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Porotic hyperostosis A new perspective.

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AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 87:3947 (1992)
Porotic Hyperostosis: A New Perspective
PATTY STUART-MACADAM
Department ofdnthropology, University of Toronto, Toronto, Ontario
M5S 1A1, Canada
KEY WORDS
stress markers
Anemia, Cribra orbitalia, Pathogen load, Skeletal
ABSTRACT
Porotic hyperostosis is a paleopathologic condition that has
intrigued researchers for over a century and a half. It is now generally accepted
that anemia, most probably an iron deficiency anemia, is the etiologic factor
responsible for lesion production. Although there can be a number of factors
involved in the development of iron deficiency anemia, a dietary explanation
has often been invoked to explain the occurrence of porotic hyperostosis in past
human skeletal populations. In fact, porotic hyperostosis has been referred to
as a “nutritional” stress indicator. Traditionally those groups with a higher
incidence of porotic hyperostosis have been considered to be less successful in
adapting to their environment or more nutritionally disadvantaged than other
groups.
A new perspective is emerging that is challenging previous views of the role
of iron in health and disease, thus having profound implications for the
understanding of porotic hyperostosis. There is a new appreciation of the
adaptability and flexibility of iron metabolism; as a result it has become
apparent that diet plays a very minor role in the developmentof iron deficiency
anemia. It is now understood that, rather than being detrimental, hypoferremia (deficiency of iron in the blood) is actually an adaptation to disease and
microorganism invasion. When faced with chronic andlor heavy pathogen
loads individuals become hypoferremic as part of their defense against these
pathogens, thus increasing their susceptibility to iron deficiency anemia.
Within the context of this new perspective porotic hyperostosis is seen not as a
nutritional stress indicator, but as a indication that a population is attempting
to adapt to the pathogen load in its environment.
Progress in science occurs by a number of
means, including the development of new
techniques of investigation, the accumulation of data, and the gradual development of
thought based on the work of numerous researchers. However, one of the most vital
means of scientific progress is the application of new perspectives-that is, the introduction of novel frameworks, concepts, or
ideas. New perspectives applied to existing
data promote new insights and pave the way
for new directions of thought and research.
The present paper explores the development
of thought with regard to a paleopathologic
condition, porotic hyperostosis, and illustrates how the emergence of a new perspective can have a profound impact on the per-
@ 1992 WILEY-LISS,INC
ception of and understanding of this
condition.
Porotic hyperostosis is a paleopathologic
condition that has intrigued researchers for
over a century and a half. The skull vault,
particularly the frontal, parietal, and occipital bones, as well as the orbital roof are
affected. Macroscopically what is evident is a
number of small holes of varying size and
distribution that penetrate the outer compact bone of the skull. This corresponds with
an increase in the middle table of bone, or
diploe, and a thinning of the outer table of
bone. Microscopically the spaces between
bone trabeculae are enlarged and open
Received July 25,1990; accepted June 20,1991,
40
P. STUART-MACADAM
widely onto the bone surface. Radiographically there are a number of changes: on the
horizontal plates of the frontal bone (orbital
roof)there is an increase in thickness seen in
lateral views, and alterations of the orbital
rim on anterior-posterior views, while on the
skull vault thinning and/or disappearance of
the outer compact bone, increased granularity, an increase in the middle table of bone,
and sometimes a “hair-on-end” pattern of
trabeculation are seen (Stuart-Macadam,
1982,1987).
The literature pertaining to this condition
abounds with views concerning etiology and
terminology. Just a few of the names that
have been suggested are “symmetrical osteoporosis” (Hrdlicka, 1914), “spongy hyperostosis” (Muller, 1935), and “external cribra
cranii” (Koganei, 1912). Suggestions for etiology have ranged from the effects of carrying water jugs on the head (Wood-Jones,
1910), a toxic disorder (Hrdlicka, 1914), a
racial trait (Welcker, 18881,or dietary problems (Williams, 1929). Owen (18591, who
was one of the first to comment on the condition, said that a skull from Nepal with the
lesions “is chiefly remarkable as exemplifying the rare disease of hypertrophous thickening of the parietal bones.” In 1924 Morant
attributed lesions on the same skull to a
“hypertrophy,osteitis, acrocephaly or a more
specific but unknown pathological state.”
