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Second Thoughts about Peppered Moths

Every student of biological evolution learns about peppered moths. The dramatic increase in dark forms of this species during the industrial revolution, and experiments pointing to differential bird predation as the cause, have become the classical story of evolution by natural selection. The same careful scientific approach which established the classical story in the first place, however, has now revealed major flaws in it. It is time to take another look. The peppered moth, Biston betularia, comes in various shades of gray. One hundred and fifty years ago, the species consisted almost entirely of “typical” forms, with predominantly light gray scales interspersed with black (hence the name, “peppered”). In 1848, a coal-black “melanic” form was collected near Manchester, England, and by 1950 melanic forms made up more than 90% of the peppered moths in that area. A similar change was reported in many other species of moths, as well as in ladybird beetles, spiders, and even some birds. Since the phenomenon was observed not only around Manchester but also near other industrial centers such as Birmingham and Liverpool, it became known as “industrial melanism.” The Classical Story Before 1950, the cause of industrial melanism was largely a matter of speculation. According to Tutt (1896), the cause was cryptic coloration and differential predation. Tutt theorized that in unpolluted woodlands, typicals are well camouflaged against the light-colored lichens that grow on tree trunks; but in woodlands where industrial pollution has killed the lichens and exposed the dark brown tree trunks, melanics are better camouflaged (Figure 1). Since predatory birds are more likely to eat the most conspicuous moths, melanic forms would increase as a result of natural selection. Tutt’s theory, though plausible, was not widely accepted at the time because entomologists and ornithologists had no evidence that birds were major predators of camouflaged day-resting moths.
[gallery link="none" size="full" ids="19833,19834,19835"] Figure 1. Peppered moths resting on three different tree trunks. (top) Two moths (one typical and one melanic) resting on the dark bark of an oak tree near the industrial city of Liverpool, U.K. (middle) The same two moths on a nearby beech tree covered by a combination of green algae and lichen. (bottom) Typical and melanic moths resting on light-colored lichen on an oak tree in rural Wales. Note the striking differences in camouflage efficiency (Bishop and Cook 1975; used by permission).
Harrison (1920) rejected Tutt’s natural selection theory, and proposed instead that melanism was induced directly by airborne industrial pollutants. Although he did not work on Biston betularia, Harrison reported that melanism could be produced in several other moth species if their larvae were fed on leaves contaminated with metallic salts. Critics pointed out, however, that some of the species Harrison used did not exhibit industrial melanism in the wild. Ford (1937) rejected Harrison’s induction theory in favor of natural selection; but he also rejected Tutt’s theory that the selective agent was bird predation, and maintained that melanic forms in polluted environments enjoyed a physiological advantage unrelated to their color (reviewed in Majerus 1998). Kettlewell’s experiments. In the 1950’s, British entomologist Bernard Kettlewell set out to resolve the issue empirically. Like Tutt, Kettlewell believed that industrial melanism was due to cryptic coloration and selective predation, and he used three experimental approaches to test the theory. First, he estimated the moths’ camouflage efficiency on various backgrounds, as judged by the human eye. Second, he directly observed bird predation through binoculars. Third, he marked and released larger numbers of moths, then recaptured some and compared the pre-release to post-recapture proportions. Kettlewell’s first experiment was conducted in an aviary containing a pair of nesting birds and their young. He released peppered moths into the aviary, and watched through binoculars as they settled onto resting sites and were subsequently eaten by the birds. Kettlewell (1955) thus established that birds do, in fact, prey on resting peppered moths. The second experiment consisted of marking several hundred peppered moths, including typicals as well as melanics, and releasing them into a polluted woodland near Birmingham, England. Kettlewell watched through binoculars as the moths settled on nearby trees; he observed that melanics were much less conspicuous than typicals, as judged by the human eye, and that birds took conspicuous moths more readily than inconspicuous ones. That night he set out traps to recapture as many as he could. Of 447 released melanics he recaptured 123, while of 137 released typicals he recaptured only 18. In other words, he recaptured 27.5% of the melanics, but only 13.0% of the typicals, suggesting that a much higher proportion of melanics had survived predation. Kettlewell concluded that “birds act as selective agents, as postulated by evolutionary theory” (Kettlewell 1955, p. 342). In Kettlewell’s third experiment, the same procedure was repeated in an unpolluted woodland in Dorset, England. Once again he released moths, scored them for crypsis, and watched for selective predation. Ethologist Niko Tinbergen accompanied him and made movies of birds picking the moths off tree trunks. As expected, melanic moths were much more conspicuous than typicals on the lichen-covered Dorset trees, and thus more readily taken by predatory birds. Kettlewell also repeated his mark-release-recapture experiment, and the results were the opposite of those obtained in the Birmingham experiment. He recaptured 62 of 496 released typicals (12.5%), but only 30 of 473 released melanics (6.3%), so the 2:1 recapture ratio which he had found in Birmingham was completely reversed. Kettlewell concluded that typicals enjoyed a selective advantage in Dorset because their superior camouflage improved their chances of surviving bird predation. He then returned to Birmingham so Tinbergen could make movies of selective predation in a polluted woodland to complement the movies he had made in an unpolluted one (Kettlewell 1956). Further support for Kettlewell’s theory. Other biologists conducted experiments with peppered moths on tree trunks to test Kettlewell’s theory that industrial melanism was due to cryptic coloration and selective predation (e.g., Clarke and Sheppard 1966, Bishop 1972, Lees and Creed 1975, Bishop and Cook 1975, Steward 1977b, Murray et al. 1980). Their conclusions generally agreed with Kettlewell’s. Following the passage of anti-pollution legislation in the 1950’s, industrial melanism began to decline. The percentage of melanics on the Wirral Peninsula, west of Liverpool, dropped from 93% in 1959 to 90% in 1962 (Clarke and Sheppard 1966, Kettlewell 1973). A decade later, Bishop and Cook (1975) reported that the reversal of industrial melanism was well under way. A reversal was also noted in other urban areas as air quality improved (reviewed in Lees 1981). By 1984, the percentage of melanics on the Wirral Peninsula had decreased to 61% (Clarke et al. 1985), and in 1996 the percentage was only 8.5% (Grant et al. 1998). Since pollution-control legislation would be expected to restore the typicals’ cryptic advantage by enabling lichens to return to the trees, the decline of industrial melanism was consistent with cryptic coloration and selective predation, and was thus widely regarded as further confirmation of Kettlewell’s theory. The textbook example of evolution in action. Kettlewell described industrial melanism in moths as “the most striking evolutionary change ever actually witnessed in any organism” (Kettlewell 1955, p. 323). Two decades later, British geneticist P. M. Sheppard called it “the most spectacular evolutionary change ever witnessed and recorded by man, with the possible exception of some examples of pesticide resistance” (Sheppard 1975, p. 70), and famed population geneticist Sewall Wright called it “the clearest case in which a conspicuous evolutionary process has actually been observed” (Wright 1978, p. 186). Industrial melanism in peppered moths thereby became “the textbook example of natural selection in action” (Jones 1982, p. 109). According to Majerus, “everyone knows the basic peppered moth story, because it is in all the textbooks” (Majerus 1998, p. 97). One recent evolution textbook calls it “a classic example of natural selection” which is “perhaps the best-known story in evolutionary biology,” though the story is “now known to be more complex” than originally thought (Ridley 1996, pp. 103-109). According to Majerus, however, evidence gathered in the 40 years since Kettlewell’s work shows that “the basic peppered moth story is wrong, inaccurate, or incomplete, with respect to most of the story’s component parts” (Majerus 1998, p. 116). What follows is a review of some of the flaws that have been discovered in the classical story.

