Evolutionary Anthropology 21:176181 (2012)

Crotchets & Quiddities

Dracula! A Paradigm Shift in Evolutionary Genetics

Death of a theory at the hands of the undead?

KENNETH M. WEISS
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 theyd 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 Boccaccios
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
Ken Weiss is Evan Pugh Professor of Anthropology and Genetics at Pennsylvania
State University. Email: kenweiss@psu.edu

C 2012 Wiley Periodicals, Inc.

V

DOI 10.1002/evan.21330
Published online in Wiley Online Library
(wileyonlinelibrary.com).

sketched a fragment of a novel on

vampires.2
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 Byrons personal physician,
J. W. Polidori, who was at the 1816
gathering. Polidoris study influenced many subsequent authors
and vampire ethnography captured
European imagination (see Wikipedia: Vampire).
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 Grays,5,6 Ill refer to the authoritative source on vampires as
Stoker. His volume was so thorough
that, unlike Grays, there has been no
need for revised editions.

VAMPIRE NATURAL HISTORY

Stoker presents vampire science
through a detailed case study of the
title individual. The lineage of
Stokers 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 diesonly
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

Crotchets & Quiddities

Dracula! A Paradigm Shift in Evolutionary Genetics 177

VAMPIROGENESIS: THE
DEVELOPMENTAL GENETICS
OF BECOMING UNDEAD

Figure 1. Impaled skeleton from Bulgarian

Museum of Natural History. [Color figure
can be viewed in the online issue, which is
available at wileyonlinelibrary.com.]

their gene pool. That explains their

relevance for readers of this journal,
but Stokers 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.

Figure 2. 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.]

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 hardand
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 cant 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 vampires lust for it
may not require genetic change,
though it may be relevant that blutwurst is most popular in central and
eastern Europe.

Figure 3. 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.]

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.

THE EVOLUTION OF VAMPIRE

DNA (vDNA)
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

178 Weiss

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).

Mutation
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 Darwins idea of gemmules, but
not genes as we know them today,
and challenges a central principle of
evolutionary geneticsunless that
principle is quaintly outdated.

Gene Flow
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.

Crotchets & Quiddities

However, among vampires theres

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 cant predict who will
immigrate, we cant 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.

Genetic Drift
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,
thats 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.

Unnatural Selection
Does selection affect the vampire
gene pool? We dont 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 vampires 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 Darwins 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.
Thats because theres 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 Darwins,
who said, in his autobiography,8 that
in the Malthusian struggle for survival favourable variations would

Crotchets & Quiddities

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.

A PROBLEM IN CRYPTOGRAPHY:
DECODING CAUSATION vDNA
Each organism has parents, and
similarity due to the chain of parentoffspring 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 varia-

Dracula! A Paradigm Shift in Evolutionary Genetics 179

tion, 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
thats actually not so clear. You might
be aware (though many geneticists
dont seem to be) that controls are
defined as being unaffected by the
trait in question, like diabetes, at the
time theyre sampled, but many of
them will eventually become affected
in the future. So until we know who
will become undead in the future, we
dont know whose DNA doesnt 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
wont 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 doesnt 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 wouldnt 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 arent 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?

180 Weiss

The bottom line is that we dont

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 cant just randomly raid mausoleums, dig up graveyards, or rummage around everybodys 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 sexmatching of controls to cases. But

Crotchets & Quiddities

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 cant
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 wouldnt immune resistance
have evolved long ago? Could stillliving 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.

FINALLY, A REAL PARADIGM SHIFT

IN EVOLUTIONARY BIOLOGY?
Dracula is a wickedly stealthful
treatise of Victorian science, so different from Darwins 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

Figure 4. With a stake in our story, Vlad the

Impaler dines before his victims. Public
domain.

sees farther than the rest of us to

make a revolutionary discovery.
Thomas Kuhn introduced the term
paradigm shift for such scientific
earthquakes.1113 Darwin has seemed
to be a perfect example. Ever since
Kuhn, our pattern of modest selfevaluation 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.
Sadly, most of the time its selfdelusion: 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 its to be found in the
rediscovery of Stoker, who failed to
explore evolutionary topics or was
unaware of their impact.

Death Be Proud!
John Donnes famous poem was
wrong. He said, And death shall be no
more, death, thou shalt die. To the
contrary, weve seen that the key difference between vampires and real life is
that in both development and evolution

Dracula! A Paradigm Shift in Evolutionary Genetics 181

Crotchets & Quiddities

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
dont 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.

NOTES
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.

REFERENCES
1 Weiss KM. 2008. Joseph Adams in the Judgment
of Paris: evolutions remarkable little book 45 years
before Darwin. Evol Anthropol 17:245249.
2 Byron L. 1819. Mazeppa: a poem. London:
John Murray.
3 Polidori JW. 1819. The vampyre. London:
Sherwood, Neely, and Jones.
4 Stoker B. 1897. Dracula. London: Hutchinson.
5 Gray H. 1974. Anatomy, descriptive and surgical. Philadelphia: Running Press Book Publishers.

Articles in Forthcoming Issues

Fossil Apes from the Valle`s-Penede`s Basin

David M. Alba

The Real Females of Human Evolution

Adrienne L. Zihlman

Primate Origins, Human Origins, and the End of Higher Taxa

Matt Cartmill

Higher Taxa: An Alternative Perspective

Ian Tattersall

Pandoras Growing Box: Inferring the Evolution and Development

of Hominin Brains from Endocasts
Christoph P.E. Zollikofer and Marcia S. Ponce de Leon

Early Primate Evolufion in Afro-Arabia

Erik Seiffert

6 Weiss KM. 2009. Grays anatomy. Evol

Anthropol 18:241246.
7 Weiss KM, Kurland JA. 2007. Going on an
antedate: a strange history of imperfect perfect
proportions. Evol Anthropol 16:204209.
8 Barlow N. 1958. The autobiography of
Charles Darwin (18091882). London: Collins.
9 Weiss KM. n.d. Little orphans nanny. Evol
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10 Weiss KM. 2010. Seeing the forest through
the gene-trees. Evol Anthropol 19:210221.
11 Kuhn T. 1962. The structure of scientific
revolutions. Chicago: University of Chicago
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12 Fleck L. 1935. Genesis and development of a
scientific fact. Chicago: University of Chicago
Press.
13 Weiss KM. 2003. Ludwik Fleck and the artof-fact. Evol Anthropol 12:168172.
14 Weiss K. 1996. Is there a paradigm shift in
genetics? Lessons from the study of human diseases. Mol Phylogenet Evol 5:259265.
C 2012 Wiley Periodicals, Inc.
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