The concensus at present favors the terms
“porotichyperostosis” (after Angel, 1966) for
lesions of either the vault or orbit, or “cribra
orbitalia” (after Welcker, 1888)for lesions of
the orbit. Researchers now feel that porotic
hyperostosis is the result of an anemia and,
in the majority of populations, most probably
an acquired iron deficiency anemia. This is
not to say that the genetic anemias such as
thalassemia and sickle cell anemia did not
occur in the past, but that their relatively
low incidence in populations would not
account for the high frequency of porotic
hyperostosis seen in populations from many
geographic areas and time periods (StuartMacadam, 1982,1990).
Iron deficiency anemia can be defined as a
reduction below normal in levels of hemoglobin and hematocrit (packed red cell volume)
in blood. This can occur for a variety of
reasons including blood loss, accelerated demands as a result of factors such as growth or
pregnancy, inadequate absorption of iron,
and nutritional deficiencies (Robinson,
1972).However, since Williams first put for-
ward the suggestion in 1929 anthropologists
have emphasized a dietary explanation for
the occurrence of porotic hyperostosis (hence
anemia) in the archaeological record. In fact,
porotic hyperostosis has often been referred
to as a nutritional stress indicator (Armelagos, 1990; Goodman et al., 1988; Huss-Ashmore et al., 1982; Mensforth et al., 1978;
Martin et al., 1985). It is true that the term
nutrition encompasses more than just diet;
the problem is that this has not been made
explicit in discussions of porotic hyperostosis
and as a result the assumption has often
been made that diet is of paramount importance. However, it is easily understood how
porotic hyperostosis could be interpreted in
this manner.
For example, there appears to be a strong
correlation between the occurrence of porotic
hyperostosis and both the introduction of
‘cereal grains in the Neolithic (Cohen and
Armelagos, 1984), and subsistence on cereal
grains, particularly maize. Cereal grains
contain phytates, which can inhibit the absorption of dietary iron by the intestine.
El-Najjar (1976), El-Najjar and Robertson,
(19761, and El-Najjar and colleagues (1975,
1976, 1982) popularized the “maize dependency” hypothesis, which stressed that porotic hyperostosis was most common in
groups that had a high proportion of maize in
their diet. Since that time there has been a
greater appreciation of the complexity of the
story (Lallo et al., 1977; Mensforth et al.,
1978; etc.), but diet is still invoked as a factor
in almost every discussion of porotic hyperostosis (exceptions are Kent, 1986; StuartMacadam, 1988,1989,1990).
The dietary hypothesis fit the data well
enough in the past, but now new data, and
more importantly a new perspective, have
emerged which shed a different light on porotic hyperostosis. The new perspective involves a reappraisal of the role of iron in
health and disease. There is a greater appreciation of the flexibility and complexity of
iron absorption by the intestine and a new
understanding of the adaptive features of
iron metabolism. It is now known that iron
plays an important role in the defense system of the human body. Two important
points have emerged as a result:
1. Except in cases of outright malnutrition,
diet plays a minor role, if any, in the development of iron deficiency anemia.