Problems with the Classical Story

When biologists looked beyond Birmingham and Dorset, where Kettlewell had conducted his experiments, they found discrepancies between Kettlewell's theory and the actual geographical distribution of melanic moths. For example, if melanic moths in polluted woodlands enjoyed as much of a selective advantage as Kettlewell's experiments seemed to indicate, then they should have completely replaced typicals in heavily polluted areas such as Manchester (Bishop and Cook 1980, Mani 1990). This never happened, however, indicating that factors other than selective predation must be affecting melanic frequencies. Some investigators attributed the discrepancy to heterozygote advantage (Clarke and Sheppard 1966, Lees and Creed 1975), but it has since been established that there is no evidence for this (Creed et al. 1980, Lees 1981, Mani 1982, Cook et al. 1986). [caption id="" align="alignright" width="262"]pepfig2.gif - 5660 Bytes Figure 2. Problems with the classical story: The U.K. and The Netherlands. (a) Despite theoretical predictions, the proportion of melanics around heavily-polluted Manchester never reached 100% (Bishop and Cook 1980, Mani 1990). (b) The proportion of melanics in East Anglia reached 80% despite the absence of any apparent pollution (Lees and Creed 1975); after the introduction of pollution control legislation, typicals became predominant before lichens returned to the trees (Grant and Howlett 1988). (c) South of latitude 52*N, the relatively poor correlation of melanism with sulfur dioxide concentration suggested that non-industrial factors were of greater importance than selective predation (Steward 1977a,b); after the introduction of pollution control legislation, the proportion of melanics decreased in the north, as expected, but increased in the south (Bishop and Cook 1980, Jones 1982). (d) The frequency of typicals on the Wirral Peninsula increased dramatically before the return of lichens to tree trunks (Clarke et al. 1985, Grant et al. 1998). (e) The decline of melanism in The Netherlands has been accompanied by an increase not only in typicals, but also in an intermediate form almost as dark as melanics. (Brakefield 1990).[/caption] Some other distribution features were inconsistent with Kettlewell's explanation, as well. In rural Wales, the frequency of melanics was higher than expected, leading Bishop to conclude that "as yet unknown factors" were involved (Bishop 1972, p. 240). In rural East Anglia, where there was little industrial pollution and typicals seemed better camouflaged, melanics reached a frequency of 80%, prompting Lees and Creed to write: "We conclude therefore that either the predation experiments and tests of conspicuousness to humans are misleading, or some factors or factors in addition to selective predation are responsible for maintaining the high melanic frequencies" (Lees and Creed 1975, pp. 75-76). On the other hand, melanics in south Wales were better camouflaged than typicals, yet comprised only about 20% of the population (Steward 1977a,b). Compiling data from 165 separate sites in Britain, Steward found a correlation between melanism and the concentration of sulfur dioxide (an airborne pollutant) north of latitude 52*N (Figure 2), but concluded that "in the south of Britain non-industrial factors may be of greater importance" than selective predation. Steward cautioned that "it may not be possible to generalize from the results for one area, to explain geographic variation over the rest of Britain" (Steward 1977a, pp. 239, 242). After the passage of anti-pollution legislation, the proportion of melanics decreased north of London (as expected), but inexplicably increased to the south (Bishop and Cook 1980; Jones 1982). In The Netherlands, the decline of melanism took another twist. As air pollution declined, not only did the frequency of typicals increase, but also the frequency of an intermediate form which was almost as dark as melanics, suggesting a more complex change than was seen in Britain (Brakefield 1990). Various theoretical models have been proposed to account for the discrepancies. Some include the effects of gene flow due to migration, though according to Jones "gene flow alone cannot explain... why melanics are so common in some unpolluted parts of Britain" (Jones 1982, p. 109). Mani (1990), like Steward (1977a), obtained a good fit between melanism and sulfur dioxide concentration, but cautioned that "such a correlation does not define causal connection. It only says that SO2 concentration can be used as an approximate measure of the level of pollution that affects the morphs differentially in some unknown way" (Mani 1990, p. 368; emphasis in original). Whatever the actual causes may be, Berry concluded, "it is clear that melanic peppered moth frequencies are determined by much more than differential visual predation by birds" (Berry 1990, p. 312). [caption id="" align="alignright" width="262"]pepfig3.gif - 5660 Bytes Figure 3. Problems with the classical story: The U. S. (a) In the 1970’s, the frequency of melanics in an unspoiled forest in southwestern Virginia was about double the frequency in polluted Blacksburg 18 km away; neither lichen cover nor gene flow could explain the difference (West 1977). (b) From 1971 to 1978, melanics remained at about 52% in a low-pollution area in central eastern Pennsylvania (Manley 1981). (c) Melanics occurred at low frequencies in western and central Massachusetts even though trees were neither devoid of lichens nor blackened by soot (Sargent 1974, Treat 1979). (d) Between the 1960’s and 1990’s, melanics in southeastern Michigan increased and decreased in parallel with those in England, but without any perceptible changes in lichen cover (Grant et al. 1996).[/caption] In the United States, the first melanic peppered moth was reported in Philadelphia in 1906, and melanism increased until by 1959 it was over 90% in some areas (Owen 1962). Yet the geographical distribution did not fit the classical story any better than it did in the U.K. (Figure 3). In the 1970’s, the frequency of melanics in a seemingly unspoiled forest in southwestern Virginia was more than double the frequency at polluted Blacksburg, 18 km away. The difference was not related to lichen cover, and could not be explained by pollution levels or gene flow (West 1977). In a low-pollution area in central eastern Pennsylvania, melanics remained at about 52% from 1971 to 1978 (Manley 1981), and in western and central Massachusetts melanics persisted at low frequencies even though the trees there were neither devoid of lichens nor blackened by soot (Sargent 1974, Treat 1979). In southeastern Michigan, the frequency of melanics was over 90% in the early 1960's, then dropped to less than 20% by 1995 (Grant et al. 1995), thus paralleling the decline of melanism in the U.K. Yet the decline in Michigan "occurred in the absence of perceptible changes in local lichen floras" (Grant et al. 1996, p. 351). Recently, Grant and his colleagues reported a good correlation between sulfur dioxide levels and melanic frequencies in southwestern Virginia, central eastern Pennsylvania, and southeastern Michigan. In fact, the decline of melanism in both the U.S. and the U.K. appears to be "correlated primarily with reductions in atmospheric sulfur dioxide" (Grant et al. 1998, p. 465). The lack of correlation between between melanic frequencies and lichen cover, however, is a serious problem for the theory that industrial melanism is due to cryptic coloration and selective predation. This aspect of the story warrants a closer look. Is there a correlation between melanism and lichen cover? In the 1970's, Kettlewell noted that melanism began declining on the Wirral Peninsula before lichens returned to the trees (Kettlewell 1973). Lees and his colleagues surveyed melanism in peppered moths at 104 sites throughout Britain, and found a lack of correlation with lichen cover which they considered "surprising in view of the results of Kettlewell's selection experiments" (Lees et al. 1973). As noted above, American biologists during the same period reported that melanism was also unrelated to lichen cover in the U.S. (Sargent 1974, West 1977, Treat 1979). The discrepancy has persisted. In the early 1980's, Clarke and his colleagues found "a reasonable correlation" in the U.K. between the decline in melanism and decrease in sulfur dioxide pollution, but were surprised to note "that throughout this time the appearance of the trees in Wirral does not seem to have changed appreciably" (Clarke et al. 1985, p. 198). According to Grant and Howlett, if the rise of industrial melanism was originally due to the demise of lichens on trees, then "the prediction is that lichens should precede the recovery of the typical morph as the common form. That is, the hiding places should recover before the hidden. But, this is clearly not the case in at least two regions where the recovery of typicals has been especially well documented in the virtual absence of these lichens: on the Wirral..., and in East Anglia" (Grant and Howlett 1988, pp. 230-231). Ten years later, the situation on the Wirral Peninsula remains the same; Grant and his colleagues note that "even now lichen coverage on trees in that region is sparse, yet the typicals exceed 93%" (Grant et al. 1998, p. 466). The decline of melanism in the U.S. without perceptible changes in the lichen cover prompted Grant and his colleagues to conclude that "the role of lichens has been inappropriately emphasized in chronicles about the evolution of melanism in peppered moths" (Grant et al. 1996, p. 351). Sargent and his colleagues note that "the recent declining frequency of melanism in B. betularia in North America, where the hypothesis of a cryptic advantage of melanism never seemed applicable," is "perplexing" in view of the classical story (Sargent et al. 1998, pp. 316-317). So melanism declined in the U.K. before lichens returned to the trees. In the U.S., melanism occurred in the presence of lichens and declined without any perceptible change in them. Clearly, the rise and fall of industrial melanism did not depend on the presence or absence of lichens. Yet their presence or absence seemed highly significant in Kettlewell's experiments. Why the discrepancy? The normal resting places of peppered moths. In most of Kettlewell's experiments, moths were released in the morning and observed during the day. Recaptures were made at night. In only one experiment (June 18, 1955) did Kettlewell release moths before sunrise; he abandoned this approach because of practical difficulties such as having to warm the cold moths beforehand on the engine of his car (Kettlewell 1973). But peppered moths are night-fliers, and normally find resting places on trees before dawn. Artificial daytime releases might have disoriented the moths, causing them to fly immediately to exposed tree trunks where they became unnaturally easy targets for predatory birds. Regarding his release methods, Kettlewell wrote: "To the obvious criticism that the releases were not free to take up their own choice of resting site for the first day, I must answer that there were no other alternative backgrounds available for an insect that has to spend its days on trunks and boughs in this wood. I admit that, under their own choice, many would have taken up position higher in the trees, and... in so doing they would have avoided concentrations such as I produced.... [O]thers have shown the importance to cryptic insects of avoiding too high a density level, but this is no argument against the findings for the relative advantages" of the light and dark forms. Kettlewell granted, however, "that, under natural conditions, predation, though selective, might take place at a lower tempo" (Kettlewell 1955, p. 340; emphasis in original). In other words, Kettlewell assumed (1) that the main defect of his release method was an unnaturally high density of moths, affecting merely the tempo of predation; and (2) that he could disregard the observation that many moths would have preferred to take up positions higher in the trees. Before the 1980's most investigators shared Kettlewell's second assumption, and many of them found it convenient to conduct predation experiments using dead specimens glued or pinned to tree trunks (e.g., Clarke and Sheppard 1966, Bishop 1972, Lees and Creed 1975, Bishop and Cook 1975, Steward 1977b, Murray et al. 1980). Kettlewell himself considered this a bad idea (Kettlewell 1973), and some biologists who used dead moths suspected that the technique was unsatisfactory. For example, Bishop and Cook conducted predation experiments using dead moths glued to trees; but they noted discrepancies in their results which "may indicate that we are not correctly assessing the true nature of the resting sites of living moths when we are conducting experiments with dead ones" (Bishop and Cook 1975, p. 9). Figure 1, which is taken from Bishop and Cook's 1975 article, shows live moths rather than dead ones, but because peppered moths are quite torpid during the day it was easy to place them manually on the desired backgrounds (L. M. Cook, 1998, personal communication. University of Manchester, Manchester, U.K.). Indeed, close inspection of Figure 1 reveals that the pattern of gray-and-black scales in the typical form, and the pattern of wing veins in the melanic form, are identical in the top two panels. Clearly, the same two moths were placed on two different backgrounds. Most textbook photographs of peppered moths similarly show specimens which have been manually placed on tree trunks (Sargent et al. 1998). Since 1980, however, evidence has accumulated showing that peppered moths do not normally rest on tree trunks. Using caged moths, Mikkola observed that "the normal resting place of the Peppered Moth is beneath small, more or less horizontal branches (but not on narrow twigs), probably high up in the canopies, and the species probably only exceptionally rests on tree trunks." He noted that "night-active moths, released in an illumination bright enough for the human eye, may well choose their resting sites as soon as possible and most probably atypically." Thus "the results of Kettlewell (1955, 1956) fail to demonstrate the qualitative predation of the morphs of the Peppered Moth by birds or other predators in natural conditions" (Mikkola 1984, pp. 416-418). Mikkola used caged moths, but data on wild moths support his conclusion. In twenty-five years of field work, Clarke and his colleagues found only one peppered moth on a tree trunk, and admitted that they knew primarily "where the moths do not spend the day" (Clarke et al. 1985, p. 197; emphasis in original). When Howlett and Majerus studied the natural resting sites of peppered moths in various parts of England, they found that Mikkola's observations on caged moths were valid for wild moths, as well. They concluded: " seems certain that most B. betularia rest where they are hidden.... [and] that exposed areas of tree trunks are not an important resting site for any form of B. betularia" (Howlett and Majerus 1987, p. 40). In a separate study, Liebert and Brakefield confirmed Mikkola's observations that "the species rests predominantly on branches.... Many moths will rest underneath, or on the side of, narrow branches in the canopy" (Liebert and Brakefield 1987, p. 129). In a recent book on melanism, Majerus criticizes the "artificiality" of much previous work in this area, noting that "in most predation experiments peppered moths have been positioned on vertical tree trunks, despite the fact that they rarely chose such surfaces to rest upon in the wild" (Majerus 1998, p. 116). If peppered moths normally rest under horizontal branches in the upper canopy, then observations of differential bird predation on moths which are placed on tree trunks probably have little relevance to their survival in the wild. It appears that the classical example of natural selection is actually be an example of unnatural selection!


