Social disadvantage, genetic sensitivity, and children’s telomere length

Abstract

Significance This paper makes two contributions to research on the link between the social environment and health. Using data from a birth cohort study, we show that, among African American boys, those who grow up in highly disadvantaged environments have shorter telomeres (at age 9) than boys who grow up in highly advantaged environments. We also find that the association between the social environment and telomere length (TL) is moderated by genetic variation within the serotonin and dopamine pathways. Boys with the highest genetic sensitivity scores had the shortest TL when exposed to disadvantaged environments and the longest TL when exposed to advantaged environments. To our knowledge, this report is the first to document a gene–social environment interaction for TL, a biomarker of stress exposure.

Lifespan adversity and later adulthood telomere length in the nationally representative US Health and Retirement Study

“…Although rich in immune cells, saliva also has other cell types, such as epithelial buccal cells, making it a less pure measure of immune cell telomere length. However, a recent study demonstrated a highly significant correlation (r = 0.72) between telomere length from saliva and blood (65). Additionally, a large study with 100,000 participants that used salivary telomere length as a marker of cell aging found that salivary Bolded ORs include all significant associations.…”

Plastic and immobile: Unequal intergenerational mobility by genetic sensitivity score within sibling pairs

“…Furthermore, experimental research suggests variation at these genes is associated with financial decision making (e.g., Carpenter et al 2011;Dreber et al 2009;Zhong et al 2009aZhong et al , 2009b. Because individual alleles are not likely to have strong enough effects on complex outcomes for statistical detection (Pearson-Fuhrhop et al 2014) and to conform to the increasingly common practice of using polygenic or additive genetic measures (Mitchell et al 2014;Pearson-Fuhrhop et al 2013;Stice et al 2012; Belsky and Beaver 2011), I create a genetic sensitivity score by summing all of the sensitive alleles held by an individual. Throughout the paper, I refer to this measure as genetic sensitivity score (GSS), but an alternative term is cumulative genetic plasticity score (Belsky and Beaver 2011).…”

“…In the case of DAT1, Laucht et al (2007) found that ADHD symptoms among those carrying the 10-repeat allele are more sensitive to psychosocial adversity than among others. Mitchell et al (2014) found evidence that the DAT1 10-repeat allele, in combination with others, increased sensitivity to family socioeconomic status. Similarly for DRD2, evidence suggests the A1 allele increases sensitivity to maternal sensitivity (Mills-Koonce et al 2007;Propper et al 2008) and birth weight (Keltikangas-Jarvinen et al 2007) when predicting child behavior, physiological reaction to maternal separation, and educational attainment.…”

“…Consistent with the idea that these alleles all similarly increase sensitivity to context but that individual effects may be too weak to detect without huge samples, it is becoming increasingly common to create a polygenic or additive index of sensitive alleles (Mitchell et al 2014;Pearson-Fuhrhop et al 2013;Stice et al 2012). Belsky and Beaver (2011), for example, create a cumulative index of the five alleles discussed above and find that the index increases sensitivity to parenting.…”

Er en belastet barndom knyttet til kortere telomerer?

“…Studiene var hovedsakelig tverrsnittstudier med retrospektiv angivelse av hendelser i barndommen. Belastning i barndommen ble registrert longitudinelt i fire studier (16,17,19,26), og i en av disse målte man også telomerlengde over tid (17). I to studier ble det ikke funnet noen sammenheng mellom barndomserfaringer og telomerlengde (20,26), hvorav den ene målte belastninger longitudinelt i en fødsels-kohort (26).…”