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{{mergeto|Race and health|Talk:Race and health}} |
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#REDIRECT ] |
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{{Cleanup|December 2005}} |
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{{Redirect category shell|1= |
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The role of '''race in biomedicine''' is actively debated among ]s. |
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{{R from merge}} |
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Several questions are considered: |
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* can the concept of "race" be considered ]? |
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* When should ] be taken into account when studying humans? |
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* What definition of race is appropriate for biomedical research? |
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* Do the biological differences between races justify the use of racial categories in research? |
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* Can genetic assignment to population groups be used in lieu of self-identified race? |
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* What are the ] implications of using race in research? |
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The primary impetus for considering race in biomedical research is the possibility of improving the prevention and treatment of ]s. Many previous studies have observed that disease susceptibility and environmental responses vary by race. Thus, some researchers believe that race may be an informative category for biomedical research. Other researchers believe that racial categories have no valid biomedical applications, and may be socially harmful (Jackson, 2004). |
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== Racial, ethnic, and ancestral categories in genetics research == |
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=== The effects of racial and ethnic identities on health === |
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Racial and ethnic groups can exhibit substantial average differences in disease incidence, disease severity, disease progression, and response to treatment (LaVeist 2002). In the United States, African Americans have higher rates of mortality than does any other racial or ethnic group for 8 of the top 10 causes of death (Hummer ''et al.'' 2004). U.S. Latinos have higher rates of death from diabetes, liver disease, and infectious diseases than do non-Latinos (Vega and Amaro 1994). Native Americans suffer from higher rates of diabetes, tuberculosis, pneumonia, influenza, and alcoholism than does the rest of the U.S. population (Mahoney and Michalek 1998). European Americans die more often from heart disease and cancer than do Native Americans, Asian Americans, or Hispanics (Hummer ''et al.'' 2004). |
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Considerable evidence indicates that the racial and ethnic health disparities observed in the United States arise mostly through the effects of discrimination, differences in treatment, poverty, lack of access to health care, health-related behaviors, racism, stress, and other socially mediated forces. The infant mortality rate for African Americans is approximately twice the rate for European Americans, but, in a study that looked at members of these two groups who belonged to the military and received care through the same medical system, their infant mortality rates were essentially equivalent (Rawlings and Weir 1992). Recent immigrants to the United States from Mexico have better indicators on some measures of health than do Mexican Americans who are more assimilated into American culture (Franzini ''et al.'' 2001). Diabetes and obesity are more common among Native Americans living on U.S. reservations than among those living outside reservations (Cooper ''et al.'' 1997). Rates of heart disease among African Americans are associated with the segregation patterns in the neighborhoods where they live (Fang ''et al.'' 1998). Furthermore, the risks for many diseases are elevated for socially, economically, and politically disadvantaged groups in the United States, suggesting that socioeconomic inequities are the root causes of most of the differences (Cooper ''et al.'' 2003; Cooper 2004). |
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However, differences in allele frequencies certainly contribute to group differences in the incidence of some monogenic diseases, and they may contribute to differences in the incidence of some common diseases (Risch ''et al.'' 2002; Burchard ''et al.'' 2003; Tate and Goldstein 2004). For the monogenic diseases, the frequency of causative alleles usually correlates best with ancestry, whether familial (for example, Ellis–van Creveld syndrome among the Pennsylvania Amish), ethnic (Tay-Sachs disease among Ashkenazi Jewish populations), or geographical (hemoglobinopathies among people with ancestors who lived in malarial regions). To the extent that ancestry corresponds with racial or ethnic groups or subgroups, the incidence of monogenic diseases can differ between groups categorized by race or ethnicity, and health-care professionals typically take these patterns into account in making diagnoses. |
