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Cranial thickening in an Australian hominid as a possible palaeoepidemiological indicator.

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Cranial Thickening in an Australian Hominid As a Possible
Palaeoepidemiological Indicator
Centre For Australian Studies, School of Humanities and Social
Sciences, Bond University Private Bag 10, Gold Coast Mail Centre,
Queensland 421 7, Australia
Palaeoepidemiology, Australia, Cranial ThickenKEY WORDS
ing, Palaeopathology, Blood dyscrasias
This paper describes the cranial thickening of a late Pleistocene hominid (Willandra Lakes Hominid 50) from Australia. The unusual
development of the vault structures in this individual has few, if any, equals
among other hominids or more recent populations from around the world. The
vault morphology is, therefore, described in terms of a pathologically related
condition associated with the modern haemolytic blood dyscrasias, typical of
sickle cell anamia and thalassemia. A possible palaeoepidemiology for these
genetic adaptations among early Australasian populations is proposed together with a discussion of similar changes observed in the vault of the Singa
calvarium from the Sudan. It is tentatively suggested that the cranial thickening of the Australian hominid has its origins in some form of genetic blood
disease and that if this diagnosis is correct, this individual provides a rare
glimpse of human biological adaptation in the late Upper Pleistocene.
It is a well-known fact, and
one often reported, that the
skull capsoffossil hominids appear considerably thicker than
those of modern man. But as
yet . . . no one has provided actual figures or deemed the entire phenomenon worth consideration. (Weidenreich 1943:
This paper discusses the extraordinary
vault thickening in a fossilised human calvarium from the Willandra Lakes region of
Western New South Wales, Australia (Map)
(Thorne, in pre .). It was found as a surface
find in 1980 an$ lacks all but a few scra s of
long bone and art of the left elbow o the
post-cranial ske eton. The individual, known
as Willandra Lakes Hominid (WLH) 50, is a
very robust adult male. All cranial sutures
have been completely fused and, with the
exception of a small section of the saggital
suture, obliterated both endo- and exocranially, placing in an old adult category. It is
now art of the WLH series of 135 individuals iocumented from that area (Webb,
1989a). A date of 29,000 k 5,000B.P. has
Map 1. Willandra Lakes Region
been obtained for these remains using the
electron spin resonance (ESR) method
(Caddie et al., 1987:175).Other datingmethods for direct dating of the bone have proven
unsuitable for cross-reference of the ESR
date. The reason for this is the highly fossilised condition of the bone from which all
Received March 2,1989; accepted September 20, 1989
Fig. 1. This xeroradiograph taken in the sagittal
plane, shows clearly the uniform thickening of the WLH
50 vault. A small patch of vertically aligned bone spicules
can be seen in the prebregmatic region ofthe frontal bone
producing a hair-on-end image.
T A B L E 1. Maximum Cranial Thickness at Eight Anatomical Points for Various Hominids and Ancient and
Modern Populations (nim)'.'
Hominid or
WLH 50
WLH Series min.
WLH Series max.:'
Coobool Creek (1)
Kow Swamp (2)
Lake Tandou (3)
New Year Island (4)
Cossack (5)
Recent Aborigines (6)
Recent Europeans (7)
British Neolithic (7)
Mesoamericans (7)
Niah (8)
Neanderthals (7)
Ngandong (Solo) (9)
Choukoutien (10)
Kabwe (Broken Hill)
' A , frontal boss-; B, mid-frontal; C, Bregma; D, Ohelion; E, parietal boss'; F, asterion; G , lambda; H, inion ( - S e e footnote 4).
'Numbers in parenthesesare references: ( I ) Brown (19x2); ( 2 )Thorne (1975);(3) Freedman a n d Lofgren (1983); (4) Murray rt al (198'; (5)
Freedman andLofgren(1979);(6)Browneta1.(1979);
(7) Ivanhoe(1979);(8)Brothwell(l960);(9)Weidenreich(1951);(10)Weidenreich(1943).
