Advances in Anthropology
2012. Vol.2, No.3, 157-160
Published Online August 2012 in SciRes (http://www.SciRP.org/journal/aa) http://dx.doi.org/10.4236/aa.2012.23018
Copyright © 2012 SciRe s . 157
Extirpolation of the Mythology That Porotic Hyperostosis Is
Caused by Iron Deficiency Secondary to Dietary Shift to Maize
1Biodiversity Institute, University of Kansas, Lawrence, USA
2Anthropology Department, University of Kansas, Lawr enc e, USA
3Department of Medicine, Nor t h ea st Ohio Medical Uni versity, Rootstown, USA
Email: bmr@ k u.edu
Received May 18th, 2012; revised Jun e 20th, 2012; accepted July 6th, 2012
Diagnosing a shift to a maize-dominant diet, on the basis of recognition of high population frequencies of
porotic hyperostosis, has unfortunately entered the “collective consciousness” of anthropology—because
of the mythology that iron deficiency is a common cause of that phenomenon. Skull changes in patients
with all forms (both primary and secondary) of iron deficiency are actually extremely rare (0.68%!). That
frequency certainly does not support iron deficiency as the explanation for the high frequency of porotic
hyperostosis noted (approximating 50%) in some populations. Isotopic analysis further reveals that C4
grasses (e.g., maize) actually did not become a significant part of North American human diets until the
past 1000 years, long after notation of high frequency porotic hyperostosis. This further falsifies claims of
earlier maize diets (predicated on frequency of porotic hyperostosis) and negates the perception that
maize-induced iron deficiency is the cause of porotic hyperostosis. The latter speculation is not only con-
trary to medical evidence, but that misdirection gave false impressions of ancient populations/civilizations
and compromised use of a valuable observation. That mythology must be extirpated from the “collective
consciousness”. Perhaps now attention can be appropriately directed to exploration of genetic hemolytic
anemia, hemoglobinopathies and parasitic infestations which are known causes of porotic hyperostosis.
Keywords: Iron Deficiency; Porotic Hyperostosis; Cribra Orbitalia; Maize; Diet; Parasite;
Hemolytic Anemia; Mythology
The Importance of Scientific Methodology
This editorial makes recommendation for deletion of the
mythology that maize consumption is the dietary implication of
porotic hyperostosis. The term mythology is used herein to
describe perspectives attributed to authority, but which are
contrary to the scientific evidence. The mythology (that pri-
mary iron deficiency is the cause of porotic hyperostosis) ap-
pears embedded in anthropology’s “collective consciousness”
(Angel, 1978; El-Najjar et al., 1975; Grmek, 1989; Hill & Ar-
melagos, 1990; Von Endt & Ortner, 1982). This persistence
needs to be reexamined in view of the observations by Claude
Bernard and Will Rogers that it is not what we don’t know that
gets us into trouble, so much as what we know that ain’t so
(Spodick, 1975). When one’s life work is predicated on a per-
spective/technique, it takes tremendous intellectual integrity to
accept that the premise for that life’s work was fatally flawed in
a manner that renders it moot, thus negating a large portion of
his/her past intellectual efforts. I am impressed by medical col-
leagues who had the integrity to accept an article documenting
the failure of standard radiological examination to distinguish
sacroiliac pathology, an article which invalidated literally
thousands of articles which utilized the x-ray to identify study
groups (Rothschild et al., 1994). The reviewers understood that
falsifying the underlying premise for such work was what sci-
ence does and that it did not reflect negatively on the reporters
of past work. Failing to accept documentation/evidence would
have been contrary to the fundamental premise of scientific
study, despite the new information rendering moot so many
previous studies. The reviewers cared more for the integrity of
science than for the perceived value of their own contributions
(based upon the now falsified data) and by doing so actually
enhanced their own reputations as scientists. For researchers
without a “personal stake” in an issue, replacing authoritative
statements with data-based statements is mindful of the child’s
comment related to “the emperor’s new clothes”. While “eld-
ers” should be respected, it is unclear that their pronouncements
should be blindly followed?
Primary Iron Deficiency Does Not Cause Porotic
Relating porotic hyperostosis to primary iron deficiency is
contrary to the medical evidence: The radiological (medically
recognized) equivalent of porotic hyperostosis is the “hair on
end” or “crew cut” phenomenon (Resnick, 2002). Porotic hy-
perostosis is the result of marrow hyperplasia (Resnick, 2002),
a process that increases consumption of basic nutrients, espe-
cially iron (Fairbanks & Beutler, 1972). Iron deficiency is the
result, not the cause of the marrow hyperplasia that produces
the porotic hyperostosis. This contrasts with primary iron defi-
ciency, which causes hypo-regenerative (atrophic) marrow and
no skull alterations (Fairbanks & Beutler, 1972).
