used, or misused, examples. Just because we do not understand the function of an organ doesn’t mean that it serves no function. The appendix was once thought to be an evolutionary leftover, but today we know it serves an important immunological function. Most of the organs that were once thought to be vestigial have been shown to have functions.
3:9 When is a whale a whale? Gish, www.icr.org/article/379
Evolutionists predict the presence of billions of transitional life forms that have existed in earth’s history. Despite the presence of 250,000 fossil species, clear transitional forms, which would bolster evolutionary theory, are virtually absent. The situation of transitional forms is glaringly obvious in the case of whales and other marine mammals. The gap in transitional forms was supposedly filled by a partial fossil specimen named Pakicetus inachus. Even though the fossil was only a fraction of the skull and a few teeth, the media and scientists portrayed it as a whale-like transitional form. The fact that it was found in a deposit that was likely from a river area puts the interpretation of Pakicetus in doubt. (More complete specimens have been found that show Pakicetus as a dog-like land animal.)
Fossils of Ambulocetus natans were later discovered, and this creature was considered to be a walking whale. Despite the lack of a pelvic girdle (a partial pelvis was found in later specimens), Ambulocetus is described as having walked on land much as sea lions do and swimming with a combined motion much as otters and seals do. Why a whale would have hooves on its rear feet and be living near the seashore are questions that are not answered by the fossils.
The deposits containing Ambulocetus were found 400 feet higher than where Pakicetus was found, but both are supposedly 52 million years old. Pakicetus is called the oldest whale (cetacean), but Ambulocetus is supposed to display transitional features as land animals turned into whales. Based on teeth alone, several other wolf-like carnivores (mesonychids) are thought to be ancestors as well. The exact arrangement of these groups is disputed, and some consider the mesonychids to be a branch separate from whales.
This interpretation of scant fossil evidence is very imaginative and totally necessary to support the notion that whales evolved from land animals. Such imaginative claims of evolutionary history have been claimed in the past only to be shown false. Further evidence will certainly change the current thinking in drastic ways.
3:10 Are mutations part of the “engine” of evolution? Hodge, available at http://www.answersingenesis.org/articles/wow/are-mutations-the-engine
This chapter of War of the Worldviews details the common mechanisms of genetic mutation and explains how the mechanisms actually provide examples of a loss of information rather than the creation of new information necessary to explain molecules-to-man evolution. In evolutionary theory, mutations are described as the mechanism that fuels the engine of natural selection, creating new organisms as a result. However, the vast majority of mutations are either neutral or cause a loss of information in the genetic code of an individual.
Evolution teaches that mutations have accumulated over millions of years to increase the complexity of organisms on the earth. The Bible teaches that, as a result of Adam’s sin, all of creation is in a downward slide—including the genetic information that is in every living cell. The law against marrying close relations was not given to Israel until Leviticus 18. Up to this point, the accumulation of genetic mistakes was apparently not significant enough to cause genetic disorders in the offspring of close family members. Today, with thousands of years of accumulated genetic mistakes in the human gene pool, intermarriage would be much more likely to produce children with genetic disorders. So it seems that the explanation of a genetic degradation since the Curse of Adam actually fits the evidence better than the evolution model of increasing complexity.
3:11 Does the beak of the finch prove Darwin was right? Morris, www.icr.org/article/1135
While on his journey aboard the Beagle, Darwin had an extended stay in the Galapagos Islands. He observed a group of finches that were similar to ones he had seen on the mainland 600 miles away. Darwin concluded that these birds were related to the birds on the mainland but had developed unique traits suited to the islands. The structure of the beaks was one of the key characteristics he studied. This interpretation was contrary to some creationists of his day who believed species could not change.
Darwin’s conclusion concerning finches matches that of the modern creationist models and demonstrates the variation within a kind that is observed in nature—the finches are still finches. Studies by Drs. Peter and Rosemary Grant over the past decades have shown that the beak size of the finches changes with the climate of the islands they inhabit. Beaks got larger during droughts and smaller during wet periods. All the while, the birds were observed to interbreed. This cannot be considered evidence of evolution in the molecules-to-man sense because there was no net change in the population, even though rapid changes in beak size were observed. The Grants’ work is an example of a good study using the principles of operational science arriving at a faulty interpretation based on evolutionary presuppositions.
