This paper aims to widen the history of blood disease research beyond sickle cell anemia, situating it at the intersection of US racial politics and public health, and international malaria eradication campaigns in the Third World. It focuses on studies of G6PD deficiencies in the Mixtecos of the Mexican Pacific coast, and the Lacandones of the Mayan region in Chiapas. Two medical geneticists, Rubén Lisker and James E. Bowman, developed research projects that engaged these populations, looking for answers to evolutionary, biomedical, and genetics questions. Their practices and the context of knowledge production about these indigenous groups—how they were made objects of inquiry and intervention (Populations of Cognition)—are in full view in both cases.1
Between December 14 and 20, 1965, the World Health Organization Scientific Group on Haemoglobinopathies and Allied Disorders met at the Geneva agency’s headquarters. The group comprised eight well-known physicians including Tulio Arends, a leading Latin American human geneticist from the Venezuelan Institute for Scientific Investigations. Others came from North America, Northern and Southern Europe, the Middle East and South East Asia, an array that reflected the delicate geopolitical equilibriums of postwar international health programs, but also the development of highly specialized biomedical research around the globe. They elected Herman Lehmann, from the Abnormal Haemoglobin Research Unit of the Medical Research Council at Cambridge, as Chairman of their meeting.2
Their final report described the state of knowledge on the three main types of inherited disorders affecting “with appreciable frequency” the function of human red blood cells across “large areas of the world,” and presenting “a series of problems of considerable public health importance” (WHO 1966, pp. 5–6). These disorders included the well-known haemoglobinopathies or structurally abnormal hemoglobin disorders (like sickle cell hemoglobin or HbS, but also types C and E), the different thalassaemias (affecting the rate of synthesis of hemoglobin α- and β- chains), and the unruly group of glucose-6-phosphate dehydrogenase (G6PD) deficiencies involved in glucose metabolism and related—among other diseases—to favism, a type of hemolytic anemia affecting Mediterranean boys (see below). While only some of these “abnormalities” were associated with severe clinical disorders (like the regular pain crisis and low life-expectancy rates affecting many patients with sickle cell anemia), all of them had important implications for the study of and worldwide efforts to eradicate the different forms of malaria, a mostly tropical disease affecting human populations in the underdeveloped areas of Latin America, Asia, and Africa. The relatively high frequency of all and each of these blood-related genetic mutations was predicated on a hypothesized immunity of carriers to malaria infection, in particular to the aggressive type transmitted by Plasmodium falciparum in African populations. As research over the previous decade had shown, the distribution of human populations affected by sickle cell anemia, favism, and thalassemia, not only paralleled malaria epidemiology, but also reflected patterns of ancestry, migration, and ultimately, the history of human populations, which genetic researchers—armed with new molecular techniques—were eager to investigate. From worldwide surveys knowledge about a complex distribution of blood diseases across populations, and of related scientific projects, had emerged.
Although sickle cell has been painted as the blockbuster in the historical literature, by the mid-1960s a second group of blood diseases—G6PD deficiencies—gained prominence among human geneticists and public health officials and institutions. The number of evolutionary, biomedical, and public health issues related to G6PD research was large and, as I will detail below, ranged from basic academic research in evolutionary theory and population genetics, to the practicalities of implementing public health in rural areas. Indeed, the main conclusion in the WHO Technical Report (1966) was that equivalent attention was needed with regard to the study of G6PD deficiencies, a chaotic set of relatively frequent mutations that affected different human populations. Nevertheless, and despite the range of interesting questions related to this group of blood diseases, scholars of the history of science have paid little attention to the history and trajectory of G6PD research.
Following the model of HbS research, human geneticists extended their surveys of human populations around the globe, not just to map the regional and racial distribution of G6PD variants, but also to test selection hypotheses about the connection between genetic frequencies and malaria immunity. As mentioned before, in terms of the severity of its clinical manifestations, G6PD deficiency was best known as the cause of favism in populations of Mediterranean origin.3 However, the discovery ten years before by Paul E. Carson and his colleagues at the University of Chicago (Carson et al. 1956), that “deficiency of this enzyme was responsible for sensitivity of certain American Negro subjects to the hemolytic effect of primaquine” (WHO 1966, p. 10), placed G6PD research on a different foot. Primaquine, a derivative of the broad group of 8-aminoquinoline antimalarials introduced forty years before, was probably the most popular artificial antimalarial drug used in massive campaigns to eradicate the disease starting in the 1950s and up to the mid-1960s. But the acute response it provoked in some G6PD-deficiency carriers—called hemolytic anemia—had become the prime example of the new field of pharmacogenetics, as defined by one of its founders, the medical geneticist Arno Motulsky (Motulsky 1957). G6PD deficiency surveys thus were required as a preliminary step before allowing the use of primaquine treatment in specific malaria affected populations. Even worse: by the mid-1960s hemolytic reactions of G6PD deficiency carriers to a host of new antimalarial drugs had been reported, widening the range of potential backfire in eradication campaigns (Annex 1 of the WHO Report 366 enlisted those drugs).
