Extirpolation of the Mythology that Porotic Hyperostosis is Caused by Iron Deficiency Secondary to D

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

Extirpolation of the Mythology That Porotic Hyperostosis Is

Caused by Iron Deficiency Secondary to Dietary Shift to Maize

Bruce Rothschild1,2,3

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?

Misconceptions

Primary Iron Deficiency Does Not Cause Porotic

Hyperostosis

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,

B. ROTHSCHILD

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

porotic hyperostosis!

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

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

issue.

What then Is the Significance of Porotic

Hyperostosis?

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-

158

B. ROTHSCHILD

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-

logical study.

Accuracy of Dietary Maize Attributions: Isotope

Implications

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

time.

Eliminating Mythology

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

scientist.

B. ROTHSCHILD

160

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