3:12 Reticulate evolution, Cumming,www.icr.org/article/418
The Grants began studying the finch population of the Galapagos Islands in 1973. They monitored breeding, feeding, and physical data in the birds. The finches’ beak shape and size are the main characteristics that are used in classifying them. Even this is difficult with the variability seen in the beaks. One of the biggest problems for the finch studies is the extensive hybridization that occurs between the alleged species. The fact that these hybrids also reproduced should suggest that the three interbreeding species are actually one species. This conclusion was set aside to suggest that hybridization is essential for and accelerates the rate of evolutionary change. The standard species concept was rejected to promote evolution. The hybridization demonstrates the common gene pool that these finches all share and the high degree of variability that was present in the first birds on the islands. The branches and stems in the finch tree of life seem to be more like a thicket with interconnecting lines (termed reticulate evolution). The range of explanations for the process of evolution—it is a “fact” that it has occurred— now includes rapid or gradual, directed or undirected, tree or thicket. The creationist model can still be said to accommodate the data in a much more complete way. Variation within the created kind is confirmed in Darwin’s finches.
3:13 Change, yes; evolution, no, Parker, 2.5 Mutations, Yes; Evolution, No
The most persuasive—and dangerous—definition for evolution is “change through time.” Just because organisms can be observed to change over a period of time does not mean that all life has a common ancestor. If we think of the classic peppered moth example, we started with light and dark moths (Biston betularia) and ended up with light— and dark—colored moths of the same species in different proportions. This exemplifies the creationist idea of variation within a kind.
The natural selection that produces the variety of living things we see today began after Adam rebelled against God. The concept of natural selection was published in a biblical context by Edward Blyth 24 years before Darwin published Origin of Species. Blyth is forgotten and Darwin is remembered because of the philosophic and religious implications of his idea, not the scientific applications.
Natural selection has been shown to change organisms but always within the boundaries of the created kinds. This type of change is often termed “microevolution,” and the hypothetical type of change that turns fish into philosophers is known as “macroevolution.” The large-scale changes through time are simply dramatic extrapolations of the observed phenomenon of natural selection. This degree of extrapolation has no basis in operational science. There are limits to the amount and type of genetic change that can occur—no matter what amount of time is allowed. As an illustration: if you can pedal a bicycle at 10 mph, how long would it take to reach the moon? Bicycles have limits that would make this goal impossible regardless of the time you have to accomplish it.
3:14 Henry Zuill on biology, Ashton, Henry Zuill, Biology
When we look at the world, we see a complex interaction between living things, from bacteria to grizzly bears; all life depends on other life around it. The complexities of relationships in the ecosystems that make up the earth are just as complex as those seen inside each living cell. Biodiversity and the relationships that it incorporates are a hallmark of the design of the Creator. The more diverse and complex an ecosystem is, the more stable it is. Each species in an ecosystem provides a service, but often providers of that service overlap and each species may perform several services. Removal of one of the species has an impact on all other species. This interdependency is supposed to demonstrate how organisms have evolved alongside one another. But how did the first organism survive without the second, and vice versa?
Being created together is a simple explanation, and evolution has great difficulty explaining the many instances of species that absolutely depend on one another for their survival. When cells were described as simple blobs of jelly, it was easy to imagine that they arose spontaneously. Today, the complexity of a single cell defies an origin from simple matter. As we understand more about ecological interactions, it is apparent that the evolutionary relationships that were once assumed to be simplistic are now known to have many layers of complexity. The coevolution of complex symbiotic relationships required the existence of relationships. This provides no answer to the origin of the relationships. If the two organisms were created to coexist, a fine-tuning of the relationship would be expected in the creationist framework. Predators and parasites developed in response to the degraded world after the Flood. The created kinds may have changed, but the general relationships present before the Fall probably remained intact to some degree. The relationships seen are a testament to the Creator who instilled order and flexibility into the system. Evolutionary views cannot adequately explain the symbiotic nature of all living things.