In the context of development programs in the Third World and international public health campaigns, the study of G6PD deficiencies thus suddenly became relevant, as it became particularly clear that this group of genetic anomalies was scarcely understood. In contrast to the straightforward mechanism of sickle cell inheritance (a single autosomal dominant allele, in genetic parlance), by the mid-1960s scientists could not even agree on the number of alleles involved in the transmission of the G6PD variants being described, much less on how these potential alleles could explain the inheritance of an increasing number of disease conditions. To make matters worse, international efforts were hampered by a variety of nomenclatures, diagnostic tools, and local approaches to the study of G6PD deficiencies. Highly standardized methods had been established for the identification of sickle cell hemoglobin decades before, but the study of G6PD deficiency lacked generally agreed upon diagnostic tools and classification rules: not only might additional variants have existed that had not been properly characterized, but supposedly “new” variants may have actually been described without scientists in different countries having taken notice. Urgent research was needed also on their global distribution particularly in Third World areas, clinical manifestations, possible treatment, and diagnosis. In light of all this, the main recommendation of the WHO Group was to convene a second group of experts on G6PD deficiency the following year. The WHO Scientific Group on Standardization of Procedures for the Study of Glucose-6-Phosphate Dehydrogenase met again in Geneva (December 5–10, 1966) to elaborate international guidelines and a report on the state-of-the-art of knowledge on this group of diseases (WHO 1967). This time around, Motulsky, now at the University of Washington, was elected as chairman.
As the WHO Reports suggest, by the mid-1960s the study of G6PD deficiencies had been transformed from a secondary subject carried by the sickle cell anemia research bandwagon, to an international priority in and of itself.4 National and international agencies and research laboratories around the world committed human and material resources in a molecular-genetics research attack on this group of blood diseases. The aim of this paper is to widen the history of such studies beyond sickle cell anemia, situating these efforts in the context of transnational public health and development programs. It does so by focusing on two research surveys of G6PD deficiencies in Mexican indigenous populations undertaken in the mid-1960s. The first was led by Mexican geneticist Rubén Lisker, Director of the Genetics Department at the National Institute of Nutrition, and the second by James E. Bowman, Director of the Blood Bank, and member of the Pathology Department at the University of Chicago. Eventually, the results of both teams pointed to a neglected African ancestry component of Mexican indigenous populations, but each posed different questions in their study of G6PD deficiencies. Their complementary research, however, provides an entry point to different networks and exchanges involved in the local and global production of knowledge at a time of surging technical assistance and public health programs around the globe.
Toward this aim, I introduce some across-borders connections in the research on the overlapping afflicted populations of the southern United States and those of the Mexican coasts. I use the historically and politically charged notion of “America’s backyard” in order to bring out these connections. Though the concept of the American backyard is often used to refer to the “sphere of influence” of the United States in Latin America, there is a strong historical argument to link the “backward” Southern US states with the rest of the “underdeveloped” continent (Wang 2015) and also in terms of shared public health concerns (Birn 2006), as others have shown. In this paper, thus, I aim to show the continuities evident in epidemiological, public health, and other development programs spanning across national borders. Equally important for this special issue, my essay aims to draw attention to the material and conceptual practices by which a few Mexican indigenous populations, namely, the Lacandones of Chiapas, and the inhabitants of the Costa Chica of Oaxaca and Guerrero, were framed as subjects of inquiry, and became objects for the study of different aspects of G6PD deficiencies.
In what follows, I briefly introduce blood diseases as a highly politicized group of malaises, tracing connections between the Third World and the “backward” states of the Southern United States, with an international army of geneticists, anthropologists, physicians, and their institutions (section one).5 Supported by secondary literature, I argue that in the1960s the racial politics of public health in the Southern United States had a global counterpart in technical assistance offered in connection with development programs, particularly the malaria eradication campaign of the WHO launched at the Eighth World Health Assembly in Mexico City in 1955. Sections two and three focus on why and how particular Mexican indigenous populations became the subjects and objects of research carried out by Lisker and Bowman. These investigators’ different projects illustrate the tensions and synergies between the internationalization of postwar science and the highly localized nature of their research on human populations. As it will become clear in the text, the requirements of their research eventually made the African-Indigenous admixed Mixteca populations of the Costa Chica in the southern states of Guerrero and Oaxaca, and the Lacandon Mayan groups of the Chiapas rain forest, subjects of scientific interrogation, and objects of potential and actual intervention. In so doing, these populations also became instruments in the experimental and collection practices of Bowman and Lisker. In different ways, they became “Populations of Cognition” used to investigate the evolutionary, genetic, and biomedical aspects of G6PD variants.
2. Blood Diseases in the Era of Technical Assistance
Sickle cell anemia occupies an outstanding place in the history of science and medicine as a pivot-disease linking developments in biomedicine, molecular biology, evolutionary genetics, medicine, and the racial politics of the United States’ health care system in the 1950s and 1960s. Though rarely connected, these diverse fields of research and intervention triggered sickle cell anemia’s role as a research bandwagon for other related blood diseases around the world, comparable to—though different in meaningful ways—with regard to how cancer research garnered global resources in the very same period. Where radiation-related cancer represented middle-class white Americans’ anxieties amidst a growing awareness of atomic fallout (De Chadarevian 1996; Creager 2013), I argue that sickle cell anemia and related blood diseases condensed anxieties of social unrest about both the African American populations of the American South (Wailoo 2001; Nelson 2011) and the unruly, communism, and malaria infected-prone masses of the Third World.6
A malaise affecting malaria-ridden populations around the globe, sickle cell anemia became a symbol of the potentialities of the post-Second World War biomedical approach to medicine. In 1949 recognized chemist Linus Pauling and his colleagues at Caltech characterized it as a molecular disease, soon to be explained by one of them—Harvey Itano in 1956—as the result of the substitution of a single amino acid residue in one of the hemoglobin chains (De Chadarevian 1998; Strasser  2002). Human geneticist James Neel, head of the Genetics Department at the University of Michigan and in charge of the Atomic Bomb Casualty Commission, in a paper also published in 1949 that followed the one by Pauling, explained the hereditary pattern of sickle hemoglobin (HbS) as the result of a single autosomal dominant mutation, which accounted for the mild heterozygous form, and the acute homozygous condition (Lindee 1992). Together, the two developments provided a simple molecular-genetic account for a complex disease.7
It took a decade before the disease would evolve into a symbol of deep political and economic inequalities in the United States. As the civil rights movement gained traction in the Southern states of the American union, segregationist policies were challenged not only in the context of schools and public transportation, but also at medical facilities and hospitals around the country. Keith Wailoo (1999, chap. 5; 2001) and Alondra Nelson (2011) have given detailed accounts of how, in this highly politicized context, the painful intermittent crises of African American patients of sickle cell anemia were tackled with increasing funds, private and public, which Wailoo has thoroughly characterized as the “commodification” of the disease. In the 1960s this meant that theories of evolutionary genetics and physical anthropology, along with the use of new molecular techniques, “gave the malady a far wider currency—and a greater popular resonance.”8 As sickle cell anemia became a role model for postwar biomedical research and investment, it reinforced a vision of public health that involved highly reductionist research on protein chemistry and genetics (a single amino acid substitution in the hemoglobin chain was responsible for the sickled appearance of red blood cells) linked with new technological advances in diagnosis, saliently including gel zone-electrophoresis (Chiang 2009; Suárez-Díaz 2017 online). In the case of sickle cell anemia, the United States public health care regime adopted a biomedical research program underpinned primarily by molecular biology and a human population genetics’ approach. This approach sidelined research on the connection between the molecular mechanism and its organismic (anatomic, physiological) manifestations, as well as the search for improvements on the clinical and at home treatment of pain crisis associated with the disease.