2. Mild iron deficiency, or hypoferremia, is
POROTIC HYPEROSTOSIS
41
1988; Strauss, 1978) have written on the
mechanism of iron withholding and its advantages in the face of micro-organism invasion. Many micro-organisms require iron for
The data to support these contentions their own replication, yet lack their own
have accumulated in the medical literature stores. They rely on supplies of iron that they
over a number of years. Wadsworth (see can obtain from the host with their own
1975 review) was one of the first researchers manufactured iron-chelators. The human
to deemphasize the importance of diet in the body is able to minimize the iron available to
development of iron deficiency anemia. He micro-organisms by decreasing serum iron,
noted that many studies showed absolutely which is more readily available t o microno correlation between dietary intake of iron organisms, and decreasing absorption of diand presence or absence of iron deficiency etary iron by the intestinal mucosa. Serum
anemia. Davidson et al. (1933) also noted iron is decreased by binding the available
that in a large population of individuals from iron to the transport protein, transferrin, or
Aberdeen there were no obvious differences sending it into storage in the reticuloendoin iron consumption between those who de- thelial system. A short-term reduction in
veloped iron deficiency anemia and those absorption of dietary iron does not comprowho did not. Arthur and Isbister (1987) state mise iron metabolism because there is still
that “even if iron intake was reduced to nil, ample iron available from the destruction of
which is virtually impossible even with the old red blood cells. In fact, iron metabolism is
most frugal diets, it would still take at least almost a closed system with as much as 90%
two to three years to develop iron deficiency of the iron required for the production of new
anemia, and probably even longer because red blood cells being obtained by the turnlosses would decline as levels declined.” In over of senescent red blood cells.
There are in vivo, in vitro, and population
addition, as iron levels in the diet decrease,
the proportion absorbed increases (Wads- studies that support the concept that being
iron deficient is an advantage during expoworth, 1990).
The fact is that the intestine is capable of a sure to many disease organisms, including a
wide range of levels of absorption of iron number of bacteria, fungi, and parasites. In
from the same diet, depending on factors the past thirty years, several hundred studsuch as age, sex, physiological status, and ies on animals and a number on humans
disease status. Studies have shown that iron have shown that hosts whose iron withholdabsorption from an adequate diet can vary ing system is compromised are at increased
from a fraction of a milligram to as much as 3 risk of infection (Weinberg, 1990). Several
or 4 milligrams a day, depending on body dozen reports have shown that strengtheniron content. For example, hyperferremia, or ing the iron withholding system results in
iron overload, is associated with a decrease decreased risk of infection (see reviews in
in absorption of iron from the diet. When an Weinberg, 1974,1978,1984). Iron withholdincreased supply of iron is needed by the ing is also associated with conditions such as
body, the levels of intestinal absorption can inflammation and neoplasia, and seems to
increase concomitantly. This is particularly be a generalized stress response. The data
the case with women and children, who have are not always clear-cut, and the concept is
much greater physiological needs for iron still controversial, but the evidence increasthan men. Studies have shown that 5-10% of ingly supports the concept of iron withholddietary iron is absorbed by healthy Western ing as a positive, adaptive response to invadadult males, whereas as much as 25% is ing micro-organisms.
Data from the anthropological literature
absorbed by iron deficient adults (Arthur
and Isbister, 1987). The same flexibility oc- can also provide support for the concepts of
curs with iron loss; normal males lose ap- diet being a minor factor in the development
proximately .9 milligrams per day and hy- of iron deficiency anemia and the occurrence
perferremic males lose about 2 milligrams of iron deficiency being a defense against
micro-organisms. If the occurrence of porotic
per day (Finch, 1989).
Weinberg (1974, 1977, 1978, 1984, 1990) hyperostosis is examined through time and
and others (Bullen and Griffiths, 1987;Crosa, space three major trends are apparent: tem1987;Griffiths and Bullen, 1987; Kluger and poral, geographic, and ecological (StuartBullen, 1987; Martinez et al., 1990; Payne, Macadam, 1990). Porotic hyperostosis is
not necessarily a negative condition; in fact
it is one of the body’s defenses against disease.
42
P. STUART-MACADAM
very uncommon before the Neolithic period
(Angel, 1978; Meiklejohn et al., 1984;
Kennedy, 1984). The frequency then increases during the Neolithic (Angel, 1978)or
with the adoption of agriculture (Lallo et al.,
1977; Cohen and Armelagos, 1984). Although the picture becomes very complex,
there does appear to be a general reduction
in prevalence towards the 20th century (Angel, 1978; Hengen, 1971; Henschen, 1961).