,'Excluding WLH 50.
:Average of left a n d right sides.
Measured through occipital torus a n d internal occipital protuberance.
or anic components have been removed. A
fu 1 description of this individual is being
documented by Dr. Alan Thorne of the Australian National University.
WLH 50 is very robustly constructed, with
a large browridge and substantial cranial
buttressing. A comparison of WLH 50 with
other individuals in the Willandra Hominid
series; other Australia fossil crania; modern
populations; as well as a selection of Middle
and Upper Pleistocene hominids from
around the world, shows that it possesses an
unusually thick vault (Fig. 1,Table 1).This
paper describes the vault morphology and
explores the possibility that the exaggerated
thickness may be caused by pathology.
The vault of WLH 50 is uniformly thick
(Fig. 1).Measurements taken through the
cranial walls show that the thickness ranges
from 15mm at obelion and lambda to 19mm
on the frontal squama at a point just posterior to the frontal boss. Certain individuals
in the Willandra series and other late Pleistocene Australian populations almost equal
the thickness of WLH 50 at one or other
anatomical point on the vault. Indeed, two
individuals (WLH 19 and 28) in the Willandra Hominid series have a thickness at inion
exceeding that of WLH 50 (Table 1).Because
of the variability of bone development in this
region of the occipital, however, it is not
worthwhile comparing crania using this particular anthropometric point or, for similar
reasons, thicknesses at asterion and lambda.
Many modern Australian crania, particularly male individuals, have thickening
somewhere on the vault, but this is usually
confined to one spot and rarely exceeds
l l m m (Brown et al., 1979). Personal observations of Melanesian crania have shown
that thickening, particularly at asterion and
lambda, produces measurements close to
those noted for modern Australian crania.
None of these crania, however, are uniformally thick, as WLH 50 is, nor do they show
the same order of development (Fig. 2).
Thickening in some regions of the vault
has been noted in the late Pleistocene Kow
Swamp (9-12,000B.P.) and Coobool Creek
(ca. 12,000B.P.) populations from the Murray River (Thorne and Macumber, 1972;
Brown, 1987).Although the extent and pattern of this development has not been ade-
Fig, 2. The uniform thickening through the left parietal of WLH 50.
quately described, the overall thickness
among these groups does not equal that of
WLH 50. The largest thickness measurement from Kow Swamp is 13.5 mm on the
mid-frontal of KS 9, an individual dated to
around 9,500B.P. (Thorne and Macumber,
1972:318; Thorne, 1975:62). Measurements
up to and including 13 mm at some point on
the cranial vault, however, are not unusual
for late Pleistocene Australian crania. While
a maximum of 16.3mm has been claimed for
the mid-frontal region of one individual from
Coobool Creek, the extent and uniformity of
this thickening has not been fully described
(Brown, 1987). It is worth noting also that
there is no mention of whether this cranium
has been subjected to headbinding, as have a
number of other individuals from Coobool
Creek (Brown, 1981). One result of headbinding is a thickening of posterior areas of
the frontal squama, particularly in the prebregmatic region. In the light of the changes,
it appears that a separation of headbound
from nonheadbound crania is necessary before comparisons of cranial thickness can be
The massiveness of cranial bones among
Chinese and Javan Homo erectus groups and
the Ngandong (Solo) series is of some interest here inasmuch as these groups have been
proposed as ancestors of Australoid peoples
(Thorne, 1977; Thorne and Wolpoff, 1981;
Wolpoff et al., 1984).Vault thickness among
these hominids has been discussed by Weidenreich (1943, 1951). His general conclusion was that cranial vaults of Middle Pleistocene hominids had massive walls and that,
although thick crania are occasionallyfound
in modern humans, the human calvarium
had become thinner as modern humans
emerged. Some of the measurements taken
by Weidenreich approach those of WLH 50,
however, no individual from the Chinese and
Javan series actually achieves the thickness
of WLH 50 at any of the points discussed
here and uniformity of thickening seems to
be, once again, lacking.