Comparable and contemporary reductionist strategies were being followed in the fight against other diseases, most saliently malaria, by international and national agencies. DDT spraying of house’s walls to decimate the Anopheles mosquito vector, and the ingestion of preventive and therapeutic drugs, became the main tools for disease control and eradication around the world, versus previous programs that had encompassed social and economic development, both in America (Cuba, Jamaica, the US South) and in Europe (Spain and Italy). US agencies alone (without the WHO campaigns) “spent roughly $1.2 billion on malaria control activities, almost all of which employed DDT or other pesticides” (Packard 2007, p. 146). At first, the new strategy seemed to work, and perhaps more importantly, “local governments perceived control as an instrument for gaining popular political support” and “a sense of social progress” (Packard 2007, p. 146).
As historians have thoroughly argued, the politics of the Cold War shaped malaria control programs around the world, narrowing what before the war had been a thriving field of differing approaches to public health (Packard 2007; Cueto 2007; Cueto and Palmer 2015).9 Postwar public health programs not only reinforced this magic-bullet approach to malaria vector control by means of pesticides, supplemented by drugs like quinine and the new artificial anti-malarials, but they also “prevented the linking of malaria control programs with broader efforts at social and economic development, despite the fact that many public health experts […] argued for such a linkage” (Packard 2007, p. 146).
As control campaigns became eradication campaigns—also against the opinion of malariologists and public health experts—after the World Health Assembly in 1955, Mexico took the lead in committing to this new credo, starting its own national malaria eradication campaign, Campaña Nacional de Erradicación del Paludismo (CNEP), in 1956.10 However, as years passed, the disease persisted in areas where poverty, humid environments, “poor” or “traditional” agricultural methods, and high temperatures provided optimal conditions for the already DDT-resistant Anopheles mosquito. The use of synthetic drugs became even more important in this context. In Mexico alone, between 1957 and 1962, 11.2 million pills of antimalarial drugs (including primaquine) had been provided to the rural population (Cueto 2007, p. 116). But here awaited a menace; though many individuals carrying G6PD deficiency were known to be asymptomatic, and seemed to show some degree of immunity to the disease, one of the gene’s variants predisposed them to deadly hemorrhagic surges when treated with antimalarial drugs used by the CNEP.
G6PD deficiency seemed to be a sex-linked character that expressed fully in males, and so estimates of its frequency should “therefore be based on surveys carried out on males” (WHO 1966). In contrast to the single mutation linked to sickle cell anemia, G6PD deficiency comprised an extensive group of genetic polymorphisms with mortality rates on the order of 10% reported in localized regions of Africa, the Mediterranean, and Latin America. Moreover, as mentioned before, the number of alleles involved, transmission mechanism, and distribution of G6PD deficiencies presented a serious challenge for an unified attack. The most prevalent type among both Caucasians and “black African” populations was the “normal” electrophoretic type B. But while Caucasians of Mediterranean origins—like Sardinia, Greece and Sephardic Jews—showed a G6PD deficiency with the same electrophoretic mobility of B (type B−, known as favism), the B− deficiency found in African populations was not as severe, and so it was considered “undoubtedly” biochemically and genetically different. By contrast, African populations showed a G6PD deficiency with increased electrophoretic mobility (type A−), while “10% of American Negroes” showed the same high mobility type, but with no G6PD deficiency, designated A+, or simply A. While A− deficiency posed no serious therapeutic problem in “naturally occurring” populations, its carriers often showed the violent hemolytic reaction associated with a growing number of synthetic drugs, now not only primaquine, but the recent generation of synthetic anti-malarials and many other drugs, used by the international and national malaria eradication campaigns targeting Third World countries.