Bernard Kettlewell was a good scientist. Even now, almost half a century after his initial experiments, Kettlewell's scientific papers make exciting reading. But science doesn't stop with initial experiments. Kettlewell's successors, who were also good scientists, found unexpected problems with his conclusion that industrial melanism is due to cryptic coloration and selective predation. The geographic distribution of melanic peppered moths did not fit the theory: the frequency of melanics was not as high as it should have been in some places, and higher than it should have been in others. Furthermore, melanism is not correlated with lichen cover; in the U.K., it declined before lichens returned to the trees, while in the U.S., it occurred despite the presence of lichens and declined without any perceptible changes in lichen cover. Finally, peppered moths do not normally rest on tree trunks: instead, they normally rest under horizontal branches high in the canopy, not where Kettlewell and his successors had carried out their experiments on selective predation. These findings do not entirely rule out a role for cryptic coloration and selective predation in industrial melanism, but at the very least they deprive Kettlewell's explanation of empirical support. As one recent review concludes, "there is little persuasive evidence, in the form of rigorous and replicated observations and experiments, to support this explanation at the present time" (Sargent et al. 1998, p. 318). In at least one insect (the ladybird beetle, Adalia bipunctata), industrial melanism has nothing to do with cryptic coloration and selective predation. Ladybird beetles are extremely distasteful to most birds, and exhibit warning coloration rather than cryptic coloration; there is no evidence that they are significantly affected by selective predation (Creed 1966, Ford 1975). Industrial melanism in ladybird beetles has been attributed to non-visual selection on the ability of melanic and non-melanic forms to absorb solar radiation -- a phenomenon known as "thermal melanism" (Brakefield 1985). This does not mean that the same explanation applies to peppered moths, but it clearly indicates that cryptic coloration and selective predation are not the only possible explanations for industrial melanism. Some biologists continue to believe, like Harrison (1920), that melanism might be directly induced by environmental factors (reviewed in Sargent et al. 1998). Most biologists, however, believe that natural selection is responsible, though no one knows what traits are being selected or what factors in the environment are doing the selecting. The very prominence of the peppered moth story in the teaching of evolution requires that it be scrupulously accurate. According to Grant and Howlett, "as Biston betularia has served as a paradigm of evolution, it demands the closest possible scrutiny" (Grant and Howlett 1988, p. 231). Yet this classical story of evolution by natural selection, as it continues to be retold in many textbooks, is seriously flawed. In particular, the illustrations which typically accompany the story (like the photographs in Figure 1) mislead students by portraying peppered moths on tree trunks where they do not normally rest. Unknown to Kettlewell, his experiments had less to do with natural selection than with unnatural selection, and the true causes of industrial melanism in peppered moths remain largely unknown. The classical story, elegant and appealing though it may be, should no longer be presented as a textbook example of evolution in action. If the purpose of science education is to teach students how to do good science, then instead of re-telling the classical story textbooks would do better to focus on how science revealed its flaws.


The author thanks Laurence M. Cook for helpful comments and for permission to use his 1975 photograph of peppered moths, and thanks Bruce Grant for supplying a preprint of his 1998 article in Journal of Heredity. The author also thanks Lucy Wells and Roberta Bidinger for their assistance with the manuscript. Research for this article was funded by a grant from The Discovery Institute, Seattle, WA.


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West DA. 1977. Melanism in Biston (Lepidoptera: Geometridae) in the rural central Appalachians. Heredity 39: 75-81.

Wright S. 1978. Evolution and the Genetics of Populations. Volume 4: Variability Within and Among Natural Populations. Chicago: The University of Chicago Press.

Jonathan Wells, Expanded from The Scientist 13, no. 11 (May 24, 1999)

List of Textbooks Evaluated

(All have copyright dates of 1998 or later. Books are listed alphabetically by first author's last name.)
  1. Alton Biggs, Chris Kapicka & Linda Lundgren, Biology: The Dynamics of Life (Westerville, OH: Glencoe/McGraw-Hill, 1998). ISBN 0-02-825431-7
  2. Neil A. Campbell, Jane B. Reece & Lawrence G. Mitchell, Biology, Fifth Edition (Menlo Park, CA: The Benjamin/Cummings Publishing Company, 1999). ISBN 0-8053-6573-7
  3. Douglas J. Futuyma, Evolutionary Biology, Third Edition (Sunderland, MA: Sinauer Associates, 1998). ISBN 0-87893-189-9
  4. Burton S. Guttman, Biology, (Boston: WCB/McGraw-Hill, 1999). ISBN 0-697-22366-3
  5. George B. Johnson, Biology: Visualizing Life, Annotated Teacher's Edition (Orlando, FL: Holt, Rinehart & Winston, 1998). ISBN 0-03-016724-8
  6. Sylvia Mader, Biology, Sixth Edition (Boston: WCB/McGraw-Hill, 1998). ISBN 0-697-34080- 5
  7. Kenneth R. Miller & Joseph Levine, Biology, Fifth Edition (Upper Saddle River, NJ: Prentice-Hall, 2000). ISBN 0-13-436265-9
  8. Peter H. Raven & George B. Johnson, Biology, Fifth Edition (Boston: WCB/McGraw-Hill, 1999). ISBN 0-697-35353-2
  9. William D. Schraer & Herbert J. Stoltze, Biology: The Study of Life , Seventh Edition (Upper Saddle River, NJ: Prentice Hall, 1999). ISBN 0-13-435086-3
  10. Cecie Starr & Ralph Taggart, Biology: The Unity and Diversity of Life, Eighth Edition (Belmont, CA: Wadsworth Publishing Company, 1998). ISBN 0-534-53001-X.
Darwin's tree of life
Vertebrate limb homology
Haeckel's embryos
Peppered moths
Darwin's finches

Specific Evaluation Criterion

In general, an "A" requires full disclosure of the truth, discussion of relevant scientific controversies, and a recognition that Darwin's theory — like all scientific theories — might have to be revised or discarded if it doesn't fit the facts. An "F" indicates that the textbook uncritically relies on logical fallacy, dogmatically treats a theory as an unquestionable fact, or blatantly misrepresents published scientific evidence.

Icons of Evolution Explained

The Miller-Urey Experiment

Many modern scientists believe that living cells arose from chemical building-blocks that formed on the early Earth. In 1953, Stanley Miller used an electric spark to simulate lightning in a mixture of gasses thought to resemble the Earth's primitive atmosphere, and produced some of the chemical building-blocks of life. The experiment is pictured in many biology textbooks to show that scientists now understand an important early step in the origin of life. But scientists determined over a decade ago that the Earth's primitive atmosphere was probably nothing like the mixture of gasses Miller used, and now acknowledge that the origin of life's building-blocks remains unexplained.

A = does not include a picture or drawing of the Miller-Urey apparatus, or else accompanies it with a caption pointing out that the experiment (though historically interesting) is probably irrelevant to the origin of life because it did not simulate conditions on the early Earth; text mentions the controversy over oxygen in the primitive atmosphere, and includes extensive discussion of the other problems faced by origin-of-life research, acknowledging that they remain intractable.

B = does not include a picture or drawing of the Miller-Urey apparatus, or else accompanies it with a caption pointing out that the experiment (though historically interesting) is probably irrelevant to the origin of life because it did not simulate conditions on the early Earth; text includes at least some discussion of other problems in origin-of-life research, and does not leave the student with the impression that scientists are on the verge of understanding the origin of life.

C = includes a picture or drawing of the Miller-Urey apparatus, but the caption does not claim that the Miller-Urey experiment simulated conditions on the early Earth; the accompanying text points out that the experiment fails even if other starting mixtures are used, and does not leave the student with the impression that the experiment (or some variant of it) demonstrated how life's building-blocks formed on the early earth; does not discuss other problems with origin-of-life research.

D = includes a picture or drawing of the Miller-Urey apparatus with a misleading caption claiming or implying that the experiment simulated conditions on the early Earth; but the accompanying text explicitly points out that this was probably not the case (merely listing other gasses, and leaving it to the student to spot the discrepancy, is not sufficient); may leave the student with the impression that the experiment (or some variant of it) demonstrated how life's building-blocks formed on the early earth.

F = includes a picture or drawing of the Miller-Urey apparatus with a misleading caption claiming or implying that the experiment simulated conditions on the early Earth; the text contains no mention of the experiment's flaws, and leaves the student with the impression that it demonstrated how life's building-blocks formed on the early earth.

Darwin's Tree of Life

Darwin believed that all living things are modified descendants of one or a few original forms. Most biology textbooks show the branching-tree pattern that would result from such "descent with modification," and tell students that it is so thoroughly confirmed by the fossil and molecular evidence that it may be called a "scientific fact." But the fossil record of the "Cambrian explosion" shows that the major groups of animals appeared at about the same time -- a "lawn" rather than a tree; and recent molecular evidence suggests a "tangled thicket" instead of the branching pattern of Darwin's tree of life.

A = explicitly treats universal common ancestry as a theory rather than a fact; clearly points out that the "top-down" Cambrian explosion contradicts the "bottom-up" pattern of Darwinian evolution, and acknowledges the theoretical possibility of multiple origins and separate lines of descent; also mentions problems for universal common ancestry posed by recent evidence from molecular phylogeny.

B = explicitly treats universal common ancestry as a theory rather than a fact; clearly points out that the "top-down" Cambrian explosion contradicts the "bottom-up" pattern of Darwinian evolution, and acknowledges the theoretical possibility of multiple origins and separate lines of descent; but does not mention recent problems in molecular phylogeny.

C = explicitly treats universal common ancestry as a theory rather than a fact; discusses the Cambrian explosion as a problem for Darwinian evolution, but does not mention the theoretical possibility of multiple origins and separate lines of descent.