What then are the observations that have been misinterpreted
as suggesting that primary iron deficiency causes porotic hy-
perostosis at population frequencies approaching 50% (Angel,
1978; El-Najjar et al., 1975)? I have no idea and can identify
nothing in the literature that documents (rather than simply
espouses) the misconception/mythology of a relationship to
Examining the medical literature on iron deficiency-related
skeletal phenomena is mos t illumin ating. Iro n deficienc y is an
extremely common affliction among patients admitted to the
Cape To wn and R ed C ros s War Me moria l Ch ildr en’s Hospita l
in South Africa. Yet Lanzkowsky (1968) could identify only
15 cases among the thousands identified and found no rela-
tionship to severity of the iron deficien cy. Even the diagnosi s
of primary iron deficiency is questioned in those cases (see
comments below on secondary iron deficiency related to
parasitism and hemoglobinopathies). Agarwal et al. (1970)
revealed a frequency of porotic hyperostosis-relatable skull
changes in only 0.68% of individuals with iron deficiency and
no atrophy of parietal bones! Only 16 cases of skull changes
were added to the literature (from among thousands of indi-
viduals with iron deficiency) in the ensuing years (Rothschild,
2000), certainly an insufficient number upon which to base
frequent occurrence of porotic hyperostosis. Eng (1958) docu-
mented that the iron deficiency was the result of another proc-
ess, even when those rare skull changes happened to occur in
individuals with iron deficiency. Interestingly, Agarwal et al.
(1970) noted a significant frequency of frontal bone thinning,
with only occasional parietal bone thinning in his population
study of iron deficiency. This differs from porotic hyperosto-
sis in two fundamental aspects. It was the frontal bone that
was affected in their study, as contrasted with predominantly
parietal involvement in porotic hyperostosis. Further, they
described cortical thinning and no thickening of the diploic
space, which contrast with the thickening characteristic of
porotic hyperosto si s.
The intellectual challenge promulgating the mythology ap-
pears related to failure to recognize that iron deficiency can be
caused not only by inadequate ingestion but by processes that
increase its utilization. Any process which causes marrow hy-
perplasia increases consumption of basic nutrients (Fairbanks &
Beutler, 1972). The result is a secondary deficiency of those
nutrients. Hyperplasia is the physiologic response of bone mar-
row to any phenomenon which consumes red blood cells, proc-
esses which increase red blood cell fragility or those that reduce
the ability of red blood cell hemoglobin to carry and transfer
oxygen. Certain abnormalities of hemoglobin production result
in only partially or non-functioning molecules. Thus, nutrients
(especially iron) are consumed, but the hematologic deficiency
“(anemia) persists, stimulating more consumption, but not re-
solving the stimulus (e.g., anemia). The process is referred to as
ineffective erythropoiesis. One such genetic disorder causing
hemolytic anemia is thalassemia major, a known cause of the
“hair on end” phenomenon recognized as porotic hyperostosis
(Caffey, 1957; Resnick, 2002). Such afflicted individuals may
become deficient of usable iron stores (Fairbanks & Beutler,
1972), but that is the result, not the cause of the process pro-
ducing the skull changes. This is in contrast to other hemoglo-
bin abnormalities (e.g., sickle cell anemia) which cause damage
by physically blocking circulation, but are neither associated
with ineffective erythropoiesis, nor with porotic hyperostosis.
Oxenham and Cavill (2010) suggest that iron deficiency
produces ineffective erythropoiesis, self-citing a review (Cavil
2002), which itself cites his own chapter (Cavill & Ricketts,
1980), but unfortunately provide no primary reference evidence
to support their claim. As these publications do not present
actual data (only opinion) and do not address the above-refe-
renced radiological evidence, they do not seem to have any per-
tinence to the question.
Analysis of Skull Pathology
What Is the Cause of Skul l Changes, alth ou g h R are,
in Individuals with Iron Deficiency?