A thorough understanding of the genetics of G6PD deficiencies, and the setting of standardized approaches to include diagnosis as part of public health programs in malaria eradication thus became entwined with priorities for intervention in the context of Cold War polarization and fears of communism. The biomedicalization of public health was seen and used as a powerful political instrument, manifested in the WHO scientific groups and guidelines mentioned in the previous section. Equally important, this highly technoscientific view of blood diseases linked victims’ fortunes across national borders. Southern African-Americans (from Mississippi, Tennessee, and Alabama), Western and Central African populations, and Afro-Caribbean and other Latin American populations alike, shared not only the presence of hemoglobin S, G6PD (A−) and other deleterious genetic traits (soon to be shown to result from their shared African ancestry), but also the recurrent presence of malaria.11
3. The Mixtecos of the Coast: Lisker’s Translation of G6PD Deficiency
In 1962, Ruben Lisker, then recently appointed at the hematology section of the Instituto Nacional de Nutrición (National Institute of Nutrition, INN) found and reported a case of G6PD deficiency in a Sephardic Jewish boy in Mexico City (Lisker et al. 1962). This finding prompted him to shift his focus from hematological research on anticoagulants, to a long-term project on the distribution of blood traits among Mexican populations. Fully aware of recent developments with regard to the biomedical and pharmaceutical implications of the distribution of genetic traits through his long acquaintance with Motulsky, he set out to investigate the racial components of the “Mexican population.”12 Like many of his contemporaries around the world, Lisker started with clinical electrophoretic surveys of structurally abnormal hemoglobins (hemoglobinopathies), which he soon extended to surveys of mestizo and indigenous populations departing “from the main linguistic groups” (Lisker 1963, p. 292). As the quotation makes clear, Lisker’s sampling design stood out, as it was based on the linguistic or glotto-chronological classification of the major Mexican ethnic groups; moreover, his data interpretation was supported by careful attention to cultural anthropological research and the history of the Mexican Indians (Anaya et al. 2017).13
Since his first survey of hemoglobins S and C, Lisker noticed their presence in “admixed” individuals from the Mexican coasts (Tabasco, Veracruz and Sinaloa), which he interpreted as evidence of African immigration (“sujetos de raza negra”) during the Spanish colonial rule. This explanation, which privileged ancestry over malaria selection, eventually permeated his entire view of the genetic and anthropological diversity of the Mexican population (Lisker 1981).
In his 1963 study, Lisker reported data on 1,043 individuals from the Tarasco, Nahua, Tarahumara and Mixteco groups, among others (Rodriguez et al. 1963). However, he took good care to split the Mixteco into two different groups: the Mixtecos of the mountains (Mixtecos serranos) and the Mixtecos of the coast (Mixtecos costeños). This division reflected the simple fact that there were two different Centros de Coordinación Indígena (CCI) set up by the indigenista authorities of the Instituto Nacional Indigenista (INI, created in 1948) in order to implement its policies of indigenous “management” (Suárez-Díaz and Barahona 2013). This aspect of Lisker’s surveying practices was instrumental not only in setting the conditions under which specific results were obtained, but also for his characterization of the inhabitants of the coast as that of carrying an important African ancestral component. To do this, he also relied on previous historical accounts of their migration, studies in cultural anthropology, and of course his own medical and anthropological genetics approach (Anaya et al. 2017).
In contrast to Bowman’s approach (see next section), Lisker relied on middle-level officials, local anthropologists, and rural teachers for cultural mediation and logistical support. With their help he was able to gain access—in the era before informed consent—to thousands of adult men that he and his colleagues personally blood-sampled. He travelled with his team and friends, driving his own car back and forth from his laboratory in Mexico City, where he tested his samples—using both electrophoresis and chemical methods. Moreover, it was because of his reliance on the INI’s cultural anthropologists, and their acquaintance with local populations, that he distinguished the samples taken at the two separate CCI’s: one at the village of Jamiltepec in the Pacific coast, and the second at the mountain town of Tlaxiaco. Thanks to these “fortuitous” dual locations of the centers, Lisker realized that the linguistic sampling criterion that he had previously applied was, in this case, secondary to the location of the Mixteca people.14 The most useful group regarding the distribution of G6PD deficiency was to be found on the Mexican coasts, where the African slave trade had taken place in the seventeenth century, as cultural anthropologists and historians had previously established to be the case.
Lisker’s overlapping interests in the medical and anthropological genetics of the Mexican indigenous groups opportunistically—with regard to geography and temporality—intersected with Mexico’s anti-malaria campaigns. As Marcos Cueto (2007) has described, the 1960s were the decade of the mexicanization of the above-mentioned malaria eradication campaign (CNEP). The campaign was first driven by the Rockefeller Foundation (RF), the Pan American Health Organization (PAHO) and a battery of international and bilateral aid and development agencies (International Cooperation Agency or ICA, the antecedent of USAID, the WHO and UNICEF, etc.). But later on the campaign was gradually taken up by the Mexican government, through the Secretaría de Salud (Health Secretariat) and other national agencies, including the Secretaría de Educación Pública (Education Secretariat). Lisker soon saw the potential to align his survey project’s objectives to this national campaign in order to take advantage of available research funds from the CNEP, and he set out to conduct a broader survey to test the presence of G6PD deficiency in the larger area of the Pacific states of Oaxaca and Guerrero (Lisker et al. [1965a] [1965b] 1969) and then the Gulf of Mexico and other regions (Lisker et al. 1966).