D = assumes the truth of universal common ancestry without questioning it (and may call it a "fact"); mentions the Cambrian explosion in the body of the text (briefly mentioning it in a note at the end of the chapter, without explaining what it is, is not sufficient), but does not discuss the problem it poses for Darwinian evolution.

F = assumes the truth of universal common ancestry without questioning it (and may call it a "fact"); does not even mention the Cambrian explosion.

Homology in Vertebrate Limbs

A bat's wing, a porpoise's flipper, a horse's leg, and a human hand all contain bones that are structurally similar. Before Darwin, biologists called this "homology," and considered it evidence for a common design, but Darwin attributed it to a common ancestor. Modern Darwinists have re-defined homology as similarity due to common ancestry, but now homology cannot serve as evidence for common ancestry without arguing in a circle. Many biology textbooks use circular reasoning anyway: We know that two features are homologous because they come from a common ancestor, and we know they come from a common ancestor because they're homologous.

A = defines homology as similarity of structure and position, and explains that this was historically attributed to a common archetype; mentions a biological ancestor as one possible meaning of "archetype," but acknowledges that there are others, and that the concept of homology continues to be controversial; clearly explains out that the two biological mechanisms proposed so far to account for homology (similar genes and similar developmental pathways) are inconsistent with the evidence.

B = defines homology as similarity of structure and position due to a common archetype, and identifies "archetype" with a biological ancestor without explaining that there are other possibilities; points out that the two biological mechanisms proposed so far to account for it (similar genes and similar developmental pathways) are inconsistent with the evidence.

C = defines homology as similarity of structure and position, and cites it as evidence for common ancestry; attributes homology to similar genes or similar developmental pathways, but at least hints that there are problems with the evidence.

D = defines homology as similarity of structure and position, and cites it as evidence for common ancestry; may attribute homology to similar genes or similar developmental pathways, but fails to mention that the evidence does not fit the claim.

F = defines homology as similarity due to common ancestry, then engages in circular reasoning by citing homology as evidence for common ancestry.

Haeckel's Embryos

Darwin believed that all animals with backbones (including humans) evolved from fish-like ancestors, and he thought the best evidence for this was that the early embryos of amphibians, reptiles, birds and mammals are similar to fish embryos. Many biology textbooks carry drawings (originally by Ernst Haeckel) to illustrate this, and claim that human embryos possess "gill slits." But embryologists have known for over a century that such drawings are false, and that early embryos of amphibians, reptiles, birds and mammals do NOT resemble fish. Human embryos pass through a stage when they have wrinkles in their necks, but they never have "gill slits."

A = does not use misleading drawings or photos, and does not call pharyngeal pouches "gill slits"; points out that vertebrate embryos are most similar midway through development, after being dissimilar in their earliest stages; acknowledges this as an unresolved problem for Darwinian evolution, and considers the possibility that Darwin's theory of vertebrate origins could be wrong.

B = does not use misleading drawings or photos, and does not call pharyngeal pouches "gill slits"; points out that vertebrate embryos are most similar midway through development, after being dissimilar in their earliest stages; acknowledges this as an unresolved problem for Darwinian evolution, but does not explicitly consider the possibility that Darwin's theory of vertebrate origins could be wrong.

C = does not use misleading drawings or photos; points out that vertebrate embryos are most similar midway through development, after being dissimilar in their earliest stages, but explains away this fact in order to reconcile it with Darwinian evolution; may call pharyngeal pouches "gill slits."

D = uses actual photos rather than Haeckel's drawings, but chooses those which best fit the theory; fails to mention that earlier stages are dissimilar, and claims that early similarities in vertebrate embryos are evidence for common ancestry and Darwinian evolution; may call pharyngeal pouches "gill slits."

F = uses Haeckel's drawings (or a re-drawn version of them) without mentioning the dissimilarity of earlier stages; claims that early similarities in vertebrate embryos are evidence for common ancestry and Darwinian evolution; may call pharyngeal pouches "gill slits."

Archaeopteryx - The Missing Link

Darwin believed that modern species were linked in the past by innumerable transitional forms, but when he published his theory in 1859 those transitional links were missing. The discovery of Archaeopteryx, a fossil bird with reptile-like teeth, helped to persuade many people that Darwin's theory was true, and many biology textbooks still feature Archaeopteryx as the "missing link" between reptiles and birds. Yet paleontologists no longer believe that Archaeopteryx was the ancestor of modern birds, and its own ancestors are the subject of heated controversy. The "missing link" between reptiles and birds, it seems, is still missing.

A = explains that the status of Archaeopteryx as a transitional link between reptiles and birds is controversial; points out that modern birds are probably not descended from it; mentions the controversy over whether birds evolved from dinosaurs or from a more primitive group; points out that the supposed dinosaur ancestors of Archaeopteryx do not appear in the fossil record until tens of millions of years after it.

B = explains that the status of Archaeopteryx as a transitional link between reptiles and birds is controversial; points out that modern birds are probably not descended from it; mentions the controversy over whether birds evolved from dinosaurs or from a more primitive group; but fails to point out that the supposed dinosaur ancestors of Archaeopteryx do not appear in the fossil record until tens of millions of years after it.

C = explains that the status of Archaeopteryx as a transitional link between reptiles and birds is controversial; points out that modern birds are probably not descended from it; but does not mention the controversy over whether birds evolved from dinosaurs or from a more primitive group.

D = presents Archaeopteryx as the transitional link between reptiles (or dinosaurs) and modern birds; does not point out that modern birds are probably not descended from it, but at least hints at the fact that there is a controversy over its ancestry or its transitional status.

F = presents Archaeopteryx as the transitional link between reptiles (or dinosaurs) and modern birds; does not point out that modern birds are probably not descended from it, and does not even hint at the fact that there is a controversy over its ancestry or its transitional status.

Peppered Moths

Darwin had no direct evidence for natural selection, the principal mechanism in his theory of evolution. Experiments in the 1950s seemed to provide the missing evidence by showing that light-colored peppered moths were more easily seen and eaten by predatory birds on pollution-darkened tree trunks, leaving mostly dark-colored moths to survive and reproduce. Many biology textbooks carry photographs of light and dark peppered moths on tree trunks to illustrate this famous story. Yet biologists have known for over a decade that the story has problems. Among other things, peppered moths don't normally rest on tree trunks, and the textbook photographs have been staged.

A = uses photos of moths in their natural resting places; does not use staged photos of moths on tree trunks (except as illustrations of how the classical story was wrong); clearly discusses unresolved problems with Kettlewell's experiments and the classical story, and points out that these problems raise serious doubts about whether peppered moths provide direct evidence for natural selection.

B = uses photos of moths in their natural resting places; does not use staged photos of moths on tree trunks (except as illustrations of how the classical story was wrong); mentions unresolved problems with Kettlewell's experiments and the classical story, but does not discuss the possibility that peppered moths do not provide direct evidence for natural selection.

C = uses staged photos but clearly explains that they were staged, because moths do not rest on tree trunks in the wild; describes Kettlewell's experiments, but briefly mentions that they and the classical story are now in doubt.

D = uses staged photos without mentioning that they misrepresent the natural situation; but the accompanying text at least hints at the fact that there are problems with Kettlewell's experiments or the classical story.

F = uses staged photos without mentioning that they misrepresent the natural situation; describes Kettlewell's experiments as a demonstration of natural selection, without mentioning their flaws or problems with the classical story.

Darwin's Finches

Many biology textbooks claim that finches on the Galapagos Islands, whose beak sizes are correlated with the foods they eat, helped to convince Darwin of evolution by natural selection in 1835. But the legend of "Darwin's finches" was actually contrived a century later. Some textbooks also tell students that a slight increase in the average size of finch beaks, observed after a severe drought in the 1970s, shows how natural selection could produce a new species in only two hundred years. But the textbooks fail to mention that the change was reversed when the rains returned, and no net evolution occurred.

A = explicitly points out that the Galapagos finches had little to do with the formulation of Darwin's theory; explains that selection on finch beaks oscillates between wet and dry years, producing no net evolutionary change; points out both that the genes affecting finch beaks are unknown and that hybrids between several species are now more fit than their parents, suggesting that those species may be merging.

B = explicitly points out that the Galapagos finches had little to do with the formulation of Darwin's theory; explains that selection on finch beaks oscillates between wet and dry years, producing no net evolutionary change; points out either that the genes affecting finch beaks are unknown or that hybrids between several species are now more fit than their parents, suggesting that those species may be merging.

C = describes the Galapagos finches as a good example of adaptive radiation (the origin of species by natural selection); but points out both that selection on finch beaks oscillates between wet and dry years and that the finches did not play an important role in the formulation of Darwin's theory.

D = describes the Galapagos finches as a good example of adaptive radiation (the origin of species by natural selection); but points out either that selection on finch beaks oscillates between wet and dry years or that the finches did not play an important role in the formulation of Darwin's theory.

F = describes the Galapagos finches as a good example of adaptive radiation (the origin of species by natural selection); but fails to mention that selection on finch beaks oscillates between wet and dry years, and implies that the finches played an important role in the formulation of Darwin's theory.

Intelligent Design theory (ID) can contribute to science on at least two levels. On one level, ID is concerned with inferring from the evidence whether a given feature of the world is designed. This is the level on which William Dembski's explanatory filter and Michael Behe's concept of irreducible complexity operate. It is also the level that has received the most attention in recent years, largely because the existence of even one intelligently designed feature in living things (at least prior to human beings) would overturn the Darwinian theory of evolution that currently dominates Western biology. On another level, ID could function as a "metatheory," providing a conceptual framework for scientific research. By suggesting testable hypotheses about features of the world that have been systematically neglected by older metatheories (such as Darwin's), and by leading to the discovery of new features, ID could indirectly demonstrate its scientific fruitfulness. In November 2002, Bill Dembski, Paul Nelson and I visited the Detroit headquarters of Ideation, Inc. Ideation is a thriving business based on TRIZ, an acronym for the Russian words meaning "Theory of Inventive Problem Solving." Based on a survey of successful patents, TRIZ provides guidelines for finding solutions to specific engineering or manufacturing problems. When Ideation's president took us out to lunch, he told us that before ID could be taken seriously it would have to solve some real problems.


