Elucidating Mechanisms of Familial Transmission for Chronic Pain: Results from a Nuclear Twin Family Study

• In Event: Poster Session 04
  In Poster Session: PS 04 Topic - Biological Processes: Neuroscience and Genetics

Abstract

Evidence of the familial aggregation of chronic pain is well-documented, primarily by studies examining intergenerational transmission from parents to their adult offspring (Edwards et al., 1985). However, mounting evidence highlights substantial prevalence rates of chronic pain in pediatric populations (King et al., 2011). More research is needed to elucidate genetic and environmental mechanisms underlying the transmission of chronic pain from parents to their young children in an effort to identify risk factors associated with early onset chronic pain and to disrupt intergenerational cycles of suffering. The current study aimed to determine whether parent and child chronic pain were related in a community-based sample of 9 to 10 year-old twins and their parents and to examine the genetic and environmental mechanisms of familial transmission utilizing the nuclear twin family design (Figure 1). This model is an extension of the classical twin model, which parses the variance in a trait into additive genetic influence (A, the sum of the average effects of individual alleles across the genotype), nonadditive genetic influence (D, the interaction of alleles at the same loci), shared environmental influence (C, environmental factors common to co-twins and contributing to their similarity), and nonshared environmental influence (E, environmental factors specific to one co-twin and contributing to within-pair differences, plus measurement error). Furthermore, the nuclear twin family design can parse shared environmental variance into sibling-specific (S) and familial (F) environmental variance and determine whether familial environmental transmission from parents to offspring significantly accounts for the intergenerational resemblance on a trait above and beyond the influence of shared genetics.

Participants were drawn from an ongoing longitudinal twin study based in the southwestern United States (N=351 twin pairs (Mage = 9.72 years, SD = .87; 52% female; 31% identical, 34% same-sex fraternal, 35% opposite-sex fraternal; 56% White, 22% Latinx, 22% Other). Chronic multisite pain was defined as number of body locations with pain once a month or more for at least 3 months. Parents reported on their own and their children’s chronic pain. Child pain was significantly related to maternal (r = .25, p < .001) but not paternal pain (r = .034, ns). Model fitting results for a series of nested nuclear twin family models of chronic pain are presented in Table 1. The best fitting reduced model was the ASE model. Final ASE model estimates indicated that additive genetic influences on chronic pain were moderate in magnitude (A = .29). Sibling-specific shared environmental influences were moderate (S = .54) and nonshared environmental influences were modest (E = .17). Lastly, results suggest that the etiology of chronic pain is not substantially influenced by assortative mating (μ = -.02). Overall, genetics was the primary mechanism for parent-offspring chronic pain transmission.

In sum, very little is known regarding the etiology of pediatric chronic pain and the mechanisms that contribute to its emergence across generations. Results from the current study provide novel insight into an area of research that may inform treatment of early-onset chronic pain conditions, disrupt intergenerational cycles, and ultimately mitigate personal suffering.

Authors

• Veronica Oro, University of Oregon
  Presenting Author

• Mary Davis, Arizona State University
  Non-Presenting Author

• Kathryn Lemery-Chalfant, Arizona State University
  Non-Presenting Author