I turn now to an examination of the construction of the cranial wall in WLH 50. The
proposition is common amongst biological
anthropologists that thick cranial walls are
associated with antiquity and archaic hominids. A simple comparison of the thickness of
Middle Pleistocene crania with that of modern humans shows that there has been an
overall reduction in massiveness during that
time (see Table 1).The way in which the
vault walls are constructed in the early hom-
inids, such as the Choukoutien and Javan
H. erectus groups, follows a pattern, however, whereby “all three constituents of the
bone take equal part in the thickening, the
two tables slightly more than the diploe”
(Weidenreich, 1943:164).This pattern seems
to be typical of vault construction in other
Middle Pleistocene crania and the Ngandong
(Solo)series also. The vault walls of WLH 50
are constructed quite differently, however.
The inner and outer cranial tables are extremely thin (1-2 mm each), leaving the
greater proportion of the thickness (87.5%)
made up from diploeic or cancellous tissue
(Figs. 2,3). This pattern does not conform to
that found in the older grou s. Therefore, the
massive thickness observe in WLH 50 may
not necessarily be used as a trait t o demonstrate its antiquity.
A fundamental question emerges within
the context of the above. What does the
massive cranial thickening of WLH 50 indicate if it is not an archaic trait? It could be
su gested that WLH 50’s thickened vault
inficates its links with earlier, robust groups
in Indonesia, particularly the Ngandon series. It is logical that the general ro ust
appearance of this individual, and some
other Australian hominids, is reminiscent of
this population. Moreover, it is understandable that a thick cranial vault might be
expected as part of a suite of robust traits
associated with this Javan population. I suggest, however, that the extra thickening and
altered construction of the WLH 50 vault
indicates something different. One of the
traits now commonly associated with late
Pleistocene robust individuals from Australia is a well developed cranial thickness
(Thorne and Wolpoff, 1981). The difference,
however, between the vault thickness of
WLH 50 and much earlier hominids from
outside Australia, can be described as an
extra thickening of the cranium and a relacement of external and internal tabular
one with cancellous or diploeic tissue.
In modern humans, thickening of the cranium, particularly the diploeic or cancellous
tissue, is usually associated with some form
of pathological condition. Hyperostosis of the
internal structures of the cranial vault can
result from a number of pathologies, including Pa et’s disease of bone (osteitis deformans), yperostosis frontalis interna, leontiasis ossea and various hemoglobinopathies
(Jaffe, 1975). The latter include the geneti-
Fig. 3. A closeup view of the vault wall shows the
predominance of diploeic structures. The bone is upside
down in this view so that the thin inner bone table is at
top right and the outer is at bottom.
call determined balanced polymorphisms
s uc i as sickle cell anaemia, the thalassemias, and other haemoglobin variants
(Brittonet al., 1960;Aksoyet al., 1966;Jaffe,
Both the rarity and the distinctive nature
of the first three conditions mentioned above
almost certainly preclude their implication
in the cranial thickening of WLH 50. Moreover, none of the typical diagnostic changes
t o diploeic structures in those suffering from
Paget’s disease can be detected. Also, the
distinctive areas of rarefaction and new bone
formation that are produced in those suffering from Paget’s (osteitis deformans), are not
visible in WLH 50 (Hamdy, 1981).Hyperostosis frontalis interna, which largely affects
the anterior sections of the calvarium and
leontiasis ossea, “was only occasionally encountered in the past and is very rarely
encountered now” (Jaffe, 1975:278). Both
conditions are characterised also by substantial alterations to external and internal bone
surface architecture; do not occur uniformly
throughout the vault; and, more often than
not, they induce gross morphological
changes t o the cranium which substantial1
alter the appearance of the whole skull. A[
though some thickening of the human cranial vault occurs with age (Adeloye et al.,
19751, the massive thickening of WLH 50
must be beyond reasonable acceptance of
personal age as a cause.