I was inspired by this to sketch out something I called a Theory of Organismal Problem-Solving (TOPS). Strictly speaking, I suppose the biological equivalent of TRIZ would survey successful experiments for guidelines to solve research problems posed by existing hypotheses. I chose to try a different approach, however: As I formulated it, TOPS suggests how ID could lead to new hypotheses and scientific discoveries. TOPS begins with the observation that the evidence is sufficient to warrant at least provisional acceptance of two propositions: (1) Darwinian evolution (the theory that new features of living things originate through natural selection acting on random variations) is false, and (2) ID (the theory that many features of living things could only have originated through intelligent agency) is true. TOPS then explicitly rejects several implications of Darwinian evolution. These include: (1a) The implication that living things are best understood from the bottom up, in terms of their molecular constituents. (1b) The implications that DNA mutations are the raw materials of macroevolution, that embryo development is controlled by a genetic program, that cancer is a genetic disease, etc. (1c) The implication that many features of living things are useless vestiges of random processes, so it is a waste of time to inquire into their functions. Finally, TOPS assumes as a working hypothesis that various implications of ID are true. These include: (2a) The implication that living things are best understood from the top down, as irreducibly complex organic wholes. (2b) The implications that DNA mutations do not lead to macroevolution, that the developmental program of an embryo is not reducible to its DNA, that cancer originates in higher structural features of the cell rather than in its DNA, etc. (2c) The implication that all features of living things should be presumed to have a function until proven otherwise, and that reverse engineering is the best way to understand them. It is important to note that "implication" is not the same as "logical deduction." Darwinian evolution does not logically exclude the ID implications listed here, nor does ID logically exclude every implication of Darwinian evolution. A Darwinian may entertain the idea that other features of an embryo besides DNA influence its development, and Darwinians can (and do) use reverse engineering to understand the functions of features in living things. Furthermore, an ID viewpoint does not logically rule out genetic programs or the idea that some features of living things may be useless vestiges of evolution. The differences between Darwinian evolution and ID that form the starting-point for TOPS are not mutually exclusive logical entailments, but differences in emphasis. The goal of TOPS is not to show that Darwinian evolution leads logically to false conclusions, but to explore what happens when ID rather than evolutionary theory is used as a framework to ask research questions. Take, for example, research on the vast regions of vertebrate genomes that do not code for proteins. From a neo-Darwinian perspective, DNA mutations can provide the raw materials for evolution because DNA encodes proteins that determine the essential features of organisms. Since non-coding regions do not produce proteins, Darwinian biologists have been dismissing them for decades as random evolutionary noise or "junk DNA." From an ID perspective, however, it is extremely unlikely that an organism would expend its resources on preserving and transmitting so much "junk." It is much more likely that non-coding regions have functions that we simply haven't discovered yet. Recent research shows that "junk DNA" does, indeed, have previously unsuspected functions. Although that research was done in a Darwinian framework, its results came as a complete surprise to people trying to ask Darwinian research questions. The fact that "junk DNA" is not junk has emerged not because of evolutionary theory but in spite of it. On the other hand, people asking research questions in an ID framework would presumably have been looking for the functions of non-coding regions of DNA all along, and we might now know considerably more about them.

TOPS and Cancer

In November 2002, I decided to apply TOPS to a specific biomedical problem. Not being one to proceed timidly, I chose to tackle cancer. I quickly learned from reviewing the recent scientific literature that cancer is not correlated with any consistent pattern of DNA mutations, but it iscorrelated with abnormalities at the chromosomal level -- a phenomenon called "chromosomal instability" (Lengauer et al., 1998). Chromosomal instability, in turn, is correlated with centrosome abnormalities -- particularly the presence of extra or enlarged centrosomes. A growing number of researchers regard cancer not as a DNA disease, but as a "centrosomal disease" (Brinkley and Goepfert, 1998; Pihan et al., 1998; Lingle and Salisbury, 2000). In 1985, I had published a hypothesis about how centrosomes might produce a force in dividing cells that pushes chromosomes away from the spindle poles (Wells, 1985). Cell biologists have long been aware of this "polar ejection force" or "polar wind" (Rieder et al., 1986; Rieder and Salmon, 1994), but its mechanism remains unknown. The force has been attributed to microtubule elongation and/or microtubule-associated motor proteins, but neither of these explanations fits all the facts (Wells, 2004). In the hypothesis I proposed in 1985, magnetic interactions in the centrosome would cause spindle microtubules to "wobble" like a laboratory vortexer, though at a much higher frequency and much smaller amplitude, producing a centrifugal-like force directed away from spindle poles. I subsequently realized (with help from physicist David Snoke) that the magnetic interactions I had proposed in 1985 would not work. In 2002 it occurred to me, however, that the still-viable vortexer concept might help to explain the link between centrosomes and cancer: Centrosomes that are too numerous or too large would produce too strong a polar ejection force, damaging chromosomes and leading to chromosomal instability. If the polar ejection force were really the link between centrosomes and cancer, however, and the polar ejection force were due to a vortexer-like motion of spindle microtubules, what could be the mechanism producing this motion? My attention quickly turned to centrioles. Centrosomes in animal cells contain centrioles, tiny organelles less than a millionth of a meter long. Except for their role in nucleating eukaryotic cilia and flagella, their precise functions remain mysterious (Preble et al., 2000). They have never been a favorite object of study within the framework of Darwinian theory, because even though they replicate every time a cell divides they contain no DNA (Marshall and Rosenbaum, 2000), and they have no evolutionary intermediates from which to reconstruct phylogenies (Fulton, 1971). The cells of higher plants do not contain centrioles (Luykx, 1970; Pickett- Heaps, 1971); nor do they produce a polar ejection force like the one observed in animal cells (Khodjakov et al., 1996). It occurred to me that the correlation might not be accidental. Centrioles might be the source of the polar ejection force, and they might hold the clue to understanding cancer. In the electron microscope, centrioles look like tiny turbines. Using TOPS as my guide, I concluded that if centrioles look like turbines they might actuallybe turbines. I then used reverse engineering to formulate a testable, quantitative hypothesis linking centrioles, polar ejection forces, and cancer. That hypothesis is summarized below, and the detailed technical version (Wells, 2004) has been submitted for publication in a biology journal.

Centrioles as tiny turbines

Centrioles are roughly cylindrical in shape, and when mature they typically have a diameter of about 0.2 μm and a length of about 0.4 μm. The end of a centriole closest to the center of the cell is called "proximal," and the other end is called "distal." The organelle is composed of nine clusters of microtubules. These are organized as triplets in the proximal half, but the outermost microtubule in each triplet terminates about halfway toward the distal end, which consists of doublet microtubules (Stubblefield and Brinkley, 1967; De Harven, 1968; Wheatley, 1982; Bornens, et al., 1987). The triplet microtubules making up the proximal half of a centriole form blades that are tilted about 45 degrees relative to the circumference. Various authors have noted that the triplet microtubules have a turbine-like disposition. If the centriole were actually a tiny turbine, fluid exiting through the blades would cause the organelle to rotate clockwise when viewed from the proximal end. In order for the centriolar turbine to turn, there must be a mechanism to pump fluid through the blades. Helical structures have been observed in the lumens of centrioles (Stubblefield and Brinkley, 1967; Paintrand et al., 1992). Helical structures have also been observed associated with the central pair apparatus that rotates inside a ciliary or flagellar axoneme (Goodenough and Heuser, 1985; Mitchell, 2003), and axonemes are nucleated by basal bodies that are interconvertible with centrioles (Preble et al., 2000). If the helix inside a centriole rotates like the central apparatus of an axoneme, it could function as an "Archimedes' screw," a corkscrew-action pump that would draw fluid in through the proximal end and force it out through the triplet-microtubule turbine blades. The helical pump could be powered by dynein. Dynein produces microtubule-mediated movements in the axonemes of cilia and flagella, though its mode of action in centrioles would have to be different from the former. Cilia and flagella move because of dynein-based sliding between doublet microtubules (Brokaw, 1994; Porter and Sale, 2000). In centrioles, however, the only dynein-like structures appear to be associated with internal columns in the lumen. (Paintrand et al., 1992) Dynein molecules in those columns could drive an internal Archimedes' screw pump by interacting with its helical blades. By analogy with the central pair apparatus in axonemes, the helix inside a centriole would presumably rotate at about 100 Hz.

Dynamics of a centriole pair

Most centrosomes contain a pair of centrioles connected near their proximal ends and oriented at right angles to each other (Bornens, et al., 1987; Paintrand et al., 1992; Bornens, 2002). The older member ("mother") of a centriole pair is distinguished from the younger ("daughter") by various structures, including "distal appendages" that project at an angle from the distal-most edges of the doublet microtubules, and "subdistal appendages" that form a thick collar around most of the distal half of the mother centriole and serve as an anchor for microtubules that extend into the spindle (Paintrand et al., 1992; Piel et al., 2000). When centrioles are isolated under low calcium conditions, the subdistal appendages dissociate from the wall of the mother centriole while the distal appendages remain connected to it (Paintrand et al., 1992). These characteristics are consistent with a model in which the subdistal appendages form a bearing connected to the cell's cytoskeleton, and the distal appendages form a flange holding the mother centriole in its bearing. (Figure 1) page6image1087641280 Figure 1. Cross-section of a centriole pair. (M) Mother centriole. (D) Daughter centriole. Note the internal helices in each. (a) Subdistal appendages. (b) Spindle microtubules (which are anchored to the subdistal appendages). (c) Distal appendages. In the hypothesis presented here, the subdistal appendages function as a bearing and the distal appendages function as a flange. The large ellipse is the centromatrix capsule enclosing the centriole pair. The daughter centriole, constrained by its proximal connection to the mother, would not rotate on its own axis; instead, it would swing bodily around the long axis of the mother centriole. Nevertheless, the daughter would still function as a turbine, producing a torque that would press the mother centriole laterally against the inner wall of its bearing. The daughter's torque would thereby cause the centriole pair to revolve eccentrically, producing a wobble resembling the motion of a laboratory vortexer. The centriole pair is surrounded by a structural network of 12- to 15-nm diameter filaments called the "centromatrix" (Schnackenberg et al., 1998). The fluid inside the centromatrix capsule would not remain stationary, but would be stirred in a circle by the revolving daughter centriole. It might seem that friction against the inner wall of the centromatrix would offer enormous resistance to such movement; surprisingly, however, the resistance could be quite low because of ""nanobubbles" (Tyrrell and Attard, 2001; Steitz et al., 2003; Ball, 2003). Nanobubbles 200 nm in diameter and 20 nm thick could render a surface composed of hydrophobic 12-15 nm filaments almost frictionless. With power being continually supplied by the helical pump inside the mother centriole, calculations show that the centriole pair could reach an angular velocity of more than 10 kHz midway through cell division (see Mathematical Appendix, below).