Porotic hyperostosis occurs in skeletal collections from every country and continent, but
Hengen’s analysis of over 5,000 skulls shows
that the closer the country of origin is to the
equator, the greater the incidence of porotic
hyperostosis. Porotic hyperostosis occurs
more frequently in individuals from lowland
or coastal sites than those from highland
sites. This has been observed by a number of
researchers including HrdliEka (1914), ElNajjar et al. (19761, Ubelaker (19841, and
Angel (1972).
What clues do these trends provide about
the picture of anemia in the past? First, it is
unlikely that dietary differences alone could
account for these broad trends in time, space,
and ecology. Even though the prevalence of
porotic hyperostosis does increase with the
introduction of agriculture, closer analysis of
the data shows that groups with a heavy
reliance on agriculture (hence cereal grains)
have a varying prevalence of porotic hyperostosis, as do groups that are known to rely
more heavily on animal protein food sources.
For example, Ubelaker (1984) found little
porotic hyperostosis in an Ecuador highland
site where there was intensive agriculture,
and in some areas in North America where
maize and cereal grains were intensely cultivated, porotic hyperostosis has been found in
only a few individuals (Larsen, 1987). However, Walker (1986)found a high prevalence
of porotic hyperostosis in a group from the
Santa Barbara Channel Islands having an
iron-rich marine diet. The data also show
that both proximity to the equator and altitude correlate with incidence of porotic hyperostosis regardless of subsistence base.
If diet is not the major etiological factor in
porotic hyperostosis, then what is? Consideration of the trends in occurrence of porotic
hyperostosis and the new perspective suggests that a different factor, pathogen load,
is much more critical in the development of
anemia in past populations. Pathogen load
refers to the total number of micro-organisms in the local environment, including
fungi, viruses, bacteria, and parasites. This,
in turn, is dependent on innumerable factors
such as climate, geography, topography,
population size and density, hygiene, food
resources, seasonality, customs, and subsistence patterns. Pathogen load can have both
direct and indirect effects on the iron status
of individuals. The direct effects are evident
when an individual develops anemia as a
result of pathogens that are responsible for
blood loss or the destruction of red blood
cells. For example,the malarial parasite invades the red blood cell and causes its premature destruction. The hookworm parasite
(either Ancylostoma duodenale or Necator
americanus)attaches directly onto the small
intestine and can result in anemia through
chronic blood loss. The indirect effects are
evident when an individual contracts either
an acute or chronic disease. In the case of
many acute diseases, the body becomes temporarily hypoferremic as part of its defense
system. In this case, iron absorption from the
diet is decreased, serum iron is bound to the
iron-transporting protein, transferrin, and
excess iron is taken into storage. With
chronic diseases there is often an associated
anemia; again this is probably associated
with attempts on the part of the body to
defend itself against pathogens. Anemia of
chronic disease is one of the most common
forms of anemia, and is associated with a
number of diseases that would have affected
past populations, such as chronic mycotic
infections, tuberculosis, and osteomyelitis.
Pathogen load being a major factor in the
development of porotic hyperostosis satisfactorily explains the observed trends through
time and space. The increase in porotic hyperostosis during the Neolithic and with agriculture is a function not of iron-poor diets,
but of increased sedentism, aggregation, and
population density which resulted in greater
exposure to pathogens. A decrease in porotic
hyperostosis towards the 20th century could
be explained by improvements in sanitation
and hygiene. The increase in porotic hyperostosis with increasing proximity to the
equator reflects the increased viability of
many micro-organisms with warm, humid
conditions. A decrease with altitude is associated with less favorable conditions for
pathogens.