3:15 Genetics: no friend of evolution, Lester, www.answersingenesis.org/creation/v20/i2/genetics.asp
Mendel and Darwin were contemporaries whose theories were formulated in different ways and clashed with one another. Mendel used careful observations of traits and calculations to develop his theory of inheritance, while Darwin’s ideas were based on erroneous ideas about inheritance. Four factors can be considered in genetic variation: environment, recombination, mutation, and creation. It has long been known that environmental effects on individuals cannot be passed on to offspring as the information is not contained in the DNA. Mendel recognized the constancy of traits with variation, while Darwin, to some degree, accepted environmental influence on variation. This is evident from Darwin’s discussion of the giraffe’s neck becoming longer by “the inherited effects of the increased use of parts.”
Mendel showed that traits are reorganized independently when they are passed on to offspring. The variation would not always be evident, but it would only reappear if the trait was present in a previous generation. The amount of variation is limited by the information in the parents. Darwin’s finches offer an example of this recombination of traits. Mutations are rare in a given gene, and the cell has elaborate machinery to correct mistakes when they occur. Mutations, when they do occur, tend to be neutral but others are harmful. In the creation model, mistakes in the DNA would be expected to have harmful effects. In evolution, these mistakes are supposed to increase information even though in over 3,000 known fruit fly mutations not one produces a fly that has a survival advantage. Examples of mutations that are beneficial to the individual or population are shown to be a loss of information. Natural selection acts to preserve or eliminate traits that are beneficial or harmful, as the creation model would predict. Creation of organisms by a divine Creator is the only mechanism that is adequate to account for the variation seen in the world today. Each of the created kinds started with considerable genetic variability that has caused the variety of life we see today.
3:16 Copying confusion, Williams, www.answersingenesis.org/creation/v25/i4/DNAduplication.asp
Molecules-to-man evolution requires the production of large amounts of new genetic information. In searching for possible mechanisms, evolutionists have sometimes pointed to the ability of cells to make, and retain, multiple copies of their DNA. If this were the source of evolution, one would expect to find a general increase in the amount of DNA as you move up the evolutionary tree of life. This, however, is not the case. Humans are certainly more complex organisms than bacteria and plants, but they have less DNA in general. The organism with the most DNA is actually a bacterium (Epulopiscium fishelsoni) that has at least 25 times as much DNA as a human cell. There are also 85,000 copies of one of its genes per cell. If these extra copies of genes were indeed the raw material for evolutionary mechanisms to act on, this bacterium should be a hallmark of evolutionary adaptation—but it is still a bacterium.
3:17 Man: the image of God, Rendle-Short, www.answersingenesis.org/creation/v4/i1/man.asp
Evolutionists suggest that evolution is a meaningless, undirected process and that humans are a mere accident with no purpose or meaning in the universe. If humans evolved, then there is no eternal life and no God. This obviously flies in the face of Christian beliefs; we were created in the image of God. This view of creation gives our life meaning and purpose. Without God, there is no foundation for morality and each person can do what seems right at the time with no real consequences regarding eternity— eternity does not exist. Man shares characteristics with both animals and God. The Bible equates man and animals on a certain level, but the presence of a spirit and the ability to communicate ideas are attributes man shares with God. We also see God’s attributes in human creativity, reasoning, and the ability to express love and pursue the holiness that existed before sin entered the world. The impulse to survive seen in every living thing cannot be described in biological terms; a divine Creator must have instilled this desire in each organism. Evolutionists suggest that the hope of an afterlife is a coping mechanism that has developed as a response to the bleakness of our existence, but God says it is a promise to all. Some will be in the presence of God and others will be cast into Hell.