Centrioles and the polar ejection force

The subdistal appendages that form the bearing for the revolving centriole pair also anchor microtubules that extend into the spindle (Paintrand et al., 1992; Piel et al., 2000). Other microtubules are anchored in the pericentriolar material surrounding the centromatrix. Just as a vortexer imparts its wobble to a test tube placed in it, so the centrosome would impart its wobble to the microtubules emanating from it. Spindle microtubules would presumably not transmit this motion as uniformly as the rigid glass walls of a test tube, but they may be rigid enough to induce objects within the spindle to undergo movements not unlike the contents of a test tube in a vortexer. It is worth noting in this regard that microtubules in ordered arrays exhibit more stiffness than would be expected from non-interacting rigid rods (Sato et al., 1988). Objects within the spindle would then undergo high frequency, small amplitude circular movements perpendicular to polar microtubules, as originally proposed by Wells (1985). Objects in the middle of a bipolar spindle would thus experience a centrifugal force laterally outward from the long axis of the spindle. Calculations (see Mathematical Appendix, below) show that this force could be more than five times as strong as the force of gravity. The conical arrangement of the microtubules would convert part of this to a component parallel to the spindle axis, producing a smaller force tending to move objects radially away from the pole. The wobble produced by a revolving centriole pair could thereby generate a polar ejection force.

Implications for cancer

If centrioles generate a polar ejection force, the presence of too many centriole pairs at either pole could result in an excessive polar ejection force that subjects chromosomes to unusual stresses that cause breaks and translocations. Even more serious than the presence of extra centrioles would be a failure of the control mechanisms that normally shut down centriolar turbines at the beginning of anaphase, since centriole pairs would then continue to accelerate and generate polar ejection forces far greater than normal. A centriole-generated polar ejection force could be regulated in part by intracellular calcium levels. In dividing animal cells, the onset of anaphase is normally accompanied by a transient rise in intracellular Ca2+ concentration (Poenie et al., 1986). Elevated Ca2+ concentrations can lead to asymmetrical bending or quiescence in sea urchin sperm flagella axonemes (Brokaw, 1987). This may be due to a Ca2+-induced change in the direction of the power stroke of dynein arms (Ishijima et al., 1996), or to an effect on the central pair apparatus (Bannai, et al., 2000). If the helical pump inside a centriole is driven by dynein, then a rise in intracellular calcium concentration could shut it down. It is worth noting in this regard that a number of recent studies have reported a link between calcium and vitamin D deficiency and various types of cancer. Dietary calcium supplements can modestly reduce the risk of colorectal cancer (McCullough et al., 2003), and there appears to be an inverse correlation between vitamin D levels and prostate cancer (Konety et al., 1999). Analogs and metabolites of vitamin D inhibit the growth of prostate cancer cells in vitro (Krishnan et al., 2003) and in vivo (Vegesna et al., 2003), and they have similar inhibitory effects on breast cancer cells (Flanagan et al., 2003). If centrioles generate a polar ejection force, the correlation between calcium and vitamin D levels and cancer could be a consequence -- at least in part -- of the role of calcium in turning off centriolar turbines at the onset of anaphase.


Stubblefield and Brinkley (1967) proposed that sequential movements of the centriole's triplet microtubules turn an internal helix, which they believed to be DNA, in order to facilitate microtubule assembly. It has since become clear, however, that centrioles do not contain DNA (Marshall and Rosenbaum, 2000). In the hypothesis proposed here, a centriole is a tiny turbine composed of triplet microtubule blades and powered by an internal helical pump. This is the reverse of Stubblefield and Brinkley's idea that the triplet microtubules turn the internal helix. Bornens (1979) suggested that rapidly rotating centrioles, powered by an ATPase in cartwheel structures at their proximal ends, function like gyroscopes to provide an inertial reference system for the cell and generate electrical oscillations that coordinate cellular processes. In the hypothesis proposed here, rapidly rotating centrioles would produce small-amplitude, high-oscillations in spindle microtubules that are mechanical, not electrical as Bornens proposed. There are several ways to test this hypothesis. Two ways are:
  1. It should be possible to detect oscillations in spindle microtubules early in prometaphase by immunofluorescence microscopy and high-speed camera technology.
  2. It should be possible to regulate the polar ejection force by raising the concentration of intracellular calcium during prometaphase or blocking its rise at the beginning of anaphase.
If the hypothesis presented here withstands these and other experimental tests, then it may contribute to a better understanding not only of cell division, but also of cancer.


The author gratefully acknowledges helpful suggestions from David W. Snoke, Keith Pennock, and Lucy P. Wells. The author also thanks Joel Shoop for producing the illustration and Peter L. Maricich for assisting with the mathematical analysis.


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Mathematical Appendix

This is only a summary; for details see Wells (2004). A rotating helical pump would cause a fluid flow U into the proximal end of the centriole of

U = 4πφRotanθ(Ro2 – Ri2) (A1)

in which φ and θ are the angular velocity and pitch of the helix, respectively; Ro is the radius of the centriolar lumen (and thus the outer radius of the helix blades); and Ri is the radius of the central column around which the blades wind. Neglecting the thickness of the blades, and using values derived from electron micrographs of centrioles and measurements of central pair rotations in cilia, the fluid flow can be calculated to be of the order of U ≈ 10–19 m3 sec-1. The torque τ produced by the centriolar turbine would be the tangential component of the product of the velocity and the mass of fluid moving through the slits per second, multiplied by the distance of the turbine blades from the axis of rotation (approximately the outer radius of the centriole). The velocity and mass flow can be calculated from U, the approximate area of the slits between the turbine blades, and the density of the fluid being pumped through them. Since the outer radius of a centriole is approximately 0.1 μm, the resulting torque would be of the order of τ ≈ 10–28 kg m2 sec-2. In the rotational equivalent of Newton's force law, the angular acceleration α would be

α = τ/I (A2)

in which I is the effective moment of inertia of the revolving centriole pair. This would be of the order of 10-29 kg m2 (for derivation see Wells, 2004), so the angular acceleration produced by the torque of the mother centriole would be of the order of α ≈ 10 sec-2. Assuming negligible friction (because of nanobubbles), this torque would cause the angular velocity of the centriole pair to increase about 10 Hz every second. One minute after start-up, the centriole pair would be revolving about 600 Hz; after twenty minutes (i.e., about halfway through cell division), the pair would be revolving about 12,000 Hz. Orthogonally oriented centrioles would impart a wobble to the spindle microtubules and produce a centrifugal acceleration β given by

β = (αt)2 dtanε (A3)

in which t is the number of seconds that have elapsed since the turbines started, d is an object's distance from the centrosome, and ε is the eccentricity of the wobble. If the eccentricity of the wobble is 1°, then twenty minutes after start-up an object 20 μm from the spindle pole would be subjected to a centrifugal acceleration β of approximately 50 m sec-2, about five times greater than the acceleration due to gravity.

If you had asked me during my years studying science at Berkeley whether or not I believed what I read in my science textbooks, I would have responded much as any of my fellow students: puzzled that such a question would be asked in the first place. One might find tiny errors, of course, typos and misprints. And science is always discovering new things. But I believed — took it as a given — that my science textbooks represented the best scientific knowledge available at that time.

It was only when I was finishing my Ph.D. in cell and development biology, however, that I noticed what at first I took to be a strange anomaly. The textbook I was using prominently featured drawings of vertebrate embryos — fish, chickens, humans, etc. — where similarities were presented as evidence for descent from a common ancestor. Indeed, the drawings did appear very similar. But I’d been studying embryos for some time, looking at them under a microscope. And I knew that the drawings were just plain wrong.

I re-checked all my other textbooks. They all had similar drawings, and they were all obviously wrong. Not only did they distort the embryos they pictured; they omitted earlier stages in which the embryos look very different from one another.

Like most other science students, like most scientists themselves, I let it pass. It didn’t immediately affect my work, and I assumed that while the texts had somehow gotten this particular issue wrong, it was the exception to the rule. In 1997, however, my interest in the embryo drawings was revived when British embryologist Michael Richardson and his colleagues published the result of their study comparing the textbook drawings with actual embryos. As Richardson himself was quoted in the prestigious journal Science: “It looks like it’s turning out to be one of the most famous fakes in biology.”

Worse, this was no recent fraud. Nor was its discovery recent. The embryo drawings that appear in most every high school and college textbook are either reproductions of, or based on, a famous series of drawings by the 19th century German biologist and fervent Darwinian, Ernst Haeckel, and they have been known to scholars of Darwin and evolutionary theory to be forgeries for over a hundred years. But none of them, apparently, have seen fit to correct this almost ubiquitous misinformation.

Still thinking this an exceptional circumstance, I became curious to see if I could find other mistakes in the standard biology texts dealing with evolution. My search revealed a startling fact however: Far from being exceptions, such blatant misrepresentations are more often the rule. In my recent book I call them “Icons of Evolution,” because so many of them are represented by classic oftrepeated illustrations which, like the Haeckel drawings, have served their pedagogical purpose only too well — fixing basic misinformation about evolutionary theory in the public’s mind.

We all remember them from biology class: the experiment that created the “building blocks of life” in a tube; the evolutionary “tree,” rooted in the primordial slime and branching out into animal and plant life. Then there were the similar bone structures of, say, a bird’s wing and a man’s hand, the peppered moths, and Darwin’s finches. And, of course, the Haeckel embryos.

