Mixed Race Studies

Dispensing of Heart Drug Not ‘Black and White’

University of Alabama Research Magazine
2005-10-10

Chris Bryant

Think we’ve advanced too far in Civil Rights issues and medical care to resort to making health judgments based on skin color? Don’t be so sure, says Dr. Gregory Dorr, an assistant professor of history at The University of Alabama, who has joined scholars at the Massachusetts Institute of Technology researching so-called “designer medicines” and the possibilities they could lead to racial medicine.

When a recent study of a heart medicine claimed to show the drug reduced the mortality rate of blacks with severe cardiac disease by 43 percent, but had no effect on whites, controversy erupted.

“According to the study, BiDil (the cardiac disease drug) gave a marked increase in lowering the morbidity rates among black patients with end-stage heart disease,” Dorr said. “White people didn’t show any benefit from it. There were problems with the way the study was done that seemed to suggest that it may not be so clear cut.”…

…“In order to understand pharmacogenetics, you have to understand the longer history of race and medicine in America and how they interacted over time,” Dorr said. “I think there is a lot of potential good in genetic medicine. But, when people conflate race and genetics, we get into a very dangerous and murky area.”

Read the entire article here.

The short life of a race drug

The Lancet
Volume 379, Issue 9811 (2012-01-14 through 2012-01-20)
pages 114-115
DOI: 10.1016/S0140-6736(12)60052-X

Sheldon Krimsky, Professor of Urban & Environmental Policy & Planning; Adjunct Professor of Public Health and Family Medicine
Tufts School of Medicine
Tufts University, Medford, Massachusetts

The headlines back in June, 2005, read “FDA approves a heart drug for African Americans”. The decision that gave the company NitroMed approval for its drug BiDil exclusively to a “racial group” represented a milestone in US drug policy. The decision ignited a debate that polarised the African American community, confounded proponents of personalised medicine, and dismayed groups opposed to reinscribing racial categories into science. Ever since Ashley Montagu published Man’s Most Dangerous Myth: The Fallacy of Race in 1964 [1942?], scientists have reached a broad consensus that “race” applied to human populations has no standing in science…

…In a historical context too, the use of such racial classification is shown to be a subjective process. The concept of “race” in the USA grew out of slavery when state laws dictated racial identity by percentage admixture. A person who self-identifies as African American could have one great-grandfather (or about one-eighth of his or her genome) as the exclusive source of that identity. Homer Plessy was the plaintiff in an 1896 US Supreme Court decision (Plessy v. Ferguson) that established the “separate but equal” foundations of segregation in the USA. Plessy, who was escorted off a train for whites only, was considered black based on the infamous “one drop rule”, even though he considered himself seven-eighths white. By contrast, Jean Toomer, author of the 1923 book Cane, which chronicled the lives of black Americans, sometimes identified himself as black and sometimes as white. Thus, two individuals, both with one-eighth African ancestry, might either be defined by others as black or self-identify as white or black. Why should the drug’s approval for a differentiated group be based upon such quixotic criteria? Despite all the reasons why “race” has no role in science, it was a science-based agency that approved BiDil for a racial group…

…While many commentators who supported the approval of BiDil for black patients state that “race” is not a scientifically precise term for identifying relevant genomic or physiological characteristics that differentiate population groups, nevertheless, they argue that “self-identified race” is a useful proxy for those characteristics. However, what is the evidence that the proxy “self-identified race” is a reliable surrogate? The best evidence derives from the fact that genetic variation conferring disease susceptibility is not equally distributed among ancestral populations. For example, sickle cell anaemia is more prevalent in populations whose ancestry can be traced to sub-Saharan Africa. However, “self-identified race” is a subjective term, influenced by cultural factors, and not even grounded in the ancestral genomics of, for example, the International HapMap Project. For the purpose of the clinical trials, “self-identified race” is interpreted as a dichotomous variable (black or non-black). If race were used as a proxy for ancestral African genomics it should be a continuous function (10%, 30%, 70%, etc). It makes no scientific sense to map a continuous function onto a dichotomous variable…

Read the entire article here or here.

Are medical and nonmedical uses of large-scale genomic markers conflating genetics and ‘race’?

Nature Genetics
Volume 36, Number 11s (2004)
pages S43-S47
DOI: 10.1038/ng1439

Charles N. Rotimi, Director
Center for Research on Genomics and Global Health

“…with each birth and each death we alter the genetic attributes of human populations and drawing a line around an ephemeral entity like a human race is an exercise in futility and idiocy.” —Pat Shipman, The Evolution of Racism

We now have the tools to describe the pattern of genetic variation across the whole genome and its relationship to the history of human origins and the differential distribution of diseases across populations and geography. We can begin to dissect common complex diseases and devise new therapeutic strategies to reduce adverse drug reactions, a key public health problem ranking between the fourth and sixth leading cause of death in the US. At the social level, the new genomic tools can help us to better appreciate the fluidity of social identity, including ‘race’, ‘ethnicity’ and the more complex notion of ancestry. Challenges surrounding the design of large-scale genotyping projects such as the international HapMap initiative and their future applications illustrate the complexities and ambiguities associated with the use of group labels in genomic research. Depending on how we use this information, the potential exists to describe simultaneously our similarities and differences without reaffirming old prejudices…

…Genetic variation and social identity

To reap the full benefits of the Human Genome Project and spin-offs like the HapMap project, we must be willing to move beyond old and simplistic interpretations of differential frequencies of disease variants by poorly defined social proxies of genetic relatedness like ‘race’. We should allow the genome to teach us the extent of our evolutionary history without abbreviating it with preconceived notions of population boundaries and social identities. We must recognize that social identities are formed in various ways—ancestry, ethnic and tribal background, geopolitical boundaries, language, and other social and behavioral activities. Identities change over time and from one context to another. Their use as markers of ‘relatedness’ in genetic research without appreciation for how they were formed is likely to produce misleading information concerning the distribution of genetic variation.

