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W1994736118 abstract "Just as evolution had its doubters before Darwin and Wallace put diverse existing ideas together in a definitive way,1 scientists today are dismissive of the repeated references to vampires that regularly appear even in the major media. Readers of Evolutionary Anthropology probably share that view. However, could we be disregarding important facts that have long been at hand but that challenge accepted evolutionary theory? I was led to this surprising question when the major science news media reported the finding of medieval skeletons housed in the Bulgarian National History Museum in Sofia. These had been pierced through the chest with metal rods (Fig. 1). Archeologists suggested they'd been staked to stop them from wreaking havoc as vampires. Interestingly, much of what we know about vampires traces back not to a scientist but to the poet Lord Byron. In 1816, he hosted a gathering of friends at his place by Lake Geneva. As the party huddled out of relentless rainstorms, Byron suggested that they pass the time taking turns, in the style of Boccaccio's Decameron, relating ghost hypotheses. One guest was Mary Wollstonecraft Shelley, and Frankenstein was hatched. In 1813, Byron had written a poem, “The Giaour,” recounting a Turkish tale that included vampires, and after the 1816 gathering he sketched a “fragment of a novel” on vampires.2 Impaled skeleton from Bulgarian Museum of Natural History. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.] He never developed that, but another guest did, and in 1819 published perhaps the first major treatment of vampire life (Fig. 2),3 in which the evil predator chased vulnerable young women, while an unfortunate protagonist who realized what was going on always a bite too late. The book was attributed to Byron, which was good marketing, but it was actually written by Byron's personal physician, J. W. Polidori, who was at the 1816 gathering. Polidori's study influenced many subsequent authors and vampire ethnography captured European imagination (see Wikipedia: Vampire). The little-known founder document: The Vampyre (by Polidori, but with the original false attribution to Byron). Public domain. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.] This increasing body of data never really got a grip on mainstream thinking until Bram Stoker (Fig. 3) documented vampire science in his stark, readable, yet scientifically rigorous treatise, Dracula.4 Hereafter, as is common in science, such as when we refer to things anatomical by reference to “Gray's,”5, 6 I'll refer to the authoritative source on vampires as “Stoker.” His volume was so thorough that, unlike Gray's, there has been no need for revised editions. Bram Stoker (1847-1912), Father of the new science. Public domain. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.] Stoker presents vampire science through a detailed case study of the title individual. The lineage of Stoker's eponymous type specimen goes back at least to Vlad the Impaler, who ruled the area in the 1400s, roughly contemporary with the Bulgarian skeletons. He was infamous for brutal impalement as a means of tortured execution of his enemies, perhaps contributing to ideas on how to dispose of vampires. A vampire is a person who has been transformed into the state known as ‘undead.’ Vampires seek new victims, who invite their initial attack, then increasingly hunger for further encounters, fatal though they will be. Victims can be of any age and sex, but nubile young women are the preferred diet. After several feedings, the new victim ‘dies’—only to become a vampire. With some exceptions, vampires must lie by day in a casket of their native earth, as if in death, but they roam by night as if alive. They have eerie red eyes and sharp teeth, which you can see, yet their bodies make no shadow or reflection in mirrors. They can assume various forms, such as a vicious dog, a huge bat with ominously flapping wings, or a slithering white mist. In their nocturnal prowls, they use their fangs to feed on human blood. Fortunately, vampires can be kept at bay by a crucifix, the scent of garlic, or wafers of the sacred Host. They are called undead because they stay in their state immortally, being periodically rejuvenated by the blood of young victims. However, a vampire can be driven from the undead to be really, truly dead. The proven method is to behead it and then drive a stake through its heart, as we have seen. Thanks to Darwin, we have an evolutionary science of long standing. Indeed, Stoker, writing in 1897, must have been aware of that science. Thus, it is curious that he makes no mention of Darwin in his treatise because the facts he presents affect the population of vampires over time, which means the evolution of their gene pool. That explains their relevance for readers of this journal, but Stoker's omission leaves it to us to examine whether vampire life has anything to teach us about evolutionary theory. If his facts are accurate, they might not force us to revise Stoker, but we will have to revise Darwin. But before we address those questions, we must consider the nature of the morphological changes induced in vampires. Essentially, they involve developmental