As it happens, all of these examples, as well as many others purportedly standing as evidence of evolution, turn out to be incorrect. Not just slightly off. Not just slightly mistaken. On the subject of Darwinian evolution, the texts contained massive distortions and even some faked evidence. Nor are we only talking about high-school textbooks that some might excuse (but shouldn’t) for adhering to a lower standard. Also guilty are some of the most prestigious and widely used college texts, such as Douglas Futuyma’s Evolutionary Biology, and the latest edition of the graduate-level textbook Molecular Biology of the Cell, coauthored by the

president of the National Academy of Sciences, Bruce Alberts. In fact, when the false “evidence” is taken away, the case for Darwinian evolution, in the textbooks at least, is so thin it’s almost invisible.

Life in a Bottle

Today, there is near concensus among geochemists that the Earth’s atmosphere consisted of volcanic gases. Put those gases in the Miller-Urey apparatus and the experiment doesn’t work. (From Biology: The Dynamics of Life, McGraw-Hill.)

Anyone old enough in 1953 to understand the import of the news remembers how shocking, and to many, exhilarating, it was. Scientists Stanley Miller and Harold Urey had succeeded in creating “the building blocks” of life in a flask. Mimicking what were believed to be the natural conditions of the early Earth’s atmosphere, and then sending an electric spark through it, Miller and Urey had formed simple amino acids. As amino acids are the “building blocks” of life, it was thought just a matter of time before scientists could themselves create living organisms.

At the time, it appeared a dramatic confirmation of evolutionary theory. Life wasn’t a “miracle.” No outside agency or divine intelligence was necessary. Put the right gasses together, add electricity, and life is bound to happen. It’s a common event. Carl Sagan could thus confidently predict on PBS that the planets orbiting those “billlllions and billlllions” of stars out there must be just teeming with life.

There were problems, however. Scientists were never able to get beyond the simplest amino acids in their simulated primordial environment, and the creation of proteins began to seem not a small step or couple of steps, but a great, perhaps impassable, divide.

The telling blow to the Miller-Urey experiment, however, came in the 1970’s, when scientists began to conclude that the Earth’s early atmosphere was nothing like the mixture of gasses used by Miller and Urey. Instead of being what scientists call a “reducing,” or hydrogen-rich environment, the Earth’s early atmosphere probably consisted of gasses released by volcanoes. Today there is a near consensus among geochemists on this point. But put those volcanic gasses in the Miller-Urey apparatus, and the experiment doesn’t work — in other words, no “building blocks” of life.

What do textbooks do with this inconvenient fact? By and large, they ignore it and continue to use the Miller-Urey experiment to convince students that scientists have demonstrated an important first step in the origin of life. This includes the above-mentioned Molecular Biology of the Cell, co-authored by the National Academy of Sciences president, Bruce Alberts. Most textbooks also go on to tell students that origin-of-life researchers have found a wealth of other evidence to explain how life originated spontaneously — but they don’t tell students that the researchers themselves now acknowledge that the explanation still eludes them.

Faked Embryos

Haeckel’s faked embryos, presented as evidence of evolution in Molecular Biology of the Cell, 3rd Edition, by Bruce Alberts, president of the National Academy of Sciences, et al. (Garland Publishing)

Darwin thought “by far the strongest single class of facts in favor of” his theory came from embryology. Darwin was not an embryologist, however, so he relied on the work of German biologist Ernst Haeckel, who produced drawings of embryos from various classes of vertebrates to show that they are virtually identical in their earliest stages, and become noticeably different only as they develop. It was this pattern that Darwin found so convincing.

This may be the most egregious of distortions, since biologists have known for over a century that vertebrate embryos never look as similar as Haeckel drew them. In some cases, Haeckel used the same woodcut to print embryos that were supposedly from different classes. In others, he doctored his drawings to make the embryos appear more alike than they really were. Haeckel’s contemporaries repeatedly criticized him for these misrepresentations, and charges of fraud abounded in his lifetime. In 1997, British embryologist Michael Richardson and an international team of experts compared Haeckel’s drawings with photographs of actual vertebrate embryos, demonstrating conclusively that the drawings misrepresent the truth.

The drawings are misleading in another way. Darwin based his inference of common ancestry on the belief that the earliest stages of embryo development are the most similar. Haeckel’s drawings, however, entirely omit the earliest stages, which are much different, and start at a more similar midway point. Embryologist William Ballard wrote in 1976 that it is “only by semantic tricks and subjective selection of evidence,” by “bending the facts of nature,” that one can argue that the early stages of vertebrates “are more alike than their adults.”

Yet some version of Haeckel’s drawings can be found in most current biology textbooks. Stephen Jay Gould, one of evolutionary theory’s most vocal proponents, recently wrote that we should be “astonished and ashamed by the century of mindless recycling that has led to the persistence of these drawings in a large number, if not a majority, of modern textbooks.” (I will return below to the question of why it is only now that Mr. Gould, who has known of these forgeries for decades, has decided to bring them to widespread attention.)

Darwin's Tree of Life

Darwin’s branching “Tree of Life” has been seriously undermined by the fossil record and modern molecular biology. (From Biology, by Miller and Levine, published by Prentice Hall.)

Darwin wrote in The Origin of Species: “I view all beings not as special creations, but as the lineal descendants of some few beings” that lived in the distant past. He believed that the differences among modern species arose primarily through natural selection, or survival of the fittest, and he described the whole process as “descent with modification.”

No one doubts, of course, that a certain amount of descent with modification occurs within species. But Darwin’s theory claims to account for the origin of new species – in fact, for every species since the first cells emerged from the primordial ooze.

This theory does have the virtue of making a prediction: If all living things are gradually modified descendants of one or a few original forms, then the history of life should resemble a branching tree. Unfortunately, despite official pronouncements, this prediction has in some important respects turned out to be wrong.

The fossil record shows the major groups of animals appearing fully formed at about the same time in a “Cambrian explosion,” rather than diverging from a common ancestor. Darwin knew this, and considered it a serious objection to his theory. But he attributed it to the imperfection of the fossil record, and he thought that future research would supply the missing ancestors.

But a century and a half of continued fossil collecting has only aggravated the problem. Instead of slight differences appearing first, then greater differences emerging later, the greatest differences appear right at the start. Some fossil experts describe this as “top-down evolution,” and note that it contradicts the “bottom-up” pattern predicted by Darwin’s theory. Yet most current biology textbooks don’t even mention the Cambrian explosion, much less point out the challenge it poses for Darwinian evolution.

Then came the evidence from molecular biology. Biologists in the 1970’s began testing Darwin’s branchingtree pattern by comparing molecules in various species. The more similar the molecules in two different species are, the more closely related they are presumed to be. At first this approach seemed to confirm Darwin’s tree of life. But as scientists compared more and more molecules, they found that different molecules yield conflicting results. The branching-tree pattern inferred from one molecule often contradicts the pattern obtained from another.

Canadian molecular biologist W. Ford Doolittle doesn’t think the problem will go away. Maybe scientists “have failed to find the ‘true tree’,” he wrote in 1999, “not because their methods are inadequate or because they have chosen the wrong genes, but because the history of life cannot properly be represented as a tree.” Nevertheless, biology textbooks continue to assure students that Darwin’s Tree of Life is a scientific fact overwhelmingly confirmed by evidence. Judging from the real fossil and molecular evidence, however, it is an unsubstantiated hypothesis masquerading as a fact.

They All Look Alike: Homology in Vertebrate Limbs

Most introductory biology textbooks carry drawings of vertebrate limbs showing similarities in their bone structures. Biologists before Darwin had noticed this sort of similarity and called it “homology,” and they attributed it to construction on a common archetype or design. In The Origin of Species, however, Darwin argued that the best explanation for homology is descent with modification, and he considered it evidence for his theory.

Darwin’s followers rely on homologies to arrange fossils in branching trees that supposedly show ancestordescendant relationships. In his 1990 book, Evolution and the Myth of Creationism, biologist Tim Berra compared the fossil record to a series of Corvette models: “If you compare a 1953 and a 1954 Corvette, side by side, then a 1954 and a 1955 model, and so on, the descent with modification is overwhelmingly obvious.”

Darwin’s branching “Tree of Life” has been seriously undermined by the fossil record and modern molecular biology. (From Biology, by Miller and Levine, published by Prentice Hall.)

But Berra forgot to consider a crucial, and obvious, point: Corvettes, so far as anyone has yet been able to determine, don’t give birth to little Corvettes. They, like all automobiles, are designed by people working for auto companies. In other words, an outside intelligence. So although Berra believed he was supporting Darwinian evolution rather than the pre-Darwinian explanation, he unwittingly showed that the fossil evidence is compatible with either. Law professor (and critic of Darwinism) Phillip E. Johnson dubbed this : “Berra’s Blunder.”

The lesson of Berra’s Blunder is that we need to specify a natural mechanism before we can scientifically exclude designed construction as the cause of homology. Darwinian biologists have proposed two mechanisms: developmental pathways and genetic programs. According to the first, homologous features arise from similar cells and processes in the embryo; according to the second, homologous features are programmed by similar genes.

But biologists have known for a hundred years that homologous structures are often not produced by similar developmental pathways. And they have known for thirty years that they are often not produced by similar genes, either. So there is no empirically demonstrated mechanism to establish that homologies are due to common ancestry rather than common design.

Without a mechanism, modern Darwinists have simply defined homology to mean similarity due to common ancestry. According to Ernst Mayr, one of the principal architects of modern neo-Darwinism: “After 1859 there has been only one definition of homologous that makes biological sense: Attributes of two organisms are homologous when they are derived from an equivalent characteristic of the common ancestor.”

This is a classic case of circular reasoning. Darwin saw evolution as a theory, and homology as its evidence. Darwin’s followers assume evolution is independently established, and homology is its result. But you can’t then use homology as evidence for evolution except by reasoning in a circle: Similarity due to common ancestry demonstrates common ancestry.

Philosophers of biology have been criticizing this approach for decades. As Ronald Brady wrote in 1985: “By making our explanation into the definition of the condition to be explained, we express not scientific hypothesis but belief. We are so convinced that our explanation is true that we no longer see any need to distinguish it from the situation we were trying to explain. Dogmatic endeavors of this kind must eventually leave the realm of science.”

So how do the textbooks treat this controversy? Once again, they ignore it. In fact, they give students the impression that it makes sense to define homology in terms of common ancestry and then turn around and use it as evidence for common ancestry. And they call this “science.”