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Even with common diseases involving numerous genetic variants and environmental factors, investigators point to evidence suggesting the involvement of differentially distributed alleles with small to moderate effects. Frequently cited examples include hypertension (Douglas ''et al.'' 1996), diabetes (Gower ''et al.'' 2003), obesity (Fernandez ''et al.'' 2003), and prostate cancer (Platz ''et al.'' 2000). However, in none of these cases has allelic variation in a susceptibility gene been shown to account for a significant fraction of the difference in disease prevalence among groups, and the role of genetic factors in generating these differences remains uncertain (Mountain and Risch 2004). |
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=== The allelic architecture of disease === |
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The genetic architecture of common diseases is an important factor in determining the extent to which patterns of genetic variation influence group differences in health outcomes (Reich and Lander 2001; Pritchard and Cox 2002; Smith and Lusis 2002). According to the common disease/common variant hypothesis, common variants present in the ancestral population before the dispersal of modern humans from Africa play an important role in human diseases (Goldstein and Chikhi 2002). Genetic variants associated with Alzheimer disease, deep venous thrombosis, Crohn disease, and type 2 diabetes appear to adhere to this model (Lohmueller ''et al.'' 2003). However, the generality of the model has not yet been established and, in some cases, is in doubt (Weiss and Terwilliger 2000; Pritchard and Cox 2002; Cardon and Abecasis 2003). Some diseases, such as many common cancers, appear not to be well described by the common disease/common variant model (Kittles and Weiss 2003; Wiencke 2004). |
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Another possibility is that common diseases arise in part through the action of combinations of variants that are individually rare (Pritchard 2001; Cohen ''et al.'' 2004). Most of the disease-associated alleles discovered to date have been rare, and rare variants are more likely than common variants to be differentially distributed among groups distinguished by ancestry (Risch ''et al.'' 2002; Kittles and Weiss 2003). However, groups could harbor different, though perhaps overlapping, sets of rare variants, which would reduce contrasts between groups in the incidence of the disease. |
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The number of variants contributing to a disease and the interactions among those variants also could influence the distribution of diseases among groups. The difficulty that has been encountered in finding contributory alleles for complex diseases and in replicating positive associations suggests that many complex diseases involve numerous variants rather than a moderate number of alleles, and the influence of any given variant may depend in critical ways on the genetic and environmental background (Risch 2000; Weiss and Terwilliger 2000; Altmüller ''et al.'' 2001; Hirschhorn ''et al.'' 2002). If many alleles are required to increase susceptibility to a disease, the odds are low that the necessary combination of alleles would become concentrated in a particular group purely through drift (Cooper 2004). |
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=== Population substructure in genetics research === |
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One area in which racial and ethnic categories can be important considerations in genetics research is in controlling for confounding between population substructure, environmental exposures, and health outcomes. Association studies can produce spurious results if cases and controls have differing allele frequencies for genes that are not related to the disease being studied (Cardon and Palmer 2003; Marchini ''et al.'' 2004), although the magnitude of this problem in genetic association studies is subject to debate (Thomas and Witte 2002; Wacholder ''et al.'' 2002). Various methods have been developed to detect and account for population substructure (Morton and Collins 1998; Hoggart ''et al.'' 2003), but these methods can be difficult to apply in practice (Freedman ''et al.'' 2004). |
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Population substructure also can be used to advantage in genetic association studies. For example, populations that represent recent mixtures of geographically separated ancestral groups can exhibit longer-range linkage disequilibrium between susceptibility alleles and genetic markers than is the case for other populations (Hoggart ''et al.'' 2004; Patterson ''et al.'' 2004; Smith ''et al.'' 2004; McKeigue 2005). Genetic studies can use this admixture linkage disequilibrium to search for disease alleles with fewer markers than would be needed otherwise. Association studies also can take advantage of the contrasting experiences of racial or ethnic groups, including migrant groups, to search for interactions between particular alleles and environmental factors that might influence health (Chaturvedi 2001; Collins ''et al.'' 2003). |
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==Disease association studies== |
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Race is associated with differential disease susceptibility and environmental responses. Many highly penetrant Mendelian diseases that are caused by mutations in a single gene are known to be found at higher frequencies in certain races. The HbS allele that causes ] is found at higher frequencies in sub-Saharan Africans and Southern Europeans. Similarly, the ΔF508 allele of '']'' that causes ] is found in higher frequencies in Northern Europeans. It is believed that many of these mutations first occurred in the population that is most affected. |