genetics. The most consistent vampirogenic change is dental. I would include a figure to show the effect, but there is too little consensus, and Stoker is without illustrations. All available images are fanciful costume-shop mock-ups. They could not be real, because the fangs are often imagined to be second upper incisors, yet we know (and Stoker is definitive on this point, too) that the enlarged biting teeth were canines. Likewise, though many Halloween dentitions have multiple pointy teeth, Stoker is clear that victims show precisely two toothmarks over their jugular veins. Adding a bit of length and pointiness to canines might not seem very difficult. But the enamel coating of teeth is laid down embryologically by cells called ameloblasts. These cells express specific genes whose coded proteins capture calcium molecules and form them into crystals during tooth-germ development. But the ameloblasts then die, the proteins are degraded, and the resulting enamel layer becomes hard—and deader than, well, a vampire. It is no longer a living cellular tissue. This makes it hard to explain how anything transmitted by a vampire could induce the gene expression changes needed to produce new enamel. Limb morphology similarly depends on orchestrated sequential hierarchies of gene expression starting in cells at the earliest, rudimentary limb-bud stage of an embryo. Adult arms can't just be remodeled into bat wings by any known developmental genetic process. Limbs and teeth require local gene expression changes. However the morphogenic transformation that leaves the vampire visible but able to cast no shadow or reflection affects the whole body and is wholly inexplicable in known genetic terms. Some human populations habitually dine on blood, so the vampire's lust for it may not require genetic change, though it may be relevant that blütwurst is most popular in central and eastern Europe. A changed diurnal activity pattern to make vampires active at night and asleep by day has plenty of precedents in the natural world. Circadian clock genes are widespread in many species (http://expression.gnf.org/ cgi-bin/circadian/index.cgi) and the transition to vampire state might simply require modifying their expression. Developmentally, life depends on death! We are built by changes in the hierarchy of gene expression during embryological development. Each individual starts life by building its traits anew. The field of ‘EvoDevo,’ the evolution of development, is showing how this works at the gene level. Vampires, shrouded in undeath, seem so different that we must consider how that would be reflected in their gene pool. Evolution is about inheritance, because noninherited traits perish with the organisms that carry them. We can immediately see a problem, because according to Stoker vampires do not perish except by human agency (that is, impalement). That has serious implications for our understanding of the evolutionary process, as we can see by considering how the four basic causes of evolution would be reflected in vampire DNA (vDNA). Evolution depends on the transmission of mutational change in DNA from one generation to the next. But the changes induced in vampires' victims are transmitted through the neckline rather than the germline, and the recipients are children or adults, not fertilized eggs. The morphological effects such as those in teeth require tissue-specific, embryologically ordered cascades of gene expression, so that whatever is transmitted must cause somatic (body cell) genetic changes. In standard theory, such changes die with those who acquire them. But if somatic mutations are not transmitted across generations of people, they are transmitted in the generation of vampires, in a chain of somatic vDNA descent without parallel in the Darwinian world. This is important: evolutionary theory is adamant that there is no Lamarckian inheritance. Experience acquired during life cannot induce heritable genetic change to serve some prespecified or anticipated purpose. The somatic changes new vampires acquire, such as the remodeling of teeth or developing bat wings, clearly serve adaptive purposes and are transmitted to their victims. This Lamarckian-like inheritance resembles Darwin's idea of ‘gemmules,’ but not genes as we know them today, and challenges a central principle of evolutionary genetics—unless that principle is quaintly outdated. Gene flow is the introduction by immigrants of new genetic variants (alleles) into a population, or their loss by emigration. If you know the alleles that enter, you can predict their frequency in the offspring of the next generation in the host population in terms of mixing proportions of local and incoming variation. However, among vampires there's blood flow but no gene flow into the next generation because there are no offspring. Vampire allele frequencies are due strictly to the accumulation of new victims taking their place in the crypt. Since we can't predict who will immigrate, we can't use vDNA to predict vampires' future allele frequencies from their current ones as we can with living populations. Still, we can use vDNA variation to reconstruct the source of the immigrants; for example, they should resemble eastern Europeans. Drift is the random change