It has been known for some time that
sufferers of genetic or chronic blood disease
(hemoglobinopathies) display certain distinctive changes t o the skeleton (Cooley and
Lee, 1925; Williams, 1929). These include
thickening of the cranial vault in the form of
bossing of the parietal and frontal squamae,
and often there is an accompanying symmetrical osteoporosis, or extensive pitting, of the
outer cranial table of these bones (Hrdlicka,
1914; Cooley and Lee, 1925; Williams, 1929;
Hooton, 1930; Angel, 1964, 1967). These
changes are caused by the genetically determined deficiency in erythrocyte production,
which induces hematopoietic hyperostosis.
This results in enlargement of the marrow
cavity between the cranial tables, which, in
turn, produces exaggerated cranial bossing
and expansion of diploeic tissues in other
bones of the postcranial skeleton where bone
marrow is stored. Enlargement of the cranial
diploe induces pressure atrophy (particularly of the outer table) resulting in resorption, thinning and, occasionally, complete
destruction of the compact bone. The condition can affect all major cranial bones, but
usually not the whole bone, and never the
complete cranial vault. Radiologically, the
internal structures of the affected bone
present a brush or hair-on-end appearance
when viewed in norma lateralis (Steinbock,
1976). The latter is caused by the formation
of bone spicules within the diploe at right
angles to the table, which results from osteoclastic and osteoblastic activity during the
proliferation process (Jaffe, 1975). A norma
lateralis radiographic examination of the
vault of WLH 50 has revealed a small patch
of the hair-on-end morphology in the prebregmatic region (see Fig. 1).
In their heterozy ous form, some genetically determined H variants, or balanced
polymor hisms, such as thalassemia and
sickle ce 1 anaemia, confer a degree of immunity to malaria (Flint et al., 1986). Their
distribution is normally confined to human
populations living in latitudes between 45N
to 20S, where malaria is endemic (Bodmer
and Cavalli-Sforza, 1976). It seems likely
that these polymorphisms arose, in the form
of a random mutation, as an adaptive response amon human populations living in
areas in whic malaria was a problem. Noth-
ing is known, however, of how or when they
first arose, although 50,000 years ago has
been proposed (Zaino, 1964). They may have
arisen primarily as a sin le or precursor
condition that then mutate into a number of
variants, over a long period of time, among
human populations who took
migattoO r different
parts of the world. Alternatively, each variant we are familiar with
today could have been produced as a separate adaptation in a particular area where
malaria was endemic. This suggestion supposes, however, that the present world distribution of these conditions has altered little since the time they arose.
As far as we know, malaria was never
endemic in prehistoric Australia. Outbreaks
have been re orted in the north of the continent from t e time of the first Euro ean
settlers, but these were mainly due to eliberate changes to the environment; alterations in the size and settlement of populations and the influx of malaria sufferers
from outside Australia (Breinl, 1912; Breinl
and Holmes, 1915; Cilento, 1942). It is believed that the low population density and
nomadic nature of Aboriginal populations in
the north presented an unsuitable ecology
for the transmission and spread of malaria.
Strongest support for the idea that this disease was never endemic among late Holocene Aboriginal people comes from the
complete absence of abnormal hemoglobins
among recent Aboriginal groups (Horsfall
and Lehmann, 1953,1956; Kirk, 1981). The
palaeopatholopcal evidence also supports
this finding (Webb 198933). Nevertheless,
could malaria and its associated athologies
have existed in Australia more t an 30,000
years ago, disappearing by the Holocene?