Lanzkowsky (1968) identified hemolytic anemias (on the ba-
sis of shortening of the intravascular life span of red blood cells)
in 8 of 14 individuals with iron deficiency. Red blood cell
half-life is not shortened in primary iron deficiency anemia
(Kaplan & Zuelzer, 1950; Temperley & Sharp, 1962). The
other six individuals also had rickets, a disorder that Silverman
(1985) documented and that Lanzkowsky (1968) emphasized
can cause these same skull changes. Eng’s (1958) report of iron
deficiency related skull changes was in an individual with pe-
ripheral blood spherocytes and splenomegaly, a disorder re-
ferred to as spheroscytosis and a recognized cause of hemo-
lytic anemia (Young et al., 1951). Thus, the thought that pri-
mary iron deficiency causes porotic hyperostosis “has no
clothes”. Porotic hyperostosis in individuals who happen to be
iron deficient cannot be blamed on that deficiency.
Cribra Orbitalia Is a Separate Phenomenon from
Porotic hyperostosis and cribra orbitalia are independent phe-
nomena, both on an intra- and inter-population basis. A team of
senior investigators (Rothschild et al., 2005) even documented
an inverse relationship between cribra orbitalia and porotic
hyperostosis in skulls from the Wedda of Sri Lanka and from
geographically and other chronologically disparate sites, in-
cluding Bonnell, Pindi Pueblo, McCutchan-McLaughlin, Lake
Bronson, Warner Mound, Peter Lee Mound, Blue Blanket Point
Altern, Morrison’s Island, Greenville and Seh Gabi. It is quite
clear that cribra orbitalia and porotic hyperostosis could not
represent the same phenomenon. Therefore, the topic of cribra
orbitalia, which clearly has a variety of forms and likely causes
(Rothschild & Martin, 2006), is beyond the scope of the current
What then Is the Significance of Porotic
To what potential condition(s) does the presence of porotic
hyperostosis actually provide insight? The clinical literature
provides a possible explanation. Accentuated bone marrow red
cell production is the source of porotic hyperostosis (Goodhart
& Shils, l982; Jaffe, l972; Resnick, 2002; Rothschild & Martin,
2006). What causes increased red cell production? Blood loss
or red blood cell destruction are the processes that have been
identified. The former complicates some parasitic infections;
the latter, caused by hemolytic anemia. Enzyme deficiencies
(e.g., pyruvate kinase and glucose-6-phosphate dehydrogenase
abnormalities reducing function), abnormal red cell membranes
(e.g., hereditary spherocytosis) increasing red blood cell fragil-
ity and hemoglobinopathies (e.g., thalassemia and sickle cell
anemia) are the most common causes for the latter (Resnick,
2002; Rothschild & Martin, 2006). Hemoglo binopathies (though
sickle cell only rarely) are characterized by ineffective ery-
Copyright © 2012 SciRe s .
thropoiesis (Caffey, 1957; Resnick, 2002). Afflicted individuals
may become deficient of usable iron stores (Fairbanks & Beut-
ler, 1972), developing a secondary iron deficiency—after the
marrow hyperplasia has consumed the iron.
Hemolytic anemia is well recognized in the Old World, es-
pecially that related to fava bean ingestion among individuals
with the “inborn error of metabolism,” glucose-6-phosphate
dehydrogenase deficiency (Grmek, 1989; Kattamis et al., 1969).
Parasitic infections/infestations are especially important to con-
sider in New World populations. Although they generally pro-
duce direct blood loss from the host (e.g., from Ancyclostoma),
some (e.g., the fish tapeworm Diphyllobothrium) also consume
large quantities of vitamin B12 resulting in host deficiency
(Nyberg et al., 1961). Vitamin B12 deficiency produces “inef-
fective erythropoiesis” in which bone marrow keeps producing
cells, which are not very effective in transporting oxygen, thus
stimulating hyperplasia (Aslinia et al. , 2006) .
