Cranial thickening in an Australian hominid as a possible palaeoepidemiological indicator

AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 82:403411 (1990)

Cranial Thickening in an Australian Hominid As a Possible Palaeoepidemiological Indicator

STEPHEN WEBB Centre For Australian Studies, School of Humanities and Social Sciences, Bond University Private Bag 10, Gold Coast Mail Centre, Queensland 421 7, Australia

KEY WORDS ing, Palaeopathology, Blood dyscrasias

Palaeoepidemiology, Australia, Cranial Thicken-

ABSTRACT This paper describes the cranial thickening of a late Pleis- tocene 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 to- gether 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 ap- pear considerably thicker than those of modern man. But as yet . . . no one has provided ac- tual figures or deemed the en- tire phenomenon worth consid- eration. (Weidenreich 1943: 161)

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

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 exocrani- ally, 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

P $ post-cranial ske 7 eton. The individual, known

‘d Map 1. Willandra Lakes Region

been obtained for these remains using the electron spin resonance (ESR) method (Caddie et al., 1987:175). Other datingmeth- ods 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

@ 1990 WILEY-LISS. INC

404 s. WEBB

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 Hu.man Populations (nim)'.'

Hominid or population A B C D E F G H

WLH 50 19 17 17 15 16 17 15 18 WLH Series min. 5 6 4 4 4 6 5 7 WLH Series max.:' 13 12 10 10 14 14 12 19

- - 12 - Coobool Creek (1) - 9 11 10 Kow Swamp (2) - 14 12 - 10 12 12 -

New Year Island (4) - 6 - 5 7 - 15 - Cossack (5) - 14 12 11 11 11 11 - Recent Aborigines (6) 11 9 10 8 8 9 9 Recent Europeans (7) 6 5 6 6 6 4 7 British Neolithic (7) 7 6 7 8 7 6 9 Mesoamericans (7) 7 11 11 8 7 10 10 - Niah (8) 4 5 - 5 9 6 6 9

Singa - - -

- 9 - 14 17 - 38' Ngandong (Solo) (9) - Choukoutien (10) 16 11 10 11 16 18 15 20

- 10 10 Kabwe (Broken Hill) - - - Swanscombe -

- Lake Tandou (3) - 10 8 10 - 14 -

- - -

Neanderthals (7) 11 8 9 11 11 9 10 24 - - - - 14

- - - - 7 7 11 9 10

' 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 and right sides.

Measured through occipital torus and internal occipital protuberance.

PALEOEPIDEMIOLOGICAL INDICATOR 405

or anic components have been removed. A

documented by Dr. Alan Thorne of the Aus- tralian 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.

fu k 1 description of this individual is being

DESCRIPTION

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 Pleis- tocene 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 Willan- dra 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 lmm (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 Mur- ray 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.

406 S. WEBB

quately described, the overall thickness among these groups does not equal that of WLH 50. The largest thickness measure- ment 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 16.3 mm 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 made.

The massiveness of cranial bones among Chinese and Javan Homo erectus groups and the Ngandong (Solo) series is of some inter- est 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 Wei- denreich (1943, 1951). His general conclusion was that cranial vaults of Middle Pleis- tocene hominids had massive walls and that, although thick crania are occasionally found 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

not necessarily be used as a trait t o demon- strate its antiquity.

massive thickness observe a in WLH 50 may

DIFFERENTIAL DIAGNOSIS

A fundamental question emerges within the context of the above. What does the massive cranial thickening of WLH 50 indi- cate 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 se-

appearance of this individual, and some other Australian hominids, is reminiscent of this population. Moreover, it is understand- able 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 Austra- lia 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 re-

lacement of external and internal tabular one with cancellous or diploeic tissue. In modern humans, thickening of the cra-

nium, 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 defor-

asis ossea and various hemoglobinopathies (Jaffe, 1975). The latter include the geneti-

ries. It is logical that the general ro t ust

g

mans), fl yperostosis frontalis interna, leonti-


Fig. 3. A closeup view of the vault wall shows the predominance of diploeic structures. The bone is upside

call determined balanced polymorphisms suci as sickle cell anaemia, the thal- assemias, and other haemoglobin variants (Brittonet al., 1960;Aksoyet al., 1966; Jaffe, 1975).

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. More- over, none of the typical diagnostic changes to 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

down in this view so that the thin inner bone table is at top right and the outer is at bottom.

visible in WLH 50 (Hamdy, 1981). Hyperos- tosis 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 to 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.,

408 S. WEBB

19751, the massive thickening of WLH 50 must be beyond reasonable acceptance of personal age as a cause.

HEMOGLOBINOPATHIES

It has been known for some time that sufferers of genetic or chronic blood disease (hemoglobinopathies) display certain distinctive changes to 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 resorp- tion, 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 osteo- clastic 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

nity 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 re- sponse amon human populations living in

sickle ce P 1 anaemia, confer a degree of immu-

areas in whic a 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

variants, over a long period of time, among human populations who took

tively, each variant we are familiar with today could have been produced as a sepa- rate adaptation in a particular area where malaria was endemic. This suggestion sup- poses, 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 conti-

settlers, but these were mainly due to elib- erate 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 be- lieved 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 Ho- locene 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

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

endemic malaria for a very long time and, second, and perhaps more importantly, In- donesia 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

condition that then mutate f into a number of

them migat to Ordr ifferent parts of the world. Alterna-

c f nent from t R e time of the first Euro ean

have existed in Australia more t R an 30,000

archipelago is a P most sure to have supported


ancestors and other primates suffered from it for a very long time (Bruce-Chwatt 1965; Toft 1986). Moreover,

it has been found out that of the 65 species of An0 heles recognised as vectors of human malaria, not pess than 21 were natural or experimental vectors of simian malaria. (Bruce-Chwatt 1965:369).