3:18 Evolution—atheism, Provine, Evolution = Atheism
“Let me summarize my views on what modern evolutionary biology tells us loud and clear … . There are no gods, no purposes, no goal-directed forces of any kind. There is no life after death. When I die, I am absolutely certain that I am going to be dead. That’s the end for me. There is no ultimate foundation for ethics, no ultimate meaning to life, and no free will for humans, either.” —Dr. William B. Provine, Professor of Biological Sciences, Cornell University
3:19 Natural selection, yes; evolution, no, Parker, 2.5 Mutations, Yes; Evolution, No
The definition of the “fittest” individuals makes the notion of natural selection true based on circular reasoning. The fittest are the ones that survive, and you can tell which are the fittest by seeing which ones survive. (The fact that survival of the fittest is based on circular reasoning does not necessarily mean that the idea is false.) Fitness is controlled by many factors that allow the organism to survive and reproduce. The fastest zebra may be deaf and have a poor sense of smell. This combination would tend to eliminate his genes from a population. The only way to understand fitness is to study the first generation and then track the presence of those traits through time as successive generations are born.
Numerical values can be used to represent the fitness of individuals based on the ratio of individuals with different traits. These numbers can explain fitness, but they have no predictive power—you can only determine the fittest after they survive. Mice that hold still to avoid being seen by a soaring hawk are better able to survive, except when it is safer to run to their burrows to avoid being eaten—each may provide an advantage. If the fact that the survivors survived is used to prove evolution, the circular reasoning becomes a logic problem.
Another misconception is that the fittest variety must be increasing in number. Natural selection can still be acting on a population as its numbers are declining. There is no direction implied in natural selection—you can be the highest scorer (most fit) on the losing team. Competition happens between species (interspecific competition), but natural selection acts within species (intraspecific competition). The struggle for survival is not between lions and zebras, it is within the zebra population. This intraspecific struggle allows for change within kinds, but not from one kind to another.
One shortcoming is that natural selection cannot plan ahead—an advantage one day may become a hindrance as the environment changes. This can ultimately lead to the extinction of a population despite its current success in the environment. Natural selection favors specialization into distinct niches; when the environment changes, the specialization becomes a disadvantage. It seems impossible that this process of undirected elimination could lead to an increase in variety and complexity.
Adaptations are usually presented in a way that makes them seem like a natural extension of natural selection. There is limited evidence to suggest that natural selection can lead to new adaptations, but ample evidence shows that adaptations can lead to natural selection. An adaptation must appear before natural selection can act on it. Evolution cannot explain the appearance of these traits, but the Creator provided the variety needed in the original created kinds.
The presence of irreducible complexity in biological systems is another roadblock for naturalistic theories of evolution. It is hard to imagine how you could get to the top of the Empire State Building if you had to jump, but the task becomes easier when you learn that there are stairs. This slow and gradual idea is how evolutionists explain the molecules-to-man idea that once seemed impossible to imagine. This works if all of the steps can be used to build on one another, but what if this were not the case?
Darwin recognized this limit and acknowledged it in Origin of Species. In his book Darwin’s Black Box, Michael Behe describes the biochemical details of several systems that need all of their parts present to function. Since removing one of the proteins involved in blood-clotting causes catastrophic results, the system has irreducible complexity. This irreducible complexity is not only present within living organisms but also between them in ecological interactions. The interaction of fish and shrimp in cleaning symbiosis is one example. A large fish allows a small fish or shrimp to clean parasites from its mouth and then swims off without eating the cleaner. How could this relationship, and other irreducibly complex systems, have evolved one step at a time?
Even if Darwin’s ideas can explain the maintenance of traits and variation within a kind, they do not address the actual origin of the traits in the first place. Darwin used the phrase “from use and disuse, from the direct and indirect actions of the environment” to describe the origin of traits. This is exactly the view held by Lamarck, who is often contrasted with Darwin. Using a trait does not mean it will be passed to the offspring in a different form (stretching giraffe necks is often used as an example). As science has gathered more information about heredity, the idea of use and disuse has been shown to be false.
The origin of this new information is thought by neo- Darwinists to occur by random mutation—random mutations are the raw material for evolution. The cases of fruit fly mutation and flu virus are often used as examples to support evolution. However, these mutations cannot explain the increase or origin of information in living systems. The creationist model—that information was created by the Supreme Designer—fits the observations much better than naturalistic evolution.