The larger surveys were framed so as to provide grounds for future interventions as part of the malaria eradication campaign, but furthermore to advance Lisker’s own research on the distribution of genetic traits among Mexican populations. Between 1963 and 1966, Lisker’s research provided systematic genetic and blood groups frequency data on numerous Mexican indigenous populations throughout the country, including the Mixtecos costeños who had provided him with his first clue to the distribution of G6PD deficiency; later on he found the mutation among the Nahuas, Cora, Huicholes, and Chontales, among others, a finding that contributed to his appreciation of the admixed character of all Mexican populations.15 In the end Lisker’s surveys included more than 6,000 adult men, a sample big enough to allow him to calculate the frequency of G6PD of the A− type deficiency in indigenous populations. His approach mixed biomedicine with anthropology, and his data helped transform the previous characterization of Amerindian populations as a rather homogenous group (Suárez-Díaz 2014). More importantly, he extended his previous conclusions with regard to the Mixtecos costeños to other indigenous groups living on the coast of the Gulf of Mexico: the G6PD anomaly was due to African admixture and the history of slave trading, not to the action of natural selection against malaria infection.16 The Mixtecos’ geographical distribution had provided the original clue, leading to Lisker’s interrogation of other indigenous groups living in the Gulf of Mexico and the Pacific coasts. By incorporating the Mixtecos—and in particular the genetic distinction between the populations of the coast and those at the mountains—as an instrument to interrogate the biological versus the historical presence of G6PD deficiency in other groups, Lisker rendered them Population of Cognition.
4. A Convoluted Mediation: Bowman and Genetics Research on the Lacandones
In obituaries and institutional recollections of his career, James E. Bowman (1923–2011) has been depicted as a “trailblazing African American physician-scientist, a pioneer in genetics and bioethics” (Medicine on the Midway 2012). He was, indeed, the first African American to become a faculty member in medicine, and to hold a tenured position at the Biological Sciences Division at the University of Chicago (Medicine on the Midway 2012). His scientific career reflected the changing politics of segregationist health care and medical training in the United States (Wailoo 2001), as well as the internationalization of research, characteristic of the postwar period.
Just after entering Howard Medical School in 1946, Bowman had been drafted by the US Army, which paid for his medical education. Later on, the Department of Defense decided that “they did not want any black officers,” and so he was discharged (Easton 2011). Very soon, however, he was offered an internship at the St. Luke’s Hospital in Chicago, becoming the first African American resident to train in a major Chicago hospital. After finishing his internship and military duties, he married and decided to go overseas, accepting a post as chairman of pathology at Namazee Hospital in Shiraz, Iran, from 1955 to 1961. It was there, in Iran, where he became familiar with favism, or G6PD type B− deficiency.17
Bowman’s Iranian surveys helped him to reestablish relations and collaborations with researchers at the University of Chicago, where—as mentioned above—Paul E. Carson was responsible for the genetic and biochemical pioneering work on G6PD deficiency.18 Like Lisker, Bowman belonged to the first-generation of geneticists to use the revolutionary technology of starch-gel (zone) electrophoresis in the analysis of human blood components. With Carson’s intervention, the university invited him as an associate professor, and put him in charge of the Blood Bank, a hospital facility created in 1937 in the wake of a growing demand for blood transfusions for sickle cell anemia patients. As with other blood banks and biochemical collections around the world, this became a privileged spot to pursue research on abnormal hemoglobins and other blood diseases.19 Soon, with the aid of electrophoresis, Bowman established new G6PD variants in the Chicago collection, in particular one that he had first detected in a Caucasian male of European origin, then later among “Negroes” of the United States, and finally in a sample received from Turkey. This same variant was later to be found in his first expedition among the Lacandones in Chiapas, Mexico.
Bowman was interested in the distribution of G6PD variants, and in those years he continued his extensive research on populations of the Mediterranean and the Middle East, Asia (Vietnam, Iran), and North America (“Negro” and Mexico) (Bowman et al. 1971).20 But he was also interested in establishing the genetic mechanism to explain the transmission of G6PD deficiencies, a problem that—as I described in the first section—had eluded scientists and public health officials thus far. A recent population study in Great Britain, for instance, reported the presence of an A-B phenotype (it showed a slow and a fast electrophoretic band), and the authors suggested that those individuals might be “heterozygous for a gene pair with co-dominant autosomal transmission” (Bowman et al. 1966, p. 811). Bowman’s own research produced a number of new “bands” of differing electrophoretic mobility that required an alternative genetic hypothesis as to the number of alleles and protein chains involved in the discovery of seemingly endless variants of G6PD. Where Lisker was adamant in finding distribution frequencies and ancestry patterns, Bowman’s quest for G6PD’s hereditary mechanisms required him to look for a population that filled specific requirements to test his hypotheses. Based on their reportedly small population size and isolated location in the Chiapas mountains, he concluded that the Lacandones of Chiapas were a suitable group.
However, getting to the Lacandonian region, and more importantly, getting the Lacandones’ cooperation, was not an easy task. “The tunic-clad forest people [were] famous for being among the most elusive in Mesoamerica” (Rugeley 2001, p. 295). They inhabited the deep tropical rain forest, a region considered a “borderline” from the times of imperial maps. The very idea of “the jungle” associated with the Lacandonian region is also deeply rooted, in different ways, in Western imagination (Gollnick 2008). Plenty of legends and myths plagued the history of this group. However, in anthropologist Jan de Vos’s account, the contemporary populations did not represent the historic Lacandones, who had been wiped out in the seventeenth century through relocations, epidemic diseases, administrative resettlements (“reduction” in colonial administrative parlance), and eventually confined to the Guatemalan and Chiapas highlands (de Vos 1980; also Gollnick 2008). Moreover, during the early twentieth century archaeologists had already come to the conclusion that today’s Lacandones were not directly related to the people of the same name that had been described in the missionary records of the sixteenth century (Gollnick 2008). Notwithstanding these findings, in Bowman’s view the Lacandonians most important traits were still both their small populations size and their relative isolation.