Indonesian gibbons (Hylobates sp.) are natural hosts for malaria (Toft, 1986). It is therefore likely that Javan primate populations must have provided a suitable 001 of suscep-

a very long time. From time to time humans or hominids living there could have become infected and a precursor polymorphism evolved as an adaptive mutation over hun- dreds of generations. Moreover, the un- changing nature of the tropical environment durin the Pleistocene in places like Java

aptation by roviding uninterrupted selec-

that when people moved from Java to Aus- tralia (Thorne, 1975; Thorne and Wolpoff, 1981; Wolpoff et al., 1984; Webb, 1989a), any polymorphisms they had would have come with them. With small numbers of people, individual deaths and the long periods of time involved in the migration process we might expect a very low frequency of the gene to reach Australia, however (Webb, 1989a). This would be even lower if we consider that even in modern populations the gene frequency of these polymorphisms is compara- tively small. Furthermore, consider the added rarety of the homozygous condition.

The question remains: Could the cranial thickening of WLH 50 be a manifestation of a precursor balanced polymorphism among humans? If so, is it likely that the early variants produced somewhat different skeletal changes to those we are familiar with today? Alternatively, would these changes have manifest themselves in the same way among people with a robust cranial vault?

THE FOSSIL EVIDENCE

tibles for the transmission oft R is disease for

must a ave enhanced the success of this ad-

tion during t R at time. It seems logical, then,

The only other example of a similar type of cranial thickening in an archaic or modern human to that described for WLH 50, that I am aware of, is that in the U per Pleistocene Singa calvarium from the # udan (Stringer, 1979; Stringer et al., 1985). The cranial vault of this individual measures 14 mm through the parietal bosses (WLH 50 is 16 mm) and 15 mm at asterion (WLH 50 is 17 mm). Personal observation of this specimen re-

vealed a heart-shaped appearance to the calvarium when viewed in both norma verti- calis and norma occipitalis. This is due, in part, to the prominence of bilateral thickening at the parietal bosses, which tends to accentuate the sagittal depression and wid- ens the cranial breadth. In this way, it has a morphological similarity to more recent cra-

metrical osteoporosis, althou h nia Singa with lac sY s the distinctive pitting of t fl e outer cranial table which normally accompa- nies this condition. There is an ex ansion of

nence to the forehead. Both the inner and outer bone tables are extremely thin (less than one millimeter). Eighty percent of its thickness consists of diploeic bone compared to a maximum of 87.5% in WLH 50.

A previous study of the singa calvarium revealed that

. . . with the exception of the diploeic thickening of the parietals, the Singa skull did not exhibit any of the other radiographic criteria associated with bone changes in anaemia. (Stringer et al., 1985:354)

This study concluded that the thickening was unusual and that Singa’s morphology needed further study. Nevertheless, in their concluding remarks Stringer and his col- lea es su gested that “certain cranial and

a pathological cause.” (Stringer et al., 1985:357). My observations support the find- ings of Stringer and his colleagues. Radio- graphs of this individual, taken some years ago, however, are too opaque to clearly show the intracranial detail that might have helped secure a firm diagnosis. Further radiographic examination should be carried out in an effort to discover the nature of this condition. Nevertheless, the hyperostotic features described above suggest that this individual suffered from some form of a he- mo lobinopathy or severe anaemia.

8 L H 50 does not overtly displa symmetrical hy erostosis, cribra orbitaga, or lo-

squamae. Normally these are important palaeo athological indicators of chronic ane-

gest, at this point, that if WLH 50’s thick vault is due to some form of hemoglobinopa- thy, the disease did not have the same aeti- ology at that time or its effects on the cranium were different from those encountered today.

Although WLH 50 and Singa lack any sign

the Singa vault in the re ‘on o f t K e frontal bosses, presenting a we Y l-rounded promi-

en r ocrania 4 characteristics may be due to

calised g ossing of the parietal or frontal

mia. T K erefore, it seems reasonable to sug-

410 s. vl

of cribra orbitalia the both have an exagger-

whelming predominance of cancellous over cortical tissue. It is felt that these similari- ties 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.

CONCLUSION

I would not be the first biological anthro- pologist 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 sease today; or that we are dealin with something we have no

the older the fossil remains are the more likely that an or all of these factors and

d L 50 does not display skeletal changes conforming exactly to those observed in recent populations suffering genetical1 deter-

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

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 thou- sand years (R.L. Kwk, personal communica-

ated thickening o f t g e vault and an over-

knowledge of. %I oreover, it seems likely that

man more wi P 1 come into play.

mined anaemias, but the thickene B diploe

vau P t is caused by a condition closely allied

(EBB

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 Pleis- tocene 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 re- ciate the antiquity of human biological a a ap- tiveness.

ACKNOWLEDGMENTS

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 thickening in an Australian hominid as a possible palaeoepidemiological indicator

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