We all have a common birthplace somewhere in Africa and this common origin is the reason why we share most of our genetic information. Our common history also explains why contemporary African populations have more genetic variation than younger human populations that migrated out of Africa 100,000 years ago to populate other parts of the world, carrying with them a subset of the existing genetic information.

Given this shared history, why do we interpret human genetic variation data as though our differences rise to the level of subspecies? Two facts are relevant: (i) as a result of different evolutionary forces, including natural selection, there are geographical patterns of genetic variations that correspond, for the most part, to continental origin; and (ii) observed patterns of geographical differences in genetic information do not correspond to our notion of social identities, including ‘race’ and ‘ethnicity’. In this regard, no matter what categorical framework is applied, we cannot consistently use genetics to define racial groups without classifying some human populations as exceptions. Our evolutionary history is a continuous process of combining the new with the old, and the end result is a mosaic that is modified with each birth and death. This is why the process of using genetics to define ‘race’ is like slicing soup: “You can cut wherever you want, but the soup stays mixed”.

How can we grasp the population structure of our species? I believe this requires universal awareness that genomic information cannot be used either to confirm or to refine old social, political and economic classifications such as ‘race’. In particular, we should understand the following points: (i) individuals in genetics studies may have membership in more than one biogeographical clusters; (ii) the borders of these clusters are not distinct; and (iii) population clusters are influenced by sampling strategies. For example, the inference drawn from a study with one or two African populations will probably be very different from that drawn from a study with 100 African populations sampled from north, east, west, central and south Africa. As Steve Olson observed, “Not only do all people have the same set of genes, but all groups of people also share the major variants of those genes. Geneticists have never found a genetic marker that is of one type in all the members of one large group and of a different type in all the members of another large group”50. Furthermore, because most alleles are widespread, genetic differences among human populations are the result of gradations in allele frequencies rather than distinctive diagnostic genotypes…

Read the entire perspective here.

Grassroots Marketing in a Global Era: More Lessons from BiDil

The Journal of Law, Medicine & Ethics
Volume 39, Issue 1, Spring 2011
pages 79–90
DOI: 10.1111/j.1748-720X.2011.00552.x

Britt M. Rusert, External Humanities Fellow
Center for the Humanities
Temple University

Charmaine D. M. Royal, Associate Research Professor
Institute for Genome Sciences & Policy; Department of African and African American Studies
Duke University

BiDil, a heart failure drug for African Americans, emerged five years ago as the first FDA approved drug targeted at a specific racial group. While critical scholarship and the popular media have meticulously detailed the history of BiDil from its inauspicious beginnings as a generic combination drug for the general population to its dramatic resuscitation as a racial medicine, the enthusiastic support shown by some African American interest groups has been too little understood, as has their argument that BiDil was an important response to race-based health disparities. In this essay, we show how the drugmaker, NitroMed, used the support it had solicited from black advocacy groups and community members to market BiDil as a unique “grassroots” pharmaceutical to the African American community. We go on to situate BiDil, which relied on a domestic, U.S.-centered conception of race, within the context of the global nature of both race and health disparities. Ironically, the grassroots angle of the BiDil case ultimately obscured the global crisis in health disparities. Furthermore, we argue that the grassroots model initiated by NitroMed should be taken note of, as it marks a potential avenue for the marketing of other drugs in the future.

Read the entire article here.

While many commentators who supported the approval of BiDil for black patients state that “race” is not a scientifically precise term for identifying relevant genomic or physiological characteristics that differentiate population groups, nevertheless, they argue that “self-identified race” is a useful proxy for those characteristics. However, what is the evidence that the proxy “self-identified race” is a reliable surrogate? The best evidence derives from the fact that genetic variation conferring disease susceptibility is not equally distributed among ancestral populations. For example, sickle cell anaemia is more prevalent in populations whose ancestry can be traced to sub-Saharan Africa. However, “self-identified race” is a subjective term, influenced by cultural factors, and not even grounded in the ancestral genomics of, for example, the International HapMap Project. For the purpose of the clinical trials, “self-identified race” is interpreted as a dichotomous variable (black or non-black). If race were used as a proxy for ancestral African genomics it should be a continuous function (10%, 30%, 70%, etc). It makes no scientific sense to map a continuous function onto a dichotomous variable…

Sheldon Krimsky, “The short life of a race drug,” The Lancet, Volume 379, Issue 9811 (2012-01-14 through 2012-01-20): 114. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60052-X/fulltext.

The controversial connection between race, genetics and medicine

Minnesota Public Radio News
Midmorning Broadcast: 2010-02-03, 09:06 CST

Kerri Miller, Host

Dorothy Roberts, George A. Weiss University Professor of Law and Sociology; Raymond Pace and Sadie Tanner Mossell Alexander Professor of Civil Rights
University of Pennsylvania

David Goldstein, Professor of Genetics and Director of the Institute for Genome Sciences & Policy Center for Human Genome Variation
Duke University

[From Steven F. Riley: This is an excellent “must listen to” discussion!]

As scientists explore the human genome and medicines tailored to particular genes, a provocative question emerges about whether there is a genetic marker that could explain why some treatments work better for different racial groups. And some say the narrow focus on race misses the point of social disparities and what we now know about genetics. (00:54:12)

(Interview suspends at 00:26:40 for a short news update, then restarts at 00:30:23.)

Download the interview (00:54:12) here.