User:Ferahgo the Assassin/race in biomedicine

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The consideration of race by doctors and researchers in modern medicine has seen a marked increase since the turn of the millennium, due mostly to developments in genetics. The primary impetus for considering race in biomedical research is the possibility of improving the prevention and treatment of diseases by predicting hard-to-ascertain factors on the basis of more easily ascertained characteristics. Since medical judgment often involves decision-making under uncertain conditions,[1] many doctors consider it useful to take race into account when treating disease because diseases and treatment responses tend to cluster by ethnicity.[2] Diseases that are typically correlated with racial identification include Cystic fibrosis, Lactose intolerance, Tay-Sachs Disease, sickle cell anemia, and Crohn disease, which are genetically linked and more prevalent in some populations than others.[1] A substantial degree of consensus among medical professionals exists that the ability to treat diseases improves with greater specificity of genetic analysis, and that racial groups are a fairly imperfect and unspecific way to identify genetic clusters which correlate with disease risk. However, until cheaper and more widely available methods of genetic analysis are commonplace, the consideration of race remains a worthwhile practice for many doctors and researchers.[3]

The perceived benefit to using race as a consideration in biomedicine is based on the series of surrogate relationships between self-identified race and disease risk.[3] Analysis of microsatellite DNA markers and SNPs from human populations have shown that it is possible to assign geographic regions with a high degree of accuracy to humans using a combination of these polymorphic genes. Furthermore, analyzing the fraction of human genetic variation that lies within and between geographically separated populations has shown that the genes that are geographically highly differentiated in their allelic frequencies are not typical of the human genome in general.[4] Since race can be seen as an imperfect surrogate for ancestral geographic reason, it is in turn a surrogate for variation across one's genome. There is therefore some amount of correlation between genome-wide variation and variation at specific loci associated with disease. The ways in which these variants interact with environmental factors can subsequently give a less-than-perfect approximation of propensity for disease or treatment response.[3]

distribution of the sickle cell trait
distribution of Malaria

A classic example of a disease that tends to correlate with ethnic clusters is Tay-Sachs, an autosomal recessive disorder which is shown to be more frequent among Ashkenazi Jews than among other Jewish groups and non-Jewish populations, though it has been shown to occur in other groups as well.[5] Sickle-cell anemia, another well-known genetic disorder, has been shown to be most prevalent among individuals of sub-Saharan African ancestry, though there is also ample recorded instance of lesser prevalence among Hispanics, Indians, Saudi Arabs, and Mediterraneans. The sickle cell trait offers some resistance to malaria, since in regions where malaria is present, sickle cell has been positively selected and consequently the proportion of people with it is greater.[6] Race-based medicine comes into play when a medicine is specifically intended for ethnic clusters which are shown to have a propensity for a certain disorder. A recent example of this practice in action is the FDA approval of BiDil, a medication for congestive heart failure targeted at black people in the United States.[7] BiDil is based on the substantial evidence that African Americans with congestive heart failure respond less effectively to traditional treatments than Caucasians.[8]

The continued use of racial categories as proxies for knowledge about genetically determined health concerns in populations has been criticized widely. Outram and Ellison have identified the most common concerns related to this practice. Most genetic variation is found within racial groups whereas very little genetic variation loosely coincides with racial groups, but without making any well-defined genetic criteria for ascription of individuals to racial groups possible. Completely genetically homogenous racial groups have never existed; phenotypic traits, and variation between them, do not translate directly to similar variation in genotypic traits; and the continued use of racial categories as proxies for genetic variation has a social function of cementing socially constructed racial categories as if they were natural classes, which could result in increased stereotyping and discrimination in society.[9] In many cases, health disparities will be caused by environmental factors common to certain populations and geographic areas, such as differences in culture, diet, education, socioeconomic status, and access to health care, rather than by allele clusters.[3] Another concern is that the way in which research emphasizes differences in health risk and health care need among racial groups can lead to the development of racial discrimination in health services.[9]

Many researchers agree that a goal of health-related genetics should be to move past the weak surrogate relationships of racial health disparity and get to the root causes of health and disease. This largely includes research which strives to define human variation with greater specificity across the world.[3] One such emerging method is known as ethnogenetic layering, which is a non-typological alternative to depending on the racial paradigm in biomedicine. It works by focusing on geographically identified microethnic groups, which are far more nuanced and sensitive than simple race analyses.[10]

  1. ^ a b Ian Whitmarsh and David S. Jones, 2010, What's the Use of Race? Modern Governance and the Biology of Difference, MIT press. Chapter 9.
  2. ^ Satel, Sally. "I Am a Racially Profiling Doctor". The New York Times, published May 5, 2002
  3. ^ a b c d e Collins, Francis S. What we do and don't know about 'race', 'ethnicity', genetics and health at the dawn of the genome era. Nature Genetics Supplement, volume 36 No. 11, November 2004.
  4. ^ Revisiting race in a genomic age. By Barbara A. Koenig, Sandra Soo-Jin Lee, Sarah S. Richardson. Rutgars University Press, 2008. Chapter 5.
  5. ^ Myrianthopoulos NC and Aronson SM (July 1, 1966). "Population dynamics of Tay-Sachs disease. I. Reproductive fitness and selection.". American Journal of Human Genetics 18 (4): 313–327. PMID 5945951.
  6. ^ http://www.ornl.gov/sci/techresources/Human_Genome/posters/chromosome/sca.shtml
  7. ^ Taylor AL, Ziesche S, Yancy C, et al. (November 2004). "Combination of isosorbide dinitrate and hydralazine in blacks with heart failure". The New England Journal of Medicine 351 (20): 2049–57. doi:10.1056/NEJMoa042934. PMID 15533851.
  8. ^ Exner DV, Dries DL, Domanski MJ, Cohn JN (2001). "Lesser response to angiotensin-converting-enzyme inhibitor therapy in blacks as compared with white patients with left ventricular dysfunction". N Engl J Med 344 (18): 1351–7. doi:10.1056/NEJM200105033441802. PMID 11333991.
  9. ^ a b Ian Whitmarsh and David S. Jones, 2010, What's the Use of Race? Modern Governance and the Biology of Difference, MIT press. Chapter 5.
  10. ^ Jackson, F.L.C. Ethnogenetic layering (EL): an alternative to the traditional race model in human variation and health disparity studies. Annals of Human Biology, March–April 2008; 35(2): 121–144 http://informahealthcare.com/doi/abs/10.1080%2F03014460801941752