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Race has also been found to be associated with susceptibility to complex, multifactorial and multigenic diseases. The incidence and death rate of ] and ] ]s are significantly higher in African-Americans than European-Americans. Higher proportions of individual African ancestry is associated with increased susceptibility to both ] and abnormal levels of ] secretion. Likewise, Hispanic, American Indian, African American, Pacific Island, and South Asian ancestry is considered a risk factor for ]. Also, the incidence of ] and ] is higher in African-Americans than European-Americans. |
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The ] (often abbreviated CD-CV) hypothesis predicts common disease causing alleles will be found in all populations. An often cited example is an allele of ] E, ''APOE'' ε4, which is associated in a dose-dependent manner with susceptibility to ]. This allele is found in Africans, Asians and Europeans. However, many disease causing alleles are found to have different (technically called ]) effects in different populations. For example, the increased risk of ] that is associated with the ''APOE'' ε4 allele is 5-fold higher in individuals with Asian rather than African ancestry. |
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Polymorphisms in the regulatory region of the '']'' gene affect the rate of progression to ] and death in ] infected patients. While some CCR5 ]s are beneficial in multiple populations, other haplotypes have population-specific effects. For example, the HHE haplotype of CCR5 is associated with delayed disease progression in European-Americans, but accelerated disease progression in African-Americans. Similarly, alleles of the ''CARD15'' (also called ''NOD2'') gene are associated with ], an inflammatory bowel disorder, in European-Americans. However, none of these or any other alleles of CARD15 have been associated with Crohn's disease in African-Americans or Asians. |
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{| class="wikitable" |
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|+ Diseases that differ in frequency by race or ethnicity (Halder & Shriver, 2003). |
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! Disease || High-risk groups || Low-risk groups || Reference(s) |
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| ] || African women, Native Americans South Asians, Pacific Islanders, Aboriginal Australians || Europeans || McKeigue, ''et al.'' (1991); Hodge & Zimmet (1994) |
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| Obesity/BMI || African-Americans || European-Americans || <ref>Hodge, A. M. & Zimmet, P. Z. The epidemiology of obesity. Baillieres Clin. Endocrinol. Metab. 8, 577-599 (1994). </ref> |
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| Non-insulin dependent ] || South Asians, West Africans, Peninsular Arabs, Pacific Islanders and Native Americans || Europeans || Songer & Zimmet (1995); Martinez (1993) |
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| Non-insulin dependent diabetes || African-Americans || European-Americans || <ref>Gupta, V. ''et al.'' Racial differences in thoracic aorta atherosclerosis among ischemic stroke patients. Stroke 34, 408-412 (2003).; Songer, T. J. & Zimmet, P. Z. Epidemiology of type II diabetes: an international perspective. Pharmacoeconomics 8 (Suppl. 1), 1-11 (1995).</ref> |
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| ] || African Americans, West Africans || Europeans || Douglas ''et al.'' (1996); Gaines & Burke (1995) |
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| ] || South Asians || West African men || McKeigue, ''et al.'' (1989); Zoratti (1998) |
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| Coronary artery disease || European-Americans || African-Americans || <ref>Gupta, V. ''et al.'' Racial differences in thoracic aorta atherosclerosis among ischemic stroke patients. Stroke 34, 408-412 (2003).</ref> |
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| End-stage ] || Native Americans and African populations || Europeans || Ferguson & Morrissey (1993) |
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| End-stage renal disease || African-Americans || European-Americans || <ref>Klag, M. J. ''et al.'' End-stage renal disease in African-American and white men. 16-year MRFIT findings. JAMA 277, 1293-1298 (1997). </ref> |
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| ] || Europeans || African Americans, Hispanic Americans || Hargrave, ''et al.'' (2000) |
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| Dementia || African-Americans || European-Americans || <ref>Demirovic, J. ''et al.'' Prevalence of dementia in three ethnic groups: the South Florida program on aging and health. Ann. Epidemiol. 13, 472-478 (2003).</ref> |
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| Systemic ] || West Africans, Native Americans || Europeans || Molokhia & McKeigue (2000) |
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| ] || Europeans || || Boni, ''et al.'' (2002) |
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| ] || Africans, European Americans(Caucasians)|| Chinese, Japanese || Schwartz & Swanson (1997); Shimizu, ''et al.'' (1985) |
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| ] || Africans and African Americans || || Hoffman, ''et al.'' (2001) |