3:20 Learning the right tricks about life’s origin,www.answersingenesis.org/creation/v13/i4/tricks.asp
A Scientific American article admits (way back in 1991) that the “chicken and egg” problem of DNA and proteins has not been solved by the RNA hypothesis. DNA requires proteins to function, and proteins are made from DNA. The actual laboratory observations are highly artificial with a “great deal of help from the scientists.” Miller’s and Fox’s experiments on the origin of proteins and proteinoids, which supposedly produced “protocells,” are essentially dead ends. Clever attempts at producing life in the lab only demonstrate that life can be produced by intelligence. The stories of life originating in clay crystals and deep-ocean vents are just stories, with no observational data to confirm them. In all, much more research is needed to even begin to answer the question of the origin of life in a materialistic framework. Creationists need only accept that God has created life and study the changes that have occurred since the creation.
3:21 Startling plant discovery presents problems for evolution, DeWitt, www.answersingenesis.org/docs2005/0406mutation_fixing.asp
An amazing discovery in genetics has shown that a certain plant (Arabidopsis thaliana) can actually fix a mutation in a recessive allele even when it doesn’t have a copy of the correct sequence in its genome. In a well-designed study, the mutation was shown to be corrected in a “templatedirected process,” not by random mutations. Organisms that have a better DNA correction system would have a survival advantage, but the irreducible complexity of the system makes it highly improbable that it evolved. This correction mechanism has never been seen before and seems to defy evolution by natural selection. How do you select for the ability to fix a mutation that you don’t have? This trait could easily be lost from the population by genetic drift or random mutation in organisms that lack the mutation (assuming it is a DNA-encoded trait). A system that fixes random mutations would stop, or at least slow down, the evolutionary process.
The authors of the study suggest stress induces the repair. Stress has been shown to change mutation rates in certain bacteria, but in the other direction—more mutations are produced to create a variant that can survive the stress. RNA is a candidate for the correction mechanism, but many properties of RNA make it improbable. The RNA may be acting with other proteins, but more research needs to be done. Evolution is such a plastic theory that a “just so” story will probably come about as a result of this correction mechanism. The problem is that it would be just as likely to fix beneficial mutations as it would harmful ones. A creationist can accept this new mechanism as another way of maintaining the created kinds in light of genetic variability.
3:22 Is bacterial resistance to antibiotics an appropriate example of evolutionary change? Anderson, www.trueorigin.org/bacteria01.asp
[Summary quoted directly from the actual paper] Resistance to antibiotics and other antimicrobials is often claimed to be a clear demonstration of “evolution in a Petri dish.” However, analysis of the genetic events causing this resistance reveals that they are not consistent with the genetic events necessary for evolution (defined as common “descent with modification”). Rather, resistance resulting from horizontal gene transfer merely provides a mechanism for transferring pre-existing resistance genes. Horizontal transfer does not provide a mechanism for the origin of those genes. Spontaneous mutation does provide a potential genetic mechanism for the origin of these genes, but such an origin has never been demonstrated. Instead, all known examples of antibiotic resistance via mutation are inconsistent with the genetic requirements of evolution. These mutations result in the loss of pre-existing cellular systems/activities, such as porins and other transport systems, regulatory systems, enzyme activity, and protein binding. Antibiotic resistance may also impart some decrease of “relative fitness” (severe in a few cases), although for many mutants this is compensated by reversion. The real biological cost, though, is loss of pre-existing systems and activities. Such losses are never compensated, unless resistance is lost, and cannot validly be offered as examples of true evolutionary change.
3:23 Can genetic mutations produce positive changes in living creatures? Demick, www.christiananswers.net/q-eden/geneticmutations.html
Richard Dawkins used the idea of a “blind watchmaker” to describe how genetics can create new features in organisms through evolutionary processes. Actual observations show that natural selection acts more like a “blind gunman” as mutations occur. Mutations occur when the genetic code of DNA changes and come in many different forms. Only the mutations in the germ cells (eggs and sperm) can be considered in inherited diseases. In a large protein, a mutation at many positions in a gene may cause a defective protein to be formed. In one cholesterol disorder, 350 disease-producing mutations have been documented to cause various problems with cell membrane receptors.