New data from anthropological studies
also support the concepts that diet does not
play a major role in the incidence of porotic
hyperostosis and that pathogen load is a
critical factor in the story of anemia in the
past. Reinhard (1990) analyzed coprolites
POROTIC HYPEROSTOSIS
from some of the same Southwest Anazasi
Indian sites that El-Najjar et al. (1976) used
to generate their “maize dependency” hypothesis. On the basis of that data Reinhard
could find no relationship between maize
consumption and the occurrence of porotic
hyperostosis. He did, however, find a very
high correlation between pinworm prevalence in coprolites and porotic hyperostosis,
which he felt provided evidence for a relationship with microparasitism (protozoal,
bacterial, and viral infection). Ubelaker
(1990) has obtained data on a range of sites
in Ecuador within a broad, complex culturaltemporal framework that includes coastal
and highland sites spanning nearly 8,000
years. He found no evidence for porotic hyperostosis in earlier sites (i.e., hunting and
gatheringhorticulture) or in highland areas,
but found that porotic hyperostosis was confined to skeletal material from relatively
recent coastal sites. These sites do not appear to be associated with an iron-poor diet
as there is evidence for a heavy reliance on
oysters and clams, and utilization of reptiles,
birds, deer, and rodents. Ubelaker found
that evidence for porotic hyperostosis in Ecuador loosely follows a temporal trend, but
does not correlate closely with increasing
time or reliance upon maize agriculture.
The idea that environmental and cultural
conditions could have an important affect on
anemia in the past is not a new one. Hengen
(1971) was probably the first to suggest this
when he said:
Changes in the hygienic conditions and of the incidence of iron deficiency anemias in former times
depended without doubt largely on deviations of
the climate, differences in the habits of daily life,
procuring and preparation of food, types of housing,
keeping of domestic animals, disposal of excrement
and so on.
Other researchers have touched on this issue, but even so, diet has been considered t o
be an important etiological factor in producing porotic hyperostosis in most studies. The
time has come for diet to be de-emphasized
as a factor and pathogen load to be emphasized. The complex interaction between environmental and cultural factors that is involved in generating pathogen load in any
one population can be appreciated from a
study by Dunn (1972). Dunn surveyed the
prevalence and density of intestinal parasitism in Malayan aborigines inhabiting the
southern Malay peninsula. A great diversity
43
of habitat and culture was represented as
villages are found in a variety of ecosystems
including primary forest, secondary forest or
scrub vegetation, or near rubber estates and
large towns. Dunn was able to compare parasitism between those aborigines who had
left their traditional forest environment and
those who were still forest dwellers and subsistence cultivators.
Dunn examined the relationships among
cultural-ecological groups, sanitation, and
intestinal parasitism. Sanitary status was
estimated for each group by considering not
only the excreta and rubbish disposal practices but also a number of other environmental and cultural variables that interacted
with sanitary behavior t o produce different
sanitary conditions. These were:
1. Population density and crowding: the
larger and denser the population, the more
heavily contaminated were their living conditions.
2. Land availability around the village:
large tracts of land around the village minimized contamination.
3. Community mobility: the greater the
mobility of the community, the cleaner the
environment.
4. Subsistence: agriculturalists had more
contact with the land and a greater chance of
being exposed to soil pathogens.
5. House style: ground level housing as
opposed to pile housing meant a greater
chance of exposure to pathogens.
6. Domestic animals: these animals can
act as scavengers and reduce environmental
contamination.
7. Helminth viability: at cooler, higher
elevations the viability of helminth eggs is
reduced.
When villages were assessed for overall sanitary status they ranged from fairly good to
poor. When Dunn examined the prevalence
and abundance of intestinal parasites he
found a general correspondence between the
sanitary score and the intestinal burden.
The lower the sanitary assessment the
heavier the intestinal burden. Unfortunately there was no information on differences in the iron status among these groups.
It was mentioned that severe anemia is rare
in Malayan aborigines but that marginal
anemia is common and seemed to be the
product of a group of contributory factors
(including hookwork and perhaps Trichuris)
that vary in relative importance from one
44
P. STUART-MACADAM
cultural-ecologicalsetting to another (Dunn,
1972).