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| ] || Europeans || Chinese, Japanese, African Americans, Turkmens, Uzbeks, Native Siberians, New Zealand Maoris || Rosati (2001) |
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| ] || European Americans || African Americans || Bohannon (1999) |
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| Atrial fibrillation || European-Americans || African-Americans || <ref>Ruo, B., Capra, A. M., Jensvold, N. G. & Go, A. S. Racial variation in the prevalence of atrial fibrillation among patients with heart failure: the Epidemiology, Practice, Outcomes, and Costs of Heart Failure (EPOCH) study. J. Am. Coll. Cardiol. 43, 429-435 (2004).</ref> |
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| Carotid artery disease || European-Americans || African-Americans || <ref>Gupta, V. ''et al.'' Racial differences in thoracic aorta atherosclerosis among ischemic stroke patients. Stroke 34, 408-412 (2003).</ref> |
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| Focal segmental glomerulosclerosis || African-Americans || European-Americans || <ref>Kopp, J. B. & Winkler, C. HIV-associated nephropathy in African Americans. Kidney Int. S43-S49 (2003). </ref> |
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| Hepatitis C clearance || European-Americans || African-Americans || <ref>Thomas, D. L. ''et al.'' The natural history of hepatitis C virus infection: host, viral, and environmental factors. JAMA 284, 450-456 (2000). </ref> |
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| HIV progression || African-Americans || European-Americans || <ref>McGinnis, K. A. ''et al.'' Understanding racial disparities in HIV using data from the veterans aging cohort 3-site study and VA administrative data. Am. J. Public Health 93, 1728-1733 (2003).</ref> |
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| HIV vertical transmission || European-Americans || African-Americans || <ref>Tess, B. H., Rodrigues, L. C., Newell, M. L., Dunn, D. T. & Lago, T. D. Breastfeeding, genetic, obstetric and other risk factors associated with mother-to-child transmission of HIV-1 in Sao Paulo State, Brazil. Sao Paulo collaborative study for vertical transmission of HIV-1. Aids 12, 513-520 (1998). </ref> |
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| Hypertensive heart disease || African-Americans || European-Americans || <ref>Davey Smith, G., Neaton, J. D., Wentworth, D., Stamler, R. & Stamler, J. Mortality differences between black and white men in the USA: contribution of income and other risk factors among men screened for the MRFIT. Lancet 351, 934-939 (1998). </ref> |
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| Hypertensive retinopathy || African-Americans || European-Americans || <ref>Wong, T. Y. ''et al.'' Racial differences in the prevalence of hypertensive retinopathy. Hypertension 41, 1086-1091 (2003). </ref> |
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| Intracranial haemorrhage || African-Americans || European-Americans || <ref>Davey Smith, G., Neaton, J. D., Wentworth, D., Stamler, R. & Stamler, J. Mortality differences between black and white men in the USA: contribution of income and other risk factors among men screened for the MRFIT. Lancet 351, 934-939 (1998). </ref> |
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| Lupus nephritis with systemic lupus erythematosus || African-Americans || European-Americans || <ref>Bastian, H. M. ''et al.'' Systemic lupus erythematosus in three ethnic groups. XII. Risk factors for lupus nephritis after diagnosis. Lupus 11, 152-160 (2002). </ref> |
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| Myeloma || African-Americans || European-Americans || <ref>Davey Smith, G., Neaton, J. D., Wentworth, D., Stamler, R. & Stamler, J. Mortality differences between black and white men in the USA: contribution of income and other risk factors among men screened for the MRFIT. Lancet 351, 934-939 (1998). </ref> |
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| Pregnancy-related death || African-Americans || European-Americans || <ref>Harper, M. A. ''et al.'' Racial disparity in pregnancy-related mortality following a live birth outcome. Ann. Epidemiol. 14, 274-279 (2004).</ref> |
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| Stroke || African-Americans || European-Americans || <ref>Davey Smith, G., Neaton, J. D., Wentworth, D., Stamler, R. & Stamler, J. Mortality differences between black and white men in the USA: contribution of income and other risk factors among men screened for the MRFIT. Lancet 351, 934-939 (1998).; Kissela, B. ''et al.'' Stroke in a biracial population: the excess burden of stroke among blacks. Stroke 35, 426-431 (2004).</ref> |
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| Systemic lupus erythematosus || African-Americans || European-Americans || <ref>Molokhia, M. & McKeigue, P. Risk for rheumatic disease in relation to ethnicity and admixture. Arthritis Res. 2, 115-125 (2000). </ref> |
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| Systemic sclerosis || African-Americans || European-Americans || <ref>Reveille, J. D. Ethnicity and race and systemic sclerosis: how it affects susceptibility, severity, antibody genetics, and clinical manifestations. Curr. Rheumatol. Rep. 5, 160-167 (2003).</ref> |
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==Concept of race== |
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:''Main article: ].'' |
