Dr. Edna Suárez-Díaz, Resident Scholar


Dr. Edna Suárez-Díaz delivering her Resident Scholar lecture at the Valley Library, Oregon State University.

Dr. Edna Suárez-Díaz is the most recent individual to complete a term as resident scholar in the Oregon State University Libraries Special Collections and Archives Research Center. A professor in the Department of Evolutionary Biology at the Universidad Nacional Autónoma de México in Mexico City, Suárez-Díaz is an accomplished scholar of molecular evolution and molecular disease who serves on the editorial boards of Osiris and Perspectives on Science, among other publications.

Dr. Suárez-Díaz’ current research focus is the geopolitics of disease with a particular interest in approaches taken toward blood diseases in the twentieth century. This project brought her to Corvallis to study components of the Ava Helen and Linus Pauling Papers, focusing on Linus Pauling’s work on sickle cell anemia.

Pauling is, of course, well known for his discovery that sickle cell anemia traces its origin to the molecular level, a concept first published in 1949 with Harvey Itano, S. J. Singer and Ibert Wells. As Suárez-Díaz noted in her resident scholar lecture, the group’s finding that the basis of a complex physiological disease could emerge from a simple change in a single molecule made a profound impact on the history of biomedicine. Indeed, it is not an overstatement to suggest that the concept of a molecular disease led to massive shifts in post-war research and public policy.

Importantly, these shifts were accompanied by technological breakthroughs that enabled many other laboratories to explore new ideas related to molecular disease. In particular, the modernization of gel electrophoresis techniques served to democratize research in a way that had previously not been possible. When the Pauling group was conducting their initial experiments, electrophoresis was a tool that lay within the grasp of only a handful of well-funded laboratories. As the equipment and methodology required to do this work became less expensive, practitioners around the world began to enter the field and the impact was profound.

Suárez-Díaz is particularly interested in blood diseases and malaria in developing countries, noting that these afflictions were to the “Third World” what cancer was for industrialized societies and the middle classes. It is important to note as well that there exists a strong connection between blood diseases (like sickle cell anemia) and malaria, as the mutations that gave rise to blood diseases also provide a certain degree of immunity to malaria. As such, the geographic distribution of blood diseases correlates closely with malaria epidemiology, a phenomenon that has had consequences for public health campaigns over time, including decisions to use DDT on a massive scale in attempting to eradicate the mosquitoes that carry the disease.


Harvey Itano and Linus Pauling, ca. 1980s.

It is also interesting to chart Linus Pauling’s role – or lack thereof – in the further development of molecular disease as a field of study. Though he and three colleagues essentially created a new discipline with their 1949 paper, Pauling gradually became marginalized within the community, in part because he devoted so much of his time to political activism during the 1950s. His departure from Caltech in 1963 further distanced his scientific activities from what had, by then, become a truly international body of work.

As such, while undeniably important, Pauling’s contributions to the field might now be seen as one of many important nodes in a transnational network of scientists and practices. Moving forward, Suárez-Díaz’ work will continue to explore this transnational network, touching upon several other key issues including G6PD deficiency and the genetic consequences of atomic fallout.

Now in its eleventh year, the Resident Scholar Program at OSU Libraries has provided research support for more than two dozen visitors traveling from locations across the United States as well as international scholars from Germany, Brazil and, now, Mexico. New applications are generally accepted between January and April. To learn more, please see the Resident Scholar Program homepage.


Mutations and Malaria: Pauling’s Adventure in Genetics

Pastel drawing of Hemoglobin at 100 angstroms, 1964.

During the 1940s, Pauling had established sickle-cell anemia as a molecular disease, a pioneering concept that synthesized biology and chemistry in a revolutionary manner. Other interests had pulled him away from this important work, however, for the better part of a decade.

Then, in the early 1960s, he was introduced to research suggesting that rates of malaria infection in areas with a high rate of sickle-cell anemia were greatly reduced. On top of this existing research, Pauling also came across a reference to a particularly interesting African legend regarding the origin of malaria resistance. Intrigued, he decided to dig a little deeper and, before long, he had dedicated a small portion of his lab to the problem.