Cystic fibrosis (CF) is caused by a group of mutations in an ion pump in the cell membrane. The protein consists of 1,480 amino acids and the deletion of three bases at codon 508 causes most cases of CF. Nearly 200 other mutations have been shown to cause CF as well. Cancer is another disease that demonstrates the danger that mutations can cause to organisms. Many types of germ-line and somatic (body) cell mutations cause the cells to grow without the normal regulations on size and cell division.
If evolution has led from microbes to man, there should be some evidence that mutations can cause such an increase in information. Sickle-cell anemia is often used as an example to support Darwinian evolution, but the mutation clearly causes a loss of normal function with no new ability or information. Cancer cells are fitter than other cells around them but can hardly be considered as proof of evolution. The fact remains that observational science shows that mutations cause negative effects without a single example of a mutation that improves the function of a protein in support of evolution.
If we start from the Bible, the effects of mutations and the continued decay of the human genome is a clear example of the Curse that resulted from Adam’s sin. The human genome will become increasingly corrupted as time passes. Christ’s return and the fact that He conquered death offers the world hope for the future.
3:24 What does the fossil record teach us about evolution? Van Bebber and Taylor, www.christiananswers.net/q-eden/edn-c006.html
When deciding if the fossil record actually supports the evolution of life on earth, many factors need to be considered. Animals and plants appear very abruptly in the fossil record. Evolution would predict the fossils we find should show a vast array of transitional forms—few if any are found. Despite the extensive number of fossils found, it is believed that few new fossil types will be discovered. The lack of order in the geologic layers presents another challenge for evolutionists. The fossil record is much more consistent with the occurrence of a global Flood and special creation than with an evolutionary history.
3:25 Evidence for a young world, Humphreys, www.icr.org/article/1842
Many of the dating techniques that can be used to determine the age of the universe and the earth point to a maximum amount of time less than the billions of years required by naturalistic evolution. Galaxies wind themselves up much too fast to be billions of years old. There are too few visible supernova remnants. Comets disintegrate too rapidly and have no mechanism to reform. There is too little sediment on the sea floor to account for erosion and not enough sodium in the sea to account for billions of years. The earth’s magnetic field is decaying too rapidly. Rock layers are bent to extreme degrees, suggesting they folded rapidly while still soft. DNA and other biologic materials should decay and not be found in fossils—bacteria alleged to be 250 million years old should have no intact DNA left, yet they were able to grow.
Radioactive halos present in rocks show a time of rapid radioactive decay in the past. Too much helium resides in minerals that are supposed to be very old. Carbon-14 is found in diamonds and coal that are supposed to be millions or billions of years old. There are too few skeletons of Stone Age humans to support the alleged 200,000-year timespan. Agriculture and historical writings have been around for too short a period. In combination, this short list demonstrates that many dating methods defy the billions of years needed to support evolution’s house of cards.
3:26 Gallup poll on creationism,poll.gallup.com/content/default.aspx?ci=18748
A poll conducted by the Gallup Organization in 2005 found that 29% of Americans believe that creationism (including life originating 6,000 years ago) is definitely true with respect to explaining the origin of life on earth. About 20% consider evolution definitely true, and only 8% believe intelligent design is definitely true. The results also indicate that many people still have mixed views on the compatibility of evolution and creation.
By 58% to 26%, a majority of Americans express their belief in creationism; by 55% to 34%, a majority also accept evolution. But 32% of Americans tend to reject intelligent design, while 31% say it is probably true. The statistics make it clear that many Americans are blending ideas of creation and evolution together in an attempt to make sense of the conflicting messages. (Standing on the authority of the Bible will lead to an acceptance of creationism as the only position consistent with Scripture.)
3:27 Natural selection, Parker, 2.2 Natural Selection
Darwin based his idea of natural selection on the changes he observed in selective breeding by farmers and animal breeders. It can be observed that artificial selection can lead to the expression of hidden traits. Darwin suggested that if man can produce such changes in a short time, over millions of years natural selection could produce entirely new species. Darwin was right about the ability of natural selection to change populations, but he was wrong about the extent of change that could occur.