Today almost all countries to the north
and east of Australia are affected by malaria
(Manson-Bahr, 1961; Flint et al., 1986). The
distribution of balanced polymorphisms in
this area follows a basic pattern whereby the
HbE variant occurs throughout southeast
Asia, while in Java and Melanesia
thalassemia is dominant (Harrison et al.,
1977; Flint et al., 1986). The position of Java
in this discussion is important for two reasons. Firstly, I ropose that the Indonesian
archipelago is a most sure to have supported
endemic malaria for a very long time and,
second, and perhaps more importantly, Indonesia is the most likely place of origin for
Australia’s first human populations.
The zoonotic origins of malaria are poorly
established, but it seems likely that our early
ancestors and other primates suffered from vealed a heart-shaped appearance to the
it for a very long time (Bruce-Chwatt 1965; calvarium when viewed in both norma vertiToft 1986).Moreover,
calis and norma occipitalis. This is due, in
part, to the prominence of bilateral thickenit has been found out that of the 65 species of ing at the parietal bosses, which tends to
An0 heles recognised as vectors of human malaria,
not pess than 21 were natural or experimental vec- accentuate the sagittal depression and widens the cranial breadth. In this way, it has a
tors of simian malaria. (Bruce-Chwatt 1965:369).
morphological similarity to more recent crametrical osteoporosis, althou h
Indonesian gibbons (Hylobates sp.) are natuSinga
withlac s the distinctive pitting of t e
ral hosts for malaria (Toft, 1986). It is there- nia
fore likely that Javan primate populations outer cranial table which normally accompamust have provided a suitable 001 of suscep- nies this condition. There is an ex ansion of
tibles for the transmission oft is disease for the Singa vault in the re ‘on o f t e frontal
a very long time. From time to time humans bosses, presenting a we l-rounded promior hominids living there could have become nence to the forehead. Both the inner and
infected and a precursor polymorphism outer bone tables are extremely thin (less
evolved as an adaptive mutation over hun- than one millimeter). Eighty percent of its
dreds of generations. Moreover, the un- thickness consists of diploeic bone compared
changing nature of the tropical environment to a maximum of 87.5% in WLH 50.
A previous study of the singa calvarium
durin the Pleistocene in places like Java
must ave enhanced the success of this ad- revealed that
aptation by roviding uninterrupted selec. . . with the exception of the diploeic thickening of
tion during t at time. It seems logical, then,
the parietals, the Singa skull did not exhibit any of
that when people moved from Java to Austhe other radiographic criteria associated with bone
tralia (Thorne, 1975; Thorne and Wolpoff,
changes in anaemia. (Stringer et al., 1985:354)
1981;Wolpoff et al., 1984;Webb, 1989a),any
polymorphisms they had would have come This study concluded that the thickening
with them. With small numbers of people, was unusual and that Singa’s morphology
individual deaths and the long periods of needed further study. Nevertheless, in their
time involved in the migration process we concluding remarks Stringer and his colmight expect a very low frequency of the gene lea es su gested that “certain cranial and
t o reach Australia, however (Webb, 1989a). en ocrania characteristics may be due to
This would be even lower if we consider that a pathological cause.” (Stringer et al.,
even in modern populations the gene fre- 1985:357).My observations support the findquency of these polymorphisms is compara- ings of Stringer and his colleagues. Radiotively small. Furthermore, consider the graphs of this individual, taken some years
added rarety of the homozygous condition.
ago, however, are too opaque to clearly show
The question remains: Could the cranial the intracranial detail that might have
thickening of WLH 50 be a manifestation of a helped secure a firm diagnosis. Further raprecursor balanced polymorphism among diographic examination should be carried
humans? If so, is it likely that the early out in an effort to discover the nature of this
variants produced somewhat different skel- condition. Nevertheless, the hyperostotic
etal changes to those we are familiar with features described above suggest that this
today? Alternatively, would these changes individual suffered from some form of a hehave manifest themselves in the same way mo lobinopathy or severe anaemia.
among people with a robust cranial vault?