Dunn noted that the number of species of
parasite was closely related to the complexity of the ecosystem; the greater the complexity, the greater the number of species of
parasite. For example, the Negritos, who
subsisted on hunting and gathering and
fishing in the complex ecosystem of the Malayan rain forest, had more species of intestinal parasite than any other ethnic group.
Where that ecosystem was simplified by settlement and cultivation some species of human parasite that depend on intermediate
hosts disappeared because they could not
adapt. However, the more adaptable parasites, such as Ascaris, Trichuris, Giardia,
and Entamoeba histolytica became much
more successful in terms of prevalence and
intensity.
DISCUSSION
The acceptance of the two concepts, that
diet is of little importance in the development of iron deficiency anemia, and that iron
deficiency is an adaptive response to stress,
has a profound effect on the interpretation of
porotic hyperostosis. In the past a high prevalence of porotic hyperostosis in a population
has often been interpreted to mean a diet low
in iron or bioavailable iron, even if other
factors were considered to be operative. Porotic hyperostosis has also been interpreted
to be indicative of maladaptation. However,
viewing porotic hyperostosis in the light of
the new perspective provides alternative interpretations. First, it suggests that a high
incidence in a group is indicative of a heavy
pathogen load in the environment of that
group, for whatever reason. Secondly, it suggests that as part of their attempt to adapt,
those individuals with porotic hyperostosis
have gone into the iron-deficiency mode,
where dietary absorption of iron is inhibited
and serum iron decreased, making it more
difficult for pathogens to obtain the necessary iron for growth and development. When
this happens, the amount of iron in the diet is
irrelevant; absorption of iron by the intestine
will still be diminished. The hypoferremic
situation could be prolonged because of high
levels of andor chronic exposure to microorganisms, and iron deficiency anemia
would ensue, stimulating the formation of
new red blood cells, and increasing the size of
the marrow (marrow hyperplasia) to produce the bone changes known as porotic
hyperostosis. These lesions probably devel-
oped exclusively in childhood when the bone
is particularly susceptible to alterations associated with anemia (Stuart-Macadam,
1985).
There is a real problem in attempting to
ascertain blood measures (i.e., the severity of
anemia) from skeletal changes. There does
not appear to be any consistency between the
severity of the clinical disease and the severity of the skull changes. Caffey (1951) has
documented cases of patients of the same age
and with similar clinical and hematological
findings who show very different degrees of
skull change. This appears to be the result of
individual variability, perhaps associated
with differences in amount and distribution
of hematopoietic (red) marrow in the skull.
Severity of bone change as well as distribution of bone change can be affected. Some
individuals develop changes of the vault
only, some the orbit only, or sometimes
changes are more pronounced in one area of
the vault than another (Caffey, 1937; McAfee, 1958; Middlemiss, 1961).
Acceptance of the new perspective dramatically alters the way porotic hyperostosis
can be perceived with respect to the interaction of a population and its environment.
Porotic hyperostosis does not indicate a diet
that is low in iron or bioavailable iron and so
cannot be called upon t o provide information
about the dietary status of a population. It is
not just an indicator of nutritional stress. It
certainly is an indicator of stress; however,
the stress that is more often involved is the
pathogen load encountered by a population.
The occurrence of porotic hyperostosis reflects the attempts of that population to cope
with and adapt to its environment. It suggests that there was a primary response of
iron withholding as an adaptation to disease
and/or pathogen load, followed by the development of iron deficiency anemia as the
threshold between hypoferremia and anemia was surmounted. This would occur particularly when other factors such as physiological status (for example, pregnancy),
growth requirements, blood loss (as in parasitic infestation), or in rare cases diet, tipped
the balance. It could be said that chronic
hypoferremia is an evolutionary response to
persistent microbial invasion (Kent and
Weinberg, 1989; Sturat-Macadam 1988).