A popular example in textbooks is the case of the peppered moth. The proportion of moths of different color was shown to change as pollution changed the environment they lived in. It has also been recently revealed that the photos of moths showed dead or stunned moths glued to trees and that the moths do not land on the trunks. Despite the fraud, the concept still fails to prove evolution in the molecules-to-man sense.
3:28 Mutation, yes; evolution, no, Parker, 2.5 Mutations, Yes; Evolution, No
There are three limits to accepting mutations as a mechanism for molecules-to-man evolution. First, there are mathematical limits to the probability of evolution occurring. Mutations occur once in every 10 million duplications of DNA, so it is very likely that every cell in your body contains at least one mutation since you were born. The problem for evolution is that you need multiple, related mutations to cause a change in a structure. If mutations occur at a rate of one in 107, the odds of getting two related mutations is 1014. The likelihood of evolution quickly becomes unreasonable. In bacteria that are resistant to four different antibiotics, the probability would be 1 in 1028. It has been shown that the bacteria already had the information for resistance built into them—the trait was selected for, not created by mutations. Those bacteria that do become resistant by mutation are less fit and don’t survive outside relatively sterile environments. This is not evidence for evolution.
Second, mutations are moving in the wrong direction to support the advancement of complexity required by evolution. Almost every mutation we know of has been identified based on the disease it causes. Mutations explain the decline seen in genetic systems since the Fall of mankind in Adam. The time, chance, and random mutations simply serve to tear things apart. Shortly after creation, there would have been few genetic mistakes present in the human population, and marrying a close relative would not have been a problem. Today, the likelihood of a shared mutation causing a disease is too great a risk to allow close marriages.
The advantage of avoiding severe malaria symptoms by those with sickle-cell anemia is often given as evidence of beneficial mutations. The overall effect of the mutation is not beneficial to the human race, however, and will not lead to a more fit population.
Third, mutations can only act on genes that already exist. Natural selection cannot explain the origin of genes because there was no information for natural selection to act on. Mutation and natural selection simply produce variation within a kind—just as the biblical creation model suggests. No genetic mechanism can increase the amount of information that is needed to demonstrate evolution from particles to people. Mutations do not add information to an organism’s genome. Thousands of mutations would need to add information to change even “simple” cells into more complex cells. Even when genes mutate, they still pair up with similar alleles and are controlled by the same regulators. Mutations may affect the degree of a trait, but they do not cause new traits.
It is not the amount of time or the number of mutations, but the direction of change and the origin of information that are the biggest stumbling blocks for evolution. All of the evidence continues to point to the design and information originally provided by the Creator.
3:29 Scientific roadblocks to whale evolution, Sherwin, www.icr.org/article/433
One of the popular stories of evolution tells of how land animals evolved into whales and their cousins. Darwin suggested that a race of bears became more and more aquatic until they were whales. Other stories are full of details that have no basis in any facts. To produce whales from small land mammals would require countless changes. These gradual changes are not preserved in the fossil record to any degree.
There are many suggested ancestors to the whales, from wolf-like creatures to hippos. All require amazing changes that must have happened at an astonishing rate to fit the evolutionary timescale. Blubber, temperature regulation, special metabolism, countercurrent blood flow, and other functions would have to be present before natural selection could act on these traits. The development of one- or two-holed breathing structures stretches the limits of the evidence in fossils. Whale tails move up and down, while the alleged ancestors did not have this ability. The pelvis would have to be minimized while the flukes were expanded. The fossils to document these changes are absent.
The lack of consistency between molecular data and morphological data is a strike against evolution in general. The inconsistency is evident where certain proteins suggest whales and hippos should be grouped together, while the fossils suggest a carnivorous ancestor for whales. Neither natural selection nor mutations are sufficient to explain the alleged transformation from anything to a whale. The biblical model still provides the best explanation.
3:30 Camels—confirmation of creation, Weston, www.answersingenesis.org/creation/v19/i4/camels.asp