of allele frequencies due to the probabilistic aspects of reproduction. Since allele frequencies refer to variation within a finite population, there are what are known as statistical ‘absorbing boundaries’. Once an allele is lost, that's forever; it cannot return, so to speak, from the dead. And when one allele is fixed, it necessarily replaces all other alleles in the process. It can be mathematically proven that in these conditions the descendant lineage of every allele will eventually either be lost or fixed. By stark contrast, even an allele that is lost from the living population is never lost from the crypt. That implies that an allele is never fixed there, either. Variation may change frequency, but there are no absorbing boundaries: there is accumulation rather than replacement. Like vampires themselves, their alleles are forever. Similarly, the genotype frequencies — how alleles in the population are paired in individual people — usually follow the Hardy-Weinberg principle that if there is random mating alleles pair up based on their frequency alone.7 If, instead, there is assortative mating whereby bearers of a given genotype preferentially exchange fluids with others with the same genotype, the offspring genotype distribution will deviate from Hardy-Weinberg expectations. But with vampires, there is no mating so that Hardy-Weinberg proportions will deviate from those expectations in ways that would be very difficult to explain in a living population. Instead, vampire genotype patterns will be affected by whether there is random versus assortative recruiting. These are grave differences from the central role of genetic drift in standard theory. Does selection affect the vampire gene pool? We don't know, and Stoker is mute on the topic. We might think of predator-prey dynamics, but there are important differences. Vampires may selectively prey on victims who make themselves available because of their genotype, much as females in some species ‘present’ for males. Genotypes that lead someone to invite embrace would constitute victim-driven selection; the vampire population would gradually be enriched for these genotypes. But this would be quite different from natural selection. As Darwin made clear, in natural selection to be favored is to survive, but with vampire victim-based selection, to be favored is to die! Alternatively, the vampire's genotype might be responsible for its choice, perhaps because it prefers victims whose blood tastes good, or by ‘sexual’ selection for luscious appearance. Indeed, unlike Darwin's plodding volume, Victorian sexual innuendos abound in Stoker. But while this would enrich the vampire population with genotypes for tasting good, there is no mechanism for raising the frequency of genotypes for good taste. That's because there's no guarantee that chosen victims who join the vDNA pool will preferentially have the same choosing-genotypes. There are other challenging issues as well. For example, natural selection has clearly endowed organisms with genetic mechanisms that make them hungry and steer them to seek their prey. Vampires are no exception. But in their case, they prey on individuals who hunger to be eaten. Try to find that in ‘real’ nature! Stoker unearthed facts that go against a central tenet of Darwin's, who said, in his autobiography,8 that in the Malthusian struggle for survival “favourable variations would tend to be preserved, and unfavourable ones to be destroyed.” He used an oddly prescient choice of words, because the evolution of undeath is very different from that of life. Among vampires all variation is “preserved,” as if embalmed, forever. Since the vampire population does not turn over (in daytime) as living populations do, the selection-related variants from their entire past history accumulate rather than being replaced. Death! Again, replacement by death is fundamental to Darwinian evolutionary dynamics of life. With this in mind, we can turn our attention to the problem of identifying the responsible variation in the vampire genome. Each organism has parents, and similarity due to the chain of parent-offspring connections is vital to our ability to trace ancestry and reconstruct development and its evolution from genetic data. Even a vampire has parental origins, in the sense that Dracula was the ‘parent’ of his victims. In what was perhaps a deeper understanding of inheritance than even biologists seem to have, he called his victim “flesh of my flesh; blood of my blood; kin of my kin.” However, while there may be genealogical continuity, there is no genetic continuity in this case. Unlike Darwin, Stoker does not explain the origin of the first vampire. He must have thought about that, but perhaps information was too limited for him to have certainty. Most likely, vampires arose by gradual evolution the way species do, and we have many analytic tools to reconstruct genetic origins and functions. The vampires reported in Stoker, and skeletons such as those in Bulgaria, are recent enough to contain vDNA in good condition to be sequenced. What will it show? How should we design studies to provide adequate samples to find the genes for becoming a vamp? These are not easy questions. There must be susceptibility variation, because the NY