8 L H 50 does not overtly displa symmetrical
hy erostosis, cribra orbitaga, or loTHE FOSSIL EVIDENCE
calised ossing of the parietal or frontal
The only other example of a similar type of squamae. Normally these are important
cranial thickening in an archaic or modern palaeo athological indicators of chronic anehuman to that described for WLH 50, that I mia. T erefore, it seems reasonable to sugam aware of, is that in the U per Pleistocene gest, at this point, that if WLH 50’s thick
Singa calvarium from the udan (Stringer, vault is due to some form of hemoglobinopa1979;Stringer et al., 1985).The cranial vault thy, the disease did not have the same aetiof this individual measures 14 mm through ology at that time or its effects on the crathe parietal bosses (WLH 50 is 16 mm) and nium were different from those encountered
15 mm at asterion (WLH 50 is 17 mm). today.
Personal observation of this specimen reAlthough WLH 50 and Singa lack any sign
s. vl(EBB
of cribra orbitalia the both have an exaggerated thickening o f t e vault and an overwhelming predominance of cancellous over
cortical tissue. It is felt that these similarities are more than coincidental. The major
difference between the two is that some areas of the Singa vault are not particularly
thick (9 mm on the parietals), whereas WLH
50 is uniformally so. Is it possible that these
two individuals provide some evidence for
the initial biological adaptation of humans in
coping with endemic malaria? Today the
areas from which they or their gene pools
originated are malarial. Whether this was
the case in the late, Upper Pleistocene is a
matter for speculation.
I would not be the first biological anthropologist to point out the difficulties associated with diagnosing disease from dry bone.
This task becomes exceedingly difficult if we
consider that a particular disease may have
been somewhat different in the distant past;
displayed different sym toms than those associated with the same i s e a s e today; or that
we are dealin with something we have no
knowledge of. %
I it seems likely that
the older the fossil remains are the more
likely that an or all of these factors and
man more wi 1 come into play.
d L 50 does not display skeletal changes
conforming exactly to those observed in recent populations suffering genetical1 determined anaemias, but the thickene diploe
strongly indicates its need for hematopoietic
“reinforcement.”I propose that the intracranial bone architecture of WLH 50 is an adaptation to exactly that need. It is tentatively
sug ested, therefore, that the thickened
vau t is caused by a condition closely allied
with, or a precursor to, the modern genetically derived haemoglobinopathies. I also
propose that such a condition arose some
time before 30,000 years ago, probably as a
local adaptation in tropical areas to the
north of Australia. This condition was
brought to greater Australia as part of the
genetic baggage of migrations from areas
such as Indonesia, where it played an important adaptive role in helping people cope
with malaria. In the absence of a selective
agent for this polymorphism in Australia,
and considering Australia’s minimal population prior to 30,000B.P., the variant might
have easily been selected out from the gene
pool quite early, perhaps within a few thousand years (R.L. Kwk, personal communica-
tion). With the low frequencies of this condition likely at that time, there is no reason to
expect to find a multitude of fossil crania
bearing a similar morphology.
One last point should be emphasised. The
vault thickening seen among many late
Pleistocene and Holocene Australian crania
is not at issue here as a pathological phenomenon; the extraordinary thickening of WLH
50 is. It is proposed, therefore, that normally
this individual might have had a thick vault
commensurate with its other robust features, as have a number of other late Pleistocene Australians fossil crania, but in WLH
50’s case there is further thickening caused
by some form of genetic blood disorder. Little
or nothing is known of the palaeoepidemiology of our commonest diseases or human
responses to them. It may be possible, however, that the sort of evidence presented here
allows us to speculate on the age and distribution of one of those diseases and to ap reciate the antiquity of human biological a aptiveness.
I would like to thank Dr Chris Stringer
and the Natural History Museum in London
for access to the Singa cranium. WLH 50 is
being described by Dr Alan Thorne at the
Australian National University, Canberra. I
greatfully acknowledge his cooperation in
allowing me to present these arguments before his fuller description is available.
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cranial, possible, palaeoepidemiological, indicators, australia, thickening, hominis
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