Populations that were chronically exposed to
heavy pathogen loads have adapted by lowering their iron status, resulting in an increased susceptibility to iron deficiency anemia. Rather than being seen as a sign of
45
POROTIC HYPEROSTOSIS
weakness or maladaptation, porotic hyperostosis should be viewed as a sign that the
population is attempting to adapt to adverse
environmental conditions.
The term adaptive must, of course, be
considered in context. What is adaptive in
one situation or environment may not be in
another. This is certainly true in the case of
hypoferremia and so porotic hyperostosis
must always be viewed in the light of human
iron metabolism and body physiology. The
critical feature of human iron metabolism is
conservation; there is a fine line between too
much and too little. The body is constantly
striving to maintain a balance. Too little iron
can be associated with severe anemia which
impairs the quality of life and can eventually
lead to a failure of the cardiac and respiratory systems, while too much iron can produce fibrotic scarring, and eventual failure
of several organs, including the liver, pancreas, heart, and endocrine system (Cook,
1990). The immune system is compromised
in both situations, either from too much iron
or too little. In between the more obvious
extremes there is a grey area which is more
ambiguous; some studies suggest detrimental effects while others argue against them.
For example, some studies (Aukett et al.,
1986; Pollitt, 1989, Pollitt et al., 1989) suggest that mild iron deficiency may affect
mental achievement. However, the presence
of parasitic infestation was a confounding
factor in one study by Pollitt (1989).Dallman
(1989) and Wadsworth (1990) suggest that
an overall improvement in nutrition could
have been associated with improved mental
facilities. Apparently ingestion of oral iron
stimulates the appetite and those children in
the study by Aukett et al. who showed improved mental development with increased
hemoglobin levels also gained weight. So it is
possible that the increase in calories and
other nutrients could also have affected
mental achievement. There is epidemiological evidence that suggests that anemia during pregnancy is associated with an increased risk to the fetus; however, the data
are far from conclusive (Dallman, 1989). It is
well documented that iron deficiency impairs work performance and exercise capacity (Dallman, 1989).When the body is at rest
the cardiovascular and metabolic effects of
mild iron deficiency anemia are barely detectable, but with agricultural work and
standardized exercise, tachycardia and lactic acidosis develop.
These data indicate that there are cer-
tainly negative aspects of iron deficiency,
and this must always be considered when
talking about adaptation. However, in an
area of endemic disease or very high pathogen load the problems associated with iron
deficiency may be minor compared with the
morbidity and mortality associated with severe bacterial disease. In a different environment, one with low pathogen load and few
diseases, the negative effects of iron deficiency would loom larger. In terms of human
evolutionary history, hypoferremia would
have been advantageous in times and places
where the diseaselpathogen load was heavy.
Then it would be expected that iron deficiency anemia would occur with the most
frequency. It is precisely this pattern which
occurs in the archaeological record with respect to porotic hyperostosis. For example,
porotic hyperostosis occurs with greater frequency in lowland areas compared with
highland, in tropical areas compared with
temperate, and in areas of greater population density.
However, as it has been aptly pointed out
(Mensforth et al., 1978; Lallo et al., 1977)the
etiology of porotic hyperostosis is not simplistic but can best be understood in terms of
synergistic interactions. It is incorrect to
focus exclusively on any one factor in terms
of an explanatory model. However, with respect to porotic hyperostosis the emphasis
has traditionally been on diet to the exclusion of andlor neglect of other factors. This
paper attempts to redress the balance by
illustrating that new perspectives can lead
to different interpretations of the same data.
The story of porotic hyperostosis is not yet
complete, but perhaps some new pages have
been written.
ACKNOWLEDGMENTS
I would like to thank Dr. Suichi Nagata for
bringing to my attention the article by Dunn,
Dr. Susan Kent for stimulating me to further
develop my ideas, and Dr. Roy Stuart for his
welcome editorial assistance. Thanks also to
Dr. Matt Cartmill and the two anonymous
reviewers who provided some stimulating
and useful criticisms.
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