Genetic arguments Flashcards
Rehkopf & Adler. (2010). Commentary: It’s not all means and genes - socioeconomic position, variation, and genetic confounding.
Gist: Commentary on Johnson et al. was that (1) it demonstrates the value of examining variation in health as a phenomenon of interest in & of itself; (2) it provides empirical evidence challenging the assertion that the association of SEP & health is due primarily to shared genetic predispositions.
Difference in variance: Johnson et al. found greater variation in physical health at lower levels of SEP (genetics explain why some individuals remain healthy at low levels of education while others don’t).
Genetic causation: Johnson et al. found that prior common causes of education & health are not due to genotype at the lower end of the educational distribution; speculation (not supported).
Kuzawa & Sweet. (2013). Epigenetics and the embodiment of race: Developmental origins of U.S. racial disparities in cardiovascular health.
Gist:
Cooper. (2004). Genetic factors in ethnic disparities in health.
Gist: Can we separate the genetic and environmental risks associated with susceptibility to disease? First, race is a social construct that informs popular discourse & shapes policy; it’s based on social & historical forces & allows the justification of divisions among people based on particular backgrounds. A second use of race is within population genetics; the question being whether global variation in the human genome can be aggregated into subunits & whether those units correspond to racial categories. There is no way to map racial categories directly onto genetic subpopulations.
Deficiency model: Expectation of poorer outcomes fro groups other than whites; “Hispanic paradox” & high health status of Asian groups doesn’t match.
Heritability hang-up: No logical basis, but idea that a trait must be heritable if it varies systematically between groups.
Subtraction method: attempts to partial out environmental factors by adjusting for covariates & assumes that anything “left over” must be attributed to genetic differences.
Molecular approaches: (1) genome scan approach; (2) candidate gene approach - identify a large # of candidate genes; (3) pharmacogenetics - whether response to therapeutic drugs can be predicted by genotype.
Common disease-common variant hypothesis: assumed that susceptibility to complex disease involves sum of many variants & the variants occur at relatively high frequency in pop.
Slavery hypothesis: selective mortality caused by salt-wasting disorders created genetic susceptibility to hypertension among surviving blacks who retained salt.
Thrifty gene hypothesis: selection advantage against starvation conferred by an ability to store excess calories as fact is the cause of diabetes in Native Americans & Pacific Islanders.
Overall, race is not a reliable marker of disease.
Crimmins, Kim, Alley, Karlamangla, & Seeman. (2007). Hispanic paradox in biological risk profiles.
Gist: Research shows a better-than-expected health & mortality profile for Hispanics despite their lower SES.
Healthy immigrant hypothesis: Migrants who immigrate are different from persons from the same country of origin who don’t migrate & this plays large role in Hispanic health advantages.
Salmon hypothesis: Sick persons return to their place of origin.
Both hypotheses assume that the Hispanic health advantage is a feature exclusive to foreign-born Hispanics. Hispanics overall had a higher biological risks than whites for 3/4 scores (true for all Hispanics & Mexican Americans specifically). When controlling for SES, foreign-born Mexican immigrants had similar biological risk profiles to white & better than US-born Mexicans. This doesn’t indicate evidence of Hispanic paradox. It’s suggested that US-born Hispanics may suffer from the same social inequities that are the basis of differences found between blacks & whites.
Goodman. (2000). Why genes don’t count (for racial differences in health).
Gist: Race does not account for human genetic variation, which continuous, complexly structured, constantly changing, & predominantly within “races”. Despite disproof of race-as-biology, genetic variation continues to be used to explain racial differences. Using race as a proxy for genetic differences limits understandings of the complex interactions among political-economic processes, lived experiences, & human biologies.
Frank. (2007). What of make of it? The (re)emergence of a biological conceptualization of race in health disparities research.
Gist: Although previously refuted, the idea that race/ethnicity does have a genetic basis has been enjoying a resurgence. There are 3 main claims in the genetic & biomedical literature to explain relationship between race, genetics, & health disparities.
Claim 1: Inference of ancestry from genetic markers
Claim 2: Identification of genotypes that vary across population groups (major issue of confounding with other non-genetic risk factors)
Claim 3: Genetics and racial disparities in health (example with lung cancer as an issue)