Times (and other major science journals) routinely inform us that absolutely everything must have a genetic basis. So we want to identify the genetic reason why some women are more genetically susceptible than others to being vamped, and the genetic basis of the transformed morphology. One challenge is that our usual approach of taking a blood sample might greatly satisfy the vampire, but not reveal relevant mutations that had arisen or been introduced only in specific tissues like teeth or limbs. The gene-mapping searches we need will compare affected and unaffected individuals to find causal sites in the genome where a variant occurs more often among one group than the other. Here the ‘affected’ means vampire. Because we have to sort through millions of potential sites in the genome to find the causally associated ones, the test of the evidence is necessarily statistical, which means we need adequate sample sizes. Surface-dwelling, unbatlike nonvampire controls, like you and me, might seem amply available, but that's actually not so clear. You might be aware (though many geneticists don't seem to be) that controls are defined as being unaffected by the trait in question, like diabetes, at the time they're sampled, but many of them will eventually become affected in the future. So until we know who will become undead in the future, we don't know whose DNA doesn't contain the variants we want to identify in vampires. If there is selection, as we considered earlier, the vampire gene pool will have been increasingly enriched over time by susceptibility genotypes. Meanwhile, those genotypes would have been removed from the living population. This should make for a favorable case-control difference in the frequency of the relevant variants. However, gene mapping remains a challenge, because we know that any two copies of the human genome, even the two any individual carries, differ by millions of nucleotides. We hope that we won't have to search such a mass of variation to find a single variant buried somewhere in a isolated orphan gene,9 the frequency of which differs between cases and controls. Confirming candidate variants by shared effects in families is a powerful adjunct to association studies in humans, but doesn't apply to vampires, who have no families. Speaking of families, given what we know about the origin of genes by duplication events,9 a typical procedure would search for a ‘family’ of evolutionarily related genes (call them Vam1, Vam2, and so on) that are responsible. All human genes are already known, so we must have mislabeled Vam genes by not understanding their functions. This wouldn't be surprising, since the functions of many genes are unknown. However, one must ask why, from an evolutionary perspective, Vam genes exist in the first place. This is a problem because, as mentioned earlier, if evolution has no Lamarckian foresight, how could such genes have evolved for their future adaptive value in Carpathians? The answer, if evolutionary theory is correct, is that there aren't really any specifically “Vam” genes. Instead, we must search for variation in existing genes with some other function that were later recruited to take on new vampire-related functions. Such contingent states are sometimes called exaptations. Evolutionary theory holds that they are a genetic reservoir exploited by selection to produce new functions. Finding them will be difficult because they would be members of families with other routine functions. Thus, perfectly ordinary genes that confer long, luscious necks on women or that make women want to wear temptingly revealing low-necked blouses could easily have provided the allure needed for their bearers (so to speak) to be among the chosen. It might seem hopeless to look for genes with amorphous functions like neck delicacy, but, after all, the genetics literature contains a veritable flood of papers searching for the genes ‘for’ comparably vague traits, including similarly subtle behaviors. Not everybody is aware of its hopelessness, since such studies are widely if uncritically accepted. Why not here, as well? The bottom line is that we don't yet know the genes ‘for’ normal necks (much less a preference for low-neck shirts), but what countless genome-wide mapping studies have clearly shown is that traits such as that are affected by many different genes, typically no one of which contributes more than small effects.10 We also know that under these conditions even strong selection, such as might be conferred by genetically based recruitment, would not leave strong case-control differences even at the individual responsible sites.10 We know from disorders like diabetes, heart disease, and intelligence that we need very large samples to dig out the many critical causal variants in the sea of millions of uninvolved variants each of us carries. The current NIH state-of-the-art for genome mapping normal disorders such as hypertension, or even just human stature, is that we need hundreds of thousands of cases. Therein lie two serious kinds of challenge that, in general, evolutionary anthropologists perhaps need to take more seriously. First, how on or under the earth this side of the Styx, could we find such a horde? We need to sample the undead cadavers of a huge