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In biomedical research conducted in the U.S., the ] definition of race is often applied. This grouping recognizes five ''races'': ] or ], ], ], ] or other ], and ] or ]. However, this definition is inconsistently applied across the range of studies that address race as a medical factor, making assessment of the utility of racial categorization in medicine more difficult. |
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From the perspective of ], ] structure is the result of patterns of ]. Historically, the greatest influence on mating patterns is ]. Genetic research has shown that the greatest genetic differentiation among humans corresponds with continental groupings.{{cn}} To the extent that racial labels correspond to continental groups, some argue that they are informative for biomedical research. ] between continents in the last two centuries, with consequent racial ] has caused some to question the significance of this notion of race to medicine. |
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In multiracial societies such as that of the ], racial groups also differ by social and cultural correlates such as ] and access to ]. These factors are believed to explain some of the differential health care outcomes among races. An open area of investigation is whether racial differences persist in studies where social and cultural correlates are taken into account. |
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==Genetic differences among races== |
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The biomedical relevance of genetic differences among races is a matter of debate. The existence of genetic differences among races is well accepted.{{cn}} In general, genetic clusters exist that correspond tightly to the census definition of race and to self-identified ]. One large exception to this correspondence is that South, Central, and West Asians (e.g. Asian Indians) cluster with Europeans and are separate from East Asians. The association between ''race'' and genetics also breaks down for groups, such as ]s, that exhibit a pattern of geographical stratification of ancestry. Some researchers argue that the available evidence supports the notion that some of the genetic differences between races have biomedical significance, and thus should be studied. |
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==Genetic labelling== |
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An alternative view argues that the underlying genetic-cluster categories can be used in lieu of racial labels for biomedical purposes. Proponents of this view argue that by directly examining the ], the problem of using racial labels can be avoided. Moreover, they argue that genotyping is more reliable than using self-identified race as a ] for ancestry.{{cn}} Some fear that the use of racial labels in biomedical research runs the risk of unintentionally exasperating health disparities. |
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Proponents of using race in biomedical research argue that ignoring race will be detrimental to the health of ] groups. They argue that disease ]s differ substantially between racial groups, that relying only on genotypical classes ignores non-genetic racial factors that impact health, and, furthermore, that minorities would be poorly represented in ]s if race were ignored.{{cn}} |
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==Research== |
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The ] (]) has attempted to map the ] that varies between humans. In the future, ] could possibly reveal new data in ], ] and ]. ] could unlock secrets behind and create new strategies for managing the vulnerability of ]s to certain ]s. It could also show how human ]s have adapted to these vulnerabilities.{{dubious}}<!--The head of the Human Genome Diversity Project has cautioned researchers about making hasty conclusions about race ... so this is just off topic and OR. Unless there is a source that can be cited linking the HGDP to claims about race (not population groups!) --> To date, HGDP research has resulted in a representative world distribution of 52 distinct ]tic markers. |
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== References == |
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* Bohannon, A.D. (1999), ‘Osteoporosis and African American women’, J. Women's Health Gend. Based Med. Vol. 8, pp. 609-615. |
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* Boni, R., Schuster, C., Nehrhoff, B. and Burg, G. (2002), ‘Epidemiology of skin cancer’, Neuroendocrinol. Lett. Vol. 23 (Suppl. 2), pp. 48-51. |
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* Douglas, J.G., Thibonnier, M. and Wright, Jr., J.T. (1996), ‘Essential hypertension: Racial/ethnic differences in pathophysiology’, J. Assoc. Acad. Minor. Phys. Vol. 7, pp. 16-21. |
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* Editorial. Genes, drugs and race. ''Nature Genetics'' 29, 239 - 240 (2001). |
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* Farrer, L. A. ''et al.'' Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease Meta Analysis Consortium. ''JAMA'' 278, 1349-1356 (1997). |
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* Ferguson, R. and Morrissey, E. (1993), ‘Risk factors for end-stage renal disease among minorities’, Transplant. Proc. Vol. 25, pp. 2415-2420. |
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* Fernandez, J. R. ''et al.'' Association of African genetic admixture with resting metabolic rate and obesity among women. ''Obes. Res.'' 11, 904-911 (2003). |