Identification of hemolytic anemia on the basis of red blood
cell osmotic fragility or identification of reduction of red blood
cell half-life (Lanzkowsky, 1968) is not possible to for study in
ancient bones. However, DNA studies may identify the respon-
sible mutations for genetically-transmitted sources of hemolysis
and the role of parasites may be amenable to DNA and eco-
Accuracy of Dietary Maize Attributions: Isotope
Lee-Thorp (2008: p. 932) reported that there is “no isotope
shift consistent with significant consumption of C4 maize until
about AD 1000”, in contrast to the claims based on occurrence
of porotic hyperostosis by Angel (1978), Hill and Armelagos
(1990), Stuart-Macadam and Kent (1992) and by Buikstra
(Wilbur et al., 2008). This isotope observation should put to
rest the mythology that porotic hyperostosis identifies nutri-
tionally (maize)-related iron deficiency anemia (El-Najjar et al.,
1975; Mensforth et al., 1978; Stuart-Macadam, 1989). Accord-
ing to Lee-Thorp (2008: p. 925), the advantage of stable isotope
analysis is that it “reflects the foods actually eaten…, rather
than a palimpsest of waste of uncertain duration that typically
preserves only a tiny fraction of the original material and over-
looks those organic remains with low survival rates”. Thus,
maize was at most only a small component of diet prior to that
The misdirection related to the porotic hyperostosis-iron de-
ficiency-maize speculation has for too long compromised the
ability and opportunity of anthropology to contribute to under-
standing of ancient populations/civilizations. Greenberg (2009)
discussed how citation distortions create unfounded authority,
by establishing citation networks. Failure to incorporate “in-
convenient” publications documents delayed promulgation of
important ideas and corrections. A decade after Rothschild
(2000) exposed the fallacy of primary iron deficiency-related
porotic hyperostosis, Walker and colleagues (2009) acknow-
ledged that porotic hyperostosis does not have the long ascribed
(e.g., Stuart-Macadam, 1989) nutritional (e.g., maize “econo-
mies”) implications. Could this be analogous to the Bruce effect
in geladas (Roberts et al., 2012), another unpopular truism?
Unfortunately, promulgation of the mythology has persisted,
compromising anthropologic analyses for more than a decade.
Despite this evidence, editors of major journals (e.g., American
Journal of Physical Anthropology and the International Journal
of Osteoarchaeology) have continued to publish articles predi-
cated upon that erroneous premise (Dabbs, 2011; de la Cova,
2011; Meyer et al., 2011). Acceptance of those publications
was based on the erroneous authoritative notion that presence
of porotic hyperostosis identifies primary iron deficiency pro-
duced by maize ingestion, as repeatedly suggested by Buikstra
(Wilbur et al., 2008) and others (Angel, 1978; Hill & Armela-
gos, 1990; Scherer et al., 2007; Stuart-Macadam & Kent, 1992;
Wright & Chew, 1999).
Extirpation of this mythology has been hindered by those
who consider it a viewpoint. Gravity is not a viewpoint and
neither is recognizing that primary iron deficiency does not
produce porotic hyperostosis. Both represent scientifically
validated, evidential observations. Lockyer et al. (2011) noted
the difficulty weaning anthropologists away from this mytho-
logy. The current exposé should finally convince (assuming
they pursue an intellectually honest review of the data) those
still clinging to the mythology that porotic hyperostosis can be
used as a measure of broad biologic processes like population
migration and diffusion of genes, origin of agriculture and the
relationship between economic transition and evolutionary
processes, in addition to defining the health of populations
(Angel, 1966; Bishop, 2011; Dabbs, 2011; De la Cova, 2011;
El-Najjar et al., 1975; Lewis, 2011; Mensforth et al., 1978;
Meyer et al., 2011; Scherer et al., 2007; Wilbur et al., 2008;
Wright & Chew, 1999).
The scholarly thing to do is to identify as compromised, all
articles characterizing diet on the basis of porotic hyperostosis,
in favor of reanalysis on the basis of what is actually known to
produce the phenomenon. Misdirection has compromised use of
a valuable observation-porotic hyperostosis. As Stuart-Maca-
dam’s 1989 attribution of porotic hyperostosis to maize has
been falsified, perhaps it is now time to investigate the possibi-
lity of parasitic infections related to sanitary conditions and
fecal-oral contamination? Perhaps now attention can be appro-
priately directed to exploration of genetic hemolytic anemias,
hemoglobinopathies and parasitic infestations, which are known
causes of porotic hyperostosis. Identifying parasite exposure
and congenitally-transmitted hemolytic anemias could actually
provide greater understanding of past cultures than the false
suggestion of maize dietary implications ever did.
The challenge of what to do with articles subsequently in-
validated or documented as compromised has been brewing in
the natural and medical sciences for a few years now, and per-
haps it is time that biological anthropology considers its stand
on this issue. Should journal editors and/or reviewers be ob-
ligated to reject publication of articles whose premises have
been documented as invalid and which selectively fail to cite
pertinent literature? Doing nothing has allowed perpetration
and promulgation of the myth that is the subject of this editorial.
While this does not reflect positively on those who have suc-
cumbed and participated in allowing this mythology to persist,
there is the opportunity for them to illustrate one of the best
attributes of science: To admit that they had been misled and
that their past perceptions on the subject were wrong. That
would be in the finest tradition of science and identify within
themselves the intellectual integrity that is the measure of a true
Copyright © 2012 SciRe s . 159
Copyright © 2012 SciRe s .
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