To get their cooperation, Bowman and his colleagues required local facilitators, and so they got in touch with Alfonso León de Garay, acting Director of the Program of Genetics and Radiobiology of the National Nuclear Energy Commission (PGR-CNEN), a well-known character in diplomatic and international scientific exchanges (Barahona 2015).21 De Garay also was interested in surveying indigenous populations in the Oaxacan Mixteca, and the Chamula zones in Southeast Mexico.22 However, for the visitors from Chicago, whose research—like Lisker’s—was now supported by the United States Public Health Service, the main interest were the Lacandones and, more specifically, the detection of new electrophoretic variants of G6PD and their hereditary mechanism.
De Garay used his INI and other local connections, including contacts with the Instituto Lingüista de Verano (Summer Institute of Linguistics), as well as the CNEN resources, to take the Chicago scientists to the Lacandonian region. However, his mediating practices and monetary expenses soon raised more than one eyebrow among his peers at the CNEN.23 They seem to have followed a pattern.24 De Garay’s petitions included airplane tickets from Mexico City to Tuxtla Gutiérrez in Chiapas, as well as private plane rentals to arrive at the Lacandon zone. But more noticeably, he included solicitations for dinner arrangements to honor his guests and “local” connections. Such expenses amounted to the equivalent of today’s $1,000 USD per dinner.25
Among the people to be entertained was “the queen” of the jungle and the Lacandones, “la indiscutible ‘reina’ de ambos” (de Vos 2002, p. 96). Indeed, in those years the single most important step in having access to the Lacandones was to obtain the help of the person who acted as “their contact with the world”: photojournalist—later ecologist—Gertrude Duby Blom. Travelers to the Lacandonian jungle in the 1960 and 1970s recall making payments to Duby, who had arrived in Chiapas in 1945 with her husband, anthropologist Frans Blom. She was “in charge” of the communities’ exchanges with the “outside” world.26 Still other documents account for De Garay’s petitions to Alfonso Caso, Director of the Institute of Indigenous Affairs (INI), in order to use the infrastructure and human resources of the institute, whose personnel sometimes took the blood samples themselves.27 It was all these people, payoffs, and power plays that made the Lacandones accessible to the Chicago scientists.
With De Garay’s help, between 1964 and early 1966, Bowman and other members of the Department of Medicine and Pathology at the University of Chicago (Carson himself, as well as pathologist Henri Frischer), participated in three expeditions to Chiapas, where they sampled approximately 150 “Lacandon Indians,” whom they described as living “in two separate breeding groups” (Bowman et al. 1966, p. 813). The Lacandon met the theoretical requirements common to contemporary human genetics research: a purported isolated population, organized in small groups made up of a few dozen individuals and characterized by inbreeding practices.28 By all accounts, their total number may have been around 300 in those years, organized across about 66 families living in villages in two separate regions.
As recounted by Bowman, the Lacandones’ purported isolated character increased the chances of finding homozygous deleterious individuals for rare alleles. As he finally reported in 1966, the comparison of the Lacandones and the African American population of the United States led him to establish the two-allele hypothesis for G6PD deficiency, as a high genetic frequency of mutations was expressed in the small Lacandon populations. The Lacandones’ role in the electrophoretic and family studies was described as follows:
The survey of the Lacandones, a markedly inbred Mayan Indian population, provided direct as well as indirect support for the view that the new variant of this report is homozygous 6-PGD-B. These Indians number approximately 200 and live in scattered small family and clan groups in the jungles of Chiapas; 150 members were available for study. (Bowman et al. 1966, p. 813)
Bowman’s research in the Mayan groups was clearly motivated by a context of major political and public health concerns across national borders. In stark contrast to other contemporary studies, as I argued, it had nothing to do with the competing political issue of the effects of atomic fallout on human populations and the need to measure the rate of mutation in “primitive” populations (de Souza and Ventura Santos 2014). Bowman, however, was thankful for De Garay’s provision of access to the Lacandones, and probably understood his difficult position and need to justify the indigenous surveys for the CNEN authorities. By De Garay’s request, in May 1965 Bowman wrote a letter to the CNEN President, José Gorostiza, describing a conversation he had recently had with William Schull, a long-time collaborator of James Neel. The exchange had taken place after giving a lecture at the Department of Human Genetics of the University of Michigan, in Ann Arbor. Schull had enthusiastically praised the Mexican indigenous surveys (“[w]hy the Atomic Energy Commission of Mexico [sic] is indeed to be congratulated for wisely supporting such work. It is a tragedy that more countries are not so wise,” he claimed), and De Garay used Bowman’s account to justify the expeditions and other related expenses (CNEN [1965a] 1965c). In any case, the letter and its political use by De Garay give a sense of the range of interests and concerns to which Latin American indigenous populations could be put to work during the Cold War era.
5. Concluding Remarks
This paper aimed to introduce the field of research around G6PD as a revealing space for historical inquiry, and in particular as a way to interrogate itineraries of knowledge production about human groups in a world of political and economic asymmetries not restricted by national borders. In doing so, it highlights the central role played by a significantly small number of human populations as they became construed as subjects and as instruments for research on the genetic anomalies of the blood’s components. Blood diseases affected the deprived African-American population in the segregationist US South, inasmuch as the Third World malaria-infested populations of Latin America, Africa, and Asia. There was not respect for national borders, as these otherwise different groups shared common ancestry lines due to historically (forced) migrations and slave trade.
Research communities at the highest levels also displayed a disregard for national frontiers: Lisker and Bowman, like Tulio Arends and Hermann Lehmann—mentioned at the beginning of this paper—belonged to global circuits of international academic research and public health. But despite the obvious international and transnational character of blood disease research, the study of genetic variants demanded engagement with highly localized groups of peoples. Ironically, though, the very specific, “isolated” groups that caught Lisker and Bowman’s attention emerged from their studies as highly admixed groups: the Lacandones revealing both the Mediterranean and the African G6PD variants; the Mixtecos highlighting genetic differences within the same linguistic group, and illustrating the historical connection of the peoples of the Mexican coasts and those of Africa and Asia.
