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    • The racial disparity in US rates of cancer among

    2018-11-14

    The racial disparity in US rates of cancer (among other diseases) has been well-characterized and continues to persist with African-Americans having generally worse cancer incidence and mortality than Whites (). While many researchers have identified proximal causes for this disparity current research remains unable to completely explain the frequent and dramatic differences in cancer rates between US racial/ethnic subgroups, prompting researchers in molecular epidemiology to undertake new studies of this problem. Many of the risk factors thought to contribute to racial health disparities in the US (e.g., socioeconomic status/health care access, stress, environmental exposures) have also been associated with shorter telomeres (), however most studies comparing telomere length (TL) across racial/ethnic groups have found that in general African-Americans tend to have longer telomeres than Whites (). This counterintuitive finding has led researchers to hypothesize that these differences are due to genetic ancestry, specifically polymorphisms related to genes that regulate TL, or possibly unaccounted-for environmental factors such as pollutant exposure (). Previous studies, including genome-wide association studies (GWAS), have identified numerous genes associated with TL through mechanisms including shelterin, DNA repair, helicases, and telomerase () but few have explored variation in the UM171 of these genes by race/ethnicity. In this issue of , Hamad et al. () attempt to answer the question of genetic vs. environmental interplay in racial TL differences via a cross-sectional exploration of genes associated with TL and various sociodemographic characteristics including race/ethnicity. Using genetic data from 11,141 participants in the Health and Retirement Study (HRS) collected in 2006 and 2008 they construct a polygenic risk score (PRS) of seven single nucleotide polymorphisms following the method developed by Codd et al. (). They then identify racial and ethnic differences in PRS, with African-Americans having a lower PRS (predicting longer telomeres) and Hispanics having higher PRS (predicting shorter telomeres) compared to Whites. These findings were independent of socioeconomic factors (education and total assets), age, and gender and confirmed using a genetic principal components approach with components strongly associated with race/ethnicity. Interestingly, self-reported race performed nearly as well as genetic ancestry for these telomere-associated polymorphisms. In a subset of 5808 HRS participants with available data on TL, the authors also confirmed longer telomeres in African-Americans, and intriguing associations between TL and select genetic principal components. Data on individual SNPs presented in the supplementary tables will also fuel future research.
    A wide range of human brain imaging techniques has provided the opportunity to explore in vivo the neurophysiological processes of the brain (). This neuroimaging research has shown neuronal plasticity, which refers to the possibility of the central nervous system including the brain to adapt but also to maladapt structure, function and organization (). Subsequently, the role of maladaptive brain alterations in the persistent complaints of various chronic pain conditions (e.g., fibromyalgia, chronic low back pain, temporomandibular disorders) has been gradually elucidated (). Emerging evidence indicates that different chronic pain conditions are each associated with distinct brain reorganization, which is referred to as the neural pain signature (). In addition, changes in resting state interactions between brain networks implicated in default states, salience, attention, and reward have been demonstrated in chronic pain patients (). The results of longitudinal imaging studies suggest that brain alterations are involved in the transition to chronic pain (). In particular, the corticolimbic circuitry, which is a key system for reward and motivated behavior, has been reported as a mediator for this transition ().