number of vampires. We have no idea, of course, how many vampires even exist; Stoker provides no statistics. We can't just randomly raid mausoleums, dig up graveyards, or rummage around everybody's cellar, because how would we know which corpses were, or might have been, vampires? This parallels the difficulty mentioned earlier of deciding who is an adequate control. Faced with this complexity, some biomedical investigators suggest that a safer approach is to compare the extreme tails of the trait distribution, such as those with very high and low blood pressure in relation to heart disease. Anthropologists might adopt a similar approach, comparing known vampires to controls consisting of, say, women who typically wear turtlenecks and are least likely carry the susceptibility variants. Another standard way to reduce needless complexity is age- and sex-matching of controls to cases. But since vampires unlive forever, there is no clear meaning to age matching. Secondly, if it turns out that hundreds of genes in vDNA contain relevant variants, we will face the horrifying prospect that, as with susceptibility to diabetes or behaviors, we all carry some of the variants, which normally are harmless, but we can't really know which they are. A geneticist, even the usual type seeking media attention, should be reluctant to stick his or her neck out with only such weak evidence. An entirely different idea, considering the tissue-specific transformations that occur, is that viral transmission may be responsible. Viruses infect only some tissues, the way flu affects respiratory epithelium. Viruses were unknown to Stoker, but could be consistent with salivary transmission. However, there has been no definitive literature on the subject, and there are several questions about how the epidemiology of this partially communicable vector might work. How could a virus revitalize ameloblasts that no longer exist? How would the pool of susceptibles be maintained? And wouldn't immune resistance have evolved long ago? Could still-living victims infect their unbidden, and hence unbitten, contemporaries? Similar questions are often open wounds even in normal infectious-disease epidemiology. We might here also just note that while not usually referred to as undead, viruses are not really alive until they prey on the bodies of living hosts, and some can be transmitted in bodily fluids like saliva. Dracula is a wickedly stealthful treatise of Victorian science, so different from Darwin's dry, relentless listing of facts as not to be missed. I have noted some of its striking challenges to entrenched evolutionary theory. We have as much a stake in the outcome in our age as Vlad the Impaler did in his time (Fig. 4). For more than a century, science has romanticized the lone genius who sees farther than the rest of us to make a revolutionary discovery. Thomas Kuhn introduced the term “paradigm shift” for such scientific earthquakes.11-13 Darwin has seemed to be a perfect example. Ever since Kuhn, our pattern of modest self-evaluation has led almost everybody I know to feel that he or she is a key figure in a paradigm shift. After all, we want our lives to have more meaning than if we merely worked as drudges turning out research papers the way factory workers turn out pencils or paper towels. With a stake in our story, Vlad the Impaler dines before his victims. Public domain. Sadly, most of the time it's self-delusion: there really has been no paradigm shift in evolutionary genetics, which has been built steadily for a century.14 There has been a wealth of striking new knowledge and understanding of genetic mechanisms, but nothing that overthrows evolutionary theory… unless it's to be found in the rediscovery of Stoker, who failed to explore evolutionary topics or was unaware of their impact. John Donne's famous poem was wrong. He said, “And death shall be no more, death, thou shalt die.” To the contrary, we've seen that the key difference between vampires and real life is that in both development and evolution life depend on death and replacement, always starting over with new organisms. The fundamental fact that real life depends on real death lies silently encased within in our theories of life. Some readers may still harbor the illusion that Stoker is fiction. And not all our students have a sound evolutionary background, and many in the public who turn to us for information don't understand how the facts of biology constrain speculations about life. For these reasons, considering vDNA can help show how difficult it would be for vampires to pose any sort of paradigm shift in our understanding of how evolution works at the gene level, above ground, in the light of day. I welcome comments on this column: kenweiss@psu.edu. I co-author a blog on relevant topics at EcoDevoEvo.blogspot.com. I thank Anne Buchanan, Holly Dunsworth, Jen Wagner, and John Fleagle for critically reading this manuscript." @default.
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W1994736118 date "2012-09-01" @default.
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W1994736118 title "Dracula! A paradigm shift in evolutionary genetics: Death of a theory at the hands of the undead?" @default.
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