It is in this ample sense that I have used the figure of the “American backyard” to emphasize the overlapping maps of disease and public health programs, but also of scientific research circuits, and of transnational fears of social unrest. All of these processes linked the Southern United States’ and Latin American (Mexico’s) “backward” populations. Such overlapping distributions provided the funds and the rationale for Lisker’s extensive research, and also for Bowman’s study of the distribution of blood diseases around the world, including haemoglobinopathies and G6PD deficiencies in Vietnam (Bowman et al. 1971).
In contrast to the large historical corpus on sickle cell anemia and sickle cell hemoglobin research, accounts of the motivations, development, and impact of G6PD deficiency research are lacking. This group of blood diseases played an important role as part of the sickle cell anemia research bandwagon, where biomedicine and malaria eradication programs became entangled in the technoscientific approach to diseases characteristic of the postwar period. Moreover, as a research subject, the unruly group of G6PD deficiencies constituted a challenging topic for scientists, to be tackled with the new molecular methods of protein research (in particular, gel electrophoresis). But in contrast to sickle cell’s theoretical relevance for population genetics and evolutionary biology in relation to malaria, G6PD research had practical, immediate implications for the management of highly specific populations.
In Lisker’s case, linguistic and anthropological criteria shaped his overall extensive surveys’ design; nevertheless, it was the local infrastructure of go-betweens between the INI centers which were instrumental in bringing on the Mixtecos of the coast as a subject and as an instrument for ancestry and biomedical inquiry. He concluded that historical processes like the African slave trade—not “human migrations,” shared language, or malaria selection, but a specific historical event in the seventeenth century—accounted for the coastal distribution of G6PD deficiency. In Bowman’s research, on the other hand, it was the small size and the supposedly inbreeding practices of the Lacandon families that made them an attractive subject of study. Most noticeably in this case, however, is that the Lacandones became a hypotheses-testing instrument, a technological element in the experimental arrangement with very strong neo-colonial underpinnings. The practice and the context of knowledge production about both populations—namely, how they were characterized, classified, and made objects of intervention—is in full view in both cases.
In memory of Rubén Lisker Yourkowitsky (April 1931–December 2015).
On Lehmann’s trajectory in the creation of the first collection of abnormal hemoglobin after World War II and its connection to molecular structural studies at Cambridge University, see De Chadarevian 1998. In the 1950s, Arends collaborated with Miguel Layrisse to establish the Diego antigen, a genetic/immunological marker shared by Asian and Amerindian populations. A brief reference to Arends (1918–1990) as part of the Latin American network of medical geneticists is included in Suárez-Díaz 2014. See WHO 1966.
G6PD was characterized as “an important enzyme in the metabolism of glucose by the red cells and other tissues” in the WHO Report. The already mentioned favism was described as a severe acute hemolytic anemia that results from ingestion of fava beans and related legumes. It was the most severe G6PD deficiency, affecting Mediterranean boys, and could even result in death (WHO 1966, p. 17)
Here I use the phrase research bandwagon in a straightforward way, inspired by Joan Fujimura’s characterization of the molecular biological bandwagon in cancer research, but without committing to her sociological account. In my historical perspective, “a scientific bandwagon exists when large numbers of people, laboratories, and organizations commit their resources to one approach to a problem” (Fujimura 1988, p. 261).
In compliance with contemporary uses, and the actors’ language, I refer to Third World countries (a term with broad political meanings, and adopted and mobilized by these countries’ actors), and the underdeveloped or backward regions of the world, including those in the United States, as depicted by contemporary analysts (See Wang 2015 on the latter). Notably for the present paper, Alfred Sauvy (1952) first defined the Third World, or underdeveloped countries (his words), in terms of low-life expectancy areas, related to diseases like malaria and the lack of economic opportunities. Sauvy also claimed to have found the first reference to this “third world” in a Brazilian journal on Latin America and the Cold War, see Katz (2004), and Gilbert (2008).
As sociologists and historians of molecular biology and medicine have argued, cancer research concentrated enormous material and human resources, and became a powerful symbol of the West’s progress with the so-called War on Cancer (Fujimura 1988). The United Kingdom Cancer Act had been passed by Parliament years before in 1939. In the United States, President Richard Nixon signed the National Cancer Act in 1971, and the National Sickle Cell Anemia Control Act in 1972.
This brief account of research on sickle cell anemia is purposely biased towards the molecular aspects of the disease. Keith Wailoo differentiates between research on the theoretical aspects of sickle cell anemia and hemoglobin, on which historians of molecular biology and populations genetics have focused (De Chadarevian 1998; Dietrich 1998; Strasser 1999; 2002; Suárez-Díaz 2017 online), from medical research on the domestic and clinical treatment of the painful intermittent crisis and on anemia’s consequences for the organism. “For such theorists”—writes Wailoo—“sickle cell anemia embodied an entirely different way of talking about race. Rather than speaking of ‘racial groups,’ it was far more accurate to speak of ‘gene pools’ and ‘gene frequencies’ in a multitude of discrete populations” (Wailoo 2001, p. 145).
Wailoo (Wailoo 2001, p. 144) explores the commodification of sickle cell anemia, becoming a crucial node for biomedical, political, and patients’ aims in the decades between 1920s and 1980s. Nelson’s (2011) account of the Black Panther Party’s screening and the health care campaigns of the early 1970s provides the context where, a decade after the events here narrated, Bowman would contribute to the bioethical implications of genetic screening for African Americans, promoted in the National Sickle Cell Anemia Control Act of 1972.