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* Gaines, K. and Burke, G. (1995), ‘Ethnic differences in stroke: Black-white differences in the United States population. SECORDS Investigators. Southeastern Consortium on Racial Differences in Stroke’, Neuroepidemiology Vol. 14, pp. 209-239. |
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* Gonzalez, E. ''et al.'' Race-specific HIV-1 disease-modifying effects associated with CCR5 haplotypes. ''Proc. Natl Acad. Sci. USA.'' 96, 12004-12009 (1999). |
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* Gower, B. A. ''et al.'' Using genetic admixture to explain racial differences in insulin-related phenotypes. ''Diabetes'' 52, 1047-1051 (2003). |
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* Halder I, Shriver MD. (2003). Measuring and using admixture to study the genetics of complex diseases. Hum Genomics 1, 52-62. |
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* Hardy, J., Singleton, A. & Gwinn-Hardy, K. Ethnic differences and disease phenotypes. ''Science'' 300, 739-740 (2003). |
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* Hargrave, R., Stoeklin, M., Haan, M. and Reed, B. (2000), ‘Clinical aspects of dementia in African-American, Hispanic, and white patients’, J. Nat. Med. Assoc. Vol. 92, pp. 15-21. |
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* Hodge, A.M. and Zimmet, P.Z. (1994), ‘The epidemiology of obesity’, Baillieres Clin. Endocrinol. Metab. Vol. 8, pp. 577-599. |
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* Hoffman, R.M., Gilliland, F.D., Eley, J.W. ''et al.'' (2001), ‘Racial and ethnic differences in advanced-stage prostate cancer: The Prostate Cancer Outcomes Study’, J. Nat. Cancer Inst. Vol. 93, pp. 388-395. |
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* Holden, C. Race and medicine. ''Science'' 302, 594-596 (2003). |
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* Hugot, J. P. ''et al.'' Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease. ''Nature'' 411, 599-603 (2001). |
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* Inoue, N. Lack of common NOD2 variants in Japanese patients with Crohn's disease. ''Gastroenterology'' 123, 86-91 (2002). |
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* Jackson, F. L. C. (2004). Book chapter: '''' '''British Medical Bulletin 2004; 69: 215–235''' DOI: 10.1093/bmb/ldh012. Retrieved 29 December 2006. |
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* Martin, M. P. ''et al.'' Genetic acceleration of AIDS progression by a promoter variant of CCR5. ''Science'' 282, 1907-1911 (1998). |
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* Martinez, N.C. (1993), ‘Diabetes and minority populations. Focus on Mexican Americans’, Nurs. Clin. North Am. Vol. 28, pp. 87-95. |
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* Martinson, J. J., Chapman, N. H., Rees, D. C., Liu, Y. T. & Clegg, J. B. Global distribution of the CCR5 gene 32-basepair deletion. ''Nature Genet.'' 16, 100-103 (1997). |
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* McKeigue, P.M., Miller, G.J. and Marmot, M.G. (1989), ‘Coronary heart disease in south Asians overseas: A review’, J. Clin. Epidemiol. Vol. 42, pp. 597-609. |
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* McKeigue, P.M., Shah, B. and Marmot, M.G. (1991), ‘Relation of central obesity and insulin resistance with high diabetes prevalence and cardiovascular risk in South Asians’, Lancet Vol. 337, pp. 382-386. |
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* Molokhia, M. and McKeigue, P.M. (2000), ‘Risk for rheumatic disease in relation to ethnicity and admixture’, Arthritis Res. Vol. 2, pp. 115-125. |
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* Ogura, Y. ''et al.'' A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease. ''Nature'' 411, 603-606 (2001). |
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* Risch, N.; Burchard, E.; Ziv, E. & Tang, H. (2002). Categorization of humans in biomedical research: genes, race and disease. ''Genome Biol.'' 3, comment2007. |
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* Rosati, G. (2001), ‘The prevalence of multiple sclerosis in the world: An update’, Neurol. Sci. Vol. 22, pp. 117-139. |
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* Schwartz, A.G. and Swanson, G.M. (1997), ‘Lung carcinoma in African Americans and whites. A population-based study in metropolitan Detroit, Michigan’, Cancer Vol. 79, pp. 45-52. |
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* Shimizu, H., Wu, A.H., Koo, L.C. ''et al.'' (1985), ‘Lung cancer in women living in the Pacific Basin area’, Nat. Cancer Inst. Monogr. Vol. 69, pp. 197-201. |
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* Songer, T.J. and Zimmet, P.Z. (1995), ‘Epidemiology of type II diabetes: An international perspective’, Pharmacoeconomics Vol. 8 (Suppl. 1), pp. 1-11. |
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* Wiencke, J. K. Impact of race/ethnicity on molecular pathways in human cancer. ''Nature Rev. Cancer'' 4, 79-84 (2003). |
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* Yancy, C. D. Does race matter in heart failure. ''Am. Heart J.'' 146, 203-206 (2003). |
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* Zoratti, R. (1998), ‘A review on ethnic differences in plasma triglycerides and high-density-lipoprotein cholesterol: Is the lipid pattern the key factor for the low coronary heart disease rate in people of African origin?’, Eur. J. Epidemiol. Vol. 14, pp. 9-21. |
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== See also == |
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== External link == |
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