Early in his research, Pauling found that the protozoan parasites responsible for malaria were not able to penetrate and replicate in sickled blood cells — e.g, cells containing deformed hemoglobin. Even more interesting, Pauling discovered that individuals with only one sickle-cell allele did not suffer from the effects of sickle-cell anemia but were still highly resistant to the malaria disease.

By examining these findings, Pauling developed a set of basic rules explaining the sickle-cell and malaria interactions. They are as follows:

1. Individuals with only normal hemoglobin do not possess the deformed hemoglobin molecules present in individuals possessing either one or two sickle-cell alleles. As a result, these individuals are not resistant to malaria.
2. Those with the homozygous recessive sickle-cell trait suffer from sickled blood cells, resulting in a variety of health complications including stroke, ulcers, bacterial bone infection, kidney failure, and heart problems. Victims of the dominant form of sickle-cell anemia have a significantly shorter lifespan than the average human, often dying in infancy. Nevertheless, these individuals are not afflicted by the malaria disease.
3. Other individuals are heterozygous for the sickle-cell trait, meaning that they experience some sickling of the blood cells, but enough of their blood cells appear normal that they are able to survive without experiencing the health difficulties associated with sickle-cell anemia. Like those with the full sickle-cell anemia disease, these individuals enjoy significant resistance to the malarial disease.

Pauling stated that the human populations inhabiting malarial zones in Central Africa were becoming predominantly comprised of heterozygotes. He explained that an individual homozygous recessive for the sickle-cell trait would probably die before reaching sexual maturity, therefore not producing any children with the sickle-cell disease. Those without the sickle-cell trait would be vulnerable to malaria. In malarial regions, this group would have a high mortality rate, many of them dying before reproducing. The third group, those with only one sickle-cell allele, does not suffer from the effects of full sickle-anemia and are immune to malaria. As a result, these individuals are best suited to malarial regions and are able to procreate, giving birth to more heterozygotes who can, in turn, continue the genetic trend.

The sickle-cell trait is a hereditary disease, passed from parent to child in the Mendelian fashion. Each parent provides the child with one of the two alleles which will determine whether the child will have normal or sickled blood. Two individuals with sickle-cell anemia will invariably produce children with sickle-cell anemia. A pair in which one parent has sickle-cell anemia and the other is a carrier (meaning they have one trait rather than two) will have a 50% chance of producing a child with sickle-cell anemia and a 50% chance of producing a child with only one sickle-cell allele. A couple in which both parents carry only one sickle-cell allele will have a 25% chance of producing a child with sickle-cell anemia, a 25% chance of producing a child without the sickle-cell trait, and a 50% chance of producing a child with only one sickle-cell allele.

The following series of Punnett squares demonstrates the transfer of alleles in the case of sickle-cell anemia:

Sickle-Cell Anemia Punnett Square

Based on this thinking, Pauling argued that only the people with one sickle-cell allele would live to have children, approximately 50% of which would be born with one sickle-cell allele. He argued that this trend could continue indefinitely, probably until a mutation eliminated the sickle-cell disease entirely, leaving all peoples in malarial zones homozygous for an anti-malarial gene.

Listen: Pauling on the effect of sickle cell disease on the spread of malaria

With his theory firmly in place, Pauling turned his attention to sickle-cell anemia in non-malarial zones. Pauling was primarily concerned with the presence of sickle-cell anemia in the African American population of the southeastern United States. Because malaria is not endemic to the southern U.S., Pauling feared that a positive mutation was unlikely to occur, and the sickle cell mutation was not being removed from the gene pool as quickly as new, harmful mutations were occurring. As a result, the number of individuals suffering from sickle-cell anemia could only continue to increase.

In order to counteract this trend, Pauling spoke out in support of eugenics as a means of controlling and gradually diminishing the presence of sickle-cell anemia in the United States.

In the 1960s and 1970s, Pauling made headlines by giving talks on the subject. He was introducing the concept of beneficial mutations to a public not necessarily comfortable with certain implications of the phenomena. The humanitarian components of his efforts earned him praise from various medical groups, though his advocacy of eugenics created some concern among politicians, religious conservatives, and secular ethicists alike.

For more information on Pauling’s work with sickle-cell anemia and malaria, visit It’s in the Blood or take a look at the OSU Special Collections homepage.