According to Cueto (2007), the Mexican physicians preferred to use the French word, paludism.
Lisker’s papers’ titles often made reference to “the Mexican population,” though he would focus on specific indigenous groups. He and Motuslky had studied under the supervision of hematologist Carl Singer, at the Michael Reese Hospital of Chicago in the mid-1950s (Motuslky a couple of years before). They had been introduced by Lily Singer, Carl’s wife, herself a notable hematologist and the laboratory’s “soul.” A timeline of Lisker’s career and its context is provided in Suárez-Diaz 2014.
This sampling criterion, a framing device, represented a phylogenetic account of indigenous languages, and thus allowed Lisker a systematic way to look at genetic frequencies and gave meaning to his results. I am in debt to Francisco Vergara Silva for this important information on the value of the method originally developed in the 1950s by cultural anthropologist Morris Swadesh.
On the linguistic criterion used in Lisker’s research see Suárez-Díaz 2014.
His research on this subject was published in at least nineteen papers appearing in the American Journal of Human Genetics, Blood, and American Journal of Physical Anthropology. Lisker’s results were incorporated into the International Biological Program through his collaboration with Francisco Salzano (see Dent and Ventura this issue). Lisker became a salient figure among the regional network of Latin American geneticists. In 1969 he attended the Wenner Gren conference on “The ongoing evolution of Latin American Populations” (Salzano 1971).
The adscription of sickle-cell anemia to race is problematic. As Harriet Washington writes sickle cell anemia “also affects nearly every ethnicity in South America, Cuba, Central America, Saudi Arabia, India, Turkey, Greece, and Italy–in fact anywhere malaria is found. For the common denominator of sickle-cell disease is not race, but living in proximity to the malaria-bearing Anopheles mosquito” (Washington 2006, p. 155, my emphasis).
Bowman’s daughter, Valerie Jarrett (born Bowman) was born there. She acted as Senior Advisor to President Barack Obama (2009–2017). Because of her position in government, the FBI records of her father are available online. For many years Bowman was investigated as a suspect of communism; his father–in-law (Valerie’s maternal grandfather) being a member of the Communist Party.
Elise K. Burton is currently working on related aspects of Bowman’s research, as part of her ongoing project on Middle-East genetics.
“I have often heard rumors from the Program Directors and Laboratory Heads, in which my research on indigenous populations is questioned, as if not being related with the projects and purposes of Nuclear Energy […]. [I]t would be convenient to confirm if this research must be pursued, and if we will have the support of the Commission, given that we need to make two more expeditions during the present year. If the Commission decides otherwise, we should request funds from other institutions” (CNEN 1965d).
In his autobiography, Hans Kalmus refers to his trips to Mexico in a chapter titled “The Pleasures of Playfulness,” where he recounts sampling “the high life,” furnished with a diplomatic passport, and enjoying receptions and banquets as he was welcomed by De Garay in Mexico City. Kalmus says nothing of his scientific collaborations with the PGR members (Kalmus 1991, pp. 134–36). Another example is De Garay’s leadership at the Committee and Seminar for the Study of the Athletes of the XIX Olympic Games of Mexico City, in 1968. The anthropological and genetic study involved a number of prestigious scientists from different countries, who lavishly enjoyed dinners and first-class travels to Mexico despite their open skepticism about the scientific merits of the whole enterprise. Against De Garay’s wishes, Lisker was invited to join the seminar by architect Pedro Ramírez Vázquez, local chair of the Olympic Games (Lisker, Personal communication on August 3, 2015).
“In attention to the urgency I have in preparing our next trip to the Mayan zone with the researchers of the University of Chicago […], I calculate that I need some $18,000.00 Mexican pesos [some 85,000 USD in today’s currency] for the cost of the expedition, and I ask you for an advancement of $5,000.00 for the upcoming expenses” (CNEN 1964).
Similarly, in the late 1960s the historian of science Marsha Richmond and her then fiancé, traveled to Chiapas pursuing their “romantic” quest for the Mexican indígenas. They met Duby and paid her to stay a few days at the Lacandon region and met her protégés (Richmond, Personal communication July 2015, Montreal, Canada).
Alfonso Caso (director of the INI) facilitated the help of local anthropologists in getting De Garay blood samples; this was not the case with the Chicago expeditioners. See the letters sent to Alfonso León de Garay, by Agustín Romero Delgado, and letter from Léon de Garay to Caso (Alfonso Caso Archive 1963a, 1963b, 1963c). Also, in letters to Manuel Sandoval Vallarta, De Garay states that during the expeditions he and his team would make use of the infrastructure of the Centro Coordinador Tzeltal Tzotzil of the INI at San Cristóbal Las Casas (founded in 1951), with the mediation of anthropologist Armando Aguirre (CNEN 1965b).
On isolates, see Lipphardt 2014.
Both Lisker and Bowman contributed to the debate on the bioethical implications of genetic screening in their own countries, with the latter coming to national attention (and becoming a Presidential advisor) in the US as the 1970’s sickle cell anemia campaigns unfolded. Eventually, Bowman became a scientific advisor to several African and Asian countries: Nigeria, Laos, Iran, Ethiopia, Egypt, and United Arab Emirates. Lisker presided the National Bioethics Committee and became a member of the International Bioethics Committee at UNESCO; he was also a member of the Mexican Presidential Advisory Committee (Consejo Consultivo de Ciencias de la Presidencia) (Lisker, Personal communication on June 24, 2015.).
This research was possible thanks to UNAM-PAPIIT grant IN401017.