Nothing a Little Glue Can’t Fix: The Peppered Moths

Fabricated evidence: Since peppered moths don't naturally rest on tree trunks, researches simply glued them in place. (From Biology, by Burton S. Guttman, published by McGraw-Hill.)

Darwin was convinced that in the course of evolution, “Natural Selection has been the most important, but not the exclusive means of modification,” but he had no direct evidence of this. The best he could do in The Origin of Species was give “one or two imaginary illustrations.”

In the 1950’s, however, British physician Bernard Kettlewell provided what seemed to be conclusive evidence of natural selection. During the previous century, peppered moths in England had gone from being predominantly light-colored to being predominantly dark-colored. It was thought that the change occurred because dark moths are better camouflaged on pollution-darkened tree trunks, and thus less likely to be eaten by predatory birds.

To test this hypothesis experimentally, Kettlewell released light and dark moths onto nearby tree trunks in polluted and unpolluted woodlands, then watched as birds ate the more conspicuous moths. As expected, birds ate more light moths in the polluted woodland, and more dark moths in the unpolluted one. In an article written for Scientific American, Kettlewell called this “Darwin’s missing evidence.” Peppered moths soon became the classic example of natural selection in action, and the story is still retold in most introductory biology textbooks, accompanied by photographs of the moths on tree trunks.

In the 1980’s, however, researchers discovered evidence that the official story was flawed – including the pertinent fact that peppered moths don’t normally rest on tree trunks. Instead, they fly by night and apparently hide under upper branches during the day. By releasing moths onto nearby tree trunks in daylight, Kettlewell had created an artificial situation that does not exist in nature. Many biologists now consider his results invalid, and some even question whether natural selection was responsible for the observed changes.

So where did all those textbook photos of peppered moths on tree trunks come from? They were all staged. To expedite things, some photographers even glued dead moths to trees. Of course, the people who staged them before the 1980’s thought they were accurately representing the true situation, but we now know they were mistaken. Yet a glance at almost any current biology textbook reveals that they are all still being used as evidence for natural selection.

In 1999, a Canadian textbook-writer justified the practice: “You have to look at the audience. How convoluted do you want to make it for a first time learner?” Bob Ritter was quoted as saying in the April 1999 Alberta Report Newsmagazine. High school students “are still very concrete in the way they learn,” continued Ritter. “We want to get across the idea of selective adaptation. Later on, they can look at the work critically.”

Apparently, the “later” can be much later. When University of Chicago Professor Jerry Coyne learned the truth in 1998, he was well into his career as an evolutionary biologist. His experience illustrates how insidious the icons of evolution really are, since they mislead experts as well as novices.

Beaks and Birds: Darwin’s Finches

The sort of distortion that would land a stock promoter in jail. (From Biology, 5th Edition, by Raven & Johnson, published by McGraw-Hill.)

A quarter of a century before Darwin published The Origin of Species, he was formulating his ideas as a naturalist aboard the British survey ship H.M.S. Beagle. When the Beagle visited the Galapagos Islands in 1835, Darwin collected specimens of the local wildlife, including some finches.

Though the finches had little in fact to do with Darwin’s development of evolutionary theory, they have attracted considerable attention from modern evolutionary biologists as further evidence of natural selection. In the 1970’s, Peter and Rosemary Grant and their colleagues noted a 5 percent increase in beak size after a severe drought, because the finches were left with only hard-tocrack seeds. The change, though significant, was small; yet some Darwinists claim it explains how finch species originated in the first place.

A 1999 booklet published by the U.S. National Academy of Sciences describes Darwin’s finches as “a particularly compelling example” of the origin of species. The booklet cites the Grants’ work, and explains how “a single year of drought on the islands can drive evolutionary changes in the finches.” The booklet also calculates that “if droughts occur about once every 10 years on the islands, a new species of finch might arise in only about 200 years.”

But the booklet fails to point out that the finches’ beaks returned to normal after the rains returned. No net evolution occurred. In fact, several finch species now appear to be merging through hybridization, rather than diverging through natural selection as Darwin’s theory requires.

Withholding evidence in order to give the impression that Darwin’s finches confirm evolutionary theory borders on scientific misconduct. According to Harvard biologist Louis Guenin (writing in Nature in 1999), U.S. securities laws provide “our richest source of experiential guidance” in defining what constitutes scientific misconduct. But a stock promoter who tells his clients that a particular stock can be expected to double in value in twenty years because it went up 5 percent in 1998, while concealing the fact that the same stock declined 5 percent in 1999, might well be charged with fraud. As Berkeley law professor Phillip E. Johnson wrote in The Wall Street Journal in 1999: “When our leading scientists have to resort to the sort of distortion that would land a stock promoter in jail, you know they are in trouble.”

From Apes to Humans

Darwin’s theory really comes into its own when it is applied to human origins. While he scarcely mentioned the topic in The Origin of Species, Darwin later wrote extensively about it in The Descent of Man. “My object,” he explained, “is to show that there is no fundamental difference between man and the higher animals in their mental faculties” — even morality and religion. According to Darwin, a dog’s tendency to imagine hidden agency in things moved by the wind “would easily pass into the belief in the existence of one or more gods.”

Of course, the awareness that the human body is part of nature was around long before Darwin. But Darwin was claiming much more. Like materialistic philosophers since ancient Greece, Darwin believed that human beings are nothing more than animals.

Darwin, however, needed evidence to confirm his conjecture. Although Neanderthals had already been found, they were not then considered ancestral to humans, so Darwin had no fossil evidence for his view. It wasn’t until 1912 that amateur paleontologist Charles Dawson announced that he had found what Darwinists were looking for, in a gravel pit at Piltdown, England.

Dawson had found part of a human skull and part of an apelike lower jaw with two teeth. It wasn’t until forty years later that a team of scientists proved that the Piltdown skull, though perhaps thousands of years old, belonged to a modern human, while the jaw fragment was more recent, and belonged to a modern orangutan. The jaw had been chemically treated to make it look like a fossil, and its teeth had been deliberately filed down to make them look human. Piltdown Man was a forgery.

Most modern biology textbooks do not even mention Piltdown. When critics of Darwinism bring it up, they are usually told that the incident merely proves that science is self-correcting. And so it was, in this case — though the correction took over forty years. But the more interesting lesson to be learned from Piltdown is that scientists, like everyone else, can be fooled into seeing what they want to see.

The same subjectivity that prepared the way for Piltdown continues to plague human-origins research. According to paleoanthropologist Misia Landau, theories of human origins “far exceed what can be inferred from the study of fossils alone and in fact place a heavy burden of interpretation on the fossil record – a burden which is relieved by placing fossils into pre-existing narrative structures.” In 1996, American Museum of Natural History Curator Ian Tattersall acknowledged that “in paleoanthropology, the patterns we perceive are as likely to result from our unconscious mindsets as from the evidence itself.” Arizona State University anthropologist Geoffrey Clark echoed this view in 1997 when he wrote: “We select among alternative sets of research conclusions in accordance with our biases and preconceptions.” Clark suggested that “paleoanthropology has the form but not the substance of science.”

Biology students and the general public are rarely informed of the deep-seated uncertainty about human origins that is reflected in these statements by scientific experts. Instead, they are simply fed the latest speculation as though it were a fact. And the speculation is typically illustrated with fanciful drawings of cave men, or pictures of human actors wearing heavy make-up.

What's Going on Here?

Most of us assume that what we hear from scientists is comparatively trustworthy. Politicians might distort or shave the truth to support a preconceived agenda, but scientists, we are told, deal with facts. Sure they might sometimes get it wrong, but the beauty of science is that it’s empirically testable. If a theory is wrong, this will be discovered by other scientists performing independent experiments either to replicate or disprove their results. In this way the data are constantly reviewed and hypotheses become widely accepted theories. So how do we explain such a pervasive and long-standing distortion of the specific facts used to support evolutionary theory?

Perhaps Darwinian evolution has taken on a significance in our culture that has little to do with its scientific value, whatever that may be. An indication of this was seen in the nearly universal and censorious reaction to the Kansas School Board’s decision to allow room for dissent in the standard teaching of evolution (much of which, as we have just seen, is plain wrong).

According to the news media, only religious fundamentalists question Darwinian evolution. People who criticize Darwinism, we are told, want to bomb science back to the Stone Age and replace it with the Bible. The growing body of scientific evidence contradicting Darwinian claims is steadfastly ignored. When biochemist Michael Behe pointed out in The New York Times last year that the embryo “evidence” for evolution was faked, Harvard Darwinist Stephen Jay Gould admitted that he had known this for decades (as noted above) – but accused Behe of being a “creationist” for pointing it out.

Now, although Behe supports the idea that some features of living things are best explained by intelligent design, he is not a “creationist” as that word is normally used. Behe is a molecular biologist whose scientific work has convinced him that Darwinian theory doesn’t conform to observation and experimental evidence. Why does Gould, who knows Haeckel’s drawings were faked, dismiss Behe as a creationist for criticizing them?

I suspect that there’s an agenda other than pure science at work here. My evidence is the more or less explicit materialist message woven into many textbook accounts. Futuyma’s Evolutionary Biology is characteristic of this, informing students that “it was Darwin’s theory of evolution,” together with Marx’s theory of history and Freud’s theory of human nature, “that provided a crucial plank to the platform of mechanism and materialism” that has since been “the stage of most Western thought.” One textbook quotes Gould, who openly declares that humans are not created, but are merely fortuitous twigs on a “contingent” (i.e. accidental) tree of life. Oxford Darwinist Richard Dawkins,though not writing in a textbook, puts it even more bluntly: “Darwin made it possible to be an intellectually fulfilled atheist.”

These are obviously philosophical rather than scientific views. Futuyma, Gould, and Dawkins have a right to their philosophy. But they do not have the right to teach it as though it were science. In science, all theories — including Darwinian evolution — must be tested against the evidence.

Since Gould knows that the real embryological evidence contradicts the faked drawings in biology textbooks, why doesn’t he take a more active role in cleaning up science education? The misrepresentations and omissions I’ve examined here are just a small sampling. There are many more. For too long the debate about evolution has assumed “facts” that aren’t true. It’s time to clear away the lies that obstruct popular discussion of evolution, and insist that theories conform to the evidence. In other words, it’s time to do science as it’s supposed to be done.

Originally appeared in the The American Spectator - December 2000/January 2001. PDF Version.